◀ Back to EGF
EGF — HRAS
Pathways - manually collected, often from reviews:
-
NCI Pathway Database a6b1 and a6b4 Integrin signaling:
EGF/EGFR complex (EGF-EGFR)
→
HRAS/GTP complex (HRAS)
(modification, activates)
Russell et al., J Cell Sci 2003, Yoon et al., Cancer Res 2006
Evidence: assay
-
NCI Pathway Database a6b1 and a6b4 Integrin signaling:
EGF/EGFR complex (EGF-EGFR)
→
HRAS/GDP complex (HRAS)
(modification, activates)
Russell et al., J Cell Sci 2003, Yoon et al., Cancer Res 2006
Evidence: assay
-
NCI Pathway Database EGFR-dependent Endothelin signaling events:
HRAS/GDP complex (HRAS)
→
EGF/EGFR dimer/SHC/GRB2/SOS1 complex (EGF-EGFR-SHC1-GRB2-SOS1)
(modification, collaborate)
Iwasaki et al., Endocrinology 1999, Daub et al., Nature 1996
Evidence: mutant phenotype, other species
-
NCI Pathway Database Internalization of ErbB1:
RAS family/GDP complex (HRAS_KRAS_HRAS_KRAS_NRAS)
→
EGFR/EGFR/EGF/EGF/GRB2/SOS1 complex (EGFR-EGF-GRB2-SOS1)
(modification, collaborate)
Haugh et al., J Biol Chem 1999, Pennock et al., Mol Cell Biol 2003, Wiley et al., J Biol Chem 1991, Di Guglielmo et al., EMBO J 1994, Herbst et al., J Biol Chem 1994
Evidence: assay
-
NCI Pathway Database Internalization of ErbB1:
EGFR/EGFR/EGF/EGF/GRB2/SOS1 complex (EGFR-EGF-GRB2-SOS1)
→
RAS family/GTP complex (HRAS_KRAS_HRAS_KRAS_NRAS)
(modification, activates)
Haugh et al., J Biol Chem 1999, Pennock et al., Mol Cell Biol 2003, Wiley et al., J Biol Chem 1991, Di Guglielmo et al., EMBO J 1994, Herbst et al., J Biol Chem 1994
Evidence: assay
-
NCI Pathway Database Internalization of ErbB1:
RAS family/GDP complex (HRAS_KRAS_HRAS_KRAS_NRAS)
→
EGFR/EGFR/EGF/EGF/p46 SHC/GRB2/SOS1 complex (EGFR-EGF-SHC1-GRB2-SOS1)
(modification, collaborate)
Haugh et al., J Biol Chem 1999
Evidence: assay
-
NCI Pathway Database Internalization of ErbB1:
EGFR/EGFR/EGF/EGF/p46 SHC/GRB2/SOS1 complex (EGFR-EGF-SHC1-GRB2-SOS1)
→
RAS family/GTP complex (HRAS_KRAS_HRAS_KRAS_NRAS)
(modification, activates)
Haugh et al., J Biol Chem 1999
Evidence: assay
-
NCI Pathway Database Internalization of ErbB1:
RAS family/GDP complex (HRAS_KRAS_HRAS_KRAS_NRAS)
→
EGFR/EGFR/EGF/EGF/p52 SHC/GRB2/SOS1 complex (EGFR-EGF-SHC1-GRB2-SOS1)
(modification, collaborate)
Haugh et al., J Biol Chem 1999
Evidence: assay
-
Reactome Reaction:
EGF
→
HRAS
(reaction)
Paez et al., Science 2004, Sordella et al., Science 2004, Shimamura et al., Cancer Res 2005, Janes et al., Oncogene 1994, Chardin et al., Science 1993, Xie et al., J Biol Chem 1995
-
WikiPathways TGF-beta Receptor Signaling:
EGF
→
HRAS
(activation)
Text-mined interactions from Literome
Ammit et al., Am J Respir Cell Mol Biol 1999
:
EGF rapidly
activated p21ras within 30 s and was sustained for up to 30 min
Ding et al., Int J Cancer 2000
(Astrocytoma...) :
Mitogens, such as
epidermal growth factor and
activation of
p21-Ras , previously demonstrated to be relevant in astrocytoma proliferation and induction of VEGF, also induce Npn-1 expression
Pons et al., FEBS Lett 2001
:
In these cells, no increase of
Ras-GTP levels,
induced by
EGF or TPA, was detected
Elad-Sfadia et al., J Biol Chem 2002
:
Here we show that in comparison with Ras transfectants, H-Ras/galectin-1 or K-Ras4B/galectin-1 co-transfectants exhibit enhanced and prolonged
epidermal growth factor (EGF) stimulated increases in
Ras-GTP , Raf-1 activity, and active extracellular signal regulated kinase
Yin et al., Mol Cell Biochem 1992
(Mammary Neoplasms, Experimental) :
Neither insulin nor
epidermal growth factor increased mRNA levels of
c-Ha-ras or actin gene
Elad-Sfadia et al., J Biol Chem 2004
:
Co-transfectants of K-Ras/galectin-3, but not of H-Ras/galectin-3, exhibited enhanced and prolonged
epidermal growth factor stimulated increases in
Ras-GTP , Raf-1 activity, and PI3-K activity ... Galectin-3 antisense RNA inhibited the
epidermal growth factor stimulated increase in
K-Ras-GTP but enhanced ERK activation and augmented K-Ras ( G12V ) transformation activity
Jenei et al., Exp Cell Res 2005
:
In the present study, we found that overexpression of e3B1 in NIH3T3/EGFR cells sensitized EGF induced activation of Rac1, whereas it had no impact on
EGF induced activation of
p21Ras
Amos et al., Cell Death Differ 2006
(Glioblastoma) :
FTA also significantly reduced the amount of
EGF induced
Ras-GTP as reflected by a decrease in the level of Ras bound to Raf-RBD-GST
Qiu et al., Neuron 1991
:
NGF and
EGF rapidly
activate p21ras in PC12 cells by distinct, convergent pathways involving tyrosine phosphorylation ... Activation of
p21ras , demonstrated directly as an increase in p21ras associated GTP, was
induced rapidly but transiently by both nerve growth factor (NGF) and
epidermal growth factor (EGF) in PC12 cells
Theodorescu et al., Cancer Res 1991
(Carcinoma, Transitional Cell...) :
Ha-ras induction of the invasive phenotype
results in up-regulation of
epidermal growth factor receptors and altered responsiveness to epidermal growth factor in human papillary transitional cell carcinoma cells
Eisenberg et al., Mol Cell Biol 2011
:
HA-GPI clustering enhanced the Golgi compartment ( GC ) accumulation and signaling of
epidermal growth factor (EGF) stimulated
N-Ras-GTP
Kost et al., J Cell Physiol 1990
:
Effect of
epidermal growth factor on the expression of protooncogenes c-myc and
c-Ha-ras in short-term primary hepatocyte culture ... We have characterized the
effect of the hepatomitogen
epidermal growth factor (EGF) on the expression of the cellular protooncogenes
c-Ha-ras and c-myc in short-term ( 48 hours ) primary hepatocyte culture
Pragnell et al., Proc R Soc Lond B Biol Sci 1985
(Cell Transformation, Neoplastic...) :
While enhanced expression of the normal
Ha-ras gene did
result in a decrease in
EGF receptors on these transfectants, in contrast, the transfectants with enhanced expression of the c-myc and v-myc oncogenes did not display any significant changes in available EGF receptors although the cells were tumorigenic when tested in the nude mouse
Lichtner et al., J Cell Physiol 1988
(Adenocarcinoma...) :
Pyrimido-pyrimidine modulation of
EGF growth
promoting activity and
p21ras expression in rat mammary adenocarcinoma cells
Kamata et al., Nature 1984
(Cell Transformation, Neoplastic) :
We report here the evidence that
epidermal growth factor enhances the guanine nucleotide binding activity of activated
c-Ha-ras or v-Ha-ras p21, and phosphorylation of v-Ha-ras p21, suggesting that some mitogenic growth factors may regulate those activities
van den Berghe et al., Mol Cell Biol 1994
:
However, despite the strong
activation of
Ras-GTP formation and MAP kinase by
EGF and thrombin, glucose uptake was not stimulated by these agonists, in contrast to the eightfold stimulation of 2-deoxy-D- [ 14C ] glucose uptake by insulin
Fujimoto et al., J Steroid Biochem Mol Biol 1995
(Adenocarcinoma...) :
In these cells,
epidermal growth factor (EGF)
increased c-Ha-ras expression as did estradiol
Langlois et al., J Biol Chem 1995
:
Negative feedback regulation and desensitization of insulin- and
epidermal growth factor stimulated
p21ras activation ... Insulin or
epidermal growth factor stimulation
induces a rapid increase in
p21ras levels, but after several minutes levels decline toward basal despite ongoing hormone stimulation
Luttrell et al., J Biol Chem 1995
:
The IGF1, LPA, and
EGF receptor mediated signals are all sensitive to inhibitors of tyrosine protein kinases,
require p21ras activation, and are independent of protein kinase C
van Corven et al., Proc Natl Acad Sci U S A 1993
:
LPA- and peptide induced p21ras activation is inhibited by the tyrosine kinase inhibitor genistein, at doses that do not affect
epidermal growth factor induced
p21ras activation
Medema et al., Mol Cell Biol 1994
:
Calcium inhibits
epidermal growth factor induced activation of
p21ras in human primary keratinocytes ... In this study, we measured the
effect of both
EGF and calcium treatment on activation of
p21ras and ERK2 ... We observed that calcium treatment inhibited
EGF induced
p21ras activation
Langlois et al., Endocrinology 1994
:
Both insulin and
epidermal growth factor (EGF) significantly
increased the activation of
p21Ras in Rat-1 fibroblasts transfected with human insulin receptors
Minden et al., Science 1994
:
Activation of JNK by
epidermal growth factor (EGF) or nerve growth factor (NGF) was
dependent on
H-Ras activation, whereas JNK activation by tumor necrosis factor alpha (TNF-alpha) was Ras independent
Pronk et al., Mol Cell Biol 1994
:
Involvement of Shc in insulin- and
epidermal growth factor induced activation of
p21ras ... We have studied the role of Shc in insulin- and
EGF induced activation of
p21ras in NIH 3T3 cells overexpressing human insulin receptors ( A14 cells ) ... From these results, we conclude that after insulin and EGF treatment, Shc associates with both Grb2 and mSOS and therefore may mediate, at least in part, insulin- and
EGF induced activation of
p21ras
Medema et al., Mol Cell Biol 1993
:
Activation of
p21ras by insulin and
EGF in intact cells was abolished in cells infected with a recombinant vaccinia virus expressing p21ras ( Asn-17 ) ... From these data, we conclude that the activation of a guanine nucleotide exchange factor is involved in insulin- and
EGF induced activation of
p21ras
Fujimoto et al., Ann Clin Biochem 1995
:
Epidermal growth factor (EGF) , an activator of TK, also
increased c-Ha-ras expression
Kato et al., Eur J Cancer 1998
(Endometrial Neoplasms) :
Furthermore,
EGF caused elevation of
Ras-GTP levels in Ishikawa, but not HHUA cells