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PAK7 — RAC1
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Yoshii et al., Oncogene 1999
(MAP Kinase Signaling System) :
The recently identified
PAK interacting exchange factor ( PIX ) acts as a guanine nucleotide exchange factor on
Rac , and colocalizes with PAK in a focal complex, but little is known about the associated signaling cascades, including upstream activators of PIX
Tang et al., J Biol Chem 2000
:
Akt stimulation of
Pak was not
inhibited by dominant negative mutants of either
Rac or Cdc42 suggesting that Akt activated Pak through a GTPase independent mechanism
del Pozo et al., EMBO J 2000
:
An activated
Rac mutant lacking a membrane targeting sequence did not
activate PAK in adherent cells, while mutations that forced membrane targeting restored PAK activation in suspended cells
Taylor et al., Hematol Oncol Clin North Am 2000
(MAP Kinase Signaling System) :
Ras thus binds PI3 kinase and potentiates its activation, whereas the
Rac dependent protein kinase
PAK phosphorylates MEK and thereby stabilizes its association with Raf
He et al., Cancer J 2001
(Sarcoma, Experimental) :
Using four distinct, cell-permeable, and highly specific inhibitors, namely WR-PAK18, which blocks the PAK-PIX interaction ; AG 1478, which inhibits ErbB1 kinase activity ; and AG 825 or AG 879, which inhibits ErbB2 kinase activity, we demonstrate that ( 1 ) the PAK-PIX interaction is essential for v-Ha-RAS induced malignant transformation ; ( 2 ) v-Ha-RAS requires not only ErbB1 but also ErbB2, which are activated through two independent autocrine pathways to induce both the
PIX/Rac/CDC42 dependent
PAK activation and malignant transformation in vitro ; and ( 3 ) a combination of AG 879 and the Src family kinase-specific inhibitor PP1 suppresses almost completely the growth of RAS induced sarcomas in nude mice
Brzeska et al., J Biol Chem 2001
:
In this paper, we report the expression in insect cells of full-length, fully regulated Acanthamoeba MIHCK and further characterize the
regulation of this
PAK by
Rac , calmodulin, and autoinhibition
Feng et al., J Biol Chem 2002
:
Three members of the Cool/Pix family have shown distinct regulatory activities : ( i ) p50 ( Cool-1 ) inhibits
Cdc42/Rac stimulated
PAK activity, ( ii ) p85 ( Cool-1 ) /beta-Pix has a permissive effect on Cdc42/Rac stimulated activity, and ( iii ) p90 ( Cool-2 ) /alpha-Pix strongly activates PAK
Vidal et al., Blood 2002
:
Inhibition of Cdc42 and
Rac1 with clostridial toxin B
inhibits PAK activation and lamellae spreading ... These results suggest that
Cdc42/Rac1 dependent activation of
PAK may trigger early platelet shape change, at least in part through the regulation of cortactin binding to PAK
Krautkrämer et al., J Virol 2004
:
Notably,
activation of
Pak by its physiological activators, Cdc42 and
Rac , also occurred in lipid rafts and required raft integrity
Stofega et al., Mol Biol Cell 2004
(Breast Neoplasms) :
PAK kinase activity and subcellular distribution are tightly
regulated by rapid and transient localized
Rac and Cdc42 activation, and by interactions mediated by adapter proteins
Chi et al., Biochem Biophys Res Commun 2004
:
Activation of endogenous
Pak by platelet derived growth factor or the constitutively active
Rac1 mutant, Rac1 ( G12V ), also inhibited degradation
Feng et al., EMBO J 2004
:
The binding of either
PAK ( p21 activated kinase ) or Cbl ( Casitas B-lymphoma ) to the SH3 domain of monomeric Cool-2 is
necessary for the functional interactions between GDP bound Cdc42 or
Rac and the Cool-2 monomer
Fryer et al., J Biol Chem 2006
:
Although
Pak is primarily
activated by
Rac and Cdc42, there are additional proteins that regulate Pak activity and localization, including three AGC protein kinase family members, Akt-1, PDK-1, and cAMP dependent protein kinase
Lessmann et al., Exp Hematol 2006
:
Ins/IGF-1, like antigen ( Ag ), also stimulates the
Rac dependent activation of
PAK as well as the production of hydrogen peroxide ( H2O2 )
Lozano et al., J Cell Sci 2008
:
Interestingly,
PAK1 can not be
activated by
Rac1b , suggesting that this may contribute to the inability of Rac1b to disrupt cell-cell contacts in keratinocytes
Thirone et al., Am J Physiol Cell Physiol 2009
:
Hyperosmolarity provoked cofilin phosphorylation was mediated by the Rho/Rho kinase ( ROCK ) /LIM kinase ( LIMK ) but not the Rac/PAK/LIMK pathway, because 1 ) dominant negative ( DN ) Rho and DN-ROCK but not
DN-Rac and DN-PAK inhibited cofilin phosphorylation ; 2 ) constitutively active ( CA ) Rho and CA-ROCK but not CA-Rac and
CA-PAK induced cofilin phosphorylation ; 3 ) hyperosmolarity induced LIMK-2 phosphorylation, and 4 ) inhibition of ROCK by Y-27632 suppressed the hypertonicity triggered LIMK-2 and cofilin phosphorylation.We thenexamined whether cofilin and its phosphorylation play a role in the hypertonicity triggered F-actin changes
Flaiz et al., Exp Neurol 2009
(Neurilemmoma) :
We used a novel small-molecule PAK inhibitor, IPA-3, to investigate the
role of
PAK activation on
Rac1/Cdc42 activity, cell spreading and adhesion in human primary schwannoma and Schwann cells
Manser et al., J Biol Chem 1995
:
The purified serine/threonine kinase
p65PAK has been shown to be directly
activated by
GTP-Rac1 or GTP-Cdc42
Knaus et al., J Biol Chem 1998
:
In addition, our results indicate that a basic region in PAK is required for
PAK activation and that binding of
Rac/Cdc42 to PAK is not
sufficient for kinase activation