CACNA1C (aa 1150_1200)
- Known as:
- CACNA1C (aa 1150_1200)
- Catalog number:
- NBP1-42820SS
- Product Quantity:
- 0.025 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CACNA1C ( 1150_1200)
Related 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)
- Suicidal behavior is a complex and multifactorial phenomenon rooted in both psychological and biological mechanisms. In recent years, there has been an increasing focus on epigenetic factors, which modulate the influence of environmental factors on the expression of genes associated with emotional and cognitive regulation. - Source: PubMed
Publication date: 2026/03/02
Tussupova AruzhanTatayeva RozaKoygeldinova SholpanBazarbayeva ZhannatSembaeva ZhibekMussina Aiman - Mood and psychotic disorders are associated with disrupted circadian rhythms in sleep and activity. While mood and psychosis risk-associated genes (MPRGs) have been linked with sleep and circadian phenotypes, their contributions to molecular clock pathways and cellular circadian rhythms remain unknown. - Source: PubMed
Publication date: 2026/07/27
Xue XiangningAdelsheim ZoeGorczyca Michael TWei HeatherLeone Michael JLogan Ryan WMcCarthy Michael J - Natural products are a valuable source of antihypertensive agents; however, most studies have focused on multitarget effects or extract-level activity, limiting mechanism-specific interpretation and drug development. Here, a structure-driven screening strategy was applied to identify phytochemicals targeting CACNA1C, ADRB1, and AGTR1, key pharmacological targets of antihypertensive therapy. Quantitative structure-activity relationship models were developed using ChEMBL datasets (11,452 for CACNA1C, 612 for ADRB1, and 291 for AGTR1) and demonstrated robust predictive performance (AUC = 0.973), which was maintained under scaffold split and cross-validation. The SHAP-based interpretation revealed target-specific structural features, followed by pharmacophore profiling, chemical space analysis, and network-based prioritization. Overall, 10,586 natural compounds were screened and the top 5% per target (530 compound-target edges) were selected, revealing that 83.5% of the compounds were target-specific. Chemical space analysis revealed the predicted compounds occupied diverse and partially orthogonal regions compared with approved drugs, indicating scaffold diversification. Representative compounds selected based on docking, ADMET, and structural criteria predicted to form stable binding interactions in 100 ns molecular dynamics simulations, with consistent RMSD stabilization and favorable MM-PBSA binding free energies (-29.17 to -36.59 kJ/mol). Although source plants have reported antihypertensive effects, direct evidence in the literature linking individual compounds to specific pharmacological targets remains limited. Overall, this study presents a multilayer validation framework for the computational prioritization of antihypertensive phytochemicals, facilitating their potential integration of natural products into established pharmacological paradigms. This approach provides a strategy for prioritizing structurally diverse and computationally target-aligned candidates and may facilitate the translation of traditional herbal knowledge into modern target-based drug discovery. - Source: PubMed
Publication date: 2026/07/22
Park JunkyuShin SujinKim YoungminYoo JahyunLee KyungjinChoi Ho-Young - Congenital long QT syndrome (LQTS) is a heterogeneous disorder in which genotype and QTc duration modulate the risk of major arrhythmic events (MAEs), but contemporary paediatric outcome data remain limited. This study aimed to characterize clinical features, management strategies, and predictors of MAEs in a nationwide paediatric LQTS cohort. - Source: PubMed
Publication date: 2026/07/17
Perin FrancescaCartón Antonio JBermúdez-Jiménez Francisco JoseFernández-Barrio Bárbara CEsmel-Vilomara RogerMarcos-Fuentes LauraRueda Nuñez FernandoRodríguez Vázquez Del Rey Maria Del MarMontañés Delmás ElenaAyerza-Casas AriadnaFernández-Tudela BelénViadero Maria TeresaCastro FranciscoSiles AnaBlanca-Jover EnriqueCaravaca-Pantoja LauraBueno-Gómez AndreaSalamanca-Zarzuela BeatrizDe Vera McMullan PaulaLópez Blanco GloriaPlata-Izquierdo BeatrizJimenez Casso SoledadSerrano Robles Maria IsabelMatamala Morillo Miguel ÁngelDel Rey Megias LauraRocamora Salort SandraAparicio Fernández de Gatta CarlotaVillares Alonso MartaArroyas Sánchez MariaOrtega Montes AngelesGreco AndreaMartínez-Barrios EstefaníaJiménez-Jáimez JuanRoses-Noguer FerranSarquella-Brugada Georgia - Major depressive disorder (MDD) remains a leading cause of disability; however, monoaminergic models do not fully explain delayed treatment onset, incomplete remission, or rapid responses to glutamatergic interventions. In this study, we proposed a system-level ionic homeostasis framework for MDD. In this model, genetic susceptibility, chronic stress, metabolic burden, and neuroinflammation converge in neuronal and glial ion-channel systems, disrupting calcium, potassium, chloride, and purinergic homeostasis. These disturbances alter intrinsic excitability, synaptic integration, inhibitory tone, glial buffering, and neuron-glia signaling, thereby promoting excitation-inhibition imbalance, impaired plasticity, and corticolimbic network instability. We reviewed the evidence implicating the CACNA1C/Cav1.2, TREK-1, KCNQ, NKCC1/KCC2, HCN, transient receptor potential/acid-sensing ion channels, and glial mediators, including P2X7R, Kir4.1, and AQP4. We also discuss how ketamine-related mechanisms, chloride-restoring strategies, anti-inflammatory ion channel targeting, neuromodulation, EEG biomarkers, and AI/multiomics approaches support mechanism-informed precision therapeutics. MDD could be conceptualized as a distributed failure of ionic homeostasis that links neuroinflammation, E/I imbalance, network instability, and impaired adaptive plasticity. - Source: PubMed
Publication date: 2026/07/07
Seo Yohan