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EGF — SMAD2

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: SMAD2 → EGF (increases)
  Evidence: Significantly, phosphorylation of Ser240 was observed in vivo upon treatment of cells with epidermal growth factor (EGF) or platelet-derived growth factor (PDGF).

Text-mined interactions from Literome

Kretzschmar et al., Genes Dev 1999 (Cell Transformation, Neoplastic...) : EGF , which is weaker than oncogenic mutations at activating Ras, induces a less extensive phosphorylation and cytoplasmic retention of Smad2 and Smad3
Esguerra et al., Development 2007 : Stimulation of Alk4/EGF-CFC receptor complexes by Nodal activates Smad2/3 , leading to left sided expression of target genes that promote asymmetric placement of certain internal organs
Yang et al., Am J Physiol Lung Cell Mol Physiol 2008 (MAP Kinase Signaling System) : We show that EGF does not prevent the TGF-beta induced nuclear accumulation of Smad2/3 ; rather, EGF stabilizes the short lived Smad transcriptional corepressor TG-interacting factor (TGIF) via EGFR/Mek/Erk mediated phosphorylation of TGIF
Diamond et al., J Cell Sci 2008 (Carcinoma, Squamous Cell...) : Mechanistically, EGF enhanced Smad phosphorylation in the linker region, and attenuated TGFbeta1 mediated phosphorylation of Smad at the C-terminus, localization of Smad to the nucleus as well as Smad-driven promoter activity exclusively in oral keratinocytes but not in OSCC cells ... The effect of EGF on TGFbeta1 mediated Smad-driven promoter activity and N-cadherin expression was reversed when activation of ERK1/2 was blocked
Yeo et al., Biol Reprod 2009 : Inhibition of SMAD2/3 signaling in the presence of FSH/EGF significantly reduced fetal survival but had no effect on implantation or fetal and placental dimensions and morphology
Iwayama et al., Nephron extra 2011 : Inhibition of p38MAPK but not of ERK abolished the protective effect of EGF on CyA induced nuclear translocation of p-Smad2/3 and apoptosis
de Caestecker et al., Genes Dev 1998 : We demonstrate here that HGF and EGF , which signal through RTKs, can also mediate SMAD dependent reporter gene activation and induce rapid phosphorylation of endogenous SMAD proteins by kinase ( s ) downstream of MEK1