Gene interactions and pathways from curated databases and text-mining

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EGFR — EREG

Pathways - manually collected, often from reviews:

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