期刊
CURRENT PROTEIN & PEPTIDE SCIENCE
卷 12, 期 1, 页码 52-67出版社
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/138920311795659452
关键词
FAK; cell motility; tyrosine kinases; mouse models; signal transduction
资金
- AHA [0735543T]
- Texas A&M Health Science Center
- NIH [HL73394, GM52890, GM48050]
Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that has been shown to have key roles in cell migration, proliferation and survival. FAK activity can be stimulated in response to several types of extracellular ligands, including components of the extracellular matrix and growth factors, suggesting that FAK is an important integrator of multiple cues in the extracellular milieu. Recently, major progress has been made in understanding the molecular mechanisms regulating FAK activity. In particular, several novel proteins have been identified that can bind to FAK and inhibit its activity and associated cellular functions, including cell motility and invasion. Consistent with its critical functions in signal transduction, FAK also plays a pivotal role in mouse development. The inactivation of FAK in mice results in embryonic lethality around E8.5; this early embryonic lethal phenotype limits the use of the FAK total knockout mouse model for studying FAK function in later embryonic development stages and in adult mice. To overcome this problem, three independent groups created FAK/flox mice and generated several different FAK tissue-specific knockout mice models. Here we summarize the progress that has been made regarding the regulation of FAK-mediated signaling events in cell-based systems and also highlight the in vivo functions of FAK in a number of terminally differentiated cell lineages, including vascular endothelial cells, cardiomyocytes, neuronal cells, keratinocytes and several cancerous cell types.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据