Ask about this productRelated genes to: CACNB1 Blocking Peptide
- Gene:
- CACNB1 NIH gene
- Name:
- calcium voltage-gated channel auxiliary subunit beta 1
- Previous symbol:
- CACNLB1
- Synonyms:
- -
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1992-03-27
- Date modifiied:
- 2016-02-04
Related products to: CACNB1 Blocking Peptide
Related articles to: CACNB1 Blocking Peptide
- The primary aim of this study was to explore the involvement of miRNAs in the anti-tumor effects of borax through high-throughput sequencing analysis. - Source: PubMed
Publication date: 2026/06/12
Zhou WenboSheng FenZhou JiaoWang JinjinHuang XuefeiChen QinhuaLi JinchaoLi HuizhenLiu MingxingZhu JunyingLiu JingjianWei YingWu Lun - Coronary artery disease (CAD) causes irreversible myocardial dysfunction and progressive heart failure due to loss of contractile function and limited endogenous regenerative capacity. Current therapeutic strategies fail to restore lost myocardium or regenerate damaged cardiac tissue. Identifying dysregulated contractility-related genes may reveal actionable targets for stem cell engineering, iPSC-derived cardiomyocyte design, and tissue regeneration aimed at restoring myocardial contractility and function. - Source: PubMed
Publication date: 2026/03/31
Qu FangzhouAn XifengLei YaqiLu ChongLiu HanxiuMa HuayanLi Yongle - This study aimed to identify prognostic genes related to palmitoylation and explore their value in predicting outcomes and treatment response in lung adenocarcinoma (LUAD). We employed the single-sample Gene Set Enrichment Analysis (ssGSEA) algorithm to compute the palmitoylation pathway score(PPS) and utilized lasso regression for feature selection to identify hub palmitoylation pathway score-related genes(PPSGs). A palmitoylation-related prognostic risk score model(PM model) was developed and validated across cohorts. Functional enrichment analysis, immune profiling, and drug sensitivity analyses were performed. Additionally, the expression levels of hub PPSGs were evaluated using qPCR in lung adenocarcinoma cell lines and patient tissue samples. Fifteen hub PPSGs were used to construct the PM model, which demonstrated moderate but consistent predictive accuracy (AUCs: 0.737, 0.693, 0.676 for 1-, 2-, 5-year survival). The risk score derived from the PM model (PM score) correlated with immune suppression and cytoskeleton-related pathways. Clinically, high PM score was associated with advanced stage, male patients, reduced immunotherapy response, and enhanced sensitivity to select chemotherapies. Five key genes (TPPP, FAAH, CACNB1, GLOD5, CCNA2) were validated in local LUAD samples. The PM model serves as a clinically relevant tool for prognosis and treatment prediction in LUAD, highlighting the potential role of palmitoylation in tumor progression and therapy stratification. - Source: PubMed
Publication date: 2026/02/16
Jiang JianjunLi ZichaoYan TianbaoHe YujingZhu JiaqiJin XinRao ShuanRao Xuguang - Autism spectrum disorder (ASD) exhibits remarkable genetic heterogeneity involving hundreds of risk genes; however, the mechanism by which these genes organize within biological networks to contribute to disease pathogenesis remains incompletely understood. This study aims to elucidate these organizational principles and identify critical network bottlenecks using a novel integrative computational framework. We analyzed 893 SFARI genes using a three-pronged computational approach: (1) a Machine Learning Dynamic Perturbation Propagation algorithm; (2) a hypergraph construction method explicitly modeling multi-gene complexes by integrating protein-protein interactions, co-expression modules, and curated pathways; and (3) Hypergraph Neural Network embeddings for gene clustering. Validation was performed using hub-independent features to address potential circularity, followed by a druggability assessment to prioritize therapeutic targets. The hypergraph construction captured 3847 multi-way relationships, representing a 45% increase in biological relationships compared to pairwise networks. The perturbation algorithm achieved a 51% higher correlation with TADA genetic evidence than random walk methods. Analysis revealed a hierarchical organization where 179 hub genes exhibited a 3.22-fold increase in degree centrality and a 4.71-fold increase in perturbation scores relative to non-hub genes. Hypergraph Neural Network clustering identified five distinct gene clusters, including a "super-hub" cluster of 10 genes enriched in synaptic signaling (4.2-fold) and chromatin remodeling (3.9-fold). Validation confirmed that 8 of these 10 genes co-cluster even without topological information. Finally, we identified high-priority therapeutic targets, including , , and . These findings establish hierarchical network organization principles in ASD, demonstrating that hub genes maintain substantially elevated perturbation states. The identification of critical network bottlenecks and pharmacologically tractable targets provides a foundation for understanding autism pathogenesis and developing precision medicine approaches. - Source: PubMed
Publication date: 2026/01/09
Batrancea Larissa MargaretaAkgüller ÖmerBalcı Mehmet AliGaban Lucian - Myocardial ischemia/reperfusion injury (MIRI) is a challenging cardiovascular disease. Mepivacaine, a common local anesthetic, exacerbates myocardial injury during ischemia‑reperfusion (IR). Understanding the underlying mechanisms of MIRI and potential therapeutic targets is important to treat this disease. In the present study, differentially expressed genes (DEGs) from the GSE19339 dataset were identified and analyzed. The expression of calcium voltage‑gated channel auxiliary subunit β1 () was measured in myocardial infarction samples and the effects of different doses of mepivacaine on cell cycle progression, apoptosis, cell viability, inflammatory response and oxidative stress were evaluated in H9c2 cells. Hypoxia‑reoxygenation (H/R) treatment simulated MIRI, highlighting the role of in mepivacaine‑induced cellular inflammation and injury. The present study identified 2,396 upregulated and 1,230 downregulated DEGs enriched in pathways such as inflammatory response and chemokine signaling. Mepivacaine induced apoptosis, G phase arrest and increased oxidative stress markers, including elevated ROS and MDA levels together with decreased SOD activity, as well as inflammatory cytokines (TNF‑α, IL‑1β and IL‑6), in a dose‑dependent manner in H9c2 cells. CACNB1 knockdown reduced mepivacaine‑ and H/R‑induced damage, inhibiting inflammation and apoptosis via the CACNB1/NOD‑like receptor protein 3 (NLRP3)/Nuclear factor erythroid 2‑related factor 2 (Nrf2) axis. Furthermore, knockdown enhanced Nrf2 nuclear translocation, indicating a stress response mechanism. Mepivacaine exacerbated MIRI by inducing apoptosis, G phase arrest, oxidative stress and inflammation in H9c2 cells. knockdown reduced these effects. Targeting the CACNB1/NLRP3/Nrf2 axis may be a potential strategy for mitigating myocardial injury caused by mepivacaine and IR. - Source: PubMed
Publication date: 2025/12/19
Shao QingboZhang JiWang Huaying