anti p s2814  (Alomone Labs)


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    Alomone Labs anti p s2814
    Knockdown of TRPC7 decreased the activity of <t>RyR2</t> and SERCA without affecting the activity of IP3R in mESC-CMs. Representative CaTs recorded from the control group a before and b after applying ryanodine. Representative CaTs recorded from TRPC7 knockdown group c before and d after applying ryanodine. e , f Bar charts showing the normalized frequency and the V max-upstroke calculated from a – d . The decrease of the frequency and the V max-upstroke caused by ryanodine was less in TRPC7 knockdown group. Representative CaTs recorded from the control group g before and h after applying thapsigargin (TG). Representative CaTs recorded from TRPC7 knockdown group i before and j after applying TG. k , l Bar charts showing the normalized frequency and V max-decay calculated from g – j . The decrease of the frequency and the V max-decay and amplitude caused by TG was less in TRPC7 knockdown group. Representative CaTs recorded from the control group m before and n after applying 2-aminoethoxydipheylborate (2-APB). Representative CaTs recorded from TRPC7 knockdown group o before and p after applying 2-APB. q , r Bar charts showing the normalized frequency and the V max-upstroke calculated from m – p . The decrease of the frequency and the V max-upstroke caused by 2-APB was similar between control and TRPC7 knockdown groups. Data were presented as mean ± SEM ( n = 10 cells; cells were from 3 independent batches of differentiation). * P < 0.05, ** P < 0.01 vs control
    Anti P S2814, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti p s2814/product/Alomone Labs
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti p s2814 - by Bioz Stars, 2023-03
    86/100 stars

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    1) Product Images from "TRPC7 regulates the electrophysiological functions of embryonic stem cell-derived cardiomyocytes"

    Article Title: TRPC7 regulates the electrophysiological functions of embryonic stem cell-derived cardiomyocytes

    Journal: Stem Cell Research & Therapy

    doi: 10.1186/s13287-021-02308-7

    Knockdown of TRPC7 decreased the activity of RyR2 and SERCA without affecting the activity of IP3R in mESC-CMs. Representative CaTs recorded from the control group a before and b after applying ryanodine. Representative CaTs recorded from TRPC7 knockdown group c before and d after applying ryanodine. e , f Bar charts showing the normalized frequency and the V max-upstroke calculated from a – d . The decrease of the frequency and the V max-upstroke caused by ryanodine was less in TRPC7 knockdown group. Representative CaTs recorded from the control group g before and h after applying thapsigargin (TG). Representative CaTs recorded from TRPC7 knockdown group i before and j after applying TG. k , l Bar charts showing the normalized frequency and V max-decay calculated from g – j . The decrease of the frequency and the V max-decay and amplitude caused by TG was less in TRPC7 knockdown group. Representative CaTs recorded from the control group m before and n after applying 2-aminoethoxydipheylborate (2-APB). Representative CaTs recorded from TRPC7 knockdown group o before and p after applying 2-APB. q , r Bar charts showing the normalized frequency and the V max-upstroke calculated from m – p . The decrease of the frequency and the V max-upstroke caused by 2-APB was similar between control and TRPC7 knockdown groups. Data were presented as mean ± SEM ( n = 10 cells; cells were from 3 independent batches of differentiation). * P < 0.05, ** P < 0.01 vs control
    Figure Legend Snippet: Knockdown of TRPC7 decreased the activity of RyR2 and SERCA without affecting the activity of IP3R in mESC-CMs. Representative CaTs recorded from the control group a before and b after applying ryanodine. Representative CaTs recorded from TRPC7 knockdown group c before and d after applying ryanodine. e , f Bar charts showing the normalized frequency and the V max-upstroke calculated from a – d . The decrease of the frequency and the V max-upstroke caused by ryanodine was less in TRPC7 knockdown group. Representative CaTs recorded from the control group g before and h after applying thapsigargin (TG). Representative CaTs recorded from TRPC7 knockdown group i before and j after applying TG. k , l Bar charts showing the normalized frequency and V max-decay calculated from g – j . The decrease of the frequency and the V max-decay and amplitude caused by TG was less in TRPC7 knockdown group. Representative CaTs recorded from the control group m before and n after applying 2-aminoethoxydipheylborate (2-APB). Representative CaTs recorded from TRPC7 knockdown group o before and p after applying 2-APB. q , r Bar charts showing the normalized frequency and the V max-upstroke calculated from m – p . The decrease of the frequency and the V max-upstroke caused by 2-APB was similar between control and TRPC7 knockdown groups. Data were presented as mean ± SEM ( n = 10 cells; cells were from 3 independent batches of differentiation). * P < 0.05, ** P < 0.01 vs control

    Techniques Used: Activity Assay

    Knockdown of TRPC7 decreased while overexpression of TRPC7 increased the phosphorylation of RyR2 and PLN, respectively, in NRVMs. Western blotting showing the expression of a total RyR2, b p(S2814)RyR2, c total PLN, and d p(T17) PLN in NRVMs infected with different adenoviruses to knockdown or overexpress TRPC7. e – h Bar charts showing the quantification of each protein from a – d . To eliminate the loading bias, intensity of each target protein was normalized to that of its corresponding β-tubulin. The change of TRPC7 expression did not alter the expression of total RyR2 and PLN. However, knockdown of TRPC7 decreased while overexpression of TRPC7 increased the phosphorylation form of RyR2 [p(S2814)RyR2] and PLN [p(T17)PLN]. Data were presented as mean ± SEM ( n = 4). * P < 0.05, *** P < 0.001 vs corresponding controls
    Figure Legend Snippet: Knockdown of TRPC7 decreased while overexpression of TRPC7 increased the phosphorylation of RyR2 and PLN, respectively, in NRVMs. Western blotting showing the expression of a total RyR2, b p(S2814)RyR2, c total PLN, and d p(T17) PLN in NRVMs infected with different adenoviruses to knockdown or overexpress TRPC7. e – h Bar charts showing the quantification of each protein from a – d . To eliminate the loading bias, intensity of each target protein was normalized to that of its corresponding β-tubulin. The change of TRPC7 expression did not alter the expression of total RyR2 and PLN. However, knockdown of TRPC7 decreased while overexpression of TRPC7 increased the phosphorylation form of RyR2 [p(S2814)RyR2] and PLN [p(T17)PLN]. Data were presented as mean ± SEM ( n = 4). * P < 0.05, *** P < 0.001 vs corresponding controls

    Techniques Used: Over Expression, Western Blot, Expressing, Infection

    Schematic diagram illustrating the mechanism through which TRPC7 positively regulates the automaticity of cardiomyocytes. G protein-coupled receptors (GPCRs) locating on the plasma membrane (PM) sense the external ligands such as hormones, neurotransmitters, and growth factors, transduce the signal to activate phospholipase C (PLC) which hydrolyzes the phosphatidylinositol 4,5-bisphosphate (PIP 2 ) into inositol trisphosphate (IP 3 ) and diacylglycerol (DAG). TRPC7 is then directly activated by DAG, mediating the Ca 2+ influx. Ca 2+ permeated through TRPC7 may activate the forward mode of the Na + -Ca 2+ exchanger (NCX), leading Na + influx and depolarization. This depolarization would then accelerate diastolic depolarization (DD) and increase AP firing rate. On the other hand, Ca 2+ permeated through TRPC7 may also increase the activity of ryanodine receptor 2 (RyR2) locating on the SR, probably through CaMKII and phosphorylation of RyR2, leading to an increase of the localized calcium releases (LCRs). These LCRs are then coupled to inward NCX current, and subsequently accelerate the DD and AP firing rate. At the same time, CaMKII may also increase the phosphorylation of PLN, which subsequently increases the activity of SERCA. The enhancement of the activity of both RyR2 and SERCA result in the acceleration of CaTs
    Figure Legend Snippet: Schematic diagram illustrating the mechanism through which TRPC7 positively regulates the automaticity of cardiomyocytes. G protein-coupled receptors (GPCRs) locating on the plasma membrane (PM) sense the external ligands such as hormones, neurotransmitters, and growth factors, transduce the signal to activate phospholipase C (PLC) which hydrolyzes the phosphatidylinositol 4,5-bisphosphate (PIP 2 ) into inositol trisphosphate (IP 3 ) and diacylglycerol (DAG). TRPC7 is then directly activated by DAG, mediating the Ca 2+ influx. Ca 2+ permeated through TRPC7 may activate the forward mode of the Na + -Ca 2+ exchanger (NCX), leading Na + influx and depolarization. This depolarization would then accelerate diastolic depolarization (DD) and increase AP firing rate. On the other hand, Ca 2+ permeated through TRPC7 may also increase the activity of ryanodine receptor 2 (RyR2) locating on the SR, probably through CaMKII and phosphorylation of RyR2, leading to an increase of the localized calcium releases (LCRs). These LCRs are then coupled to inward NCX current, and subsequently accelerate the DD and AP firing rate. At the same time, CaMKII may also increase the phosphorylation of PLN, which subsequently increases the activity of SERCA. The enhancement of the activity of both RyR2 and SERCA result in the acceleration of CaTs

    Techniques Used: Activity Assay

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    • anti p s2814  (Alomone Labs)
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    Alomone Labs anti p s2814
    Knockdown of TRPC7 decreased the activity of <t>RyR2</t> and SERCA without affecting the activity of IP3R in mESC-CMs. Representative CaTs recorded from the control group a before and b after applying ryanodine. Representative CaTs recorded from TRPC7 knockdown group c before and d after applying ryanodine. e , f Bar charts showing the normalized frequency and the V max-upstroke calculated from a – d . The decrease of the frequency and the V max-upstroke caused by ryanodine was less in TRPC7 knockdown group. Representative CaTs recorded from the control group g before and h after applying thapsigargin (TG). Representative CaTs recorded from TRPC7 knockdown group i before and j after applying TG. k , l Bar charts showing the normalized frequency and V max-decay calculated from g – j . The decrease of the frequency and the V max-decay and amplitude caused by TG was less in TRPC7 knockdown group. Representative CaTs recorded from the control group m before and n after applying 2-aminoethoxydipheylborate (2-APB). Representative CaTs recorded from TRPC7 knockdown group o before and p after applying 2-APB. q , r Bar charts showing the normalized frequency and the V max-upstroke calculated from m – p . The decrease of the frequency and the V max-upstroke caused by 2-APB was similar between control and TRPC7 knockdown groups. Data were presented as mean ± SEM ( n = 10 cells; cells were from 3 independent batches of differentiation). * P < 0.05, ** P < 0.01 vs control
    Anti P S2814, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti p s2814/product/Alomone Labs
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti p s2814 - by Bioz Stars, 2023-03
    86/100 stars
    		  Buy from Supplier

    Image Search Results


    Knockdown of TRPC7 decreased the activity of RyR2 and SERCA without affecting the activity of IP3R in mESC-CMs. Representative CaTs recorded from the control group a before and b after applying ryanodine. Representative CaTs recorded from TRPC7 knockdown group c before and d after applying ryanodine. e , f Bar charts showing the normalized frequency and the V max-upstroke calculated from a – d . The decrease of the frequency and the V max-upstroke caused by ryanodine was less in TRPC7 knockdown group. Representative CaTs recorded from the control group g before and h after applying thapsigargin (TG). Representative CaTs recorded from TRPC7 knockdown group i before and j after applying TG. k , l Bar charts showing the normalized frequency and V max-decay calculated from g – j . The decrease of the frequency and the V max-decay and amplitude caused by TG was less in TRPC7 knockdown group. Representative CaTs recorded from the control group m before and n after applying 2-aminoethoxydipheylborate (2-APB). Representative CaTs recorded from TRPC7 knockdown group o before and p after applying 2-APB. q , r Bar charts showing the normalized frequency and the V max-upstroke calculated from m – p . The decrease of the frequency and the V max-upstroke caused by 2-APB was similar between control and TRPC7 knockdown groups. Data were presented as mean ± SEM ( n = 10 cells; cells were from 3 independent batches of differentiation). * P < 0.05, ** P < 0.01 vs control

    Journal: Stem Cell Research & Therapy

    Article Title: TRPC7 regulates the electrophysiological functions of embryonic stem cell-derived cardiomyocytes

    doi: 10.1186/s13287-021-02308-7

    Figure Lengend Snippet: Knockdown of TRPC7 decreased the activity of RyR2 and SERCA without affecting the activity of IP3R in mESC-CMs. Representative CaTs recorded from the control group a before and b after applying ryanodine. Representative CaTs recorded from TRPC7 knockdown group c before and d after applying ryanodine. e , f Bar charts showing the normalized frequency and the V max-upstroke calculated from a – d . The decrease of the frequency and the V max-upstroke caused by ryanodine was less in TRPC7 knockdown group. Representative CaTs recorded from the control group g before and h after applying thapsigargin (TG). Representative CaTs recorded from TRPC7 knockdown group i before and j after applying TG. k , l Bar charts showing the normalized frequency and V max-decay calculated from g – j . The decrease of the frequency and the V max-decay and amplitude caused by TG was less in TRPC7 knockdown group. Representative CaTs recorded from the control group m before and n after applying 2-aminoethoxydipheylborate (2-APB). Representative CaTs recorded from TRPC7 knockdown group o before and p after applying 2-APB. q , r Bar charts showing the normalized frequency and the V max-upstroke calculated from m – p . The decrease of the frequency and the V max-upstroke caused by 2-APB was similar between control and TRPC7 knockdown groups. Data were presented as mean ± SEM ( n = 10 cells; cells were from 3 independent batches of differentiation). * P < 0.05, ** P < 0.01 vs control

    Article Snippet: Antibodies used were anti-TRPC7 1:500 (HPA031126, Sigma), anti-β-tubulin 1:1000 (15,115, Cell Signaling, Danvers, Massachusetts, USA), anti-HCN4 1:200 (APC-052, Alomone), anti-Cav1.3 1:100 (ACC-005, Alomone), anti-Cav3.1 1:200 (ACC-021, Alomone), anti-Cav3.2 1:200 (ACC-025, Alomone), anti-RyR2 1:1000 (MA3-916, Invitrogen), anti-SERCA 1:200 (sc-30110, Santa Cruz), anti-IP3R 1:500 (ACC-019, Alomone), anti-p(S2814)RyR2 1:5000 (A010-31, Badrilla), anti-phospholamban (PLN) 1:1000 (A010-14, Badrilla), anti-p(T17) PLN 1:5000 (A010-13, Badrilla), HRP-conjugated goat anti-rabbit secondary antibody 1:5000 (Dako, Zug, Switzerland), and HRP-conjugated goat anti-mouse secondary antibody 1:5000 (Dako).

    Techniques: Activity Assay

    Knockdown of TRPC7 decreased while overexpression of TRPC7 increased the phosphorylation of RyR2 and PLN, respectively, in NRVMs. Western blotting showing the expression of a total RyR2, b p(S2814)RyR2, c total PLN, and d p(T17) PLN in NRVMs infected with different adenoviruses to knockdown or overexpress TRPC7. e – h Bar charts showing the quantification of each protein from a – d . To eliminate the loading bias, intensity of each target protein was normalized to that of its corresponding β-tubulin. The change of TRPC7 expression did not alter the expression of total RyR2 and PLN. However, knockdown of TRPC7 decreased while overexpression of TRPC7 increased the phosphorylation form of RyR2 [p(S2814)RyR2] and PLN [p(T17)PLN]. Data were presented as mean ± SEM ( n = 4). * P < 0.05, *** P < 0.001 vs corresponding controls

    Journal: Stem Cell Research & Therapy

    Article Title: TRPC7 regulates the electrophysiological functions of embryonic stem cell-derived cardiomyocytes

    doi: 10.1186/s13287-021-02308-7

    Figure Lengend Snippet: Knockdown of TRPC7 decreased while overexpression of TRPC7 increased the phosphorylation of RyR2 and PLN, respectively, in NRVMs. Western blotting showing the expression of a total RyR2, b p(S2814)RyR2, c total PLN, and d p(T17) PLN in NRVMs infected with different adenoviruses to knockdown or overexpress TRPC7. e – h Bar charts showing the quantification of each protein from a – d . To eliminate the loading bias, intensity of each target protein was normalized to that of its corresponding β-tubulin. The change of TRPC7 expression did not alter the expression of total RyR2 and PLN. However, knockdown of TRPC7 decreased while overexpression of TRPC7 increased the phosphorylation form of RyR2 [p(S2814)RyR2] and PLN [p(T17)PLN]. Data were presented as mean ± SEM ( n = 4). * P < 0.05, *** P < 0.001 vs corresponding controls

    Article Snippet: Antibodies used were anti-TRPC7 1:500 (HPA031126, Sigma), anti-β-tubulin 1:1000 (15,115, Cell Signaling, Danvers, Massachusetts, USA), anti-HCN4 1:200 (APC-052, Alomone), anti-Cav1.3 1:100 (ACC-005, Alomone), anti-Cav3.1 1:200 (ACC-021, Alomone), anti-Cav3.2 1:200 (ACC-025, Alomone), anti-RyR2 1:1000 (MA3-916, Invitrogen), anti-SERCA 1:200 (sc-30110, Santa Cruz), anti-IP3R 1:500 (ACC-019, Alomone), anti-p(S2814)RyR2 1:5000 (A010-31, Badrilla), anti-phospholamban (PLN) 1:1000 (A010-14, Badrilla), anti-p(T17) PLN 1:5000 (A010-13, Badrilla), HRP-conjugated goat anti-rabbit secondary antibody 1:5000 (Dako, Zug, Switzerland), and HRP-conjugated goat anti-mouse secondary antibody 1:5000 (Dako).

    Techniques: Over Expression, Western Blot, Expressing, Infection

    Schematic diagram illustrating the mechanism through which TRPC7 positively regulates the automaticity of cardiomyocytes. G protein-coupled receptors (GPCRs) locating on the plasma membrane (PM) sense the external ligands such as hormones, neurotransmitters, and growth factors, transduce the signal to activate phospholipase C (PLC) which hydrolyzes the phosphatidylinositol 4,5-bisphosphate (PIP 2 ) into inositol trisphosphate (IP 3 ) and diacylglycerol (DAG). TRPC7 is then directly activated by DAG, mediating the Ca 2+ influx. Ca 2+ permeated through TRPC7 may activate the forward mode of the Na + -Ca 2+ exchanger (NCX), leading Na + influx and depolarization. This depolarization would then accelerate diastolic depolarization (DD) and increase AP firing rate. On the other hand, Ca 2+ permeated through TRPC7 may also increase the activity of ryanodine receptor 2 (RyR2) locating on the SR, probably through CaMKII and phosphorylation of RyR2, leading to an increase of the localized calcium releases (LCRs). These LCRs are then coupled to inward NCX current, and subsequently accelerate the DD and AP firing rate. At the same time, CaMKII may also increase the phosphorylation of PLN, which subsequently increases the activity of SERCA. The enhancement of the activity of both RyR2 and SERCA result in the acceleration of CaTs

    Journal: Stem Cell Research & Therapy

    Article Title: TRPC7 regulates the electrophysiological functions of embryonic stem cell-derived cardiomyocytes

    doi: 10.1186/s13287-021-02308-7

    Figure Lengend Snippet: Schematic diagram illustrating the mechanism through which TRPC7 positively regulates the automaticity of cardiomyocytes. G protein-coupled receptors (GPCRs) locating on the plasma membrane (PM) sense the external ligands such as hormones, neurotransmitters, and growth factors, transduce the signal to activate phospholipase C (PLC) which hydrolyzes the phosphatidylinositol 4,5-bisphosphate (PIP 2 ) into inositol trisphosphate (IP 3 ) and diacylglycerol (DAG). TRPC7 is then directly activated by DAG, mediating the Ca 2+ influx. Ca 2+ permeated through TRPC7 may activate the forward mode of the Na + -Ca 2+ exchanger (NCX), leading Na + influx and depolarization. This depolarization would then accelerate diastolic depolarization (DD) and increase AP firing rate. On the other hand, Ca 2+ permeated through TRPC7 may also increase the activity of ryanodine receptor 2 (RyR2) locating on the SR, probably through CaMKII and phosphorylation of RyR2, leading to an increase of the localized calcium releases (LCRs). These LCRs are then coupled to inward NCX current, and subsequently accelerate the DD and AP firing rate. At the same time, CaMKII may also increase the phosphorylation of PLN, which subsequently increases the activity of SERCA. The enhancement of the activity of both RyR2 and SERCA result in the acceleration of CaTs

    Article Snippet: Antibodies used were anti-TRPC7 1:500 (HPA031126, Sigma), anti-β-tubulin 1:1000 (15,115, Cell Signaling, Danvers, Massachusetts, USA), anti-HCN4 1:200 (APC-052, Alomone), anti-Cav1.3 1:100 (ACC-005, Alomone), anti-Cav3.1 1:200 (ACC-021, Alomone), anti-Cav3.2 1:200 (ACC-025, Alomone), anti-RyR2 1:1000 (MA3-916, Invitrogen), anti-SERCA 1:200 (sc-30110, Santa Cruz), anti-IP3R 1:500 (ACC-019, Alomone), anti-p(S2814)RyR2 1:5000 (A010-31, Badrilla), anti-phospholamban (PLN) 1:1000 (A010-14, Badrilla), anti-p(T17) PLN 1:5000 (A010-13, Badrilla), HRP-conjugated goat anti-rabbit secondary antibody 1:5000 (Dako, Zug, Switzerland), and HRP-conjugated goat anti-mouse secondary antibody 1:5000 (Dako).

    Techniques: Activity Assay