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EGFR — SOAT1
Text-mined interactions from Literome
Olayioye et al., J Biol Chem 1999
:
The mechanism underlying
ErbB1 induced
Stat activation and whether Stats are downstream targets of other ErbB receptors have not been explored
Garcia et al., Oncogene 2001
(Breast Neoplasms) :
While EGF-R kinase activity is not required for constitutive Stat3 activation in breast cancer cells, EGF stimulation further increases STAT DNA binding activity, consistent with an important
role for
EGF-R in
STAT signaling and malignant progression
Sriuranpong et al., Cancer Res 2003
(Carcinoma, Squamous Cell...) :
Even in the EGFR positive cell lines,
STAT3 activation was not
dependent on
EGFR activation, as STAT3 tyrosine phosphorylation levels persisted after treatment with AG1478, a chemical inhibitor of EGFR activity
Burova et al., Tsitologiia 2003
:
Herein, we postulate also that H2O2 induced
STAT activation in carcinoma cells
involves Src dependent
EGFR transactivation
Andl et al., Am J Physiol Gastrointest Liver Physiol 2004
:
Herein, we demonstrate that
EGFR overexpression in primary esophageal keratinocytes
activates STAT in a JAK dependent fashion with the functional consequence of enhanced cell migration, which can be abolished by use of a JAK-specific inhibitor, AG-490
Alvarez et al., Cancer Res 2006
(Carcinoma, Non-Small-Cell Lung...) :
In non-small-cell lung cancer cells,
STAT3 activity is
regulated by
EGFR through modulation of STAT3 serine phosphorylation
Quesnelle et al., J Cell Biochem 2007
(Neoplasms) :
STAT mediated
EGFR signaling in cancer ...
EGFR likely
activates STAT in a manner distinctive from other mechanisms of STAT activation ; STAT5 can be phosphorylated in an EGF dependent manner at unique sites, conferring novel functions
Yuan et al., J Biol Chem 2010
(Breast Neoplasms...) :
Our data suggest PTPN9 as a negative regulator of breast cancer cells by targeting ErbB2 and
EGFR and
inhibiting STAT activation
Bauer et al., Cell Host Microbe 2012
:
We find that hBD3 is highly active against H. pylori in vitro and is rapidly induced during early infection via
EGFR dependent activation of MAP kinase and
JAK/STAT signaling