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EGFR — HRG

Text-mined interactions from Literome

Noguchi et al., Gastroenterology 1999 : HRG-alpha activated tyrosine phosphorylation of epidermal growth factor receptor (EGFR), erbB2, and erbB3 and induced not only erbB3/erbB2 but also erbB3/EGFR and erbB2/EGFR heterodimer formation in MKN-28 cancer cells
Campiglio et al., J Cell Biochem 1999 (Ovarian Neoplasms) : These findings reveal a distinct pattern of HRG induced EGFR family interaction in ovarian cancer that is distinct from that described in human breast cancer
Stoica et al., Oncogene 2003 : Experiments employing selective ErbB inhibitors demonstrate that the effect of HRG-beta1 on ER-alpha expression and activity is also mediated by ErbB2 and not by EGFR , demonstrating that ErbB2 is the primary mediator of the effects of HRG-beta1 on ER-alpha regulation
Birtwistle et al., Molecular systems biology 2007 : To help understand ErbB signaling quantitatively, in this work we combine traditional experiments with computational modeling, building a model that describes how stimulation of all four ErbB receptors with epidermal growth factor (EGF) and heregulin (HRG) leads to activation of two critical downstream proteins, extracellular-signal regulated kinase ( ERK ) and Akt
Kumar et al., Mol Pharmacol 2008 : We show that integrating measurements of signals across three key kinase pathways involved in regulating migration of human mammary epithelial cells, downstream of ErbB system receptor activation by epidermal growth factor (EGF) or heregulin (HRG) , significantly improves prediction of cell migration changes resulting from treatment with the small-molecule inhibitors 2- ( 4-morpholinyl ) -8-phenyl-4H-1-benzopyran-4-one ( LY294002 ) and 2'-amino-3'-methoxyflavone ( PD98059 ) for both normal and HER2 overexpressing cells
Nakakuki et al., Cell 2010 : Activation of ErbB receptors by epidermal growth factor (EGF) or heregulin (HRG) determines distinct cell-fate decisions, although signals propagate through shared pathways
Huang et al., Biochem J 1998 : HRG also triggers association of epidermal-growth-factor receptors (EGFR) with a kinase-inactive ErbB2 subset while reducing EGFR association with active ErbB2