◀ Back to EGFR
EGFR — EREG
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
EGFR
→
Complex of EGFR-EREG
(directlyIncreases, EGFR/EREG Activity)
Evidence: Depsipeptide Depsipeptide was originally isolated from a strain of Chromobacterium violaceum. Initial studies with this bicyclic peptide demonstrated a selective decrease in c-myc expression. However, growth inhibition of the Ha-rastransformed NIH-3T3 clonal cell line Ras-1 was also observed in the absence of altered Ha-ras mRNA expression [67]. Depsipeptide appears to regulate the cell cycle at several points, including cell cycle arrest at G0/G1 and inhibition of signal transduction through mi...
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OpenBEL Selventa BEL large corpus:
Complex of EGFR-ERBB2
→
EREG
(directlyIncreases)
Evidence: the second group betacellulin (BTC), heparin-binding EGF (HB-EGF), and epiregulin (EPR), which exhibit dual specificity in that they bind ErbB1 and ErbB4.
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OpenBEL Selventa BEL large corpus:
Complex of EGFR-ERBB4
→
EREG
(directlyIncreases)
Evidence: the second group betacellulin (BTC), heparin-binding EGF (HB-EGF), and epiregulin (EPR), which exhibit dual specificity in that they bind ErbB1 and ErbB4.
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KEGG ErbB signaling pathway:
EREG
→
Complex of EGFR
(protein-protein, activation)
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KEGG ErbB signaling pathway:
EREG
→
EGFR
(protein-protein, activation)
-
NCI Pathway Database ErbB receptor signaling network:
EGFR (EGFR)
→
EGFR/ErbB2/epiregulin complex (EGFR-ERBB2-EREG)
(modification, collaborate)
Komurasaki et al., Oncogene 1997
Evidence: physical interaction
-
NCI Pathway Database ErbB receptor signaling network:
EGFR (EGFR)
→
epiregulin (EREG)
(modification, collaborate)
Komurasaki et al., Oncogene 1997
Evidence: physical interaction
-
NCI Pathway Database ErbB receptor signaling network:
EGFR/ErbB2/epiregulin complex (EGFR-ERBB2-EREG)
→
ErbB2 (ERBB2)
(modification, collaborate)
Komurasaki et al., Oncogene 1997
Evidence: physical interaction
-
NCI Pathway Database ErbB receptor signaling network:
EGFR/ErbB2/epiregulin complex (EGFR-ERBB2-EREG)
→
epiregulin (EREG)
(modification, collaborate)
Komurasaki et al., Oncogene 1997
Evidence: physical interaction
-
NCI Pathway Database ErbB receptor signaling network:
EGFR (EGFR)
→
EGFR/EGFR/epiregulin/epiregulin complex (EGFR-EREG)
(modification, collaborate)
Zhuang et al., American journal of physiology. Renal physiology 2007*, Komurasaki et al., Oncogene 1997
Evidence: assay, physical interaction
-
NCI Pathway Database ErbB receptor signaling network:
EGFR (EGFR)
→
epiregulin (EREG)
(modification, collaborate)
Zhuang et al., American journal of physiology. Renal physiology 2007*, Komurasaki et al., Oncogene 1997
Evidence: assay, physical interaction
-
NCI Pathway Database ErbB receptor signaling network:
EGFR/EGFR/epiregulin/epiregulin complex (EGFR-EREG)
→
epiregulin (EREG)
(modification, collaborate)
Zhuang et al., American journal of physiology. Renal physiology 2007*, Komurasaki et al., Oncogene 1997
Evidence: assay, physical interaction
-
NCI Pathway Database ErbB receptor signaling network:
EGFR/ErbB3/epiregulin complex (EGFR-ERBB3-EREG)
→
EGFR (EGFR)
(modification, collaborate)
Komurasaki et al., Oncogene 1997
Evidence: physical interaction
-
NCI Pathway Database ErbB receptor signaling network:
EGFR/ErbB3/epiregulin complex (EGFR-ERBB3-EREG)
→
ErbB3 (ERBB3)
(modification, collaborate)
Komurasaki et al., Oncogene 1997
Evidence: physical interaction
-
NCI Pathway Database ErbB receptor signaling network:
EGFR/ErbB3/epiregulin complex (EGFR-ERBB3-EREG)
→
epiregulin (EREG)
(modification, collaborate)
Komurasaki et al., Oncogene 1997
Evidence: physical interaction
-
NCI Pathway Database ErbB receptor signaling network:
EGFR (EGFR)
→
epiregulin (EREG)
(modification, collaborate)
Komurasaki et al., Oncogene 1997
Evidence: physical interaction
-
Reactome Reaction:
EGFR
→
EREG
(reaction)
Vijapurkar et al., Exp Cell Res 2003, Walton et al., J Biol Chem 1990, Li et al., Cell Signal 2007, Xu et al., Mol Cell Biol 2007, Hazan et al., Cell Growth Differ 1990, Kaushansky et al., Chem Biol 2008, Helin et al., J Biol Chem 1991, Margolis et al., J Biol Chem 1989, Ricci et al., Oncogene 1995, Wallasch et al., EMBO J 1995, Prigent et al., EMBO J 1994, Soler et al., Oncogene 1994, Segatto et al., Oncogene 1993, Cohen et al., J Biol Chem 1996, Pinkas-Kramarski et al., EMBO J 1996
-
Reactome Reaction:
EGFR
→
EREG
(indirect_complex)
Cohen et al., J Biol Chem 1996
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Yamanaka et al., Biochem Biophys Res Commun 2001
:
Among four EGF-receptor (EGFR) family members, the
EGFR was solely
activated by EGF, heparin binding EGF (HB-EGF), transforming growth factor alpha ( TGF alpha ),
epiregulin (ER) , and betacellulin (BTC), resulting in induction of phenotypic modulation of SMCs
Komurasaki et al., Growth Factors 2002
(MAP Kinase Signaling System) :
In vivo, increased production of
epiregulin was noted in extracts of the remnant liver obtained 24 h after partial hepatectomy, and
EGFR phosphorylation by these extracts was partially
inhibited by anti-epiregulin antibody
Kuntz et al., Growth Factors 2005
:
Finally, in the two cell lines expressing ErbB receptors, we demonstrated that only
EGFR/ErbB1 was
activated by
epiregulin
Charalambous et al., Carcinogenesis 2007
(Neoplasms) :
Epidermal growth factor receptor (EGFR) ligands ( transforming growth factor alpha ( TGFalpha ), heparin binding EGF-like growth factor and
epiregulin ) are constitutively
induced by LMP1, leading to
EGFR phosphorylation but also down-regulation, degradation or turn-over, with the appearance of cleaved EGFR fragments
Zhang et al., Cancer prevention research (Philadelphia, Pa.) 2008
(Carcinoma, Non-Small-Cell Lung...) :
Collectively, these findings show that
epiregulin expression correlated with advanced disease, was
EGFR dependent , and conferred invasive properties on NSCLC cells
White et al., Cardiovasc Res 2010
(Atherosclerosis) :
We have demonstrated two novel and important functions of CX3CL1 on primary human SMCs : anti-apoptosis and proliferation, both mediated via
epiregulin induced
EGFR signalling
Bade et al., J Cell Sci 2011
(Breast Neoplasms...) :
Here, we investigated whether the FGFR1 induced increase in AREG and
EREG expression might coordinately
increase EGFR signaling to promote mammary tumorigenesis ... Taken together, these data suggest that AREG and
EREG mediate tumorigenic phenotypes by activating EGFR signaling, and that the oncogenic potential of FGFR1
requires EGFR activation to promote mammary tumorigenesis
Modjtahedi et al., Int J Cancer 1998
:
Like EGF, we found that both the
epiregulin induced growth inhibition of HN5 and MDA-MB468 cells and tyrosine phosphorylation of the 170 kDa
EGFR on HN5 cells are reversed in the presence of anti-EGFR MAbs ICR62 and ICR80