The integrin adhesome: from genes and proteins to human disease

被引:464
作者
Winograd-Katz, Sabina E. [1 ]
Faessler, Reinhard [2 ]
Geiger, Benjamin [1 ]
Legate, Kyle R. [2 ,3 ]
机构
[1] Weizmann Inst Sci, Dept Mol Cell Biol, IL-76100 Rehovot, Israel
[2] Max Planck Inst Biochem, Dept Mol Med, D-82152 Martinsried, Germany
[3] Univ Munich, Dept Appl Phys, Ctr Nanosci, D-80799 Munich, Germany
基金
欧洲研究理事会;
关键词
FOCAL ADHESION KINASE; ALPHA; 3; BETA-1-INTEGRIN; LEUKOCYTE ADHESION; LINKED KINASE; GLANZMANN THROMBASTHENIA; CARDIAC-HYPERTROPHY; EXTRACELLULAR-MATRIX; MISSENSE MUTATION; BETA-3; INTEGRIN; MYOSIN-II;
D O I
10.1038/nrm3769
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The adhesive interactions of cells with their environment through the integrin family of transmembrane receptors have key roles in regulating multiple aspects of cellular physiology, including cell proliferation, viability, differentiation and migration. Consequently, failure to establish functional cell adhesions, and thus the assembly of associated cytoplasmic scaffolding and signalling networks, can have severe pathological effects. The roles of specific constituents of integrin-mediated adhesions, which are collectively known as the 'integrin adhesome', in diverse pathological states are becoming clear. Indeed, the prominence of mutations in specific adhesome molecules in various human diseases is now appreciated, and experimental as well as in silico approaches provide insights into the molecular mechanisms underlying these pathological conditions.
引用
收藏
页码:273 / 288
页数:16
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