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CDC42 — VAV3
Pathways - manually collected, often from reviews:
-
KEGG T cell receptor signaling pathway:
VAV1/VAV2/VAV3
→
CDC42/RHOA
(protein-protein, activation)
-
KEGG Fc gamma R-mediated phagocytosis:
VAV1/VAV2/VAV3
→
CDC42
(protein-protein, activation)
-
KEGG Leukocyte transendothelial migration:
VAV1/VAV2/VAV3
→
CDC42
(protein-protein, activation)
-
KEGG Chemokine signaling pathway:
VAV1/VAV2/VAV3
→
CDC42
(protein-protein, activation)
-
NCI Pathway Database Regulation of CDC42 activity:
CDC42/GDP complex (CDC42)
→
VAV3 (VAV3)
(modification, collaborate)
Aoki et al., Mol Biol Cell 2005*
Evidence: assay
-
Reactome Reaction:
CDC42
→
VAV3
(reaction)
Reid et al., J Biol Chem 1999, Schmidt et al., Genes Dev 2002, Jaffe et al., Annu Rev Cell Dev Biol 2005, Ramos-Morales et al., Oncogene 1995, Pasteris et al., Cell 1994, Hart et al., J Biol Chem 1994, Hart et al., J Biol Chem 1996, Zheng et al., J Biol Chem 1996, Van Aelst et al., Genes Dev 1997, Ren et al., J Biol Chem 1998
-
WikiPathways Chemokine signaling pathway:
VAV1/VAV2/VAV3
→
CDC42
(activation)
Text-mined interactions from Literome
Zeng et al., Mol Cell Biol 2000
(Cell Transformation, Neoplastic) :
In vitro binding assays using glutathione S-transferase-fusion polypeptides containing the GTPase binding domains of Rok-alpha, Pak, or Ack revealed that overexpression of
Vav3 in NIH 3T3 cells
resulted in the activation of Rac-1 and
Cdc42 whereas a deletion mutant lacking the N-terminal calponin homology and acidic region domains activated RhoA and Rac-1 but lost the ability to activate Cdc42
Aoki et al., Mol Biol Cell 2005
:
Local phosphatidylinositol 3,4,5-trisphosphate accumulation recruits Vav2 and
Vav3 to
activate Rac1/Cdc42 and initiate neurite outgrowth in nerve growth factor stimulated PC12 cells ... Depletion of Vav2 and
Vav3 by RNA interference significantly
inhibited both
Rac1/Cdc42 activation and the formation of short processes leading to neurite outgrowth ... At the NGF induced protrusions, local phosphatidylinositol 3,4,5-trisphosphate accumulation recruited Vav2 and Vav3 to activate Rac1 and
Cdc42 , and conversely, Vav2 and
Vav3 were
required for the local activation of PI3-kinase