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BCL2 — EGFR

Text-mined interactions from Literome

Jost et al., J Biol Chem 2001 : Epidermal growth factor receptor dependent control of keratinocyte survival and Bcl-xL expression through a MEK dependent pathway ... This protection is, at least in part, due to EGFR dependent expression of the antiapoptotic Bcl-2 family member, Bcl-x ( L )
Wang et al., Zhonghua Zhong Liu Za Zhi 2003 (Glioblastoma) : Bcl-2 and Bax, being nuclear matrix associated proteins, are probably involved in the EGFR-cDNA induced malignant conversion of glioblastoma cells by introducing EGFR cDNA into the tumor cells
Bernal et al., Gastroenterology 2006 : Epidermal growth factor receptor signaling regulates Bax and Bcl-w expression and apoptotic responses during intestinal adaptation in mice
Yan et al., Gastroenterology 2009 (Disease Models, Animal...) : Furthermore, H pylori induced EGFR phosphorylation stimulated phosphotidylinositol-3'-kinase dependent activation of the antiapoptotic factor Akt, increased expression of the antiapoptotic factor Bcl-2 , and decreased expression of the proapoptotic factor Bax
Lucas et al., Biol Reprod 2010 : E2 and G-1 decreased BAX and increased BCL2 expression and these effects were blocked by MAP2K1/2 inhibitor and EGFR kinase inhibitor
Zhao et al., J Lipid Res 2012 : Further studies showed that TNF-a decreased expression of the antiapoptotic proteins Bcl-2 and Bcl-xL , decreased I?Ba and PPAR?, and also inhibited PI3K dependent Akt and EGFR signaling
Rodeck et al., Proc Natl Acad Sci U S A 1997 : Regulation of Bcl-xL expression in human keratinocytes by cell-substratum adhesion and the epidermal growth factor receptor
Stoll et al., Oncogene 1998 : Furthermore, stimulation of EGFR signaling through two natural ligands, transforming growth factor (TGF)-alpha and epidermal growth factor (EGF), increased the expression of Bcl-XL in quiescent keratinocytes and HaCaT cells