Campa Carlo C, Ciraolo Elisa, Ghigo Alessandra, Germena Giulia, Hirsch Emilio
a Molecular Biotechnology Center; Department of Molecular Biotechnology and Health Sciences; University of Torino ; Torino , Italy.
Small GTPases. 2015;6(2):71-80. doi: 10.4161/21541248.2014.989789. Epub 2015 May 5.
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.
Rac和PI3K是细胞内信号转导分子,能够调节对细胞行为至关重要的多种信号通路。PI3K是脂质激酶,可产生磷酸化脂质,进而在细胞内转导细胞外信号,而Rac是一种小G蛋白,影响肌动蛋白的组织。有力证据表明,在多种情况下,这两条信号通路似乎相互交织。例如,PI3K产生的磷酸化脂质招募并激活GEF和GAP蛋白,这些是Rac功能的关键调节因子。相反,PI3K与激活的Rac相互作用,导致Rac信号放大。本综述总结了在细胞迁移和ROS产生这两个不同过程中,Rac和PI3K信号之间相互作用的分子机制。