SCN5A antibody - C-terminal region (ARP35542_P050)
- Known as:
- SCN5A (anti-) - C-terminal region (ARP35542_P050)
- Catalog number:
- arp35542_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- SCN5A antibody - C-terminal region (ARP35542_P050)
Related genes to: SCN5A antibody - C-terminal region (ARP35542_P050)
- Gene:
- SCN5A NIH gene
- Name:
- sodium voltage-gated channel alpha subunit 5
- Previous symbol:
- CMD1E
- Synonyms:
- Nav1.5, LQT3, HB1, HBBD, PFHB1, IVF, HB2, HH1, SSS1, CDCD2, CMPD2, ICCD
- Chromosome:
- 3p22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-04-10
- Date modifiied:
- 2019-04-23
Related products to: SCN5A antibody - C-terminal region (ARP35542_P050)
Related articles to: SCN5A antibody - C-terminal region (ARP35542_P050)
- Myocardial fibrosis (MF), a common pathological consequence of cardiovascular diseases, compromises cardiac function and elevates the risk of heart failure and arrhythmias. Considering the limited therapeutic options, this study explored the antifibrotic potential of Obacunone (OB), focusing on its links to lipid metabolism pathways. Potential OB targets, MF-associated genes, and lipid metabolism-related genes were curated from databases and literature. Transcriptomic datasets were analyzed to identify differentially expressed genes (DEGs) in MF, and lipid metabolism-related DEGs (LMDEGs) were subsequently intersected with these target sets to identify OB-associated targets. These core targets were further investigated via protein-protein interaction (PPI) network, consensus clustering, functional enrichment, and molecular docking analysis. Key findings were validated via western blotting. Intersection analysis identified ten LMDEGs associated with OB. Moreover, PPI network analysis highlighted a subnetwork of seven strongly interacting targets-CYP19A1, STAT3, LGALS3, PDGFRA, SCN5A, SLC9A1, and SERPINE1. Functional enrichment indicated OB's involvement in the epidermal growth factor receptor (EGFR), advanced glycation end-product-receptor for advanced lycation end-products (AGE-RAGE), and hypoxia-inducible factor-1 (HIF-1) signaling pathways. Furthermore, consensus clustering revealed distinct subtypes of MF. Molecular docking confirmed strong binding affinities between OB and core targets. In vivo, OB attenuated fibrosis, downregulated SLC9A1 and SERPINE1 expression, and upregulated CYP19A1, LGALS3, PDGFRA, and SCN5A. This integrated study demonstrates that OB exerts antifibrotic effects by regulating lipid metabolism-related genes and pathways. The identification of MF subtypes supports personalized therapy, positioning OB as a promising candidate for MF treatment. - Source: PubMed
Publication date: 2026/05/28
Liang GuanfengLin YongchunLi LipingCai JingyueLiu Xiaoping - Individuals of African ancestry are underrepresented in genetic studies, contributing to disproportionately higher rates of variants of uncertain significance (VUS) and fewer actionable results in genetic testing for cardiomyopathies and arrhythmias. We aimed to determine whether ancestry-enriched VUS confer measurable cardiovascular risk among individuals of African ancestry. - Source: PubMed
Publication date: 2026/05/27
Abe Temidayo ALancaster Megan CRoden Dan M - Cardiovascular and cerebrovascular diseases, encompassing cardiac arrhythmias, atherosclerosis, and ischaemic stroke, remain the foremost causes of death and long-term disability globally. Despite improved outcomes with conventional therapy, substantial residual risk persists, providing the impetus for gene-based intervention. KCNQ1/KCNH2 suppression-and-replacement, SCN5A base editing, and structural protein restoration via PKP2 and TMEM43 have each demonstrated capacity to re-establish electrophysiological stability in arrhythmia models. For atherosclerosis, RNA-based agents, notably inclisiran, alongside in vivo editing strategies such as VERVE-101, offer durable lipid reduction and attenuation of vascular inflammation. In ischaemic stroke, cGAS-STING silencing, AAV-NeuroD1-mediated neuronal reprogramming, and delivery of neurotrophic factors, including VEGF and BDNF, extend the therapeutic window well beyond reperfusion. Collectively, these approaches position gene therapy as a meaningful complement to standard care, capable of addressing root molecular pathology rather than downstream consequences. This review synthesises current mechanistic understanding, translational obstacles, and emerging directions across these three disease domains, arguing that, delivery and safety challenges notwithstanding, gene therapy stands to substantially reshape how cardiovascular and cerebrovascular diseases are prevented and treated. - Source: PubMed
Publication date: 2026/05/18
Liu ZixuLiu RuiqiYing YingNie Jing - The risk of atrial fibrillation (AF) is higher in endurance athletes. Pulmonary vein isolation (PVI) is effective in this group, implicating pulmonary vein (PV) remodelling, but underlying mechanisms are unclear. This study investigated if endurance training remodels PV sleeves and the PV-left atrial (LA) junction to promote PV triggers and a permissive peri-antral substrate for AF. - Source: PubMed
Publication date: 2026/05/25
Soattin LucaTopal LeilaTikhomirov RomanLagomarsino-Oneto DanieleAl-Othman SamiLee Angela W CSaluja SushantHornyik TiborHusti ZoltánPintér Jenő AntalMohammed Aiman Saleh ASmith MatthewFrancis Alice JMcKie MeganTorre EleonoraPolyák AlexandraFarkas AttilaBentzen Bo HjorthKeavney BernardNagy NorbertJost NorbertCasadei BarbaraMangoni Matteo EBoyett Mark RColman Michael ANiederer Steven AVarró AndrásMorris Gwilym MBaczkó IstvánD'Souza Alicia - Brugada phenocopy is a reversible Brugada pattern on an electrocardiogram (ECG) caused by identifiable clinical conditions (such as fever, electrolyte abnormalities, or drug exposure) in patients without true congenital Brugada syndrome, which is an inherited arrhythmogenic disorder often associated with SCN5A mutations. - Source: PubMed
Publication date: 2026/03/16
Haque Obaid IUr Rehman ObaidOthman LeenMozayan MansoorAronis Konstantinos N