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躯干受体酪氨酸激酶可通过一条不依赖Ras的途径激活Raf。

The torso receptor tyrosine kinase can activate Raf in a Ras-independent pathway.

作者信息

Hou X S, Chou T B, Melnick M B, Perrimon N

机构信息

Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA.

出版信息

Cell. 1995 Apr 7;81(1):63-71. doi: 10.1016/0092-8674(95)90371-2.

Abstract

Activation of the receptor tyrosine kinase (RTK) torso defines the spatial domains of expression of the transcription factors tailless and huckebein. Previous analyses have demonstrated that Ras1 (p21ras) operates upstream of the D-Raf (Raf1) serine/threonine kinase in this signaling pathway. By using a recently developed technique of germline mosaics, we find that D-Raf can be activated by torso in the complete absence of Ras1. This result is supported by analysis of D-Raf activation in the absence of either the exchange factor Son of sevenless (Sos) or the adaptor protein drk (Grb2), as well as by the phenotype of a D-Raf mutation that abolishes binding of Ras1 to D-Raf. Our study provides in vivo evidence that Raf can be activated by an RTK in a Ras-independent pathway.

摘要

受体酪氨酸激酶(RTK)躯干的激活决定了转录因子无尾和胡凯宾的表达空间域。先前的分析表明,在该信号通路中,Ras1(p21ras)在D-Raf(Raf1)丝氨酸/苏氨酸激酶的上游发挥作用。通过使用最近开发的种系嵌合体技术,我们发现,在完全没有Ras1的情况下,躯干也能激活D-Raf。在没有交换因子七less之子(Sos)或衔接蛋白drk(Grb2)的情况下对D-Raf激活的分析,以及消除Ras1与D-Raf结合的D-Raf突变的表型,均支持了这一结果。我们的研究提供了体内证据,表明Raf可以通过一条不依赖Ras的途径被RTK激活。

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