Title : S-nitrosylation of c-Src via NMDAR-nNOS module promotes c-Src activation and NR2A phosphorylation in cerebral ischemia/reperfusion.

Pub. Date : 2012 Jun

PMID : 22422045






2 Functional Relationships(s)
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1 Taken together, the S-nitrosylation of c-Src is provoked by NO derived from endogenous nNOS, which is activated by Ca(2+) influx from NMDA receptors, and promotes the auto-phosphorylation at tyrosines and further phosphorylates NR2A. Tyrosine SRC proto-oncogene, non-receptor tyrosine kinase Rattus norvegicus
2 Previous studies suggested that activated c-Src promote the tyrosine phosphorylation of NMDA receptor subunit NR2A, and thus aggravate the injury induced by transient cerebral ischemia/reperfusion (I/R) in rat hippocampus CA1 region. Tyrosine SRC proto-oncogene, non-receptor tyrosine kinase Rattus norvegicus