CACNA1C Antibody
- Known as:
- CACNA1C Antibody
- Catalog number:
- AF1175a
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- CACNA1C Antibody
Related genes to: CACNA1C Antibody
- 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 Antibody
Related articles to: CACNA1C Antibody
- Dilated cardiomyopathy (DCM) is a primary myocardial disorder characterized by progressive ventricular dilatation and impaired myocardial systolic contractility, and it represents the most common form of cardiomyopathy globally. DCM drives a substantial worldwide disease burden, thus presenting a formidable and persistent challenge to global public health systems. The pathogenesis of DCM is marked by extreme etiological heterogeneity: 30%-50% of cases have a familial origin, with genetic determinants serving as the core driver of disease onset and progression. With the rapid advancement and widespread application of next-generation sequencing (NGS) technologies, a growing repertoire of DCM-causative genes has been successfully identified. These genes encode key functional proteins that regulate multiple core physiological processes in cardiomyocytes, including sarcomeric structure maintenance, intracellular signal transduction, and myocardial energy homeostasis. DCM-causing genes can be classified into multiple categories according to their functions. Sarcomeric protein genes (such as TTN, MYH7, and TNNT2) disrupt sarcomere assembly and contractile function through mechanisms such as haploinsufficiency and the toxic peptide hypothesis; mutations in nuclear membrane protein genes (such as LMNA and EMD) cause abnormal nuclear structure and disordered mechanotransduction signals; ion channel genes (such as SCN5A, CACNA1C, and RYR2) affect electrophysiological balance and calcium handling; desmosome-related genes (such as DSC2 and DSP) are associated with abnormal cell junctions and dysregulation of the Wnt/β-catenin pathway; KLF13, ETS1, and BMP10 are possible candidate genes for DCM with limited research; loss of function of RBM20 leads to abnormal splicing of TTN, CamkIIδ, RyR2, etc. and causes nuclear import defects as well as cytoplasmic RBM20-RNP granule toxicity, thereby driving ventricular dilation. These genes drive myocardial remodeling through common signaling pathways (such as ERK and TGF-β). Potential treatment strategies include gene-level interventions, targeted pathway inhibitors, and myosin activators. However, genetic heterogeneity results in a narrow applicable population for single-gene therapies. Future research needs to shift from targeting individual genes to improving the common pathological environment to achieve broad-spectrum treatment. Exploring upstream prevention of mutations or activation of endogenous repair mechanisms provides new directions for the treatment of DCM. - Source: PubMed
Publication date: 2026/03/28
Zhang XiaoZhang XinyuChen YunruHuan NaWang ChenglongZhang Dawu - Dopamine signaling is critical for cognitive and emotional regulation and is implicated in multiple neuropsychiatric disorders. One downstream effector of dopamine is the L-type calcium channel CaV1.2, encoded by the risk gene . Genome-wide association studies have consistently linked single nucleotide polymorphisms to schizophrenia, bipolar disorder, and related conditions. We previously showed that homozygous deletion of in dopamine receptor 1 (D1)-expressing cells enhances remote (30 days post-training) contextual fear memory in male mice. Here, we extend these findings by examining sex- and gene dosage-dependent behavioral consequences of loss in D1 cells. We find a sex-dependent dissociation, where females show enhanced aversive memory up to 30 days post-training even with partial loss, whereas males require complete loss to show enhanced fear. In contrast, males show impaired spatial memory in the Water Y-maze following heterozygous or homozygous deletion, an effect not observed in females. Cue-associated fear memory was transiently elevated in females but unaffected in males. Locomotor activity was reduced in females during the initial minutes of testing, with no effects in males, while social interaction and anxiety-like behaviors were unchanged across groups. These findings indicate that Ca 1.2 signaling in D1-expressing cells differentially regulates aversive versus spatial memory in a sex-dependent manner, providing insight into how risk variants may contribute to sex-specific cognitive phenotype. - Source: PubMed
Publication date: 2026/04/08
Walsh Josiah DScala-Chavez DiegoLee Andrew SMartínez-Rivera ArleneRajadhyaksha Anjali M - The cross-disorder risk gene encoding the α1 subunit of the L-type calcium channel Ca1.2 has repeatedly been associated with various psychiatric disorders. is expressed in parvalbumin positive (PV) neurons which play an important role in regulating excitation-inhibition (E/I) balance and their dysregulation has been implicated in different psychiatric conditions. To address the cell type-specific contribution of Ca1.2 to endophenotypes related to psychiatric disorders, we generated mice with a conditional deletion in PV neurons (Ca1.2-PV). Male knockout mice exhibited increased anxiety-like behavior, and a more passive stress-coping strategy in the forced swim test, while locomotion, social behavior, and cognitive performance were unaffected. In contrast, mice lacking Ca1.2 in forebrain glutamatergic neurons (Ca1.2-Nex) displayed enhanced active stress-coping, revealing a bidirectional, cell type-specific role of Ca1.2 in stress-induced behaviors. cFos mapping following stress exposure identified distinct activation patterns in stress-responsive brain regions, suggesting distinct circuit mechanisms underlying these opposing behavioral phenotypes. Together, these findings identify Ca1.2 in PV neurons as a critical regulator of anxiety and stress-coping behavior and highlight complementary contributions of inhibitory and excitatory circuits to stress adaptation, with implications for targeted therapeutic strategies in psychiatric disorders. - Source: PubMed
Publication date: 2026/04/20
Loganathan SrivaishnaviZhao ChenDeussing Jan M - 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