Gene interactions and pathways from curated databases and text-mining

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MAPK1 — SMAD2

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Wrana et al., Science's STKE : signal transduction knowledge environment 2000 : In the cytosol, Smad translocation might be inhibited by mitogen activated protein kinase dependent phosphorylation, whereas in the nucleus Smads interact with a number of transcription factors that themselves are primary targets of other signaling pathways
Yang et al., Am J Pathol 2003 (Fibrosis) : Inhibition of Erk-1/2 activation by Mek kinase inhibitor PD98059 restored TGF-beta1 mediated Smad-2/3 nuclear accumulation and myofibroblast activation
Lee et al., Int J Oncol 2004 (Stomach Neoplasms) : Smad2 mediates Erk1/2 activation by TGF-beta1 in suspended, but not in adherent, gastric carcinoma cells ... In this study, we examined effects of cell adhesion status on the TGF-beta1 mediated Erk1/2 regulation, and roles of Smad proteins on the cell adhesion mediated effects, using a gastric carcinoma cell variant
Rhyu et al., J Am Soc Nephrol 2005 (Fibrosis...) : Chemical inhibition of ERK but not p38 MAPK inhibited TGF-beta1 induced Smad 2 phosphorylation, and both MAPK inhibitors inhibited TGF-beta1- and H ( 2 ) O ( 2 ) -induced EMT
Galliher et al., Cancer Res 2007 (MAP Kinase Signaling System...) : Interestingly, although the expression of Y284F-TbetaR-II mutants in breast cancer cells had no effect on TGF-beta stimulation of Smad2/3 , this TbetaR-II mutant completely abrogated p38 MAPK activation by TGF-beta
Zhao et al., Mol Cell Biochem 2008 (Fibrosis...) : Additionally, the inhibition of MAPK signaling had no effect on Smad activation elicited by chymase
Zhang et al., Exp Dermatol 2009 (Fibrosis) : Activation of Smad2 required p38 MAPK but not p42/p44 MAPK or the epidermal growth factor receptor
Schievenbusch et al., Biochem Biophys Res Commun 2009 (Fibrosis) : As previously shown, Erk1/2 phosphorylation results in Smad-linker phosphorylation, thereby antagonizing cellular signals induced by TGFbeta
Zhu et al., Prostate 2010 (MAP Kinase Signaling System) : These findings suggest a dual role for PHB as a downstream determinant of the cellular response to TGF-beta via Smad dependent pathway ( apoptosis ) and MAPK intracellular signaling ( survival )
Rodrigues Díez et al., PloS one 2010 (Fibrosis) : In cultured rat VSMCs, direct AngII/Smad pathway activation was mediated by p38 MAPK and ROCK activation
Ungefroren et al., Int J Oncol 2011 (Carcinoma, Pancreatic Ductal...) : Biochemically, dnSrc inhibition failed to block TGF-ß1/ALK5 induced activation of Smad2 and Smad3, but partially inhibited transcriptional activation of TGF-ß/Smad-responsive reporter genes, and effectively blocked basal and TGF-ß1 induced activation of p38 MAPK
Mottershead et al., Mol Hum Reprod 2012 : The GDF9/BMP15 synergistic signalling response was inhibited by the SMAD2/3 phosphorylation inhibitor SB431542, as well as inhibition of the mitogen activated protein kinase or rous sarcoma oncogene (SRC) signalling pathways, but not the nuclear factor kappa B pathway
Liu et al., J Agric Food Chem 2012 (Carcinoma, Non-Small-Cell Lung...) : EGCG decreased the phosphorylation of Smad2 and Erk1/2 , inhibited the nuclear translocation of Smad2 , and repressed the expression of transcription factors ZEB1, Snail, Slug, and Twist, and up-regulated the expression of E-cadherin