Caspase cleavage of the MET receptor generates an HGF interfering fragment

被引：20

作者：

Deheuninck, Julien ^{[1
,2
]}

Foveau, Benedicte ^{[1
,2
]}

Goormachtigh, Gautier ^{[1
,2
]}

Leroy, Catherine ^{[1
,2
]}

Ji, Zongling ^{[1
,2
]}

Tulasne, David ^{[1
,2
]}

Fafeur, Veronique ^{[1
,2
]}

机构：

[1] Univ Lille 1, Inst Biol, CNRS, UMR 8161, F-59021 Lille, France

[2] Univ Lille 2, Inst Pasteur, F-59021 Lille, France

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2008年 / 367卷 / 03期

基金：

澳大利亚研究理事会;

关键词：

HGF; C-MET; caspase; tyrosine kinase receptor; apoptosis;

D O I：

10.1016/j.bbrc.2007.12.177

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The MET tyrosine kinase receptor activated by its ligand HGF/SF, induces several cellular responses, including survival. Nonetheless, the MET receptor is cleaved in stress conditions by caspases within its intracellular region, generating a 40 kDa fragment, p40 MET, with pro-apoptotic properties. Here, we established that this cleavage splits the receptor at the juxtamembrane ESVD site, causing the concomitant generation of p100 MET, corresponding to the entire extracellular region of the MET receptor still spanning the membrane. This fragment is able to bind HGF/SF and to prevent HGF-dependent signaling downstream of full MET, demonstrating its function as a decoy receptor. (C) 2008 Elsevier Inc. All rights reserved.

引用

页码：573 / 577

页数：5

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