Focal Adhesion Kinase Versus p53: Apoptosis or Survival?
Focal Adhesion Kinase Versus p53: Apoptosis or Survival?
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DOI：
10.1126/stke.120pe22
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发表时间：
2008-05-20
影响因子：
7.3
通讯作者：
Golubovskaya, Vita M.
中科院分区：
文献类型：
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作者：
Cance, William G.;Golubovskaya, Vita M.
粘着斑激酶(FAK)是一种酪氨酸激酶，可与多种信号伙伴相互作用，帮助细胞在各种促凋亡信号的作用下存活。FAK最重要的相互作用之一是与肿瘤抑制蛋白P53的相互作用。P53不仅能与FAK的氨基末端结合，还能与FAK启动子结合，从而抑制其转录。一项研究现在报道了FAK与P53不依赖于激酶的相互作用的生物学意义，这开辟了未来细胞信号转导和癌症研究的前景。我们主要研究FAK和P53信号转导途径，在人类和小鼠细胞中，这些信号转导通路将细胞外基质和细胞质连接到细胞核。FAK被认为是一种关键的支架蛋白，可以隔离促凋亡蛋白，如P53，以调节细胞生存。
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.