CHRNA3 antibody
- Known as:
- CHRNA3 (anti-)
- Catalog number:
- orb35316
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- CHRNA3 antibody
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
- Recent evidence determined that acupoints frequently overlap with regions of referred somatic hypersensitivity induced by visceral disease, a phenomenon known as acupoint sensitization. This state is typically characterized by sensory hypersensitivity and functional enhancement, often accompanied by superior therapeutic outcomes following acupuncture. However, the neurobiological mechanisms that prime acupoints for enhanced responsiveness remain poorly understood. - Source: PubMed
Publication date: 2026/05/19
Xu WenjieZhang DingdanTang YuanweiWang YingWang ZijieXi HanqingGao XinyanZhu BingCui Xiang - 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