CACNA2D1 Antibody
- Known as:
- CACNA2D1 Antibody
- Catalog number:
- csb-pa004407la01hu
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- CusAb
- Gene target:
- CACNA2D1 Antibody
Related genes to: CACNA2D1 Antibody
- Gene:
- CACNA2D1 NIH gene
- Name:
- calcium voltage-gated channel auxiliary subunit alpha2delta 1
- Previous symbol:
- CACNL2A, CACNA2, MHS3, LINC01112
- Synonyms:
- lncRNA-N3
- Chromosome:
- 7q21.11
- Locus Type:
- gene with protein product
- Date approved:
- 1992-03-27
- Date modifiied:
- 2019-04-23
Related products to: CACNA2D1 Antibody
Related articles to: CACNA2D1 Antibody
- Left atrial remodeling (LAR) critically contributes to the progression of heart failure (HF) and the development of atrial fibrillation (AF) following myocardial infarction (MI). The protein α2δ1, primarily known for its role in neuropathic pain, is abundantly expressed in atrial tissue, but its involvement in post-MI LAR remains unclear. Here, LAR models were established in rats post-MI, and atrial hypertrophy was induced in HL-1 cells using angiotensin II (AngII). The role of α2δ1 in atrial hypertrophy was examined through treatment with either the α2δ1 inhibitor gabapentin or a C-terminal interfering peptide (α2δ1 CT-pep). A significant upregulation of α2δ1 expression was observed in the left atrium (LA) of MI rats and in AngII-treated HL-1 cells. Western blot analysis revealed increased α2δ1 levels in membrane fractions and decreased levels in the cytoplasmic fractions compared to controls. Both gabapentin and α2δ1 CT-pep treatment significantly reduced HL-1 cell hypertrophy and inhibited CAMKII and HDAC4 phosphorylation. Co-immunoprecipitation assays demonstrated an interaction between α2δ1 and GluN1, which was enhanced by AngII stimulation. Inhibition of α2δ1 attenuated the α2δ1-GluN1 interaction and reduced GluN1 translocation to the plasma membrane. In MI-induced HF rats, gabapentin treatment diminished atrial hypertrophy, suppressed AF inducibility and duration, and decreased membrane-associated α2δ1 and GluN1 levels. These findings suggest that the C-terminal domain of α2δ1 may contribute to left atrial hypertrophy in chronic ischemic heart failure and is associated with altered membrane GluN1 abundance and p-CAMKII/p-HDAC4 signaling. α2δ1 may therefore represent a potential therapeutic target for left atrial remodeling in ischemic heart failure. - Source: PubMed
Publication date: 2026/06/24
Wang ShaoxianLi ZhenjunYang NingXu JieYang BoDong ZengxiangZhou XiaohuiHan Wei - In the previous single-cell transcriptome analysis of goat ovulation, we identified that CACNA2D1 may play a critical role in immune cell infiltration during the ovulation process. Therefore, this study aimed to investigate the function of CACNA2D1 in ovulation. - Source: PubMed
Publication date: 2026/06/13
Guo ConghuiLiu JieChen KaihaoLiu GuangbinLiu DewuLi Yaokun - Chaihu Shugan San (CSS) is a classical traditional Chinese medicine formula widely used in improving depression. The purpose of this study was to investigate the molecular mechanisms underlying the antidepressant effects of CSS. - Source: PubMed
Wei XinHou LingchenBan ZiyunZang ShuxianZhang YuxuanWang MingyanAn FeiyuLiu YuqiLi De-PeiWang YuanyuanGao Yonggang - Human immunodeficiency virus 1 (HIV-1) infection often results in sensory neuropathy, with >60% of affected individuals developing chronic pain. Although viral proteins such as glycoprotein 120 (gp120) contribute to neuronal injury and pain hypersensitivity, their specific effects on nociceptive signaling remain unclear. Hyperactivity of -methyl-d-aspartate receptor (NMDAR) in the spinal dorsal horn is a hallmark of neuropathic pain. Here, we determined how gp120 affects synaptic NMDAR activity in spinal excitatory and inhibitory neurons in male and female mice. Intrathecal gp120 enhanced expression of α2δ-1 and GluN1 in the dorsal root ganglion (DRG) and spinal cord. Gp120 also increased α2δ-1-GluN1 interaction and their synaptic trafficking in the spinal cord. Functionally, gp120 induced hyperactivity of presynaptic NMDARs on primary afferent terminals and postsynaptic NMDARs in vesicular glutamate transporter 2-expressing excitatory, but not vesicular GABA/glycine transporter-expressing inhibitory, dorsal horn neurons. Importantly, gp120-induced hyperactivity of both presynaptic and postsynaptic NMDARs was eliminated by the α2δ-1 inhibitory ligand gabapentin or by an α2δ-1 C-terminal peptide that disrupts α2δ-1-NMDAR interactions. Correspondingly, treatment with the NMDAR antagonist, gabapentin, or α2δ-1 C-terminal peptide consistently reversed gp120-induced persistent nociceptive hypersensitivity. Furthermore, genetic deletion of or selective ablation of GluN1 in DRG neurons significantly attenuated gp120-induced nociceptive hypersensitivity. Together, these findings indicate that gp120 drives nociceptive hypersensitivity by augmenting presynaptic and postsynaptic activity of α2δ-1-bound NMDARs, thereby amplifying nociceptive transmission from primary afferents to spinal excitatory neurons. Targeting α2δ-1-associated NMDARs may therefore represent a promising therapeutic approach for HIV-associated chronic neuropathic pain. - Source: PubMed
Publication date: 2026/06/24
Gautam VipashaHuang 黄玉莹 YuyingChen 陈红 HongChen 陈少瑞 Shao-RuiPan 潘惠麟 Hui-Lin - The prevalence of coronary heart disease (CHD) continues to rise, and there is a lack of methods for early detection. To identify biomarkers for CHD, we analyzed the CACNA2D1 protein concentration in patients with different degrees of coronary artery stenosis to explore the correlation between plasma CACNA2D1 protein concentration and the severity of coronary artery stenosis. - Source: PubMed
Publication date: 2026/05/15
An LeRen YanhuiYang JinPei Zuowei