CHRNA3 Antibody (N_term)
- Known as:
- CHRNA3 Antibody (N_term)
- Catalog number:
- AP5022a
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- CHRNA3 Antibody (N_term)
Related genes to: CHRNA3 Antibody (N_term)
- 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 (N_term)
Related articles to: CHRNA3 Antibody (N_term)
- Accumulating evidence has demonstrated a significant association between e-cigarette exposure and airway epithelial damage. Nevertheless, the molecular drivers orchestrating this pathology remain unclear. Here, we demonstrated that nicotine is the key component of e-cigarette aerosols that induced pathogenic changes, including apoptosis, oxidative stress, and mucus overproduction, in mouse airway epithelium and in human bronchial epithelial (HBE) cells. We further established that the nicotine of e-cigarette aerosols induced autophagosome formation via MTOR inhibition, while concurrently suppressing autolysosomal degradation through lysosomal membrane permeabilization (LMP). Restoration of lysosomal membrane integrity reversed e-cigarette aerosol-induced LMP and the subsequent macroautophagy/autophagy inhibition, thereby alleviating airway epithelial damage. Mechanistically, nicotine of e-cigarette aerosols permeabilized lysosomal membranes via calcium-dependent activation of PLA2G4A, which hydrolyzed the sn-2 ester bond of lysosomal glycerophospholipids, generating lysophospholipids. This process was initiated by nicotine binding to CHRNA3/α3 nAChR, a ligand-gated ion channel whose activation triggered intracellular Ca overload. Genetic or pharmaceutical inhibition of CHRNA3 reduced intracellular Ca content, abolishing PLA2G4A activation. This inhibited lysosomal glycerophospholipid hydrolysis, thereby attenuating LMP and subsequently resolving autophagic flux blockade and cytotoxicity in HBE cells. Moreover, the role of CHRNA3-mediated PLA2G4A activation in e-cigarette aerosol-induced autophagy-lysosome dysfunction and cellular toxicity was validated in human lung organoids. Overall, our study underscores the importance of CHRNA3 activation, as a molecular initiating event (MIE), in the regulation of PLA2G4A-mediated hydrolysis of glycerophospholipids and autophagic flux impairment, and CHRNA3 inhibition could serve as a potential therapy for airway disorders induced by e-cigarette aerosols. - Source: PubMed
Publication date: 2026/06/13
Yu YongquanXu ShuyuYang LiuShu ShugeZhou HaojieHua ZhenchengWang LiZhu YingranShi AimingXia RongChen ChaoWang Shou-Lin - 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 - BACKGROUND: 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. METHODS: We conducted cross-trait meta-analyses of genome-wide association studies (GWAS) encompassing 23 cancer types and 14 cardiovascular diseases using MTAG and CPASSOC. Tissue-specific expression patterns were evaluated using GTEx data, while single-cell RNA sequencing analyzed differential gene expression in HF patients and LC cases compared to healthy controls. Pharmacological screening was performed using DrugBank and PharmGKB databases to identify potential therapeutic candidates. RESULTS: Our analyses identified 48 pleiotropic single nucleotide polymorphisms clustered within chromosome 15q25.1 that were significantly associated with both LC and HF (p < 1 × 10− 76). These variants implicated key genes including CHRNA3, CHRNA5, HYKK, and PSMA4, which demonstrated enrichment in neuroactive ligand-receptor interaction pathways and specific expression in cardiac tissues and immune cells. Twenty candidate drugs targeting cholinergic pathways were identified. CONCLUSIONS: These findings uncover a shared genetic locus and neural pathways underlying LC-HF comorbidity, offering mechanistic insights and therapeutic opportunities. The results highlight the need for integrated cardiology-oncology approaches in managing these complex conditions. - 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