CACNA1C (aa 1150_1200)
- Known as:
- CACNA1C (aa 1150_1200)
- Catalog number:
- NBP1-42820
- Product Quantity:
- 0.1 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CACNA1C ( 1150_1200)
Ask about this productRelated genes to: CACNA1C (aa 1150_1200)
- 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 (aa 1150_1200)
Related articles to: CACNA1C (aa 1150_1200)
- Copper oxide nanoparticles (CuONPs) are widely employed in industrial and biomedical applications; however, their long-term exposure induces severe cardiac impairments. Spiraeoside (SPD) is a naturally occurring flavonoid with diverse biological properties. The current study was designed to investigate the cardioprotective effects of SPD against CuONPs-induced cardiotoxicity. Thirty-two rats were randomly allocated into four groups: control, CuONPs (100 mg/ kg), CuONPs (100 mg/kg) + SPD (200 mg/ kg), and SPD (200 mg/kg) alone treated group. Our findings showed that CuONPs exposure substantially reduced the expression of ATP2A2, RYR2, CACNA1C, and GSK3B while upregulating CAMK2D, AXIN2, WNT3A, and CTNNB1. Moreover, CuONPs intoxication induced severe oxidative imbalance as evidenced by high levels of ROS and MDA while reducing the activities of GST, GSR, CAT, HO-1, SOD and GPx. Besides, CuONPs administration increased the levels of Troponin-I, LDH, Troponin-T, CRP, BNP, NT-proBNP, CPK, and CK-MB. Severe echocardiographic alterations were found after CuONPs exposure as indicated by significant reduction in heart rate, high EDV and ESV, as well as ventricular dilation. Similarly, CuONPs induced marked upregulation of pro-inflammatory markers including COX-2, IL-6, IL-1β and TNF-α. A significant upregulation of Bax, Caspase-3, and Caspase-9 while a marked reduction in the levels of Bcl-2 was found following the exposure of CuONPs. Histopathological analysis showed severe structural myocardial damage in response to CuONPs intoxication. Nonetheless, SPD notably protected cardiac tissues via regulating calcium-dependent signaling pathways, inflammatory and apoptotic responses, echocardiographic parameters, oxidative stress, and histopathological alterations. Collectively, these findings suggest that SPD is a promising natural bioactive molecule against cardiac injury caused by nanoparticles. All preclinical studies, such as pharmacokinetic, toxicological, and dose optimization investigation, are still needed to assess the potential clinical applicability. - Source: PubMed
Publication date: 2026/08/28
Arshad RameeshaMehreen ArifaJamil SalimHassan Hesham MHalawani Ibrahim FAlsharif Khalaf FAlzahrani Khalid J - 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