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ERBB2 — STAT3
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Biogrid Interaction:
STAT3
—
ERBB2
(direct interaction, unspecified method)
Jones et al., Nature 2006
-
IRef Biogrid Interaction:
STAT3
—
ERBB2
(physical association, affinity chromatography technology)
Ren et al., J Biol Chem 2002
-
IRef Intact Interaction:
ERBB2
—
STAT3
(association, coimmunoprecipitation)
Ren et al., J Biol Chem 2002
-
IRef Intact Interaction:
ERBB2
—
STAT3
(direct interaction, protein array)
Jones et al., Nature 2006
-
IRef Intact Interaction:
ERBB2
—
STAT3
(colocalization, confocal microscopy)
Béguelin et al., Mol Cell Biol 2010*
-
IRef Intact Interaction:
Complex of 19 proteins
(association, anti bait coimmunoprecipitation)
Hawthorne et al., Mol Cancer Res 2009*
-
IRef Intact Interaction:
Complex of UBASH3B-CDC37-EGFR-ERBB3-ERRFI1-SHC1-ERBB2-STAT3
(association, anti bait coimmunoprecipitation)
Li et al., Molecular systems biology 2013
-
IRef Intact Interaction:
Complex of 70 proteins
(association, anti bait coimmunoprecipitation)
Thelemann et al., Mol Cell Proteomics 2005
Text-mined interactions from Literome
Fernandes et al., Int J Cancer 1999
(Lung Neoplasms) :
In this report, we demonstrate that
STAT 3 is constitutively
activated in these cells by the TGF-alpha stimulated
ErbB-1/-2 heterodimer complex ... Inhibition of
ErbB-2 kinase activity by tyrphostin AG825
prevented the constitutive activation of
STAT 3 in the TGF-alpha producing, ErbB-1 expressing cell line
DeArmond et al., Oncogene 2003
(Pancreatic Neoplasms) :
Autocrine mediated
ErbB-2 kinase
activation of
STAT3 is required for growth factor independence of pancreatic cancer cell lines ... Expression of a STAT3 dominant negative prevented SFM stimulated cell proliferation of MIA PaCa-2 cells, suggesting that
activation of
STAT3 by
ErbB2 is required for a growth factor independent phenotype of these cells
Dowlati et al., Mol Cancer Ther 2004
:
Our study suggests that residual
ErbB2 activation by EGF, despite EGFR blockade, is
responsible for persistent downstream activation of
Stat-3
Hawthorne et al., Mol Cancer Res 2009
(Breast Neoplasms) :
Our data suggest that
ErbB2 overexpression can
activate STAT3 through Src leading to transcriptional up-regulation of p21 ( Cip1 ) that confers Taxol resistance of breast cancer cells
Lee et al., The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology 2008
:
In the present study, we found that specific tyrphostin inhibitors of
ErbB2 ( AG825 and AG879 ), but not ErbB1 inhibitor ( AG1478 ),
suppressed IL-6 induced tyrosine phosphorylation of
STAT3 in schwannoma cells ... Additionally, the inhibition of
ErbB2 expression, with either a specific RNAi or transfection of an ErbB2 mutant lacking the intracellular domain did not
inhibit the IL-6 induced tyrosine phosphorylation of
STAT3