Cacna1c
- Known as:
- Cacna1c
- Catalog number:
- 043084A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Cacna1c
Related genes to: Cacna1c
- 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
Anti-CACNA1Canti-CACNA1C / Cav1.2anti-CACNA1C / Cav1.2Antibodies: CACNA1C HOST: Goat Clonality: pAbBovine Voltage-dependent L-type calcium channel subunit alpha-1C(CACNA1C) ELISA kitCACB-receptor,CACH2,CACN2,CACNA1C,CACNL1A1,Calcium channel, L type, alpha-1 polypeptide, isoform 1, cardiac muscle,CCHL1A1,Oryctolagus cuniculus,Rabbit,Smooth muscle calcium channel blocker receptor,VCACH2,CACN2,CACNA1C,CACNL1A1,Calcium channel, L type, alpha-1 polypeptide, isoform 1, cardiac muscle,CCHL1A1,Homo sapiens,Human,Voltage-dependent L-type calcium channel subunit alpha-1C,Voltage-gatedCach2,Cacn2,Cacna1c,Cacnl1a1,Calcium channel, L type, alpha-1 polypeptide, isoform 1, cardiac muscle,Cchl1a1,MBC,MELC-CC,Mouse,Mouse brain class C,Mus musculus,Voltage-dependent L-type calcium channelCach2,Cacn2,Cacna1c,Cacnl1a1,Calcium channel, L type, alpha-1 polypeptide, isoform 1, cardiac muscle,Cchl1a1,Rat,Rat brain class C,Rattus norvegicus,RBC,Voltage-dependent L-type calcium channel subuniCACNA1A Gene calcium channel, voltage-dependent, P_Q type, alpha 1A subunitCACNA1C AntibodyCACNA1C antibody Ab host: RabbitCACNA1C (aa 1150_1200)CACNA1C (aa 1150_1200)CACNA1C (aa 1450_1500) Related articles to: Cacna1c
- 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 - encodes the pore-forming subunit of the L-type calcium channel Cav1.2. Common variants in are associated with psychiatric disorders, whereas rare single nucleotide variants cause -related disorder, a multisystem disorder with symptoms that include autism spectrum disorder (ASD), intellectual disability, and seizures. However, the cellular mechanisms linking dysfunction to neurodevelopmental phenotypes remain poorly understood. - Source: PubMed
Publication date: 2026/07/22
Wilkinson GemmaWood JamieRoivainen NuppuHaddon Josephine EUnderwood Jack F GHall JeremyHarwood Adrian J - CACNA1C is a risk gene for multiple psychiatric disorders and the Ca1.2 protein it encodes is a potential target for their treatment. It is known that alternative start exon usage and splicing of CACNA1C RNA results in multiple transcript isoforms. However, the identity of full-length isoforms, and their relative abundance between tissues, remains unknown. Such information is important for understanding the molecular mechanisms of illness associations and to advance the potential for Ca1.2 isoform-selective drugs. In this study we compared full-length isoforms expressed in human brain with those expressed in heart and aorta using PCR-targeted long-read nanopore amplicon sequencing. We also performed 5'-RACE to profile which CACNA1C transcription start exons are used. CACNA1C RNA splicing revealed distinct tissue-enriched isoforms in brain, heart and aorta, with the results corroborated by publicly available short-read RNA-seq data. For example, splicing of mutually exclusive exons 21 and 22 differentiated isoforms expressed in the brain from those in the heart and aorta. 5'-RACE identified a novel start exon, exon 1d, which was detected in brain and aorta but not heart, and which predicts channels with a truncated N-terminus. The full-length isoforms identified here, from both the previously known start exons and the novel start exon, are likely to impact on the function and the pharmacology of the encoded Ca1.2 channel. Identification of brain-enriched isoforms provides the possibility of designing drugs preferentially targeting Ca1.2 for psychiatric indications. - Source: PubMed
Publication date: 2026/09/11
Hall Nicola AlMould Arne WNassiri IsarKudasheva SofiaWright David JChen LiArshad Osama ATao RanKleinman Joel EWeinberger Daniel RHyde Thomas MHarrison Paul JHaerty WilfriedTunbridge Elizabeth M