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- W2149675706 abstract "GluR5-containing kainite receptor (GluR5-KAR) plays an important role in the pathophysiology of nervous system diseases, while S-nitrosylation exerts a variety of effects on biological systems. However, the mechanism of GluR5-KAR S-nitrosylation is still unclear up to now. Here our researches found that GluR5-KAR selective agonist ATPA stimulation activated the nonclassical GluR5-KAR-Gq-PLC-IP(3)R pathway and the signalling module GluR5·PSD-95·nNOS (the former is more important), led to Ca(2+) release from intracellular calcium stores endoplasmic reticulum (ER) to cytoplasm and extracellular calcium indrawal, respectively, which further resulted in nNOS activation and GluR5-KAR S-nitrosylation, and then inhibited GluR5-mediated whole-cell current attenuation and induced apoptosis in primary cultured hippocampal neurons. Clarification of the primary mechanisms of GluR5-KAR S-nitrosylation induced by ATPA and identification of critical cysteine for GluR5-2a S-nitrosylation (Cys231 and Cys804) open up a brand-new field for revealing downstream signalling pathway of GluR5-KAR and its molecular characteristics, exploring the pathogenesis of neurological diseases and searching for promising therapies." @default.
- W2149675706 created "2016-06-24" @default.
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- W2149675706 date "2012-12-01" @default.
- W2149675706 modified "2023-09-23" @default.
- W2149675706 title "ATPA induced GluR5-containing kainite receptor S-nitrosylation via activation of GluR5–Gq–PLC–IP3R pathway and signalling module GluR5·PSD-95·nNOS" @default.
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- W2149675706 doi "https://doi.org/10.1016/j.biocel.2012.09.009" @default.
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