CHRNB1 _ ACHRB
- Known as:
- CHRNB1 _ ACHRB
- Catalog number:
- Y213951
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CHRNB1 _ ACHRB
Ask about this productRelated genes to: CHRNB1 _ ACHRB
- Gene:
- CHRNB1 NIH gene
- Name:
- cholinergic receptor nicotinic beta 1 subunit
- Previous symbol:
- CHRNB
- Synonyms:
- -
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-25
- Date modifiied:
- 2016-02-04
Related products to: CHRNB1 _ ACHRB
Antibodies: CHRNB1 _ ACHRB HOST: Goat Clonality: pAbBovine Acetylcholine receptor subunit beta(CHRNB1) ELISA kitBovine Acetylcholine receptor subunit beta(CHRNB1) ELISA kitBovine Acetylcholine receptor subunit beta(CHRNB1) ELISA kit SpeciesBovineBovine cholinergic receptor, nicotinic, beta 1 (muscle) (CHRNB1) ELISA kit, Species Bovine, Sample Type serum, plasmaCanine Acetylcholine receptor subunit beta(CHRNB1) ELISA kitCanine Acetylcholine receptor subunit beta(CHRNB1) ELISA kitChicken Acetylcholine receptor subunit beta(CHRNB1) ELISA kitChicken Acetylcholine receptor subunit beta(CHRNB1) ELISA kitChicken Acetylcholine receptor subunit beta(CHRNB1) ELISA kit SpeciesChickenChicken cholinergic receptor, nicotinic, beta 1 (muscle) (CHRNB1) ELISA kit, Species Chicken, Sample Type serum, plasmaCHRNA7 Gene cholinergic receptor, nicotinic, alpha 7Chrnb1CHRNB1Chrnb1 Related articles to: CHRNB1 _ ACHRB
- Neurodegenerative diseases (NDDs), including Alzheimer's disease (AD) and Parkinson's disease (PD), are major public health challenges lacking effective therapies. To identify potential drug targets, we integrated large-scale genome-wide association studies with expression, methylation, protein, and splicing QTL datasets using Mendelian Randomization (MR) and summary-data-based MR (SMR). Colocalization analysis and machine learning were applied to prioritize candidate genes, followed by in silico druggability evaluation through molecular docking and molecular dynamics (MD) simulations. In animal models, candidate genes identified by transcriptomic analysis were further validated using integrative molecular and functional experiments. We identified several genes with potential causal links to AD (e.g., IQCE, HDHD2, ALPP) and PD (e.g., IL15, STK3, CHRNB1). Transcriptomic analyses indicated a consistent downregulation of IL-15 in PD model mice, corroborated by subsequent Western blot and immunohistochemical validation. Among predicted compounds, Prednisolone (ALPP), Sirolimus (IL15), and CHEMBL379975 (STK3) showed favorable binding affinities and stable MD trajectories, suggesting promising therapeutic relevance. Collectively, these findings highlight 12 QTL-regulated genes as promising molecular targets for further investigation in the context of NDDs. While the computational results provide a useful basis for hypothesis generation, experimental validation will be essential to determine the biological relevance and therapeutic potential of these candidate genes and compounds. - Source: PubMed
Publication date: 2026/01/16
Li XunZhang LeiXia JinyanZheng MeilingZhou ZhipengCai Jing - This study investigates the shared genetic basis between gastrointestinal (GI) diseases and neurodegenerative diseases (ND) using genome-wide association study (GWAS) data and statistical genetic methods. - Source: PubMed
Jiang YanZhang YuxiangMa LeiLi Chao - Migraine is a complex neurological disorder that severely compromises quality of life. Current therapies remain inadequate, creating an urgent need for precision medicine approaches. To bridge this gap, we integrated genome-wide association studies (GWASs) and multi-tissue expression quantitative trait loci (eQTL) data. Using Mendelian randomization (SMR/HEIDI) to identify putatively causal genes, followed by colocalization analysis, protein-protein interaction networks, and gene enrichment, we prioritized druggable targets. Phenome-wide association studies (PheWASs) further assessed their potential safety profiles. We identified 31 migraine-associated genes in whole blood, 20 in brain tissue, and 9 genes shared by both whole blood and brain regions. Among 13 druggable genes identified from the DGIdb and supporting literature, 10 passed colocalization validation. Eight genes (TGFB3, CHRNB1, BACE2, THRA, NCOR2, NR1D1, CHD4, REV3L) showed interactions with known drug targets, enabling the computational prediction of 41 potential repurposable drugs. Based on target druggability, PPI (protein-protein interaction) and favorable PheWAS profiles, NR1D1, THRA, NCOR2, and CHD4 are prioritized for drug development. Additionally, MICU1, UFL1, LY6G5C, and PPP1CC emerged as novel pathophysiological factors. This study establishes a multi-omics framework for precision migraine therapy, translating genetic insights into clinically actionable targets. - Source: PubMed
Publication date: 2025/09/29
Liu XiantingLiu QingmingZhu HaoningZhou XiaoLi XinyaoHu MingPeng FuJi JianguangYang Shu - The adult nicotinic acetylcholine receptor in muscle is a pentameric complex composed of four transmembrane subunits, and these are encoded by CHRNA1, CHRNB1, CHRND, and CHRNE, respectively. There were only a few case reports of congenital myasthenic syndromes due to CHRNA1, CHRNB1, and CHRND. We aimed to share phenotypic and genotypic features of the patients. - Source: PubMed
Publication date: 2025/08/05
Guan JingZhang MinHu ChaopingZhao LeiZhang LinmeiLi XihuaWang YiZhou ShuizhenLi Wenhui - Congenital myasthenic syndromes (CMS) are a heterogeneous group of disorders characterized by compromised neuromuscular signal transmission due to pathogenic germline variants in genes expressed at the neuromuscular junction (NMJ). A total of 40 genes have been reported in CMS (AGRN, ALG14, ALG2, CHAT, CHD8, CHRNA1, CHRNB1, CHRND, CHRNE, CHRNG, COL13A1, COLQ, DES, DOK7, DPAGT1, GFPT1, GMPPB, LAMA5, LAMB2, LRP4, MACF1, MUSK, MYO9A, PLEC, PREPL, PTPN11, PURA, RAPSN, RPH3A, SCN4A, SLC18A3, SLC25A1, SLC5A7, SNAP25, SYT2, TEFM, TOR1AIP1, UNC13A, UNC50 and VAMP1). The 40 genes are putatively classified into 13 subtypes by pathomechanical, clinical, and therapeutic features. A unique feature shared by recently identified genes is that CMS is concomitantly recognized in other mostly severer diseases. For example, four recently identified genes exhibit the following phenotypes: PURA-CMS, developmental delay; TEFM-CMS, mitochondrial disease; PTPN11-CMS, Noonan syndrome/Leopard syndrome; and DES-CMS, desmin myopathy. Conversely, these diseases are not always associated with CMS, although genetic and/or environmental factors that determine the involvement of the NMJ remain to be identified. In this review, particular emphasis will be placed on five recently identified genes (MACF1, TEFM, PTPN11, DES and UNC50). - Source: PubMed
Publication date: 2025/06/18
Ohno KinjiIto MikakoOhkawara Bisei