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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Requirement of mitogen-activated protein kinase kinase 3 (MKK3) for tumor necrosis factor-induced cytokine expression
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Requirement of mitogen-activated protein kinase kinase 3 (MKK3) for tumor necrosis factor-induced cytokine expression

机译：有丝分裂原激活的蛋白激酶激酶3（MKK3）对肿瘤坏死因子诱导的细胞因子表达的要求

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摘要

The p~38 mitogen-activated protein kinase is activated by treatment of cells with cytokines and by exposure to environmental stress. The effects of these stimuli on p38 MAP kinase are mediated by the MAP kinase kinases (MKKs) MKK3, MKK4, and MKK6. We have examined the function of the p38 MAP kinase signaling pathway by investigating the effect of targeted disruption of the Mkk3 gene. Here we report that Mkk3 gene disruption caused a selective defect in the response of fibroblasts to the proinflammatory cytokine tumor necrosis factor, including reduced p~38 MAP kinase activation and cytokine cxpression. These data demonstrate that the MKK3 protein kinase is a critical component of a tumor necrosis factor-stimulated signaling pathway that causes increased expression of inflammatory cytokines.
机译：p〜38丝裂原活化的蛋白激酶通过用细胞因子处理细胞并暴露于环境压力而被激活。这些刺激对p38 MAP激酶的作用由MAP激酶激酶（MKK）MKK3，MKK4和MKK6介导。我们已经通过调查针对性破坏Mkk3基因的影响，检查了p38 MAP激酶信号通路的功能。在这里，我们报道Mkk3基因破坏导致成纤维细胞对促炎性细胞因子肿瘤坏死因子的选择性缺陷，包括降低的p〜38 MAP激酶激活和细胞因子表达。这些数据证明，MKK3蛋白激酶是肿瘤坏死因子刺激的信号传导途径的关键组成部分，该信号传导途径导致炎症性细胞因子的表达增加。

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