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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