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抗原受体向核因子κB的信号传导。

Antigen-receptor signaling to nuclear factor kappa B.

作者信息

Schulze-Luehrmann Jan, Ghosh Sankar

机构信息

Section of Immunobiology and Department of Molecular Biophysics & Biochemistry, Yale University School of Medicine, New Haven, CT 06520, USA.

出版信息

Immunity. 2006 Nov;25(5):701-15. doi: 10.1016/j.immuni.2006.10.010.

DOI:10.1016/j.immuni.2006.10.010
PMID:17098202
Abstract

Signal transduction events leading to the survival, differentiation, or apoptosis of cells of the innate or adaptive immune system must be properly coordinated to ensure the normal mounting and termination of immune responses. One of the key transcription factors in immune responses is nuclear factor kappaB (NF-kappaB), which has been the focus of intense investigation over the past two decades. With the identification of the CARMA1-BCL10-MALT1 complex and ongoing progress in understanding the molecular mechanisms connecting T cell and B cell receptor proximal signals to the IkappaB kinase (IKK) complex, a cohesive model of antigen receptor (AgR)-dependent signaling to NF-kappaB activation is beginning to emerge. In this review, we provide an overview of the current state of research into the mechanisms that regulate AgR-mediated NF-kappaB transcriptional activity, with particular focus on the events leading to activation of the IKK complex.

摘要

导致固有免疫系统或适应性免疫系统细胞存活、分化或凋亡的信号转导事件必须得到妥善协调,以确保免疫反应的正常启动和终止。免疫反应中的关键转录因子之一是核因子κB(NF-κB),在过去二十年中它一直是深入研究的焦点。随着CARMA1-BCL10-MALT1复合物的鉴定以及在理解将T细胞和B细胞受体近端信号与IκB激酶(IKK)复合物相连接的分子机制方面的不断进展,一种将抗原受体(AgR)依赖性信号传导与NF-κB激活联系起来的连贯模型开始浮现。在本综述中,我们概述了调节AgR介导的NF-κB转录活性机制的当前研究状况,特别关注导致IKK复合物激活的事件。

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