◀ Back to MAPK3
MAPK3 — STAT3
Pathways - manually collected, often from reviews:
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OpenBEL Selventa BEL large corpus:
STAT3
→
MAPK3
(increases, MAPK3 Activity, STAT3 Activity)
Evidence: We propose that the FGF-1-induced signaling pathway that leads to promatrilysin expression is ERK-dependent and leads to phosphorylation of Ser-727 on STAT3, phosphorylated STAT3, then binds and transactivates the matrilysin promoter
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OpenBEL Selventa BEL large corpus:
STAT3
→
MAPK3
(increases, STAT3 Activity)
Evidence: We propose that the FGF-1-induced signaling pathway that leads to promatrilysin expression is ERK-dependent and leads to phosphorylation of Ser-727 on STAT3, phosphorylated STAT3, then binds and transactivates the matrilysin promoter
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BioCarta stat3 signaling pathway:
STAT3/STAT3 complex (STAT3)
→
ERK1 (MAPK3)
(modification, collaborate)
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BioCarta stat3 signaling pathway:
ERK1 (MAPK3)
→
STAT3/STAT3 (Ser727) complex (STAT3)
(modification, activates)
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BioCarta bioactive peptide induced signaling pathway:
STATs (STAT3/STAT5A/STAT1/STAT5A/STAT5B/STAT5B)
→
ERK1 (MAPK3)
(modification, collaborate)
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BioCarta bioactive peptide induced signaling pathway:
ERK1 (MAPK3)
→
STATS/STATS complex (STAT3_STAT5A_STAT1_STAT5A_STAT5B_STAT5B)
(modification, activates)
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BioCarta erk1/erk2 mapk signaling pathway:
ERK1 (MAPK3)
→
STAT3
(modification, activates)
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NCI Pathway Database PDGFR-beta signaling pathway:
Erk1-2-active (MAPK3/MAPK1)
→
STAT3 (STAT3)
(modification, activates)
Bowman et al., Proc Natl Acad Sci U S A 2001, Chung et al., Mol Cell Biol 1997
Evidence: mutant phenotype, assay, physical interaction
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WikiPathways TCA Cycle Nutrient Utilization and Invasiveness of Ovarian Cancer:
MAPK3/MAPK1
→
STAT3
(activation)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
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IRef Hprd Interaction:
MAPK3
—
STAT3
(in vitro)
Jain et al., J Biol Chem 1999, Lim et al., J Biol Chem 1999*, Deb et al., EMBO J 2001, Dolled-Filhart et al., Clin Cancer Res 2003*, Wierenga et al., Exp Hematol 2003*, Lo et al., J Biol Chem 2003*, Chung et al., Mol Cell Biol 1997, Jain et al., Oncogene 1998*
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IRef Hprd Interaction:
MAPK3
—
STAT3
(in vivo)
Jain et al., J Biol Chem 1999, Lim et al., J Biol Chem 1999*, Deb et al., EMBO J 2001, Dolled-Filhart et al., Clin Cancer Res 2003*, Wierenga et al., Exp Hematol 2003*, Lo et al., J Biol Chem 2003*, Chung et al., Mol Cell Biol 1997, Jain et al., Oncogene 1998*
Text-mined interactions from Literome
Liang et al., J Biol Chem 1999
:
In addition, we show that Ang II-induced serine phosphorylation of
STAT3 in VSMCs is
mediated by
mitogen activated protein kinase and that dephosphorylation is mediated by protein phosphatase 2A (PP2A)
van Puijenbroek et al., Exp Cell Res 1999
(Carcinoma, Embryonal) :
Using a dominant negative p21ras construct and a specific inhibitor of mitogen activated protein kinase kinase ( MEK ; PD098059 ) we demonstrated that CNTF induced
Stat3 transactivation was
independent of the p21ras-mitogen activated protein kinase (
MAPK ) pathway, while CNTF induced MAPK activation was p21ras- and MEK dependent
Schuringa et al., Biochem J 2000
(Carcinoma, Hepatocellular...) :
In conclusion, these data indicate that IL-6 induced
STAT3 transactivation and Ser ( 727 ) phosphorylation is
independent of
ERK-1 or JNK-1 activity, but involves a gp130 receptor signalling cascade that includes Vav, Rac-1, MEKK and SEK-1/MKK-4 as signal transduction components
Wang et al., Oncogene 2000
:
PD180970 did not affect
MAPK activation by PDGF or the JAK dependent
activation of
Stat3 by interleukin-6
Tancredi et al., J Neurochem 2000
(Synaptic Transmission) :
The IL-6 induced inhibition of PTP and LTP was accompanied by a simulation of
STAT3 tyrosine phosphorylation and an
inhibition of
MAPK/ERK dual phosphorylation, in the absence of changes in the state of activation of SAPK/JNK
Boeuf et al., J Biol Chem 2001
:
We have shown that LIF induced phosphorylation of RSKs in ES cells is dependent on ERKs, whereas
STAT3 phosphorylation is not
mediated by any known
MAPK activities
Frost et al., Endocrinology 2002
:
The tyrosine kinase inhibitors, genistein, PP1, and AG-490, and the
MAPK kinase inhibitor, PD98059, did not
block Stat3 or Stat5 phosphorylation
Xu et al., Mol Cell Biol 2003
:
Interleukin-13 induction of 15-lipoxygenase gene expression requires p38
mitogen activated protein kinase mediated serine 727 phosphorylation of Stat1 and
Stat3
Makuta et al., Biol Pharm Bull 2003
:
These results first indicate that
Erk1/2 and STAT-3 regulate CCR5 expression, and that Erk mediated phosphorylation of Ser is
required for full stimulation of
STAT-3 in CCR5 expression
Lo et al., J Biol Chem 2003
:
Galpha16QL induced
STAT3 activation was
enhanced by overexpression of
extracellular signal regulated kinase 1 ( ERK1 ), but was inhibited by U0126, a Raf-1 inhibitor, and coexpression of the dominant negative mutants of Ras and Rac1
Ishikawa et al., Oncogene 2005
(Multiple Myeloma...) :
Furthermore, the FGF induced activation of
ERK 1/2 contributed to the serine phosphorylation of
STAT 3 , suggesting that the signaling crosstalk between the cytokine receptor, IL-6 receptor alpha/gp 130 and the growth factor receptor tyrosine kinase, FGFR 3
Sumimoto et al., J Exp Med 2006
(MAP Kinase Signaling System...) :
Furthermore, specific DNA binding and transcriptional activity of
STAT3 were not
affected by down-regulation of the
MAPK signaling with the BRAF RNAi
Horie et al., Microbiol Immunol 2007
(Burkitt Lymphoma) :
A specific inhibitor of p38
MAPK , SB203580,
blocked simultaneously
STAT3 DNA binding activity, and IL-10 mRNA expression, IL-10 production, and then the cell growth was inhibited
Izumi-Nagai et al., Am J Pathol 2007
(Choroidal Neovascularization...) :
CNV generation was accompanied by
STAT3 activation in choroidal endothelial cells and macrophages, and IL-6 receptor blockade
resulted in selectively inhibited phosphorylation of STAT3 but not
extracellular signal regulated kinase 1/2
Wang et al., Am J Physiol Endocrinol Metab 2007
(Myocardial Reperfusion Injury...) :
Interestingly, EC
STAT3 deficiency decreased myocardial STAT3 activation but
increased myocardial p38
MAPK activation in both sexes ; however, this was seen to a greater degree in females ... This observation was associated with decreased activation of myocardial
STAT3 and increased
activation of p38
MAPK in EC STAT3KO heart after I/R
Kreis et al., Mol Cancer Res 2007
(Carcinoma, Hepatocellular...) :
Using a specific JAK inhibitor, sustained STAT3 activation was completely abrogated in all tested melanoma lines, whereas inhibition of Src or
mitogen activated protein kinase/extracellular signal regulated kinase kinase 1/2
had no effect on constitutively tyrosine phosphorylated
STAT3 levels
Liu et al., Int J Mol Med 2008
(Nasopharyngeal Neoplasms) :
Demonstration of the involvement of different kinases in LMP1 induced STAT3 activation supports the
involvement of the JAK/STAT and
mitogen activated protein kinase ( MAPK ) /ERK signaling pathways in the regulation of
STAT3 activation by LMP1
Weng et al., Alcohol 2008
:
Inhibition of
p42/44MAPK also
increased STAT3 DNA binding activity
Shamsasenjan et al., Int J Hematol 2009
(Multiple Myeloma) :
Cucurbitacin I (
STAT3 inhibitor ), but not U0126 (
MAPK inhibitor ), could abolish the effect of IL-6
Souza et al., Toxicol Lett 2009
:
MAPK promotes
STAT3 phosphorylation that could induce a protective mechanism against Cd toxicity
Yu et al., Cell Biol Int 2009
(Adenocarcinoma...) :
Growth suppression due to SOCS3 was associated with attenuated
activation of
Erk1/2 , Akt as well as
STAT3
Schaljo et al., J Immunol 2009
(Inflammation) :
We found that IL-10 initiates a
Stat3 dependent increase of TTP expression accompanied by a delayed decrease of p38
MAPK activity
Akasaka et al., Biochim Biophys Acta 2010
:
JAK2 or p38
MAPK inhibitor
suppressed leptin induced lipid oxidation and decreased
STAT3 phosphorylation in both types of myotube, respectively
Bhattacharjee et al., J Biol Chem 2011
(MAP Kinase Signaling System) :
Further, we found that Src tyrosine kinase mediated activation of p38
MAPK is
required for Stat1 and
Stat3 serine 727 phosphorylation in alternatively activated monocytes/macrophages
Imataki et al., J Immunol 2012
:
IL-21 can supplement suboptimal Lck independent
MAPK activation in a
STAT-3 dependent manner in human CD8 ( + ) T cells
Pijet et al., Cytokine 2013
(MAP Kinase Signaling System) :
Detailed acute and chronic studies with the use of metabolic inhibitors revealed that both JAK/STAT3 and
MEK/MAPK but not PI3-K/AKT/GSK-3ß signaling pathways were activated by leptin, and that
STAT3 ( Y ( 705 ) P-STAT3 ) and MEK ( T ( 202/ ) Y ( 204 ) P-ERK1/2 )
mediate these effects
Tkach et al., Endocr Relat Cancer 2013
(Breast Neoplasms) :
p42/p44
MAPK mediated
Stat3Ser727 phosphorylation is required for progestin induced full activation of Stat3 and breast cancer growth
Andrés et al., Exp Dermatol 2013
(MAP Kinase Signaling System...) :
TNFa, 12-O-Tetradecanoylphorbol 13-acetate ( TPA ) and UVB irradiation induced Ser727 phosphorylation of
STAT3 in an ERK1/2- and p38
MAPK dependent manner, which resulted in a modulatory effect on STAT3 transcriptional activity
Jain et al., Oncogene 1998
:
Repression of
Stat3 activity by activation of
mitogen activated protein kinase ( MAPK )