◀ Back to IGF1
CRK — IGF1
Pathways - manually collected, often from reviews:
-
NCI Pathway Database IGF1 pathway:
IRS2/Crk complex (IRS2-CRK)
→
IGF-1R heterotetramer/IGF1/IRS1 complex (IGF1R-IGF1-IRS1)
(modification, collaborate)
Beitner-Johnson et al., J Biol Chem 1996
Evidence: mutant phenotype, assay
-
NCI Pathway Database IGF1 pathway:
IGF-1R heterotetramer/IGF1/IRS1 complex (IGF1R-IGF1-IRS1)
→
CRK (CRK)
(modification, activates)
Butler et al., J Biol Chem 1997, Fagerström et al., J Biol Chem 1998, Casamassima et al., J Biol Chem 1998
Evidence: assay, physical interaction
-
NCI Pathway Database IGF1 pathway:
IGF-1R heterotetramer/IGF1/IRS1 complex (IGF1R-IGF1-IRS1)
→
Crk/p130 Cas/Paxillin complex (CRK-BCAR1-PXN)
(modification, activates)
Butler et al., J Biol Chem 1997, Fagerström et al., J Biol Chem 1998, Casamassima et al., J Biol Chem 1998
Evidence: assay, physical interaction
-
NCI Pathway Database IGF1 pathway:
IGF-1R heterotetramer/IGF1/IRS1 complex (IGF1R-IGF1-IRS1)
→
IRS1/Crk complex (IRS1-CRK)
(modification, activates)
Beitner-Johnson et al., J Biol Chem 1995*, Beitner-Johnson et al., J Biol Chem 1996, Koval et al., Biochem J 1998
Evidence: mutant phenotype, assay
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
STRING interaction:
CRK
—
IGF1
(interaction, mapped from kegg_pathways)
-
STRING interaction:
CRK
—
IGF1
(interaction, mapped from kegg_pathways)
-
STRING interaction:
IGF1
—
CRK
(interaction, mapped from dip)
-
STRING interaction:
IGF1
—
CRK
(interaction, mapped from dip)
Text-mined interactions from Literome
Remacle-Bonnet et al., Cancer Res 2000
(Adenocarcinoma...) :
These findings indicate that the antiapoptotic function of
IGF-I in HT29-D4 cells is based on the enhancement of the survival pathways initiated by TNF, but not Fas, and
mediated by
MAPK/p38 , MAPK/ERK, and NF-kappaB, which act in concert to suppress the proapoptotic signals
Yamagishi et al., Brain Res Mol Brain Res 2003
(Potassium Deficiency) :
BDNF and
IGF-1 suppressed the activation of
p38 and c-Jun, but not of c-Jun N-terminal kinase (JNK), caused by lowering the potassium concentration
Furundzija et al., Biochem Biophys Res Commun 2010
(Atherosclerosis) :
Pharmacological blocking experiments with specific inhibitors of Akt, PKC and p38 MAP-kinase revealed that IGF-1 dependent activation of focal adhesion kinase ( FAK ) and paxillin, and consecutively IGF-1 facilitated migration, required
IGF-1/IGF-1R mediated
PI3-kinase/PKC/p38 dependent integrin inside-out signaling
Bae et al., Biochem Biophys Res Commun 2013
:
U0126 ( ERK1/2 inhibitor ) and SB203580 (
p38 MAPK inhibitor )
inhibited IGF-1 induced MUC8 and MUC5B mRNA expression
Beitner-Johnson et al., J Biol Chem 1995
(Carcinoma, Embryonal) :
Insulin-like growth factor-I stimulates tyrosine phosphorylation of endogenous
c-Crk ... We show that
IGF-I stimulates tyrosine phosphorylation of
Crk II via stimulation of endogenous IGF-I receptors in both 293 cells and NIH-3T3 cells ...
IGF-I stimulated tyrosine phosphorylation of
Crk II in a dose- and time dependent manner
Casamassima et al., J Biol Chem 1998
:
Crk complex in
response to
IGF-I