Integrins and anoikis
Integrins and anoikis
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DOI：
10.1016/s0955-0674(97)80124-x
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发表时间：
1997-10-01
影响因子：
7.5
通讯作者：
Ruoslahti, E
中科院分区：
文献类型：
--
作者：
Frisch, SM;Ruoslahti, E
整合素介导的细胞-基质接触的丧失在某些细胞类型中诱导细胞凋亡（“失巢凋亡”）。最近的研究表明，蛋白激酶信号通路对失巢凋亡起着积极和消极的控制作用。粘着斑激酶，当被整合素激活时，可以抑制失巢凋亡。磷脂酰肌醇3-激酶和AKT癌蛋白可能介导粘着斑激酶的失巢凋亡抑制作用。相反，应激活化蛋白激酶/Jun氨基末端激酶途径促进失巢凋亡。最新的结果表明，半胱天冬酶介导的切割的第一个组成部分，这后一个途径，MEKK-1，可能会触发激活这一途径失巢凋亡。此外，某些整合素可以调节bcl-2的表达水平，可能调节失巢凋亡的阈值。
The loss of integrin-mediated cell-matrix contact induces apoptosis ('anoikis') in certain cell types. Recently it has been shown that protein kinase signaling pathways control anoikis both positively and negatively. Focal adhesion kinase, when activated by integrins, can suppress anoikis. Phosphatidylinositol 3-kinase and the AKT oncoprotein may mediate the anoikis-suppressing effects of focal adhesion kinase. Conversely, the stress-activated protein kinase/Jun amino-terminal kinase pathway promotes anoikis. Latest results indicate that caspase-mediated cleavage of the first component of this latter pathway, MEKK-1, may trigger activation of this pathway in anoikis. In addition, certain integrins may regulate bcl-2 expression levels, possibly adjusting the threshold for anoikis.