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anti-trpc7 antibody  (Alomone Labs)


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    Alomone Labs anti-trpc7 antibody
    Anti Trpc7 Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 90/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/acc-066/custom%40acc-066%4040498020?v=Alomone+Labs
    Average 90 stars, based on 2 article reviews
    anti-trpc7 antibody - by Bioz Stars, 2026-07
    90/100 stars

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    RH specifically represses hippocampal TRPC6 channel in diabetic mice. (A) Relative TRPC6 mRNA expression (n = 6) in PC12 cells cultured in medium with normal glucose concentration (NG, 5.6 mM) or medium with high glucose concentration (HG, 25 mM). NG+LG, cells cultured in NG medium and received three times of low glucose stimulation (12 hours per times, LG, 3.0 mM); HG+LG, cells cultured in HG medium and received three times of low glucose stimulation (12 hours per times, LG, 3.0 mM). (B) Representative Western blots of TRPC6 protein in PC12 cells in four groups. GAPDH served as a loading control. Quantitative data were shown on the right (n = 4). (C) Relative mRNA expression levels of TRPC6 in hippocampus from nondiabetic (ND) mice, ND mice with recurrent moderate hypoglycemia (ND‐RH), mice with STZ‐induced type 1 diabetes mellitus (DM), and DM mice with RH (DM‐RH) (n = 6 samples from six mice). (D) Representative Western blots of TRPC6 in hippocampus. GAPDH served as a loading control. Quantitative results are shown on the right (n = 3 tissues from three mice). TPRC6 −/− , TRPC6 global knockout mice. (E) Relative mRNA expression levels of TRPC1, TRPC3, TRPC4, TRPC5, and <t>TRPC7</t> in hippocampus (n = 6–8 samples from four mice). * P < .05, ** P < .01, *** P < .001. Statistical significance was assessed using a one‐way ANOVA or Kruskal‐Wallis test
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    Average 90 stars, based on 1 article reviews
    anti trpc7 antibody - by Bioz Stars, 2026-07
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    RH specifically represses hippocampal TRPC6 channel in diabetic mice. (A) Relative TRPC6 mRNA expression (n = 6) in PC12 cells cultured in medium with normal glucose concentration (NG, 5.6 mM) or medium with high glucose concentration (HG, 25 mM). NG+LG, cells cultured in NG medium and received three times of low glucose stimulation (12 hours per times, LG, 3.0 mM); HG+LG, cells cultured in HG medium and received three times of low glucose stimulation (12 hours per times, LG, 3.0 mM). (B) Representative Western blots of TRPC6 protein in PC12 cells in four groups. GAPDH served as a loading control. Quantitative data were shown on the right (n = 4). (C) Relative mRNA expression levels of TRPC6 in hippocampus from nondiabetic (ND) mice, ND mice with recurrent moderate hypoglycemia (ND‐RH), mice with STZ‐induced type 1 diabetes mellitus (DM), and DM mice with RH (DM‐RH) (n = 6 samples from six mice). (D) Representative Western blots of TRPC6 in hippocampus. GAPDH served as a loading control. Quantitative results are shown on the right (n = 3 tissues from three mice). TPRC6 −/− , TRPC6 global knockout mice. (E) Relative mRNA expression levels of TRPC1, TRPC3, TRPC4, TRPC5, and <t>TRPC7</t> in hippocampus (n = 6–8 samples from four mice). * P < .05, ** P < .01, *** P < .001. Statistical significance was assessed using a one‐way ANOVA or Kruskal‐Wallis test
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    Alomone Labs antitrpc7
    RH specifically represses hippocampal TRPC6 channel in diabetic mice. (A) Relative TRPC6 mRNA expression (n = 6) in PC12 cells cultured in medium with normal glucose concentration (NG, 5.6 mM) or medium with high glucose concentration (HG, 25 mM). NG+LG, cells cultured in NG medium and received three times of low glucose stimulation (12 hours per times, LG, 3.0 mM); HG+LG, cells cultured in HG medium and received three times of low glucose stimulation (12 hours per times, LG, 3.0 mM). (B) Representative Western blots of TRPC6 protein in PC12 cells in four groups. GAPDH served as a loading control. Quantitative data were shown on the right (n = 4). (C) Relative mRNA expression levels of TRPC6 in hippocampus from nondiabetic (ND) mice, ND mice with recurrent moderate hypoglycemia (ND‐RH), mice with STZ‐induced type 1 diabetes mellitus (DM), and DM mice with RH (DM‐RH) (n = 6 samples from six mice). (D) Representative Western blots of TRPC6 in hippocampus. GAPDH served as a loading control. Quantitative results are shown on the right (n = 3 tissues from three mice). TPRC6 −/− , TRPC6 global knockout mice. (E) Relative mRNA expression levels of TRPC1, TRPC3, TRPC4, TRPC5, and <t>TRPC7</t> in hippocampus (n = 6–8 samples from four mice). * P < .05, ** P < .01, *** P < .001. Statistical significance was assessed using a one‐way ANOVA or Kruskal‐Wallis test
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    Average 90 stars, based on 1 article reviews
    antitrpc7 - by Bioz Stars, 2026-07
    90/100 stars
      Buy from Supplier

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    RH specifically represses hippocampal TRPC6 channel in diabetic mice. (A) Relative TRPC6 mRNA expression (n = 6) in PC12 cells cultured in medium with normal glucose concentration (NG, 5.6 mM) or medium with high glucose concentration (HG, 25 mM). NG+LG, cells cultured in NG medium and received three times of low glucose stimulation (12 hours per times, LG, 3.0 mM); HG+LG, cells cultured in HG medium and received three times of low glucose stimulation (12 hours per times, LG, 3.0 mM). (B) Representative Western blots of TRPC6 protein in PC12 cells in four groups. GAPDH served as a loading control. Quantitative data were shown on the right (n = 4). (C) Relative mRNA expression levels of TRPC6 in hippocampus from nondiabetic (ND) mice, ND mice with recurrent moderate hypoglycemia (ND‐RH), mice with STZ‐induced type 1 diabetes mellitus (DM), and DM mice with RH (DM‐RH) (n = 6 samples from six mice). (D) Representative Western blots of TRPC6 in hippocampus. GAPDH served as a loading control. Quantitative results are shown on the right (n = 3 tissues from three mice). TPRC6 −/− , TRPC6 global knockout mice. (E) Relative mRNA expression levels of TRPC1, TRPC3, TRPC4, TRPC5, and TRPC7 in hippocampus (n = 6–8 samples from four mice). * P < .05, ** P < .01, *** P < .001. Statistical significance was assessed using a one‐way ANOVA or Kruskal‐Wallis test

    Journal: Clinical and Translational Medicine

    Article Title: Low‐glucose‐sensitive TRPC6 dysfunction drives hypoglycemia‐induced cognitive impairment in diabetes

    doi: 10.1002/ctm2.205

    Figure Lengend Snippet: RH specifically represses hippocampal TRPC6 channel in diabetic mice. (A) Relative TRPC6 mRNA expression (n = 6) in PC12 cells cultured in medium with normal glucose concentration (NG, 5.6 mM) or medium with high glucose concentration (HG, 25 mM). NG+LG, cells cultured in NG medium and received three times of low glucose stimulation (12 hours per times, LG, 3.0 mM); HG+LG, cells cultured in HG medium and received three times of low glucose stimulation (12 hours per times, LG, 3.0 mM). (B) Representative Western blots of TRPC6 protein in PC12 cells in four groups. GAPDH served as a loading control. Quantitative data were shown on the right (n = 4). (C) Relative mRNA expression levels of TRPC6 in hippocampus from nondiabetic (ND) mice, ND mice with recurrent moderate hypoglycemia (ND‐RH), mice with STZ‐induced type 1 diabetes mellitus (DM), and DM mice with RH (DM‐RH) (n = 6 samples from six mice). (D) Representative Western blots of TRPC6 in hippocampus. GAPDH served as a loading control. Quantitative results are shown on the right (n = 3 tissues from three mice). TPRC6 −/− , TRPC6 global knockout mice. (E) Relative mRNA expression levels of TRPC1, TRPC3, TRPC4, TRPC5, and TRPC7 in hippocampus (n = 6–8 samples from four mice). * P < .05, ** P < .01, *** P < .001. Statistical significance was assessed using a one‐way ANOVA or Kruskal‐Wallis test

    Article Snippet: The primary antibodies were used, including anti‐TRPC1 (ACC‐010, 120 kDa), anti‐TRPC3 (ACC‐016, 100 kDa), anti‐TRPC4 (ACC‐018, 97 kDa), anti‐TRPC5 (ACC‐020, 100 kDa), anti‐TRPC6 antibody (ACC‐017, 110 kDa), anti‐TRPC7 antibody (ACC‐066, 95 kDa), anti‐TRPV1 (ACC‐030, 90 kDa), and anti‐TRPV4 (ACC‐034, 100 kDa) from Alomone; anti‐LKB1 (PA5‐96062, 48 kDa), anti‐phospho‐CaMMK2 (PA5‐105225, 65 kDa), and anti‐phospho‐DRP1 (S616, PA5‐64821, predicted to react with Ser585 in rats and Ser600 in mice, 83 kDa) antibodies from Invitrogen; anti‐CaMKK2 (ab135979, 65 kDa), anti‐Drp1 (ab184247, 83 kDa), anti‐phospho‐DRP1 (S637, ab193216, predicted to react with Ser656 in rats and Ser616 in mice, 83 kDa), anti‐PSD95 (ab238135, 80 kDa), anti‐Synapsin I (ab254349, 74 kDa), and anti‐SYP (ab32127, 34 kDa) antibodies from Abcam; anti‐AMPKα (2532S, 62 kDa) and anti‐phospho‐AMPKα (Thr172, 2535S, 62 kDa) antibodies from CST, followed by incubation with the secondary antibodies (ZSGB‐BIO).

    Techniques: Expressing, Cell Culture, Concentration Assay, Western Blot, Knock-Out

    RH specifically reduces TRPC6 expression in the white blood cells from diabetic patients. (A) Relative mRNA expression of TRPC6 in human blood white blood cells from normal subject (n = 14 samples from 14 patients), type 2 diabetic patients without hypoglycemia episodes (T2DM, n = 18 samples from 18 patients) or diabetic patients with RH (T2DM‐RH, n = 8 samples from eight patients). (B‐E) Relative mRNA expression of TRPC1, TRPC3, TRPC5, and TRPC7 in human white blood cells. (F‐I) Representative image showed Ca 2+ influx in white blood cells from a normal subject (F), a T2DM patient without RH (G), and a T2DM patient with RH and quantitative data are shown on the right (I). Ca 2+ (1 mM, Cacl 2 ) and/or hyperforin (Hyp, 10 µM) was added at the point 25S; * P < 0.01, ** P < 0.01, and *** P < 0.001. Statistical significance was assessed using Kruskal‐Wallis test followed by Dunn's multiple comparisons test

    Journal: Clinical and Translational Medicine

    Article Title: Low‐glucose‐sensitive TRPC6 dysfunction drives hypoglycemia‐induced cognitive impairment in diabetes

    doi: 10.1002/ctm2.205

    Figure Lengend Snippet: RH specifically reduces TRPC6 expression in the white blood cells from diabetic patients. (A) Relative mRNA expression of TRPC6 in human blood white blood cells from normal subject (n = 14 samples from 14 patients), type 2 diabetic patients without hypoglycemia episodes (T2DM, n = 18 samples from 18 patients) or diabetic patients with RH (T2DM‐RH, n = 8 samples from eight patients). (B‐E) Relative mRNA expression of TRPC1, TRPC3, TRPC5, and TRPC7 in human white blood cells. (F‐I) Representative image showed Ca 2+ influx in white blood cells from a normal subject (F), a T2DM patient without RH (G), and a T2DM patient with RH and quantitative data are shown on the right (I). Ca 2+ (1 mM, Cacl 2 ) and/or hyperforin (Hyp, 10 µM) was added at the point 25S; * P < 0.01, ** P < 0.01, and *** P < 0.001. Statistical significance was assessed using Kruskal‐Wallis test followed by Dunn's multiple comparisons test

    Article Snippet: The primary antibodies were used, including anti‐TRPC1 (ACC‐010, 120 kDa), anti‐TRPC3 (ACC‐016, 100 kDa), anti‐TRPC4 (ACC‐018, 97 kDa), anti‐TRPC5 (ACC‐020, 100 kDa), anti‐TRPC6 antibody (ACC‐017, 110 kDa), anti‐TRPC7 antibody (ACC‐066, 95 kDa), anti‐TRPV1 (ACC‐030, 90 kDa), and anti‐TRPV4 (ACC‐034, 100 kDa) from Alomone; anti‐LKB1 (PA5‐96062, 48 kDa), anti‐phospho‐CaMMK2 (PA5‐105225, 65 kDa), and anti‐phospho‐DRP1 (S616, PA5‐64821, predicted to react with Ser585 in rats and Ser600 in mice, 83 kDa) antibodies from Invitrogen; anti‐CaMKK2 (ab135979, 65 kDa), anti‐Drp1 (ab184247, 83 kDa), anti‐phospho‐DRP1 (S637, ab193216, predicted to react with Ser656 in rats and Ser616 in mice, 83 kDa), anti‐PSD95 (ab238135, 80 kDa), anti‐Synapsin I (ab254349, 74 kDa), and anti‐SYP (ab32127, 34 kDa) antibodies from Abcam; anti‐AMPKα (2532S, 62 kDa) and anti‐phospho‐AMPKα (Thr172, 2535S, 62 kDa) antibodies from CST, followed by incubation with the secondary antibodies (ZSGB‐BIO).

    Techniques: Expressing