anti kir2 1  (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 anti kir2 1
    A. Gross appearance of cardiomyocyte induction by CSA. Six days after the Flk1 + cell culture on OP9 cells (Flk-d6). cTnT staining (brown). Left panel: control. Right panel: CSA treatment. Scale bars = 400 µm. B. Quantitative evaluation of cardiomyocyte induction by fluorescent intensity of cTnT staining. Relative fluorescent intensity is indicated (n = 4, †, p<0.001 vs control). C. Representative action potential of iPSC-derived spontaneously beating cardiomyocytes. D. Sarcomeric organization in TMRM-purified cardiomyocytes at Flk-d8. Immunostaining with anti-sarcomeric α-actinin antibody (red) and DAPI (blue). Right panel shows higher magnification of boxed area. Scale bar = 25 µm. E–H. Double immunostaining of TMRM-purified cardiomyocytes at Flk-d8 for connexin43 (Cx43) (green) and cTnT (orange) (E), Cav3.2 (green) and cTnT (orange) (F), HCN4 (green) and cTnT (orange) (G), <t>Kir2.1</t> (green) and cTnT (orange) (H). Nuclei are visualized with DAPI. Scale bars = 25 µm. I. FACS analysis for cardiac progenitor induction from mouse iPSCs by CSA. X axis: CXCR4. Y axis: Flk1. Percentages of FCV cardiac progenitor cells (double positive population; red boxes) in total Flk1 + cell progenies are indicated.
    Anti Kir2 1, 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/anti kir2 1/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti kir2 1 - by Bioz Stars, 2023-01
    94/100 stars

    Images

    1) Product Images from "Induction and Enhancement of Cardiac Cell Differentiation from Mouse and Human Induced Pluripotent Stem Cells with Cyclosporin-A"

    Article Title: Induction and Enhancement of Cardiac Cell Differentiation from Mouse and Human Induced Pluripotent Stem Cells with Cyclosporin-A

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0016734

    A. Gross appearance of cardiomyocyte induction by CSA. Six days after the Flk1 + cell culture on OP9 cells (Flk-d6). cTnT staining (brown). Left panel: control. Right panel: CSA treatment. Scale bars = 400 µm. B. Quantitative evaluation of cardiomyocyte induction by fluorescent intensity of cTnT staining. Relative fluorescent intensity is indicated (n = 4, †, p<0.001 vs control). C. Representative action potential of iPSC-derived spontaneously beating cardiomyocytes. D. Sarcomeric organization in TMRM-purified cardiomyocytes at Flk-d8. Immunostaining with anti-sarcomeric α-actinin antibody (red) and DAPI (blue). Right panel shows higher magnification of boxed area. Scale bar = 25 µm. E–H. Double immunostaining of TMRM-purified cardiomyocytes at Flk-d8 for connexin43 (Cx43) (green) and cTnT (orange) (E), Cav3.2 (green) and cTnT (orange) (F), HCN4 (green) and cTnT (orange) (G), Kir2.1 (green) and cTnT (orange) (H). Nuclei are visualized with DAPI. Scale bars = 25 µm. I. FACS analysis for cardiac progenitor induction from mouse iPSCs by CSA. X axis: CXCR4. Y axis: Flk1. Percentages of FCV cardiac progenitor cells (double positive population; red boxes) in total Flk1 + cell progenies are indicated.
    Figure Legend Snippet: A. Gross appearance of cardiomyocyte induction by CSA. Six days after the Flk1 + cell culture on OP9 cells (Flk-d6). cTnT staining (brown). Left panel: control. Right panel: CSA treatment. Scale bars = 400 µm. B. Quantitative evaluation of cardiomyocyte induction by fluorescent intensity of cTnT staining. Relative fluorescent intensity is indicated (n = 4, †, p<0.001 vs control). C. Representative action potential of iPSC-derived spontaneously beating cardiomyocytes. D. Sarcomeric organization in TMRM-purified cardiomyocytes at Flk-d8. Immunostaining with anti-sarcomeric α-actinin antibody (red) and DAPI (blue). Right panel shows higher magnification of boxed area. Scale bar = 25 µm. E–H. Double immunostaining of TMRM-purified cardiomyocytes at Flk-d8 for connexin43 (Cx43) (green) and cTnT (orange) (E), Cav3.2 (green) and cTnT (orange) (F), HCN4 (green) and cTnT (orange) (G), Kir2.1 (green) and cTnT (orange) (H). Nuclei are visualized with DAPI. Scale bars = 25 µm. I. FACS analysis for cardiac progenitor induction from mouse iPSCs by CSA. X axis: CXCR4. Y axis: Flk1. Percentages of FCV cardiac progenitor cells (double positive population; red boxes) in total Flk1 + cell progenies are indicated.

    Techniques Used: Cell Culture, Staining, Derivative Assay, Purification, Immunostaining, Double Immunostaining

    anti kir2 1  (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 anti kir2 1
    A. Gross appearance of cardiomyocyte induction by CSA. Six days after the Flk1 + cell culture on OP9 cells (Flk-d6). cTnT staining (brown). Left panel: control. Right panel: CSA treatment. Scale bars = 400 µm. B. Quantitative evaluation of cardiomyocyte induction by fluorescent intensity of cTnT staining. Relative fluorescent intensity is indicated (n = 4, †, p<0.001 vs control). C. Representative action potential of iPSC-derived spontaneously beating cardiomyocytes. D. Sarcomeric organization in TMRM-purified cardiomyocytes at Flk-d8. Immunostaining with anti-sarcomeric α-actinin antibody (red) and DAPI (blue). Right panel shows higher magnification of boxed area. Scale bar = 25 µm. E–H. Double immunostaining of TMRM-purified cardiomyocytes at Flk-d8 for connexin43 (Cx43) (green) and cTnT (orange) (E), Cav3.2 (green) and cTnT (orange) (F), HCN4 (green) and cTnT (orange) (G), <t>Kir2.1</t> (green) and cTnT (orange) (H). Nuclei are visualized with DAPI. Scale bars = 25 µm. I. FACS analysis for cardiac progenitor induction from mouse iPSCs by CSA. X axis: CXCR4. Y axis: Flk1. Percentages of FCV cardiac progenitor cells (double positive population; red boxes) in total Flk1 + cell progenies are indicated.
    Anti Kir2 1, 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/anti kir2 1/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti kir2 1 - by Bioz Stars, 2023-01
    94/100 stars

    Images

    1) Product Images from "Induction and Enhancement of Cardiac Cell Differentiation from Mouse and Human Induced Pluripotent Stem Cells with Cyclosporin-A"

    Article Title: Induction and Enhancement of Cardiac Cell Differentiation from Mouse and Human Induced Pluripotent Stem Cells with Cyclosporin-A

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0016734

    A. Gross appearance of cardiomyocyte induction by CSA. Six days after the Flk1 + cell culture on OP9 cells (Flk-d6). cTnT staining (brown). Left panel: control. Right panel: CSA treatment. Scale bars = 400 µm. B. Quantitative evaluation of cardiomyocyte induction by fluorescent intensity of cTnT staining. Relative fluorescent intensity is indicated (n = 4, †, p<0.001 vs control). C. Representative action potential of iPSC-derived spontaneously beating cardiomyocytes. D. Sarcomeric organization in TMRM-purified cardiomyocytes at Flk-d8. Immunostaining with anti-sarcomeric α-actinin antibody (red) and DAPI (blue). Right panel shows higher magnification of boxed area. Scale bar = 25 µm. E–H. Double immunostaining of TMRM-purified cardiomyocytes at Flk-d8 for connexin43 (Cx43) (green) and cTnT (orange) (E), Cav3.2 (green) and cTnT (orange) (F), HCN4 (green) and cTnT (orange) (G), Kir2.1 (green) and cTnT (orange) (H). Nuclei are visualized with DAPI. Scale bars = 25 µm. I. FACS analysis for cardiac progenitor induction from mouse iPSCs by CSA. X axis: CXCR4. Y axis: Flk1. Percentages of FCV cardiac progenitor cells (double positive population; red boxes) in total Flk1 + cell progenies are indicated.
    Figure Legend Snippet: A. Gross appearance of cardiomyocyte induction by CSA. Six days after the Flk1 + cell culture on OP9 cells (Flk-d6). cTnT staining (brown). Left panel: control. Right panel: CSA treatment. Scale bars = 400 µm. B. Quantitative evaluation of cardiomyocyte induction by fluorescent intensity of cTnT staining. Relative fluorescent intensity is indicated (n = 4, †, p<0.001 vs control). C. Representative action potential of iPSC-derived spontaneously beating cardiomyocytes. D. Sarcomeric organization in TMRM-purified cardiomyocytes at Flk-d8. Immunostaining with anti-sarcomeric α-actinin antibody (red) and DAPI (blue). Right panel shows higher magnification of boxed area. Scale bar = 25 µm. E–H. Double immunostaining of TMRM-purified cardiomyocytes at Flk-d8 for connexin43 (Cx43) (green) and cTnT (orange) (E), Cav3.2 (green) and cTnT (orange) (F), HCN4 (green) and cTnT (orange) (G), Kir2.1 (green) and cTnT (orange) (H). Nuclei are visualized with DAPI. Scale bars = 25 µm. I. FACS analysis for cardiac progenitor induction from mouse iPSCs by CSA. X axis: CXCR4. Y axis: Flk1. Percentages of FCV cardiac progenitor cells (double positive population; red boxes) in total Flk1 + cell progenies are indicated.

    Techniques Used: Cell Culture, Staining, Derivative Assay, Purification, Immunostaining, Double Immunostaining

    rabbit polyclonal antibody against kir2 1  (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 rabbit polyclonal antibody against kir2 1
    Myoblasts were transfected with either control siRNA or siEGFR. A . Percentages of transfected myoblasts with functional <t>Kir2.1</t> channels, 48 hours post-transfection. B. Current densities of the total population of myoblasts (including myoblasts with no current, i.e. <5 pA). C. Current-voltage relationships of a myoblast transfected with siEGFR. Voltage-steps were to −40, −60, −80, −100, −120 and −140 mV from a holding potential at −60 mV. The inset shows a control myoblast with no Kir2.1 current, a typical Kir2.1 current recorded from a myoblast, 48 h after transfection with siEGFR. Addition of 500 µM Ba 2+ inhibited this current. D. Myoblasts were first transfected with control siRNA or siEGFR, and 24 h later with a plasmid coding for GFP-Kir2.1. One day after, immunoprecipitation of GFP was performed. Immunoblots reveal Kir2.1 and phospho-tyrosine (P-Tyr). E . Cytoplasmic Ca 2+ was assessed with Fura-2-AM on proliferating myoblasts, 2 days after siRNA transfection. Intracellular Ca 2+ stores were depleted with 10 µM thapsigargin (Tg) in a medium containing 250 nM Ca 2+ . Then 1.8 mM Ca 2+ was subsequently added to reveal SOCE. The first part of the experiment was performed with a medium containing 30 mM KCl in order to clamp cells at around −40 mV. The second part was performed with a medium containing 5 mM KCl allowing cells to hyperpolarize. F . Quantification of peak SOCE (n = 6; * p<0.05).
    Rabbit Polyclonal Antibody Against Kir2 1, 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/rabbit polyclonal antibody against kir2 1/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit polyclonal antibody against kir2 1 - by Bioz Stars, 2023-01
    94/100 stars

    Images

    1) Product Images from "Epidermal Growth Factor Receptor Down-Regulation Triggers Human Myoblast Differentiation"

    Article Title: Epidermal Growth Factor Receptor Down-Regulation Triggers Human Myoblast Differentiation

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0071770

    Myoblasts were transfected with either control siRNA or siEGFR. A . Percentages of transfected myoblasts with functional Kir2.1 channels, 48 hours post-transfection. B. Current densities of the total population of myoblasts (including myoblasts with no current, i.e. <5 pA). C. Current-voltage relationships of a myoblast transfected with siEGFR. Voltage-steps were to −40, −60, −80, −100, −120 and −140 mV from a holding potential at −60 mV. The inset shows a control myoblast with no Kir2.1 current, a typical Kir2.1 current recorded from a myoblast, 48 h after transfection with siEGFR. Addition of 500 µM Ba 2+ inhibited this current. D. Myoblasts were first transfected with control siRNA or siEGFR, and 24 h later with a plasmid coding for GFP-Kir2.1. One day after, immunoprecipitation of GFP was performed. Immunoblots reveal Kir2.1 and phospho-tyrosine (P-Tyr). E . Cytoplasmic Ca 2+ was assessed with Fura-2-AM on proliferating myoblasts, 2 days after siRNA transfection. Intracellular Ca 2+ stores were depleted with 10 µM thapsigargin (Tg) in a medium containing 250 nM Ca 2+ . Then 1.8 mM Ca 2+ was subsequently added to reveal SOCE. The first part of the experiment was performed with a medium containing 30 mM KCl in order to clamp cells at around −40 mV. The second part was performed with a medium containing 5 mM KCl allowing cells to hyperpolarize. F . Quantification of peak SOCE (n = 6; * p<0.05).
    Figure Legend Snippet: Myoblasts were transfected with either control siRNA or siEGFR. A . Percentages of transfected myoblasts with functional Kir2.1 channels, 48 hours post-transfection. B. Current densities of the total population of myoblasts (including myoblasts with no current, i.e. <5 pA). C. Current-voltage relationships of a myoblast transfected with siEGFR. Voltage-steps were to −40, −60, −80, −100, −120 and −140 mV from a holding potential at −60 mV. The inset shows a control myoblast with no Kir2.1 current, a typical Kir2.1 current recorded from a myoblast, 48 h after transfection with siEGFR. Addition of 500 µM Ba 2+ inhibited this current. D. Myoblasts were first transfected with control siRNA or siEGFR, and 24 h later with a plasmid coding for GFP-Kir2.1. One day after, immunoprecipitation of GFP was performed. Immunoblots reveal Kir2.1 and phospho-tyrosine (P-Tyr). E . Cytoplasmic Ca 2+ was assessed with Fura-2-AM on proliferating myoblasts, 2 days after siRNA transfection. Intracellular Ca 2+ stores were depleted with 10 µM thapsigargin (Tg) in a medium containing 250 nM Ca 2+ . Then 1.8 mM Ca 2+ was subsequently added to reveal SOCE. The first part of the experiment was performed with a medium containing 30 mM KCl in order to clamp cells at around −40 mV. The second part was performed with a medium containing 5 mM KCl allowing cells to hyperpolarize. F . Quantification of peak SOCE (n = 6; * p<0.05).

    Techniques Used: Transfection, Functional Assay, Plasmid Preparation, Immunoprecipitation, Western Blot

    anti kir2 1 antibody  (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 anti kir2 1 antibody
    <t>I</t> <t>K1</t> in wt and dystrophic ventricular cardiomyocytes. (A) Typical original potassium current traces of a wt, mdx, and mdx-utr cardiomyocyte elicited from a holding potential of −100 mV by 500-ms steps to various voltages (the pulse protocol is shown in the inset of <xref ref-type=Fig. 1B ). The dashed line indicates the zero current level. (B) Current density-voltage relationships derived from a series of experiments as shown in Fig. 1A (n = 38 for wt, 36 for mdx, and 13 for mdx-utr, respectively). The current levels at the end of the test pulse were evaluated and plotted against the applied voltages. The lines through the data points represent fits with the function: y = Y0/(1 + exp((x-V05)/k)). (C) Current density values at −100 mV (means ± SEM) are compared between wt and dystrophic (mdx and mdx-utr) cardiomyocytes. *** indicates that ANOVA revealed a highly significant difference between the tested groups (p < 0.001). (D) Current density values at −100 mV of wt and dystrophic cardiomyocytes from all experiments on female (♀) mice (n = 14 for wt, 15 for mdx, and 13 for mdx-utr). ** p < 0.01, ANOVA. E : Current density values at −100 mV of wt and mdx cardiomyocytes from all experiments on male (♂) mice (n = 24 for wt and 21 for mdx). * p < 0.05 (p = 0.011), Student's t-test. " width="250" height="auto" />
    Anti Kir2 1 Antibody, 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/anti kir2 1 antibody/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti kir2 1 antibody - by Bioz Stars, 2023-01
    94/100 stars

    Images

    1) Product Images from "Decreased inward rectifier potassium current I K1 in dystrophin-deficient ventricular cardiomyocytes"

    Article Title: Decreased inward rectifier potassium current I K1 in dystrophin-deficient ventricular cardiomyocytes

    Journal: Channels

    doi: 10.1080/19336950.2016.1228498

    I K1 in wt and dystrophic ventricular cardiomyocytes. (A) Typical original potassium current traces of a wt, mdx, and mdx-utr cardiomyocyte elicited from a holding potential of −100 mV by 500-ms steps to various voltages (the pulse protocol is shown in the inset of <xref ref-type=Fig. 1B ). The dashed line indicates the zero current level. (B) Current density-voltage relationships derived from a series of experiments as shown in Fig. 1A (n = 38 for wt, 36 for mdx, and 13 for mdx-utr, respectively). The current levels at the end of the test pulse were evaluated and plotted against the applied voltages. The lines through the data points represent fits with the function: y = Y0/(1 + exp((x-V05)/k)). (C) Current density values at −100 mV (means ± SEM) are compared between wt and dystrophic (mdx and mdx-utr) cardiomyocytes. *** indicates that ANOVA revealed a highly significant difference between the tested groups (p < 0.001). (D) Current density values at −100 mV of wt and dystrophic cardiomyocytes from all experiments on female (♀) mice (n = 14 for wt, 15 for mdx, and 13 for mdx-utr). ** p < 0.01, ANOVA. E : Current density values at −100 mV of wt and mdx cardiomyocytes from all experiments on male (♂) mice (n = 24 for wt and 21 for mdx). * p < 0.05 (p = 0.011), Student's t-test. " title="I K1 in wt and dystrophic ventricular cardiomyocytes. (A) ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: I K1 in wt and dystrophic ventricular cardiomyocytes. (A) Typical original potassium current traces of a wt, mdx, and mdx-utr cardiomyocyte elicited from a holding potential of −100 mV by 500-ms steps to various voltages (the pulse protocol is shown in the inset of Fig. 1B ). The dashed line indicates the zero current level. (B) Current density-voltage relationships derived from a series of experiments as shown in Fig. 1A (n = 38 for wt, 36 for mdx, and 13 for mdx-utr, respectively). The current levels at the end of the test pulse were evaluated and plotted against the applied voltages. The lines through the data points represent fits with the function: y = Y0/(1 + exp((x-V05)/k)). (C) Current density values at −100 mV (means ± SEM) are compared between wt and dystrophic (mdx and mdx-utr) cardiomyocytes. *** indicates that ANOVA revealed a highly significant difference between the tested groups (p < 0.001). (D) Current density values at −100 mV of wt and dystrophic cardiomyocytes from all experiments on female (♀) mice (n = 14 for wt, 15 for mdx, and 13 for mdx-utr). ** p < 0.01, ANOVA. E : Current density values at −100 mV of wt and mdx cardiomyocytes from all experiments on male (♂) mice (n = 24 for wt and 21 for mdx). * p < 0.05 (p = 0.011), Student's t-test.

    Techniques Used: Derivative Assay

    Kir2.1 protein exparession and localization in wt and dystrophic ventricular cardiomyocytes. (A) Representative western blot experiment of membrane lysates from adult wt and dystrophic (mdx and mdx-utr) ventricular tissues stained for Kir2.1 and the β-subunit of a G s protein (AS7). The latter was used as loading control. (B) Relative band intensities of Kir2.1 normalized to the respective band intensities of the loading control plotted as means ± SEM for wt (n = 5) and dystrophic (mdx, n = 6; mdx-utr, n = 2) animals. A Student's t-test did not reveal a significant difference between wt and mdx (p = 0.11; n.s., not significant). (C) Typical examples of Kir2.1 immunostainings of an isolated wt (left) and mdx (right) cardiomyocyte.
    Figure Legend Snippet: Kir2.1 protein exparession and localization in wt and dystrophic ventricular cardiomyocytes. (A) Representative western blot experiment of membrane lysates from adult wt and dystrophic (mdx and mdx-utr) ventricular tissues stained for Kir2.1 and the β-subunit of a G s protein (AS7). The latter was used as loading control. (B) Relative band intensities of Kir2.1 normalized to the respective band intensities of the loading control plotted as means ± SEM for wt (n = 5) and dystrophic (mdx, n = 6; mdx-utr, n = 2) animals. A Student's t-test did not reveal a significant difference between wt and mdx (p = 0.11; n.s., not significant). (C) Typical examples of Kir2.1 immunostainings of an isolated wt (left) and mdx (right) cardiomyocyte.

    Techniques Used: Western Blot, Staining, Isolation

    kir2 1  (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 kir2 1
    Kir2 1, 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/kir2 1/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    kir2 1 - by Bioz Stars, 2023-01
    94/100 stars

    Images

    rabbit polyclonal primary antibodies against k ir 2 1  (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 rabbit polyclonal primary antibodies against k ir 2 1
    Genetic ablation of K IR 2.1 does not eliminate inward K + currents in cerebral arterial smooth muscle cells (SMCs). Whole-cell patch clamp electrophysiology was used to measure K IR current with voltage ramps from −100 to +20 mV in the absence and presence of Ba 2+ in 60 mM K + . (a,b) Representative recordings of whole-cell and Ba 2+ -subtracted K IR currents in myocytes isolated from SMC K IR 2.1 −/− mice and non-induced Cre SMC controls. (c) Summary data compare peak inward current at −100 mV between groups ( n = 9 SMCs from 6 mice in control group and n = 9 SMCs from 8 mice in knockout group; nested t -test).
    Rabbit Polyclonal Primary Antibodies Against K Ir 2 1, 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/rabbit polyclonal primary antibodies against k ir 2 1/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit polyclonal primary antibodies against k ir 2 1 - by Bioz Stars, 2023-01
    94/100 stars

    Images

    1) Product Images from "Genetic ablation of smooth muscle K IR 2.1 is inconsequential to the function of mouse cerebral arteries"

    Article Title: Genetic ablation of smooth muscle K IR 2.1 is inconsequential to the function of mouse cerebral arteries

    Journal: Journal of Cerebral Blood Flow & Metabolism

    doi: 10.1177/0271678X221093432

    Genetic ablation of K IR 2.1 does not eliminate inward K + currents in cerebral arterial smooth muscle cells (SMCs). Whole-cell patch clamp electrophysiology was used to measure K IR current with voltage ramps from −100 to +20 mV in the absence and presence of Ba 2+ in 60 mM K + . (a,b) Representative recordings of whole-cell and Ba 2+ -subtracted K IR currents in myocytes isolated from SMC K IR 2.1 −/− mice and non-induced Cre SMC controls. (c) Summary data compare peak inward current at −100 mV between groups ( n = 9 SMCs from 6 mice in control group and n = 9 SMCs from 8 mice in knockout group; nested t -test).
    Figure Legend Snippet: Genetic ablation of K IR 2.1 does not eliminate inward K + currents in cerebral arterial smooth muscle cells (SMCs). Whole-cell patch clamp electrophysiology was used to measure K IR current with voltage ramps from −100 to +20 mV in the absence and presence of Ba 2+ in 60 mM K + . (a,b) Representative recordings of whole-cell and Ba 2+ -subtracted K IR currents in myocytes isolated from SMC K IR 2.1 −/− mice and non-induced Cre SMC controls. (c) Summary data compare peak inward current at −100 mV between groups ( n = 9 SMCs from 6 mice in control group and n = 9 SMCs from 8 mice in knockout group; nested t -test).

    Techniques Used: Patch Clamp, Isolation, Knock-Out

    K I R 2.1 is negligibly expressed in cerebral vascular smooth muscle cells (SMCs) while K IR 2.2 is highly expressed at the cell membrane. Tamoxifen-induced K IR 2.1 knockout significantly reduced subunit expression but levels remained detectable by immunofluorescence. (a) Fluorescent anti-K IR 2.1 (green) exhibited a faint labeling pattern in cerebral arterial myocytes from SMC K IR 2.1 −/− and control mice with nuclei stained with DAPI (blue). (b) Summary of data compares fluorescence intensity (background subtracted) of K IR 2.1 signal between groups ( n = 10 cells from 5 animals in control group and n = 9 cells from 5 animals in knockout group; unpaired t -test). (c) Immunofluorescence labeling of SMCs for K IR 2.2. (d) Summary of data compares background-subtracted fluorescence intensity of K IR 2.2 signal between groups ( n = 8 cells pooled from 4 animals/group; unpaired t -test). Two cells were analyzed per animal with background signal subtracted using 2° antibody control.
    Figure Legend Snippet: K I R 2.1 is negligibly expressed in cerebral vascular smooth muscle cells (SMCs) while K IR 2.2 is highly expressed at the cell membrane. Tamoxifen-induced K IR 2.1 knockout significantly reduced subunit expression but levels remained detectable by immunofluorescence. (a) Fluorescent anti-K IR 2.1 (green) exhibited a faint labeling pattern in cerebral arterial myocytes from SMC K IR 2.1 −/− and control mice with nuclei stained with DAPI (blue). (b) Summary of data compares fluorescence intensity (background subtracted) of K IR 2.1 signal between groups ( n = 10 cells from 5 animals in control group and n = 9 cells from 5 animals in knockout group; unpaired t -test). (c) Immunofluorescence labeling of SMCs for K IR 2.2. (d) Summary of data compares background-subtracted fluorescence intensity of K IR 2.2 signal between groups ( n = 8 cells pooled from 4 animals/group; unpaired t -test). Two cells were analyzed per animal with background signal subtracted using 2° antibody control.

    Techniques Used: Knock-Out, Expressing, Immunofluorescence, Labeling, Staining, Fluorescence

    K IR 2.2 protein expression is unaltered in smooth muscle cell (SMC) K IR 2.1 −/− cerebral arteries. (a) Western blot of intact cerebral arteries confirmed that protein levels of K IR 2.2 are not impacted by deletion of SMC K IR 2.1. (b) Summary of data compares K IR 2.2 protein levels between control and knockout mice (normalized to actin; n = 6 mice; unpaired t -test).
    Figure Legend Snippet: K IR 2.2 protein expression is unaltered in smooth muscle cell (SMC) K IR 2.1 −/− cerebral arteries. (a) Western blot of intact cerebral arteries confirmed that protein levels of K IR 2.2 are not impacted by deletion of SMC K IR 2.1. (b) Summary of data compares K IR 2.2 protein levels between control and knockout mice (normalized to actin; n = 6 mice; unpaired t -test).

    Techniques Used: Expressing, Western Blot, Knock-Out

    K IR 2.1 and K IR 2.2 subunits are inversely expressed in cerebral endothelial and vascular smooth muscle cells. (a) K IR 2.1 and (b) K IR 2.2 subunit expression is shown as average cellular transcript counts per cell, as determined by single-cell RNA sequencing of the mouse brain vasculature. Data highlight differences in the dominant subunit between cell types. Abbreviations: PC – pericytes; SMC – smooth muscle cells; EC – endothelial cells; v – venous; c – capillary; a – arterial; aa – arteriolar. Figures provided by http://betsholtzlab.org/VascularSingleCells/database.html . 33,34
    Figure Legend Snippet: K IR 2.1 and K IR 2.2 subunits are inversely expressed in cerebral endothelial and vascular smooth muscle cells. (a) K IR 2.1 and (b) K IR 2.2 subunit expression is shown as average cellular transcript counts per cell, as determined by single-cell RNA sequencing of the mouse brain vasculature. Data highlight differences in the dominant subunit between cell types. Abbreviations: PC – pericytes; SMC – smooth muscle cells; EC – endothelial cells; v – venous; c – capillary; a – arterial; aa – arteriolar. Figures provided by http://betsholtzlab.org/VascularSingleCells/database.html . 33,34

    Techniques Used: Expressing, RNA Sequencing Assay

    Myogenic responses and K + -induced dilation are intact in cerebral arteries of smooth muscle cell (SMC) K IR 2.1 −/− mice. Cerebral arteries from control and SMC K IR 2.1 −/− mice were cannulated and intravascular pressure was elevated stepwise while vasomotor responses were measured. (a) Representative diameter traces from endothelium-denuded vessels of control and SMC K IR 2.1 −/− mice show the effect of increasing pressure on myogenic tone. (b) Summary of data highlights limited impact of smooth muscle K IR 2.1 knockout on myogenic tone development. Paired t -test was performed for 0 vs. 100 μM Ba 2+ treatment ( n = 10 vessels in the control group and n = 11 vessels in the SMC K IR 2.1 −/− group with 1 vessel/mouse; *P < 0.05). (c) K + -induced dilation, elicited by increasing extracellular K + from 5 mM to 10 mM before and after treatment with 100-μM Ba 2+ , was intact in the knockout group ( n = 6 vessels in the control group and SMC K IR 2.1 −/− group; one-way ANOVA with Sidak’s multiple comparisons test). (d) K + -induced dilation (5 mM K + to 10 mM K + ) was abrogated with exposure to low concentrations of Ba 2+ , implicating K IR 2.2 as the mediator of this response based on its Ba 2+ sensitivity profile ( n = 7 vessels from control mice; repeated measures one-way ANOVA with Sidak’s multiple comparisons test). Myogenic tone (%) was calculated as: [(passive diameter – active diameter)/(passive diameter – minimal diameter)] × 100 at each pressure step. K + -induced dilation (%) was calculated as difference between diameter at 10 mM [K + ] and 5 mM [K + ] divided by the dilatory range (passive diameter – minimal diameter).
    Figure Legend Snippet: Myogenic responses and K + -induced dilation are intact in cerebral arteries of smooth muscle cell (SMC) K IR 2.1 −/− mice. Cerebral arteries from control and SMC K IR 2.1 −/− mice were cannulated and intravascular pressure was elevated stepwise while vasomotor responses were measured. (a) Representative diameter traces from endothelium-denuded vessels of control and SMC K IR 2.1 −/− mice show the effect of increasing pressure on myogenic tone. (b) Summary of data highlights limited impact of smooth muscle K IR 2.1 knockout on myogenic tone development. Paired t -test was performed for 0 vs. 100 μM Ba 2+ treatment ( n = 10 vessels in the control group and n = 11 vessels in the SMC K IR 2.1 −/− group with 1 vessel/mouse; *P < 0.05). (c) K + -induced dilation, elicited by increasing extracellular K + from 5 mM to 10 mM before and after treatment with 100-μM Ba 2+ , was intact in the knockout group ( n = 6 vessels in the control group and SMC K IR 2.1 −/− group; one-way ANOVA with Sidak’s multiple comparisons test). (d) K + -induced dilation (5 mM K + to 10 mM K + ) was abrogated with exposure to low concentrations of Ba 2+ , implicating K IR 2.2 as the mediator of this response based on its Ba 2+ sensitivity profile ( n = 7 vessels from control mice; repeated measures one-way ANOVA with Sidak’s multiple comparisons test). Myogenic tone (%) was calculated as: [(passive diameter – active diameter)/(passive diameter – minimal diameter)] × 100 at each pressure step. K + -induced dilation (%) was calculated as difference between diameter at 10 mM [K + ] and 5 mM [K + ] divided by the dilatory range (passive diameter – minimal diameter).

    Techniques Used: Knock-Out

    Region-specific brain perfusion is not altered in smooth muscle cell (SMC) K IR 2.1 −/− mice at rest and with increased systemic blood pressure. (a) Representative arterial spin-labeled MR brain perfusion maps. Scans were done in a posterior-to-anterior direction and the volume of brain scanned was divided into 5 coronal slices. Resting cerebral blood flow was measured in control and SMC K IR 2.1 −/− mice. Scans were repeated after blood pressure challenge with an intraperitoneal phenylephrine injection. Figure shows slices from 2 regions of the brain (red boxes) spanning cerebral nuclei, hippocampus, thalamus, and hypothalamus. (b) Baseline perfusion in several major brain structures was not significantly different between control and tamoxifen-induced mice. The blood pressure challenge caused a modest but significant rise in cerebral blood flow to a similar extent in control and SMC K IR 2.1 −/− animals. Unpaired t -test was performed for control ( n = 7 mice) vs. SMC K IR 2.1 −/− ( n = 11 mice) comparison; paired t -test was performed for baseline vs. phenylephrine-treatment. *P < 0.05 compared to baseline control.
    Figure Legend Snippet: Region-specific brain perfusion is not altered in smooth muscle cell (SMC) K IR 2.1 −/− mice at rest and with increased systemic blood pressure. (a) Representative arterial spin-labeled MR brain perfusion maps. Scans were done in a posterior-to-anterior direction and the volume of brain scanned was divided into 5 coronal slices. Resting cerebral blood flow was measured in control and SMC K IR 2.1 −/− mice. Scans were repeated after blood pressure challenge with an intraperitoneal phenylephrine injection. Figure shows slices from 2 regions of the brain (red boxes) spanning cerebral nuclei, hippocampus, thalamus, and hypothalamus. (b) Baseline perfusion in several major brain structures was not significantly different between control and tamoxifen-induced mice. The blood pressure challenge caused a modest but significant rise in cerebral blood flow to a similar extent in control and SMC K IR 2.1 −/− animals. Unpaired t -test was performed for control ( n = 7 mice) vs. SMC K IR 2.1 −/− ( n = 11 mice) comparison; paired t -test was performed for baseline vs. phenylephrine-treatment. *P < 0.05 compared to baseline control.

    Techniques Used: Labeling, Injection

    kir2 1  (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 kir2 1
    ( a ) Representative AP trace of ventricular-like control BJ iPSC-CMs obtained at 1 Hz of pacing. Inset . First derivative with respect to time (dV/dt). ( b–f) Action potential properties. Recordings at 1 and 2 Hz were similar to those obtained from the healthy donor patient derived-iPSC-CMs (Control 1). ( g-i) Current traces, I/V curves, and normalized current densities for NaV1.5, CaV1.2, and <t>Kir2.1</t> ion channels, respectively. Data obtained from the control BJ iPSC-CMs (Control 2) were similar to the other control iPSC-CMs.
    Kir2 1, 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/kir2 1/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    kir2 1 - by Bioz Stars, 2023-01
    94/100 stars

    Images

    1) Product Images from "SNTA1 Gene Rescues Ion Channel Function in Cardiomyocytes Derived from Induced Pluripotent Stem Cells Reprogrammed from Muscular Dystrophy Patients with Arrhythmias"

    Article Title: SNTA1 Gene Rescues Ion Channel Function in Cardiomyocytes Derived from Induced Pluripotent Stem Cells Reprogrammed from Muscular Dystrophy Patients with Arrhythmias

    Journal: bioRxiv

    doi: 10.1101/2022.01.25.477696

    ( a ) Representative AP trace of ventricular-like control BJ iPSC-CMs obtained at 1 Hz of pacing. Inset . First derivative with respect to time (dV/dt). ( b–f) Action potential properties. Recordings at 1 and 2 Hz were similar to those obtained from the healthy donor patient derived-iPSC-CMs (Control 1). ( g-i) Current traces, I/V curves, and normalized current densities for NaV1.5, CaV1.2, and Kir2.1 ion channels, respectively. Data obtained from the control BJ iPSC-CMs (Control 2) were similar to the other control iPSC-CMs.
    Figure Legend Snippet: ( a ) Representative AP trace of ventricular-like control BJ iPSC-CMs obtained at 1 Hz of pacing. Inset . First derivative with respect to time (dV/dt). ( b–f) Action potential properties. Recordings at 1 and 2 Hz were similar to those obtained from the healthy donor patient derived-iPSC-CMs (Control 1). ( g-i) Current traces, I/V curves, and normalized current densities for NaV1.5, CaV1.2, and Kir2.1 ion channels, respectively. Data obtained from the control BJ iPSC-CMs (Control 2) were similar to the other control iPSC-CMs.

    Techniques Used: Derivative Assay

    (a) Superimposed I Na current traces for Control 1, hemizygous and heterozygous iPSC-CMs elicited by the pulse protocol shown by the inset. (b) Left , normalized current-voltage (I/V) relationships. I Na was significantly reduced in both Male 1 and Male 2 iPSC-CMs compared with control at the specified voltages. Heterozygous female iPSC-CMs showed also a very reduced current density from 35 to 10 mV. Two-way analysis of variance (ANOVA) followed by Sidak’s multiple comparisons test. Right, peak I Na density at 20 mV was reduced in all three affected groups compared to control. (c) Typical I K1 density traces from control and DMD cells elicited by the pulse protocol in the inset . (d) Left , I/V relationships. I K1 was significantly reduced in both Male 1 and Male 2 iPSC-CMs compared with control at the specified voltages. Two-way ANOVA followed by Sidak’s multiple comparisons. Right, normalized current densities at -120 mV. I K1 was decreased in Male 1 and in Male 2 cells compared to control cells. Two-tailed Mann-Whitney test. Errors bars represent SEM. The n -values are in parentheses. ****P < 0.0001, ** P < 0.005 and * P < 0.05 and *P < 0.056.
    Figure Legend Snippet: (a) Superimposed I Na current traces for Control 1, hemizygous and heterozygous iPSC-CMs elicited by the pulse protocol shown by the inset. (b) Left , normalized current-voltage (I/V) relationships. I Na was significantly reduced in both Male 1 and Male 2 iPSC-CMs compared with control at the specified voltages. Heterozygous female iPSC-CMs showed also a very reduced current density from 35 to 10 mV. Two-way analysis of variance (ANOVA) followed by Sidak’s multiple comparisons test. Right, peak I Na density at 20 mV was reduced in all three affected groups compared to control. (c) Typical I K1 density traces from control and DMD cells elicited by the pulse protocol in the inset . (d) Left , I/V relationships. I K1 was significantly reduced in both Male 1 and Male 2 iPSC-CMs compared with control at the specified voltages. Two-way ANOVA followed by Sidak’s multiple comparisons. Right, normalized current densities at -120 mV. I K1 was decreased in Male 1 and in Male 2 cells compared to control cells. Two-tailed Mann-Whitney test. Errors bars represent SEM. The n -values are in parentheses. ****P < 0.0001, ** P < 0.005 and * P < 0.05 and *P < 0.056.

    Techniques Used: Two Tailed Test, MANN-WHITNEY

    (a) Representative Western blot for each antibody used. The bands within the blue rectangles at ∼250 KDa and below 50 KDa correspond to NaV1.5 and Kir2.1, respectively. About 50K cells were collected to quantify total NaV1.5, Kir2.1 and actinin levels in control, heterozygous and hemizygous DMD cells. (b) Scatter plots of NaV1.5 and Kir2.1 detected in control, female and DMD iPSC-CMs. NaV1.5 and Kir2.1 protein levels were normalized to actinin (loading control). (c) Representative Western blot after biotinylation and protein precipitation with streptavidin magnetic beads. (d) Scatter plots of biotinylated NaV1.5 and Kir2.1 from control, female , and DMD iPSC-CMs. Fifty μg of biotinylated protein was loaded. Errors bars represent SEM. The n -values are in parentheses. Two-tailed Mann-Whitney test. *** P < 0.001, ** P < 0.01, and * P < 0.05
    Figure Legend Snippet: (a) Representative Western blot for each antibody used. The bands within the blue rectangles at ∼250 KDa and below 50 KDa correspond to NaV1.5 and Kir2.1, respectively. About 50K cells were collected to quantify total NaV1.5, Kir2.1 and actinin levels in control, heterozygous and hemizygous DMD cells. (b) Scatter plots of NaV1.5 and Kir2.1 detected in control, female and DMD iPSC-CMs. NaV1.5 and Kir2.1 protein levels were normalized to actinin (loading control). (c) Representative Western blot after biotinylation and protein precipitation with streptavidin magnetic beads. (d) Scatter plots of biotinylated NaV1.5 and Kir2.1 from control, female , and DMD iPSC-CMs. Fifty μg of biotinylated protein was loaded. Errors bars represent SEM. The n -values are in parentheses. Two-tailed Mann-Whitney test. *** P < 0.001, ** P < 0.01, and * P < 0.05

    Techniques Used: Western Blot, Magnetic Beads, Two Tailed Test, MANN-WHITNEY

    (a) Cartoon illustrating non-viral piggy-bac vector encoding SNTA1 for transfection in Male 1 iPSC-CMs. SNTA1 coding region (CDS) is driven by the CAG promoter and followed by green fluorescence protein (GFP) after an internal ribosome entry site (IRES). Control vector only expresses GFP. (b) Western blot for α-1-Syntrophin expression normalized with GAPDH. (c) Immunostaining for Kir2.1 (red), Na V 1.5 (white) and WGA (green) in control Male 1 iPSC-CM (left) and Male 1 iPSC-CM transfected with SNTA1 . Nuclei were stained with DAPI. Yellow arrows point to iPSC-CM membrane staining. Scale bar, 5 μm. (d) Quantification of Kir2.1 and Na V 1.5 colocalization with WGA at the cell membrane shows significant increase of both Kir2.1 ( *P < 0.05; n = 7–10 cells) and Na V 1.5 ( ** P < 0.01; n = 7–10 cells).
    Figure Legend Snippet: (a) Cartoon illustrating non-viral piggy-bac vector encoding SNTA1 for transfection in Male 1 iPSC-CMs. SNTA1 coding region (CDS) is driven by the CAG promoter and followed by green fluorescence protein (GFP) after an internal ribosome entry site (IRES). Control vector only expresses GFP. (b) Western blot for α-1-Syntrophin expression normalized with GAPDH. (c) Immunostaining for Kir2.1 (red), Na V 1.5 (white) and WGA (green) in control Male 1 iPSC-CM (left) and Male 1 iPSC-CM transfected with SNTA1 . Nuclei were stained with DAPI. Yellow arrows point to iPSC-CM membrane staining. Scale bar, 5 μm. (d) Quantification of Kir2.1 and Na V 1.5 colocalization with WGA at the cell membrane shows significant increase of both Kir2.1 ( *P < 0.05; n = 7–10 cells) and Na V 1.5 ( ** P < 0.01; n = 7–10 cells).

    Techniques Used: Plasmid Preparation, Transfection, Fluorescence, Western Blot, Expressing, Immunostaining, Staining

    (a–b) Normalized current-voltage (I/V) relationships for I Na and I K1 in Male 1 before (black) and after (red) syntrophin expression at the specified voltages. Two-way analysis of variance (ANOVA) followed by Sidak’s multiple comparisons test. Graphs show peak I Na density at -20 mV (a) and peak I K1 density at -120 mV (b) . The inset in B highlights the increased outward component of I K1 at less negative potentials upon syntrophin expression. Two-tailed Mann-Whitney test. (c) Effect of syntrophin expression on AP showing: i) Averaged (left) and representative (right) action potential traces of ventricular-like iPSC-cardiomyocytes derived from DMD cells before (black) and after (red) syntrophin expression, ii) maximal AP upstroke velocity (dV/dt max ), iii) Amplitude, iv) Overshoot, v) MDP and vi) APD 90 . Errors bars represent SEM. The n -values are in parentheses. * P < 0.05; ** P < 0.01; and *** P < 0.001.
    Figure Legend Snippet: (a–b) Normalized current-voltage (I/V) relationships for I Na and I K1 in Male 1 before (black) and after (red) syntrophin expression at the specified voltages. Two-way analysis of variance (ANOVA) followed by Sidak’s multiple comparisons test. Graphs show peak I Na density at -20 mV (a) and peak I K1 density at -120 mV (b) . The inset in B highlights the increased outward component of I K1 at less negative potentials upon syntrophin expression. Two-tailed Mann-Whitney test. (c) Effect of syntrophin expression on AP showing: i) Averaged (left) and representative (right) action potential traces of ventricular-like iPSC-cardiomyocytes derived from DMD cells before (black) and after (red) syntrophin expression, ii) maximal AP upstroke velocity (dV/dt max ), iii) Amplitude, iv) Overshoot, v) MDP and vi) APD 90 . Errors bars represent SEM. The n -values are in parentheses. * P < 0.05; ** P < 0.01; and *** P < 0.001.

    Techniques Used: Expressing, Two Tailed Test, MANN-WHITNEY, Derivative Assay

    anti kir2 1  (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 anti kir2 1
    Inwardly rectifying potassium current ( <t>I</t> <t>K1</t> ) and corresponding <t>Kir2.1</t> protein in 3wRbCMs. (A) Western blot of Kir2.1, inwardly rectifying channel subunit in freshly isolated, 48 h cultured, non-transduced, and 48 h cultured, GFP transduced cells. (B) Quantification of the western blots ( N = 4) shows significant downregulation of total Kir2.1 protein during 48 h of culturing with and without GFP transduction compared to freshly isolated cells. (C) Representative I K1 traces in a freshly isolated 3wRbCM. Voltage clamp protocol is shown in the insert. (D) Cumulative I K1 I–V curves of freshly isolated, 48 h cultured, non-transduced, and 48 h cultured, GFP-transduced cells. The symbol ** corresponds to p < 0.01.
    Anti Kir2 1, 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/anti kir2 1/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti kir2 1 - by Bioz Stars, 2023-01
    94/100 stars

    Images

    1) Product Images from "Three-Week-Old Rabbit Ventricular Cardiomyocytes as a Novel System to Study Cardiac Excitation and EC Coupling"

    Article Title: Three-Week-Old Rabbit Ventricular Cardiomyocytes as a Novel System to Study Cardiac Excitation and EC Coupling

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2021.672360

    Inwardly rectifying potassium current ( I K1 ) and corresponding Kir2.1 protein in 3wRbCMs. (A) Western blot of Kir2.1, inwardly rectifying channel subunit in freshly isolated, 48 h cultured, non-transduced, and 48 h cultured, GFP transduced cells. (B) Quantification of the western blots ( N = 4) shows significant downregulation of total Kir2.1 protein during 48 h of culturing with and without GFP transduction compared to freshly isolated cells. (C) Representative I K1 traces in a freshly isolated 3wRbCM. Voltage clamp protocol is shown in the insert. (D) Cumulative I K1 I–V curves of freshly isolated, 48 h cultured, non-transduced, and 48 h cultured, GFP-transduced cells. The symbol ** corresponds to p < 0.01.
    Figure Legend Snippet: Inwardly rectifying potassium current ( I K1 ) and corresponding Kir2.1 protein in 3wRbCMs. (A) Western blot of Kir2.1, inwardly rectifying channel subunit in freshly isolated, 48 h cultured, non-transduced, and 48 h cultured, GFP transduced cells. (B) Quantification of the western blots ( N = 4) shows significant downregulation of total Kir2.1 protein during 48 h of culturing with and without GFP transduction compared to freshly isolated cells. (C) Representative I K1 traces in a freshly isolated 3wRbCM. Voltage clamp protocol is shown in the insert. (D) Cumulative I K1 I–V curves of freshly isolated, 48 h cultured, non-transduced, and 48 h cultured, GFP-transduced cells. The symbol ** corresponds to p < 0.01.

    Techniques Used: Western Blot, Isolation, Cell Culture, Transduction

    anti kir2 1 extracellular  (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
  • 93

    Structured Review

    Alomone Labs anti kir2 1 extracellular
    Anti Kir2 1 Extracellular, 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/anti kir2 1 extracellular/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti kir2 1 extracellular - by Bioz Stars, 2023-01
    93/100 stars

    Images

    anti kir2 1 intracellular  (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 anti kir2 1 intracellular
    Anti Kir2 1 Intracellular, 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/anti kir2 1 intracellular/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti kir2 1 intracellular - by Bioz Stars, 2023-01
    94/100 stars

    Images

    kir2 1  (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 kir2 1
    Effects of FGF21 on Na + channel ( I Na ) and K + channel ( <t>I</t> <t>K1</t> ) currents of AC16 human cardiomyocytes. (A, B) The current density-voltage relationships curves of whole-cell sodium current ( I Na ) and potassium current ( I K1 ) were recorded in AC16 cells treatment with H 2 O 2 and H 2 O 2 +rhbFGF21. * p < 0.05 vs. Control. (C) Exemplar superimposed traces of APD recorded from myocytes, and comparison of average data of APD (F) , APD 50 (G) , and APD 90 (H) measured AC16 human cardiomyocytes from Control, rhbFGF21, H 2 O 2 , and H 2 O 2 +rhbFGF21. One-way ANOVA with Tukey’s multiple comparisons test was used to compare the difference between multiple groups, * p < 0.05; ** p < 0.01. (D, E) The APA and RMP of AC16 cells from Control, rhbFGF21, H 2 O 2 , and H 2 O 2 +rhbFGF21 group recorded by patch-clamp technique. n = 3–7, ** p < 0.01.
    Kir2 1, 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/kir2 1/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    kir2 1 - by Bioz Stars, 2023-01
    94/100 stars

    Images

    1) Product Images from "Fibroblast Growth Factor 21 Ameliorates Na V 1.5 and Kir2.1 Channel Dysregulation in Human AC16 Cardiomyocytes"

    Article Title: Fibroblast Growth Factor 21 Ameliorates Na V 1.5 and Kir2.1 Channel Dysregulation in Human AC16 Cardiomyocytes

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2021.715466

    Effects of FGF21 on Na + channel ( I Na ) and K + channel ( I K1 ) currents of AC16 human cardiomyocytes. (A, B) The current density-voltage relationships curves of whole-cell sodium current ( I Na ) and potassium current ( I K1 ) were recorded in AC16 cells treatment with H 2 O 2 and H 2 O 2 +rhbFGF21. * p < 0.05 vs. Control. (C) Exemplar superimposed traces of APD recorded from myocytes, and comparison of average data of APD (F) , APD 50 (G) , and APD 90 (H) measured AC16 human cardiomyocytes from Control, rhbFGF21, H 2 O 2 , and H 2 O 2 +rhbFGF21. One-way ANOVA with Tukey’s multiple comparisons test was used to compare the difference between multiple groups, * p < 0.05; ** p < 0.01. (D, E) The APA and RMP of AC16 cells from Control, rhbFGF21, H 2 O 2 , and H 2 O 2 +rhbFGF21 group recorded by patch-clamp technique. n = 3–7, ** p < 0.01.
    Figure Legend Snippet: Effects of FGF21 on Na + channel ( I Na ) and K + channel ( I K1 ) currents of AC16 human cardiomyocytes. (A, B) The current density-voltage relationships curves of whole-cell sodium current ( I Na ) and potassium current ( I K1 ) were recorded in AC16 cells treatment with H 2 O 2 and H 2 O 2 +rhbFGF21. * p < 0.05 vs. Control. (C) Exemplar superimposed traces of APD recorded from myocytes, and comparison of average data of APD (F) , APD 50 (G) , and APD 90 (H) measured AC16 human cardiomyocytes from Control, rhbFGF21, H 2 O 2 , and H 2 O 2 +rhbFGF21. One-way ANOVA with Tukey’s multiple comparisons test was used to compare the difference between multiple groups, * p < 0.05; ** p < 0.01. (D, E) The APA and RMP of AC16 cells from Control, rhbFGF21, H 2 O 2 , and H 2 O 2 +rhbFGF21 group recorded by patch-clamp technique. n = 3–7, ** p < 0.01.

    Techniques Used: Patch Clamp

    Effects of FGF21 on Na V 1.5 and Kir2.1 expression in human AC16 cells. (A) Protein level of Na V 1.5 and Kir2.1 in AC16 human cardiomyocytes treatment with H 2 O 2 (100 μmol) for 6 h, n = 3–4 batches of cells, * p < 0.05; ** p < 0.01. Analysis by one-way ANOVA, mean ± SEM. (B) Immunofluorescence staining of Na V 1.5 and Kir2.1 expression in AC16 human cardiomyocytes treatment with H 2 O 2 . * p < 0.05; ** p < 0.01. Analysis by one-way ANOVA, mean ± SEM. Scale bar indicates 100 μm.
    Figure Legend Snippet: Effects of FGF21 on Na V 1.5 and Kir2.1 expression in human AC16 cells. (A) Protein level of Na V 1.5 and Kir2.1 in AC16 human cardiomyocytes treatment with H 2 O 2 (100 μmol) for 6 h, n = 3–4 batches of cells, * p < 0.05; ** p < 0.01. Analysis by one-way ANOVA, mean ± SEM. (B) Immunofluorescence staining of Na V 1.5 and Kir2.1 expression in AC16 human cardiomyocytes treatment with H 2 O 2 . * p < 0.05; ** p < 0.01. Analysis by one-way ANOVA, mean ± SEM. Scale bar indicates 100 μm.

    Techniques Used: Expressing, Immunofluorescence, Staining

    Effect of FGFR on Na V 1.5 and Kir2.1 expression. (A) Protein level of Na V 1.5 and Kir2.1 in AC16 human cardiomyocytes in Control, H 2 O 2 , H 2 O 2 +rhbFGF21, and H 2 O 2 +rhbFGF21 + TKI258 group, n = 4 batches of cells, * p < 0.05; ** p < 0.01. Analysis by one-way ANOVA, mean ± SEM. (B) Immunofluorescence staining of Na V 1.5 and Kir2.1 expression in AC16 human cardiomyocytes in each group. * p < 0.05; ** p < 0.01. Analysis by one-way ANOVA, mean ± SEM. Scale bar indicates 100 μm.
    Figure Legend Snippet: Effect of FGFR on Na V 1.5 and Kir2.1 expression. (A) Protein level of Na V 1.5 and Kir2.1 in AC16 human cardiomyocytes in Control, H 2 O 2 , H 2 O 2 +rhbFGF21, and H 2 O 2 +rhbFGF21 + TKI258 group, n = 4 batches of cells, * p < 0.05; ** p < 0.01. Analysis by one-way ANOVA, mean ± SEM. (B) Immunofluorescence staining of Na V 1.5 and Kir2.1 expression in AC16 human cardiomyocytes in each group. * p < 0.05; ** p < 0.01. Analysis by one-way ANOVA, mean ± SEM. Scale bar indicates 100 μm.

    Techniques Used: Expressing, Immunofluorescence, Staining

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 94
    Alomone Labs anti kir2 1
    A. Gross appearance of cardiomyocyte induction by CSA. Six days after the Flk1 + cell culture on OP9 cells (Flk-d6). cTnT staining (brown). Left panel: control. Right panel: CSA treatment. Scale bars = 400 µm. B. Quantitative evaluation of cardiomyocyte induction by fluorescent intensity of cTnT staining. Relative fluorescent intensity is indicated (n = 4, †, p<0.001 vs control). C. Representative action potential of iPSC-derived spontaneously beating cardiomyocytes. D. Sarcomeric organization in TMRM-purified cardiomyocytes at Flk-d8. Immunostaining with anti-sarcomeric α-actinin antibody (red) and DAPI (blue). Right panel shows higher magnification of boxed area. Scale bar = 25 µm. E–H. Double immunostaining of TMRM-purified cardiomyocytes at Flk-d8 for connexin43 (Cx43) (green) and cTnT (orange) (E), Cav3.2 (green) and cTnT (orange) (F), HCN4 (green) and cTnT (orange) (G), <t>Kir2.1</t> (green) and cTnT (orange) (H). Nuclei are visualized with DAPI. Scale bars = 25 µm. I. FACS analysis for cardiac progenitor induction from mouse iPSCs by CSA. X axis: CXCR4. Y axis: Flk1. Percentages of FCV cardiac progenitor cells (double positive population; red boxes) in total Flk1 + cell progenies are indicated.
    Anti Kir2 1, 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/anti kir2 1/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti kir2 1 - by Bioz Stars, 2023-01
    94/100 stars
      Buy from Supplier

    94
    Alomone Labs rabbit polyclonal antibody against kir2 1
    Myoblasts were transfected with either control siRNA or siEGFR. A . Percentages of transfected myoblasts with functional <t>Kir2.1</t> channels, 48 hours post-transfection. B. Current densities of the total population of myoblasts (including myoblasts with no current, i.e. <5 pA). C. Current-voltage relationships of a myoblast transfected with siEGFR. Voltage-steps were to −40, −60, −80, −100, −120 and −140 mV from a holding potential at −60 mV. The inset shows a control myoblast with no Kir2.1 current, a typical Kir2.1 current recorded from a myoblast, 48 h after transfection with siEGFR. Addition of 500 µM Ba 2+ inhibited this current. D. Myoblasts were first transfected with control siRNA or siEGFR, and 24 h later with a plasmid coding for GFP-Kir2.1. One day after, immunoprecipitation of GFP was performed. Immunoblots reveal Kir2.1 and phospho-tyrosine (P-Tyr). E . Cytoplasmic Ca 2+ was assessed with Fura-2-AM on proliferating myoblasts, 2 days after siRNA transfection. Intracellular Ca 2+ stores were depleted with 10 µM thapsigargin (Tg) in a medium containing 250 nM Ca 2+ . Then 1.8 mM Ca 2+ was subsequently added to reveal SOCE. The first part of the experiment was performed with a medium containing 30 mM KCl in order to clamp cells at around −40 mV. The second part was performed with a medium containing 5 mM KCl allowing cells to hyperpolarize. F . Quantification of peak SOCE (n = 6; * p<0.05).
    Rabbit Polyclonal Antibody Against Kir2 1, 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/rabbit polyclonal antibody against kir2 1/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit polyclonal antibody against kir2 1 - by Bioz Stars, 2023-01
    94/100 stars
      Buy from Supplier

    94
      Buy from Supplier


    94
    Alomone Labs rabbit polyclonal primary antibodies against k ir 2 1
    Genetic ablation of K IR 2.1 does not eliminate inward K + currents in cerebral arterial smooth muscle cells (SMCs). Whole-cell patch clamp electrophysiology was used to measure K IR current with voltage ramps from −100 to +20 mV in the absence and presence of Ba 2+ in 60 mM K + . (a,b) Representative recordings of whole-cell and Ba 2+ -subtracted K IR currents in myocytes isolated from SMC K IR 2.1 −/− mice and non-induced Cre SMC controls. (c) Summary data compare peak inward current at −100 mV between groups ( n = 9 SMCs from 6 mice in control group and n = 9 SMCs from 8 mice in knockout group; nested t -test).
    Rabbit Polyclonal Primary Antibodies Against K Ir 2 1, 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/rabbit polyclonal primary antibodies against k ir 2 1/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit polyclonal primary antibodies against k ir 2 1 - by Bioz Stars, 2023-01
    94/100 stars
      Buy from Supplier

    93
    Alomone Labs anti kir2 1 extracellular
    Genetic ablation of K IR 2.1 does not eliminate inward K + currents in cerebral arterial smooth muscle cells (SMCs). Whole-cell patch clamp electrophysiology was used to measure K IR current with voltage ramps from −100 to +20 mV in the absence and presence of Ba 2+ in 60 mM K + . (a,b) Representative recordings of whole-cell and Ba 2+ -subtracted K IR currents in myocytes isolated from SMC K IR 2.1 −/− mice and non-induced Cre SMC controls. (c) Summary data compare peak inward current at −100 mV between groups ( n = 9 SMCs from 6 mice in control group and n = 9 SMCs from 8 mice in knockout group; nested t -test).
    Anti Kir2 1 Extracellular, 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/anti kir2 1 extracellular/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti kir2 1 extracellular - by Bioz Stars, 2023-01
    93/100 stars
      Buy from Supplier

    94
    Alomone Labs anti kir2 1 intracellular
    Genetic ablation of K IR 2.1 does not eliminate inward K + currents in cerebral arterial smooth muscle cells (SMCs). Whole-cell patch clamp electrophysiology was used to measure K IR current with voltage ramps from −100 to +20 mV in the absence and presence of Ba 2+ in 60 mM K + . (a,b) Representative recordings of whole-cell and Ba 2+ -subtracted K IR currents in myocytes isolated from SMC K IR 2.1 −/− mice and non-induced Cre SMC controls. (c) Summary data compare peak inward current at −100 mV between groups ( n = 9 SMCs from 6 mice in control group and n = 9 SMCs from 8 mice in knockout group; nested t -test).
    Anti Kir2 1 Intracellular, 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/anti kir2 1 intracellular/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti kir2 1 intracellular - by Bioz Stars, 2023-01
    94/100 stars
      Buy from Supplier

    Image Search Results


    A. Gross appearance of cardiomyocyte induction by CSA. Six days after the Flk1 + cell culture on OP9 cells (Flk-d6). cTnT staining (brown). Left panel: control. Right panel: CSA treatment. Scale bars = 400 µm. B. Quantitative evaluation of cardiomyocyte induction by fluorescent intensity of cTnT staining. Relative fluorescent intensity is indicated (n = 4, †, p<0.001 vs control). C. Representative action potential of iPSC-derived spontaneously beating cardiomyocytes. D. Sarcomeric organization in TMRM-purified cardiomyocytes at Flk-d8. Immunostaining with anti-sarcomeric α-actinin antibody (red) and DAPI (blue). Right panel shows higher magnification of boxed area. Scale bar = 25 µm. E–H. Double immunostaining of TMRM-purified cardiomyocytes at Flk-d8 for connexin43 (Cx43) (green) and cTnT (orange) (E), Cav3.2 (green) and cTnT (orange) (F), HCN4 (green) and cTnT (orange) (G), Kir2.1 (green) and cTnT (orange) (H). Nuclei are visualized with DAPI. Scale bars = 25 µm. I. FACS analysis for cardiac progenitor induction from mouse iPSCs by CSA. X axis: CXCR4. Y axis: Flk1. Percentages of FCV cardiac progenitor cells (double positive population; red boxes) in total Flk1 + cell progenies are indicated.

    Journal: PLoS ONE

    Article Title: Induction and Enhancement of Cardiac Cell Differentiation from Mouse and Human Induced Pluripotent Stem Cells with Cyclosporin-A

    doi: 10.1371/journal.pone.0016734

    Figure Lengend Snippet: A. Gross appearance of cardiomyocyte induction by CSA. Six days after the Flk1 + cell culture on OP9 cells (Flk-d6). cTnT staining (brown). Left panel: control. Right panel: CSA treatment. Scale bars = 400 µm. B. Quantitative evaluation of cardiomyocyte induction by fluorescent intensity of cTnT staining. Relative fluorescent intensity is indicated (n = 4, †, p<0.001 vs control). C. Representative action potential of iPSC-derived spontaneously beating cardiomyocytes. D. Sarcomeric organization in TMRM-purified cardiomyocytes at Flk-d8. Immunostaining with anti-sarcomeric α-actinin antibody (red) and DAPI (blue). Right panel shows higher magnification of boxed area. Scale bar = 25 µm. E–H. Double immunostaining of TMRM-purified cardiomyocytes at Flk-d8 for connexin43 (Cx43) (green) and cTnT (orange) (E), Cav3.2 (green) and cTnT (orange) (F), HCN4 (green) and cTnT (orange) (G), Kir2.1 (green) and cTnT (orange) (H). Nuclei are visualized with DAPI. Scale bars = 25 µm. I. FACS analysis for cardiac progenitor induction from mouse iPSCs by CSA. X axis: CXCR4. Y axis: Flk1. Percentages of FCV cardiac progenitor cells (double positive population; red boxes) in total Flk1 + cell progenies are indicated.

    Article Snippet: Anti-Kir2.1 (1∶200) and anti-connexin 43 (1∶200) antibodies were from Alomone (Israel) and Invitrogen (Carlsbad, CA), respectively.

    Techniques: Cell Culture, Staining, Derivative Assay, Purification, Immunostaining, Double Immunostaining

    Myoblasts were transfected with either control siRNA or siEGFR. A . Percentages of transfected myoblasts with functional Kir2.1 channels, 48 hours post-transfection. B. Current densities of the total population of myoblasts (including myoblasts with no current, i.e. <5 pA). C. Current-voltage relationships of a myoblast transfected with siEGFR. Voltage-steps were to −40, −60, −80, −100, −120 and −140 mV from a holding potential at −60 mV. The inset shows a control myoblast with no Kir2.1 current, a typical Kir2.1 current recorded from a myoblast, 48 h after transfection with siEGFR. Addition of 500 µM Ba 2+ inhibited this current. D. Myoblasts were first transfected with control siRNA or siEGFR, and 24 h later with a plasmid coding for GFP-Kir2.1. One day after, immunoprecipitation of GFP was performed. Immunoblots reveal Kir2.1 and phospho-tyrosine (P-Tyr). E . Cytoplasmic Ca 2+ was assessed with Fura-2-AM on proliferating myoblasts, 2 days after siRNA transfection. Intracellular Ca 2+ stores were depleted with 10 µM thapsigargin (Tg) in a medium containing 250 nM Ca 2+ . Then 1.8 mM Ca 2+ was subsequently added to reveal SOCE. The first part of the experiment was performed with a medium containing 30 mM KCl in order to clamp cells at around −40 mV. The second part was performed with a medium containing 5 mM KCl allowing cells to hyperpolarize. F . Quantification of peak SOCE (n = 6; * p<0.05).

    Journal: PLoS ONE

    Article Title: Epidermal Growth Factor Receptor Down-Regulation Triggers Human Myoblast Differentiation

    doi: 10.1371/journal.pone.0071770

    Figure Lengend Snippet: Myoblasts were transfected with either control siRNA or siEGFR. A . Percentages of transfected myoblasts with functional Kir2.1 channels, 48 hours post-transfection. B. Current densities of the total population of myoblasts (including myoblasts with no current, i.e. <5 pA). C. Current-voltage relationships of a myoblast transfected with siEGFR. Voltage-steps were to −40, −60, −80, −100, −120 and −140 mV from a holding potential at −60 mV. The inset shows a control myoblast with no Kir2.1 current, a typical Kir2.1 current recorded from a myoblast, 48 h after transfection with siEGFR. Addition of 500 µM Ba 2+ inhibited this current. D. Myoblasts were first transfected with control siRNA or siEGFR, and 24 h later with a plasmid coding for GFP-Kir2.1. One day after, immunoprecipitation of GFP was performed. Immunoblots reveal Kir2.1 and phospho-tyrosine (P-Tyr). E . Cytoplasmic Ca 2+ was assessed with Fura-2-AM on proliferating myoblasts, 2 days after siRNA transfection. Intracellular Ca 2+ stores were depleted with 10 µM thapsigargin (Tg) in a medium containing 250 nM Ca 2+ . Then 1.8 mM Ca 2+ was subsequently added to reveal SOCE. The first part of the experiment was performed with a medium containing 30 mM KCl in order to clamp cells at around −40 mV. The second part was performed with a medium containing 5 mM KCl allowing cells to hyperpolarize. F . Quantification of peak SOCE (n = 6; * p<0.05).

    Article Snippet: Blots were incubated with the primary antibodies diluted in 5% non-fat milk or 5% BSA TBST as follows: rabbit monoclonal antibody against EGFR (1∶1500; D38B1 XP®, or 1∶1000; 15F8, Cell Signaling), rabbit polyclonal antibody against MEF2 (1∶3000; sc-313, Santa Cruz Biotechnology), mouse polyclonal antibody against Myogenin (1∶3000; clone F5D, BD Biosciences), mouse monoclonal antibody against α-Tubulin (1∶10000; clone DM1A, Sigma), rabbit polyclonal antibody against Kir2.1 (1∶200; Alomone), mouse monoclonal against phospho-tyrosine (1∶3000; P3300, Sigma) and rabbit monoclonal antibody against phospho-p42/44 MAPK (Erk1/2; Thr2027Tyr204; 1∶1500; D13.14.4E XP®, Cell Signaling).

    Techniques: Transfection, Functional Assay, Plasmid Preparation, Immunoprecipitation, Western Blot

    I K1 in wt and dystrophic ventricular cardiomyocytes. (A) Typical original potassium current traces of a wt, mdx, and mdx-utr cardiomyocyte elicited from a holding potential of −100 mV by 500-ms steps to various voltages (the pulse protocol is shown in the inset of <xref ref-type=Fig. 1B ). The dashed line indicates the zero current level. (B) Current density-voltage relationships derived from a series of experiments as shown in Fig. 1A (n = 38 for wt, 36 for mdx, and 13 for mdx-utr, respectively). The current levels at the end of the test pulse were evaluated and plotted against the applied voltages. The lines through the data points represent fits with the function: y = Y0/(1 + exp((x-V05)/k)). (C) Current density values at −100 mV (means ± SEM) are compared between wt and dystrophic (mdx and mdx-utr) cardiomyocytes. *** indicates that ANOVA revealed a highly significant difference between the tested groups (p < 0.001). (D) Current density values at −100 mV of wt and dystrophic cardiomyocytes from all experiments on female (♀) mice (n = 14 for wt, 15 for mdx, and 13 for mdx-utr). ** p < 0.01, ANOVA. E : Current density values at −100 mV of wt and mdx cardiomyocytes from all experiments on male (♂) mice (n = 24 for wt and 21 for mdx). * p < 0.05 (p = 0.011), Student's t-test. " width="100%" height="100%">

    Journal: Channels

    Article Title: Decreased inward rectifier potassium current I K1 in dystrophin-deficient ventricular cardiomyocytes

    doi: 10.1080/19336950.2016.1228498

    Figure Lengend Snippet: I K1 in wt and dystrophic ventricular cardiomyocytes. (A) Typical original potassium current traces of a wt, mdx, and mdx-utr cardiomyocyte elicited from a holding potential of −100 mV by 500-ms steps to various voltages (the pulse protocol is shown in the inset of Fig. 1B ). The dashed line indicates the zero current level. (B) Current density-voltage relationships derived from a series of experiments as shown in Fig. 1A (n = 38 for wt, 36 for mdx, and 13 for mdx-utr, respectively). The current levels at the end of the test pulse were evaluated and plotted against the applied voltages. The lines through the data points represent fits with the function: y = Y0/(1 + exp((x-V05)/k)). (C) Current density values at −100 mV (means ± SEM) are compared between wt and dystrophic (mdx and mdx-utr) cardiomyocytes. *** indicates that ANOVA revealed a highly significant difference between the tested groups (p < 0.001). (D) Current density values at −100 mV of wt and dystrophic cardiomyocytes from all experiments on female (♀) mice (n = 14 for wt, 15 for mdx, and 13 for mdx-utr). ** p < 0.01, ANOVA. E : Current density values at −100 mV of wt and mdx cardiomyocytes from all experiments on male (♂) mice (n = 24 for wt and 21 for mdx). * p < 0.05 (p = 0.011), Student's t-test.

    Article Snippet: Thereafter, the cells were incubated with Anti-Kir2.1 antibody (APC-026, Alomone Labs; 1:500 in PBS) at 4°C overnight.

    Techniques: Derivative Assay

    Kir2.1 protein exparession and localization in wt and dystrophic ventricular cardiomyocytes. (A) Representative western blot experiment of membrane lysates from adult wt and dystrophic (mdx and mdx-utr) ventricular tissues stained for Kir2.1 and the β-subunit of a G s protein (AS7). The latter was used as loading control. (B) Relative band intensities of Kir2.1 normalized to the respective band intensities of the loading control plotted as means ± SEM for wt (n = 5) and dystrophic (mdx, n = 6; mdx-utr, n = 2) animals. A Student's t-test did not reveal a significant difference between wt and mdx (p = 0.11; n.s., not significant). (C) Typical examples of Kir2.1 immunostainings of an isolated wt (left) and mdx (right) cardiomyocyte.

    Journal: Channels

    Article Title: Decreased inward rectifier potassium current I K1 in dystrophin-deficient ventricular cardiomyocytes

    doi: 10.1080/19336950.2016.1228498

    Figure Lengend Snippet: Kir2.1 protein exparession and localization in wt and dystrophic ventricular cardiomyocytes. (A) Representative western blot experiment of membrane lysates from adult wt and dystrophic (mdx and mdx-utr) ventricular tissues stained for Kir2.1 and the β-subunit of a G s protein (AS7). The latter was used as loading control. (B) Relative band intensities of Kir2.1 normalized to the respective band intensities of the loading control plotted as means ± SEM for wt (n = 5) and dystrophic (mdx, n = 6; mdx-utr, n = 2) animals. A Student's t-test did not reveal a significant difference between wt and mdx (p = 0.11; n.s., not significant). (C) Typical examples of Kir2.1 immunostainings of an isolated wt (left) and mdx (right) cardiomyocyte.

    Article Snippet: Thereafter, the cells were incubated with Anti-Kir2.1 antibody (APC-026, Alomone Labs; 1:500 in PBS) at 4°C overnight.

    Techniques: Western Blot, Staining, Isolation

    Genetic ablation of K IR 2.1 does not eliminate inward K + currents in cerebral arterial smooth muscle cells (SMCs). Whole-cell patch clamp electrophysiology was used to measure K IR current with voltage ramps from −100 to +20 mV in the absence and presence of Ba 2+ in 60 mM K + . (a,b) Representative recordings of whole-cell and Ba 2+ -subtracted K IR currents in myocytes isolated from SMC K IR 2.1 −/− mice and non-induced Cre SMC controls. (c) Summary data compare peak inward current at −100 mV between groups ( n = 9 SMCs from 6 mice in control group and n = 9 SMCs from 8 mice in knockout group; nested t -test).

    Journal: Journal of Cerebral Blood Flow & Metabolism

    Article Title: Genetic ablation of smooth muscle K IR 2.1 is inconsequential to the function of mouse cerebral arteries

    doi: 10.1177/0271678X221093432

    Figure Lengend Snippet: Genetic ablation of K IR 2.1 does not eliminate inward K + currents in cerebral arterial smooth muscle cells (SMCs). Whole-cell patch clamp electrophysiology was used to measure K IR current with voltage ramps from −100 to +20 mV in the absence and presence of Ba 2+ in 60 mM K + . (a,b) Representative recordings of whole-cell and Ba 2+ -subtracted K IR currents in myocytes isolated from SMC K IR 2.1 −/− mice and non-induced Cre SMC controls. (c) Summary data compare peak inward current at −100 mV between groups ( n = 9 SMCs from 6 mice in control group and n = 9 SMCs from 8 mice in knockout group; nested t -test).

    Article Snippet: Rabbit polyclonal primary antibodies against K IR 2.1 (APC-026, 1:200; Alomone) and K IR 2.2 (APC-042, 1:200; Alomone) were diluted in quench solution and applied to cells for overnight incubation (4 °C).

    Techniques: Patch Clamp, Isolation, Knock-Out

    K I R 2.1 is negligibly expressed in cerebral vascular smooth muscle cells (SMCs) while K IR 2.2 is highly expressed at the cell membrane. Tamoxifen-induced K IR 2.1 knockout significantly reduced subunit expression but levels remained detectable by immunofluorescence. (a) Fluorescent anti-K IR 2.1 (green) exhibited a faint labeling pattern in cerebral arterial myocytes from SMC K IR 2.1 −/− and control mice with nuclei stained with DAPI (blue). (b) Summary of data compares fluorescence intensity (background subtracted) of K IR 2.1 signal between groups ( n = 10 cells from 5 animals in control group and n = 9 cells from 5 animals in knockout group; unpaired t -test). (c) Immunofluorescence labeling of SMCs for K IR 2.2. (d) Summary of data compares background-subtracted fluorescence intensity of K IR 2.2 signal between groups ( n = 8 cells pooled from 4 animals/group; unpaired t -test). Two cells were analyzed per animal with background signal subtracted using 2° antibody control.

    Journal: Journal of Cerebral Blood Flow & Metabolism

    Article Title: Genetic ablation of smooth muscle K IR 2.1 is inconsequential to the function of mouse cerebral arteries

    doi: 10.1177/0271678X221093432

    Figure Lengend Snippet: K I R 2.1 is negligibly expressed in cerebral vascular smooth muscle cells (SMCs) while K IR 2.2 is highly expressed at the cell membrane. Tamoxifen-induced K IR 2.1 knockout significantly reduced subunit expression but levels remained detectable by immunofluorescence. (a) Fluorescent anti-K IR 2.1 (green) exhibited a faint labeling pattern in cerebral arterial myocytes from SMC K IR 2.1 −/− and control mice with nuclei stained with DAPI (blue). (b) Summary of data compares fluorescence intensity (background subtracted) of K IR 2.1 signal between groups ( n = 10 cells from 5 animals in control group and n = 9 cells from 5 animals in knockout group; unpaired t -test). (c) Immunofluorescence labeling of SMCs for K IR 2.2. (d) Summary of data compares background-subtracted fluorescence intensity of K IR 2.2 signal between groups ( n = 8 cells pooled from 4 animals/group; unpaired t -test). Two cells were analyzed per animal with background signal subtracted using 2° antibody control.

    Article Snippet: Rabbit polyclonal primary antibodies against K IR 2.1 (APC-026, 1:200; Alomone) and K IR 2.2 (APC-042, 1:200; Alomone) were diluted in quench solution and applied to cells for overnight incubation (4 °C).

    Techniques: Knock-Out, Expressing, Immunofluorescence, Labeling, Staining, Fluorescence

    K IR 2.2 protein expression is unaltered in smooth muscle cell (SMC) K IR 2.1 −/− cerebral arteries. (a) Western blot of intact cerebral arteries confirmed that protein levels of K IR 2.2 are not impacted by deletion of SMC K IR 2.1. (b) Summary of data compares K IR 2.2 protein levels between control and knockout mice (normalized to actin; n = 6 mice; unpaired t -test).

    Journal: Journal of Cerebral Blood Flow & Metabolism

    Article Title: Genetic ablation of smooth muscle K IR 2.1 is inconsequential to the function of mouse cerebral arteries

    doi: 10.1177/0271678X221093432

    Figure Lengend Snippet: K IR 2.2 protein expression is unaltered in smooth muscle cell (SMC) K IR 2.1 −/− cerebral arteries. (a) Western blot of intact cerebral arteries confirmed that protein levels of K IR 2.2 are not impacted by deletion of SMC K IR 2.1. (b) Summary of data compares K IR 2.2 protein levels between control and knockout mice (normalized to actin; n = 6 mice; unpaired t -test).

    Article Snippet: Rabbit polyclonal primary antibodies against K IR 2.1 (APC-026, 1:200; Alomone) and K IR 2.2 (APC-042, 1:200; Alomone) were diluted in quench solution and applied to cells for overnight incubation (4 °C).

    Techniques: Expressing, Western Blot, Knock-Out

    K IR 2.1 and K IR 2.2 subunits are inversely expressed in cerebral endothelial and vascular smooth muscle cells. (a) K IR 2.1 and (b) K IR 2.2 subunit expression is shown as average cellular transcript counts per cell, as determined by single-cell RNA sequencing of the mouse brain vasculature. Data highlight differences in the dominant subunit between cell types. Abbreviations: PC – pericytes; SMC – smooth muscle cells; EC – endothelial cells; v – venous; c – capillary; a – arterial; aa – arteriolar. Figures provided by http://betsholtzlab.org/VascularSingleCells/database.html . 33,34

    Journal: Journal of Cerebral Blood Flow & Metabolism

    Article Title: Genetic ablation of smooth muscle K IR 2.1 is inconsequential to the function of mouse cerebral arteries

    doi: 10.1177/0271678X221093432

    Figure Lengend Snippet: K IR 2.1 and K IR 2.2 subunits are inversely expressed in cerebral endothelial and vascular smooth muscle cells. (a) K IR 2.1 and (b) K IR 2.2 subunit expression is shown as average cellular transcript counts per cell, as determined by single-cell RNA sequencing of the mouse brain vasculature. Data highlight differences in the dominant subunit between cell types. Abbreviations: PC – pericytes; SMC – smooth muscle cells; EC – endothelial cells; v – venous; c – capillary; a – arterial; aa – arteriolar. Figures provided by http://betsholtzlab.org/VascularSingleCells/database.html . 33,34

    Article Snippet: Rabbit polyclonal primary antibodies against K IR 2.1 (APC-026, 1:200; Alomone) and K IR 2.2 (APC-042, 1:200; Alomone) were diluted in quench solution and applied to cells for overnight incubation (4 °C).

    Techniques: Expressing, RNA Sequencing Assay

    Myogenic responses and K + -induced dilation are intact in cerebral arteries of smooth muscle cell (SMC) K IR 2.1 −/− mice. Cerebral arteries from control and SMC K IR 2.1 −/− mice were cannulated and intravascular pressure was elevated stepwise while vasomotor responses were measured. (a) Representative diameter traces from endothelium-denuded vessels of control and SMC K IR 2.1 −/− mice show the effect of increasing pressure on myogenic tone. (b) Summary of data highlights limited impact of smooth muscle K IR 2.1 knockout on myogenic tone development. Paired t -test was performed for 0 vs. 100 μM Ba 2+ treatment ( n = 10 vessels in the control group and n = 11 vessels in the SMC K IR 2.1 −/− group with 1 vessel/mouse; *P < 0.05). (c) K + -induced dilation, elicited by increasing extracellular K + from 5 mM to 10 mM before and after treatment with 100-μM Ba 2+ , was intact in the knockout group ( n = 6 vessels in the control group and SMC K IR 2.1 −/− group; one-way ANOVA with Sidak’s multiple comparisons test). (d) K + -induced dilation (5 mM K + to 10 mM K + ) was abrogated with exposure to low concentrations of Ba 2+ , implicating K IR 2.2 as the mediator of this response based on its Ba 2+ sensitivity profile ( n = 7 vessels from control mice; repeated measures one-way ANOVA with Sidak’s multiple comparisons test). Myogenic tone (%) was calculated as: [(passive diameter – active diameter)/(passive diameter – minimal diameter)] × 100 at each pressure step. K + -induced dilation (%) was calculated as difference between diameter at 10 mM [K + ] and 5 mM [K + ] divided by the dilatory range (passive diameter – minimal diameter).

    Journal: Journal of Cerebral Blood Flow & Metabolism

    Article Title: Genetic ablation of smooth muscle K IR 2.1 is inconsequential to the function of mouse cerebral arteries

    doi: 10.1177/0271678X221093432

    Figure Lengend Snippet: Myogenic responses and K + -induced dilation are intact in cerebral arteries of smooth muscle cell (SMC) K IR 2.1 −/− mice. Cerebral arteries from control and SMC K IR 2.1 −/− mice were cannulated and intravascular pressure was elevated stepwise while vasomotor responses were measured. (a) Representative diameter traces from endothelium-denuded vessels of control and SMC K IR 2.1 −/− mice show the effect of increasing pressure on myogenic tone. (b) Summary of data highlights limited impact of smooth muscle K IR 2.1 knockout on myogenic tone development. Paired t -test was performed for 0 vs. 100 μM Ba 2+ treatment ( n = 10 vessels in the control group and n = 11 vessels in the SMC K IR 2.1 −/− group with 1 vessel/mouse; *P < 0.05). (c) K + -induced dilation, elicited by increasing extracellular K + from 5 mM to 10 mM before and after treatment with 100-μM Ba 2+ , was intact in the knockout group ( n = 6 vessels in the control group and SMC K IR 2.1 −/− group; one-way ANOVA with Sidak’s multiple comparisons test). (d) K + -induced dilation (5 mM K + to 10 mM K + ) was abrogated with exposure to low concentrations of Ba 2+ , implicating K IR 2.2 as the mediator of this response based on its Ba 2+ sensitivity profile ( n = 7 vessels from control mice; repeated measures one-way ANOVA with Sidak’s multiple comparisons test). Myogenic tone (%) was calculated as: [(passive diameter – active diameter)/(passive diameter – minimal diameter)] × 100 at each pressure step. K + -induced dilation (%) was calculated as difference between diameter at 10 mM [K + ] and 5 mM [K + ] divided by the dilatory range (passive diameter – minimal diameter).

    Article Snippet: Rabbit polyclonal primary antibodies against K IR 2.1 (APC-026, 1:200; Alomone) and K IR 2.2 (APC-042, 1:200; Alomone) were diluted in quench solution and applied to cells for overnight incubation (4 °C).

    Techniques: Knock-Out

    Region-specific brain perfusion is not altered in smooth muscle cell (SMC) K IR 2.1 −/− mice at rest and with increased systemic blood pressure. (a) Representative arterial spin-labeled MR brain perfusion maps. Scans were done in a posterior-to-anterior direction and the volume of brain scanned was divided into 5 coronal slices. Resting cerebral blood flow was measured in control and SMC K IR 2.1 −/− mice. Scans were repeated after blood pressure challenge with an intraperitoneal phenylephrine injection. Figure shows slices from 2 regions of the brain (red boxes) spanning cerebral nuclei, hippocampus, thalamus, and hypothalamus. (b) Baseline perfusion in several major brain structures was not significantly different between control and tamoxifen-induced mice. The blood pressure challenge caused a modest but significant rise in cerebral blood flow to a similar extent in control and SMC K IR 2.1 −/− animals. Unpaired t -test was performed for control ( n = 7 mice) vs. SMC K IR 2.1 −/− ( n = 11 mice) comparison; paired t -test was performed for baseline vs. phenylephrine-treatment. *P < 0.05 compared to baseline control.

    Journal: Journal of Cerebral Blood Flow & Metabolism

    Article Title: Genetic ablation of smooth muscle K IR 2.1 is inconsequential to the function of mouse cerebral arteries

    doi: 10.1177/0271678X221093432

    Figure Lengend Snippet: Region-specific brain perfusion is not altered in smooth muscle cell (SMC) K IR 2.1 −/− mice at rest and with increased systemic blood pressure. (a) Representative arterial spin-labeled MR brain perfusion maps. Scans were done in a posterior-to-anterior direction and the volume of brain scanned was divided into 5 coronal slices. Resting cerebral blood flow was measured in control and SMC K IR 2.1 −/− mice. Scans were repeated after blood pressure challenge with an intraperitoneal phenylephrine injection. Figure shows slices from 2 regions of the brain (red boxes) spanning cerebral nuclei, hippocampus, thalamus, and hypothalamus. (b) Baseline perfusion in several major brain structures was not significantly different between control and tamoxifen-induced mice. The blood pressure challenge caused a modest but significant rise in cerebral blood flow to a similar extent in control and SMC K IR 2.1 −/− animals. Unpaired t -test was performed for control ( n = 7 mice) vs. SMC K IR 2.1 −/− ( n = 11 mice) comparison; paired t -test was performed for baseline vs. phenylephrine-treatment. *P < 0.05 compared to baseline control.

    Article Snippet: Rabbit polyclonal primary antibodies against K IR 2.1 (APC-026, 1:200; Alomone) and K IR 2.2 (APC-042, 1:200; Alomone) were diluted in quench solution and applied to cells for overnight incubation (4 °C).

    Techniques: Labeling, Injection