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首页> 外文期刊>Molecular and Cellular Biology >Proapoptotic Function of the MET Tyrosine Kinase Receptor through Caspase Cleavage
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Proapoptotic Function of the MET Tyrosine Kinase Receptor through Caspase Cleavage

机译：通过胱天蛋白酶裂解的MET酪氨酸激酶受体的促凋亡功能。

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The MET tyrosine kinase, the receptor of hepatocyte growth factor-scatter factor (HGF/SF), is known to be essential for normal development and cell survival. We report that stress stimuli induce the caspase-mediated cleavage of MET in physiological cellular targets, such as epithelial cells, embryonic hepatocytes, and cortical neurons. Cleavage occurs at aspartic residue 1000 within the SVD site of the juxtamembrane region, independently of the crucial docking tyrosine residues Y1001 or Y1347 and Y1354. This cleavage generates an intracellular 40-kDa MET fragment containing the kinase domain. The p40 MET fragment itself causes apoptosis of MDCK epithelial cells and embryonic cortical neurons, whereas its kinase-dead version is impaired in proapoptotic activity. Finally, HGF/SF treatment does not favor MET cleavage and apoptosis, confirming the known survival role of ligand-activated MET. Our results show that stress stimuli convert the MET survival receptor into a proapoptotic factor.
机译：MET酪氨酸激酶是肝细胞生长因子-散射因子（HGF / SF）的受体，已知对于正常发育和细胞存活至关重要。我们报告应力刺激诱导生理细胞靶标，如上皮细胞，胚胎肝细胞和皮层神经元中的半胱天冬酶介导的裂解。裂解发生在近膜区域SVD位点内的天冬氨酸残基1000处，与关键的对接酪氨酸残基Y1001或Y1347和Y1354无关。该切割产生含有激酶结构域的细胞内40kDa MET片段。 p40 MET片段本身会引起MDCK上皮细胞和胚胎皮质神经元的凋亡，而其激酶死亡形式的促凋亡活性受损。最后，HGF / SF治疗不利于MET的裂解和凋亡，从而证实了配体激活的MET的已知存活作用。我们的结果表明，应激刺激将MET生存受体转化为促凋亡因子。

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