Ask about this productRelated genes to: CACNB2 Blocking Peptide
- Gene:
- CACNB2 NIH gene
- Name:
- calcium voltage-gated channel auxiliary subunit beta 2
- Previous symbol:
- MYSB, CACNLB2
- Synonyms:
- -
- Chromosome:
- 10p12
- Locus Type:
- gene with protein product
- Date approved:
- 1992-03-27
- Date modifiied:
- 2019-04-23
Related products to: CACNB2 Blocking Peptide
Related articles to: CACNB2 Blocking Peptide
- To elucidate the genetic architecture of blood pressure (BP) and heart rate (HR) during early life and assess their potential relevance to adult health outcomes. - Source: PubMed
Publication date: 2026/04/27
Xie TianAni AlirezaVaez AhmadNolte Ilja MSu ShaoyongIshikuro MamiWang SiqiZhang WenboSoares Ana GoncalvesMotazedi EhsanCalas LucindaRonkainen JustiinaPedersen Casper-Emil TLu XuelingStinson Sara EFelix Janine FStankevic EvelinaWang Carol AThiering ElisabethFernández DietmarCalvo-Serra BeatrizStathopoulou Maria GFore RubyKumar AshishTuhkanen JohannaBilbao Jose RamonIbarluzea JesusIsaacs AaronFonvig Cilius EsmannRivadeneira FernandoLund Morten Asp VonsildHolm Louise Aasvan der Most Peter JRiese HarriëtteNarita AkiraTamiya GenFlexeder ClaudiaWiersma RikstjeArgoty-Pantoja Anna DVinding RebeccaHansen Tine WillumKümler ThomasEstarlich MarisaBustamante MarionaYuan Wen LunBoland-Augé AnneDeleuze Jean-FrançoisPetrelis Alexandros MRifas-Shiman SherylKajantie EeroFernandez-Jimenez NoraSanta-Marina LoretoArts Ilja C WLahti JariStrandberg TimoKull IngerBergström AnnaHivert Marie-FranceBønnelykke KlausKuriyama ShinichiBeilin Lawrence JMori Trevor AHartman Catharina AGrarup NielsThijs CarelRäikkönen KatriMelén ErikOken EmilyVisvikis-Siest SophieGützkow Kristine BGrazuleviciene ReginaHeude BarbaraChatzi LedaVrijheid MartineStandl MarieVrijkotte TanjaPennell Craig EOldehinkel Albertine JHansen TorbenJaddoe Vincent W VHolm Jens-ChristianSebert SylvainTimpson Nicholas JObara TakuWang XiaolingLawlor Deborah ACorpeleijn EvaAhluwalia Tarunveer SSnieder Harold - Coronary artery disease (CAD) causes irreversible myocardial dysfunction and progressive heart failure due to loss of contractile function and limited endogenous regenerative capacity. Current therapeutic strategies fail to restore lost myocardium or regenerate damaged cardiac tissue. Identifying dysregulated contractility-related genes may reveal actionable targets for stem cell engineering, iPSC-derived cardiomyocyte design, and tissue regeneration aimed at restoring myocardial contractility and function. - Source: PubMed
Publication date: 2026/03/31
Qu FangzhouAn XifengLei YaqiLu ChongLiu HanxiuMa HuayanLi Yongle - Following their domestication, chickens were translocated around the world to novel environments. Through a combination of natural and artificial selection, chickens adapted to these local conditions, creating significant genetic diversity across populations worldwide. Studying this diversity in the context of local environmental conditions may offer insights into mechanisms of adaptation to environmental stressors. In this study, we analyzed genomic data from the Chicken Genomic Diversity Consortium, applying multiple statistical approaches, including fixation index (F), nucleotide diversity (π), Tajima’s D, and runs of homozygosity (ROH), to identify selective sweeps among indigenous chickens from Afghanistan, China, Indonesia, Iran and Pakistan, compared with White Leghorn chickens. We identified sweeps in 14 genes related to heat tolerance, associated with relevant gene ontology (GO) terms and located within ROH regions. These genes, such as , , , , , , , , , , , , , , and play crucial roles in calcium signaling pathways, thermal sensation, and the plasticity of neurodevelopmental processes. These findings illustrate the significant role of selection in shaping genomic differentiation across chicken populations and provide insights into the genetic basis of adaptation to environmental stressors. - Source: PubMed
Publication date: 2026/04/07
Hosseinzadeh SevdaRafat Seyed AbbasJavanmard ArashHasanpur KarimBardou PhilippeCharles MathieuKlopp ChristopheSmith Adrian LFiddaman Steven R - Triple-negative breast cancers (TNBCs) are among the most aggressive breast tumors, due not only to the absence of clinically functional biomarkers used in other molecular subtypes, but also their marked heterogeneity and pronounced migratory and invasive behavior. The search for new molecules of interest for risk prediction, diagnosis and therapy stems from the class of long non-coding RNAs (lncRNAs), which often display context-dependent ("dual") functions and tissue specificity. Among them, lncRNA LINC01133 stands out for its dysregulation across cancer, although its molecular role in TNBC remains unclear. In the present study, we used the human TNBC cell line Hs578T to generate a cell panel comprising the parental line (Hs578T_wt), the control line (Hs578T_ctr), and the LINC01133 knockout line (Hs578T_ko). Subsequently, we performed bulk RNA-Seq to identify KO-associated Differentially Expressed Genes (DEGs) using as the primary contrast. Functional interpretation was achieved by Over-Representation Analysis (ORA) using Gene Ontology. We then conducted a comparative patient-cohort analysis using TCGA-BRCA Basal-like/TNBC cases (TCGA/BRCA n = 1098; Basal-like/TNBC n = 199), classified with the AIMS algorithm, and evaluated concordance between KO-associated signatures and patient tumor expression patterns via trend-based analyses across the LINC01133 expression levels and associated genes. A total of 265 KO-dominant DEGs were identified in Hs578T_ko, reflecting transcriptional changes consistent with tumor progression, with enrichment of pathways associated with LINC01133 knockout including cell adhesion, cell-cell interactions, epithelial-mesenchymal transition (EMT), and extracellular matrix (ECM) remodeling. The main DEGs included , , , , , , , , , and with additional candidates, such as and the lncRNA gene , which have been implicated in migration/invasion, ECM remodeling, or signaling across multiple tumor contexts. Translational analyses in TCGA-BRCA basal-like tumors suggested a descriptive association in which lower LINC01133 levels were accompanied by shifts in the expression trends of genes linked to ECM/EMT programs and modulation of genes related to cell adhesion and protease inhibition. : These results suggest a transcriptional model in which LINC01133 is associated with TNBC-related gene expression programs in a concentration-dependent manner, with loss of LINC01133 being associated with a transcriptomic shift toward pro-migratory/ECM remodeling signatures. While functional validation is required to establish causality, these data support LINC01133 as a molecule of interest in breast cancer research. - Source: PubMed
Publication date: 2026/01/24
Teodoro Júnior LeandroJesus-Ferreira Henrique César deSogayar Mari CleideNishiyama-Jr Milton Yutaka - Atrial fibrillation (AF) is the most common cardiac arrhythmia and is associated with increased morbidity and mortality due to complications such as stroke and heart failure. Cardiac fibrosis creates a pathological substrate for AF and remains inadequately addressed by current therapies. The calcium channel subunit CACNB2 has emerged as an underlying regulator of cardiac electrophysiology and fibrosis, yet its effects in the context of AF and atrial fibrosis remain poorly understood. In this study, CACNB2 was identify as a novel anti-fibrotic target in AF, demonstrating that CACNB2 overexpression in a rat AF model significantly improved electrophysiological parameters, including normalization of atrial effective refractory period (AERP), reappearance of regular P waves, and shortened AF duration, and mitigated atrial fibrosis and inflammation by reducing α-SMA, collagen I, and collagen III expression and inflammatory cytokine levels. In vitro, CACNB2 overexpression attenuated the profibrotic effects of Ang II on primary atrial fibroblasts, including reductions in cell viability and fibrotic marker expression. Also, CACNB2 overexpression modulated calcium handling and cellular oxidative stress responses in primary atrial cardiomyocytes under Ang II stimulation. This protective effect was accompanied by a modulation of the TGF-β/Smad pathway, suggesting a direct regulatory effect of CACNB2 on this fibrotic process. Collectively, our findings reveal that CACNB2 overexpression plays a protective role against AF and cardiac fibrosis by improving electrophysiological stability, reducing fibrotic remodeling, and modulating fibroblast and cardiomyocytes phenotype and function. These results highlight the novel therapeutic potential of targeting CACNB2 to treat AF and prevent its progression by addressing the underlying atrial fibrosis, offering a promising avenue for future research and development of novel AF therapies. - Source: PubMed
Publication date: 2026/02/24
Zhang DanLi ZongjuanLi NijinaZhang Hao