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SRC — VAV2
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
VAV2
→
SRC
(directlyIncreases, SRC Activity, VAV2 Activity)
Servitja et al., J Biol Chem 2003*
Evidence: We further show that Vav2 and the ubiquitously expressed Rac1 guanine nucleotide exchange factor Tiam1 are phosphorylated in tyrosine residues in cells transfected with active and oncogenic Src.Moreover, phosphorylation of Tiam1 in cells treated with pervanadate, a potent inhibitor of tyrosine phosphatases, was partially inhibited by the Src inhibitor SU6656.
-
Reactome Reaction:
SRC
→
VAV2
(indirect_complex)
Marignani et al., J Cell Biol 2001, Cowan et al., Neuron 2005
-
Reactome Reaction:
SRC
→
VAV2
(reaction)
Song et al., J Immunol 1999, Aghazadeh et al., Cell 2000, Marignani et al., J Cell Biol 2001, Marston et al., Nat Cell Biol 2003, Cowan et al., Neuron 2005, Garrett et al., Exp Cell Res 2007, Deckert et al., Immunity 1996, Teramoto et al., J Biol Chem 1997
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
STRING interaction:
SRC
—
VAV2
(interaction, mapped from bind kegg_pathways)
-
STRING interaction:
VAV2
—
SRC
(interaction, mapped from bind kegg_pathways)
Text-mined interactions from Literome
Servitja et al., J Biol Chem 2003
(Cell Transformation, Neoplastic) :
Evidence of a
role for Tiam1 and
Vav2 in Rac activation by
Src
Meng et al., EMBO J 2004
:
Here we show that DIP binds to p190RhoGAP and Vav2, and that DIP is phosphorylated by
Src and
mediates the phosphorylation of p190RhoGAP and
Vav2 upon EGF stimulation
Fukuyama et al., Oncogene 2006
:
The c-Src catalysed tyrosine phosphorylation was not sufficient for the activation of
Vav2 and the
c-Src induced activation of Rap1 was additionally
necessary for it, although activated Rap1 alone was not sufficient for the activation of non-tyrosine phosphorylated Vav2
Gavard et al., Nat Cell Biol 2006
:
This process is initiated by the activation of the small GTPase Rac by VEGFR-2 through the
Src dependent phosphorylation of
Vav2 , a guanine nucleotide-exchange factor
Murata et al., J Neurosci 2006
:
Inhibition of either FGD1 related Cdc42-guanine nucleotide exchange factor (GEF) ( FRG ) or
Vav2 , which is a GEF for Cdc42 and Rac and is
activated by
Src , also prevented the effects of CD47 on dendritic development
Garrett et al., Exp Cell Res 2007
:
Moreover,
Vav2 is tyrosine phosphorylated upon VEGF treatment, which temporally correlates with Rac1 activation and
requires VEGFR-2 signaling and
Src kinase activity
Lu et al., J Biol Chem 2008
:
In Nef infected podocytes,
Src kinase
induces phosphorylation of DIP, p190RhoGAP, and
Vav2 , leading to RhoA inhibition and Rac1 activation
Arora et al., Am J Physiol Cell Physiol 2008
:
Collagen bead binding promoted phosphorylation of
Vav2 , which temporally correlated with Rac1 activation and which
required Src kinase activity
Peng et al., Cell Signal 2010
:
Src and PI3K are both
required upstream of
Vav2 and RhoA activation