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primary anti human nav1 5 antibodies  (Alomone Labs)


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    Alomone Labs primary anti human nav1 5 antibodies
    Identifying SCN5a p.C335R and TTN truncating variants by using precision diagnostic methods. ( A ) Patient’s pedigree showing co-segregation of an SCN5a C335R variant. The index patient (III. 3) was diagnosed with DCM and sick sinus syndrome at age 59 and underwent CRT-D implantation. She only carried the SCN5a C335R variant. Patient IV.1 was diagnosed with DCM and conduction disease at age 24. He carried both SCN5a and TTN truncating variants. ( B ) Masson Trichrome stained left ventricular endomyocardial biopsy of patient IV.1 with SCN5a and TTN truncating variants. Histopathological examination demonstrated extensive cardiac fibrosis in this patient with DCM and conduction disease. ( C ) Schematic representation of the <t>Nav1.5</t> cardiac sodium channel. The variant is located in Ploop between S5 and S6 of Domain-I.
    Primary Anti Human Nav1 5 Antibodies, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/primary+anti+human+nav1+5+antibodies/pmc08657717-87-0-4?v=Alomone+Labs
    Average 93 stars, based on 1 article reviews
    primary anti human nav1 5 antibodies - by Bioz Stars, 2026-07
    93/100 stars

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    1) Product Images from "Identification of SCN5a p.C335R Variant in a Large Family with Dilated Cardiomyopathy and Conduction Disease"

    Article Title: Identification of SCN5a p.C335R Variant in a Large Family with Dilated Cardiomyopathy and Conduction Disease

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms222312990

    Identifying SCN5a p.C335R and TTN truncating variants by using precision diagnostic methods. ( A ) Patient’s pedigree showing co-segregation of an SCN5a C335R variant. The index patient (III. 3) was diagnosed with DCM and sick sinus syndrome at age 59 and underwent CRT-D implantation. She only carried the SCN5a C335R variant. Patient IV.1 was diagnosed with DCM and conduction disease at age 24. He carried both SCN5a and TTN truncating variants. ( B ) Masson Trichrome stained left ventricular endomyocardial biopsy of patient IV.1 with SCN5a and TTN truncating variants. Histopathological examination demonstrated extensive cardiac fibrosis in this patient with DCM and conduction disease. ( C ) Schematic representation of the Nav1.5 cardiac sodium channel. The variant is located in Ploop between S5 and S6 of Domain-I.
    Figure Legend Snippet: Identifying SCN5a p.C335R and TTN truncating variants by using precision diagnostic methods. ( A ) Patient’s pedigree showing co-segregation of an SCN5a C335R variant. The index patient (III. 3) was diagnosed with DCM and sick sinus syndrome at age 59 and underwent CRT-D implantation. She only carried the SCN5a C335R variant. Patient IV.1 was diagnosed with DCM and conduction disease at age 24. He carried both SCN5a and TTN truncating variants. ( B ) Masson Trichrome stained left ventricular endomyocardial biopsy of patient IV.1 with SCN5a and TTN truncating variants. Histopathological examination demonstrated extensive cardiac fibrosis in this patient with DCM and conduction disease. ( C ) Schematic representation of the Nav1.5 cardiac sodium channel. The variant is located in Ploop between S5 and S6 of Domain-I.

    Techniques Used: Diagnostic Assay, Variant Assay, Staining

    SCN5a p.C335R carriers show conduction disease and reduced left ventricular ejection fraction (LV-EF). All family members with SCN5a p.C335R variant showed significantly longer PQ ( A ) and QRS intervals ( B ), lower left ventricular EF ( C ), and higher atrial fibrillation (AF) rates ( D ) than other family members without this variant. All 4 family members carrying SCN5a p.C335R who received CRT-D were non-responders ( E , F ). T-Test; * = p ≤ 0.05, ** = p ≤ 0.01. Data are presented as mean ± SD.
    Figure Legend Snippet: SCN5a p.C335R carriers show conduction disease and reduced left ventricular ejection fraction (LV-EF). All family members with SCN5a p.C335R variant showed significantly longer PQ ( A ) and QRS intervals ( B ), lower left ventricular EF ( C ), and higher atrial fibrillation (AF) rates ( D ) than other family members without this variant. All 4 family members carrying SCN5a p.C335R who received CRT-D were non-responders ( E , F ). T-Test; * = p ≤ 0.05, ** = p ≤ 0.01. Data are presented as mean ± SD.

    Techniques Used: Variant Assay

    Functional analysis of SCN5a p.C335R variant. ( A ) Na + current traces from Nav1.5 wild-type and p.C335R transfected Xenopus oocytes. This showed a loss of function in Nav1.5 p. C335R. Sodium channel currents (INa) were evoked from −80 mV to 70 mV. Western blot analysis confirmed that the wild-type and mutated Nav1.5 were expressed and that loss of Nav1.5 function was not due to absent expression of the protein. Anti-Rad50 used as a reference. ( B , C ) Representative traces of INa in iPSC-CMs with wild-type and SCN5a p.C335R variant. Sodium channel currents (n = 9) were reduced in iPSC-CMs of the DCM patients.
    Figure Legend Snippet: Functional analysis of SCN5a p.C335R variant. ( A ) Na + current traces from Nav1.5 wild-type and p.C335R transfected Xenopus oocytes. This showed a loss of function in Nav1.5 p. C335R. Sodium channel currents (INa) were evoked from −80 mV to 70 mV. Western blot analysis confirmed that the wild-type and mutated Nav1.5 were expressed and that loss of Nav1.5 function was not due to absent expression of the protein. Anti-Rad50 used as a reference. ( B , C ) Representative traces of INa in iPSC-CMs with wild-type and SCN5a p.C335R variant. Sodium channel currents (n = 9) were reduced in iPSC-CMs of the DCM patients.

    Techniques Used: Functional Assay, Variant Assay, Transfection, Western Blot, Expressing



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    primary anti human nav1 5 antibodies  (Alomone Labs)
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    Alomone Labs primary anti human nav1 5 antibodies
    Identifying SCN5a p.C335R and TTN truncating variants by using precision diagnostic methods. ( A ) Patient’s pedigree showing co-segregation of an SCN5a C335R variant. The index patient (III. 3) was diagnosed with DCM and sick sinus syndrome at age 59 and underwent CRT-D implantation. She only carried the SCN5a C335R variant. Patient IV.1 was diagnosed with DCM and conduction disease at age 24. He carried both SCN5a and TTN truncating variants. ( B ) Masson Trichrome stained left ventricular endomyocardial biopsy of patient IV.1 with SCN5a and TTN truncating variants. Histopathological examination demonstrated extensive cardiac fibrosis in this patient with DCM and conduction disease. ( C ) Schematic representation of the <t>Nav1.5</t> cardiac sodium channel. The variant is located in Ploop between S5 and S6 of Domain-I.
    Primary Anti Human Nav1 5 Antibodies, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/primary+anti+human+nav1+5+antibodies/pmc08657717-87-0-4?v=Alomone+Labs
    Average 93 stars, based on 1 article reviews
    primary anti human nav1 5 antibodies - by Bioz Stars, 2026-07
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    Identifying SCN5a p.C335R and TTN truncating variants by using precision diagnostic methods. ( A ) Patient’s pedigree showing co-segregation of an SCN5a C335R variant. The index patient (III. 3) was diagnosed with DCM and sick sinus syndrome at age 59 and underwent CRT-D implantation. She only carried the SCN5a C335R variant. Patient IV.1 was diagnosed with DCM and conduction disease at age 24. He carried both SCN5a and TTN truncating variants. ( B ) Masson Trichrome stained left ventricular endomyocardial biopsy of patient IV.1 with SCN5a and TTN truncating variants. Histopathological examination demonstrated extensive cardiac fibrosis in this patient with DCM and conduction disease. ( C ) Schematic representation of the <t>Nav1.5</t> cardiac sodium channel. The variant is located in Ploop between S5 and S6 of Domain-I.
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    Image Search Results


    Identifying SCN5a p.C335R and TTN truncating variants by using precision diagnostic methods. ( A ) Patient’s pedigree showing co-segregation of an SCN5a C335R variant. The index patient (III. 3) was diagnosed with DCM and sick sinus syndrome at age 59 and underwent CRT-D implantation. She only carried the SCN5a C335R variant. Patient IV.1 was diagnosed with DCM and conduction disease at age 24. He carried both SCN5a and TTN truncating variants. ( B ) Masson Trichrome stained left ventricular endomyocardial biopsy of patient IV.1 with SCN5a and TTN truncating variants. Histopathological examination demonstrated extensive cardiac fibrosis in this patient with DCM and conduction disease. ( C ) Schematic representation of the Nav1.5 cardiac sodium channel. The variant is located in Ploop between S5 and S6 of Domain-I.

    Journal: International Journal of Molecular Sciences

    Article Title: Identification of SCN5a p.C335R Variant in a Large Family with Dilated Cardiomyopathy and Conduction Disease

    doi: 10.3390/ijms222312990

    Figure Lengend Snippet: Identifying SCN5a p.C335R and TTN truncating variants by using precision diagnostic methods. ( A ) Patient’s pedigree showing co-segregation of an SCN5a C335R variant. The index patient (III. 3) was diagnosed with DCM and sick sinus syndrome at age 59 and underwent CRT-D implantation. She only carried the SCN5a C335R variant. Patient IV.1 was diagnosed with DCM and conduction disease at age 24. He carried both SCN5a and TTN truncating variants. ( B ) Masson Trichrome stained left ventricular endomyocardial biopsy of patient IV.1 with SCN5a and TTN truncating variants. Histopathological examination demonstrated extensive cardiac fibrosis in this patient with DCM and conduction disease. ( C ) Schematic representation of the Nav1.5 cardiac sodium channel. The variant is located in Ploop between S5 and S6 of Domain-I.

    Article Snippet: Primary anti-human NaV1.5 antibodies (Alomone Labs, Jerusalem, Israel) and anti-Rad50 as a reference (Bethyl Laboratories Inc., Montgomery, AL, USA) were diluted in the same blocking solution and incubated with the membranes overnight.

    Techniques: Diagnostic Assay, Variant Assay, Staining

    SCN5a p.C335R carriers show conduction disease and reduced left ventricular ejection fraction (LV-EF). All family members with SCN5a p.C335R variant showed significantly longer PQ ( A ) and QRS intervals ( B ), lower left ventricular EF ( C ), and higher atrial fibrillation (AF) rates ( D ) than other family members without this variant. All 4 family members carrying SCN5a p.C335R who received CRT-D were non-responders ( E , F ). T-Test; * = p ≤ 0.05, ** = p ≤ 0.01. Data are presented as mean ± SD.

    Journal: International Journal of Molecular Sciences

    Article Title: Identification of SCN5a p.C335R Variant in a Large Family with Dilated Cardiomyopathy and Conduction Disease

    doi: 10.3390/ijms222312990

    Figure Lengend Snippet: SCN5a p.C335R carriers show conduction disease and reduced left ventricular ejection fraction (LV-EF). All family members with SCN5a p.C335R variant showed significantly longer PQ ( A ) and QRS intervals ( B ), lower left ventricular EF ( C ), and higher atrial fibrillation (AF) rates ( D ) than other family members without this variant. All 4 family members carrying SCN5a p.C335R who received CRT-D were non-responders ( E , F ). T-Test; * = p ≤ 0.05, ** = p ≤ 0.01. Data are presented as mean ± SD.

    Article Snippet: Primary anti-human NaV1.5 antibodies (Alomone Labs, Jerusalem, Israel) and anti-Rad50 as a reference (Bethyl Laboratories Inc., Montgomery, AL, USA) were diluted in the same blocking solution and incubated with the membranes overnight.

    Techniques: Variant Assay

    Functional analysis of SCN5a p.C335R variant. ( A ) Na + current traces from Nav1.5 wild-type and p.C335R transfected Xenopus oocytes. This showed a loss of function in Nav1.5 p. C335R. Sodium channel currents (INa) were evoked from −80 mV to 70 mV. Western blot analysis confirmed that the wild-type and mutated Nav1.5 were expressed and that loss of Nav1.5 function was not due to absent expression of the protein. Anti-Rad50 used as a reference. ( B , C ) Representative traces of INa in iPSC-CMs with wild-type and SCN5a p.C335R variant. Sodium channel currents (n = 9) were reduced in iPSC-CMs of the DCM patients.

    Journal: International Journal of Molecular Sciences

    Article Title: Identification of SCN5a p.C335R Variant in a Large Family with Dilated Cardiomyopathy and Conduction Disease

    doi: 10.3390/ijms222312990

    Figure Lengend Snippet: Functional analysis of SCN5a p.C335R variant. ( A ) Na + current traces from Nav1.5 wild-type and p.C335R transfected Xenopus oocytes. This showed a loss of function in Nav1.5 p. C335R. Sodium channel currents (INa) were evoked from −80 mV to 70 mV. Western blot analysis confirmed that the wild-type and mutated Nav1.5 were expressed and that loss of Nav1.5 function was not due to absent expression of the protein. Anti-Rad50 used as a reference. ( B , C ) Representative traces of INa in iPSC-CMs with wild-type and SCN5a p.C335R variant. Sodium channel currents (n = 9) were reduced in iPSC-CMs of the DCM patients.

    Article Snippet: Primary anti-human NaV1.5 antibodies (Alomone Labs, Jerusalem, Israel) and anti-Rad50 as a reference (Bethyl Laboratories Inc., Montgomery, AL, USA) were diluted in the same blocking solution and incubated with the membranes overnight.

    Techniques: Functional Assay, Variant Assay, Transfection, Western Blot, Expressing