CACNA1C
- Known as:
- CACNA1C
- Catalog number:
- Y213999
- Product Quantity:
- 200ul
- 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
- Context-induced relapse is a major barrier to recovery from alcohol use disorder (AUD). Identifying molecular targets involved in contextual memories associated with alcohol use may serve as novel pharmacotherapies. Our RNAseq profiling study of the hippocampus from rhesus monkeys with chronic alcohol use identified the voltage-gated calcium channel CACNA1C as a promising therapeutic target. However, data regarding CACNA1C expression in AUD and whether inhibition of CACNA1C can attenuate ethanol contextual memories remains limited. We tested the hypothesis that hippocampal CACNA1C expression is increased in human and nonhuman primates (NHPs) with chronic alcohol use. Further, we used a mouse conditioned place preference (CPP) paradigm to test the hypothesis that Nifedipine, a CACNA1C-selective L-type calcium channel antagonist, can attenuate ethanol-induced CPP. CACNA1C mRNA expression was increased in the hippocampus of subjects with AUD (p < 0.03). Increased densities of CACNA1C neurons (p < 0.01) and glia (p < 0.02) were observed in rhesus monkeys with chronic alcohol use. Ethanol-treated mice spent more time in the ethanol-paired chamber compared to the vehicle animals (p < 0.04), demonstrating ethanol-induced CPP. This effect was attenuated by Nifedipine, as time spent in the ethanol-paired chamber in the ethanol + Nifedipine group was not significantly different from the vehicle group. These findings demonstrate that chronic alcohol use increases CACNA1C expression in the hippocampus across species and that a CACNA1C subtype-selective antagonist reduces ethanol-induced CPP. Together, these results support CACNA1C as a promising therapeutic target for memory dysfunction in AUD. - Source: PubMed
Publication date: 2026/04/17
Pareek TanyaPham Loc MO'Donovan Sinead MZamarripa C AustinAllen Iv ObieFreeman Kevin BPlatt Donna MGrant Kathleen APantazopoulos HarryGisabella Barbara - The prevalence of Type 2 diabetes mellitus (T2DM) is rapidly increasing in India, yet molecular markers that reflect early disease susceptibility remain limited. Epigenetic modifications such as DNA methylation may reflect early metabolic vulnerability preceding overt dysglycemia. In this study, we examined genome-wide DNA methylation patterns in a pilot subset nested within a prospective Indian cohort using Nanopore sequencing and assessed their associations with previously identified metabolite predictors from the same cohort. - Source: PubMed
Publication date: 2026/04/16
Satheesh GopikaAsokan Aneesh KVijayakumar GadadharanRajavelu ArumugamRao Sudha NarayanaSivakumar Krishnankutty ChandrikaJaleel Abdul - Pathogenic variants in CACNA1C have been associated with cardiac arrhythmias and neurodevelopmental disorders, occasionally accompanied by movement disorders. Here we report the case of a 66-year-old female patient with combined dystonia-parkinsonism carrying a pathogenic CACNA1C variant. Neurological examination revealed painful tremulous cervical dystonia, blepharospasm, divergent strabismus, hypomimia, and mild dystonic posturing of left hand, action tremor, and bradykinesia of the upper limbs. Botulinum toxin type A injections provided only partial relief of cervical dystonia, so the patient underwent bilateral Deep Brain Stimulation of Globus Pallidus Internus (GPi-DBS), which resulted in dystonia improvement. Genetic analysis identified an extremely rare heterozygous nonsense variant in the CACNA1C gene (NM_199460.3: c.481C > T; NP_955630.3: p.Arg161*), predicted to introduce a premature stop codon resulting in early protein truncation. Haploinsufficiency is a known disease mechanism for this gene. This variant has previously been reported in two individuals with neurodevelopmental phenotypes. Based on ACMG guidelines, the variant was classified as pathogenic. Our findings suggest that CACNA1C variants may be associated with adult-onset movement disorders, even in the absence of a prior history of neurodevelopmental disease. This case broadens the phenotypic spectrum within CACNA1C-related disorders. GPi-DBS may represent a valuable therapeutic option in selected cases. - Source: PubMed
Publication date: 2026/04/13
Ottaviani DonatellaBacchin RuggeroPjeçi ArlendMalaguti Maria ChiaraLongo ChiaraSarubbo SilvioGiometto BrunoDzinovic IvanaZech MichaelDi Fonzo AlessioMonfrini Edoardo - Functional recovery of the hand following brachial plexus injury (BPI) is highly dependent on preventing atrophy of the intrinsic muscles of the hand. Although electrical muscle stimulation (EMS) is an effective therapeutic approach for atrophy, its underlying mechanisms remain poorly elucidated. This study investigated the biological mechanisms through which EMS-induced muscle contraction inhibits the progression of denervation-induced atrophy. Using a rat model of total BPI, we validated the protective effect of EMS against atrophy in denervated intrinsic muscles. Whole-cell patch-clamp analysis confirmed the functional role of the L-type voltage-gated calcium channel in this process. We further discovered that EMS rectifies the aberrant elevation of intracellular Ca concentration resulting from Cav1.1 dysfuntion. In vitro cellular experiments revealed that a rise in cytosolic Ca activates the translation rather than transcription of IGF-1. Crucially, long-term and regular EMS sustains elevated IGF-1 levels, which subsequently modulates protein metabolism in myocytes, thereby mitigating denervated muscle atrophy. - Source: PubMed
Yan HongzeLiao ChengpengMo GuokangRui JingGao KaimingZhao XinLao JieLiu Yuzhou - - Source: PubMed