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EGF — PAK1

Text-mined interactions from Literome

Menard et al., Cell Signal 2003 : In this study, we show that PAK1 can be stimulated by carbachol, lysophosphatidic acid (LPA), epidermal growth factor (EGF) , and phorbol 12-myristate 13-acetate ( PMA ) by multiple independent and overlapping pathways ... Studies using inhibitors of the EGF receptor tyrosine kinase, phosphatidylinositol 3-kinase ( PI3-kinase ) and protein kinase C ( PKC ) revealed that all of the cell surface agonists could activate PAK1 through pathways independent of PKC, that EGF stimulated a PI3-kinase dependent pathway to stimulate PAK1, and that muscarinic receptor stimulation of PAK1 was predominantly mediated through this EGF-R dependent mechanism ... Activation of PAK1 by LPA was independent of PI3-kinase and the EGF receptor, but was inhibited by dominant negative RhoA
Singh et al., J Biol Chem 2005 : In this report, we demonstrate the nuclear localization of Pak1 upon stimulation by epidermal growth factor
Beeser et al., J Biol Chem 2005 : Inhibition of Pak kinase activity dramatically decreased phosphorylation of Mek1 at Ser ( 298 ) in response to either PDGF or EGF , but this inhibition did not prevent Mek1 activation by EGF, suggesting that although Pak can phosphorylate Mek1 at Ser ( 298 ), this event is not required for Mek1 activation by growth factors
Beier et al., Atherosclerosis 2008 : In VSMC, EGF sequentially stimulated PAK , peaking at 5 min, and JNK, peaking at 15 min. Pretreatment of VSMC by EGF receptor specific tyrosine kinase inhibitor AG1478 and non-specific tyrosine kinase inhibitor genistein inhibited EGF induced activation of Rac1, PAK and JNK, whereas tyrosine kinase inhibitors specific for Src ( PP1 ) and specific for platelet derived growth factor ( AG1296 ) had no effect
Lightcap et al., PloS one 2009 : Here, we demonstrate that the LC8-Pak1 interaction is necessary for epidermal growth factor (EGF) induced nuclear import of Pak1 in MCF-7 cells, and that this event is contingent upon LC8 mediated Pak1 dimerization
Yang et al., Journal of biomedical research 2011 : Activation of Rac1-PI3K/Akt is required for epidermal growth factor induced PAK1 activation and cell migration in MDA-MB-231 breast cancer cells ... Blocking PI3K/Akt signalling with LY294002 or Akt siRNA remarkably inhibited both EGF induced PAK1 activation and cell migration ... Furthermore, expression of dominant negative Rac1 ( T17N ) could largely block EGF induced PI3K/Akt-PAK1 activation and cell migration ... Interestingly, EGF could induce a significant production of ROS, and N-acetyl-L-cysteine, a scavenger of ROS which abolished the EGF induced ROS generation, cell migration, as well as activation of PI3K/Akt and PAK , but not Rac1