Ask about this productRelated genes to: CHRNA3 antibody
- Gene:
- CHRNA3 NIH gene
- Name:
- cholinergic receptor nicotinic alpha 3 subunit
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 15q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1990-05-11
- Date modifiied:
- 2016-10-05
Related products to: CHRNA3 antibody
Related articles to: CHRNA3 antibody
- Chronic obstructive pulmonary disease (COPD) and cardiovascular diseases (CVDs), including hypertension (HTN), coronary heart disease (CHD), and heart failure (HF), are major global health burdens. The shared genetic mechanisms underlying the high comorbidity between COPD and CVDs remain unclear. - Source: PubMed
Publication date: 2026/01/08
Chen ShiyuLi XiaojianXie Rongfang - Lung cancer (LC) and heart failure (HF) frequently co-occur with substantial clinical consequences, yet their shared genetic architecture remains poorly characterized. Emerging evidence suggests common pathophysiological pathways may underlie this comorbidity, particularly involving neural signaling and inflammatory processes. - Source: PubMed
Publication date: 2026/01/12
Mu LinquanZhou YiLi SongpuLiu Feng - About 60% of patients with high-risk neuroblastoma relapse. Specific mRNA detection in bone marrow (BM) by reverse transcriptase quantitative PCR (RT-qPCR) is associated with survival outcomes. Peripheral blood (PB) sampling is less invasive. Therefore, we prospectively validated an RT-qPCR panel of neuroblastoma mRNA in PB of patients with high-risk neuroblastoma, treated in NB2004-HR (GPOH) and NBL2009 (DCOG). - Source: PubMed
Publication date: 2025/12/18
Gelineau Nina Uvan Zogchel Lieke M JDe Carolis Borisvan Wezel Esther MZappeij-Kannegieter LilyJavadi AhmadSchumacher-Kuckelkorn RoswithaSimon ThorstenBerthold Frankvan Noesel Max MFiocco MartaStutterheim JanineEllen van der Schoot CHero BarbaraTytgat Godelieve A M - Understanding how genomic variants contribute to lung cancer (LC) risk is key to better understanding the molecular mechanisms underlying that risk. While genome-wide association studies (GWAS) have identified numerous LC risk loci, most single nucleotide polymorphisms (SNPs) reside in non-coding regions, making the interpretation of their function challenging. We accounted for lung-specific chromatin interactions and allele-specific gene expression levels in lung tissue to identify novel interactions between LC GWAS SNPs and distal genes. Pathway enrichment analysis implicated eight target genes (CYP2A6, ADCY2, CHRNA3, CHRNA5, LATS1, RAD52, RIF1, TP53BP1) in functional networks involving caffeine metabolism, DNA ionizing radiation (IR)-double strand breaks and cellular response, and nicotine effect on dopaminergic neurons. Novel findings include a role for rs2853677 in ADCY2 dysregulation (previous attribution to TERT) and rs9322193 in targeting tumour suppressor gene LATS1 (previous attribution to RPS18P9/KATNA1). By linking germline variants to more biologically relevant gene targets and somatic processes, our results align more closely with established epidemiological and environmental risk factors for lung cancer, including a potential genetic explanation for the environmental interaction of caffeine and smoking in LC risk. This highlights the value of integrating 3D genome architecture and tissue-specific expression to refine our understanding of cancer susceptibility. - Source: PubMed
Publication date: 2025/11/13
Khoo AldricPudjihartono MichaelO'Sullivan Justin MSchierding William - Chronic obstructive pulmonary disease (COPD) is a complex condition influenced by both environmental and genetic factors. Among the genetic determinants, polymorphisms in the and genes have been implicated in nicotine dependence and susceptibility to COPD in several populations. However, evidence remains limited in admixed populations such as Brazilians. This cross-sectional study investigated the association between (rs1051730, rs8034191) and (rs2234922) polymorphisms with tobacco nicotine dependence and COPD in a Brazilian cohort. Genotyping was performed using TaqMan SNP assays, and pulmonary function was assessed via spirometry according to ATS/ERS standards. Associations between genetic variants, tobacco intake, and COPD status were evaluated using χ and Fisher's exact tests, with odds ratios (ORs) and 95% confidence intervals (CIs). Post hoc power analyses were conducted to estimate detectable effect sizes. A total of 123 active or former smokers were analyzed. The variants (rs1051730 and rs8034191) showed a trend toward higher prevalence among individuals with heavy tobacco intake (>40 pack-years), though no significant allelic or genotypic differences were found between COPD and control groups ( > 0.05). The rs2234922 A allele was significantly more frequent in COPD patients, suggesting increased disease risk ( < 0.05), while the GG genotype appeared protective. Post hoc power analyses indicated moderate power (≈0.56-0.63) for the observed associations. In this Brazilian population, the polymorphisms may influence nicotine dependence, while rs2234922 appears to be associated with COPD susceptibility. These findings support a potential genetic contribution to disease risk and tobacco nicotine dependence, warranting further large-scale studies to confirm these associations and explore their therapeutic implications. - Source: PubMed
Publication date: 2025/11/14
Prudente Bartholo ThiagoPorto Luis CristóvãoPozzan RobertoNascimento AdrianaBartholo Barbara Beatriz Garcia RaskovischRufino Rogerioda Costa Cláudia Henrique