Park Eun Jeong, Yuki Yoshikazu, Kiyono Hiroshi, Shimaoka Motomu
Department of Molecular Pathobiology and Cell Adhesion Biology, Mie University Graduate School of Medicine, Mie, 514-8507, Japan.
Division of Mucosal Immunology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
J Biomed Sci. 2015 Jul 8;22(1):51. doi: 10.1186/s12929-015-0159-6.
Integrins mediate leukocyte accumulation to the sites of inflammation, thereby enhancing their potential as an important therapeutic target for inflammatory disorders. Integrin activation triggered by inflammatory mediators or signaling pathway is a key step to initiate leukocyte migration to inflamed tissues; however, an appropriately regulated integrin deactivation is indispensable for maintaining productive leukocyte migration. While typical integrin antagonists that block integrin activation target the initiation of leukocyte migration, a novel class of experimental compounds has been designed to block integrin deactivation, thereby perturbing the progression of cell migration. Current review discusses the mechanisms by which integrin is activated and subsequently deactivated by focusing on its structure-function relationship.
整合素介导白细胞聚集到炎症部位，因此增强了它们作为炎症性疾病重要治疗靶点的潜力。由炎症介质或信号通路触发的整合素激活是启动白细胞向炎症组织迁移的关键步骤；然而，适当调节的整合素失活对于维持有效的白细胞迁移是必不可少的。虽然阻断整合素激活的典型整合素拮抗剂靶向白细胞迁移的起始阶段，但已设计出一类新型实验性化合物来阻断整合素失活，从而干扰细胞迁移的进程。当前综述通过关注整合素的结构 - 功能关系来讨论整合素被激活以及随后失活的机制。
Zotero 插件
