nav1 5  (Alomone Labs)


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    Alomone Labs nav1 5
    ( 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 <t>NaV1.5,</t> 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.
    Nav1 5, 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
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    Average 94 stars, based on 1 article reviews
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    nav1 5 - by Bioz Stars, 2023-02
    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) SCN5A mRNA expression was increased in iPSC-CMs from hemizygous and heterozygous DMD individuals (top), as well as in the human left ventricle heart tissue from a Becker MD individual compared to a healthy subject (bottom). (b) KCNJ2 mRNA levels were higher in both hemizygous and heterozygous iPSC-CMs (top), like those found in human left ventricle heart tissue from Becker DM patients (bottom) when compared to the corresponding control. (c) CACNA1C mRNA expression was not significant different among tested groups from either iPSC-CMs (top) or left ventricle tissues (bottom). mRNA levels were determined by qRT-PCR and calculated by the comparative Ct method (2 -ddCt ) normalized to the internal control 18s rRNA. Errors bars represent SEM. The n -values are in parentheses. Two-tailed Mann-Whitney test. ** P < 0.005.
    Figure Legend Snippet: (a) SCN5A mRNA expression was increased in iPSC-CMs from hemizygous and heterozygous DMD individuals (top), as well as in the human left ventricle heart tissue from a Becker MD individual compared to a healthy subject (bottom). (b) KCNJ2 mRNA levels were higher in both hemizygous and heterozygous iPSC-CMs (top), like those found in human left ventricle heart tissue from Becker DM patients (bottom) when compared to the corresponding control. (c) CACNA1C mRNA expression was not significant different among tested groups from either iPSC-CMs (top) or left ventricle tissues (bottom). mRNA levels were determined by qRT-PCR and calculated by the comparative Ct method (2 -ddCt ) normalized to the internal control 18s rRNA. Errors bars represent SEM. The n -values are in parentheses. Two-tailed Mann-Whitney test. ** P < 0.005.

    Techniques Used: Expressing, Quantitative RT-PCR, 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–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

    nav1 5  (Alomone Labs)


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    Alomone Labs nav1 5
    ( 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 <t>NaV1.5,</t> 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.
    Nav1 5, 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/nav1 5/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    nav1 5 - by Bioz Stars, 2023-02
    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) SCN5A mRNA expression was increased in iPSC-CMs from hemizygous and heterozygous DMD individuals (top), as well as in the human left ventricle heart tissue from a Becker MD individual compared to a healthy subject (bottom). (b) KCNJ2 mRNA levels were higher in both hemizygous and heterozygous iPSC-CMs (top), like those found in human left ventricle heart tissue from Becker DM patients (bottom) when compared to the corresponding control. (c) CACNA1C mRNA expression was not significant different among tested groups from either iPSC-CMs (top) or left ventricle tissues (bottom). mRNA levels were determined by qRT-PCR and calculated by the comparative Ct method (2 -ddCt ) normalized to the internal control 18s rRNA. Errors bars represent SEM. The n -values are in parentheses. Two-tailed Mann-Whitney test. ** P < 0.005.
    Figure Legend Snippet: (a) SCN5A mRNA expression was increased in iPSC-CMs from hemizygous and heterozygous DMD individuals (top), as well as in the human left ventricle heart tissue from a Becker MD individual compared to a healthy subject (bottom). (b) KCNJ2 mRNA levels were higher in both hemizygous and heterozygous iPSC-CMs (top), like those found in human left ventricle heart tissue from Becker DM patients (bottom) when compared to the corresponding control. (c) CACNA1C mRNA expression was not significant different among tested groups from either iPSC-CMs (top) or left ventricle tissues (bottom). mRNA levels were determined by qRT-PCR and calculated by the comparative Ct method (2 -ddCt ) normalized to the internal control 18s rRNA. Errors bars represent SEM. The n -values are in parentheses. Two-tailed Mann-Whitney test. ** P < 0.005.

    Techniques Used: Expressing, Quantitative RT-PCR, 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–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

    nav1 5  (Alomone Labs)


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    Alomone Labs nav1 5
    Nav1 5, 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
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    anti nav1 5  (Alomone Labs)


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    Alomone Labs anti nav1 5
    Anti Nav1 5, 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
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    Average 94 stars, based on 1 article reviews
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    nav1 5  (Alomone Labs)


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    Alomone Labs nav1 5
    Short- and long-term effects of NOC-18 on Na + channel current (I Na ) in neonatal rat cardiomyocytes. ( A ) Representative <t>I</t> <t>Na</t> traces in the control condition and during the acute (5 min) application of 1 mM NOC-18 given to the same patch are shown. I Na was recorded by a depolarization pulse of 50 ms duration, ranging from − 80 to 40 mV in 5 mV steps, applied from holding potentials of − 140 mV. Current (I)–voltage (V) relationship before (control) and after application of 1 mM NOC-18 (5 min) demonstrates the maximum inward current of the control (− 151.2 ± 14.9 pA/pF) and with NOC-18 (− 156.2 ± 9.5 pA/pF). ( B ) The steady-state inactivation and activation (conductance) curves of the control and during application of NOC-18 (5 min); Mid-points of the voltage relation for the activation ( V a,1/2 ) was − 36.0 ± 0.2 mV in the control and − 37.1 ± 0.2 mV during application of NOC-18; Midpoint of the voltage relation for the inactivation ( V i,1/2 ) was − 63.7 ± 0.2 mV in the control and − 65.6 ± 0.2 mV during application of NOC-18. ( C ) Representative I Na traces with vehicle or NOC-18 treated for 24 h. I–V relationship demonstrates the maximum inward current of vehicle (− 160.7 ± 11.6 pA/pF, n = 18) and with NOC-18 (− 122.2 ± 10.9 pA/pF). ( D ) The steady-state inactivation and activation (conductance) curves of vehicle (24 h) and NOC-18 (24 h); V a,1/2 was − 39.0 ± 0.2 mV in vehicle and − 37.4 ± 0.2 mV in NOC-18 (24 h); V i,1/2 was − 65.3 ± 0.2 mV in vehicle and − 73.8 ± 0.4 mV in NOC-18 (24 h). Values represent the mean ± SE. Numbers of cell are shown in parentheses. * p < 0.05 vs. vehicle.
    Nav1 5, 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
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    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
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    1) Product Images from "Nitric oxide down-regulates voltage-gated Na + channel in cardiomyocytes possibly through S-nitrosylation-mediated signaling"

    Article Title: Nitric oxide down-regulates voltage-gated Na + channel in cardiomyocytes possibly through S-nitrosylation-mediated signaling

    Journal: Scientific Reports

    doi: 10.1038/s41598-021-90840-0

    Short- and long-term effects of NOC-18 on Na + channel current (I Na ) in neonatal rat cardiomyocytes. ( A ) Representative I Na traces in the control condition and during the acute (5 min) application of 1 mM NOC-18 given to the same patch are shown. I Na was recorded by a depolarization pulse of 50 ms duration, ranging from − 80 to 40 mV in 5 mV steps, applied from holding potentials of − 140 mV. Current (I)–voltage (V) relationship before (control) and after application of 1 mM NOC-18 (5 min) demonstrates the maximum inward current of the control (− 151.2 ± 14.9 pA/pF) and with NOC-18 (− 156.2 ± 9.5 pA/pF). ( B ) The steady-state inactivation and activation (conductance) curves of the control and during application of NOC-18 (5 min); Mid-points of the voltage relation for the activation ( V a,1/2 ) was − 36.0 ± 0.2 mV in the control and − 37.1 ± 0.2 mV during application of NOC-18; Midpoint of the voltage relation for the inactivation ( V i,1/2 ) was − 63.7 ± 0.2 mV in the control and − 65.6 ± 0.2 mV during application of NOC-18. ( C ) Representative I Na traces with vehicle or NOC-18 treated for 24 h. I–V relationship demonstrates the maximum inward current of vehicle (− 160.7 ± 11.6 pA/pF, n = 18) and with NOC-18 (− 122.2 ± 10.9 pA/pF). ( D ) The steady-state inactivation and activation (conductance) curves of vehicle (24 h) and NOC-18 (24 h); V a,1/2 was − 39.0 ± 0.2 mV in vehicle and − 37.4 ± 0.2 mV in NOC-18 (24 h); V i,1/2 was − 65.3 ± 0.2 mV in vehicle and − 73.8 ± 0.4 mV in NOC-18 (24 h). Values represent the mean ± SE. Numbers of cell are shown in parentheses. * p < 0.05 vs. vehicle.
    Figure Legend Snippet: Short- and long-term effects of NOC-18 on Na + channel current (I Na ) in neonatal rat cardiomyocytes. ( A ) Representative I Na traces in the control condition and during the acute (5 min) application of 1 mM NOC-18 given to the same patch are shown. I Na was recorded by a depolarization pulse of 50 ms duration, ranging from − 80 to 40 mV in 5 mV steps, applied from holding potentials of − 140 mV. Current (I)–voltage (V) relationship before (control) and after application of 1 mM NOC-18 (5 min) demonstrates the maximum inward current of the control (− 151.2 ± 14.9 pA/pF) and with NOC-18 (− 156.2 ± 9.5 pA/pF). ( B ) The steady-state inactivation and activation (conductance) curves of the control and during application of NOC-18 (5 min); Mid-points of the voltage relation for the activation ( V a,1/2 ) was − 36.0 ± 0.2 mV in the control and − 37.1 ± 0.2 mV during application of NOC-18; Midpoint of the voltage relation for the inactivation ( V i,1/2 ) was − 63.7 ± 0.2 mV in the control and − 65.6 ± 0.2 mV during application of NOC-18. ( C ) Representative I Na traces with vehicle or NOC-18 treated for 24 h. I–V relationship demonstrates the maximum inward current of vehicle (− 160.7 ± 11.6 pA/pF, n = 18) and with NOC-18 (− 122.2 ± 10.9 pA/pF). ( D ) The steady-state inactivation and activation (conductance) curves of vehicle (24 h) and NOC-18 (24 h); V a,1/2 was − 39.0 ± 0.2 mV in vehicle and − 37.4 ± 0.2 mV in NOC-18 (24 h); V i,1/2 was − 65.3 ± 0.2 mV in vehicle and − 73.8 ± 0.4 mV in NOC-18 (24 h). Values represent the mean ± SE. Numbers of cell are shown in parentheses. * p < 0.05 vs. vehicle.

    Techniques Used: Activation Assay

    Concentration-dependent long-term (24 h) effects of NOC-18 and S-Nitroso-N-acetyl-DL-penicillamine (SNAP) on I Na . ( A ) Representative I Na traces with vehicle, 100 μM SNAP, 300 μM SNAP and 1000 μM SNAP applied for 24 h. ( B ) Dose–response relationships of the effects of NO donors, NOC-18 and SNAP, on the fractional I Na . The potency, e.g. half-maximum inhibitory concentration (IC 50 ), was estimated as 491 μM and 1505 μM for SNAP and NOC-18, respectively. Numbers of cell are shown in parentheses.
    Figure Legend Snippet: Concentration-dependent long-term (24 h) effects of NOC-18 and S-Nitroso-N-acetyl-DL-penicillamine (SNAP) on I Na . ( A ) Representative I Na traces with vehicle, 100 μM SNAP, 300 μM SNAP and 1000 μM SNAP applied for 24 h. ( B ) Dose–response relationships of the effects of NO donors, NOC-18 and SNAP, on the fractional I Na . The potency, e.g. half-maximum inhibitory concentration (IC 50 ), was estimated as 491 μM and 1505 μM for SNAP and NOC-18, respectively. Numbers of cell are shown in parentheses.

    Techniques Used: Concentration Assay

    Effects of an NO scavenger carboxy-PTIO (20 μM) on the action of NOC-18 for I Na modulation. ( A ) Representative I Na traces in the control condition (vehicle), 20 μM carboxy-PTIO, and 20 μM carboxy-PTIO plus 1 mM NOC-18 applied for 24 h. ( B ) I–-V relationship of I Na with vehicle, 20 μM carboxy-PTIO, and 20 μM carboxy-PTIO plus 1 mM NOC-18, demonstrating no statistical difference among three groups. Numbers of cell are shown in parentheses. Values represent the mean ± SE.
    Figure Legend Snippet: Effects of an NO scavenger carboxy-PTIO (20 μM) on the action of NOC-18 for I Na modulation. ( A ) Representative I Na traces in the control condition (vehicle), 20 μM carboxy-PTIO, and 20 μM carboxy-PTIO plus 1 mM NOC-18 applied for 24 h. ( B ) I–-V relationship of I Na with vehicle, 20 μM carboxy-PTIO, and 20 μM carboxy-PTIO plus 1 mM NOC-18, demonstrating no statistical difference among three groups. Numbers of cell are shown in parentheses. Values represent the mean ± SE.

    Techniques Used:

    Effects of a sulfhydryl-reducing agent N -ethylmaleimide (NEM) and a thiol-reducing agent dithiothreital (DTE) on NOC-18 for I Na modulation. ( A , B ) Representative I Na traces with 1 mM NOC-18 applied for 24 h in the absence or presence of NEM, and their I–V relationships of I Na . ( C , D ) Representative I Na traces with 1 mM NOC-18 applied for 24 h in the absence or presence of DTE, and their I–V relationships of I Na . In the presence of NEM or DTE, NOC-18 was unable to reduce I Na . Numbers of cell are shown in parentheses. Values represent the mean ± SE.
    Figure Legend Snippet: Effects of a sulfhydryl-reducing agent N -ethylmaleimide (NEM) and a thiol-reducing agent dithiothreital (DTE) on NOC-18 for I Na modulation. ( A , B ) Representative I Na traces with 1 mM NOC-18 applied for 24 h in the absence or presence of NEM, and their I–V relationships of I Na . ( C , D ) Representative I Na traces with 1 mM NOC-18 applied for 24 h in the absence or presence of DTE, and their I–V relationships of I Na . In the presence of NEM or DTE, NOC-18 was unable to reduce I Na . Numbers of cell are shown in parentheses. Values represent the mean ± SE.

    Techniques Used:

    Effects of a PKG inhibitor KT5823 and a guanylate cyclase inhibitor ODQ on NOC-18 for I Na modulation. ( A , B ) Representative I Na traces with 1 mM NOC-18 applied for 24 h in the absence or presence of 500 nM, and their I–V relationships of I Na . In the presence of KT5823, NOC-18 reduce the maximum inward current of I Na by 31%, indicating that I Na inhibiting effects of NOC-18 was independently of the action through PKG. ( C , D ) Representative I Na traces with 1 mM NOC-18 applied for 24 h in the absence or presence of 10 μM ODQ, and their I–V relationships of I Na . In the presence of ODQ, NOC-18 reduced the maximum inward current of I Na by 35%, indicating that I Na inhibiting effects of NOC-18 was independently of the action through GC activity. Numbers of cell are shown in parentheses. Values represent the mean ± SE. * p < 0.05 vs. KT5823 + NOC-18 or vs. ODQ + NOC-18.
    Figure Legend Snippet: Effects of a PKG inhibitor KT5823 and a guanylate cyclase inhibitor ODQ on NOC-18 for I Na modulation. ( A , B ) Representative I Na traces with 1 mM NOC-18 applied for 24 h in the absence or presence of 500 nM, and their I–V relationships of I Na . In the presence of KT5823, NOC-18 reduce the maximum inward current of I Na by 31%, indicating that I Na inhibiting effects of NOC-18 was independently of the action through PKG. ( C , D ) Representative I Na traces with 1 mM NOC-18 applied for 24 h in the absence or presence of 10 μM ODQ, and their I–V relationships of I Na . In the presence of ODQ, NOC-18 reduced the maximum inward current of I Na by 35%, indicating that I Na inhibiting effects of NOC-18 was independently of the action through GC activity. Numbers of cell are shown in parentheses. Values represent the mean ± SE. * p < 0.05 vs. KT5823 + NOC-18 or vs. ODQ + NOC-18.

    Techniques Used: Activity Assay

    Effects of a membrane-permeable analog of cGMP (8Br-cGMP) on I Na . ( A , B ) Representative I Na traces with vehicle and 500 μM 8Br-cGMP applied for 24 h, and their I–V relationships of I Na . 8Br-cGMP was unable to modify I Na . Numbers of cell are shown in parentheses. Values represent the mean ± SE.
    Figure Legend Snippet: Effects of a membrane-permeable analog of cGMP (8Br-cGMP) on I Na . ( A , B ) Representative I Na traces with vehicle and 500 μM 8Br-cGMP applied for 24 h, and their I–V relationships of I Na . 8Br-cGMP was unable to modify I Na . Numbers of cell are shown in parentheses. Values represent the mean ± SE.

    Techniques Used:

    FOXO1 as a possible link between NO and Nav1.5. ( A ) Changes of SCN5A mRNA- and FOXO1 mRNA-expression were examined by NO donors SNAP and NOC-18. SNAP (500 μM) and NOC-18 (1 mM) significantly reduced mRNA levels of SCN5A, although both NO donors were without effects on FOXO1 mRNA levels. Effects of 25 μM H 2 O 2 were assessed as positive controls. ( B ) Effects of NOC-18 on SCN5A and FOXO1 protein expression evaluated by Western blot analysis. Nav1.5 protein levels (whole cell) were significantly reduced, whereas FOXO1 protein levels (nucleus) were significantly increased by 1 mM NOC-18 applied for 24 h. Numbers of sample are shown in parentheses. Data were expressed as mean ± SD. * p < 0.05. See the supplemental file for the complete gel/blot images. ( C , D ) Actions of a FOXO1 activator paclitaxel and NOC18 for I Na . ( C ) Representative I Na traces with vehicle, 1 μM paclitaxel and 1 μM paclitaxel with 1 mM NOC-18 applied for 24 h, and ( D ) their I–V relationships. Numbers of cell are shown in parentheses. ( E ) Expression and distribution of Nav1.5 and FOXO1 as assessed by immunocytochemistry procedure. Cardiomyocytes were exposed to vehicle or 1 mM NOC-18 for 24 h. Nav1.5 for stained in green, FOXO1 in red, and DAPI staining to visualize nuclei in blue. Scale bar = 20 μm.
    Figure Legend Snippet: FOXO1 as a possible link between NO and Nav1.5. ( A ) Changes of SCN5A mRNA- and FOXO1 mRNA-expression were examined by NO donors SNAP and NOC-18. SNAP (500 μM) and NOC-18 (1 mM) significantly reduced mRNA levels of SCN5A, although both NO donors were without effects on FOXO1 mRNA levels. Effects of 25 μM H 2 O 2 were assessed as positive controls. ( B ) Effects of NOC-18 on SCN5A and FOXO1 protein expression evaluated by Western blot analysis. Nav1.5 protein levels (whole cell) were significantly reduced, whereas FOXO1 protein levels (nucleus) were significantly increased by 1 mM NOC-18 applied for 24 h. Numbers of sample are shown in parentheses. Data were expressed as mean ± SD. * p < 0.05. See the supplemental file for the complete gel/blot images. ( C , D ) Actions of a FOXO1 activator paclitaxel and NOC18 for I Na . ( C ) Representative I Na traces with vehicle, 1 μM paclitaxel and 1 μM paclitaxel with 1 mM NOC-18 applied for 24 h, and ( D ) their I–V relationships. Numbers of cell are shown in parentheses. ( E ) Expression and distribution of Nav1.5 and FOXO1 as assessed by immunocytochemistry procedure. Cardiomyocytes were exposed to vehicle or 1 mM NOC-18 for 24 h. Nav1.5 for stained in green, FOXO1 in red, and DAPI staining to visualize nuclei in blue. Scale bar = 20 μm.

    Techniques Used: Expressing, Western Blot, Immunocytochemistry, Staining

    The current hypothesis regarding NO-mediated downregulation of the Na + channel. NO is suggested to act through a suppressor gene FOXO1 for SCN5A transcription. FOXO1*: activated form of FOXO1.
    Figure Legend Snippet: The current hypothesis regarding NO-mediated downregulation of the Na + channel. NO is suggested to act through a suppressor gene FOXO1 for SCN5A transcription. FOXO1*: activated form of FOXO1.

    Techniques Used:

    primary antibodies against nav1 5  (Alomone Labs)


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    Alomone Labs primary antibodies against nav1 5
    Effects of Nav blockade on human SAN and atrial conduction
    Primary Antibodies Against Nav1 5, 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
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    1) Product Images from "Impaired neuronal sodium channels cause intranodal conduction failure and reentrant arrhythmias in human sinoatrial node"

    Article Title: Impaired neuronal sodium channels cause intranodal conduction failure and reentrant arrhythmias in human sinoatrial node

    Journal: Nature Communications

    doi: 10.1038/s41467-019-14039-8

    Effects of Nav blockade on human SAN and atrial conduction
    Figure Legend Snippet: Effects of Nav blockade on human SAN and atrial conduction

    Techniques Used:

    a Left to right: immunofluorescence image showing double staining of cNav1.5 (red) and Cx43 (green) in human heart 294050 cryosection with sinoatrial node (SAN) and right atrial (RA) regions ( n = 8) separated by white dotted line; magnification of image to show the distribution of cNav1.5 in the RA vs. the SAN; bar graph showing fluorescence signal intensity in the human SAN vs. RA. b Left to right: immunofluorescence image showing double staining of nNav1.6 (red) and Cx43 (green) in human heart cryosection with SAN and RA regions ( n = 7) separated by white dotted line; magnification of image to show the distribution of Nav1.6 in the RA vs. the SAN; bar graph showing fluorescence signal intensity in the human SAN vs. RA. c Left to right: cNav1.5 (red) and α-actinin (green; staining cardiomyocytes) dual staining; nNav1.6 (red) and α-actinin (green) dual staining confirm the cardiomyocyte-specific localization of cNav1.5 and nNav1.6. d Serial sections staining cNav1.5, nNav1.6, Cx43, and a nerve bundle labeled by anti-tyrosine hydroxylase (TH: staining sympathetic nerves) show that nNav1.6 and cNav1.5 are predominantly found in the myocytes relative to nerve bundles. All presented images a – d were collected from human heart 294050. e Left: representative immunoblotting bands for cNav1.5, α-actinin (marker of cardiomyocytes), and Cx43. Right: summary data of immunoblotting results of cNav1.5 protein distribution in the human SAN ( n = 6) and RA ( n = 6), compared with GAPDH (middle) and α-actinin (right), respectively. Cx43 connexin-43, GAPDH glyceraldehyde 3-phosphate dehydrogenase. Data were represented in mean ± SD. For immunostaining, analysis was done using lme4 and emmeans packages in R 3.4.4. Predictors included Heart (treated as random effect) and Condition (fixed effect). Pairwise tests between Condition levels were adjusted using Tukey’s method. Western blotting data analysis was done using two-sided t -test. Source data and uncropped versions of the western blot are provided as a file.
    Figure Legend Snippet: a Left to right: immunofluorescence image showing double staining of cNav1.5 (red) and Cx43 (green) in human heart 294050 cryosection with sinoatrial node (SAN) and right atrial (RA) regions ( n = 8) separated by white dotted line; magnification of image to show the distribution of cNav1.5 in the RA vs. the SAN; bar graph showing fluorescence signal intensity in the human SAN vs. RA. b Left to right: immunofluorescence image showing double staining of nNav1.6 (red) and Cx43 (green) in human heart cryosection with SAN and RA regions ( n = 7) separated by white dotted line; magnification of image to show the distribution of Nav1.6 in the RA vs. the SAN; bar graph showing fluorescence signal intensity in the human SAN vs. RA. c Left to right: cNav1.5 (red) and α-actinin (green; staining cardiomyocytes) dual staining; nNav1.6 (red) and α-actinin (green) dual staining confirm the cardiomyocyte-specific localization of cNav1.5 and nNav1.6. d Serial sections staining cNav1.5, nNav1.6, Cx43, and a nerve bundle labeled by anti-tyrosine hydroxylase (TH: staining sympathetic nerves) show that nNav1.6 and cNav1.5 are predominantly found in the myocytes relative to nerve bundles. All presented images a – d were collected from human heart 294050. e Left: representative immunoblotting bands for cNav1.5, α-actinin (marker of cardiomyocytes), and Cx43. Right: summary data of immunoblotting results of cNav1.5 protein distribution in the human SAN ( n = 6) and RA ( n = 6), compared with GAPDH (middle) and α-actinin (right), respectively. Cx43 connexin-43, GAPDH glyceraldehyde 3-phosphate dehydrogenase. Data were represented in mean ± SD. For immunostaining, analysis was done using lme4 and emmeans packages in R 3.4.4. Predictors included Heart (treated as random effect) and Condition (fixed effect). Pairwise tests between Condition levels were adjusted using Tukey’s method. Western blotting data analysis was done using two-sided t -test. Source data and uncropped versions of the western blot are provided as a file.

    Techniques Used: Immunofluorescence, Double Staining, Fluorescence, Staining, Labeling, Western Blot, Marker, Immunostaining

    a Geometry of 2D computer model. b Action potentials (AP) and their derivatives (d V /d t ) show different electrophysiological (EP) characteristics of SAN, SACP, and RA cells in the current model. Propagation of APs along the middle axis of the 2D SAN-atrium are displayed from the top to bottom with time at control conditions ( c ), Ado ( d ), and sodium current ( I Na ) 20% blockade ( e ). Blue and red numbers indicate the conduction time from SAN leading pacemaker through SAN and SACP, respectively. f Left: Ado plus I Na blockade reproduced prolonged SCL and SAN exit block. Right: representative APs and derivatives. Ado adenosine, RA right atria, SACP sinoatrial conduction pathway, SACT sinoatrial conduction time, SAN sinoatrial node.
    Figure Legend Snippet: a Geometry of 2D computer model. b Action potentials (AP) and their derivatives (d V /d t ) show different electrophysiological (EP) characteristics of SAN, SACP, and RA cells in the current model. Propagation of APs along the middle axis of the 2D SAN-atrium are displayed from the top to bottom with time at control conditions ( c ), Ado ( d ), and sodium current ( I Na ) 20% blockade ( e ). Blue and red numbers indicate the conduction time from SAN leading pacemaker through SAN and SACP, respectively. f Left: Ado plus I Na blockade reproduced prolonged SCL and SAN exit block. Right: representative APs and derivatives. Ado adenosine, RA right atria, SACP sinoatrial conduction pathway, SACT sinoatrial conduction time, SAN sinoatrial node.

    Techniques Used: Blocking Assay

    a Geometry of the 2D computer model with unexcitable fibrosis elements shown in light blue. b Action potentials (AP) and their derivatives (d V /d t ) show different electrophysiologic (EP) characteristics of SAN, SACP, and RA cells in the current model. Table results displaying combinations of adenosine dose and the percentage of sodium current ( I Na ) block in terms of cycle length, SACT, and threshold of SAN pacemaking and conduction impairment in control model ( c ) and HF model ( d ). Ado adenosine, HF heart failure, SACP sinoatrial conduction pathway, SACT sinoatrial conduction time, SAN, sinoatrial node, SCL sinus cycle length.
    Figure Legend Snippet: a Geometry of the 2D computer model with unexcitable fibrosis elements shown in light blue. b Action potentials (AP) and their derivatives (d V /d t ) show different electrophysiologic (EP) characteristics of SAN, SACP, and RA cells in the current model. Table results displaying combinations of adenosine dose and the percentage of sodium current ( I Na ) block in terms of cycle length, SACT, and threshold of SAN pacemaking and conduction impairment in control model ( c ) and HF model ( d ). Ado adenosine, HF heart failure, SACP sinoatrial conduction pathway, SACT sinoatrial conduction time, SAN, sinoatrial node, SCL sinus cycle length.

    Techniques Used: Blocking Assay

    anti nav1 5  (Alomone Labs)


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    Alomone Labs anti nav1 5
    Relaxin increases CV and reduces collagen in aged LV. ( A ) (a) RLX treatment resulted in a significant increase in CV during steady pacing (S1:S1). (b) CV restitution kinetics measured by programmed stimulation with premature pulses (S2 beats) was significantly increased by RLX, particularly during fast pacing times. *Indicates P < 0.05. 20x magnification ( B ) LV tissue sections were stained with Picro-sirius red and imaged on an Olympus Provis Light Microscope. The collagen to tissue ratio was significantly reduced in RLX (Bb, n = 6) treated animals compared to control (Ba, n = 5) by 23%. ( C ) LV tissue stained for <t>Nav1.5</t> showed that RLX (Cb, n = 6) significantly increased Nav1.5 expression compared to control hearts (Ca, n = 5). 600x magnification, scale bars = 25 µm and apply to all panels.
    Anti Nav1 5, 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
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    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 increases CV and reduces collagen in aged LV. ( A ) (a) RLX treatment resulted in a significant increase in CV during steady pacing (S1:S1). (b) CV restitution kinetics measured by programmed stimulation with premature pulses (S2 beats) was significantly increased by RLX, particularly during fast pacing times. *Indicates P < 0.05. 20x magnification ( B ) LV tissue sections were stained with Picro-sirius red and imaged on an Olympus Provis Light Microscope. The collagen to tissue ratio was significantly reduced in RLX (Bb, n = 6) treated animals compared to control (Ba, n = 5) by 23%. ( C ) LV tissue stained for Nav1.5 showed that RLX (Cb, n = 6) significantly increased Nav1.5 expression compared to control hearts (Ca, n = 5). 600x magnification, scale bars = 25 µm and apply to all panels.
    Figure Legend Snippet: Relaxin increases CV and reduces collagen in aged LV. ( A ) (a) RLX treatment resulted in a significant increase in CV during steady pacing (S1:S1). (b) CV restitution kinetics measured by programmed stimulation with premature pulses (S2 beats) was significantly increased by RLX, particularly during fast pacing times. *Indicates P < 0.05. 20x magnification ( B ) LV tissue sections were stained with Picro-sirius red and imaged on an Olympus Provis Light Microscope. The collagen to tissue ratio was significantly reduced in RLX (Bb, n = 6) treated animals compared to control (Ba, n = 5) by 23%. ( C ) LV tissue stained for Nav1.5 showed that RLX (Cb, n = 6) significantly increased Nav1.5 expression compared to control hearts (Ca, n = 5). 600x magnification, scale bars = 25 µm and apply to all panels.

    Techniques Used: Staining, Light Microscopy, Expressing

    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 < 0.01). ( C , D ) RLX significantly increased Nav1.5 expression in isolated myocytes compared to control ( n = 10–12 cells/group; 3 replicate experiments). 600x magnification, scale bars (25 µm) apply to all panels.
    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 < 0.01). ( C , D ) RLX significantly increased Nav1.5 expression in isolated myocytes compared to control ( n = 10–12 cells/group; 3 replicate experiments). 600x magnification, scale bars (25 µm) apply to all panels.

    Techniques Used: Labeling, Fluorescence, Expressing, Isolation

    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 < 0.05 compared to controls. *Indicates p < 0.05. **Indicates p < 0.01. ***Indicates p < 0.001.
    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 < 0.05 compared to controls. *Indicates p < 0.05. **Indicates p < 0.01. ***Indicates p < 0.001.

    Techniques Used: Inhibition, Expressing

    agp 008  (Alomone Labs)


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    Alomone Labs agp 008
    Agp 008, 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
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    agp 008  (Alomone Labs)


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    Alomone Labs agp 008
    Agp 008, 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
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    anti c terminal nav1 5  (Alomone Labs)


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    Alomone Labs anti c terminal nav1 5
    Anti C Terminal Nav1 5, 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 c terminal nav1 5/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
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    nav1 5  (Alomone Labs)


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    Alomone Labs nav1 5
    Nav1 5, 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
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    Average 94 stars, based on 1 article reviews
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    Alomone Labs nav1 5
    ( 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 <t>NaV1.5,</t> 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.
    Nav1 5, 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/nav1 5/product/Alomone Labs
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    Alomone Labs anti nav1 5
    ( 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 <t>NaV1.5,</t> 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.
    Anti Nav1 5, 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
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    Alomone Labs primary antibodies against nav1 5
    Effects of Nav blockade on human SAN and atrial conduction
    Primary Antibodies Against Nav1 5, 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
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    Alomone Labs agp 008
    Effects of Nav blockade on human SAN and atrial conduction
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    Alomone Labs anti c terminal nav1 5
    Effects of Nav blockade on human SAN and atrial conduction
    Anti C Terminal Nav1 5, 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
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    Image Search Results


    ( 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.

    Journal: bioRxiv

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

    doi: 10.1101/2022.01.25.477696

    Figure Lengend 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.

    Article Snippet: Primary antibodies were used at different dilutions in block solution: Troponin I (#MAB1691, Millipore) was used at 1:500, Kir2.1 (#APC-026, Alomone) antibody was used at 1:200, Nav1.5 (#AGP-008, Alomone) was used at 1:200, Dystrophin MANDRA1 (#D8043, Sigma) was used at 1:100, and Phalloidin 488 (#A12379, Invitrogen) at 1:500 (it comes with a fluorophore conjugated so no secondary Ab incubation was needed, stains F-actin).

    Techniques: 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.

    Journal: bioRxiv

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

    doi: 10.1101/2022.01.25.477696

    Figure Lengend 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.

    Article Snippet: Primary antibodies were used at different dilutions in block solution: Troponin I (#MAB1691, Millipore) was used at 1:500, Kir2.1 (#APC-026, Alomone) antibody was used at 1:200, Nav1.5 (#AGP-008, Alomone) was used at 1:200, Dystrophin MANDRA1 (#D8043, Sigma) was used at 1:100, and Phalloidin 488 (#A12379, Invitrogen) at 1:500 (it comes with a fluorophore conjugated so no secondary Ab incubation was needed, stains F-actin).

    Techniques: Two Tailed Test, MANN-WHITNEY

    (a) SCN5A mRNA expression was increased in iPSC-CMs from hemizygous and heterozygous DMD individuals (top), as well as in the human left ventricle heart tissue from a Becker MD individual compared to a healthy subject (bottom). (b) KCNJ2 mRNA levels were higher in both hemizygous and heterozygous iPSC-CMs (top), like those found in human left ventricle heart tissue from Becker DM patients (bottom) when compared to the corresponding control. (c) CACNA1C mRNA expression was not significant different among tested groups from either iPSC-CMs (top) or left ventricle tissues (bottom). mRNA levels were determined by qRT-PCR and calculated by the comparative Ct method (2 -ddCt ) normalized to the internal control 18s rRNA. Errors bars represent SEM. The n -values are in parentheses. Two-tailed Mann-Whitney test. ** P < 0.005.

    Journal: bioRxiv

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

    doi: 10.1101/2022.01.25.477696

    Figure Lengend Snippet: (a) SCN5A mRNA expression was increased in iPSC-CMs from hemizygous and heterozygous DMD individuals (top), as well as in the human left ventricle heart tissue from a Becker MD individual compared to a healthy subject (bottom). (b) KCNJ2 mRNA levels were higher in both hemizygous and heterozygous iPSC-CMs (top), like those found in human left ventricle heart tissue from Becker DM patients (bottom) when compared to the corresponding control. (c) CACNA1C mRNA expression was not significant different among tested groups from either iPSC-CMs (top) or left ventricle tissues (bottom). mRNA levels were determined by qRT-PCR and calculated by the comparative Ct method (2 -ddCt ) normalized to the internal control 18s rRNA. Errors bars represent SEM. The n -values are in parentheses. Two-tailed Mann-Whitney test. ** P < 0.005.

    Article Snippet: Primary antibodies were used at different dilutions in block solution: Troponin I (#MAB1691, Millipore) was used at 1:500, Kir2.1 (#APC-026, Alomone) antibody was used at 1:200, Nav1.5 (#AGP-008, Alomone) was used at 1:200, Dystrophin MANDRA1 (#D8043, Sigma) was used at 1:100, and Phalloidin 488 (#A12379, Invitrogen) at 1:500 (it comes with a fluorophore conjugated so no secondary Ab incubation was needed, stains F-actin).

    Techniques: Expressing, Quantitative RT-PCR, 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

    Journal: bioRxiv

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

    doi: 10.1101/2022.01.25.477696

    Figure Lengend 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

    Article Snippet: Primary antibodies were used at different dilutions in block solution: Troponin I (#MAB1691, Millipore) was used at 1:500, Kir2.1 (#APC-026, Alomone) antibody was used at 1:200, Nav1.5 (#AGP-008, Alomone) was used at 1:200, Dystrophin MANDRA1 (#D8043, Sigma) was used at 1:100, and Phalloidin 488 (#A12379, Invitrogen) at 1:500 (it comes with a fluorophore conjugated so no secondary Ab incubation was needed, stains F-actin).

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

    (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.

    Journal: bioRxiv

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

    doi: 10.1101/2022.01.25.477696

    Figure Lengend 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.

    Article Snippet: Primary antibodies were used at different dilutions in block solution: Troponin I (#MAB1691, Millipore) was used at 1:500, Kir2.1 (#APC-026, Alomone) antibody was used at 1:200, Nav1.5 (#AGP-008, Alomone) was used at 1:200, Dystrophin MANDRA1 (#D8043, Sigma) was used at 1:100, and Phalloidin 488 (#A12379, Invitrogen) at 1:500 (it comes with a fluorophore conjugated so no secondary Ab incubation was needed, stains F-actin).

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

    Effects of Nav blockade on human SAN and atrial conduction

    Journal: Nature Communications

    Article Title: Impaired neuronal sodium channels cause intranodal conduction failure and reentrant arrhythmias in human sinoatrial node

    doi: 10.1038/s41467-019-14039-8

    Figure Lengend Snippet: Effects of Nav blockade on human SAN and atrial conduction

    Article Snippet: Primary antibodies against Nav1.5 (custom-made in Dr Mohler’s lab), Nav1.6 (Alomone), Connexin-43(Cx43), Glyceraldehyde 3-phosphate dehydrogenase, and α-actinin (Sigma-Aldrich) were used to quantify corresponding proteins by western blotting and immunostaining , (Supplementary Table ).

    Techniques:

    a Left to right: immunofluorescence image showing double staining of cNav1.5 (red) and Cx43 (green) in human heart 294050 cryosection with sinoatrial node (SAN) and right atrial (RA) regions ( n = 8) separated by white dotted line; magnification of image to show the distribution of cNav1.5 in the RA vs. the SAN; bar graph showing fluorescence signal intensity in the human SAN vs. RA. b Left to right: immunofluorescence image showing double staining of nNav1.6 (red) and Cx43 (green) in human heart cryosection with SAN and RA regions ( n = 7) separated by white dotted line; magnification of image to show the distribution of Nav1.6 in the RA vs. the SAN; bar graph showing fluorescence signal intensity in the human SAN vs. RA. c Left to right: cNav1.5 (red) and α-actinin (green; staining cardiomyocytes) dual staining; nNav1.6 (red) and α-actinin (green) dual staining confirm the cardiomyocyte-specific localization of cNav1.5 and nNav1.6. d Serial sections staining cNav1.5, nNav1.6, Cx43, and a nerve bundle labeled by anti-tyrosine hydroxylase (TH: staining sympathetic nerves) show that nNav1.6 and cNav1.5 are predominantly found in the myocytes relative to nerve bundles. All presented images a – d were collected from human heart 294050. e Left: representative immunoblotting bands for cNav1.5, α-actinin (marker of cardiomyocytes), and Cx43. Right: summary data of immunoblotting results of cNav1.5 protein distribution in the human SAN ( n = 6) and RA ( n = 6), compared with GAPDH (middle) and α-actinin (right), respectively. Cx43 connexin-43, GAPDH glyceraldehyde 3-phosphate dehydrogenase. Data were represented in mean ± SD. For immunostaining, analysis was done using lme4 and emmeans packages in R 3.4.4. Predictors included Heart (treated as random effect) and Condition (fixed effect). Pairwise tests between Condition levels were adjusted using Tukey’s method. Western blotting data analysis was done using two-sided t -test. Source data and uncropped versions of the western blot are provided as a file.

    Journal: Nature Communications

    Article Title: Impaired neuronal sodium channels cause intranodal conduction failure and reentrant arrhythmias in human sinoatrial node

    doi: 10.1038/s41467-019-14039-8

    Figure Lengend Snippet: a Left to right: immunofluorescence image showing double staining of cNav1.5 (red) and Cx43 (green) in human heart 294050 cryosection with sinoatrial node (SAN) and right atrial (RA) regions ( n = 8) separated by white dotted line; magnification of image to show the distribution of cNav1.5 in the RA vs. the SAN; bar graph showing fluorescence signal intensity in the human SAN vs. RA. b Left to right: immunofluorescence image showing double staining of nNav1.6 (red) and Cx43 (green) in human heart cryosection with SAN and RA regions ( n = 7) separated by white dotted line; magnification of image to show the distribution of Nav1.6 in the RA vs. the SAN; bar graph showing fluorescence signal intensity in the human SAN vs. RA. c Left to right: cNav1.5 (red) and α-actinin (green; staining cardiomyocytes) dual staining; nNav1.6 (red) and α-actinin (green) dual staining confirm the cardiomyocyte-specific localization of cNav1.5 and nNav1.6. d Serial sections staining cNav1.5, nNav1.6, Cx43, and a nerve bundle labeled by anti-tyrosine hydroxylase (TH: staining sympathetic nerves) show that nNav1.6 and cNav1.5 are predominantly found in the myocytes relative to nerve bundles. All presented images a – d were collected from human heart 294050. e Left: representative immunoblotting bands for cNav1.5, α-actinin (marker of cardiomyocytes), and Cx43. Right: summary data of immunoblotting results of cNav1.5 protein distribution in the human SAN ( n = 6) and RA ( n = 6), compared with GAPDH (middle) and α-actinin (right), respectively. Cx43 connexin-43, GAPDH glyceraldehyde 3-phosphate dehydrogenase. Data were represented in mean ± SD. For immunostaining, analysis was done using lme4 and emmeans packages in R 3.4.4. Predictors included Heart (treated as random effect) and Condition (fixed effect). Pairwise tests between Condition levels were adjusted using Tukey’s method. Western blotting data analysis was done using two-sided t -test. Source data and uncropped versions of the western blot are provided as a file.

    Article Snippet: Primary antibodies against Nav1.5 (custom-made in Dr Mohler’s lab), Nav1.6 (Alomone), Connexin-43(Cx43), Glyceraldehyde 3-phosphate dehydrogenase, and α-actinin (Sigma-Aldrich) were used to quantify corresponding proteins by western blotting and immunostaining , (Supplementary Table ).

    Techniques: Immunofluorescence, Double Staining, Fluorescence, Staining, Labeling, Western Blot, Marker, Immunostaining

    a Geometry of 2D computer model. b Action potentials (AP) and their derivatives (d V /d t ) show different electrophysiological (EP) characteristics of SAN, SACP, and RA cells in the current model. Propagation of APs along the middle axis of the 2D SAN-atrium are displayed from the top to bottom with time at control conditions ( c ), Ado ( d ), and sodium current ( I Na ) 20% blockade ( e ). Blue and red numbers indicate the conduction time from SAN leading pacemaker through SAN and SACP, respectively. f Left: Ado plus I Na blockade reproduced prolonged SCL and SAN exit block. Right: representative APs and derivatives. Ado adenosine, RA right atria, SACP sinoatrial conduction pathway, SACT sinoatrial conduction time, SAN sinoatrial node.

    Journal: Nature Communications

    Article Title: Impaired neuronal sodium channels cause intranodal conduction failure and reentrant arrhythmias in human sinoatrial node

    doi: 10.1038/s41467-019-14039-8

    Figure Lengend Snippet: a Geometry of 2D computer model. b Action potentials (AP) and their derivatives (d V /d t ) show different electrophysiological (EP) characteristics of SAN, SACP, and RA cells in the current model. Propagation of APs along the middle axis of the 2D SAN-atrium are displayed from the top to bottom with time at control conditions ( c ), Ado ( d ), and sodium current ( I Na ) 20% blockade ( e ). Blue and red numbers indicate the conduction time from SAN leading pacemaker through SAN and SACP, respectively. f Left: Ado plus I Na blockade reproduced prolonged SCL and SAN exit block. Right: representative APs and derivatives. Ado adenosine, RA right atria, SACP sinoatrial conduction pathway, SACT sinoatrial conduction time, SAN sinoatrial node.

    Article Snippet: Primary antibodies against Nav1.5 (custom-made in Dr Mohler’s lab), Nav1.6 (Alomone), Connexin-43(Cx43), Glyceraldehyde 3-phosphate dehydrogenase, and α-actinin (Sigma-Aldrich) were used to quantify corresponding proteins by western blotting and immunostaining , (Supplementary Table ).

    Techniques: Blocking Assay

    a Geometry of the 2D computer model with unexcitable fibrosis elements shown in light blue. b Action potentials (AP) and their derivatives (d V /d t ) show different electrophysiologic (EP) characteristics of SAN, SACP, and RA cells in the current model. Table results displaying combinations of adenosine dose and the percentage of sodium current ( I Na ) block in terms of cycle length, SACT, and threshold of SAN pacemaking and conduction impairment in control model ( c ) and HF model ( d ). Ado adenosine, HF heart failure, SACP sinoatrial conduction pathway, SACT sinoatrial conduction time, SAN, sinoatrial node, SCL sinus cycle length.

    Journal: Nature Communications

    Article Title: Impaired neuronal sodium channels cause intranodal conduction failure and reentrant arrhythmias in human sinoatrial node

    doi: 10.1038/s41467-019-14039-8

    Figure Lengend Snippet: a Geometry of the 2D computer model with unexcitable fibrosis elements shown in light blue. b Action potentials (AP) and their derivatives (d V /d t ) show different electrophysiologic (EP) characteristics of SAN, SACP, and RA cells in the current model. Table results displaying combinations of adenosine dose and the percentage of sodium current ( I Na ) block in terms of cycle length, SACT, and threshold of SAN pacemaking and conduction impairment in control model ( c ) and HF model ( d ). Ado adenosine, HF heart failure, SACP sinoatrial conduction pathway, SACT sinoatrial conduction time, SAN, sinoatrial node, SCL sinus cycle length.

    Article Snippet: Primary antibodies against Nav1.5 (custom-made in Dr Mohler’s lab), Nav1.6 (Alomone), Connexin-43(Cx43), Glyceraldehyde 3-phosphate dehydrogenase, and α-actinin (Sigma-Aldrich) were used to quantify corresponding proteins by western blotting and immunostaining , (Supplementary Table ).

    Techniques: Blocking Assay