◀ Back to EGFR
EGFR — HRAS
Pathways - manually collected, often from reviews:
-
KEGG Melanoma:
EGFR/FGFR1/IGF1R/MET/PDGFRA/PDGFRB
→
HRAS/KRAS/NRAS
(protein-protein, activation)
-
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:
EGFR
→
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 ERK Pathway in Huntington's Disease:
EGFR
→
HRAS
(activation)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
STRING interaction:
EGFR
—
HRAS
(interaction, mapped from kegg_pathways mint intact)
-
STRING interaction:
HRAS
—
EGFR
(interaction, mapped from kegg_pathways mint intact)
Text-mined interactions from Literome
He et al., Cancer J 2001
(Sarcoma, Experimental) :
Using four distinct, cell-permeable, and highly specific inhibitors, namely WR-PAK18, which blocks the PAK-PIX interaction ; AG 1478, which inhibits ErbB1 kinase activity ; and AG 825 or AG 879, which inhibits ErbB2 kinase activity, we demonstrate that ( 1 ) the PAK-PIX interaction is essential for v-Ha-RAS induced malignant transformation ; ( 2 )
v-Ha-RAS requires not only
ErbB1 but also ErbB2, which are activated through two independent autocrine pathways to induce both the PIX/Rac/CDC42 dependent PAK activation and malignant transformation in vitro ; and ( 3 ) a combination of AG 879 and the Src family kinase-specific inhibitor PP1 suppresses almost completely the growth of RAS induced sarcomas in nude mice
Casanova et al., Cancer Res 2002
(Cell Transformation, Neoplastic...) :
This study reports that activated
Ha-ras results in a dramatic induction of
EGFR in epidermal tumor cells and provides experimental evidence that EGFR signaling is responsible for Ha-ras dependent vascular endothelial growth factor ( VEGF ) induction, as well as for the repression of other angiogenic factors such as angiopoietin 1
Cengel et al., Neoplasia (New York, N.Y.) 2007
(Colorectal Neoplasms...) :
Taken together, these findings suggest that
EGFR activated
H-Ras signaling is initiated by oncogenic K-Ras to promote radiation survival in pancreatic and colorectal cancers
Zushi et al., American journal of cancer research 2011
:
These results indicate that either
HRAS mutation or
activation of
EGFR in cooperation with MYC overexpression play critical roles in transformation of HTKs on a background of inactivation of the pRB and p53 pathways and telomerase activation
Okimoto et al., Oncogene 1996
:
Regulation of
epidermal growth factor receptor by activated
H-ras and V-myc oncogenes in mouse Balb/3T3 cells : possible roles of AP-1