anti nav1 5 antibody  (Alomone Labs)


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    Name:
    Guinea pig Anti Nav1 5 SCN5A Antibody
    Description:
    Guinea pig Anti NaV1 5 SCN5A Antibody AGP 008 raised in guinea pigs is a highly specific antibody directed against an epitope of the rat protein The antibody can be used in western blot and immunohistochemistry applications It has been designed to recognize NaV1 5 sodium channel from rat human and mouse samples The antigen used to immunize guinea pigs is the same as Anti NaV1 5 SCN5A 493 511 Antibody ASC 005 raised in rabbit Our line of guinea pig antibodies enables more flexibility with our products such as multiplex staining studies immunoprecipitation etc
    Catalog Number:
    AGP-008
    Price:
    397.0
    Category:
    Primary Antibody
    Applications:
    Immunofluorescence, Immunohistochemistry, Western Blot
    Purity:
    Affinity purified on immobilized antigen.
    Immunogen:
    Synthetic peptide
    Size:
    25 mcl
    Antibody Type:
    Polyclonal Primary Antibodies
    Format:
    Lyophilized Powder
    Host:
    Guinea pig
    Isotype:
    Guinea pig total IgG
    Buy from Supplier


    Structured Review

    Alomone Labs anti nav1 5 antibody
    Guinea pig Anti Nav1 5 SCN5A Antibody
    Guinea pig Anti NaV1 5 SCN5A Antibody AGP 008 raised in guinea pigs is a highly specific antibody directed against an epitope of the rat protein The antibody can be used in western blot and immunohistochemistry applications It has been designed to recognize NaV1 5 sodium channel from rat human and mouse samples The antigen used to immunize guinea pigs is the same as Anti NaV1 5 SCN5A 493 511 Antibody ASC 005 raised in rabbit Our line of guinea pig antibodies enables more flexibility with our products such as multiplex staining studies immunoprecipitation etc
    https://www.bioz.com/result/anti nav1 5 antibody/product/Alomone Labs
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti nav1 5 antibody - by Bioz Stars, 2021-09
    92/100 stars

    Images

    1) Product Images from "Relaxin reverses maladaptive remodeling of the aged heart through Wnt-signaling"

    Article Title: Relaxin reverses maladaptive remodeling of the aged heart through Wnt-signaling

    Journal: Scientific Reports

    doi: 10.1038/s41598-019-53867-y

    Relaxin up-regulates Nav1.5 in LV cardiomyocytes. ( A ) Rat ventricular myocytes treated with increasing concentrations of RLX were fixed and labeled with Nav1.5 Ab. The data show that Nav1.5 fluorescence visibly increases with RLX treatment. ( B ) Dose-response of the ratio of Nav1.5 to phalloidin fluorescence (used for normalization purposes). EC 50 ~1.3 nM, ( n = 6 wells/data point, P
    Figure Legend Snippet: Relaxin up-regulates Nav1.5 in LV cardiomyocytes. ( A ) Rat ventricular myocytes treated with increasing concentrations of RLX were fixed and labeled with Nav1.5 Ab. The data show that Nav1.5 fluorescence visibly increases with RLX treatment. ( B ) Dose-response of the ratio of Nav1.5 to phalloidin fluorescence (used for normalization purposes). EC 50 ~1.3 nM, ( n = 6 wells/data point, P

    Techniques Used: Labeling, Fluorescence

    Relaxin signals through Wnt signaling to increase Nav1.5. ( A ) Less than 10% of untreated myocytes exhibit nuclear β-catenin ( A a,c); however, cells treated with RLX for 24 or 48 hours showed a significant increase in cells positive for nuclear β-catenin ( A b,c). 60x magnification. Data obtained from 3–4 separate preparations, 62–148 cells counted per sample. ( B ) Cells treated with RLX or CHIR, an inhibitor of GSK3β and Wnt pathway activator, significantly increased Nav1.5 by more than 2-fold ( B a–e, n ≥ 8 cells/group). Inhibition of canonical Wnt signaling by DKK1 blocked the effects of RLX 9 n ≥ 24 cells/group) and Wnt1 (n ≥ 17 cells/group) on Nav1.5 expression ( B f–o). 600x magnification, scale bars = 25 µm and apply to all panels. *Indicates p
    Figure Legend Snippet: Relaxin signals through Wnt signaling to increase Nav1.5. ( A ) Less than 10% of untreated myocytes exhibit nuclear β-catenin ( A a,c); however, cells treated with RLX for 24 or 48 hours showed a significant increase in cells positive for nuclear β-catenin ( A b,c). 60x magnification. Data obtained from 3–4 separate preparations, 62–148 cells counted per sample. ( B ) Cells treated with RLX or CHIR, an inhibitor of GSK3β and Wnt pathway activator, significantly increased Nav1.5 by more than 2-fold ( B a–e, n ≥ 8 cells/group). Inhibition of canonical Wnt signaling by DKK1 blocked the effects of RLX 9 n ≥ 24 cells/group) and Wnt1 (n ≥ 17 cells/group) on Nav1.5 expression ( B f–o). 600x magnification, scale bars = 25 µm and apply to all panels. *Indicates p

    Techniques Used: Inhibition, Expressing

    2) Product Images from "An East Asian Common Variant Vinculin P.Asp841His Was Associated With Sudden Unexplained Nocturnal Death Syndrome in the Chinese Han Population"

    Article Title: An East Asian Common Variant Vinculin P.Asp841His Was Associated With Sudden Unexplained Nocturnal Death Syndrome in the Chinese Han Population

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    doi: 10.1161/JAHA.116.005330

    Voltage‐dependent gating for cardiac sodium channel ( SCN 5A) coexpressed with vinculin ( VCL ) in HEK 293 cells. A, Between each group, no significant difference in activation of SCN5A was observed. B, Under pH 7.0, D841H showed a significant repolarizing shift by 3.0 mV in inactivation of SCN5A compared to WT at pH 7.4.
    Figure Legend Snippet: Voltage‐dependent gating for cardiac sodium channel ( SCN 5A) coexpressed with vinculin ( VCL ) in HEK 293 cells. A, Between each group, no significant difference in activation of SCN5A was observed. B, Under pH 7.0, D841H showed a significant repolarizing shift by 3.0 mV in inactivation of SCN5A compared to WT at pH 7.4.

    Techniques Used: Activation Assay

    Electrophysiological properties of cardiac sodium channel (SCN5A) in HEK 293 cells coexpressing SCN 5A and either wild‐type vinculin ( VCL ‐ WT ) or VCL ‐D841H. A, Representative whole‐cell current traces showing peak sodium current ( I N a ) under both normal ( pH 7.4) and acidosis ( pH 7.0) conditions in HEK 293 cells expressing SCN 5A and either WT or variant VCL ‐D841H. B, Summary data of peak I N a densities from every group. The number of tested cells is indicated above the bar. * P
    Figure Legend Snippet: Electrophysiological properties of cardiac sodium channel (SCN5A) in HEK 293 cells coexpressing SCN 5A and either wild‐type vinculin ( VCL ‐ WT ) or VCL ‐D841H. A, Representative whole‐cell current traces showing peak sodium current ( I N a ) under both normal ( pH 7.4) and acidosis ( pH 7.0) conditions in HEK 293 cells expressing SCN 5A and either WT or variant VCL ‐D841H. B, Summary data of peak I N a densities from every group. The number of tested cells is indicated above the bar. * P

    Techniques Used: Expressing, Variant Assay

    3) Product Images from "Vinculin variant M94I identified in sudden unexplained nocturnal death syndrome decreases cardiac sodium current"

    Article Title: Vinculin variant M94I identified in sudden unexplained nocturnal death syndrome decreases cardiac sodium current

    Journal: Scientific Reports

    doi: 10.1038/srep42953

    Co-localization of VCL and SCN5A in human ventricular tissue slice. ( A , B ) Immunofluorescence staining of SCN5A (green), VCL (red) and overlay channel from control and case (SUNDS patient, VCL–M94I variant carrier) human ventricular tissue slices. The second row shows a higher magnification view of the area outlined in yellow the first row. The yellow color from overlay panel indicates co-localization of VCL and SCN5A. ( C and D ) Signal intensity profile of signals from selected areas (outlined with yellow dashed rectangle in second row of ( A and B ) were calculated and plotted from control and case slices respectively. Integrity of the fluorescence signals of both SCN5A (blue line) and VCL (red line) along transverse direction was aligned and plotted.
    Figure Legend Snippet: Co-localization of VCL and SCN5A in human ventricular tissue slice. ( A , B ) Immunofluorescence staining of SCN5A (green), VCL (red) and overlay channel from control and case (SUNDS patient, VCL–M94I variant carrier) human ventricular tissue slices. The second row shows a higher magnification view of the area outlined in yellow the first row. The yellow color from overlay panel indicates co-localization of VCL and SCN5A. ( C and D ) Signal intensity profile of signals from selected areas (outlined with yellow dashed rectangle in second row of ( A and B ) were calculated and plotted from control and case slices respectively. Integrity of the fluorescence signals of both SCN5A (blue line) and VCL (red line) along transverse direction was aligned and plotted.

    Techniques Used: Immunofluorescence, Staining, Variant Assay, Fluorescence

    Electrophysiological properties of cardiac sodium channel in HEK293 cells co-expressing SCN5A and either WT or mutant VCL. ( A ) Representative whole-cell current traces showing peak I Na under both normal (pH 7.4) and moderate acidosis (pH 7.0) condition in HEK293 cells expressing SCN5A and either WT or mutant VCL. ( B ) Summary data of peak I Na densities from every group. The number of tested cells is indicated above the bar. * p
    Figure Legend Snippet: Electrophysiological properties of cardiac sodium channel in HEK293 cells co-expressing SCN5A and either WT or mutant VCL. ( A ) Representative whole-cell current traces showing peak I Na under both normal (pH 7.4) and moderate acidosis (pH 7.0) condition in HEK293 cells expressing SCN5A and either WT or mutant VCL. ( B ) Summary data of peak I Na densities from every group. The number of tested cells is indicated above the bar. * p

    Techniques Used: Expressing, Mutagenesis

    VCL directly interacts with SCN5A. ( A ) Mouse liver and heart (HT) tissue lysates were immunoprecipitated (IP) using VCL or SCN5A antibody and analyzed by Western blotting using the indicated antibodies; ( B ) Wild-type VCL (VCL-WT) and SCN5A were transfected into HEK293 cells for 24 h, cell lysates were IP using VCL or SCN5A antibody and analyzed by Western blotting using the indicated antibodies; ( C ) Mutant VCL (VCL-M94I) and SCN5A were transfected into HEK293 cells for 24 h, cell lysates were IP using VCL or SCN5A antibody and analyzed by Western blotting using the indicated antibodies; ( D ) VCL-WT, VCL-M94I and SCN5A were transfected into HEK293 cells for 24 h, cell lysates were IP using VCL or SCN5A antibody and analyzed by Western blotting using the indicated antibodies. The results are representative of three independent experiments.
    Figure Legend Snippet: VCL directly interacts with SCN5A. ( A ) Mouse liver and heart (HT) tissue lysates were immunoprecipitated (IP) using VCL or SCN5A antibody and analyzed by Western blotting using the indicated antibodies; ( B ) Wild-type VCL (VCL-WT) and SCN5A were transfected into HEK293 cells for 24 h, cell lysates were IP using VCL or SCN5A antibody and analyzed by Western blotting using the indicated antibodies; ( C ) Mutant VCL (VCL-M94I) and SCN5A were transfected into HEK293 cells for 24 h, cell lysates were IP using VCL or SCN5A antibody and analyzed by Western blotting using the indicated antibodies; ( D ) VCL-WT, VCL-M94I and SCN5A were transfected into HEK293 cells for 24 h, cell lysates were IP using VCL or SCN5A antibody and analyzed by Western blotting using the indicated antibodies. The results are representative of three independent experiments.

    Techniques Used: Immunoprecipitation, Western Blot, Transfection, Mutagenesis

    Voltage–dependent gating for SCN5A co-expressed with VCL in HEK293 cells. ( A ) Under normal pH condition, M94I caused a statistically significant depolarizing shift in activation of cardiac sodium channel by 2.7 mV compared to WT. Vrev = 84.8 mV. ( B ) Under pH 7.0, M94I showed a significant repolarizing shift by 4.1 mV in inactivation of cardiac sodium channel compared with WT at pH 7.4.
    Figure Legend Snippet: Voltage–dependent gating for SCN5A co-expressed with VCL in HEK293 cells. ( A ) Under normal pH condition, M94I caused a statistically significant depolarizing shift in activation of cardiac sodium channel by 2.7 mV compared to WT. Vrev = 84.8 mV. ( B ) Under pH 7.0, M94I showed a significant repolarizing shift by 4.1 mV in inactivation of cardiac sodium channel compared with WT at pH 7.4.

    Techniques Used: Activation Assay

    Related Articles

    Staining:

    Article Title: Vinculin variant M94I identified in sudden unexplained nocturnal death syndrome decreases cardiac sodium current
    Article Snippet: .. Sections were stained with commercially available antibodies: Guinea Pig anti-Nav1.5 (polyclonal, Alomone labs, 1:200) and Alexa Fluor 488 Goat anti-Guinea Pig IgG (H + L) (ThermoFisher, Cat# a11073); Mouse anti-VCL (monoclonal, Sigma-Aldrich, 1:200) and Alexa Fluor 568 Goat anti-Mouse IgG (H + L) (ThermoFisher, Cat# a11004). ..

    Expressing:

    Article Title: Relaxin reverses maladaptive remodeling of the aged heart through Wnt-signaling
    Article Snippet: .. Guinea Pig and Rabbit anti-Nav1.5 (AGP-008, Alomone Labs, 1:200 in tissue and ab56240, Abcam, 1:200 in cells), rabbit anti-β-catenin (ab32572, Abcam, 1:250), mouse anti-Cx43 (sc-13558, Santa Cruz Biotechnology, Inc, 1:100), rabbit anti-collagen I (ab34710, Abcam, 1:200), mouse anti-Wnt1 (10C8, Thermo Fisher, 1:200) antibodies were used to measure protein expression. ..

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  • 92
    Alomone Labs anti nav1 5 antibody
    Relaxin up-regulates <t>Nav1.5</t> in LV cardiomyocytes. ( A ) Rat ventricular myocytes treated with increasing concentrations of RLX were fixed and labeled with Nav1.5 Ab. The data show that Nav1.5 fluorescence visibly increases with RLX treatment. ( B ) Dose-response of the ratio of Nav1.5 to phalloidin fluorescence (used for normalization purposes). EC 50 ~1.3 nM, ( n = 6 wells/data point, P
    Anti Nav1 5 Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti nav1 5 antibody/product/Alomone Labs
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti nav1 5 antibody - by Bioz Stars, 2021-09
    92/100 stars
      Buy from Supplier

    Image Search Results


    Relaxin up-regulates Nav1.5 in LV cardiomyocytes. ( A ) Rat ventricular myocytes treated with increasing concentrations of RLX were fixed and labeled with Nav1.5 Ab. The data show that Nav1.5 fluorescence visibly increases with RLX treatment. ( B ) Dose-response of the ratio of Nav1.5 to phalloidin fluorescence (used for normalization purposes). EC 50 ~1.3 nM, ( n = 6 wells/data point, P

    Journal: Scientific Reports

    Article Title: Relaxin reverses maladaptive remodeling of the aged heart through Wnt-signaling

    doi: 10.1038/s41598-019-53867-y

    Figure Lengend Snippet: Relaxin up-regulates Nav1.5 in LV cardiomyocytes. ( A ) Rat ventricular myocytes treated with increasing concentrations of RLX were fixed and labeled with Nav1.5 Ab. The data show that Nav1.5 fluorescence visibly increases with RLX treatment. ( B ) Dose-response of the ratio of Nav1.5 to phalloidin fluorescence (used for normalization purposes). EC 50 ~1.3 nM, ( n = 6 wells/data point, P

    Article Snippet: Guinea Pig and Rabbit anti-Nav1.5 (AGP-008, Alomone Labs, 1:200 in tissue and ab56240, Abcam, 1:200 in cells), rabbit anti-β-catenin (ab32572, Abcam, 1:250), mouse anti-Cx43 (sc-13558, Santa Cruz Biotechnology, Inc, 1:100), rabbit anti-collagen I (ab34710, Abcam, 1:200), mouse anti-Wnt1 (10C8, Thermo Fisher, 1:200) antibodies were used to measure protein expression.

    Techniques: Labeling, Fluorescence

    Relaxin signals through Wnt signaling to increase Nav1.5. ( A ) Less than 10% of untreated myocytes exhibit nuclear β-catenin ( A a,c); however, cells treated with RLX for 24 or 48 hours showed a significant increase in cells positive for nuclear β-catenin ( A b,c). 60x magnification. Data obtained from 3–4 separate preparations, 62–148 cells counted per sample. ( B ) Cells treated with RLX or CHIR, an inhibitor of GSK3β and Wnt pathway activator, significantly increased Nav1.5 by more than 2-fold ( B a–e, n ≥ 8 cells/group). Inhibition of canonical Wnt signaling by DKK1 blocked the effects of RLX 9 n ≥ 24 cells/group) and Wnt1 (n ≥ 17 cells/group) on Nav1.5 expression ( B f–o). 600x magnification, scale bars = 25 µm and apply to all panels. *Indicates p

    Journal: Scientific Reports

    Article Title: Relaxin reverses maladaptive remodeling of the aged heart through Wnt-signaling

    doi: 10.1038/s41598-019-53867-y

    Figure Lengend Snippet: Relaxin signals through Wnt signaling to increase Nav1.5. ( A ) Less than 10% of untreated myocytes exhibit nuclear β-catenin ( A a,c); however, cells treated with RLX for 24 or 48 hours showed a significant increase in cells positive for nuclear β-catenin ( A b,c). 60x magnification. Data obtained from 3–4 separate preparations, 62–148 cells counted per sample. ( B ) Cells treated with RLX or CHIR, an inhibitor of GSK3β and Wnt pathway activator, significantly increased Nav1.5 by more than 2-fold ( B a–e, n ≥ 8 cells/group). Inhibition of canonical Wnt signaling by DKK1 blocked the effects of RLX 9 n ≥ 24 cells/group) and Wnt1 (n ≥ 17 cells/group) on Nav1.5 expression ( B f–o). 600x magnification, scale bars = 25 µm and apply to all panels. *Indicates p

    Article Snippet: Guinea Pig and Rabbit anti-Nav1.5 (AGP-008, Alomone Labs, 1:200 in tissue and ab56240, Abcam, 1:200 in cells), rabbit anti-β-catenin (ab32572, Abcam, 1:250), mouse anti-Cx43 (sc-13558, Santa Cruz Biotechnology, Inc, 1:100), rabbit anti-collagen I (ab34710, Abcam, 1:200), mouse anti-Wnt1 (10C8, Thermo Fisher, 1:200) antibodies were used to measure protein expression.

    Techniques: Inhibition, Expressing

    Voltage‐dependent gating for cardiac sodium channel ( SCN 5A) coexpressed with vinculin ( VCL ) in HEK 293 cells. A, Between each group, no significant difference in activation of SCN5A was observed. B, Under pH 7.0, D841H showed a significant repolarizing shift by 3.0 mV in inactivation of SCN5A compared to WT at pH 7.4.

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    Article Title: An East Asian Common Variant Vinculin P.Asp841His Was Associated With Sudden Unexplained Nocturnal Death Syndrome in the Chinese Han Population

    doi: 10.1161/JAHA.116.005330

    Figure Lengend Snippet: Voltage‐dependent gating for cardiac sodium channel ( SCN 5A) coexpressed with vinculin ( VCL ) in HEK 293 cells. A, Between each group, no significant difference in activation of SCN5A was observed. B, Under pH 7.0, D841H showed a significant repolarizing shift by 3.0 mV in inactivation of SCN5A compared to WT at pH 7.4.

    Article Snippet: Sections were stained with antibodies: mouse anti‐VCL (monoclonal, 1:200; Sigma‐Aldrich, St. Louis, MO) and Guinea Pig anti‐Nav1.5 (polyclonal, 1:200; Alomone Labs Ltd, Jerusalem, Israel).

    Techniques: Activation Assay

    Electrophysiological properties of cardiac sodium channel (SCN5A) in HEK 293 cells coexpressing SCN 5A and either wild‐type vinculin ( VCL ‐ WT ) or VCL ‐D841H. A, Representative whole‐cell current traces showing peak sodium current ( I N a ) under both normal ( pH 7.4) and acidosis ( pH 7.0) conditions in HEK 293 cells expressing SCN 5A and either WT or variant VCL ‐D841H. B, Summary data of peak I N a densities from every group. The number of tested cells is indicated above the bar. * P

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    Article Title: An East Asian Common Variant Vinculin P.Asp841His Was Associated With Sudden Unexplained Nocturnal Death Syndrome in the Chinese Han Population

    doi: 10.1161/JAHA.116.005330

    Figure Lengend Snippet: Electrophysiological properties of cardiac sodium channel (SCN5A) in HEK 293 cells coexpressing SCN 5A and either wild‐type vinculin ( VCL ‐ WT ) or VCL ‐D841H. A, Representative whole‐cell current traces showing peak sodium current ( I N a ) under both normal ( pH 7.4) and acidosis ( pH 7.0) conditions in HEK 293 cells expressing SCN 5A and either WT or variant VCL ‐D841H. B, Summary data of peak I N a densities from every group. The number of tested cells is indicated above the bar. * P

    Article Snippet: Sections were stained with antibodies: mouse anti‐VCL (monoclonal, 1:200; Sigma‐Aldrich, St. Louis, MO) and Guinea Pig anti‐Nav1.5 (polyclonal, 1:200; Alomone Labs Ltd, Jerusalem, Israel).

    Techniques: Expressing, Variant Assay

    Co-localization of VCL and SCN5A in human ventricular tissue slice. ( A , B ) Immunofluorescence staining of SCN5A (green), VCL (red) and overlay channel from control and case (SUNDS patient, VCL–M94I variant carrier) human ventricular tissue slices. The second row shows a higher magnification view of the area outlined in yellow the first row. The yellow color from overlay panel indicates co-localization of VCL and SCN5A. ( C and D ) Signal intensity profile of signals from selected areas (outlined with yellow dashed rectangle in second row of ( A and B ) were calculated and plotted from control and case slices respectively. Integrity of the fluorescence signals of both SCN5A (blue line) and VCL (red line) along transverse direction was aligned and plotted.

    Journal: Scientific Reports

    Article Title: Vinculin variant M94I identified in sudden unexplained nocturnal death syndrome decreases cardiac sodium current

    doi: 10.1038/srep42953

    Figure Lengend Snippet: Co-localization of VCL and SCN5A in human ventricular tissue slice. ( A , B ) Immunofluorescence staining of SCN5A (green), VCL (red) and overlay channel from control and case (SUNDS patient, VCL–M94I variant carrier) human ventricular tissue slices. The second row shows a higher magnification view of the area outlined in yellow the first row. The yellow color from overlay panel indicates co-localization of VCL and SCN5A. ( C and D ) Signal intensity profile of signals from selected areas (outlined with yellow dashed rectangle in second row of ( A and B ) were calculated and plotted from control and case slices respectively. Integrity of the fluorescence signals of both SCN5A (blue line) and VCL (red line) along transverse direction was aligned and plotted.

    Article Snippet: Sections were stained with commercially available antibodies: Guinea Pig anti-Nav1.5 (polyclonal, Alomone labs, 1:200) and Alexa Fluor 488 Goat anti-Guinea Pig IgG (H + L) (ThermoFisher, Cat# a11073); Mouse anti-VCL (monoclonal, Sigma-Aldrich, 1:200) and Alexa Fluor 568 Goat anti-Mouse IgG (H + L) (ThermoFisher, Cat# a11004).

    Techniques: Immunofluorescence, Staining, Variant Assay, Fluorescence

    Electrophysiological properties of cardiac sodium channel in HEK293 cells co-expressing SCN5A and either WT or mutant VCL. ( A ) Representative whole-cell current traces showing peak I Na under both normal (pH 7.4) and moderate acidosis (pH 7.0) condition in HEK293 cells expressing SCN5A and either WT or mutant VCL. ( B ) Summary data of peak I Na densities from every group. The number of tested cells is indicated above the bar. * p

    Journal: Scientific Reports

    Article Title: Vinculin variant M94I identified in sudden unexplained nocturnal death syndrome decreases cardiac sodium current

    doi: 10.1038/srep42953

    Figure Lengend Snippet: Electrophysiological properties of cardiac sodium channel in HEK293 cells co-expressing SCN5A and either WT or mutant VCL. ( A ) Representative whole-cell current traces showing peak I Na under both normal (pH 7.4) and moderate acidosis (pH 7.0) condition in HEK293 cells expressing SCN5A and either WT or mutant VCL. ( B ) Summary data of peak I Na densities from every group. The number of tested cells is indicated above the bar. * p

    Article Snippet: Sections were stained with commercially available antibodies: Guinea Pig anti-Nav1.5 (polyclonal, Alomone labs, 1:200) and Alexa Fluor 488 Goat anti-Guinea Pig IgG (H + L) (ThermoFisher, Cat# a11073); Mouse anti-VCL (monoclonal, Sigma-Aldrich, 1:200) and Alexa Fluor 568 Goat anti-Mouse IgG (H + L) (ThermoFisher, Cat# a11004).

    Techniques: Expressing, Mutagenesis

    VCL directly interacts with SCN5A. ( A ) Mouse liver and heart (HT) tissue lysates were immunoprecipitated (IP) using VCL or SCN5A antibody and analyzed by Western blotting using the indicated antibodies; ( B ) Wild-type VCL (VCL-WT) and SCN5A were transfected into HEK293 cells for 24 h, cell lysates were IP using VCL or SCN5A antibody and analyzed by Western blotting using the indicated antibodies; ( C ) Mutant VCL (VCL-M94I) and SCN5A were transfected into HEK293 cells for 24 h, cell lysates were IP using VCL or SCN5A antibody and analyzed by Western blotting using the indicated antibodies; ( D ) VCL-WT, VCL-M94I and SCN5A were transfected into HEK293 cells for 24 h, cell lysates were IP using VCL or SCN5A antibody and analyzed by Western blotting using the indicated antibodies. The results are representative of three independent experiments.

    Journal: Scientific Reports

    Article Title: Vinculin variant M94I identified in sudden unexplained nocturnal death syndrome decreases cardiac sodium current

    doi: 10.1038/srep42953

    Figure Lengend Snippet: VCL directly interacts with SCN5A. ( A ) Mouse liver and heart (HT) tissue lysates were immunoprecipitated (IP) using VCL or SCN5A antibody and analyzed by Western blotting using the indicated antibodies; ( B ) Wild-type VCL (VCL-WT) and SCN5A were transfected into HEK293 cells for 24 h, cell lysates were IP using VCL or SCN5A antibody and analyzed by Western blotting using the indicated antibodies; ( C ) Mutant VCL (VCL-M94I) and SCN5A were transfected into HEK293 cells for 24 h, cell lysates were IP using VCL or SCN5A antibody and analyzed by Western blotting using the indicated antibodies; ( D ) VCL-WT, VCL-M94I and SCN5A were transfected into HEK293 cells for 24 h, cell lysates were IP using VCL or SCN5A antibody and analyzed by Western blotting using the indicated antibodies. The results are representative of three independent experiments.

    Article Snippet: Sections were stained with commercially available antibodies: Guinea Pig anti-Nav1.5 (polyclonal, Alomone labs, 1:200) and Alexa Fluor 488 Goat anti-Guinea Pig IgG (H + L) (ThermoFisher, Cat# a11073); Mouse anti-VCL (monoclonal, Sigma-Aldrich, 1:200) and Alexa Fluor 568 Goat anti-Mouse IgG (H + L) (ThermoFisher, Cat# a11004).

    Techniques: Immunoprecipitation, Western Blot, Transfection, Mutagenesis

    Voltage–dependent gating for SCN5A co-expressed with VCL in HEK293 cells. ( A ) Under normal pH condition, M94I caused a statistically significant depolarizing shift in activation of cardiac sodium channel by 2.7 mV compared to WT. Vrev = 84.8 mV. ( B ) Under pH 7.0, M94I showed a significant repolarizing shift by 4.1 mV in inactivation of cardiac sodium channel compared with WT at pH 7.4.

    Journal: Scientific Reports

    Article Title: Vinculin variant M94I identified in sudden unexplained nocturnal death syndrome decreases cardiac sodium current

    doi: 10.1038/srep42953

    Figure Lengend Snippet: Voltage–dependent gating for SCN5A co-expressed with VCL in HEK293 cells. ( A ) Under normal pH condition, M94I caused a statistically significant depolarizing shift in activation of cardiac sodium channel by 2.7 mV compared to WT. Vrev = 84.8 mV. ( B ) Under pH 7.0, M94I showed a significant repolarizing shift by 4.1 mV in inactivation of cardiac sodium channel compared with WT at pH 7.4.

    Article Snippet: Sections were stained with commercially available antibodies: Guinea Pig anti-Nav1.5 (polyclonal, Alomone labs, 1:200) and Alexa Fluor 488 Goat anti-Guinea Pig IgG (H + L) (ThermoFisher, Cat# a11073); Mouse anti-VCL (monoclonal, Sigma-Aldrich, 1:200) and Alexa Fluor 568 Goat anti-Mouse IgG (H + L) (ThermoFisher, Cat# a11004).

    Techniques: Activation Assay