◀ Back to MAPK1
MAPK1 — SMAD1
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
SMAD1
→
MAPK1
(decreases, MAPK1 Translocation, SMAD1 Activity)
Evidence: Erk phosphorylates serine residues in the linker regions of Smad1 (Kretzschmar et al., 1997), Smad2 and Smad3 (Kretzschmar et al., 1999), and substitution of these serines by negatively charged residues inhibits nuclear translocation of Smads and thus signalling.
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OpenBEL Selventa BEL large corpus:
SMAD1
→
MAPK1
(directlyIncreases, MAPK1 Activity, SMAD1 Activity)
Qiu et al., EMBO J 2007*
Evidence: We found that BMPs/Smad1 signaling inhibits the growth of androgen-sensitive prostate cancer cells.
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KEGG TGF-beta signaling pathway:
MAPK1/MAPK3
→
Complex of SMAD1-SMAD4-SMAD5-SMAD9
(protein-protein, inhibition)
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NCI Pathway Database ErbB1 downstream signaling:
Erk1-2-active (MAPK3/MAPK1)
→
SMAD1 (SMAD1)
(modification, activates)
Kretzschmar et al., Nature 1997*
Evidence: assay
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NCI Pathway Database BMP receptor signaling:
ERK2 (MAPK1)
→
SMAD1 (SMAD1)
(modification, activates)
Sapkota et al., Mol Cell 2007
Evidence: assay
-
WikiPathways ESC Pluripotency Pathways:
Complex of SMAD5-SMAD1-SMAD9-SMAD4
→
MAPK7/MAPK1/MAPK6/MAPK4/MAPK12
(inhibition)
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
Lee et al., Int J Oncol 2004
(Stomach Neoplasms) :
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
Kano et al., Endocrinology 2005
:
BMPs
induced both
Smad1/5/8 phosphorylation and Tlx2-Luc activation, whereas activin stimulated 3TP-Luc activity and p38
MAPK phosphorylation
Zhao et al., Mol Cell Biochem 2008
(Fibrosis...) :
Additionally, the inhibition of
MAPK signaling
had no effect on
Smad activation elicited by chymase
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 )
Zhou et al., Dev Cell 2010
:
BMP2 induction of
Smad1/5/8 phosphorylation and Runx2 expression, but not noncanonical p38
MAPK activation , was reduced in chondrocytes from neogenin mutant mice
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