Ask about this productRelated genes to: CHRNB3 Blocking Peptide
- Gene:
- CHRNB3 NIH gene
- Name:
- cholinergic receptor nicotinic beta 3 subunit
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 8p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1990-05-11
- Date modifiied:
- 2016-02-04
Related products to: CHRNB3 Blocking Peptide
Related articles to: CHRNB3 Blocking Peptide
- Tobacco consumption remains a leading global health challenge, driving chronic diseases such as cancer, cardiovascular disorders, and metabolic dysfunction through intricate molecular mechanisms. This study investigates the multifaceted effects of tobacco exposure on genetic, epigenetic, and metabolic pathways, focusing on its role in carcinogenesis. Tobacco smoke, laden with carcinogens like benzopyrene, nitrosamines, and reactive oxygen species (ROS), induces genetic mutations and impairs DNA repair by downregulating tumor suppressor genes like tumor protein 53 (P53), ataxia-telangiectasia mutated (ATM), ataxia telangiectasia and Rad3-related (ATR), and poly (ADP-ribose) polymerase 1 (PARP1), leading to genomic instability and heightened cancer risk. Dysregulation of apoptosis-regulating genes B-cell lymphoma 2 (BCL-2), CL2 associated X (BAX), and cysteinyl aspartate specific proteinase 3 and 9 (CASPASE-3, CASPASE-9) further promotes tumor cell survival, while nicotine addiction genes cholinergic receptor nicotinic beta 3 subunit (CHRNB3), dopamine receptor D2 (DRD2), catechol-O-methyltransferase (COMT), and dopamine beta-hydroxylase (DBH) reinforce dependency via dopaminergic pathways. Metabolically, tobacco disrupts glycolysis, oxidative phosphorylation, and folate metabolism by altering cytochrome P450 family 2 subfamily A member 6 (CYP2A6), methylenetetrahydrofolate reductase (MTHFR), and hypoxia-inducible factor 1-alpha (HIF-1α) expression, resulting in insulin resistance, mitochondrial dysfunction, and lipid peroxidation, which exacerbate systemic diseases and cancer progression (Warburg effect). Epigenetic changes, including DNA methylation and histone modifications via histone deacetylase 1 (HDAC1), enhancer of zeste 2 polycomb repressive complex 2 subunits (EZH2), and suppressor of variegation 3-9 homolog 1 (SUV39H1), silence tumor suppressors cyclin-dependent kinase inhibitor 2A (CDKN2A), creating a long-term oncogenic imprint. Mitochondrial genes, mitochondrially encoded NADH: ubiquinone oxidoreductase core subunit 1 & 4 (MT-ND1 and MT-ND4) and mitochondrially encoded cytochrome c oxidase I (MT-CO1), suffer, reducing ATP synthesis and increasing ROS, which drives apoptosis evasion and inflammatory nuclear factor kappa B (NF-κB), interleukin 6 (IL-6), and tumor necrosis factor-α (TNF-α). This research uniquely integrates these molecular disruptions, emphasizing novel insights into metabolic reprogramming (CYP2A6, MTHFR, HIF-1α) and epigenetic mechanisms in tobacco-induced pathogenesis. Additionally, it explores impacts on stem cell genes, SRY-box transcription factor 2 (SOX2), octamer-binding transcription factor 4 (OCT4), and Nanog homeobox (NANOG), linking tobacco to cancer stem cell proliferation and metastasis (e.g., oral squamous cell carcinoma). The study also highlights tobacco's role in aging, telomere shortening - telomerase reverse transcriptase (TERT downregulation) - and thymic involution, accelerating immunosenescence and disease susceptibility. These findings underscore the need for targeted interventions, such as epigenetic therapies, metabolic reprogramming, and robust tobacco control policies, to mitigate the global burden of tobacco-related diseases. By providing a unified framework for understanding tobacco's molecular impact, this research advocates for precision medicine and public health strategies to address the pervasive effects of tobacco on human health. - Source: PubMed
Publication date: 2026/01/31
Kumar UjjwalJahnavi GBiswas BijitAlam BenazirVarshney Saurabh - Rare coding variants that alter protein function and confer beneficial health effects can suggest potential drug targets. CHRNB3 encodes the β3 subunit of nicotinic acetylcholine receptors that bind nicotine and mediate its action in the brain. Here we report an exome-wide association study of number of cigarettes smoked per day (cig per day) in 37,897 current smokers from the Mexico City Prospective Study. We identify a deleterious missense variant in CHRNB3, p.Glu284Gly, that associates with a significant reduction in daily cigarette consumption. The missense variant is enriched in people of Indigenous Mexican ancestry but rare in other ancestries. We further identify a predicted loss-of-function variant in CHRNB3 that significantly associates with reduction in number of smoked cigarettes per day in participants of Japan Biobank. This variant is enriched in people of East Asian ancestry but is rare in other ancestries. Finally, we find that rare deleterious missense and predicted loss-of-function variants in aggregate associate with a reduction in the number of smoked cigarettes per day in individuals of European ancestry from the UK Biobank. Our results suggest that loss of function of CHRNB3 significantly associates with daily cigarette smoking, proposing β3 inhibition as a potential therapeutic strategy for nicotine addiction. - Source: PubMed
Publication date: 2026/02/24
Rajagopal Veera MZiyatdinov AndreyJoseph TylerAyer ArianeAhmed MohsinMbatchou JoelleZou YuxinAveritt Amelia JBanerjee NilanjanaCantor MichaelTorres Jason MChen EstebanVarela Jennifer Rico Jones MarcusOverton JohnHarari OlivierLotta LucaAbecasis GonçaloBaras ArisBerumen JaimeKuri-Morales PabloAlegre-Díaz JesúsTapia-Conyer RobertoCollins RoryEmberson Jonathan RMarchini JonathanCoppola Giovanni - Aniridia-associated keratopathy (AAK) leads to loss of corneal transparency because of epithelial, inflammatory, and pathological vascular changes. Here, we sought to understand this process at the transcriptomic level while evaluating an experimental pharmacotherapy for potential modulatory effects. - Source: PubMed
Javidjam DinaMoustardas PetrosDashti AvaAberdam DanielSchweitzer-Chaput ArnaudCisternino SalvatoreBremond-Gignac DominiqueLagali Neil - The world has recognized the significance of sustainable animal production, especially in terms of mitigating methane emissions. Developing strategies to mitigate methane without compromising productivity presents a significant challenge for nutritionists and breeders. However, measuring methane emissions at the individual level can be expensive and laborious. Therefore, the use of genomic approaches combined with whole-genome information may be an alternative to overcome these challenges. This study aimed to use sequencing data to carry out GWAS to identify genomic regions and candidate genes involved in biological processes and metabolic pathways of enteric methane emission-related traits (ME: daily methane emission, RME: residual methane emission, MY: methane yield, MI: methane intensity, and MM: methane metabolic). For this, 1042 Nellore animals with phenotypic information and 2744 imputed for sequence genotypes belonging to three breeding programs from Brazil were used. The SNP significance was estimated through frequentist statistics using the single-step GBLUP approach. For ME, a total of 27 significant SNPs were deemed significant (p < 3.55 × 10 ), harboring 89 positional candidate genes. For RME, 21 SNPs showed significant association, and 48 genes were mapped. Regarding MY, 20 SNPs were deemed significant and surrounded 76 candidate genes. For MI, 5 significant SNPs mapped 15 potential candidate genes, while in MM, 10 significant SNPs were located near 50 positional candidate genes. Various statistically significant SNPs and genomic regions on BTA 5, 6, 8, 10, 11, 13, 19, and 27 were shared between methane emission-related traits. Comparing QTL regions affecting methane-related traits showed common genomic regions with QTL previously related to feed efficiency, growth, and enteric methane emission. In general, the potential candidate genes (DUOX1, DUOX2, FRMD4A, NOS2, CHRNB3, CHRNA6, CALM2, EPCAM, MSH2, MSH6, KCNK12, MUC4, MUC20, LDHAL6B, SLC20A2, LIPC, EDNRA, ACOXL, MAP4K4, IL1R1, IL1R2, PLCB3, ESRRA, and BAD) are involved in several biological processes and signaling pathways related to gastrointestinal motility, salivary secretion, enteric nervous system, mucosal barrier integrity, epithelial transport, olfactory receptors, lipid metabolism, oxidative stress, cAMP, cGMP-PKG, MAPK cascade, among others. Our results highlight the complexity of methane emission as a polygenic phenotype, suggesting that bovine genetics can modulate methane emissions by controlling the ruminal ecosystem. These findings may serve as a basis for future research focused on developing selection strategies for more sustainable beef cattle production. - Source: PubMed
Publication date: 2025/12/17
Arikawa Leonardo MMota Lucio F MFonseca Larissa F SFernandes Júnior Gerardo ANasner Sindy L CValente Júlia P SSoares Tainara L SBorges Marcelo SSilva Joel APelaez Amalia MMercadante Maria E ZAlbuquerque Lucia G - The circadian clockwork is implicated in the etiology of addiction, with circadian rhythm disruptions bidirectionally linked to substance abuse, but the molecular mechanisms that underlie this connection are not well known. - Source: PubMed
Publication date: 2024/12/20
Khan AyubMinbay MeteAttia ZiadAy Ahmet AliIngram Krista K