◀ Back to MAPK8
MAP3K7 — MAPK8
Pathways - manually collected, often from reviews:
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OpenBEL Selventa BEL large corpus:
MAPK8
→
MAP3K7
(increases, MAP3K7 Activity, MAPK8 Activity)
Evidence: The IRAK4:IRAK1:TRAF6 complex then interacts at the membrane with another preformed complex consisting of TAK1, TAB1 and TAB2. This interaction induces phosphorylation of TAB2 and TAK1. TAK1 is subsuequently activated in the cytoplasm, leading to the activation of IKK. Activation leads to phosphorylation and degradation of IKB and consequent release of NFKB. Activation of TAK1 also results in the activation of MAP kinases and JNK.
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OpenBEL Selventa BEL large corpus:
MAPK8
→
MAP3K7
(increases, MAP3K7 Activity, MAPK8 Activity)
Evidence: In IRAK1-deficient mice, cytokine production in response to IL-1 and LPS was diminished but not abolished25-27, whereas IRAK4-deficient mice showed virtually no response to IL-1, LPS or other bacterial components, demonstrating that IRAK4 has an important role in IL-1R/TLR signalling28. Recently, patients with an inherited IRAK4 deficiency have been identified29. These patients failed to respond to IL-1, to IL-18 or to stimulation of each of five TLRs (TLR2, TLR3, TLR4, TLR5 and TLR9). Together,...
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KEGG NOD-like receptor signaling pathway:
Complex of MAP3K7-TAB1-TAB2-TAB3
→
MAPK10/MAPK8/MAPK9
(protein-protein, activation)
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KEGG Toxoplasmosis:
MAP3K7
→
MAPK10/MAPK8/MAPK9
(protein-protein, activation)
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WikiPathways EBV LMP1 signaling:
Complex of MAP3K7-TAB1-MAP3K3-TRAF6
→
MAPK8
(activation)
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WikiPathways NLR Proteins:
MAP3K7
→
MAPK8
(activation)
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WikiPathways DNA Damage Response (only ATM dependent):
Complex of MAP3K4-MAP3K7
→
MAPK8
(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:
MAP3K7
—
MAPK8
(physical association, affinity chromatography technology)
Sanna et al., Mol Cell Biol 2002*
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IRef Hprd Interaction:
Complex of 26 proteins
(in vivo)
Blanco et al., PloS one 2008
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IRef Hprd Interaction:
MAP3K7
—
MAPK8
(in vitro)
Sanna et al., Mol Cell Biol 2002*
-
IRef Hprd Interaction:
MAP3K7
—
MAPK8
(in vivo)
Sanna et al., Mol Cell Biol 2002*
-
IRef Hprd Interaction:
Complex of 37 proteins
(in vivo)
Blanco et al., PloS one 2008
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IRef Innatedb Interaction:
MAPK8
—
MAP3K7
(unknown, -)
Sanna et al., Mol Cell Biol 2002*
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IRef Intact Interaction:
Complex of MAP2K7-MAPK8-MAP3K7
(physical association, molecular sieving)
Blanco et al., Mol Cell Biol 2007*
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IRef Intact Interaction:
Complex of MAPK8-MAP2K7-TAB1-MAP3K7-MAPK8IP1
(association, molecular sieving)
Blanco et al., PloS one 2008
-
IRef Intact Interaction:
Complex of MAP3K7-MAPK8IP1-VRK2-MAPK8
(association, pull down)
Blanco et al., PloS one 2008
-
IRef Intact Interaction:
Complex of VRK2-MAPK8IP1-MAPK8-MAP2K7-TAB1-MAP3K7
(association, molecular sieving)
Blanco et al., PloS one 2008
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IRef Intact Interaction:
Complex of MAPK8-VRK2-MAP3K7-TAB1-MAPK8IP1-MAP2K7
(association, molecular sieving)
Blanco et al., PloS one 2008
-
IRef Ophid Interaction:
MAPK8
—
MAP3K7
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
Text-mined interactions from Literome
Goswami et al., Dev Biol 2001
(MAP Kinase Signaling System) :
Overexpression of
TAK1 led to a reduction in
MAPK activity in early gastrula ectoderm
McDermott et al., J Biol Chem 2002
:
In addition we found a
role for
TAK-1 in the activation of p38
MAPK by IL-1, with TAK-1 also associating with active Ras
Kettner-Buhrow et al., Biochem Biophys Res Commun 2006
(MAP Kinase Signaling System) :
dsiRNA against TAK1 or TAB1 significantly suppressed their target proteins as well as
TAK1 mediated activation of NFkappaB, p38
MAPK , and JNK, and of IL-8 transcription
Kim et al., American journal of physiology. Renal physiology 2007
:
TGF-beta activated kinase 1 and TAK1 binding protein 1 cooperate to
mediate TGF-beta1 induced MKK3-p38
MAPK activation and stimulation of type I collagen ... Transient overexpression of
TAK1 with TAB1
enhanced the activation of MKK3 and p38
MAPK with or without TGF-beta(1) stimulation, whereas a dominant negative mutant of TAK1 ( TAK1DN ) suppressed TGF-beta(1) induced activation of MKK3 and p38 MAPK
Windheim et al., Biochem J 2007
:
We also show that RIP2
induces the activation of the protein kinase
TAK1 ( transforming-growth-factor-beta activated kinase-1 ), that a dominant negative mutant of TAK1 inhibits RIP2 induced activation of JNK ( c-Jun N-terminal kinase ) and p38alpha
MAPK , and that signalling downstream of NOD2 or RIP2 is reduced by the TAK1 inhibitor ( 5Z ) -7-oxozeaenol or in TAK1-deficient cells
Adhikari et al., Oncogene 2007
:
Stimulation of cells with cytokines and microbial pathogens results in the activation of
TAK1 , which subsequently
activates the I-kappa B kinase complex (IKK) and
mitogen activated protein ( MAP ) kinases , culminating in the activation of NF-kappaB and AP-1, respectively
Kodym et al., RNA 2008
(MAP Kinase Signaling System) :
Activation of
TAK1-D leads to the downstream activation of the p38
MAPK and of SAPK/JNK but not the NFkappaB pathway
Kumar et al., J Immunol 2009
(Inflammation) :
In this study, we tested the hypothesis that
TAK1 ( TGF-beta activated kinase 1 ) is
involved in TWEAK induced activation of NF-kappaB and
MAPK and expression of proinflammatory protein
Mikkelsen et al., J Biol Chem 2009
:
We also observed that TRAF2 and
TAK1 were
essential for RIG-I mediated activation of p38
MAPK
Korchnak et al., Cell Signal 2009
:
Mixed lineage kinase 3 (MLK3) is a mitogen activated protein kinase kinase kinase (
MAP3K ) that
activates multiple mitogen activated protein kinase (
MAPK ) pathways in response to growth factors, stresses and the pro-inflammatory cytokine, tumor necrosis factor (TNF)
Cheng et al., J Biomed Mater Res A 2010
(Inflammation...) :
The critical
role for
TAK1 in
p38MAPK and NFkappaB activation was as well confirmed by the inhibition of p38MAPK and NFkappaB activity following 5Z-7-oxozeaenol, a selective inhibitor of TAK1
Qian et al., J Immunol 2011
(Parkinson Disease) :
Salmeterol significantly inhibited LPS induced production of microglial proinflammatory neurotoxic mediators, such as TNF-a, superoxide, and NO, as well as the inhibition of
TAK1 mediated phosphorylation of
MAPK and p65 NF-?B
Avila et al., Innate Immun 2012
:
Lyn kinase controls TLR4 dependent IKK and
MAPK activation
modulating the activity of
TRAF-6/TAK-1 protein complex in mast cells
Tran et al., J Biol Chem 2012
(MAP Kinase Signaling System) :
In agreement with this, overexpression of ASK1 or
TAK1 resulted in enhanced
p38MAPK activation, and their knockdown inhibited p38MAPK in C2C12 cells ... Overexpression of
TAK1 or ASK1 in Cdo ( -/- ) myoblasts and Cdo depleted C2C12 cells
restored p38MAPK activation as well as myotube formation
Yumoto et al., J Biol Chem 2013
(Cleft Palate) :
Our studies show that in neural crest derived craniofacial ecto-mesenchymal cells,
Tak1 is not only
required for TGF-ß- and bone morphogenetic protein induced p38
Mapk activation but also plays a role in agonist induced C-terminal and linker region phosphorylation of the receptor mediated R-Smads
Hirata et al., J Immunol 2013
:
TAK1 , a member of MAPK kinase kinase ( MAPKK-K ) family, can
activate JNK, p38
MAPK , and NF-?B signaling pathways