◀ Back to CRK
CRK — SRC
Pathways - manually collected, often from reviews:
-
NCI Pathway Database Nectin adhesion pathway:
Src (SRC)
→
CRK (CRK)
(modification, activates)
Fukuyama et al., J Biol Chem 2005*
Evidence: mutant phenotype
-
NCI Pathway Database Signaling events mediated by focal adhesion kinase:
FAK/Src-Yes-Fyn/p130 CAS complex (PTK2-YES1_SRC_FYN-BCAR1)
→
CRK (CRK)
(modification, collaborate)
Oktay et al., J Cell Biol 1999, Barberis et al., J Biol Chem 2000
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Signaling events mediated by focal adhesion kinase:
FAK/Src-Yes-Fyn/p130 CAS complex (PTK2-YES1_SRC_FYN-BCAR1)
→
FAK/Src-Yes-Fyn/p130 CAS/CRK complex (PTK2-YES1_SRC_FYN-BCAR1-CRK)
(modification, collaborate)
Oktay et al., J Cell Biol 1999, Barberis et al., J Biol Chem 2000
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Signaling events mediated by focal adhesion kinase:
CRK (CRK)
→
FAK/Src-Yes-Fyn/p130 CAS/CRK complex (PTK2-YES1_SRC_FYN-BCAR1-CRK)
(modification, collaborate)
Oktay et al., J Cell Biol 1999, Barberis et al., J Biol Chem 2000
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Signaling events mediated by focal adhesion kinase:
None
→
FAK/Src-Yes-Fyn/p130 CAS/CRK/DOCK1/ELMO1 complex (PTK2-YES1_SRC_FYN-BCAR1-CRK-DOCK1-ELMO1)
(modification, collaborate)
Cho et al., J Cell Biol 2002, Hsia et al., J Cell Biol 2003, Sharma et al., BMC cell biology 2008, Kiyokawa et al., Genes Dev 1998, Dolfi et al., Proc Natl Acad Sci U S A 1998
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Signaling events mediated by focal adhesion kinase:
RAC1/GDP complex (RAC1)
→
FAK/Src-Yes-Fyn/p130 CAS/CRK/DOCK1/ELMO1 complex (PTK2-YES1_SRC_FYN-BCAR1-CRK-DOCK1-ELMO1)
(modification, collaborate)
Cho et al., J Cell Biol 2002, Hsia et al., J Cell Biol 2003, Sharma et al., BMC cell biology 2008, Kiyokawa et al., Genes Dev 1998, Dolfi et al., Proc Natl Acad Sci U S A 1998
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Signaling events mediated by focal adhesion kinase:
FAK/Src-Yes-Fyn/p130 CAS/CRK/DOCK1/ELMO1 complex (PTK2-YES1_SRC_FYN-BCAR1-CRK-DOCK1-ELMO1)
→
None
(modification, activates)
Cho et al., J Cell Biol 2002, Hsia et al., J Cell Biol 2003, Sharma et al., BMC cell biology 2008, Kiyokawa et al., Genes Dev 1998, Dolfi et al., Proc Natl Acad Sci U S A 1998
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Endothelins:
p130Cas/CRK/Src/PYK2 complex (BCAR1-SRC-CRK-PTK2B)
→
PYK2 (PTK2B)
(modification, collaborate)
Kodama et al., Hypertension 2003
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database Endothelins:
p130Cas/CRK/Src/PYK2 complex (BCAR1-SRC-CRK-PTK2B)
→
p130Cas (BCAR1)
(modification, collaborate)
Kodama et al., Hypertension 2003
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database Endothelins:
p130Cas/CRK/Src/PYK2 complex (BCAR1-SRC-CRK-PTK2B)
→
Src (SRC)
(modification, collaborate)
Kodama et al., Hypertension 2003
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database Endothelins:
p130Cas/CRK/Src/PYK2 complex (BCAR1-SRC-CRK-PTK2B)
→
CRK (CRK)
(modification, collaborate)
Kodama et al., Hypertension 2003
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database Endothelins:
Src (SRC)
→
CRK (CRK)
(modification, collaborate)
Kodama et al., Hypertension 2003
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database Signaling events mediated by focal adhesion kinase:
FAK/Src-Yes-Fyn/p130 CAS/CRK/DOCK1/ELMO1 complex (PTK2-YES1_SRC_FYN-BCAR1-CRK-DOCK1-ELMO1)
→
DOCK1/ELMO1 complex (DOCK1-ELMO1)
(modification, collaborate)
Hsia et al., J Cell Biol 2003
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Signaling events mediated by focal adhesion kinase:
FAK/Src-Yes-Fyn/p130 CAS/CRK/DOCK1/ELMO1 complex (PTK2-YES1_SRC_FYN-BCAR1-CRK-DOCK1-ELMO1)
→
FAK/Src-Yes-Fyn/p130 CAS/CRK complex (PTK2-YES1_SRC_FYN-BCAR1-CRK)
(modification, collaborate)
Hsia et al., J Cell Biol 2003
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Signaling events mediated by focal adhesion kinase:
DOCK1/ELMO1 complex (DOCK1-ELMO1)
→
FAK/Src-Yes-Fyn/p130 CAS/CRK complex (PTK2-YES1_SRC_FYN-BCAR1-CRK)
(modification, collaborate)
Hsia et al., J Cell Biol 2003
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database E-cadherin signaling in the nascent adherens junction:
Src (SRC)
→
CRK (CRK)
(modification, activates)
Fukuyama et al., Oncogene 2006
Evidence: mutant phenotype, physical interaction, other species
-
NCI Pathway Database Endothelins:
p130Cas/CRK/Src/PYK2 complex (BCAR1-SRC-CRK-PTK2B)
→
JNK1 (MAPK8)
(modification, activates)
Kodama et al., Hypertension 2003
Evidence: mutant phenotype, assay
-
Reactome Reaction:
SRC
→
CRK
(indirect_complex)
Mochizuki et al., J Biol Chem 2000, Parsons et al., J Cell Sci 2003, Vallés et al., J Biol Chem 2004, Defilippi et al., Trends Cell Biol 2006, Klemke et al., J Cell Biol 1998*
-
Reactome Reaction:
SRC
→
CRK
(reaction)
Mochizuki et al., J Biol Chem 2000, Parsons et al., J Cell Sci 2003, Vallés et al., J Biol Chem 2004, Defilippi et al., Trends Cell Biol 2006, Klemke et al., J Cell Biol 1998*
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Blaukat et al., J Biol Chem 1999
:
Pyk2 induced activation of
Src is
necessary for phosphorylation of Shc and p130Cas and their association with Grb2 and
Crk , respectively, and for the activation of ERK and JNK cascades
Tai et al., Arterioscler Thromb Vasc Biol 2002
:
Previously, we showed that flow mediated tyrosine phosphorylation of p130
Crk associated substrate (Cas) required calcium dependent
c-Src activation
Gerthoffer et al., Am J Physiol Gastrointest Liver Physiol 2005
:
Src activation also
leads to activation of ERK and
p38 MAPKs
Carini et al., J Hepatol 2006
(Anoxia...) :
ATPgammaS activated Src and promoted a
Src dependent stimulation of both ERK1/2 and
p38MAPK
Bouchard et al., Apoptosis 2008
:
We report that : ( 1 ) Anoikis causes a down-activation of Fak,
Src , Akt-1 and Erk1/2, a loss of Fak-Src association, and a sustained/enhanced
activation of
p38beta , which is required as apoptosis/anoikis driver ; ( 2 ) PI3-K/Akt-1 up-regulates the expression of Bcl-X ( L ) and Mcl-1, down-regulates Bax and Bak, drives Bad phosphorylation ( both serine112/136 residues ) and antagonizes p38beta activation ; ( 3 ) MEK/Erk up-regulates Bcl-2, drives Bad phosphorylation ( serine112 residue ), but does not antagonize p38bactivation ; ( 4 ) PI3-K/Akt-1 is required for survival, whereas MEK/Erk is not ; ( 5 ) Src acts as a cornerstone in the engagement of both pathways by beta1 integrins/Fak, and is crucial for survival ; and ( 6 ) beta1 integrins/Fak and/or Src regulate Bcl-2 homologs as both PI3-K/Atk-1 and MEK/Erk combined
Sachdev et al., BMC cancer 2009
(Colonic Neoplasms...) :
Specifically, in the absence of FAK,
Src induced higher phosphorylation of p190RhoGAP, paxillin ( poY118 ) and
Crk irrespective of adhesion state, PKC-delta ( poY311 ), connexin-43 ( poY265 ) and Sam68 only under adherent conditions, and p56Dok-2 ( poY351 ) and p120catenin ( poY228 ) only under suspension conditions
Watanabe et al., Cell Res 2009
:
Furthermore,
Crk induced the phosphorylation of
Src-Y416 ; accordingly the interaction between Crk and Csk was increased
Watanabe et al., Mol Cancer Res 2009
(Sarcoma, Synovial) :
Adaptor protein
Crk induces
Src dependent activation of p38 MAPK in regulation of synovial sarcoma cell proliferation ... The present study shows that
Crk induced activation of
Src and subsequent signaling by p38 mitogen activated protein kinase ( MAPK ) contribute to the enhanced proliferation of human synovial sarcoma cells
Samoylenko et al., Carcinogenesis 2012
(Adenocarcinoma...) :
Thereby, Ruk ( l )
/CIN85 led to a more rapid and prolonged epidermal growth factor dependent activation of
Src , Akt and ERK1/2 and treatment with the Src inhibitor PP2 and the PI3K inhibitor LY294002 abolished the Ruk ( l ) /CIN85 dependent changes in cell motility