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GRAP2 — RAC1

Pathways - manually collected, often from reviews:

• Reactome Reaction: GRAP2 → RAC1 (indirect_complex) Tybulewicz et al., Immunol Rev 2003, Bos et al., Cell 2007
• Reactome Reaction: GRAP2 → RAC1 (reaction) Abe et al., J Biol Chem 2000, Zeng et al., Mol Cell Biol 2000, Chong et al., J Biol Chem 2001, Parrini et al., Mol Cell 2002, Tybulewicz et al., Immunol Rev 2003, Bos et al., Cell 2007

Text-mined interactions from Literome

Philips et al., J Biol Chem 2000 : Differential effect of Rac and Cdc42 on p38 kinase activity and cell cycle progression of nonadherent primary mouse fibroblasts
Versteeg et al., J Biol Chem 2000 : In turn Rac mediates p38 mitogen activated protein ( MAP ) kinase activation and cytoskeletal reorganization, whereas factor VIIa induced p42/p44 MAP kinase stimulation required PI3K enzymatic activity but was not inhibited by dominant negative Rac proteins
Grill et al., Blood 2002 (MAP Kinase Signaling System) : Overexpression of constitutively active mutants of p21 Ras, or Rac-1 , but not of PI-3K, was sufficient for activation of p38 mitogen activated protein kinase ( MAPK ) in cells of hemopoietic origin
Honda et al., Genes Cells 2003 : Cdc42, and presumably Rac , activated in this way, induced the activation of c-Jun N-terminal kinase (JNK), but not p38 mitogen activated protein ( MAP ) kinase or extracellular signal regulated kinase ( ERK )
Fessler et al., J Biol Chem 2004 : Methyl-beta-cyclodextrin induces activation of p38 and Cdc42, but not Rac , in the nonstimulated PMN, yet inhibits subsequent lipopolysaccharide induced activation of p38 and Cdc42
Natal et al., Apoptosis 2006 : In turn, Rac mediates the increase of both JNK and p38 activities in a sustained fashion, as well as the phosphorylation levels of their respective substrates c-Jun and ATF-2
Wu et al., Mol Med 2007 (Neoplasm Recurrence, Local...) : Surprisingly, Rac1 mediated phosphorylation of p38 mitogen activated kinase in papilloma cells but not normal cells, and inhibition of p38 with the specific inhibitor SB202190 suppressed COX-2 expression in papilloma cells but had no effect on low-level COX-2 expression in normal cells
Zuluaga et al., FEBS Lett 2007 : We have investigated the cross-talk between p38alpha and Rac-1 and found that p38alpha regulates the association between Rac-1 and caveolin-1 in serum deprived cardiomyocytes
Zhang et al., J Biol Chem 2009 (Breast Neoplasms...) : Silencing of D4-GDI results in constitutive Rac1 activation and translocation from the cytosol to cellular membrane compartments and in sustained activation of p38 and JNK kinases
Schreiber et al., Innate Immun 2013 : Furthermore, inhibiting Rac in HRV exposed macrophages attenuated activation of the stress kinase p38 and release of the pro-inflammatory cytokine CCL2, but inhibiting Rac did not affect release of the pro-inflammatory cytokine CCL5