The Role of Crk Adaptor Proteins in T-Cell Adhesion and Migration.
The Role of Crk Adaptor Proteins in T-Cell Adhesion and Migration.
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DOI：
10.3389/fimmu.2015.00509
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发表时间：
2015
影响因子：
7.3
通讯作者：
Isakov N
中科院分区：
文献类型：
--
作者：
Braiman A;Isakov N
Crk衔接蛋白是多种细胞表面受体信号转导的关键分子。它们通过SH 2介导的与信号转导效应分子如Cbl、ZAP-70、CasL和STAT 5的瞬时相互作用参与淋巴细胞活化的早期步骤。此外，它们通过它们的SH 3结构域与效应分子如C3 G组成型缔合，所述效应分子介导细胞粘附并调节淋巴细胞外渗和募集至炎症部位。最近的研究表明，CrkII的构象和功能受到免疫亲素的调节，这也影响CrkII依赖的T细胞粘附到纤连蛋白和趋化因子的迁移。本文讨论了机制，调节CrkII的构象和功能，一般情况下，并强调受体偶联的信号通路，控制T淋巴细胞粘附和迁移到炎症部位的Crk蛋白的作用。
Crk adaptor proteins are key players in signal transduction from a variety of cell surface receptors. They are involved in early steps of lymphocyte activation through their SH2-mediated transient interaction with signal transducing effector molecules, such as Cbl, ZAP-70, CasL, and STAT5. In addition, they constitutively associate, via their SH3 domain, with effector molecules, such as C3G, that mediate cell adhesion and regulate lymphocyte extravasation and recruitment to sites of inflammation. Recent studies demonstrated that the conformation and function of CrkII is subjected to a regulation by immunophilins, which also affect CrkII-dependent T-cell adhesion to fibronectin and migration toward chemokines. This article addresses mechanisms that regulate CrkII conformation and function, in general, and emphasizes the role of Crk proteins in receptor-coupled signaling pathways that control T-lymphocyte adhesion and migration to inflammatory sites.