CACNA1C antibody
- Known as:
- CACNA1C (anti-)
- Catalog number:
- orb87787
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- 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
- 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
Kransdorf Evan PMathias MarcoNakamura KotokaChugh HarpriyaNguyen DavidTyrer JonathanPharoah Paul DReinier KyndaronAkdemir ZeynepBoerwinkle EricYu BingChugh Sumeet S - Gastrointestinal (GI) motility is coordinated by multiple neurotransmitter systems acting on distinct post-junctional cells within the smooth muscle-interstitial cell-PDGFRα⁺ (SIP) syncytium. This study integrates physiological, pharmacological, and single-cell transcriptomic data to define the cellular mechanisms underlying inhibitory and excitatory neuromuscular transmission in the human colon. Inhibitory signaling involves purinergic (P2Y₁) and adrenergic (α₁A) receptors, which activate SKCa channels in PDGFRα⁺ cells, while nitrergic (nitric oxide (NO)-soluble guanylate cyclase (sGC)-cGMP) pathways are primarily mediated by interstitial cells of Cajal (ICCs) and smooth muscle cells (SMCs). VIPergic signaling also contributes to relaxation through cAMP-dependent mechanisms possibly located in PDGFRα⁺ cells. Excitatory transmission is mainly driven by muscarinic M3 and M2 receptors expressed in ICCs and SMCs, leading to calcium-dependent contractions. Pharmacologically, hyoscine butylbromide (HBB) reduces acetylcholine (ACh)-induced contractions by blocking M2/M3 receptors, whereas neostigmine enhances cholinergic transmission to restore motility. Blockade of voltage-gated calcium channels (Cav1.2, CACNA1C) by agents such as otilonium bromide further contributes to spasmolytic effects. These findings provide an integrated framework linking receptor expression, cellular mechanisms, and drug actions that modulate GI motility. - Source: PubMed
Publication date: 2026/05/06
Guzman PerePenchova MihaelaVergara PatriJimenez Marcel - High-Grade Serous Ovarian Cancer (HGSOC) is the most lethal gynecological malignancy due to aggressive growth, widespread metastases, and high intra-tumoral heterogeneity. Poor prognosis is largely due to late diagnosis, hence there is an urgent need to identify novel biomarkers for screening, diagnosis, and monitoring. Here, we propose the voltage-dependent calcium channel hCaV1.2 encoded by CACNA1C as a potential biomarker and therapeutic target in HGSOC. Using IHC analysis for ten ovarian cancer patients, cytotoxicity assay, TCGA gene expression and survival analyses, homology modeling, molecular docking, Calcium channel membrane assembly and molecular dynamics simulations, we tested CACNA1C's role in HGSOC progression and the effect of blocking on cancer cell survival. We show that nifedipine (NIFE), a calcium channel blocker (CCB), had a tumor suppressive effect based on binding models predicted by three-dimensional computer assisted molecular modeling and in vitro validation using human HGSOC cell line. Using The Cancer Genome Atlas ovarian public cohort, we found CACNA1C mRNA expression strongly correlated with poor patient survival for late-stage and metastasis than primary. We also show strong correlation of CACNA1C protein expression using immunohistochemistry correlating with COH ovarian carcinomas patients' disease progression. This research demonstrates that targeting HGSOC via CCBs may be therapeutically beneficial. By establishing further in vitro, in vivo, and clinical trials using FDA approved NIFE may be repurposed to target CACNA1C for HGSOC. - Source: PubMed
Publication date: 2026/04/22
Hammad Mohamed AWu Kingsley YAbd El-Fattah Eslam EAboody Karen SChang Chia-En A