CHRNA3 antibody - N-terminal region (ARP34964_P050)
- Known as:
- CHRNA3 (anti-) - N-terminal region (ARP34964_P050)
- Catalog number:
- arp34964_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CHRNA3 antibody - N-terminal region (ARP34964_P050)
Related genes to: CHRNA3 antibody - N-terminal region (ARP34964_P050)
- 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-terminal region (ARP34964_P050)
Related articles to: CHRNA3 antibody - N-terminal region (ARP34964_P050)
- Bladder cancer is the ninth most common cancer worldwide, caused by genetic and environmental risk factors. Here, we report the findings of a multi-population meta-analysis of genome-wide association studies, including 32,470 individuals with and 1,753,462 without bladder cancer. We identify 70 independent risk loci, of which 43 are novel. Using a 70-marker polygenic risk score (HR = 1.63 per standard deviation), we increase the area under the curve from 0.71 (baseline risk model) to 0.75. Integrative analyses reveal the enrichment of the associated variants within accessible chromatin regions, and of the prioritized genes within pathways for xenobiotic metabolism and smoking behavior. Specifically, we show that the 15q25.1 variant rs71581744-ACCCC/A co-localizes with tissue-specific CHRNA3 expression, modulates mRNA stability, and associates with risk of muscle-invasive bladder cancer among current smokers. Together, these findings substantially expand the known genetic architecture of bladder cancer risk and highlight the germline regulation of smoking behavior as a mechanism driving bladder cancer susceptibility. - Source: PubMed
Publication date: 2026/08/08
Prokunina-Olsson LudmilaFlorez-Vargas OscarLevin Michael GDutta DiptavoBreeze Charles EHurwitz Lauren MYan WushengLamy PhilippePapenberg Brenen WWang KevinLee Chia-HanMilne Roger LGu JianUm Caroline YJoseph VijaiFurberg HelenaLe Calvez-Kelm FlorenceLori AdrianaChoudhury Parichoy PalAfshar NinaKogevinas ManolisOffit KennethVermeulen Sita HLópez de Maturana EvangelinaAlbanes DemetriusPurdue Mark PCortessis Victoria KKaragas Margaret RKooperberg CharlesBjurlin MarcTadesse Deborah AMoore Steven CHuang Wen-YiHaiman Christopher AStern Mariana CEliassen A HeatherMucci Lorelei AAben Katja KGalesloot Tessel E Verma AnuragYoshino SoichiroHikino KeikoTerao ChikashiRafnar ThorunnMatsuda KoichiShuin TaroGarcia-Closas MontserratReal Francisco XKiemeney Lambertus AChanock Stephen JMalats NúriaSilverman Debra TDyrskjot LarsRothman NathanielDamrauer Scott MKoutros StellaDamrauer Jeffrey S - [This corrects the article DOI: 10.3389/fnhum.2026.1845376.]. - Source: PubMed
Publication date: 2026/08/21
Rueckels MarkusBoreddy Srinivas ReddyPicard-Maureau Marcus - Epilepsy is a complex disorder with multiple provoking factors and etiologies. Certain genetic alterations in certain genes have been related to the development of various types of epilepsy. We performed a systematic review to evaluate associations between four nAChR alpha subunit genes (CHRNA2/3/5/6) and epilepsy subtypes. - Source: PubMed
Publication date: 2026/08/11
Daas AhmadAl-Zu'bi Laith MarwanDarweesh Aisheh FatehiKhrisat Rama AbdullahALsharafat Hadeel DakhalalahBarhoush Rahaf MalekAl-Zoubi Raed MAl-Batayneh KhalidAl Zoubi Mazhar Salim - Neuroblastoma is characterized by frequent involvement of bone marrow (BM) as a site of cell dissemination and spread. In this study, single-cell RNA sequencing (scRNA-seq) was used to analyze the cellular heterogeneity of a subset of metastatic BM samples collected at initial diagnosis. Comparison of the single-cell data with bulk RNA sequencing further refined the analysis. An enrichment of regulatory T cells relative to a healthy control and activation of the CD24, CD47, and CD200 "don't eat me" signals were documented. Computational analyses highlighted communication between neuroblastoma and myeloid cells via the amyloid precursor protein (APP) and midkine (MK) signaling networks. Within neuroblastoma cells, mutually exclusive adrenergic and transitory cell states were identified, and ten sub-clusters were denoted. In addition, common and unique tumor cell antigens were investigated. CNTFR and CHRNA3, as high-ranking candidates, were validated, confirming their strong selectivity for neuroblastoma cells. Taken together, these findings support the existence of a significant tumor-dependent modulation of the BM ecosystem, which should be considered when introducing immunotherapy. Furthermore, they highlight the potential to investigate new antigens at the single-cell resolution. - Source: PubMed
Publication date: 2026/06/23
Aveic SanjaDavini AlessandroMenegazzo SaraPantile MarcellaZanon CarloCorrà AnnaFaggin GiovanniCorallo DianaPellin DaniloSantoro LuisaFrasson ChiaraZin AngelicaFrancescato SamuelaRossi BartolomeoNeculaescu Ioana AncutaPigazzi MartinaBuldini BarbaraViscardi ElisabettaBiffi Alessandra - Conditioned immune responses demonstrate that learned sensory cues can modulate peripheral immunity without re-exposure to the original immunological trigger. In 2026, this research area reaches the centennial of early Pavlovian immune-reflex experiments that already reported conditioned leukocyte shifts and enhancement-like resistance to infection. Although modern psychoneuroimmunology has been shaped largely by conditioned immunosuppression, conditioned immune enhancement remains comparatively less explored despite its relevance to anticipatory host defense, immune surveillance, tumor biology, and neuroimmune regulation. This mini review focuses on the efferent, or recall, pathways of conditioned immune enhancement and separates them from afferent acquisition signals and central cue-immune-state representations. Classical odor-conditioning paradigms using camphor and the viral mimic polyinosinic:polycytidylic acid identified interferon- as an acquisition-related signal, whereas recall studies implicated β-endorphin, -opioid receptor, glutamatergic/NMDA, monoaminergic, catecholaminergic, cholinergic, serotonergic, ACTH-related, interferon--related, and endocrine mechanisms. Conditioned enhancement has been shown for natural killer cell activity, cytotoxic T-lymphocyte responses, neutrophil activity, antibody responses, and tumor-model readouts. We further integrate recent circuit-level studies of insular immune-state retrieval, brain-to-spleen humoral control, vagal cytokine coding, and descending sympathetic inflammatory pathways, together with transcriptomic data from a gene-agnostic multi-tissue pilot study assessing post-recall gene-expression dynamics. Together, these findings argue against a simple hypothalamic-pituitary-adrenal axis model and instead support a temporally organized, multi-channel efferent architecture. Dissecting and understanding this emerging architecture may provide the mechanistic basis for translating the efferent arm of conditioned immune enhancement into future therapeutic concepts with clinical impact. - Source: PubMed
Publication date: 2026/06/25
Rueckels MarkusBoreddy Srinivas ReddyPicard-Maureau Marcus