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GIT1 — SRC
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
GIT1
→
SRC
(directlyIncreases, GIT1 Activity)
Haendeler et al., J Biol Chem 2003*
Evidence: Here we show that the GPCR kinase-interacting protein-1 (GIT1) is a substrate for c-Src that undergoes tyrosine phosphorylation in response to angiotensin II (AngII) and EGF in vascular smooth muscle and 293 cells.
-
OpenBEL Selventa BEL large corpus:
GIT1
→
SRC
(directlyIncreases, GIT1 Activity)
Yin et al., Mol Cell Biol 2004*
Evidence: Here we show that the GPCR kinase-interacting protein 1 (GIT1) is a substrate for c-Src that associates with MEK1 in vascular smooth-muscle cells and human embryonic kidney 293 cells.
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Reactome Reaction:
GIT1
→
SRC
(indirect_complex)
Zhang et al., J Cell Biol 2003, Segura et al., Nat Neurosci 2007
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Reactome Reaction:
GIT1
→
SRC
(reaction)
Bokoch et al., Annu Rev Biochem 2003, Zhang et al., J Cell Biol 2003, Zhang et al., J Neurosci 2005, Segura et al., Nat Neurosci 2007
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
van Nieuw Amerongen et al., Circ Res 2004
:
Thrombin stimulated
GIT1 tyrosine phosphorylation with a time course similar to FAK phosphorylation in a Rho kinase- and
Src dependent manner
Yin et al., J Biol Chem 2005
:
Because
Src is
required for both
GIT1 tyrosine phosphorylation and focal adhesion disassembly, we studied the effects of Src on GIT1-ERK1/2 interactions
Wang et al., Arterioscler Thromb Vasc Biol 2009
:
Because
GIT1 is a substrate of c-Src, and podosome formation is
c-Src dependent , we hypothesized that GIT1 plays an important role in VEGF induced EC podosome formation and cell migration