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原癌基因Cot激酶通过NF-κB诱导激酶和IκB激酶参与CD3/CD28诱导的NF-κB激活。

The proto-oncogene Cot kinase participates in CD3/CD28 induction of NF-kappaB acting through the NF-kappaB-inducing kinase and IkappaB kinases.

作者信息

Lin X, Cunningham E T, Mu Y, Geleziunas R, Greene W C

机构信息

Gladstone Institute of Virology and Immunology, University of California San Francisco, 94141, USA.

出版信息

Immunity. 1999 Feb;10(2):271-80. doi: 10.1016/s1074-7613(00)80027-8.

Abstract

The proto-oncogene Cot/Tpl-2 encodes a MAP3K-related serine-threonine kinase. Expression of wild type Cot activates the IkappaB kinases (IKK) leading to induction of NF-kappaB. Conversely, expression of kinase-deficient Cot inhibits CD3/CD28 but not TNF alpha induction of NF-kappaB. These findings suggest the selective involvement of Cot/Tpl-2 or a closely related kinase in the CD3/CD28 costimulatory pathway leading to induced nuclear expression of NF-kappaB. In contrast, a kinase-deficient mutant of the NF-kappaB-inducing kinase (NIK) inhibits both CD3/CD28 and TNF alpha signaling, indicating that these pathways converge at or prior to the action of NIK. Consistent with such a sequential function of these two kinases, Cot physically assembles with and phosphorylates NIK in vivo.

摘要

原癌基因Cot/Tpl-2编码一种与丝裂原活化蛋白激酶激酶3(MAP3K)相关的丝氨酸-苏氨酸激酶。野生型Cot的表达激活IκB激酶(IKK),从而导致核因子κB(NF-κB)的诱导。相反,激酶缺陷型Cot的表达抑制CD3/CD28,但不抑制肿瘤坏死因子α(TNFα)诱导的NF-κB。这些发现表明Cot/Tpl-2或一种密切相关的激酶选择性地参与了导致NF-κB核表达诱导的CD3/CD28共刺激途径。相比之下,NF-κB诱导激酶(NIK)的激酶缺陷型突变体抑制CD3/CD28和TNFα信号传导,表明这些途径在NIK作用时或之前汇聚。与这两种激酶的这种顺序功能一致,Cot在体内与NIK物理组装并使其磷酸化。

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