The carboxyl terminal tyrosine 417 residue of NOK has an autoinhibitory effect on NOK-mediated signaling transductions.
The carboxyl terminal tyrosine 417 residue of NOK has an autoinhibitory effect on NOK-mediated signaling transductions.
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DOI：
10.1016/j.bbrc.2007.02.154
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发表时间：
2007-05
影响因子：
3.1
通讯作者：
Yinghua Li;S. Zhong;Zhili Rong;Yongming Ren;Zhiyong Li;Shuping Zhang;Z. Chang;Li Liu
中科院分区：
文献类型：
--
作者：
Yinghua Li;S. Zhong;Zhili Rong;Yongming Ren;Zhiyong Li;Shuping Zhang;Z. Chang;Li Liu
受体蛋白酪氨酸激酶（RPTKs）是细胞生长、分化、迁移和代谢的必需介质。最近，一个新的RPTK命名为NOK已被克隆和表征。在本研究中，我们研究了NOK羧基端酪氨酸417残基在不同信号通路激活中的作用。Y417位点酪氨酸突变为苯丙氨酸（Y417F）不仅显著增强了ERK的激活，而且显著促进了STAT1和STAT3的激活。NIH3T3-NOK（Y417F）稳定细胞的增殖能力明显高于NIH3T3-NOK。总之，我们的研究结果表明，酪氨酸Y417残基的羧基尾巴的NOK表现出自身抑制作用的NOK介导的信号转导。
Receptor protein tyrosine kinases (RPTKs) are essential mediators of cell growth, differentiation, migration, and metabolism. Recently, a novel RPTK named NOK has been cloned and characterized. In current study, we investigated the role of the carboxyl terminal tyrosine 417 residue of NOK in the activations of different signaling pathways. A single tyrosine to phenylalanine point mutation at Y417 site (Y417F) not only dramatically enhanced the NOK-induced activation of extracellular signal-regulated kinase (ERK), but also markedly promoted the NOK-mediated activation of both signal transducer and activator of transcription 1 and 3 (STAT1 and 3). Moreover, the proliferation potential of NIH3T3-NOK (Y417F) stable cells were significantly elevated as compared with that of NIH3T3-NOK. Overall, our results demonstrate that the tyrosine Y417 residue at the carboxyl tail of NOK exhibits an autoinhibitory role in NOK-mediated signaling transductions.