CACNA1C antibody
- Known as:
- CACNA1C (anti-)
- Catalog number:
- orb87786
- Product Quantity:
- 50 ug
- Category:
- -
- Supplier:
- 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
- Annexin A4 (A4) is a negative modulator of adenylyl cyclase type 5 (AC5) with increased expression in failing human hearts. Here, we investigated whether A4 deficiency contributes to cardiac electrical and structural remodeling induced by chronic stimulation of β-adrenergic receptors (βAR). A4-deficient mice (gene trapped, GT) and wild-type (WT) were infused for 7 days with isoprenaline (ISO) or NaCl as control. Myocytes of ISO-treated GT (GT) displayed more hypertrophy, increased action potential duration, reduced K-current I, preserved L-type Ca current I with a negative shift of voltage dependence of activation, in line with increased AC/cAMP/PKA signaling, and increased NCX1 versus WT. At the molecular level, mRNA levels for Kcnd3, Kcnip2, Cacna1c decreased at unchanged protein levels of Kv4.2, Kv4.3, KChIP2, α1C, independent of genotype, suggesting posttranslational modifications of the channels underlying I and I. Chronic ISO-induced βAR desensitization and redox stress were confirmed by decreased cAMP production and lower mRNA levels of Adrb1, Adcy5/6, and Sod2, and reduced response to acute ISO, with no additional genotype-dependent effects on calcium handling or contractility. Nevertheless, GT cardiomyocytes retained a greater cAMP response to acute ISO, in line with AC5 disinhibition and preserved β2AR and Gαs/i, suggesting genotype-dependent differences in β-adrenergic signaling under stress. mRNA levels of Anxa4 were increased in hypertrophied WT vs. normal WT hearts, supporting a protective role for A4. Overall, the advanced remodeling in A4-deficient myocytes detected in response to chronic βAR stimulation proposes using A4 peptide as a therapeutic tool to prevent the progression of cardiac electrical remodeling. - Source: PubMed
Pluteanu FlorentinaHeinick AlexanderDomnik-Lehnert ManuelMüller Frank UHermes Christina - Excitation-contraction coupling is central to cardiovascular physiology, but the prospective relevance of circulating proteins involved in this pathway remains uncertain. - Source: PubMed
Publication date: 2026/08/12
Hu DanGao YangWang JingGuo QuanShi ZhuochengChen DonghuiXia DongshengLi MuweiWang XiaohuGeng Bingchuan - Premenstrual disorders (PMDs) are characterized by affective and physical symptoms before menses, likely due to abnormal sensitivity to normal hormone fluctuations. While sizable heritability has been indicated in twin studies, there are no genome-wide association studies (GWASs) to inform the genetic architecture of PMDs. - Source: PubMed
Publication date: 2026/06/29
Hysaj ElgetaJaholkowski PiotrShadrin Alexey ABergstedt JacobLu YiBertone-Johnson ElizabethBulik Cynthia MLandén MikaelSandin SvenKowalec KaarinaHägg SaraDi Florio AriannaGoldman DavidSchmidt Peter JValdimarsdóttir Unnur AAndreassen Ole ALu Donghao - Alternative splicing is a critical determinant of protein diversity in the heart, where it drives the postnatal functional maturation of cardiomyocytes and specifies the ion-channel and calcium-handling isoforms required for mature contractile function; dysregulated splicing programs have in turn been implicated in cardiomyopathies and arrhythmias. However, the splicing regulators that control cardiomyocyte calcium handling remain largely unknown. - Source: PubMed
Publication date: 2026/07/28
Murphy SeanWang HanwenZureick NadineKoakutsu MisatoSuh DavidLee Dong IkKwon Chulan - High cholesterol is a key cardiovascular risk factor that can modulate cardiac electrophysiology and promote acquired long QT syndrome (acLQTS)-related cardiotoxicity, a potentially life-threatening condition associated with QT prolongation, torsade de pointes, and sudden cardiac death. This study investigated the effects of cholesterol overload on human Ether-à-go-go-Related Gene (hERG/Kv11.1; encoded by KCNH2) potassium channels and L-type calcium channels (LTCC; mainly Cav1.2/CACNA1C in cardiomyocytes), as well as the underlying mechanisms of acLQTS-related cardiotoxicity, using human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs), whole-cell patch clamp, quantitative real-time PCR (qRT-PCR), Western blotting, immunoprecipitation, fluorescence imaging, and a high-cholesterol diet guinea pig model with rosuvastatin intervention combined with optical mapping. The results showed that transient cholesterol exposure inhibited hERG tail current amplitude and accelerated channel inactivation, with the effect showing a Y652-dependent component, while also enhancing LTCC activity. Mechanistically, cholesterol overload triggered endoplasmic reticulum (ER) stress, impaired hERG proteostasis, and promoted ER-to-lysosome-associated degradation (ERLAD) of hERG. This process was associated with CANX-mediated recognition of abnormal hERG and FAM134B-LC3B-related autophagic-lysosomal processing, contributing to reduced total hERG expression and membrane-localized mature hERG. FAM134B overexpression partially preserved hERG expression and attenuated cholesterol-induced ER stress/autophagy-related abnormalities. In vivo, rosuvastatin improved lipid profiles and cardiac remodeling in high-cholesterol guinea pigs but was associated with more pronounced action potential duration (APD) and QT interval prolongation under high-cholesterol conditions. These findings suggest that cholesterol overload may increase susceptibility to hERG-related repolarization abnormalities during rosuvastatin exposure and highlight the importance of cholesterol management and electrocardiographic (ECG) monitoring in hypercholesterolemic settings. - Source: PubMed
Publication date: 2026/08/12
Ma LuTeng WeiLiu Xin-YuSong YingYi Ze-ShuaiLi Xiao-XuLi Yue-XinDing Qi-RuiZhou Yu-YanSun XiangHong Hai-YingLi Bao-Xin