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EGFR — SERPINE1

Text-mined interactions from Literome

Kutz et al., Exp Cell Res 2006 : TGF-beta 1-induced PAI-1 expression is E box/USF dependent and requires EGFR signaling ... Maximal immediate-early PAI-1 induction upon exposure to TGF-beta1 required EGFR , p21ras, MEK and pp60(c-src) signaling as pharmacologic or dominant negative inhibition of any of the four intermediates ( EGFR, p21ras, MEK, pp60(c-src) ) virtually eliminated TGF-beta1 augmented PAI-1 levels
Du et al., Microbes Infect 2007 (Carcinoma, Squamous Cell...) : The cag PAI was not necessary for EGFR signal transactivation
Samarakoon et al., J Mol Cell Cardiol 2008 : TGF-beta1 induced PAI-1 expression in both primary cultures and in an established line ( R22 ) of vascular smooth muscle cells ( VSMC ) was completely blocked by inhibition of epidermal growth factor receptor (EGFR) activity or adenoviral delivery of a kinase-dead EGFR ( K721A ) construct
Freytag et al., J Invest Dermatol 2010 (MAP Kinase Signaling System) : Moreover, EGFR signaling blockade or EGFR knockdown attenuated TGF-beta1 induced PAI-1 expression, implicating EGFR transactivation in TGF-beta1 stimulated PAI-1 expression, and reduced colony dispersal in TGF-beta1+EGF treated cultures
Shih et al., Mol Cancer Res 2012 (MAP Kinase Signaling System) : Furthermore, PAI-1 upregulation in shDLC1 cells is EGFR-MEK pathway dependent and is able to promote in vitro angiogenesis