Goat Anti-Human CACNA1C, (C Terminus) Antibodies
- Known as:
- Goat Antibody toHuman CACNA1C, (C Terminus) Antibodies
- Catalog number:
- ER-14-1610
- Product Quantity:
- 100 μg
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Goat Anti-Human CACNA1C ( Terminus) Antibodies
Related genes to: Goat Anti-Human CACNA1C, (C Terminus) Antibodies
- 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: Goat Anti-Human CACNA1C, (C Terminus) Antibodies
Related articles to: Goat Anti-Human CACNA1C, (C Terminus) Antibodies
- Anorexia nervosa (AN) is a severe metabo-psychiatric disorder with the highest mortality rate among psychiatric conditions. Its characteristic onset during adolescence suggests that disrupted neurodevelopmental processes during critical periods may contribute to disease pathophysiology. In this exploratory study, we conducted an integrated multi-layered omics analysis to identify molecular alterations affecting neurodevelopmental pathways in individuals with AN. We employed three complementary approaches: DNA methylation sequencing via Reduced Representation Bisulfite Sequencing (RRBS), microRNA (miRNA) expression profiling using panel-based qPCR, and microbiome characterization through 16S rRNA sequencing in a sample of 38 patients with AN and 40 healthy controls. Analyses focused on molecular mechanisms involved in neurodevelopmental processes. RRBS analysis identified methylation differences in neurodevelopmentally relevant genes, particularly (voltage-gated calcium channel) and (transcription factor). miRNA profiling revealed extensive dysregulation, with 74 miRNAs showing altered levels in the AN pools. Network analysis highlighted that miR-135 family targets (SK3 channel involved in neuronal excitability), while miR-374b regulates (IGF-1 signaling modulator). Microbiome analysis revealed that 42% of the AN group exhibited dramatic oral dysbiosis characterized by Proteobacteria dominance. Our findings demonstrate coordinated multi-level dysregulation of mechanisms governing neural circuit maturation during adolescence, supporting a neurodevelopmental framework for understanding AN. The convergence of molecular alterations on ion channels and growth factor signaling suggests systems-level perturbations in developmental regulatory mechanisms. The identified miRNAs represent potential biomarkers and therapeutic targets, while microbiome heterogeneity suggests distinct clinical subgroups. While exploratory in nature, this work provides novel insights into AN molecular architecture and generates testable hypotheses for future mechanistic studies incorporating individual-level data essential to validate these candidates and establish robust clinical correlations. - Source: PubMed
Publication date: 2026/05/19
Gilardini FedericaSabatucci AnnalauraCifani CarloSegura-Garcia CristinaPucci MariangelaRania MariannaD'Addario Claudio - Autism spectrum disorder (ASD) may be a predisposing factor in the development of catatonia, which has been demonstrated to be effectively treated using electroconvulsive therapy (ECT). CACNA1 channelopathy mutations have been associated with autism spectrum disorder, intellectual disability, and epilepsy. The single published case report of ECT use in CACNA1 subunit mutations demonstrated a negative outcome, and no current case reports on CACNA1B, CACNA1C, CACNA1D, or CACNA1E mutations have been published. We present a case of an adolescent with a known CACNA1D mutation and symptoms of excited catatonia who experienced a reduction in the frequency and severity of self-injurious and violent behavior following treatment with ECT. Our case demonstrates the use of ECT for catatonia in an individual with a CACNA1 mutation without complication and with a positive therapeutic response. - Source: PubMed
Publication date: 2026/05/26
Mancine RyleyKuang JoannaRaghunandan ChristinaPalffy Alexander - Painful diabetic neuropathy (PDN) is frequently accompanied by anxiety, yet the neural circuit mechanisms associated with nociceptive hypersensitivity to affective dysfunction remain unclear. Here we combined brain-wide c-Fos mapping, viral tracing, in vivo fiber photometry, whole-cell recordings, and projection-specific opto/chemogenetics in a mouse model of streptozotocin-induced PDN to define a thalamo-cortex circuit for pain-anxiety comorbidity. Within the posterior insular cortex (pIC), CaMKIIα⁺ excitatory neurons were recruited in PDN mice with comorbid anxiety, exhibiting heightened neuronal excitability and enhanced excitatory synaptic input. Bidirectional chemogenetic modulation of pIC neurons oppositely regulated anxiety-like behavior and mechanical hypersensitivity without locomotor or glycemic confounds. Circuit mapping identified a monosynaptic excitatory projection from the paraventricular thalamus (PVT) to the pIC; PVT neurons were hyperactive in PDN, and projection-defined manipulation of the PVT to pIC pathway bidirectionally controlled the behavioral phenotypes. Cacna1c was upregulated in the PVT of PDN mice; its knockdown in pIC-projecting PVT neurons attenuated both pain and anxiety-like behaviors. Together, these results delineate a thalamo-cortex excitatory pathway that couples nociceptive and affective dimensions of PDN and suggest that selective targeting of the PVT to pIC circuit may provide coordinated relief of pain and anxiety-related symptoms. - Source: PubMed
Publication date: 2026/05/27
Wei MinShou JiayinYang JingCai SiqingBai QiyuanHou JinwenJiang YeShen ShixiongYu ZhuoyingZhao XinruHan YongzhengCai JieYang Xue-WeiLi ZhengqianMa DaqingXing Guo-GangLi Min - Chronic stress is a major risk factor for cognitive decline and blood-brain barrier (BBB) disruption, yet the underlying molecular mechanisms remain elusive. This study aimed to investigate the specific role of the metabolic intermediate homocysteine (Hcy) in chronic stress-induced BBB dysfunction and cognitive impairment. We utilized a male Sprague-Dawley rat model of chronic unpredictable mild stress (CUMS) and administered vitamin B complex to lower Hcy levels in vivo. Regional Hcy accumulation, BBB permeability, and cognitive behaviors were assessed. In vitro, primary rat brain microvascular endothelial cells (BMECs) were exposed to Hcy to evaluate barrier-forming function, transcriptomic alterations, DNA methylation patterns, Cav1.2 expression, and reactive oxygen species (ROS) production. CUMS selectively induced BBB hyperpermeability and significant Hcy accumulation predominantly within the rat hippocampus, which correlated intimately with cognitive deficits. Lowering Hcy levels via vitamin B supplementation successfully restored hippocampal BBB integrity and alleviated cognitive impairment. In addition, elevated Hcy severely impaired the barrier function of BMECs. Mechanistically, Hcy reduced global DNA methylation in BMECs and specifically induced targeted DNA hypomethylation at the intro region of . This epigenetic shift caused the transcriptional derepression and overexpression of the Cav1.2 calcium channel. Upregulated Cav1.2 subsequently triggered a robust ROS burst, leading to tight junction degradation. Our findings unveil a novel metabolic-epigenetic axis where Hcy-driven hypomethylation directly disrupts BMECs function to dismantle the hippocampal BBB. Lowering Hcy or targeting this Hcy-Cav1.2 pathway establishes a promising therapeutic strategy for mitigating stress-related neurovascular damage and cognitive disorders. - Source: PubMed
Publication date: 2026/04/30
Zhou Mao-YangLi Jin-ShanSun Zhao-XinYin JieZhao YunXie FangWang XueZhang Sheng-HuiSun Zhao-WeiQian Ling-Jia - More than 360,000 Americans experience sudden cardiac arrest (SCA) annually. A subgroup is caused by rare genetic variants, but existing studies are not population based and have been limited to nonsurvivors. - Source: PubMed
Publication date: 2026/04/06
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