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Last update 08 May 2025

CHRNA9

Last update 08 May 2025

Basic Info

Synonyms

acetylcholine receptor, nicotinic, alpha 9 (neuronal), cholinergic receptor nicotinic alpha 9 subunit, cholinergic receptor, nicotinic alpha 9

+ [7]

Introduction

Ionotropic receptor with a probable role in the modulation of auditory stimuli. Agonist binding induces a conformation change that leads to the opening of an ion-conducting channel across the plasma membrane (PubMed:11752216, PubMed:25282151). The channel is permeable to a range of divalent cations including calcium, the influx of which may activate a potassium current which hyperpolarizes the cell membrane (PubMed:11752216, PubMed:25282151). In the ear, this may lead to a reduction in basilar membrane motion, altering the activity of auditory nerve fibers and reducing the range of dynamic hearing. This may protect against acoustic trauma. May also regulate keratinocyte adhesion (PubMed:11021840).

Drugs associated with CHRNA9

GAT-2710

Target

CHRNA9

Mechanism

CHRNA9 agonists

Active Org.

Bouvé College of Health Sciences

Originator Org.

Bouvé College of Health Sciences

Active Indication

Chronic Pain

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

1HA-78

Target

CHRNA9

Mechanism

CHRNA9 agonists

Active Org.

Bouvé College of Health Sciences

Originator Org.

Bouvé College of Health Sciences

Active Indication

Chronic Pain

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

1HA-84

Target

CHRNA9

Mechanism

CHRNA9 agonists

Active Org.

Bouvé College of Health Sciences

Originator Org.

Bouvé College of Health Sciences

Active Indication

Chronic Pain

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CHRNA9

100 Translational Medicine associated with CHRNA9

0 Patents (Medical) associated with CHRNA9

120

Literatures (Medical) associated with CHRNA9

29 Apr 2025·Proceedings of the National Academy of Sciences

B cell–derived acetylcholine mitigates skin inflammation in mice through α9 nicotinic acetylcholine receptor–mediated signaling

Article

Author: Elia, Andrew J. ; Candi, Eleonora ; Haight, Jillian ; Ramamurthy, Nisha ; Melino, Gerry ; Helke, Simone ; Rugolo, Francesco ; Tobin, Chantal ; Berger, Thorsten ; Jafari, Soode Moghadas ; You-Ten, Annick ; Mak, Tak W. ; Foffi, Erica

Chronic inflammatory skin disorders are characterized by keratinocyte hyperproliferation and hyperactivation as well as immune cell infiltration. We investigated whether immune cell–derived acetylcholine (ACh) is a modulator of skin inflammation in mice. Here, we identify skin epithelial B cells as a key source of ACh that damps down inflammation. We used imiquimod (IMQ) to induce inflammatory skin disease (ISD) in mice lacking ACh production specifically in B cells (ChAT fl/fl;Mb1-Cre mice). Increased keratinocyte proliferation, epidermal thickening, and elevated levels of proinflammatory cytokines resulted. ACh binding to α9 nicotinic ACh receptor (encoded by Chrna9 ) expressed on wild-type mouse keratinocytes reduced their proliferation. Chrna9 -deficient mice exhibited the same exacerbated ISD phenotype as ChAT fl/fl;Mb1-Cre mice following IMQ induction. Our data suggest that B cell–derived ACh maintains skin homeostasis by modulating keratinocyte turnover and controlling immune-related inflammation. Therapeutic manipulation of this cholinergic pathway might mitigate both keratinocyte dysfunction and immune dysregulation in human patients, potentially pointing to treatments for ISDs such as psoriasis and related disorders.

01 Jan 2025·Heliyon

Identification and analysis of prognostic ion homeostasis characteristics in kidney renal clear cell carcinoma

Article

Author: Li, Liyang ; Zhang, Xiangmin ; Chu, Jian ; Ye, Maofei ; Qian, Xiongxian ; Zhao, Yong

Kidney renal clear cell carcinoma (KIRC), a prevalent primary malignant tumor within the urinary system, is characterized by significant heterogeneity. It has been shown that ion channels are important targets for anti-tumor therapy. In this study, we screened 70 selected KIRC related ion homeostasis genes with significant differential expression. We established diagnostic and prognostic models for 15 genes (PDK4, JPH4, ATP1A3, CCL7, CYP27B1, ABCB6, TNFSF11, MCHR1, TNNI3, ANGPTL3, Ednrb, SAA1, Chrna9, TMPRSS6, CCL14) by LASSO regression in the TCGA-KIRC cohort. We also provided a nomogram based on ion homeostasis for clinicians to explore the combined effect of the risk model on clinical variables. Patients in the low-risk group have a significant survival advantage. The potential clinical benefit of our predicted 15 gene signatures in clinical strategies was validated by Calibration Curves and DCA curves. Ultimately, the immune microenvironment and enrichment pathways were analyzed among individuals categorized as high-risk and low-risk. The predictable ion homeostasis-associated 15 gene signature established in this study predicts overall survival outcomes in patients with KIRC, to some extent helping clinicians to select personalized treatment regimens.

01 Nov 2024·Angiogenesis

The angiogenic role of the alpha 9-nicotinic acetylcholine receptor in triple-negative breast cancers

Article

Author: Chen, Michael ; Chang, Chun-Chao ; Rahayu, Sri ; Cheng, Chun-Chia ; Chuang, Kuo-Hsiang ; Kan, Tzu-Chun ; Hsu, Chun-Chun ; Chang, Jungshan ; Ochirbat, Sonjid ; Huang, Tzu-Hsuan

Nicotine acts as an angiogenic factor by stimulating endogenous cholinergic pathways. Several subtypes of nicotinic acetylcholine receptors (nAChRs) have been demonstrated to be closely correlated to the formation and progression of different types of cancers. Recently, several studies have found that nicotinic acetylcholine receptors α9 (α9-nAChRs) are highly expressed in breast tumors, especially in tumors derived from patients diagnosed at advanced stages. In vitro studies have demonstrated that activation of α9-nAChRs is associated with increased proliferation and migration of breast cancer. To study the tumor-promoting role of α9-nAChRs in breast cancers, we generated a novel anti-α9-nAChR and methoxy-polyethylene glycol (mPEG) bispecific antibody (α9 BsAb) for dissecting the molecular mechanism on α9-nAChR-mediated tumor progression. Unexpectedly, we discovered the angiogenic role of α9-nAChR in nicotine-induced neovascularization of tumors. It revealed α9 BsAbs reduced nicotine-induced endothelial cell tube formation, blood vessel development in Matrigel plug assay and angiogenesis in microtube array membrane murine model (MTAMs). To unbraid the molecular mechanism of α9-nAChR in nicotine-mediated angiogenesis, the α9 BsAbs were applied and revealed the inhibitory roles in nicotine-induced production of hypoxia-inducible factor-2 alpha (HIF-2α), vascular endothelial growth factor A (VEGF-A), phosphorylated vascular endothelial growth factor receptor 2 (p-VEGFR2), vascular endothelial growth factor receptor 2 (VEGFR2) and matrix metalloproteinase-9 (MMP9) from triple-negative breast cancer cells (MDA-MB-231), suggesting α9-nAChRs played an important role in nicotine-induced angiogenesis. To confirm our results, the shRNA targeting α9-nAChRs was designed and used to silence α9-nAChR expression and then evaluated the angiogenic role of α9-nAChRs. The results showed α9 shRNA also played an inhibitory effect in blocking the nicotine-induced angiogenic signaling. Taken together, α9-nAChR played a critical role in nicotine-induced angiogenesis and this bispecific antibody (α9 BsAb) may serve as a potential therapeutic candidate for treatments of the α9 positive cancers.

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CHRNA9

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