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anti-nav1.5 antibody  (Alomone Labs)


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    Alomone Labs anti-nav1.5 antibody
    Anti Nav1.5 Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 96/100, based on 135 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/asc-005/custom%40asc-005%4041846068?v=Alomone+Labs
    Average 96 stars, based on 135 article reviews
    anti-nav1.5 antibody - by Bioz Stars, 2026-07
    96/100 stars

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    (A) Volcano plot depiction of the differential proteome from ventricular tissue lysates of Popdc1 +/+ and Popdc1 fs/fs rats. Prioritization of the top targets highlighted profound downregulation of BVES (POPDC1) and the membrane scaffold Ankyrin-G (Ank3) (n=5-7). (B) KEGG pathway enrichment of the proteome identified “Cardiac muscle contraction” and “Arrhythmogenic right ventricular cardiomyopathy” and various cardiomyopathies as the top disrupted pathways. (C) Immunofluorescence staining of the myocardium demonstrates the loss of both BVES and Ankyrin-G (both in red) in Popdc1 fs/fs rats. (D) RT-qPCR gene expression analyses in cardiac tissue demonstrated reduced Popdc1 but normalized AnkG mRNA (n=5-7). (E) Western blots confirm the reduction of cardiac <t>POPDC1-Ankyrin-G-Nav1.5</t> axis and TREK-1 (KCNK2), concurrent with an upregulation of Kv4.3 and Cav1.2 in Popdc1 fs/fs rats (n=6). (F–G) Popdc1 fs/fs hearts exhibit markers of oxidative stress: elevated malondialdehyde (MDA; G) and reduced superoxide dismutase (SOD; H) activity (n=4). (F) Transmission electron microscopy (TEM) displays widened intercalated discs and myofibrillar disarray (red arrowhead) in Popdc1 fs/fs hearts (n=3). Data are mean ± SD. Statistical analyses conducted were unpaired Student’s t-test. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 respectively.
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    (A) Volcano plot depiction of the differential proteome from ventricular tissue lysates of Popdc1 +/+ and Popdc1 fs/fs rats. Prioritization of the top targets highlighted profound downregulation of BVES (POPDC1) and the membrane scaffold Ankyrin-G (Ank3) (n=5-7). (B) KEGG pathway enrichment of the proteome identified “Cardiac muscle contraction” and “Arrhythmogenic right ventricular cardiomyopathy” and various cardiomyopathies as the top disrupted pathways. (C) Immunofluorescence staining of the myocardium demonstrates the loss of both BVES and Ankyrin-G (both in red) in Popdc1 fs/fs rats. (D) RT-qPCR gene expression analyses in cardiac tissue demonstrated reduced Popdc1 but normalized AnkG mRNA (n=5-7). (E) Western blots confirm the reduction of cardiac <t>POPDC1-Ankyrin-G-Nav1.5</t> axis and TREK-1 (KCNK2), concurrent with an upregulation of Kv4.3 and Cav1.2 in Popdc1 fs/fs rats (n=6). (F–G) Popdc1 fs/fs hearts exhibit markers of oxidative stress: elevated malondialdehyde (MDA; G) and reduced superoxide dismutase (SOD; H) activity (n=4). (F) Transmission electron microscopy (TEM) displays widened intercalated discs and myofibrillar disarray (red arrowhead) in Popdc1 fs/fs hearts (n=3). Data are mean ± SD. Statistical analyses conducted were unpaired Student’s t-test. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 respectively.
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    (A) Volcano plot depiction of the differential proteome from ventricular tissue lysates of Popdc1 +/+ and Popdc1 fs/fs rats. Prioritization of the top targets highlighted profound downregulation of BVES (POPDC1) and the membrane scaffold Ankyrin-G (Ank3) (n=5-7). (B) KEGG pathway enrichment of the proteome identified “Cardiac muscle contraction” and “Arrhythmogenic right ventricular cardiomyopathy” and various cardiomyopathies as the top disrupted pathways. (C) Immunofluorescence staining of the myocardium demonstrates the loss of both BVES and Ankyrin-G (both in red) in Popdc1 fs/fs rats. (D) RT-qPCR gene expression analyses in cardiac tissue demonstrated reduced Popdc1 but normalized AnkG mRNA (n=5-7). (E) Western blots confirm the reduction of cardiac <t>POPDC1-Ankyrin-G-Nav1.5</t> axis and TREK-1 (KCNK2), concurrent with an upregulation of Kv4.3 and Cav1.2 in Popdc1 fs/fs rats (n=6). (F–G) Popdc1 fs/fs hearts exhibit markers of oxidative stress: elevated malondialdehyde (MDA; G) and reduced superoxide dismutase (SOD; H) activity (n=4). (F) Transmission electron microscopy (TEM) displays widened intercalated discs and myofibrillar disarray (red arrowhead) in Popdc1 fs/fs hearts (n=3). Data are mean ± SD. Statistical analyses conducted were unpaired Student’s t-test. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 respectively.
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    (A) Volcano plot depiction of the differential proteome from ventricular tissue lysates of Popdc1 +/+ and Popdc1 fs/fs rats. Prioritization of the top targets highlighted profound downregulation of BVES (POPDC1) and the membrane scaffold Ankyrin-G (Ank3) (n=5-7). (B) KEGG pathway enrichment of the proteome identified “Cardiac muscle contraction” and “Arrhythmogenic right ventricular cardiomyopathy” and various cardiomyopathies as the top disrupted pathways. (C) Immunofluorescence staining of the myocardium demonstrates the loss of both BVES and Ankyrin-G (both in red) in Popdc1 fs/fs rats. (D) RT-qPCR gene expression analyses in cardiac tissue demonstrated reduced Popdc1 but normalized AnkG mRNA (n=5-7). (E) Western blots confirm the reduction of cardiac <t>POPDC1-Ankyrin-G-Nav1.5</t> axis and TREK-1 (KCNK2), concurrent with an upregulation of Kv4.3 and Cav1.2 in Popdc1 fs/fs rats (n=6). (F–G) Popdc1 fs/fs hearts exhibit markers of oxidative stress: elevated malondialdehyde (MDA; G) and reduced superoxide dismutase (SOD; H) activity (n=4). (F) Transmission electron microscopy (TEM) displays widened intercalated discs and myofibrillar disarray (red arrowhead) in Popdc1 fs/fs hearts (n=3). Data are mean ± SD. Statistical analyses conducted were unpaired Student’s t-test. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 respectively.
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    (A) Volcano plot depiction of the differential proteome from ventricular tissue lysates of Popdc1 +/+ and Popdc1 fs/fs rats. Prioritization of the top targets highlighted profound downregulation of BVES (POPDC1) and the membrane scaffold Ankyrin-G (Ank3) (n=5-7). (B) KEGG pathway enrichment of the proteome identified “Cardiac muscle contraction” and “Arrhythmogenic right ventricular cardiomyopathy” and various cardiomyopathies as the top disrupted pathways. (C) Immunofluorescence staining of the myocardium demonstrates the loss of both BVES and Ankyrin-G (both in red) in Popdc1 fs/fs rats. (D) RT-qPCR gene expression analyses in cardiac tissue demonstrated reduced Popdc1 but normalized AnkG mRNA (n=5-7). (E) Western blots confirm the reduction of cardiac <t>POPDC1-Ankyrin-G-Nav1.5</t> axis and TREK-1 (KCNK2), concurrent with an upregulation of Kv4.3 and Cav1.2 in Popdc1 fs/fs rats (n=6). (F–G) Popdc1 fs/fs hearts exhibit markers of oxidative stress: elevated malondialdehyde (MDA; G) and reduced superoxide dismutase (SOD; H) activity (n=4). (F) Transmission electron microscopy (TEM) displays widened intercalated discs and myofibrillar disarray (red arrowhead) in Popdc1 fs/fs hearts (n=3). Data are mean ± SD. Statistical analyses conducted were unpaired Student’s t-test. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 respectively.
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    (A) Volcano plot depiction of the differential proteome from ventricular tissue lysates of Popdc1 +/+ and Popdc1 fs/fs rats. Prioritization of the top targets highlighted profound downregulation of BVES (POPDC1) and the membrane scaffold Ankyrin-G (Ank3) (n=5-7). (B) KEGG pathway enrichment of the proteome identified “Cardiac muscle contraction” and “Arrhythmogenic right ventricular cardiomyopathy” and various cardiomyopathies as the top disrupted pathways. (C) Immunofluorescence staining of the myocardium demonstrates the loss of both BVES and Ankyrin-G (both in red) in Popdc1 fs/fs rats. (D) RT-qPCR gene expression analyses in cardiac tissue demonstrated reduced Popdc1 but normalized AnkG mRNA (n=5-7). (E) Western blots confirm the reduction of cardiac <t>POPDC1-Ankyrin-G-Nav1.5</t> axis and TREK-1 (KCNK2), concurrent with an upregulation of Kv4.3 and Cav1.2 in Popdc1 fs/fs rats (n=6). (F–G) Popdc1 fs/fs hearts exhibit markers of oxidative stress: elevated malondialdehyde (MDA; G) and reduced superoxide dismutase (SOD; H) activity (n=4). (F) Transmission electron microscopy (TEM) displays widened intercalated discs and myofibrillar disarray (red arrowhead) in Popdc1 fs/fs hearts (n=3). Data are mean ± SD. Statistical analyses conducted were unpaired Student’s t-test. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 respectively.
    Guinea Pig Anti Nav1.5 Antibody, 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
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    (A) Volcano plot depiction of the differential proteome from ventricular tissue lysates of Popdc1 +/+ and Popdc1 fs/fs rats. Prioritization of the top targets highlighted profound downregulation of BVES (POPDC1) and the membrane scaffold Ankyrin-G (Ank3) (n=5-7). (B) KEGG pathway enrichment of the proteome identified “Cardiac muscle contraction” and “Arrhythmogenic right ventricular cardiomyopathy” and various cardiomyopathies as the top disrupted pathways. (C) Immunofluorescence staining of the myocardium demonstrates the loss of both BVES and Ankyrin-G (both in red) in Popdc1 fs/fs rats. (D) RT-qPCR gene expression analyses in cardiac tissue demonstrated reduced Popdc1 but normalized AnkG mRNA (n=5-7). (E) Western blots confirm the reduction of cardiac <t>POPDC1-Ankyrin-G-Nav1.5</t> axis and TREK-1 (KCNK2), concurrent with an upregulation of Kv4.3 and Cav1.2 in Popdc1 fs/fs rats (n=6). (F–G) Popdc1 fs/fs hearts exhibit markers of oxidative stress: elevated malondialdehyde (MDA; G) and reduced superoxide dismutase (SOD; H) activity (n=4). (F) Transmission electron microscopy (TEM) displays widened intercalated discs and myofibrillar disarray (red arrowhead) in Popdc1 fs/fs hearts (n=3). Data are mean ± SD. Statistical analyses conducted were unpaired Student’s t-test. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 respectively.
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    Image Search Results


    (A) Volcano plot depiction of the differential proteome from ventricular tissue lysates of Popdc1 +/+ and Popdc1 fs/fs rats. Prioritization of the top targets highlighted profound downregulation of BVES (POPDC1) and the membrane scaffold Ankyrin-G (Ank3) (n=5-7). (B) KEGG pathway enrichment of the proteome identified “Cardiac muscle contraction” and “Arrhythmogenic right ventricular cardiomyopathy” and various cardiomyopathies as the top disrupted pathways. (C) Immunofluorescence staining of the myocardium demonstrates the loss of both BVES and Ankyrin-G (both in red) in Popdc1 fs/fs rats. (D) RT-qPCR gene expression analyses in cardiac tissue demonstrated reduced Popdc1 but normalized AnkG mRNA (n=5-7). (E) Western blots confirm the reduction of cardiac POPDC1-Ankyrin-G-Nav1.5 axis and TREK-1 (KCNK2), concurrent with an upregulation of Kv4.3 and Cav1.2 in Popdc1 fs/fs rats (n=6). (F–G) Popdc1 fs/fs hearts exhibit markers of oxidative stress: elevated malondialdehyde (MDA; G) and reduced superoxide dismutase (SOD; H) activity (n=4). (F) Transmission electron microscopy (TEM) displays widened intercalated discs and myofibrillar disarray (red arrowhead) in Popdc1 fs/fs hearts (n=3). Data are mean ± SD. Statistical analyses conducted were unpaired Student’s t-test. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 respectively.

    Journal: bioRxiv

    Article Title: Recessive POPDC1 Truncation Causes Lethal Short-QT Pattern Arrhythmogenic Cardiomyopathy with Multi-Ion Channel Remodeling and Ankyrin-G Scaffold Disruption

    doi: 10.64898/2026.03.07.710328

    Figure Lengend Snippet: (A) Volcano plot depiction of the differential proteome from ventricular tissue lysates of Popdc1 +/+ and Popdc1 fs/fs rats. Prioritization of the top targets highlighted profound downregulation of BVES (POPDC1) and the membrane scaffold Ankyrin-G (Ank3) (n=5-7). (B) KEGG pathway enrichment of the proteome identified “Cardiac muscle contraction” and “Arrhythmogenic right ventricular cardiomyopathy” and various cardiomyopathies as the top disrupted pathways. (C) Immunofluorescence staining of the myocardium demonstrates the loss of both BVES and Ankyrin-G (both in red) in Popdc1 fs/fs rats. (D) RT-qPCR gene expression analyses in cardiac tissue demonstrated reduced Popdc1 but normalized AnkG mRNA (n=5-7). (E) Western blots confirm the reduction of cardiac POPDC1-Ankyrin-G-Nav1.5 axis and TREK-1 (KCNK2), concurrent with an upregulation of Kv4.3 and Cav1.2 in Popdc1 fs/fs rats (n=6). (F–G) Popdc1 fs/fs hearts exhibit markers of oxidative stress: elevated malondialdehyde (MDA; G) and reduced superoxide dismutase (SOD; H) activity (n=4). (F) Transmission electron microscopy (TEM) displays widened intercalated discs and myofibrillar disarray (red arrowhead) in Popdc1 fs/fs hearts (n=3). Data are mean ± SD. Statistical analyses conducted were unpaired Student’s t-test. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 respectively.

    Article Snippet: Blots were probed with primary antibodies against Cav1.2 (1:1000, MA5-45389, Thermo Fisher Scientific), Kv4.3 (1:500, PA5-93292, Thermo Fisher Scientific), Nav1.5 (1:200, ASC-005, Alomone Labs), TREK-1/KCNK2 (1:1000, PA5-115452, Thermo Fisher Scientific), AnkG (1:1000, 27980-1-AP, Proteintech), BVES (1:1000, as above, Thermo Fisher Scientific), and GAPDH (1:10000, 60004-1-Ig, Proteintech).

    Techniques: Membrane, Immunofluorescence, Staining, Quantitative RT-PCR, Gene Expression, Western Blot, Activity Assay, Transmission Assay, Electron Microscopy