◀ Back to MAPK14
MAPK14 — MEF2C
Pathways - manually collected, often from reviews:
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OpenBEL Selventa BEL large corpus:
MEF2C
→
MAPK14
(directlyIncreases, MAPK14 Activity, MEF2C Activity)
Zhao et al., Mol Cell Biol 1999
Evidence: We showed previously that the transactivation activity of MEF2C is stimulated by p38 mitogen-activated protein (MAP) kinase. In this study, we examined the potential role of the p38 MAP kinase pathway in regulating the other MEF2 family members. We found that MEF2A, but not MEF2B or MEF2D, is a substrate for p38. Among the four p38 group members, p38 is the most potent kinase for MEF2A. Threonines 312 and 319 within the transcription activation domain of MEF2A are the regulatory sites phosphoryl...
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OpenBEL Selventa BEL large corpus:
MEF2C
→
MAPK14
(directlyIncreases, MAPK14 Activity, MEF2C Activity)
Zhao et al., Mol Cell Biol 1999
Evidence: We showed previously that the transactivation activity of MEF2C is stimulated by p38 mitogen-activated protein (MAP) kinase.
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BioCarta p38 mapk signaling pathway:
p38 (MAPK14)
→
MEF2 (MEF2C/MEF2B/MEF2D/MEF2A)
(modification, activates)
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BioCarta control of skeletal myogenesis by hdac and calcium/calmodulin-dependent kinase (camk):
p38 (MAPK14)
→
MEF2/MYOD complex (MYOD1-MEF2C_MEF2B_MEF2D_MEF2A)
(modification, activates)
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KEGG MAPK signaling pathway:
MAPK11/MAPK12/MAPK13/MAPK14
→
MEF2C
(protein-protein, phosphorylation)
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NCI Pathway Database Signaling mediated by p38-alpha and p38-beta:
p38alpha-beta-active (MAPK14/MAPK11)
→
MEF2C (MEF2C)
(modification, activates)
Han et al., Nature 1997, Zhao et al., Mol Cell Biol 1999
Evidence: mutant phenotype, assay
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Reactome Reaction:
MEF2C
→
MAPK14
(reaction)
Yang et al., Mol Cell Biol 1999, Wu et al., Mol Cell Biol 2000, Han et al., Nature 1997, Zhao et al., Mol Cell Biol 1999, Zetser et al., J Biol Chem 1999
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Reactome Reaction:
MEF2C
→
MAPK14
(direct_complex)
Yang et al., Mol Cell Biol 1999, Wu et al., Mol Cell Biol 2000, Han et al., Nature 1997, Zhao et al., Mol Cell Biol 1999, Zetser et al., J Biol Chem 1999
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WikiPathways Energy Metabolism:
MAPK14
→
MEF2D/MEF2A/MEF2B/MEF2C
(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 Biogrid Interaction:
MEF2C
—
MAPK14
(direct interaction, two hybrid)
Bandyopadhyay et al., Nat Methods 2010
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IRef Hprd Interaction:
MAPK14
—
MEF2C
(in vitro)
Yang et al., Mol Cell Biol 1999, Wu et al., Mol Cell Biol 2000, Han et al., Nature 1997, Yang et al., Nucleic Acids Res 1998*
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IRef Hprd Interaction:
MAPK14
—
MEF2C
(in vivo)
Yang et al., Mol Cell Biol 1999, Wu et al., Mol Cell Biol 2000, Han et al., Nature 1997, Yang et al., Nucleic Acids Res 1998*
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IRef Intact Interaction:
MAPK14
—
MEF2C
(physical association, two hybrid pooling approach)
Bandyopadhyay et al., Nat Methods 2010
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IRef Ophid Interaction:
MAPK14
—
MEF2C
(aggregation, confirmational text mining)
Yang et al., Nucleic Acids Res 1998*
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IRef Ophid Interaction:
MAPK14
—
MEF2C
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
Text-mined interactions from Literome
Ding et al., Stem Cells Dev 2008
:
Nuclear location of
MEF2C , which played a critical role in cardiomyocyte differentiation and could be
activated by
p38MAPK , was stimulated after icariin exposure
Andrews et al., Eur J Immunol 2012
:
The transcription factor
myocyte enhancer factor-2C (MEF2C) is
regulated by both calcineurin and
mitogen activated protein kinase signaling pathways, and is essential for proliferation and survival downstream of BCR engagement in mature B cells