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CARD 蛋白对 NF-κB 的调控。

Regulation of NF-κB by the CARD proteins.

机构信息

Department of Molecular and Cellular Oncology, The University of Texas, M D Anderson Cancer Center, Houston, TX 77030, USA.

出版信息

Immunol Rev. 2012 Mar;246(1):141-53. doi: 10.1111/j.1600-065X.2012.01110.x.

DOI:10.1111/j.1600-065X.2012.01110.x
PMID:22435552
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3339759/
Abstract

Scaffold proteins play pivotal roles in the regulation of signal transduction pathways by connecting upstream receptors to downstream effector molecules. During the last decade, many scaffold proteins that contain caspase-recruitment domains (CARD) have been identified. Investigating the roles of CARD proteins has revealed that many of them play crucial roles in signaling cascades leading to activation of nuclear factor-κB (NF-κB). In this review, we discuss the contributions of CARD proteins to NF-κB activation in various signaling cascades. In particular, we share some of our personal experiences during the initial investigation of the functions of the CARMA family of CARD proteins and then summarize the roles of these proteins in signaling pathways induced by antigen receptors, G protein-coupled receptors, receptor tyrosine kinase, and C-type lectin receptors in the context of recent progress in these field.

摘要

支架蛋白通过将上游受体连接到下游效应分子,在信号转导途径的调节中发挥关键作用。在过去的十年中,已经鉴定出许多含有半胱氨酸天冬氨酸蛋白酶募集结构域 (CARD) 的支架蛋白。对 CARD 蛋白的研究表明,它们中的许多在导致核因子-κB (NF-κB) 激活的信号级联中发挥关键作用。在这篇综述中,我们讨论了 CARD 蛋白在各种信号转导途径中对 NF-κB 激活的贡献。特别是,我们分享了在最初研究 CARMA 家族 CARD 蛋白的功能时的一些个人经验,然后总结了这些蛋白在抗原受体、G 蛋白偶联受体、受体酪氨酸激酶和 C 型凝集素受体诱导的信号通路中的作用,以及这些领域的最新进展。

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本文引用的文献

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CARMA3 is crucial for EGFR-Induced activation of NF-κB and tumor progression.CARMA3 对于 EGFR 诱导的 NF-κB 激活和肿瘤进展至关重要。
Cancer Res. 2011 Mar 15;71(6):2183-92. doi: 10.1158/0008-5472.CAN-10-3626.
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NF-κB signaling pathways regulated by CARMA family of scaffold proteins.CARMA 家族衔接蛋白调控的 NF-κB 信号通路。
Cell Res. 2011 Jan;21(1):55-70. doi: 10.1038/cr.2010.182. Epub 2010 Dec 28.
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Thrombin-dependent NF-{kappa}B activation and monocyte/endothelial adhesion are mediated by the CARMA3·Bcl10·MALT1 signalosome.依赖凝血酶的 NF-κB 激活和单核细胞/内皮细胞黏附是由 CARMA3·Bcl10·MALT1 信号体介导的。
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Oncogenic CARD11 mutations induce hyperactive signaling by disrupting autoinhibition by the PKC-responsive inhibitory domain.致癌性 CARD11 突变通过破坏 PKC 反应抑制结构域的自身抑制作用,诱导信号过度激活。
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