期刊
EMBO REPORTS
卷 9, 期 12, 页码 1203-1208出版社
WILEY
DOI: 10.1038/embor.2008.202
关键词
cell adhesion; extracellular matrix; integrin; kindlin
资金
- NHLBI NIH HHS [P01 HL073311] Funding Source: Medline
- NIDCR NIH HHS [DE016099, R01 DE016099-04, R01 DE016099-03, R01 DE016099-02, R01 DE016099-01A1, R01 DE016099] Funding Source: Medline
- NIDDK NIH HHS [R01 DK054639, DK54639] Funding Source: Medline
- NIGMS NIH HHS [R01 GM065188, GM65188] Funding Source: Medline
Integrin-mediated cell-ECM (extracellular matrix) adhesion is a fundamental process that controls cell behaviour. For correct cell-ECM adhesion, both the ligand-binding affinity and the spatial organization of integrins must be precisely controlled; how integrins are regulated, however, is not completely understood. Kindlins constitute a family of evolutionarily conserved cytoplasmic components of cell-ECM adhesions that bind to beta-integrin cytoplasmic tails directly and cooperate with talin in integrin activation. In addition, kindlins interact with many components of cell-ECM adhesions-such as migfilin and integrin-linked kinase-to promote cytoskeletal reorganization. Loss of kindlins causes severe defects in integrin signalling, cell-ECM adhesion and cytoskeletal organization, resulting in early embryonic lethality (kindlin-2), postnatal lethality (kindlin-3) and Kindler syndrome (kindlin-1). It is therefore clear that kindlins, together with several other integrin-proximal proteins, are essential for integrin signalling and cell-ECM adhesion regulation.
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