Ask about this productRelated genes to: Cacng1 antibody
- Gene:
- CACNG1 NIH gene
- Name:
- calcium voltage-gated channel auxiliary subunit gamma 1
- Previous symbol:
- CACNLG
- Synonyms:
- -
- Chromosome:
- 17q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-03-27
- Date modifiied:
- 2016-02-04
Related products to: Cacng1 antibody
Related articles to: Cacng1 antibody
- Understanding the genetic regulatory mechanisms of fat accumulation is crucial for improving beef quality. Hanwoo (Korean native cattle) is renowned for its high intramuscular fat (marbling), yet the genetic regulation of adipose gene expression remains insufficiently understood. In this study, we performed expression quantitative trait loci (eQTL) analysis using RNA-Seq data and genotype data from backfat tissue of 75 Hanwoo steers to identify regulatory variants associated with adipose deposition. A total of 25,042 significant -eQTL associations (FDR < 0.05) were identified, and 5362 unique top -eQTL pairs were retained after gene-wise filtering. Key -regulated genes included , , , and , which are involved in cytoskeletal organization, muscle development and calcium signaling. Three major -regulatory hotspots were located on BTA15 (BTA15:50354741) and BTA21 (BTA21:21526143, and BTA21:21541921). Permutation-based analysis (100,000 iterations) was conducted to control false positives, identifying 12 statistically significant -eQTL hotspots (FDR q < 0.05), of which SNP 6:60512276 and SNP 21:17035557 exhibited extensive -regulatory activity influencing 429 and 161 genes, respectively. In particular, SNP 21:17035557 acted as a shared - and -regulatory hub, indicating hierarchical control of adipose gene networks. Functional enrichment analyses revealed significant involvement of cytoskeleton- and calcium-dependent pathways, highlighting the interplay between structural remodeling and metabolic regulation in adipose tissue. These findings provide a comprehensive, system-level view of adipose gene regulation in Hanwoo cattle and highlight candidate molecular targets for genome-assisted and precision breeding. Moreover, this study offers quantitative genomic resources that can support the development of prediction models and decision-support systems for improving carcass traits in Hanwoo breeding programs. - Source: PubMed
Publication date: 2025/10/24
Lee JunyoungJeong TaejoonPark WoncheoulJang SunsikLee Poong-YeonLim Dajeong - Thermogenic beige adipocytes emerge in white adipose tissue (WAT) under certain physiological and pathological conditions, leading to increased energy expenditure, insulin sensitivity, and glucose tolerance. The induction of beige adipocyte formation represents a promising therapeutic approach for obesity and associated chronic diseases; however, the mechanisms controlling WAT beiging remain incompletely understood. - Source: PubMed
Publication date: 2025/04/02
Liu YangYin AmeliaSeese KendallFu WenyanYin Hang - In diabetes, macrophages and inflammation are increased in the islets, along with β-cell dysfunction. Here, we demonstrate that galectin-3 (Gal3), mainly produced and secreted by macrophages, is elevated in islets from both high-fat diet (HFD)-fed and diabetic db/db mice. Gal3 acutely reduces glucose-stimulated insulin secretion (GSIS) in β-cell lines and primary islets in mice and humans. Importantly, Gal3 binds to calcium voltage-gated channel auxiliary subunit gamma 1 (CACNG1) and inhibits calcium influx via the cytomembrane and subsequent GSIS. β-Cell CACNG1 deficiency phenocopies Gal3 treatment. Inhibition of Gal3 through either genetic or pharmacologic loss of function improves GSIS and glucose homeostasis in both HFD-fed and db/db mice. All animal findings are applicable to male mice. Here we show a role of Gal3 in pancreatic β-cell dysfunction, and Gal3 could be a therapeutic target for the treatment of type 2 diabetes. - Source: PubMed
Publication date: 2024/05/01
Jiang QianZhao QijinChen YibingMa ChunxiaoPeng XiaohongWu XiLiu XingfengWang RuoranHou ShaocongKong LijuanWan YanjunWang ShusenMeng Zhuo-XianCui BingChen LiangyiLi Pingping - Aripiprazole is recommended for routine use in schizophrenia patients. However, the biological mechanism for the adverse drug reactions (ADRs) among schizophrenia patients with the antipsychotic drug aripiprazole is far from clear. To explore the potential genetic factors that may cause movement-related adverse antipsychotic effects in patients, we conducted an association analysis between movement-related ADRs and SNPs in schizophrenia patients receiving aripiprazole monotherapy. In this study, multiple ADRs of 384 patients were quantified within 6-week treatment, and the scores of movement-related ADRs at baseline and follow-up time points during treatment were obtained. The highest score record was used as the quantitative index in analysis, and genetic analysis at the genome-wide level was conducted. The SNP rs4149181 in SLC22A8 [P = 2.28 × 10] showed genome-wide significance, and rs2284223 in ADCYAP1R1 [P = 9.76 × 10], rs73258503 in KCNIP4 [P = 1.39 × 10], rs678428 in SMAD9 [P = 4.70 × 10], rs6421034 in NAP1L4 [P = 6.80 × 10], and rs1394796 in ERBB4 [P = 8.60 × 10] were found to be significantly associated with movement-related ADRs. The combined prediction model of these six loci showed acceptable performance in predicting adverse events [area under the curve (AUC): 0.84]. Combined with the function and network of the above genes and other candidate loci (KCNA1, CACNG1, etc.), we hypothesize that SLC22A8 and KCNIP4-Kv channel perform their respective functions as transporter or channel and participate in the in vivo metabolism or effects of aripiprazole. The above results imply the important function of ion transporters and channels in movement-related adverse antipsychotic effects in aripiprazole monotherapy schizophrenia patients. - Source: PubMed
Publication date: 2023/07/25
Wang XuepingMei DongliLu ZheZhang YuyananSun YaoyaoLu TianlanYan HaoYue Weihua - Heterogeneous genetic loci contribute to hereditary hearing loss; more than 100 deafness genes have been identified, and the number is increasing. To detect pathogenic variants in multiple deafness genes, in addition to novel candidate genes associated with hearing loss, whole exome sequencing (WES), followed by analysis prioritizing genes categorized in four tiers, were applied. - Source: PubMed
Publication date: 2022/03/05
Mutai HidekiMomozawa YukihideKamatani YoichiroNakano AtsukoSakamoto HirokazuTakiguchi TetsuyaNara KiyomitsuKubo MichiakiMatsunaga Tatsuo