焦点粘着
PTK2
细胞生物学
信号转导
生物
酪氨酸激酶
支架蛋白
细胞外基质
细胞粘附
细胞
蛋白激酶C
丝裂原活化蛋白激酶激酶
生物化学
作者
William G. Cance,Vita M. Golubovskaya
出处
期刊:Science Signaling
[American Association for the Advancement of Science (AAAS)]
日期:2008-05-20
卷期号:1 (20)
被引量:94
摘要
Focal adhesion kinase (FAK) is a tyrosine kinase that interacts with a multitude of signaling partners and helps cells to survive in the face of various proapoptotic signals. One of the most important interactions for FAK is with the tumor suppressor protein p53. p53 binds not only to the amino-terminal domain of FAK but also to the FAK promoter to inhibit its transcription. A study now reports the biological implications of the kinase-independent interaction of FAK with p53, which opens up future perspectives in cell signaling and cancer research. We focus on FAK and p53 signaling, which link signal transduction pathways from the extracellular matrix and cytoplasm to the nucleus, in human and mouse cells. FAK is proposed to be a critical scaffold protein that sequesters proapoptotic proteins, such as p53, to mediate cell survival.
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