Ask about this productRelated genes to: CHRM3 antibody
- Gene:
- CHRM3 NIH gene
- Name:
- cholinergic receptor muscarinic 3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1q43
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-04
- Date modifiied:
- 2016-03-03
Related products to: CHRM3 antibody
Related articles to: CHRM3 antibody
- Fat Mass and Obesity-Associated (FTO) is linked to multiple myeloma (MM) progression, but its action mechanisms are poorly understood. - Source: PubMed
Publication date: 2026/03/23
Lu BoBin TingDeng Xue-FeiXie MeiLin ChaoTang JingSun Tian-Tian - Acetylcholine differentially modulates anterior cingulate (ACC) and lateral prefrontal (LPFC) cortices for cognitive-emotional integration, but cell-specific expression and function of muscarinic receptors (mAChR) and corresponding CHRM1-4 genes in these areas of the primate brain are largely unknown. Our single-nucleus RNA sequencing and mRNA-protein histology in macaques revealed CHRM3 as the most enriched mAChR gene in neurons, while m1 predominates at the protein level, likely due to nuclear retention of CHRM3 and cytoplasmic trafficking of CHRM1. CHRM3 and CHRM1 showed strong co-expression and functional overlap, and were transcriptomically-distinct from CHRM2, which was uniquely enriched in deep layer excitatory and PVALB+ inhibitory neurons. Between-region comparisons showed that CHRM3 is enriched in LPFC relative to ACC excitatory neurons. Further, CHRM1-3+ neurons showed region-specific transcriptomic signatures, with upregulation of synaptic plasticity genes in ACC relative to LPFC. Functional in vitro experiments confirmed a robust cholinergic-mediated decrease in excitatory and increase in inhibitory synaptic tone specific to ACC neurons, accompanied by changes in spine morphology. In contrast, cholinergic stimulation reduced inhibitory current amplitude in LPFC, shifting the microcircuit towards a stronger excitatory tone. These findings highlight region-specific acetylcholine signaling essential for flexible processing, learning and memory, which may underlie neurochemical circuit imbalance in neuropsychiatric disorders. - Source: PubMed
Publication date: 2026/03/19
Tsolias AlexandraMojica Chromewell AYamani RaghadKhanna Sonal DAl Abdullatif SalamSnyder Benjamin JChang WayneGuillamon-Vivancos TeresaGoodliffe JosephCapriglione Angela LZhou YuxinTan Palanca Isabel LuisaMartinez JoaquinCampbell Joshua DLuebke Jennifer IZeldich EllaMedalla Maria - The Post-COVID syndrome is associated with the generation of autoantibodies to vasoregulative G-protein coupled receptors (GPCR). It remains elusive, however, whether these autoantibodies play a pathophysiological role in this disease. The present study investigates whether detection and concentration of GPCR autoantibodies are related to vascular function in patients with Post-COVID. - Source: PubMed
Publication date: 2026/02/24
Seibert Felix SKurucay MelisaWiemers LeaStervbo UlrikSander OliverSegelbacher MonikaSeidel MaximilianBertram SebastianBabel NinaWesthoff Timm H - The purpose of this study is to explore the potential mechanism of Si-Wu-Tang (SWT) against esophageal squamous cell carcinoma (ESCC). Initially, 18 active molecules and 96 related targets of SWT obtained from publicly accessible databases. Through Genecards database queries and gene differential expression analysis combined with weighted gene correlation network analysis (WGCNA) on the GSE20347 dataset of ESCC, 3649 disease targets were identified. A subsequent analysis of Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment was performed on 51 disease-drug intersection genes using the R language. Additionally, we identified 3 target hub genes (CDK1, NCOA1, and CHRM3) utilizing machine learning tools. Single-gene GSEA results suggested that hub genes may influence several signaling pathways and biological processes. Immune infiltration analysis demonstrated that SWT might impact the tumor immune microenvironment in ESCC by acting on hub targets. Molecular docking demonstrated the presence of affinity between target hub proteins and active compounds. This study revealed that SWT might exert its therapeutic effects on ESCC through multi-targets and multi-mechanisms. - Source: PubMed
Li XinboZhang ChenchenLi JingYuan JianfengXing TiantianYang HeyuanShi Huijuan - The treatment of prostate cancer (PCa) continues to pose substantial clinical challenges. The use of large language models (LLMs) to identify the key molecular determinants of PCa progression, followed by experimental biological validation, helps uncover novel therapeutic targets. We developed hierarchical knowledge-guided LLM for risk gene identification (HKLLM-RG), a PCa risk gene identification method. Among the candidate genes identified, ALKBH5 emerged as particularly noteworthy in the analysis. Reduced expression of ALKBH5 correlated with aggressive clinical features and significantly reduced survival in PCa. ALKBH5 inhibits PCa progression and promotes ferroptosis. CHRM3, which is the downstream molecule of ALKBH5, could promote PCa cell proliferation and migration. ALKBH5 regulates CHRM3 in an mA-dependent manner. Mechanistically, the ALKBH5/CHRM3 axis suppresses AKT signaling, thereby inducing the upregulation of the transcriptional repressor ZNF281. This regulatory cascade subsequently downregulates the expression of SLC3A2 and GPX4, ultimately sensitizing cells to ferroptosis. Thus, AZD5363 and RSL3 targeting the ALKBH5/CHRM3/ZNF281 axis can effectively synergize to treat PCa by promoting ferroptosis. Taken together, this study leverages LLM-guided discovery to delineate a novel ALKBH5/CHRM3/ZNF281 regulatory axis controlling ferroptotic susceptibility in PCa. Importantly, a synergistic therapeutic strategy was identified by combining RSL3 with AZD5363, providing novel therapeutic targets and directions for PCa treatment. - Source: PubMed
Publication date: 2026/02/06
Yi XianyanlingHan ZeyuLu DazhiXu HangZheng XiaonanTang YaxiongLi JinLi XuanjiLiao DazhouLi HongWei QiangYang LuPeng JiajieAi Jianzhong