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)
- 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 - 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.: AACOCF3: arachidonyl trifluoromethyl ketone; AB-PAS: Alcian Blue Periodic Acid Schiff; ANXA5: annexin V; AOP: adverse outcome pathway; ATG: autophagy related; BECN1: beclin 1; CASP3: caspase 3; CASP7: caspase 7; CASP9: caspase 9; CQ: chloroquine; CHRNA/nAChR: cholinergic receptor nicotinic alpha subunit; CTSD: cathepsin D; DHE: dihydroethidium; DMSO: dimethyl sulfoxide; E-cigarette: electronic cigarette; ENGASE/NAG: endo-beta-N-acetylglucosaminidase; FBS: fetal bovine serum; GA: geldanamycin; GSH: glutathione; HBE: human bronchial epithelial; HEX: hexamethonium; LAMP: lysosome associated membrane protein; LC-MS/MS: liquid chromatography-tandem mass spectrometry; LGALS3: galectin 3; LBD: ligand-binding domain; LMP: lysosomal membrane permeabilization; LPC: lysophosphatidylcholine; LPE: lysophosphatidylethanolamine; MAP1LC3/LC3B: microtubule associated protein 1 light chain 3 beta; MDA: malondialdehyde; MIE: molecular initiating event; MTBE: methyl tert-butyl ether; MTOR: mechanistic target of rapamycin kinase; mtROS: mitochondrial reactive oxygen species; NBR1: NBR1 autophagy cargo receptor; PBS: phosphate-buffered saline; PC: diacyl glycerophosphatidylcholine; PE: diacyl glycerophosphatidylethanolamine; Penh: pulmonary resistance; PG: propylene glycol; PLA2G4A/cPLA2: phospholipase A2 group IVA; PLA2G4E: phospholipase A2 group IVE; ROS: reactive oxygen species; siRNA: small interfering RNA; SOD: superoxide dismutase; SQSTM1/p62: sequestosome 1; TEM: transmission electron microscopy; TUNEL: terminal deoxynucleotidyl transferase dUTP nick end labeling; VG: vegetable glycerin. - Source: PubMed
Publication date: 2026/06/21
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