CACNA1C (aa 1150_1200)
- Known as:
- CACNA1C (aa 1150_1200)
- Catalog number:
- NBP1-42820
- Product Quantity:
- 0.1 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CACNA1C ( 1150_1200)
Related genes to: CACNA1C (aa 1150_1200)
- Gene:
- CACNA1C NIH gene
- Name:
- calcium voltage-gated channel subunit alpha1 C
- Previous symbol:
- CCHL1A1, CACNL1A1
- Synonyms:
- Cav1.2, CACH2, CACN2, TS, LQT8
- Chromosome:
- 12p13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1991-01-30
- Date modifiied:
- 2019-04-23
Related products to: CACNA1C (aa 1150_1200)
Related articles to: CACNA1C (aa 1150_1200)
- The advent of pharmacogenomics-guided antihypertensive therapy represents a paradigm shift in hypertension management. This study aimed to investigate the prevalence of relevant genetic variants among hypertensive patients in Hunan Province, China, and evaluate the efficacy of genotype-directed vs. clinically guided therapy. - Source: PubMed
Publication date: 2026/09/18
Wu ShaLiu WenwuChen LongXu YonglongJin JingChen FangLi JunHu WuhuiWu JieCai YongjunHuang ZiChai XiaoliShi XiangjiangLuo YanlinZeng GaofengZeng HaiyanChen ZhiGuo FugangWang LeiWu MingxinQu ZhihaoWang YuPeng Daoquan - Gestational diabetes mellitus (GDM) is a common metabolic disorder, posing serious health risks to both mother and fetus. This study aims to explore the placental endocrine mechanisms involved in GDM. - Source: PubMed
Deng LijunYang MoWang XinGong NingZhang NingYang QingGu Chengmin - Perfluorooctanoic acid (PFOA) is a persistent environmental pollutant associated with cardiovascular dysfunction, but the molecular links between PFOA exposure and atrial fibrillation (AF) remain unclear. We aimed to prioritize a candidate mediator connecting PFOA with AF and examine its associated molecular effects in atrial cardiomyocytes. - Source: PubMed
Publication date: 2026/09/03
Li DanBai ChuanfengZhao Jinping - Sperm activation and movement are essential in freshwater fishes, where limited energy reserves and a short motility duration require rapid ATP-driven motility regulated by osmolality and ions. However, the physiological and molecular mechanisms underlying osmolality and ion regulation in mandarin fish () remain unclear, and ions in aquaculture systems may exert additional effects. Here, we integrated physiology with transcriptomic and proteomic analyses to characterize the effects of osmolality and ions on sperm motility and identify key genes, proteins, and regulatory networks involved in sperm activation and movement. Low osmolality (<50 mOsm/kg) promoted sperm activation, with sperm motility progressively decreasing as osmolality increased. Although relatively high osmolality supported motility maintenance, the initial motility was comparatively low, indicating the limited energy reserves of freshwater fish spermatozoa. Na and K activation media enhanced motility, whereas Ca supplementation suppressed activation. Ca levels below a 1:500 molar ratio (<0.06 mM) did not significantly affect sperm motility, indicating the importance of limiting Ca exposure during fertilization. Multi-omics analyses identified six differentially expressed genes, including , , and , and 35 differentially expressed proteins, including ATP1B, PRKCB, and CPT1A, as key molecules associated with Na, K, and Ca signaling and energy metabolism. The calcium signaling pathway, cAMP signaling pathway, and oxidative phosphorylation were significantly enriched in KEGG enrichment analysis, while Gene Ontology (GO) enrichment analysis identified ion signaling and energy metabolism, including ion transport, the ATP metabolic process, and the glycolytic process. Our findings provide a putative regulatory network for sperm activation and movement in mandarin fish and a basis for optimizing artificial fertilization. - Source: PubMed
Publication date: 2026/09/02
Wang QinghuaZhang YuxinHuang ZhongZhang WeiweiWu YingxinLi JiajieZhang YizhengLi LuZhu ZhimingMeng Zining - Patients with early-stage myocardial infarction (MI) are at high risk of malignant ventricular arrhythmias, yet the cell-type-specific molecular landscape associated with post-infarction arrhythmogenesis has not been systematically characterized. This study integrates single-nucleus and spatial transcriptomics to define a cardiomyocyte subpopulation in early MI and dissect the -centered regulatory network driving its ion channel remodeling. Single-nucleus transcriptomic data from post-MI human hearts were re-analyzed to identify a distinct subpopulation, termed arrhythmia-potential cardiomyocytes (aCMs), within the infarct border zone, characterized by pronounced ion channel remodeling. Gene co-expression network analysis revealed two modules highly associated with aCMs, in which NEAT1 correlated with the calcium channel gene and the LIM domain protein PDLIM5. All three genes were upregulated in hypoxic rat cardiomyocytes; siRNA-mediated knockdown confirmed that silencing downregulated and expression, consistent with in silico knockout predictions. A ceRNA network further identified as a key mediator consistent with regulatory axis. These findings suggest that cardiomyocytes in the early MI border zone exhibit ion channel remodeling driven by elevated , which may modulate and through a microRNA-mediated ceRNA network, suggesting that targeting may warrant further investigation for preventing malignant arrhythmias in early-stage MI. - Source: PubMed
Publication date: 2026/09/07
Zhao JiuxiaoZhu QianLou YangZhou MingminChen YamengChen ShiquanLiu QiangJiang Chenyang