CACNA1C pSer1928 antibody Ab host: Rabbit
- Known as:
- CACNA1C pSer1928 (anti-) Antibody production species: Rabbit
- Catalog number:
- 'AP55387SU-N
- Product Quantity:
- 0.2 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CACNA1C pSer1928 antibody host: Rabbit
Related genes to: CACNA1C pSer1928 antibody Ab host: Rabbit
- 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
- Gene:
- PPP1R18 NIH gene
- Name:
- protein phosphatase 1 regulatory subunit 18
- Previous symbol:
- KIAA1949
- Synonyms:
- phostensin
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-02
- Date modifiied:
- 2016-10-05
Related products to: CACNA1C pSer1928 antibody Ab host: Rabbit
Related articles to: CACNA1C pSer1928 antibody Ab host: Rabbit
- 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 - 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