Crossroads of PI3K and Rac pathways.

Crossroads of PI3K and Rac pathways.
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DOI:
10.4161/21541248.2014.989789
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发表时间:
2015-01-01
期刊:
影响因子:
--
通讯作者:
Hirsch, Emilio
Hirsch, Emilio
中科院分区:
其他
文献类型:
--
作者:
Campa, Carlo C;Ciraolo, Elisa;Hirsch, Emilio

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Rac和PI3K是细胞内信号转导子,能够调节细胞行为的多个基本信号通路。PI3K是产生磷酸化脂质的脂质激酶,磷酸化脂质反过来抑制细胞内的细胞外信号,而Rac是影响肌动蛋白组织的小G蛋白。令人信服的证据表明,在多种情况下,这两种信号通路似乎是混合的。例如,由PI3K产生的磷酸化脂质募集并激活GEF和GAP蛋白,它们是Rac功能的关键调节剂。相反,PI3K与活化的Rac相互作用,导致Rac信号放大。本文综述了Rac和PI3K信号在细胞迁移和ROS产生两个不同过程中相互作用的分子机制。
Rac and PI3Ks are intracellular signal transducers able to regulate multiple signaling pathways fundamental for cell behavior. PI3Ks are lipid kinases that produce phosphorylated lipids which, in turn, transduce extracellular cues within the cell, while Rac is a small G protein that impacts on actin organization. Compelling evidence indicates that in multiple circumstances the 2 signaling pathways appear intermingled. For instance, phosphorylated lipids produced by PI3Ks recruit and activate GEF and GAP proteins, key modulators of Rac function. Conversely, PI3Ks interact with activated Rac, leading to Rac signaling amplification. This review summarizes the molecular mechanisms underlying the cross-talk between Rac and PI3K signaling in 2 different processes, cell migration and ROS production.