trpc5  (Alomone Labs)


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    Name:
    Anti TRPC5 Antibody
    Description:
    Anti TRPC5 Antibody ACC 020 is a highly specific antibody directed against an epitope of the human protein The antibody can be used in western blot immunoprecipitation immunocytochemistry and immunohistochemistry applications It has been designed to recognize TRPC5 from mouse rat and human samples
    Catalog Number:
    ACC-020
    Price:
    397.0
    Category:
    Primary Antibody
    Applications:
    Immunocytochemistry, Immunofluorescence, Immunohistochemistry, Immunoprecipitation, Western Blot
    Purity:
    Affinity purified on immobilized antigen.
    Immunogen:
    Synthetic peptide
    Size:
    25 mcl
    Antibody Type:
    Polyclonal Primary Antibodies
    Format:
    Lyophilized Powder
    Host:
    Rabbit
    Isotype:
    Rabbit IgG
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    Structured Review

    Alomone Labs trpc5
    Anti TRPC5 Antibody
    Anti TRPC5 Antibody ACC 020 is a highly specific antibody directed against an epitope of the human protein The antibody can be used in western blot immunoprecipitation immunocytochemistry and immunohistochemistry applications It has been designed to recognize TRPC5 from mouse rat and human samples
    https://www.bioz.com/result/trpc5/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    trpc5 - by Bioz Stars, 2021-09
    93/100 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 "A translational kidney organoid system bolsters human relevance of clinical development candidate"

    Article Title: A translational kidney organoid system bolsters human relevance of clinical development candidate

    Journal: bioRxiv

    doi: 10.1101/2019.12.30.891440

    TRPC5 inhibition protects against podocyte injury in human kidney organoids in vivo (A) Oral dosing of GFB-887 in rats results in drug exposure of transplanted, perfused human kidney organoids equivalent to rat plasma levels. Athymic nude, male rats were implanted with day 14 early differentiating organoids under the sub-capsular space. Transplanted rats were grown for 2 ( left panel ) or 4 ( right panel ) weeks and orally dosed with 10 mg/kg GFB-887 for 3 consecutive days prior to plasma, kidney and organoid collection. Data show mean ± SEM of GFB-887 exposure from at least 4 independent measurements suggest that transplanted human kidney organoids achieve maximal vascularization as well as functional connectivity to host vasculature in 2 weeks. (B) Super resolution imaging reveals PS-induced loss of synaptopodin in transplanted human organoids, which can be prevent by orally dosing with GFB-887: HBSS (Hank’s Balanced Salt solution serving as vehicle control), PS, PS + GFB-887. (C) Quantification of PS induced podocyte injury and protection by CsA or GBF-887. Synaptopodin mean intensity in podocytes was quantified from human organoids from transplant experiments for vehicle, PS, co-perfusion GFB-887 + PS, and oral dosing of GFB-887 + PS (Data show mean ± SEM; for all treatment conditions vs. PS p
    Figure Legend Snippet: TRPC5 inhibition protects against podocyte injury in human kidney organoids in vivo (A) Oral dosing of GFB-887 in rats results in drug exposure of transplanted, perfused human kidney organoids equivalent to rat plasma levels. Athymic nude, male rats were implanted with day 14 early differentiating organoids under the sub-capsular space. Transplanted rats were grown for 2 ( left panel ) or 4 ( right panel ) weeks and orally dosed with 10 mg/kg GFB-887 for 3 consecutive days prior to plasma, kidney and organoid collection. Data show mean ± SEM of GFB-887 exposure from at least 4 independent measurements suggest that transplanted human kidney organoids achieve maximal vascularization as well as functional connectivity to host vasculature in 2 weeks. (B) Super resolution imaging reveals PS-induced loss of synaptopodin in transplanted human organoids, which can be prevent by orally dosing with GFB-887: HBSS (Hank’s Balanced Salt solution serving as vehicle control), PS, PS + GFB-887. (C) Quantification of PS induced podocyte injury and protection by CsA or GBF-887. Synaptopodin mean intensity in podocytes was quantified from human organoids from transplant experiments for vehicle, PS, co-perfusion GFB-887 + PS, and oral dosing of GFB-887 + PS (Data show mean ± SEM; for all treatment conditions vs. PS p

    Techniques Used: Inhibition, In Vivo, Functional Assay, Imaging

    Double labeling with synaptopodin reveals podocyte TRPC5 protein expression in human organoids Representative glomerulus ( left panel ) and zoomed in super-resolution images TRPC5 and synaptopodin staining in individual podocytes. Synaptopodin: green, TRPC5: red, Hoechst: blue.
    Figure Legend Snippet: Double labeling with synaptopodin reveals podocyte TRPC5 protein expression in human organoids Representative glomerulus ( left panel ) and zoomed in super-resolution images TRPC5 and synaptopodin staining in individual podocytes. Synaptopodin: green, TRPC5: red, Hoechst: blue.

    Techniques Used: Labeling, Expressing, Staining

    CsA and TRPC5 inhibition protects against podocyte injury in kidney organoids in vitro (A) Representative current-voltage relationship recording during a 500 ms voltage ramp from -80 mV to +80 mV in the absence and presence of 0.1 μM GFB-887 or the reference TRPC5 inhibitor, 100 μM ML-204. (B) Concentration dependence of inhibition of human TRPC5 currents after a 3 min application of GFB-887 at +80 mV. Data points are mean ± SEM of 3-4 observations at each concentration. (C) Upregulation of TRPC5 mRNA expression during organoid differentiation in vitro (D) Double labeling with synaptopodin reveals podocyte TRPC5 protein expression in human organoids (E) CsA and GFB-887 protects against PS induced podocyte injury in in vitro D28 organoids. Representative PS injury mask for an organoid is depicted in blue and the inset box indicates and area in the region that can be used for identification of injured podocytes for quantitation ( top left panel ). Representative glomeruli identified for podocyte injury quantitation of aggregated actin for treatment with vehicle DMSO, PS alone, CsA + PS, GFB-887 + PS, and the combination of CsA and GFB-887 + PS. Synaptopodin: green; Phalloidin: red. (F) Quantification of PS induced actin aggregation. GFB-887 and CsA are non-additive, consistent with shared mechanism of action. DMSO vs. PS, p
    Figure Legend Snippet: CsA and TRPC5 inhibition protects against podocyte injury in kidney organoids in vitro (A) Representative current-voltage relationship recording during a 500 ms voltage ramp from -80 mV to +80 mV in the absence and presence of 0.1 μM GFB-887 or the reference TRPC5 inhibitor, 100 μM ML-204. (B) Concentration dependence of inhibition of human TRPC5 currents after a 3 min application of GFB-887 at +80 mV. Data points are mean ± SEM of 3-4 observations at each concentration. (C) Upregulation of TRPC5 mRNA expression during organoid differentiation in vitro (D) Double labeling with synaptopodin reveals podocyte TRPC5 protein expression in human organoids (E) CsA and GFB-887 protects against PS induced podocyte injury in in vitro D28 organoids. Representative PS injury mask for an organoid is depicted in blue and the inset box indicates and area in the region that can be used for identification of injured podocytes for quantitation ( top left panel ). Representative glomeruli identified for podocyte injury quantitation of aggregated actin for treatment with vehicle DMSO, PS alone, CsA + PS, GFB-887 + PS, and the combination of CsA and GFB-887 + PS. Synaptopodin: green; Phalloidin: red. (F) Quantification of PS induced actin aggregation. GFB-887 and CsA are non-additive, consistent with shared mechanism of action. DMSO vs. PS, p

    Techniques Used: Inhibition, In Vitro, Concentration Assay, Expressing, Labeling, Quantitation Assay

    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

    Related Articles

    Incubation:

    Article Title: Glycolysis is essential for chemoresistance induced by transient receptor potential channel C5 in colorectal cancer
    Article Snippet: .. After blocked with phosphate-buffered saline tween containing 5% non-fat milk, the PVDF membranes were incubated with the primary antibodies anti-TRPC5 (ACC-020, Alomone labs, Jerusalem, State of Israel) (1:500), anti-caspase-3 (ab32351, Abcam Biotechnology, Cambridge, MA, USA) (1:500), anti-glucose transporter 1 (GLUT1) (ab115730, Abcam Biotechnology) (1:1000), β-actin (AA128, Beyotime Biotechnology) (1:1000) and subsequently with the corresponding secondary antibodies [goat anti-rabbit IgG (A0208, Beyotime Biotechnology) and goat anti-mouse IgG (A0216, Beyotime Biotechnology)]. ..

    Staining:

    Article Title: Effects of Transient Receptor Potential Cation 5 (TRPC5) Inhibitor, NU6027, on Hippocampal Neuronal Death after Traumatic Brain Injury
    Article Snippet: .. Brain tissues were stained by TRPC5 antibodies (Alomone Laboratories, Jerusalem, Israel). ..

    other:

    Article Title: Trpc6 inactivation confers protection in a model of severe nephrosis in rats
    Article Snippet: We also used a rabbit polyclonal antibody against TRPC5 from Alomone (ACC-020).

    Plasmid Preparation:

    Article Title: TRPC5‑induced autophagy promotes the TMZ‑resistance of glioma cells via the CAMMKβ/AMPKα/mTOR pathway.
    Article Snippet: .. The following antibodies were used: Anti-β-actin (cat. no. sc-47778; 1:200) from Santa Cruz Biotechnology, Inc. (Dallas, TX, USA); anti-TRPC5 (cat. no. ACC-020; 1:200) from Alomone Labs (Jerusalem, Israel); anti-phospho-CaMKKβ (Ser286) (cat. no. 12716; 1:500), anti-CaMKKβ (cat. no. 4436; 1:500), anti-phospho-AMPKα (Ser172) (cat. no. 2535; 1:500), anti-AMPKα (cat. no. 2532S; 1:500), anti-phospho-mTOR (Ser2448) (cat. no. 2971; 1:500), anti-mTOR (cat. no. 2972; 1:500) and anti-microtubule associated protein 1 light chain 3 α (LC3; cat. no. 12741; 1:500) from Cell Signaling Technology, Inc. (Danvers, MA, USA); and AlexaFluor 488‑conjugated goat anti‑mouse IgG (cat. no. R37120; 1:2,000) and Alexa Fluor 555‑conjugated goat anti-rabbit IgG (cat. no. A21428; 1:2,000) from Thermo Fisher Scientific, Inc. Plasmid and transfection. ..

    Transfection:

    Article Title: TRPC5‑induced autophagy promotes the TMZ‑resistance of glioma cells via the CAMMKβ/AMPKα/mTOR pathway.
    Article Snippet: .. The following antibodies were used: Anti-β-actin (cat. no. sc-47778; 1:200) from Santa Cruz Biotechnology, Inc. (Dallas, TX, USA); anti-TRPC5 (cat. no. ACC-020; 1:200) from Alomone Labs (Jerusalem, Israel); anti-phospho-CaMKKβ (Ser286) (cat. no. 12716; 1:500), anti-CaMKKβ (cat. no. 4436; 1:500), anti-phospho-AMPKα (Ser172) (cat. no. 2535; 1:500), anti-AMPKα (cat. no. 2532S; 1:500), anti-phospho-mTOR (Ser2448) (cat. no. 2971; 1:500), anti-mTOR (cat. no. 2972; 1:500) and anti-microtubule associated protein 1 light chain 3 α (LC3; cat. no. 12741; 1:500) from Cell Signaling Technology, Inc. (Danvers, MA, USA); and AlexaFluor 488‑conjugated goat anti‑mouse IgG (cat. no. R37120; 1:2,000) and Alexa Fluor 555‑conjugated goat anti-rabbit IgG (cat. no. A21428; 1:2,000) from Thermo Fisher Scientific, Inc. Plasmid and transfection. ..

    Immunohistochemistry:

    Article Title: A translational kidney organoid system bolsters human relevance of clinical development candidate
    Article Snippet: .. Primary antibodies included: CD31/PECAM-1 (Bethyl Laboratories, IHC-00055), RECA-1 (BioRad, MCA970GA), synaptopodin (Progen, GP94-N), E-cadherin (R & D, AF648), TRPC5 (UC Davic/NIH NeuroMAB Facility, 75-104), TRPC5 (Alomon Labs, ACC-020). ..

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    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: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/trpc5/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    trpc5 - by Bioz Stars, 2021-09
    93/100 stars
      Buy from Supplier

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    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