NLK phosphorylates Raptor to mediate stress-induced mTORC1 inhibition.
NLK phosphorylates Raptor to mediate stress-induced mTORC1 inhibition.
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NLK 磷酸化 Raptor 介导应激诱导的 mTORC1 抑制
DOI：
10.1101/gad.265116.115
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发表时间：
2015-11-15
影响因子：
10.5
通讯作者：
Guan KL
中科院分区：
文献类型：
--
作者：
Yuan HX;Wang Z;Yu FX;Li F;Russell RC;Jewell JL;Guan KL
Yuan等人表明，Nemo样激酶（NLK）使S863上的Raptor磷酸化，以破坏其与Rag GT3的相互作用，这对mTORC 1溶酶体募集很重要。具有Nlk缺失或Raptor S863磷酸化突变体的敲入的细胞在渗透应激时的快速mTORC 1抑制中是有缺陷的。
Yuan et al. show that the Nemo-like kinase (NLK) phosphorylates Raptor on S863 to disrupt its interaction with the Rag GTPase, which is important for mTORC1 lysosomal recruitment. Cells with Nlk deletion or knock-in of the Raptor S863 phosphorylation mutants are defective in the rapid mTORC1 inhibition upon osmotic stress.