Structural basis of blocking integrin activation and deactivation for anti-inflammation

被引：32

作者：

Park, Eun Jeong ^{[1
,2
]}

Yuki, Yoshikazu ^{[2
]}

Kiyono, Hiroshi ^{[2
,3
]}

Shimaoka, Motomu ^{[1
]}

机构：

[1] Mie Univ, Grad Sch Med, Dept Mol Pathobiol & Cell Adhes Biol, Tsu, Mie 5148507, Japan

[2] Univ Tokyo, Inst Med Sci, Dept Microbiol & Immunol, Div Mucosal Immunol, Tokyo 1088639, Japan

[3] Univ Tokyo, Inst Med Sci, Int Res & Dev Ctr Mucosal Vaccine, Tokyo 1088639, Japan

来源：

JOURNAL OF BIOMEDICAL SCIENCE | 2015年 / 22卷

关键词：

Integrin; Affinity; Activation; Deactivation; Leukocyte; Inflammation; Talin; Kindlin; ACTIVE CROHNS-DISEASE; EFFECTOR T-CELLS; CYTOPLASMIC DOMAIN; LEUKOCYTE INTEGRIN; LIGAND-BINDING; ALPHA-SUBUNIT; BREAST-CANCER; BETA-SUBUNIT; METAL-ION; I-DOMAIN;

D O I：

10.1186/s12929-015-0159-6

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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.

引用

页数：9