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RAC1 — TRIO

Pathways - manually collected, often from reviews:

• BioCarta rac1 cell motility signaling pathway: 0005085 (ARHGEF1/TRIO/VAV1/ARHGEF5/CACNA1A) → RAC1 (modification, activates)
• NCI Pathway Database Netrin-mediated signaling events: RAC1/GDP complex (RAC1) → TRIO (TRIO) (modification, collaborate) Briançon-Marjollet et al., Mol Cell Biol 2008, Peng et al., J Biol Chem 2010*
  Evidence: mutant phenotype, assay
• NCI Pathway Database Regulation of RAC1 activity: RAC1/GDP complex (RAC1) → TRIO (TRIO) (modification, collaborate) Bellanger et al., Nat Cell Biol 2000*, Zhang et al., Biochem Biophys Res Commun 2005*, Charrasse et al., Mol Biol Cell 2007*, Briançon-Marjollet et al., Mol Cell Biol 2008, Debant et al., Proc Natl Acad Sci U S A 1996*
  Evidence: assay
• Reactome Reaction: TRIO → RAC1 (reaction) Harrington et al., J Neurosci 2002, Li et al., Nat Neurosci 2008, Briançon-Marjollet et al., Mol Cell Biol 2008
• Reactome Reaction: TRIO → RAC1 (indirect_complex) Li et al., Nat Neurosci 2008, Briançon-Marjollet et al., Mol Cell Biol 2008
• WikiPathways Regulation of Microtubule Cytoskeleton: TRIO → RAC1 (activation)

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: TRIO — RAC1 (direct interaction, pull down) Gao et al., J Biol Chem 2001*
• IRef Dip Interaction: RAC1 — TRIO (direct interaction, pull down) Chen et al., Proc Natl Acad Sci U S A 2011*
• IRef Hprd Interaction: TRIO — RAC1 (in vivo) Gao et al., J Biol Chem 2001*
• IRef Hprd Interaction: TRIO — RAC1 (in vitro) Gao et al., J Biol Chem 2001*
• IRef Ophid Interaction: RAC1 — TRIO (aggregation, interologs mapping) Brown et al., Bioinformatics 2005
• IRef Ophid Interaction: RAC1 — TRIO (aggregation, confirmational text mining) Gao et al., J Biol Chem 2001*

Text-mined interactions from Literome

Debreceni et al., J Biol Chem 2004 : The N1406A/D1407A mutant of Trio acted dominant negatively in vitro by retaining Rac1 binding activity but losing GEF catalytic activity and competitively inhibited Rac1 activation by wild type Trio
Briançon-Marjollet et al., Mol Cell Biol 2008 : Trio mediates netrin-1 induced Rac1 activation in axon outgrowth and guidance ... Here, we show that the RhoGEF Trio mediates Rac1 activation in netrin-1 signaling ... We found that Trio interacts with the netrin-1 receptor DCC in mouse embryonic brains and that netrin-1 induced Rac1 activation in brain is impaired in the absence of Trio
Bach et al., Mol Biol Cell 2010 : M-cadherin dependent pathways that signal through Rac1 GTPase activation via the Rho-guanine nucleotide exchange factor ( GEF ) Trio are important for myoblast fusion
Li et al., Genes & cancer 2011 : Because knockdown of CDH11 prevents the plasma membrane localization of Trio, our study indicates that CDH11 may play a role in recruiting Trio to the plasma membrane where Trio activates Rac , leading to cell migration
van Rijssel et al., Mol Biol Cell 2012 : Moreover, upon clustering of ICAM-1, the Rho-guanine nucleotide exchange factor Trio activates Rac1 , prior to activating RhoG, in a filamin dependent manner
van Rijssel et al., Cell Adh Migr 2012 : We recently reported that the Rho-GEF Trio , known to be able to exchange GTP on Rac1, RhoG and RhoA, regulates lamellipodia formation to mediate cell spreading and migration in a Rac1 dependent manner
DeGeer et al., Mol Cell Biol 2013 : The Rho guanine nucleotide exchange factor ( GEF ) Trio is essential for Rac1 activation downstream of netrin-1/DCC, but the molecular mechanisms governing Trio activity remain elusive
Bellanger et al., Oncogene 1998 : To determine whether Trio could activate Rac1 and RhoA in vivo, we measured the effect of Trio on Mitogen Activated Protein Kinase ( MAPK ) pathways and cytoskeletal rearrangements events mediated by the two GTPases
Bellanger et al., C R Seances Soc Biol Fil 1998 : [ Role of the multifunctional Trio protein in the control of the Rac1 and RhoA gtpase signaling pathways ]