Inhibition of the mitogen-activated protein kinase kinase superfamily by a Yersinia effector
Inhibition of the mitogen-activated protein kinase kinase superfamily by a Yersinia effector
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DOI：
10.1126/science.285.5435.1920
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发表时间：
1999-09-17
期刊：
影响因子：
56.9
通讯作者：
Dixon, JE
中科院分区：
文献类型：
--
作者：
Orth, K;Palmer, LE;Dixon, JE
细菌病原体耶尔森氏菌使用III型分泌系统将几种毒力因子注入靶细胞。耶尔森氏菌毒力因子之一YopJ显示直接结合MAPK（促分裂原活化蛋白激酶）激酶（MKK）超家族，阻断MKK的磷酸化和随后的活化。这些结果解释了YopJ在抑制细胞外信号调节激酶、c-Jun氨基末端激酶、p38和核因子κ B信号通路、阻止细胞因子合成和促进细胞凋亡方面的多种活性。在动物和植物的许多细菌病原体中发现的YopJ相关蛋白可以起到阻断MKK的作用，使得宿主信号传导反应可以在感染时被调节。
The bacterial pathogen Yersinia uses a type III secretion system to inject several virulence factors into target cells. One of the Yersinia virulence factors, YopJ, was shown to bind directly to the superfamily of MAPK (mitogen-activated protein kinase) kinases (MKKs) blocking both phosphorylation and subsequent activation of the MKKs. These results explain the diverse activities of YopJ in inhibiting the extracellular signal-regulated kinase, c-Jun amino-terminal kinase, p38, and nuclear factor kappa B signaling pathways, preventing cytokine synthesis and promoting apoptosis. YopJ-related proteins that are found in a number of bacterial pathogens of animals and plants may function to block MKKs so that host signaling responses can be modulated upon infection.