Ask about this productRelated genes to: CHRNA9 Blocking Peptide
- Gene:
- CHRNA9 NIH gene
- Name:
- cholinergic receptor nicotinic alpha 9 subunit
- Previous symbol:
- -
- Synonyms:
- NACHRA9
- Chromosome:
- 4p14
- Locus Type:
- gene with protein product
- Date approved:
- 2000-11-29
- Date modifiied:
- 2016-02-04
Related products to: CHRNA9 Blocking Peptide
Related articles to: CHRNA9 Blocking Peptide
- Nicotinic acetylcholine receptors (nAChRs) on immune cells are promising therapeutic targets for the treatment of inflammatory diseases and pain. Both α7 and α9* nAChRs (*denotes the potential presence of other nAChR subunits) have been implicated as mediators of the cholinergic anti-inflammatory system (CAS). This study investigated the binding sites of α7-selective ligands on these receptors and their effects on ATP-dependent release of the pro-inflammatory cytokines interleukin (IL)-1β and IL-18 by human mononuclear phagocytes. - Source: PubMed
Publication date: 2026/03/11
Mobasher MonaHone Arik JPilzecker MalinBozic DariaHecker AndreasMcIntosh J MichaelKirschner Karl NGrau VeronikaPapke Roger LAndleeb HinaRichter Katrin - The clinical interest in mechanisms controlling the biosynthesis and release of the pro-inflammatory cytokine interleukin (IL)-1β is outstanding, as IL-1β is associated with life-threatening inflammatory diseases including hyperinflammation caused by extracellular ATP originating from damaged cells. Previously, we identified a cholinergic mechanism controlling ATP-dependent IL-1β release via metabotropic signaling of unconventional nicotinic acetylcholine receptors (nAChRs) containing subunits α7 and α9* (denoting homomeric or heteromeric α9) in monocytes. This study examines whether this mechanism is active in human macrophages (THP-1 cell-derived, peripheral blood mononuclear cell-derived, and peritoneal macrophages). - Source: PubMed
Publication date: 2025/10/27
Wolf Philipp M KHanke DominikSingh Vijay KKeller Hanno LEttischer Luca JTeppe LauraAmati Anca-LauraHecker AndreasHusain-Syed FaeqRohde MariusNuber Ulrike ABüttner KathrinMcIntosh J MichaelLiese JulianeMazurek SybilleGrau VeronikaRichter Katrin - To identify novel genetic loci associated with differences in serum etonogestrel concentrations among contraceptive implant users. - Source: PubMed
Publication date: 2025/02/27
Lazorwitz AaronAquilante Christina LShortt Jonathan AGignoux Christopher RTeal StephanieSheeder Jeanelle - Triple-negative breast cancer (TNBC) lacks expression of estrogen receptor (ER), progesterone receptor (PR), and HER2, and remains one of the most aggressive and therapeutically challenging breast cancer subtypes, marked by early relapse, metastasis, and limited targeted treatment options. In a recent study published in The Journal of Pathology, Kuo et al provide compelling evidence that nicotine exposure, whether from tobacco smoke or e-cigarette vapor, drives TNBC progression by promoting stem-like and metastatic phenotypes. Integrating clinical datasets, patient tissues, cell lines, and in vivo models, the authors demonstrate that nicotine enhances tumor aggressiveness via coordinated upregulation of CHRNA9 and IGF1R. Silencing either receptor attenuates nicotine-induced stemness, invasion, and metastasis, revealing a therapeutically actionable axis. High expression of CHRNA9 and IGF1R correlates with poor clinical outcomes and may define a nicotine-exposed TNBC subgroup that could benefit from IGF1R-targeted therapy or repurposed nicotinic receptor antagonists. These findings underscore the role of environmental exposures in shaping tumor biology and offer a mechanistic basis for the poorer prognosis observed in smokers with breast cancer. © 2025 The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2025/09/09
Simpkins ChristopherToska Eneda - The early onset of peripheral deafness significantly alters the proper development of the auditory system. Likewise, exposure to loud noise during early development produces a similar disruptive effect. Before hearing onset in altricial mammals, cochlear inner hair cells (IHCs) exhibit spontaneous electrical activity that drives auditory circuit development. This activity is modulated by medial olivocochlear (MOC) efferent feedback through α9α10 nicotinic cholinergic receptors in IHCs. In adults, these receptors are restricted to outer hair cells, where they mediate MOC feedback to regulate cochlear amplification. Although the MOC system's protective role to prevent noise-induced hearing loss in adulthood is well established, its influence during early developmental stages-especially in response to exposure to loud noise-remains largely unexplored. In this study, we investigated the role of MOC feedback during early postnatal development using α9 knock-out (KO) and α9 knock-in (KI) mice of either sex, which respectively lack or exhibit enhanced cholinergic activity. Our findings reveal that both increased and absent olivocochlear activity result in altered auditory sensitivity at the onset of hearing, along with long-range alterations in the number and morphology of ribbon synapses. Early noise exposure caused lasting auditory damage in both wild-type and α9KO mice, with deficits persisting into adulthood. In contrast, α9KI mice were protected from noise-induced damage, with no long-term effects on auditory function. These results highlight the increased susceptibility of the auditory system during early postnatal development. Moreover, they indicate that an enhanced MOC feedback shields the auditory system from noise damage during this period. - Source: PubMed
Publication date: 2025/09/24
Castagna Valeria CBoero Luis EDi Guilmi Mariano NCatalano Di Meo CamilaBallestero Jimena AFuchs Paul ALauer Amanda MElgoyhen Ana BelénGomez-Casati Maria Eugenia