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ARHGDIB — RAC1

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: Complex of ARHGDIB-RAC1 (directlyDecreases, ARHGDIB/RAC1 Activity)
  Evidence: The beta2 integrin-triggered relocalization of Rac1 to the cytoskeleton was enabled by a PI 3-kinase-induced dissociation of Rac1 from LyGDI.

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: RAC1 — ARHGDIB (direct interaction, two hybrid) Vinayagam et al., Science signaling 2011
• IRef Hprd Interaction: RAC1 — ARHGDIB (in vivo) Illenberger et al., EMBO J 1998*
• IRef Intact Interaction: RAC1 — ARHGDIB (physical association, two hybrid) Vinayagam et al., Science signaling 2011
• IRef Ophid Interaction: RAC1 — ARHGDIB (aggregation, confirmational text mining) Illenberger et al., EMBO J 1998*
• IRef Ophid Interaction: RAC1 — ARHGDIB (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Groysman et al., J Biol Chem 2002 : Surprisingly, Vav1 associates with Ly-GDI , a hematopoietic cell-specific guanine nucleotide dissociation inhibitor of Rac
Klahre et al., Plant J 2006 : Nt-RhoGDI2 regulates Rac/Rop signaling and polar cell growth in tobacco pollen tubes
Huang et al., J Biomed Sci 2009 : We also demonstrated that knockdown of RhoGDIbeta expression by RNA interference blocked RhoGDIbeta induced Rac1 expression and cell migration
Wu et al., Nat Immunol 2009 : CARD9 associated with the GDP-dissociation inhibitor LyGDI in phagosomes after bacterial and fungal infection and binding of CARD9 suppressed LyGDI mediated inhibition of the GTPase Rac1 , thereby leading to ROS production and bacterial killing in macrophages
Watanabe et al., AIDS Res Hum Retroviruses 2012 (HIV Infections) : The results showed that ( 1 ) a significant portion of RhoA and Rac1, but not Cdc42, exists in the GTP bound active form under steady-state conditions, ( 2 ) ectopic ARHGDIB expression reduced the F-actin content and the active forms of both RhoA and Rac1 , and ( 3 ) HIV-1 infection was attenuated by either ectopic expression of ARHGDIB or inhibition of the RhoA signal cascade at the HIV-1 Env dependent early phase of the viral life cycle
Griner et al., Oncogene 2013 : PKCa phosphorylation of RhoGDI2 at Ser31 disrupts interactions with Rac1 and decreases GDI activity
Duan et al., J Radiat Res 2013 : Interestingly, LyGDI was discovered as a new target gene of miR-34a, and downregulation of LyGDI promoted Rac1 activation and membrane translocation, resulting in cell apoptosis