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EGFR — STAT5B
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
—
STAT5B
(coimmunoprecipitation)
Schulze et al., Molecular systems biology 2005
-
IRef Bind_translation Interaction:
EGFR
—
STAT5B
(affinity chromatography technology)
Schulze et al., Molecular systems biology 2005
-
IRef Biogrid Interaction:
EGFR
—
STAT5B
(physical association, affinity chromatography technology)
Runge et al., Biochem Biophys Res Commun 1999*
-
IRef Hprd Interaction:
Complex of 73 proteins
(in vivo)
Schulze et al., Molecular systems biology 2005
-
IRef Hprd Interaction:
EGFR
—
STAT5B
(in vitro)
Runge et al., Biochem Biophys Res Commun 1999*, Kloth et al., J Biol Chem 2002*
-
IRef Hprd Interaction:
EGFR
—
STAT5B
(in vivo)
Runge et al., Biochem Biophys Res Commun 1999*, Kloth et al., J Biol Chem 2002*
-
IRef Hprd Interaction:
Complex of 19 proteins
(in vivo)
Schulze et al., Molecular systems biology 2005
-
IRef Intact Interaction:
EGFR
—
STAT5B
(physical association, pull down)
Schulze et al., Molecular systems biology 2005
-
IRef Ophid Interaction:
EGFR
—
STAT5B
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
-
IRef Ophid Interaction:
EGFR
—
STAT5B
(aggregation, confirmational text mining)
Jones et al., Nature 2006
Text-mined interactions from Literome
Kloth et al., J Biol Chem 2003
:
We demonstrate that 1 ) activation of
STAT5b by EGF
requires overexpression of the
EGFR , 2 ) co-overexpression of c-Src alone does not result in EGF induced activation of STAT5b but enhances that seen in EGFR overexpressing cells, and 3 ) EGF induced tyrosine phosphorylation of STAT5b requires Tyr ( 845 ) of the EGFR
Peng et al., Nucleic Acids Res 2010
:
Taken together, CPEB3 has a novel function in the nucleus as to suppress
Stat5b dependent
EGFR gene transcription
Hu et al., Proc Natl Acad Sci U S A 2011
(Glioblastoma) :
The
EGFR-selective tyrosine kinase inhibitors, erlotinib and gefitinib,
blocked not only EGFRvIII signaling to ERK but also uPAR dependent
STAT5b activation