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The rare variants in CHRNA9 were significantly associated with smoking status.
Our findings support a significant interaction effect existing between the CHRNA9 gene and smoking exposure on the risk of breast cancer development.
CHRNA9 polymorphisms are associated with non-small cell lung cancer.
Thia case-control analysis revealed that an increased risk of lung cancer is associated with two SNPs in CHRNA9, rs56159866 and rs6819385.
Data suggest that the biologic activities of Alpha9 nicotinic receptor (CHRNA9) may be regulated at the splicing level, and genetic polymorphisms in CHRNA9 affecting protein levels, amino acid sequence and RNA splicing may influence the risk for lung cancer.
A two order of magnitude species difference in potency of alpha-conotoxin RgIA is reported for rat versus human alpha9alpha10 nAChR (show CHRNA4 ELISA Kits).
Estrogen receptor-alpha (show ESR1 ELISA Kits) plays a central role in mediating alpha9-nAChR (show CHRNA4 ELISA Kits) gene up-regulation in response to either nicotine or estradiol stimulation.
Significant increases in the alpha9-nAChR (show CHRNA4 ELISA Kits) mRNA and protein levels in MCF-7 cells were detected 6 h after nicotine treatment. Nicotine- and estrogen-induced alpha9-nicotinic acetylcholine receptor upregulation was blocked by (-)-epigallocatechin-3-gallate.
These results suggest that alpha9-nAChR (show CHRNA4 ELISA Kits)-mediated cyclin D3 (show CCND3 ELISA Kits) overexpression is important for nicotine-induced transformation of normal human breast epithelial cells.
The alpha9-nAChR (show CHRNA4 ELISA Kits) is important for nicotine-induced transformation of normal human breast epithelial cells. Results imply that receptor-mediated carcinogenic signals play a decisive role in biological functions related to human breast cancer development.
the present study, we show that alpha9-nAChR (show CHRNA4 ELISA Kits) KO mice, which lack cholinergic transmission between medial (MOC) and lateral (LOC (show PTPRC ELISA Kits)) olivocochlear neurons located in the brainstem.
Auditory cortex microstimulation produces an enhancement of contralateral noise suppression of auditory brainstem responses in WT mice but not in Chrna9 KO mice.
alpha9-nAChR (show CHRNA4 ELISA Kits) KO mice showed normal responses to acute noxious thermal and mechanical stimuli, and developed normal chronic cold and mechanical allodynia in inflammatory and nerve injury pain models.
Inhibition of N-type Ca(2 (show CA2 ELISA Kits)+) channel channels by Vc1.1 and RgIA conotoxins is not mediated by the expression of alpha9 nAChRs in dorsal root ganglia neurons.
Relative to their wild-type littermates, Chrna9(L9'T/L9'T) mice showed less permanent hearing loss following exposure to intense noise. Thus, a point mutation designed to alter alpha9alpha10 receptor gating has provided an animal model.
In nAChR (show CHRNA4 ELISA Kits) alpha9 null mice there is premature, effusive innervation to the synaptic pole of outer hair cells coinciding with delayed expression of cell adhesion proteins.Collapse of ectopic innervation coincides with age-related hyperexpression pattern.
description of the role of alpha9 nAChR (show CHRNA4 ELISA Kits) subunit in the development of the olivocochlear system and efferent function
This gene is a member of the ligand-gated ionic channel family and nicotinic acetylcholine receptor gene superfamily. It encodes a plasma membrane protein that forms homo- or hetero-oligomeric divalent cation channels. This protein is involved in cochlea hair cell development and is also expressed in the outer hair cells (OHCs) of the adult cochlea.
, cholinergic receptor, nicotinic, alpha polypeptide 9
, neuronal acetylcholine receptor subunit alpha-9
, nicotinic acetylcholine receptor subunit alpha-9
, NACHR alpha 9
, acetylcholine receptor, neuronal nicotinic, alpha-9 subunit
, neuronal acetylcholine receptor protein, alpha-9 subunit
, nicotinic acetylcholine receptor subunit alpha 9
, acetylcholine receptor alpha 9 subunit (nAChR)
, cholinergic receptor, nicotinic, alpha 9