trpc5  (Alomone Labs)


Bioz Verified Symbol Alomone Labs is a verified supplier
Bioz Manufacturer Symbol Alomone Labs manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 94

    Structured Review

    Alomone Labs trpc5
    Effect of candesartan or telmisartan but not amlodipine on TRPC expression in mesenteric arterioles. Long-term administration of angiotensin AT1 receptor antagonist telmisartan or candesartan, but not of calcium channel blocker amlodipine reduces TRPC1, TRPC3 and <t>TRPC5</t> channel protein expression in vivo. The angiotensin AT1 receptor antagonist telmisartan (5 mg/kg per day) or candesartan (4 mg/kg per day), calcium channel blocker amlodipine (10 mg/kg per day), or placebo were administered to SHR by gavage for 16 weeks. Representative immunoblottings of TRPC channel protein expressions in mesenteric arterioles from treated SHR (Fig. 7A) and summary data are shown (Fig. 7B). * P
    Trpc5, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 30 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/trpc5/product/Alomone Labs
    Average 94 stars, based on 30 article reviews
    Price from $9.99 to $1999.99
    trpc5 - by Bioz Stars, 2022-08
    94/100 stars

    Images

    1) Product Images from "Increased rhythmicity in hypertensive arterial smooth muscle is linked to transient receptor potential canonical channels"

    Article Title: Increased rhythmicity in hypertensive arterial smooth muscle is linked to transient receptor potential canonical channels

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/j.1582-4934.2009.00890.x

    Effect of candesartan or telmisartan but not amlodipine on TRPC expression in mesenteric arterioles. Long-term administration of angiotensin AT1 receptor antagonist telmisartan or candesartan, but not of calcium channel blocker amlodipine reduces TRPC1, TRPC3 and TRPC5 channel protein expression in vivo. The angiotensin AT1 receptor antagonist telmisartan (5 mg/kg per day) or candesartan (4 mg/kg per day), calcium channel blocker amlodipine (10 mg/kg per day), or placebo were administered to SHR by gavage for 16 weeks. Representative immunoblottings of TRPC channel protein expressions in mesenteric arterioles from treated SHR (Fig. 7A) and summary data are shown (Fig. 7B). * P
    Figure Legend Snippet: Effect of candesartan or telmisartan but not amlodipine on TRPC expression in mesenteric arterioles. Long-term administration of angiotensin AT1 receptor antagonist telmisartan or candesartan, but not of calcium channel blocker amlodipine reduces TRPC1, TRPC3 and TRPC5 channel protein expression in vivo. The angiotensin AT1 receptor antagonist telmisartan (5 mg/kg per day) or candesartan (4 mg/kg per day), calcium channel blocker amlodipine (10 mg/kg per day), or placebo were administered to SHR by gavage for 16 weeks. Representative immunoblottings of TRPC channel protein expressions in mesenteric arterioles from treated SHR (Fig. 7A) and summary data are shown (Fig. 7B). * P

    Techniques Used: Expressing, In Vivo

    Inhibition of norepinephrine-induced vasomotion in mesenteric arterioles from SHR by specific anti-TRPC antibodies Representative tracings of norepinephrine-induced vasomotion in mesenteric arterioles from SHR under control conditions (A), in the presence of anti-TRPC1 antibodies (B), anti-TRPC3 antibodies (C), anti-TRPC3 antibodies with antigenic peptide (D), anti-TRPC5 antibodies (E), anti-TRPC1 plus anti-TRPC3 antibodies (F) or in the presence of anti-β-actin antibodies (G). Representative tracings of norepinephrine-induced vasomotion in mesenteric arterioles from SHR under control conditions after short-term exposure to hypotonic 0.45% NaCl without antibody (H), or after short-term exposure to hypotonic 0.45% NaCl plus TRPC3 antibody (I). Summary data (J) show that inhibition of TRPC channels by specific anti-TRPC antibodies significantly attenuates norepinephrine-induced vasomotion in SHR. Data are mean ± S.E.M. of n = 6 independent experiments. * P
    Figure Legend Snippet: Inhibition of norepinephrine-induced vasomotion in mesenteric arterioles from SHR by specific anti-TRPC antibodies Representative tracings of norepinephrine-induced vasomotion in mesenteric arterioles from SHR under control conditions (A), in the presence of anti-TRPC1 antibodies (B), anti-TRPC3 antibodies (C), anti-TRPC3 antibodies with antigenic peptide (D), anti-TRPC5 antibodies (E), anti-TRPC1 plus anti-TRPC3 antibodies (F) or in the presence of anti-β-actin antibodies (G). Representative tracings of norepinephrine-induced vasomotion in mesenteric arterioles from SHR under control conditions after short-term exposure to hypotonic 0.45% NaCl without antibody (H), or after short-term exposure to hypotonic 0.45% NaCl plus TRPC3 antibody (I). Summary data (J) show that inhibition of TRPC channels by specific anti-TRPC antibodies significantly attenuates norepinephrine-induced vasomotion in SHR. Data are mean ± S.E.M. of n = 6 independent experiments. * P

    Techniques Used: Inhibition

    Expression of TRPC1, TRPC3 and TRPC5 channels in mesenteric arterioles from SHR. Representative immunoblottings (A) and summary data (B) of TRPC1, TRPC3, TRPC4, TRPC5,TRPC6 channels and TRPC3 antibody with its respective antigenic peptide the protein expression in mesenteric arterioles from WKY (open bars) and SHR (filled bars). Data are mean ± S.E.M. of n = 4 independent experiments. * P
    Figure Legend Snippet: Expression of TRPC1, TRPC3 and TRPC5 channels in mesenteric arterioles from SHR. Representative immunoblottings (A) and summary data (B) of TRPC1, TRPC3, TRPC4, TRPC5,TRPC6 channels and TRPC3 antibody with its respective antigenic peptide the protein expression in mesenteric arterioles from WKY (open bars) and SHR (filled bars). Data are mean ± S.E.M. of n = 4 independent experiments. * P

    Techniques Used: Expressing

    Inhibition of norepinephrine-induced calcium increase in mesenteric arterioles from SHR by specific anti-TRPC antibodies. Representative tracings of norepinephrine-induced calcium increase in mesenteric arterioles from SHR under control conditions and in the presence of anti-TRPC1 antibodies (A), anti-TRPC3 antibodies (B), anti-TRPC5 antibodies (C), anti-TRPC1 plus anti-TRPC3 plus anti-TRPC5 antibodies (D), anti-TRPC3 antibodies plus TRPC3 antigenic peptide (E) or anti-β-actin antibodies (F). Summary data (G) shows the effects of specific anti-TRPC antibodies on norepinephrine-induced calcium influx in mesenteric arterioles from SHR. Data are mean ± S.E.M. of n = 8 independent experiments. * P
    Figure Legend Snippet: Inhibition of norepinephrine-induced calcium increase in mesenteric arterioles from SHR by specific anti-TRPC antibodies. Representative tracings of norepinephrine-induced calcium increase in mesenteric arterioles from SHR under control conditions and in the presence of anti-TRPC1 antibodies (A), anti-TRPC3 antibodies (B), anti-TRPC5 antibodies (C), anti-TRPC1 plus anti-TRPC3 plus anti-TRPC5 antibodies (D), anti-TRPC3 antibodies plus TRPC3 antigenic peptide (E) or anti-β-actin antibodies (F). Summary data (G) shows the effects of specific anti-TRPC antibodies on norepinephrine-induced calcium influx in mesenteric arterioles from SHR. Data are mean ± S.E.M. of n = 8 independent experiments. * P

    Techniques Used: Inhibition

    2) Product Images from "Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion"

    Article Title: Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2018.00813

    Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.
    Figure Legend Snippet: Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.

    Techniques Used:

    Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p
    Figure Legend Snippet: Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p

    Techniques Used: Expressing, Western Blot

    Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p
    Figure Legend Snippet: Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p

    Techniques Used: Inhibition, Activation Assay, Western Blot, Expressing, AST Assay, Transfection

    I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (
    Figure Legend Snippet: I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (

    Techniques Used: Proximity Ligation Assay, Incubation

    3) Product Images from "TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line"

    Article Title: TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line

    Journal:

    doi:

    TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following
    Figure Legend Snippet: TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following

    Techniques Used:

    Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP
    Figure Legend Snippet: Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP

    Techniques Used: Transfection

    Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were
    Figure Legend Snippet: Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were

    Techniques Used: Over Expression, Transfection

    4) Product Images from "TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line"

    Article Title: TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line

    Journal:

    doi:

    TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following
    Figure Legend Snippet: TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following

    Techniques Used:

    Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP
    Figure Legend Snippet: Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP

    Techniques Used: Transfection

    Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were
    Figure Legend Snippet: Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were

    Techniques Used: Over Expression, Transfection

    5) Product Images from "Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion"

    Article Title: Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2018.00813

    Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.
    Figure Legend Snippet: Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.

    Techniques Used:

    Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p
    Figure Legend Snippet: Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p

    Techniques Used: Expressing, Western Blot

    Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p
    Figure Legend Snippet: Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p

    Techniques Used: Inhibition, Activation Assay, Western Blot, Expressing, AST Assay, Transfection

    I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (
    Figure Legend Snippet: I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (

    Techniques Used: Proximity Ligation Assay, Incubation

    6) Product Images from "TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line"

    Article Title: TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line

    Journal:

    doi:

    TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following
    Figure Legend Snippet: TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following

    Techniques Used:

    Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP
    Figure Legend Snippet: Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP

    Techniques Used: Transfection

    Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were
    Figure Legend Snippet: Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were

    Techniques Used: Over Expression, Transfection

    7) Product Images from "TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line"

    Article Title: TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line

    Journal:

    doi:

    TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following
    Figure Legend Snippet: TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following

    Techniques Used:

    Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP
    Figure Legend Snippet: Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP

    Techniques Used: Transfection

    Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were
    Figure Legend Snippet: Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were

    Techniques Used: Over Expression, Transfection

    8) Product Images from "Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion"

    Article Title: Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2018.00813

    Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.
    Figure Legend Snippet: Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.

    Techniques Used:

    Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p
    Figure Legend Snippet: Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p

    Techniques Used: Expressing, Western Blot

    Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p
    Figure Legend Snippet: Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p

    Techniques Used: Inhibition, Activation Assay, Western Blot, Expressing, AST Assay, Transfection

    I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (
    Figure Legend Snippet: I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (

    Techniques Used: Proximity Ligation Assay, Incubation

    9) Product Images from "Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion"

    Article Title: Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2018.00813

    Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.
    Figure Legend Snippet: Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.

    Techniques Used:

    Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p
    Figure Legend Snippet: Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p

    Techniques Used: Expressing, Western Blot

    Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p
    Figure Legend Snippet: Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p

    Techniques Used: Inhibition, Activation Assay, Western Blot, Expressing, AST Assay, Transfection

    I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (
    Figure Legend Snippet: I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (

    Techniques Used: Proximity Ligation Assay, Incubation

    10) Product Images from "Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion"

    Article Title: Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2018.00813

    Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.
    Figure Legend Snippet: Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.

    Techniques Used:

    Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p
    Figure Legend Snippet: Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p

    Techniques Used: Expressing, Western Blot

    Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p
    Figure Legend Snippet: Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p

    Techniques Used: Inhibition, Activation Assay, Western Blot, Expressing, AST Assay, Transfection

    I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (
    Figure Legend Snippet: I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (

    Techniques Used: Proximity Ligation Assay, Incubation

    11) Product Images from "TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line"

    Article Title: TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line

    Journal:

    doi:

    TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following
    Figure Legend Snippet: TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following

    Techniques Used:

    Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP
    Figure Legend Snippet: Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP

    Techniques Used: Transfection

    Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were
    Figure Legend Snippet: Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were

    Techniques Used: Over Expression, Transfection

    12) Product Images from "TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line"

    Article Title: TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line

    Journal:

    doi:

    TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following
    Figure Legend Snippet: TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following

    Techniques Used:

    Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP
    Figure Legend Snippet: Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP

    Techniques Used: Transfection

    Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were
    Figure Legend Snippet: Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were

    Techniques Used: Over Expression, Transfection

    13) Product Images from "TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line"

    Article Title: TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line

    Journal:

    doi:

    TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following
    Figure Legend Snippet: TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following

    Techniques Used:

    Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP
    Figure Legend Snippet: Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP

    Techniques Used: Transfection

    Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were
    Figure Legend Snippet: Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were

    Techniques Used: Over Expression, Transfection

    14) Product Images from "Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion"

    Article Title: Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2018.00813

    Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.
    Figure Legend Snippet: Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.

    Techniques Used:

    Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p
    Figure Legend Snippet: Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p

    Techniques Used: Expressing, Western Blot

    Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p
    Figure Legend Snippet: Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p

    Techniques Used: Inhibition, Activation Assay, Western Blot, Expressing, AST Assay, Transfection

    I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (
    Figure Legend Snippet: I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (

    Techniques Used: Proximity Ligation Assay, Incubation

    15) Product Images from "TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line"

    Article Title: TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line

    Journal:

    doi:

    TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following
    Figure Legend Snippet: TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following

    Techniques Used:

    Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP
    Figure Legend Snippet: Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP

    Techniques Used: Transfection

    Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were
    Figure Legend Snippet: Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were

    Techniques Used: Over Expression, Transfection

    16) Product Images from "Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion"

    Article Title: Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2018.00813

    Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.
    Figure Legend Snippet: Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.

    Techniques Used:

    Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p
    Figure Legend Snippet: Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p

    Techniques Used: Expressing, Western Blot

    Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p
    Figure Legend Snippet: Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p

    Techniques Used: Inhibition, Activation Assay, Western Blot, Expressing, AST Assay, Transfection

    I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (
    Figure Legend Snippet: I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (

    Techniques Used: Proximity Ligation Assay, Incubation

    17) Product Images from "Genetic Deletion of KLHL1 Leads to Hyperexcitability in Hypothalamic POMC Neurons and Lack of Electrical Responses to Leptin"

    Article Title: Genetic Deletion of KLHL1 Leads to Hyperexcitability in Hypothalamic POMC Neurons and Lack of Electrical Responses to Leptin

    Journal: Frontiers in Neuroscience

    doi: 10.3389/fnins.2021.718464

    Overexpression of Ca V 3.1 T-type calcium channels in KLHL1-KO mice hypothalamus. (A) Pleiotropic signaling of leptin in POMC hypothalamic neurons. Leptin binding to its receptor LRb results in the downstream activation of JAK2. STAT3 is subsequently phosphorylated and mobilized to the nucleus resulting in de novo gene expression. Activation of insulin receptor substrate (IRS) stimulates Akt- and mTOR pathways via activation of phosphorylated PI3K and the production of PIP3. The activation of PLCλ1 by PIP3 mediates the activation of TRPC1/5 channels, recruiting T-type CaV3.1/2 channels thought membrane depolarization. (B) Western blot analysis from hypothalamic extracts assessing TRPC1, TRPC5, Ca V 3.2 and Ca V 3.1 channel levels; Ca V 3.1 protein levels are doubled in KLHL1-KO hypothalamus. Bars show densitometric quantification normalized to GAPDH. Data represent means ± S.E.M (TRPC1, n = 3 each; TRPC5, n = 4 each; Ca V 3.2, n = 5 each; Ca V 3.1, n = 5 each). * P
    Figure Legend Snippet: Overexpression of Ca V 3.1 T-type calcium channels in KLHL1-KO mice hypothalamus. (A) Pleiotropic signaling of leptin in POMC hypothalamic neurons. Leptin binding to its receptor LRb results in the downstream activation of JAK2. STAT3 is subsequently phosphorylated and mobilized to the nucleus resulting in de novo gene expression. Activation of insulin receptor substrate (IRS) stimulates Akt- and mTOR pathways via activation of phosphorylated PI3K and the production of PIP3. The activation of PLCλ1 by PIP3 mediates the activation of TRPC1/5 channels, recruiting T-type CaV3.1/2 channels thought membrane depolarization. (B) Western blot analysis from hypothalamic extracts assessing TRPC1, TRPC5, Ca V 3.2 and Ca V 3.1 channel levels; Ca V 3.1 protein levels are doubled in KLHL1-KO hypothalamus. Bars show densitometric quantification normalized to GAPDH. Data represent means ± S.E.M (TRPC1, n = 3 each; TRPC5, n = 4 each; Ca V 3.2, n = 5 each; Ca V 3.1, n = 5 each). * P

    Techniques Used: Over Expression, Mouse Assay, Binding Assay, Activation Assay, Expressing, Western Blot

    18) Product Images from "TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line"

    Article Title: TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line

    Journal:

    doi:

    TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following
    Figure Legend Snippet: TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following

    Techniques Used:

    Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP
    Figure Legend Snippet: Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP

    Techniques Used: Transfection

    Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were
    Figure Legend Snippet: Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were

    Techniques Used: Over Expression, Transfection

    19) Product Images from "Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion"

    Article Title: Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2018.00813

    Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.
    Figure Legend Snippet: Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.

    Techniques Used:

    Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p
    Figure Legend Snippet: Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p

    Techniques Used: Expressing, Western Blot

    Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p
    Figure Legend Snippet: Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p

    Techniques Used: Inhibition, Activation Assay, Western Blot, Expressing, AST Assay, Transfection

    I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (
    Figure Legend Snippet: I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (

    Techniques Used: Proximity Ligation Assay, Incubation

    20) Product Images from "Rat Hypocretin/Orexin Neurons Are Maintained in a Depolarized State by TRPC Channels"

    Article Title: Rat Hypocretin/Orexin Neurons Are Maintained in a Depolarized State by TRPC Channels

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0015673

    The TRPC5 antibody occludes the effect of FFA in hcrt/orx neurons. (A) Transient (2 min) bath-application of 100 µM flufenamic acid (FFA), a non specific blocker of cationic currents, produces a strong membrane hyperpolarization and cessation of firing; inset: in voltage-clamp this hyperpolarization corresponds to an outward current. (B) Voltage-clamp ramps in absence (Ctrl) and presence (FFA) of flufenamic acid. The subtraction of voltage-clamp ramps shown in the inset suggests the presence of a voltage-dependent cationic current. (C–D) In hcrt/orx neurons loaded with a TRPC5 antibody, bath-application of FFA had only a small additional effect either in current-clamp (C) or in voltage-clamp (D).
    Figure Legend Snippet: The TRPC5 antibody occludes the effect of FFA in hcrt/orx neurons. (A) Transient (2 min) bath-application of 100 µM flufenamic acid (FFA), a non specific blocker of cationic currents, produces a strong membrane hyperpolarization and cessation of firing; inset: in voltage-clamp this hyperpolarization corresponds to an outward current. (B) Voltage-clamp ramps in absence (Ctrl) and presence (FFA) of flufenamic acid. The subtraction of voltage-clamp ramps shown in the inset suggests the presence of a voltage-dependent cationic current. (C–D) In hcrt/orx neurons loaded with a TRPC5 antibody, bath-application of FFA had only a small additional effect either in current-clamp (C) or in voltage-clamp (D).

    Techniques Used:

    Dual immunohistochemical staining for TRPC5 and hcrt/orx. (A–B) Photomicrographs from a dual-immunostained section combining an hcrt/orx antibody from Santa Cruz (A) and a TRPC5 antibody from Alomone Labs (B). Examples of double labelled hcrt/orx-TRPC5 cells are indicated by white arrowheads and one such cell by a double circle (enlarged in the corresponding small panels to the right). Some hcrt/orx cells do not express TRPC5, as shown by an example indicated with a single circle. It is noteworthy that many hcrt/orx-negative cells also expressed TRPC5, as shown by an example indicated with a downward arrow (in panels A and B). (C–D) Same as in A and B with an hcrt/orx antibody from Phoenix Pharmaceuticals (C) and a TRPC5 antibody from NeuroMab (D). (Scale bars: 20 µm).
    Figure Legend Snippet: Dual immunohistochemical staining for TRPC5 and hcrt/orx. (A–B) Photomicrographs from a dual-immunostained section combining an hcrt/orx antibody from Santa Cruz (A) and a TRPC5 antibody from Alomone Labs (B). Examples of double labelled hcrt/orx-TRPC5 cells are indicated by white arrowheads and one such cell by a double circle (enlarged in the corresponding small panels to the right). Some hcrt/orx cells do not express TRPC5, as shown by an example indicated with a single circle. It is noteworthy that many hcrt/orx-negative cells also expressed TRPC5, as shown by an example indicated with a downward arrow (in panels A and B). (C–D) Same as in A and B with an hcrt/orx antibody from Phoenix Pharmaceuticals (C) and a TRPC5 antibody from NeuroMab (D). (Scale bars: 20 µm).

    Techniques Used: Immunohistochemistry, Staining

    The depolarized state of hcrt/orx neurons is blocked by a TRPC5 antibody. (A–C) In voltage-clamp configuration, intracellular application of either a TRPC1 (A) or a TRPC3 (B) or a TRPC4 (C) antibody (AbTRPC1, AbTRPC3 and AbTRPC4 respectively, all from Alomone Labs) has no effect on the current needed to clamp the cell at −50 mV. (D–E) Intracellular application of a TRPC5 antibody (Alomone Labs), in contrast, induces an outward current (D) that is blocked by co-application of a TRPC5 antigen (E). (F–G) In current-clamp configuration, intracellular application of a TRPC5 antibody alone (from either Alomone Labs (F) or NeuroMab (inset in F) induces an important membrane hyperpolarization and cessation of firing. In contrast, intracellular co-application of the TRPC5 antibody (Alomone Labs) together with its appropriate antigen (AgTRPC5) has no effect (G, to compare with F). (H) Voltage-clamp ramps in absence (Ctrl) and presence of a TRPC5 antibody (AbTRPC5, Alomone Labs). In the inset, subtraction of voltage-clamp ramps (Ctrl - AbTRPC5) suggests the presence of a voltage-dependent TRPC5 current.
    Figure Legend Snippet: The depolarized state of hcrt/orx neurons is blocked by a TRPC5 antibody. (A–C) In voltage-clamp configuration, intracellular application of either a TRPC1 (A) or a TRPC3 (B) or a TRPC4 (C) antibody (AbTRPC1, AbTRPC3 and AbTRPC4 respectively, all from Alomone Labs) has no effect on the current needed to clamp the cell at −50 mV. (D–E) Intracellular application of a TRPC5 antibody (Alomone Labs), in contrast, induces an outward current (D) that is blocked by co-application of a TRPC5 antigen (E). (F–G) In current-clamp configuration, intracellular application of a TRPC5 antibody alone (from either Alomone Labs (F) or NeuroMab (inset in F) induces an important membrane hyperpolarization and cessation of firing. In contrast, intracellular co-application of the TRPC5 antibody (Alomone Labs) together with its appropriate antigen (AgTRPC5) has no effect (G, to compare with F). (H) Voltage-clamp ramps in absence (Ctrl) and presence of a TRPC5 antibody (AbTRPC5, Alomone Labs). In the inset, subtraction of voltage-clamp ramps (Ctrl - AbTRPC5) suggests the presence of a voltage-dependent TRPC5 current.

    Techniques Used:

    21) Product Images from "Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion"

    Article Title: Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2018.00813

    Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.
    Figure Legend Snippet: Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.

    Techniques Used:

    Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p
    Figure Legend Snippet: Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p

    Techniques Used: Expressing, Western Blot

    Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p
    Figure Legend Snippet: Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p

    Techniques Used: Inhibition, Activation Assay, Western Blot, Expressing, AST Assay, Transfection

    I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (
    Figure Legend Snippet: I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (

    Techniques Used: Proximity Ligation Assay, Incubation

    22) Product Images from "TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line"

    Article Title: TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line

    Journal:

    doi:

    TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following
    Figure Legend Snippet: TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following

    Techniques Used:

    Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP
    Figure Legend Snippet: Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP

    Techniques Used: Transfection

    Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were
    Figure Legend Snippet: Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were

    Techniques Used: Over Expression, Transfection

    23) Product Images from "Rat Hypocretin/Orexin Neurons Are Maintained in a Depolarized State by TRPC Channels"

    Article Title: Rat Hypocretin/Orexin Neurons Are Maintained in a Depolarized State by TRPC Channels

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0015673

    The TRPC5 antibody occludes the effect of FFA in hcrt/orx neurons. (A) Transient (2 min) bath-application of 100 µM flufenamic acid (FFA), a non specific blocker of cationic currents, produces a strong membrane hyperpolarization and cessation of firing; inset: in voltage-clamp this hyperpolarization corresponds to an outward current. (B) Voltage-clamp ramps in absence (Ctrl) and presence (FFA) of flufenamic acid. The subtraction of voltage-clamp ramps shown in the inset suggests the presence of a voltage-dependent cationic current. (C–D) In hcrt/orx neurons loaded with a TRPC5 antibody, bath-application of FFA had only a small additional effect either in current-clamp (C) or in voltage-clamp (D).
    Figure Legend Snippet: The TRPC5 antibody occludes the effect of FFA in hcrt/orx neurons. (A) Transient (2 min) bath-application of 100 µM flufenamic acid (FFA), a non specific blocker of cationic currents, produces a strong membrane hyperpolarization and cessation of firing; inset: in voltage-clamp this hyperpolarization corresponds to an outward current. (B) Voltage-clamp ramps in absence (Ctrl) and presence (FFA) of flufenamic acid. The subtraction of voltage-clamp ramps shown in the inset suggests the presence of a voltage-dependent cationic current. (C–D) In hcrt/orx neurons loaded with a TRPC5 antibody, bath-application of FFA had only a small additional effect either in current-clamp (C) or in voltage-clamp (D).

    Techniques Used:

    Dual immunohistochemical staining for TRPC5 and hcrt/orx. (A–B) Photomicrographs from a dual-immunostained section combining an hcrt/orx antibody from Santa Cruz (A) and a TRPC5 antibody from Alomone Labs (B). Examples of double labelled hcrt/orx-TRPC5 cells are indicated by white arrowheads and one such cell by a double circle (enlarged in the corresponding small panels to the right). Some hcrt/orx cells do not express TRPC5, as shown by an example indicated with a single circle. It is noteworthy that many hcrt/orx-negative cells also expressed TRPC5, as shown by an example indicated with a downward arrow (in panels A and B). (C–D) Same as in A and B with an hcrt/orx antibody from Phoenix Pharmaceuticals (C) and a TRPC5 antibody from NeuroMab (D). (Scale bars: 20 µm).
    Figure Legend Snippet: Dual immunohistochemical staining for TRPC5 and hcrt/orx. (A–B) Photomicrographs from a dual-immunostained section combining an hcrt/orx antibody from Santa Cruz (A) and a TRPC5 antibody from Alomone Labs (B). Examples of double labelled hcrt/orx-TRPC5 cells are indicated by white arrowheads and one such cell by a double circle (enlarged in the corresponding small panels to the right). Some hcrt/orx cells do not express TRPC5, as shown by an example indicated with a single circle. It is noteworthy that many hcrt/orx-negative cells also expressed TRPC5, as shown by an example indicated with a downward arrow (in panels A and B). (C–D) Same as in A and B with an hcrt/orx antibody from Phoenix Pharmaceuticals (C) and a TRPC5 antibody from NeuroMab (D). (Scale bars: 20 µm).

    Techniques Used: Immunohistochemistry, Staining

    The depolarized state of hcrt/orx neurons is blocked by a TRPC5 antibody. (A–C) In voltage-clamp configuration, intracellular application of either a TRPC1 (A) or a TRPC3 (B) or a TRPC4 (C) antibody (AbTRPC1, AbTRPC3 and AbTRPC4 respectively, all from Alomone Labs) has no effect on the current needed to clamp the cell at −50 mV. (D–E) Intracellular application of a TRPC5 antibody (Alomone Labs), in contrast, induces an outward current (D) that is blocked by co-application of a TRPC5 antigen (E). (F–G) In current-clamp configuration, intracellular application of a TRPC5 antibody alone (from either Alomone Labs (F) or NeuroMab (inset in F) induces an important membrane hyperpolarization and cessation of firing. In contrast, intracellular co-application of the TRPC5 antibody (Alomone Labs) together with its appropriate antigen (AgTRPC5) has no effect (G, to compare with F). (H) Voltage-clamp ramps in absence (Ctrl) and presence of a TRPC5 antibody (AbTRPC5, Alomone Labs). In the inset, subtraction of voltage-clamp ramps (Ctrl - AbTRPC5) suggests the presence of a voltage-dependent TRPC5 current.
    Figure Legend Snippet: The depolarized state of hcrt/orx neurons is blocked by a TRPC5 antibody. (A–C) In voltage-clamp configuration, intracellular application of either a TRPC1 (A) or a TRPC3 (B) or a TRPC4 (C) antibody (AbTRPC1, AbTRPC3 and AbTRPC4 respectively, all from Alomone Labs) has no effect on the current needed to clamp the cell at −50 mV. (D–E) Intracellular application of a TRPC5 antibody (Alomone Labs), in contrast, induces an outward current (D) that is blocked by co-application of a TRPC5 antigen (E). (F–G) In current-clamp configuration, intracellular application of a TRPC5 antibody alone (from either Alomone Labs (F) or NeuroMab (inset in F) induces an important membrane hyperpolarization and cessation of firing. In contrast, intracellular co-application of the TRPC5 antibody (Alomone Labs) together with its appropriate antigen (AgTRPC5) has no effect (G, to compare with F). (H) Voltage-clamp ramps in absence (Ctrl) and presence of a TRPC5 antibody (AbTRPC5, Alomone Labs). In the inset, subtraction of voltage-clamp ramps (Ctrl - AbTRPC5) suggests the presence of a voltage-dependent TRPC5 current.

    Techniques Used:

    24) Product Images from "Rat Hypocretin/Orexin Neurons Are Maintained in a Depolarized State by TRPC Channels"

    Article Title: Rat Hypocretin/Orexin Neurons Are Maintained in a Depolarized State by TRPC Channels

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0015673

    The TRPC5 antibody occludes the effect of FFA in hcrt/orx neurons. (A) Transient (2 min) bath-application of 100 µM flufenamic acid (FFA), a non specific blocker of cationic currents, produces a strong membrane hyperpolarization and cessation of firing; inset: in voltage-clamp this hyperpolarization corresponds to an outward current. (B) Voltage-clamp ramps in absence (Ctrl) and presence (FFA) of flufenamic acid. The subtraction of voltage-clamp ramps shown in the inset suggests the presence of a voltage-dependent cationic current. (C–D) In hcrt/orx neurons loaded with a TRPC5 antibody, bath-application of FFA had only a small additional effect either in current-clamp (C) or in voltage-clamp (D).
    Figure Legend Snippet: The TRPC5 antibody occludes the effect of FFA in hcrt/orx neurons. (A) Transient (2 min) bath-application of 100 µM flufenamic acid (FFA), a non specific blocker of cationic currents, produces a strong membrane hyperpolarization and cessation of firing; inset: in voltage-clamp this hyperpolarization corresponds to an outward current. (B) Voltage-clamp ramps in absence (Ctrl) and presence (FFA) of flufenamic acid. The subtraction of voltage-clamp ramps shown in the inset suggests the presence of a voltage-dependent cationic current. (C–D) In hcrt/orx neurons loaded with a TRPC5 antibody, bath-application of FFA had only a small additional effect either in current-clamp (C) or in voltage-clamp (D).

    Techniques Used:

    Dual immunohistochemical staining for TRPC5 and hcrt/orx. (A–B) Photomicrographs from a dual-immunostained section combining an hcrt/orx antibody from Santa Cruz (A) and a TRPC5 antibody from Alomone Labs (B). Examples of double labelled hcrt/orx-TRPC5 cells are indicated by white arrowheads and one such cell by a double circle (enlarged in the corresponding small panels to the right). Some hcrt/orx cells do not express TRPC5, as shown by an example indicated with a single circle. It is noteworthy that many hcrt/orx-negative cells also expressed TRPC5, as shown by an example indicated with a downward arrow (in panels A and B). (C–D) Same as in A and B with an hcrt/orx antibody from Phoenix Pharmaceuticals (C) and a TRPC5 antibody from NeuroMab (D). (Scale bars: 20 µm).
    Figure Legend Snippet: Dual immunohistochemical staining for TRPC5 and hcrt/orx. (A–B) Photomicrographs from a dual-immunostained section combining an hcrt/orx antibody from Santa Cruz (A) and a TRPC5 antibody from Alomone Labs (B). Examples of double labelled hcrt/orx-TRPC5 cells are indicated by white arrowheads and one such cell by a double circle (enlarged in the corresponding small panels to the right). Some hcrt/orx cells do not express TRPC5, as shown by an example indicated with a single circle. It is noteworthy that many hcrt/orx-negative cells also expressed TRPC5, as shown by an example indicated with a downward arrow (in panels A and B). (C–D) Same as in A and B with an hcrt/orx antibody from Phoenix Pharmaceuticals (C) and a TRPC5 antibody from NeuroMab (D). (Scale bars: 20 µm).

    Techniques Used: Immunohistochemistry, Staining

    The depolarized state of hcrt/orx neurons is blocked by a TRPC5 antibody. (A–C) In voltage-clamp configuration, intracellular application of either a TRPC1 (A) or a TRPC3 (B) or a TRPC4 (C) antibody (AbTRPC1, AbTRPC3 and AbTRPC4 respectively, all from Alomone Labs) has no effect on the current needed to clamp the cell at −50 mV. (D–E) Intracellular application of a TRPC5 antibody (Alomone Labs), in contrast, induces an outward current (D) that is blocked by co-application of a TRPC5 antigen (E). (F–G) In current-clamp configuration, intracellular application of a TRPC5 antibody alone (from either Alomone Labs (F) or NeuroMab (inset in F) induces an important membrane hyperpolarization and cessation of firing. In contrast, intracellular co-application of the TRPC5 antibody (Alomone Labs) together with its appropriate antigen (AgTRPC5) has no effect (G, to compare with F). (H) Voltage-clamp ramps in absence (Ctrl) and presence of a TRPC5 antibody (AbTRPC5, Alomone Labs). In the inset, subtraction of voltage-clamp ramps (Ctrl - AbTRPC5) suggests the presence of a voltage-dependent TRPC5 current.
    Figure Legend Snippet: The depolarized state of hcrt/orx neurons is blocked by a TRPC5 antibody. (A–C) In voltage-clamp configuration, intracellular application of either a TRPC1 (A) or a TRPC3 (B) or a TRPC4 (C) antibody (AbTRPC1, AbTRPC3 and AbTRPC4 respectively, all from Alomone Labs) has no effect on the current needed to clamp the cell at −50 mV. (D–E) Intracellular application of a TRPC5 antibody (Alomone Labs), in contrast, induces an outward current (D) that is blocked by co-application of a TRPC5 antigen (E). (F–G) In current-clamp configuration, intracellular application of a TRPC5 antibody alone (from either Alomone Labs (F) or NeuroMab (inset in F) induces an important membrane hyperpolarization and cessation of firing. In contrast, intracellular co-application of the TRPC5 antibody (Alomone Labs) together with its appropriate antigen (AgTRPC5) has no effect (G, to compare with F). (H) Voltage-clamp ramps in absence (Ctrl) and presence of a TRPC5 antibody (AbTRPC5, Alomone Labs). In the inset, subtraction of voltage-clamp ramps (Ctrl - AbTRPC5) suggests the presence of a voltage-dependent TRPC5 current.

    Techniques Used:

    25) Product Images from "TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line"

    Article Title: TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line

    Journal:

    doi:

    TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following
    Figure Legend Snippet: TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following

    Techniques Used:

    Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP
    Figure Legend Snippet: Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP

    Techniques Used: Transfection

    Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were
    Figure Legend Snippet: Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were

    Techniques Used: Over Expression, Transfection

    26) Product Images from "TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line"

    Article Title: TRPC5/Orai1/STIM1-dependent Store-operated Entry of Ca2+ Is Linked to Degranulation in a Rat Mast Cell Line

    Journal:

    doi:

    TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following
    Figure Legend Snippet: TRPC5, STIM1, and Orai1 are essential for entry of Sr 2+ and Ca 2+ as well as degranulation in Ag-stimulated cells. A-D As in previous figures, changes in intracellular Ca 2+ and Sr 2+ were determined in Fura-2-loaded cells (in Ca 2+ -free medium) following

    Techniques Used:

    Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP
    Figure Legend Snippet: Knock down of TRPCs by shRNAs shows that entry of Sr 2+ and Ca 2+ is dependent on TRPC5. Cells were co-transfected with the indicated inhibitory RNA and YFP 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were made in EYFP

    Techniques Used: Transfection

    Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were
    Figure Legend Snippet: Overexpression of STIM1 and TRPC5 reveal that TRPC5 conveys both Sr 2+ and Ca 2+ . Cells were co-transfected with EYFP and TRPC5 alone or combination with STIM1 as indicated 48 h before measurement of Ca 2+ and Sr 2+ in Fura-2-loaded cells. Measurements were

    Techniques Used: Over Expression, Transfection

    27) Product Images from "Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion"

    Article Title: Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2018.00813

    Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.
    Figure Legend Snippet: Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.

    Techniques Used:

    Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p
    Figure Legend Snippet: Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p

    Techniques Used: Expressing, Western Blot

    Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p
    Figure Legend Snippet: Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p

    Techniques Used: Inhibition, Activation Assay, Western Blot, Expressing, AST Assay, Transfection

    I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (
    Figure Legend Snippet: I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (

    Techniques Used: Proximity Ligation Assay, Incubation

    28) Product Images from "Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion"

    Article Title: Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2018.00813

    Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.
    Figure Legend Snippet: Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.

    Techniques Used:

    Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p
    Figure Legend Snippet: Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p

    Techniques Used: Expressing, Western Blot

    Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p
    Figure Legend Snippet: Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p

    Techniques Used: Inhibition, Activation Assay, Western Blot, Expressing, AST Assay, Transfection

    I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (
    Figure Legend Snippet: I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (

    Techniques Used: Proximity Ligation Assay, Incubation

    29) Product Images from "Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion"

    Article Title: Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2018.00813

    Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.
    Figure Legend Snippet: Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.

    Techniques Used:

    Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p
    Figure Legend Snippet: Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p

    Techniques Used: Expressing, Western Blot

    Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p
    Figure Legend Snippet: Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p

    Techniques Used: Inhibition, Activation Assay, Western Blot, Expressing, AST Assay, Transfection

    I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (
    Figure Legend Snippet: I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (

    Techniques Used: Proximity Ligation Assay, Incubation

    30) Product Images from "Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion"

    Article Title: Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2018.00813

    Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.
    Figure Legend Snippet: Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.

    Techniques Used:

    Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p
    Figure Legend Snippet: Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p

    Techniques Used: Expressing, Western Blot

    Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p
    Figure Legend Snippet: Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p

    Techniques Used: Inhibition, Activation Assay, Western Blot, Expressing, AST Assay, Transfection

    I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (
    Figure Legend Snippet: I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (

    Techniques Used: Proximity Ligation Assay, Incubation

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 94
    Alomone Labs trpc5
    Effect of candesartan or telmisartan but not amlodipine on TRPC expression in mesenteric arterioles. Long-term administration of angiotensin AT1 receptor antagonist telmisartan or candesartan, but not of calcium channel blocker amlodipine reduces TRPC1, TRPC3 and <t>TRPC5</t> channel protein expression in vivo. The angiotensin AT1 receptor antagonist telmisartan (5 mg/kg per day) or candesartan (4 mg/kg per day), calcium channel blocker amlodipine (10 mg/kg per day), or placebo were administered to SHR by gavage for 16 weeks. Representative immunoblottings of TRPC channel protein expressions in mesenteric arterioles from treated SHR (Fig. 7A) and summary data are shown (Fig. 7B). * P
    Trpc5, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/trpc5/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    trpc5 - by Bioz Stars, 2022-08
    94/100 stars
      Buy from Supplier

    Image Search Results


    Effect of candesartan or telmisartan but not amlodipine on TRPC expression in mesenteric arterioles. Long-term administration of angiotensin AT1 receptor antagonist telmisartan or candesartan, but not of calcium channel blocker amlodipine reduces TRPC1, TRPC3 and TRPC5 channel protein expression in vivo. The angiotensin AT1 receptor antagonist telmisartan (5 mg/kg per day) or candesartan (4 mg/kg per day), calcium channel blocker amlodipine (10 mg/kg per day), or placebo were administered to SHR by gavage for 16 weeks. Representative immunoblottings of TRPC channel protein expressions in mesenteric arterioles from treated SHR (Fig. 7A) and summary data are shown (Fig. 7B). * P

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Increased rhythmicity in hypertensive arterial smooth muscle is linked to transient receptor potential canonical channels

    doi: 10.1111/j.1582-4934.2009.00890.x

    Figure Lengend Snippet: Effect of candesartan or telmisartan but not amlodipine on TRPC expression in mesenteric arterioles. Long-term administration of angiotensin AT1 receptor antagonist telmisartan or candesartan, but not of calcium channel blocker amlodipine reduces TRPC1, TRPC3 and TRPC5 channel protein expression in vivo. The angiotensin AT1 receptor antagonist telmisartan (5 mg/kg per day) or candesartan (4 mg/kg per day), calcium channel blocker amlodipine (10 mg/kg per day), or placebo were administered to SHR by gavage for 16 weeks. Representative immunoblottings of TRPC channel protein expressions in mesenteric arterioles from treated SHR (Fig. 7A) and summary data are shown (Fig. 7B). * P

    Article Snippet: The membranes were incubated with primary rabbit antibodies against TRPC1, TRPC3, TRPC4, TRPC5 and TRPC6 (1:200; Alomone Labs), followed by incubation with goat anti-rabbit horseradish peroxidase-conjugated secondary antibody.

    Techniques: Expressing, In Vivo

    Inhibition of norepinephrine-induced vasomotion in mesenteric arterioles from SHR by specific anti-TRPC antibodies Representative tracings of norepinephrine-induced vasomotion in mesenteric arterioles from SHR under control conditions (A), in the presence of anti-TRPC1 antibodies (B), anti-TRPC3 antibodies (C), anti-TRPC3 antibodies with antigenic peptide (D), anti-TRPC5 antibodies (E), anti-TRPC1 plus anti-TRPC3 antibodies (F) or in the presence of anti-β-actin antibodies (G). Representative tracings of norepinephrine-induced vasomotion in mesenteric arterioles from SHR under control conditions after short-term exposure to hypotonic 0.45% NaCl without antibody (H), or after short-term exposure to hypotonic 0.45% NaCl plus TRPC3 antibody (I). Summary data (J) show that inhibition of TRPC channels by specific anti-TRPC antibodies significantly attenuates norepinephrine-induced vasomotion in SHR. Data are mean ± S.E.M. of n = 6 independent experiments. * P

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Increased rhythmicity in hypertensive arterial smooth muscle is linked to transient receptor potential canonical channels

    doi: 10.1111/j.1582-4934.2009.00890.x

    Figure Lengend Snippet: Inhibition of norepinephrine-induced vasomotion in mesenteric arterioles from SHR by specific anti-TRPC antibodies Representative tracings of norepinephrine-induced vasomotion in mesenteric arterioles from SHR under control conditions (A), in the presence of anti-TRPC1 antibodies (B), anti-TRPC3 antibodies (C), anti-TRPC3 antibodies with antigenic peptide (D), anti-TRPC5 antibodies (E), anti-TRPC1 plus anti-TRPC3 antibodies (F) or in the presence of anti-β-actin antibodies (G). Representative tracings of norepinephrine-induced vasomotion in mesenteric arterioles from SHR under control conditions after short-term exposure to hypotonic 0.45% NaCl without antibody (H), or after short-term exposure to hypotonic 0.45% NaCl plus TRPC3 antibody (I). Summary data (J) show that inhibition of TRPC channels by specific anti-TRPC antibodies significantly attenuates norepinephrine-induced vasomotion in SHR. Data are mean ± S.E.M. of n = 6 independent experiments. * P

    Article Snippet: The membranes were incubated with primary rabbit antibodies against TRPC1, TRPC3, TRPC4, TRPC5 and TRPC6 (1:200; Alomone Labs), followed by incubation with goat anti-rabbit horseradish peroxidase-conjugated secondary antibody.

    Techniques: Inhibition

    Expression of TRPC1, TRPC3 and TRPC5 channels in mesenteric arterioles from SHR. Representative immunoblottings (A) and summary data (B) of TRPC1, TRPC3, TRPC4, TRPC5,TRPC6 channels and TRPC3 antibody with its respective antigenic peptide the protein expression in mesenteric arterioles from WKY (open bars) and SHR (filled bars). Data are mean ± S.E.M. of n = 4 independent experiments. * P

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Increased rhythmicity in hypertensive arterial smooth muscle is linked to transient receptor potential canonical channels

    doi: 10.1111/j.1582-4934.2009.00890.x

    Figure Lengend Snippet: Expression of TRPC1, TRPC3 and TRPC5 channels in mesenteric arterioles from SHR. Representative immunoblottings (A) and summary data (B) of TRPC1, TRPC3, TRPC4, TRPC5,TRPC6 channels and TRPC3 antibody with its respective antigenic peptide the protein expression in mesenteric arterioles from WKY (open bars) and SHR (filled bars). Data are mean ± S.E.M. of n = 4 independent experiments. * P

    Article Snippet: The membranes were incubated with primary rabbit antibodies against TRPC1, TRPC3, TRPC4, TRPC5 and TRPC6 (1:200; Alomone Labs), followed by incubation with goat anti-rabbit horseradish peroxidase-conjugated secondary antibody.

    Techniques: Expressing

    Inhibition of norepinephrine-induced calcium increase in mesenteric arterioles from SHR by specific anti-TRPC antibodies. Representative tracings of norepinephrine-induced calcium increase in mesenteric arterioles from SHR under control conditions and in the presence of anti-TRPC1 antibodies (A), anti-TRPC3 antibodies (B), anti-TRPC5 antibodies (C), anti-TRPC1 plus anti-TRPC3 plus anti-TRPC5 antibodies (D), anti-TRPC3 antibodies plus TRPC3 antigenic peptide (E) or anti-β-actin antibodies (F). Summary data (G) shows the effects of specific anti-TRPC antibodies on norepinephrine-induced calcium influx in mesenteric arterioles from SHR. Data are mean ± S.E.M. of n = 8 independent experiments. * P

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Increased rhythmicity in hypertensive arterial smooth muscle is linked to transient receptor potential canonical channels

    doi: 10.1111/j.1582-4934.2009.00890.x

    Figure Lengend Snippet: Inhibition of norepinephrine-induced calcium increase in mesenteric arterioles from SHR by specific anti-TRPC antibodies. Representative tracings of norepinephrine-induced calcium increase in mesenteric arterioles from SHR under control conditions and in the presence of anti-TRPC1 antibodies (A), anti-TRPC3 antibodies (B), anti-TRPC5 antibodies (C), anti-TRPC1 plus anti-TRPC3 plus anti-TRPC5 antibodies (D), anti-TRPC3 antibodies plus TRPC3 antigenic peptide (E) or anti-β-actin antibodies (F). Summary data (G) shows the effects of specific anti-TRPC antibodies on norepinephrine-induced calcium influx in mesenteric arterioles from SHR. Data are mean ± S.E.M. of n = 8 independent experiments. * P

    Article Snippet: The membranes were incubated with primary rabbit antibodies against TRPC1, TRPC3, TRPC4, TRPC5 and TRPC6 (1:200; Alomone Labs), followed by incubation with goat anti-rabbit horseradish peroxidase-conjugated secondary antibody.

    Techniques: Inhibition

    Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.

    Journal: Frontiers in Physiology

    Article Title: Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion

    doi: 10.3389/fphys.2018.00813

    Figure Lengend Snippet: Schematic model illustrating the cardioprotection effect of Ucn-2 from I/R injuries. Left panel summarizes the effect of I/R in rats. I/R promotes fibrosis, hypertrophy and increases the infarct size. I/R also decreases heart’s contractility (ejection fraction and cell shortening) and [Ca 2+ ] i transients. In addition, we demonstrated that I/R potentiates SOCE and upregulated several ion channels, such as Orai1 and TRPC5. Right panel illustrates the effects of the addition of Ucn-2 at the onset of reperfusion. Ucn-2 inhibits fibrosis and decreases the infarct size; it recovers significantly heart’s contraction and the amplitude of [Ca 2+ ] i transients. Moreover, Ucn-2 blocks I/R-evoked exacerbated SOCE and it inhibits I/R-induced Orai1 and TRPC5 upregulation and interaction.

    Article Snippet: Antibodies: TRPC1, TRPC4, TRPC5 and TRPC6 (Alomone Labs, Israel), Orai1 (Novus Biologicals, United States), STIM1 (Sigma-Aldrich, United States) and GAPDH (Cell Signaling, United States).

    Techniques:

    Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p

    Journal: Frontiers in Physiology

    Article Title: Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion

    doi: 10.3389/fphys.2018.00813

    Figure Lengend Snippet: Urocortin-2 regulates the expression of TRPC5, Orai1 and STIM1. (A,B,E,F) Bar graphs showing relative fold change of mRNA levels of TRPC5, Orai1, STIM1 and TRPC6 respectively. (C,D,G,H) Representative immunoblots (top) and quantification (bottom) of protein expression of TRPC5, Orai1, STIM1 and TRPC6 respectively assessed by Western Blots and normalized to their corresponding β-actin expression. Sample were from “Sham” (blue bar); remote (green) and risk (red) zones processed 1 week after I/R. Hatched bars are for rats infused with Ucn-2 (150 μg/Kg). Values are mean ± SEM from 4 to 6 rats. ∗ , ∗∗ , ∗∗∗ Indicate significance at p

    Article Snippet: Antibodies: TRPC1, TRPC4, TRPC5 and TRPC6 (Alomone Labs, Israel), Orai1 (Novus Biologicals, United States), STIM1 (Sigma-Aldrich, United States) and GAPDH (Cell Signaling, United States).

    Techniques: Expressing, Western Blot

    Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p

    Journal: Frontiers in Physiology

    Article Title: Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion

    doi: 10.3389/fphys.2018.00813

    Figure Lengend Snippet: Urocortin-2 inhibition of I/R-induced SOCE involves TRPC5 and Orai1 activation. (A) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); after I/R, and in cells treated with Ucn-2 ± 0.5 μM of astressin ( I/R + Ucn-2; I/R + Ucn-2 + Ast). (B) Representative Western Blot (top) and summary analysis (bottom) showing the expression of TRPC5 and Orai1 normalized to GAPDH examined in untreated NRVMs (control); and in cells transfected with siRNA against Orai1 (siOrai1) and TRPC5 (siTRPC5). (C) Representative traces and average data of TG-induced Ca 2+ influx in Fura-2 loaded NRVMs from “Control,” “I/R” and “I/R+Ucn-2,” and in cells transfected with siRNA of TRPC5 “I/R+siTRPC5” and Orai1 “I/R+siOrai1.” n = 100–200 cells from 6 cultures. Data are mean ± SEM. ∗ , ∗∗ , ∗∗∗ indicate significance at p

    Article Snippet: Antibodies: TRPC1, TRPC4, TRPC5 and TRPC6 (Alomone Labs, Israel), Orai1 (Novus Biologicals, United States), STIM1 (Sigma-Aldrich, United States) and GAPDH (Cell Signaling, United States).

    Techniques: Inhibition, Activation Assay, Western Blot, Expressing, AST Assay, Transfection

    I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (

    Journal: Frontiers in Physiology

    Article Title: Urocortin-2 Prevents Dysregulation of Ca2+ Homeostasis and Improves Early Cardiac Remodeling After Ischemia and Reperfusion

    doi: 10.3389/fphys.2018.00813

    Figure Lengend Snippet: I/R enhances TRPC5 and Orai1 co-localization in cardiomyocytes. (A) Representative images of NRVMs using primary antibodies against TRPC5 and Orai1 conjugated with the appropriate Proximity Ligation Assay (PLA) probes, from untreated “control” cells, “I/R” cells and from cells incubated with Ucn-2 (10 nM; I/R + Ucn-2). The left panels show NRVMs images when antibodies were conjugated with PLA probes; middle panels show merged images with DAPI (blue); and right panels show Bright Field (BF) images. Red puncta indicate that proteins are in close proximity (

    Article Snippet: Antibodies: TRPC1, TRPC4, TRPC5 and TRPC6 (Alomone Labs, Israel), Orai1 (Novus Biologicals, United States), STIM1 (Sigma-Aldrich, United States) and GAPDH (Cell Signaling, United States).

    Techniques: Proximity Ligation Assay, Incubation