【摘 要】
：
Many GPCR agonists can activate receptor-tyrosine-kinases (RTKs) through transactivation, the mechanisms of which are poorly defined.Here, we have investigated IGF-1 receptor (IGF-1R) transactivation
【机 构】
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National Center for Drug Screening, State Key Laboratory of Drug Research, Shanghai Institute of Mat
【出 处】
：
中国神经科学学会第九届全国学术会议暨第五届会员代表大会
论文部分内容阅读
Many GPCR agonists can activate receptor-tyrosine-kinases (RTKs) through transactivation, the mechanisms of which are poorly defined.Here, we have investigated IGF-1 receptor (IGF-1R) transactivation by GABAB receptor using a chemical biology approach in rat primary neurons.We show that GABAB receptor activation induces a dynamic assembly and disassembly of a protein complex, including both receptors and their downstream effectors.FAK, a non-receptor tyrosine kinase, plays a key role in coordinating this dynamic process.Importantly, such a dynamic process is critical for transactivation and transactivation-dependent neuronal survival.Our results reveal an important mechanism underlying GPCR transactivation of RTKs.
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