◀ Back to RAC1

RAC1 — RAC2

Pathways - manually collected, often from reviews:

• WikiPathways Microglia Pathogen Phagocytosis Pathway: RAC1/RAC2/RAC3 → NCF1/NCF4/NCF2/RAC1/RAC2/RAC3/CYBB/CYBA (activation)
  
• WikiPathways DNA Damage Response (only ATM dependent): Complex of RAC1-RAC2-RAC3 → MAP3K1 (activation)
• WikiPathways DNA Damage Response (only ATM dependent): Complex of RAC1-RAC2-RAC3 → MLKL (activation)

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• Gene Ontology Complexes actin filament: actin filament complex (ACTN3-DNAJA3-AIF1L-TEK-RAC2-FKBP15-RAC1-ACTC1-RCSD1-FMN1-ACKR2-CORO1A-SH2B2-MYO9B-DFNB31-FLNA-ARHGAP6-GNG12-LCP1-GAS7) Prakash et al., Hum Mol Genet 2000, Beggs et al., J Biol Chem 1992, Gatfield et al., Mol Biol Cell 2005, Eyers et al., Biochem J 2005, Bookwalter et al., J Biol Chem 2006, Kurzik-Dumke et al., Cell Signal 2007, Saharinen et al., Nat Cell Biol 2008, Schulze et al., FEBS J 2008, Zhang et al., J Immunol 2009, Debold et al., J Mol Cell Cardiol 2010, Borroni et al., Science signaling 2013

Text-mined interactions from Literome

Gu et al., J Biol Chem 2001 (Immunologic Deficiency Syndromes) : When expressed in hematopoietic cells, D57N Rac2 reduced endogenous activities of not only Rac2, but also Rac1 and decreased cell expansion in vitro in the presence of growth factors due to increased cell apoptosis
Aspenström et al., Biochem J 2004 : Cdc42, TCL ( TC10-like ), Rac1-Rac3 and RhoG induced the formation of lamellipodia, whereas Cdc42, Rac1 and Rac2 also induced the formation of thick bundles of actin filaments
Sánchez-Martín et al., J Biol Chem 2004 : We have identified Vav, a guanine nucleotide exchange factor for Rac-1, and PI3K/Akt, as regulators of the activation and inactivation phases of the activity of Rac-1, respectively, in the context of LFA-1 signaling based on the following experimental evidence : ( i ) LFA-1 induced activation of Vav and PI3K/Akt with kinetics consistent with a regulatory role for these molecules on Rac-1 , ( ii ) overexpression of a constitutively active Vav mutant induces activation of Rac independently of LFA-1 stimulation whereas overexpression of a dominant negative Vav mutant blocks LFA-1 mediated Rac activation, ( iii ) pharmacological inhibition of PI3K/Akt prevented the fall in the activity of Rac-1 after its initial activation but had no effect on Vav activity, and ( iv ) overexpression of a dominant negative or a constitutively active Akt-1 induced or inhibited, respectively, Rac-1 activity
Shyu et al., J Biomed Sci 2009 : TNF-alpha induced phosphorylation of Rac, while atorvastatin and Rac-1 inhibitor inhibited the phosphorylation of Rac induced by TNF-alpha