◀ Back to EGFR
CRK — EGFR
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Bind Interaction:
Complex of EGFR-GRB2-STAT5B-CRK
-
IRef Bind_translation Interaction:
EGFR
—
CRK
(affinity chromatography technology)
Schulze et al., Molecular systems biology 2005
-
IRef Bind_translation Interaction:
EGFR
—
CRK
(coimmunoprecipitation)
Schulze et al., Molecular systems biology 2005
-
IRef Biogrid Interaction:
EGFR
—
CRK
(physical association, affinity chromatography technology)
Katayama et al., Jpn J Cancer Res 1999*
-
IRef Biogrid Interaction:
EGFR
—
CRK
(physical association, affinity chromatography technology)
Ota et al., Cell Signal 1998*
-
IRef Biogrid Interaction:
EGFR
—
CRK
(direct interaction, unspecified method)
Jones et al., Nature 2006
-
IRef Biogrid Interaction:
EGFR
—
CRK
(physical association, affinity chromatography technology)
Schulze et al., Molecular systems biology 2005
-
IRef Biogrid Interaction:
EGFR
—
CRK
(physical association, affinity chromatography technology)
Hashimoto et al., J Biol Chem 1998*
-
IRef Biogrid Interaction:
EGFR
—
CRK
(direct interaction, enzymatic study)
Hashimoto et al., J Biol Chem 1998*
-
IRef Hprd Interaction:
Complex of 73 proteins
(in vivo)
Schulze et al., Molecular systems biology 2005
-
IRef Hprd Interaction:
Complex of 73 proteins
(in vivo)
Kao et al., J Biol Chem 2001
-
IRef Hprd Interaction:
EGFR
—
CRK
(in vitro)
Endo et al., J Biol Chem 2002*, Abassi et al., EMBO J 2002*, Wang et al., Oncogene 1996*, Koval et al., Biochem J 1998, Hashimoto et al., J Biol Chem 1998*
-
IRef Hprd Interaction:
EGFR
—
CRK
(in vivo)
Endo et al., J Biol Chem 2002*, Abassi et al., EMBO J 2002*, Wang et al., Oncogene 1996*, Koval et al., Biochem J 1998, Hashimoto et al., J Biol Chem 1998*
-
IRef Intact Interaction:
EGFR
—
CRK
(direct interaction, protein array)
Jones et al., Nature 2006
-
IRef Ophid Interaction:
EGFR
—
CRK
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
Text-mined interactions from Literome
Nicholl et al., J Vasc Surg 2005
:
Inhibition of
EGFR reduced both ERK1/2 and
p38 MAPK activation
Kuwahara et al., Am J Physiol Lung Cell Mol Physiol 2006
:
We conclude that NE increases IL-8 transcription through
p38/NF-kappaB activation via
EGFR transactivation
Jiang et al., J Ocul Pharmacol Ther 2006
:
EGF induced cell migration in a dose dependent manner ; EGF induced
EGFR phosphorylation and downstream
activation of c-Jun N-terminal protein kinase (JNK),
p38 MAP kinase ( p38 ) , extracellular signal regulated kinase ( ERK1/2 ) and AKT, were inhibited by PD153035 ( EGFR inhibitor ), JNKi ( JNK inhibitor ), SB203580 ( p38 inhibitor ), U0126 ( MEK/ERK inhibitor ), and LY294002 ( PI3K/AKT inhibitor ), respectively
Harrington et al., Obesity (Silver Spring) 2007
:
Our results show that EGFR homodimers mediate action of EGF at high abundance, but at low abundance, EGF promotes differentiation through
EGFR/EB2R heterodimer
activation of Src and
p38
Taub et al., Mol Biol Cell 2007
(MAP Kinase Signaling System) :
Continuous
EGFR signaling from late endosomes
caused sustained extracellular signal regulated kinase and
p38 signaling and resulted in hyperactivation of nuclear targets, such as Elk-1
Wakasaki et al., Neoplasia (New York, N.Y.) 2010
(Carcinoma, Squamous Cell...) :
Little is known, however, about a
role of
CIN85 in
EGFR signaling as well as its relevance to tumor development and progression of HNSCC
Schroeder et al., Mol Biol Cell 2012
:
In this study we show that
EGFR activation
leads to a pronounced src mediated tyrosine phosphorylation of
CIN85 that subsequently influences EGFR ubiquitination