Chk1 phosphorylates the tumour suppressor Mig‐6, regulating the activation of EGF signalling
作者： Ning Liu , Masaki Matsumoto , Kyoko Kitagawa , Yojiro Kotake , Sayuri Suzuki
关键词:
摘要: The tumour suppressor gene product Mig-6 acts as an inhibitor of epidermal growth factor (EGF) signalling. However, its posttranslational modifications and regulatory mechanisms have not been elucidated. Here, we investigated the phosphorylation human found that Chk1 phosphorylated in vivo well vitro. Moreover, EGF stimulation promoted without DNA damage was inhibited by depletion Chk1. also increased Ser280-phosphorylated Chk1, a cytoplasmic-tethering form, via PI3K pathway. Mass spectrometric analyses suggested Ser 251 major site vitro vivo. Substitution to alanine inhibitory activity against receptor (EGFR) activation. EGF-dependent activation EGFR cell were depletion, rescued co-depletion Mig-6. Our results suggest phosphorylates on 251, resulting inhibition Mig-6, positive regulator This is novel function
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