Entity
--
e1
cso30:c:EntityBiologicalCompartment
cso30:i:CC_PlasmaMembrane
--
--
--
csml-variable:Double
m1
0
infinite
0
--
DUSP10
--
e10
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m10
0
infinite
0
--
p38
--
e11
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m11
0
infinite
0
--
DUSP10:p38
--
e12
cso30:c:Complex
cso30:i:CC_Cytoplasm
--
--
csml-variable:Double
m12
0
infinite
0
--
JNK
--
e13
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m13
0
infinite
0
--
DUSP10:JNK
--
e14
cso30:c:Complex
cso30:i:CC_Cytoplasm
--
--
csml-variable:Double
m14
0
infinite
0
--
IL-2
--
e15
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m15
0
infinite
0
--
DUSP5
--
e16
cso30:c:mRNA
cso30:i:CC_Nucleoplasm
--
csml-variable:Double
m16
0
infinite
0
--
IL-7
--
e17
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m17
0
infinite
0
--
csml-variable:Double
m18
0
infinite
0
--
DUSP6
--
e19
cso30:c:mRNA
cso30:i:CC_Nucleoplasm
--
csml-variable:Double
m19
0
infinite
0
--
--
e2
cso30:c:EntityBiologicalCompartment
cso30:i:CC_PlasmaMembrane_ExternalSideOfPlasmaMembrane_
--
--
--
csml-variable:Double
m2
0
infinite
0
--
LPS:TLR4
--
e20
cso30:c:Complex
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m20
0
infinite
0
--
DUSP1
--
e21
cso30:c:mRNA
cso30:i:CC_Nucleoplasm
--
csml-variable:Double
m21
0
infinite
0
--
DUSP2
--
e22
cso30:c:mRNA
cso30:i:CC_Nucleoplasm
--
csml-variable:Double
m22
0
infinite
0
--
DUSP16
--
e23
cso30:c:mRNA
cso30:i:CC_Nucleoplasm
--
csml-variable:Double
m23
0
infinite
0
--
TLR ligands
--
e24
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m24
0
infinite
0
--
Ligand:M-CSF
--
e25
cso30:c:Complex
cso30:i:CC_Cytoplasm
--
--
csml-variable:Double
m25
0
infinite
0
--
DUSP1
--
e26
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m26
0
infinite
0
--
U0126
--
e27
cso30:c:SmallMolecule
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m27
0
infinite
0
--
STAT1{p}
--
e28
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m28
0
infinite
0
--
STAT1
--
e29
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m29
0
infinite
0
--
--
e3
cso30:c:EntityBiologicalCompartment
cso30:i:CC_PlasmaMembrane_IntegralToPlasmaMembrane_
--
--
--
csml-variable:Double
m3
0
infinite
0
--
LPS
--
e30
cso30:c:Protein
cso30:i:CC_Extracellular
--
--
csml-variable:Double
m30
0
infinite
0
--
TLR4
--
e31
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
--
csml-variable:Double
m31
0
infinite
0
--
PKC
--
e32
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m32
0
infinite
0
--
LPS:TLR:MyD88
--
e33
cso30:c:Complex
cso30:i:CC_Cytoplasm
--
--
csml-variable:Double
m33
0
infinite
0
--
TLR:PloyI:C:TRIF
--
e34
cso30:c:Complex
cso30:i:CC_Cytoplasm
--
--
csml-variable:Double
m34
0
infinite
0
--
JNK{active}
--
e35
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
--
csml-variable:Double
m35
0
infinite
0
--
Gluccorticoids
--
e36
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
--
csml-variable:Double
m36
0
infinite
0
--
IL-10
--
e37
cso30:c:Protein
cso30:i:CC_Extracellular
--
csml-variable:Double
m37
0
infinite
0
--
TLR:Ligand
--
e38
cso30:c:Complex
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m38
0
infinite
0
--
dexamethasone
--
e39
cso30:c:SmallMolecule
cso30:i:CC_Cytoplasm
--
--
csml-variable:Double
m39
0
infinite
0
--
--
e4
cso30:c:EntityBiologicalCompartment
cso30:i:CC_PlasmaMembrane_InternalSideOfPlasmaMembrane_
--
--
--
csml-variable:Double
m4
0
infinite
0
--
Ligand:CB2
--
e40
cso30:c:Complex
cso30:i:CC_Cytoplasm
--
--
csml-variable:Double
m40
0
infinite
0
--
MAPK
--
e41
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m41
0
infinite
0
--
MAPK{active}
--
e42
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m42
0
infinite
0
--
MAPK{p}
--
e43
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
--
csml-variable:Double
m43
0
infinite
0
--
TNF-alpha
--
e44
cso30:c:mRNA
cso30:i:CC_Nucleoplasm
--
--
csml-variable:Double
m44
0
infinite
0
--
csml-variable:Double
m45
0
infinite
0
--
IL-6
--
e46
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
--
csml-variable:Double
m46
0
infinite
0
--
IL-6
--
e47
cso30:c:mRNA
cso30:i:CC_Nucleolus
--
--
csml-variable:Double
m47
0
infinite
0
--
DUSP2
--
e48
cso30:c:Protein
cso30:i:CC_Nucleolus
--
csml-variable:Double
m48
0
infinite
0
--
p38{p}
--
e49
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m49
0
infinite
0
--
DUSP6
--
e5
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
--
csml-variable:Double
m5
0
infinite
0
--
--
e50
cso30:c:EntityBiologicalCompartment
cso30:i:CC_NuclearEnvelopeLumen
--
--
--
csml-variable:Double
m50
0
infinite
0
--
--
e51
cso30:c:EntityBiologicalCompartment
cso30:i:CC_NuclearPore
--
--
--
csml-variable:Double
m51
0
infinite
0
--
--
e52
cso30:c:EntityBiologicalCompartment
cso30:i:CC_NuclearInnerMembrane
--
--
--
csml-variable:Double
m52
0
infinite
0
--
--
e53
cso30:c:EntityBiologicalCompartment
cso30:i:CC_NuclearLumen
--
--
--
csml-variable:Double
m53
0
infinite
0
--
--
e54
cso30:c:EntityBiologicalCompartment
cso30:i:CC_NuclearOuterMembrane
--
--
--
csml-variable:Double
m54
0
infinite
0
--
--
e55
cso30:c:EntityBiologicalCompartment
cso30:i:CC_Nucleus
--
--
--
csml-variable:Double
m55
0
infinite
0
--
--
e56
cso30:c:EntityBiologicalCompartment
cso30:i:CC_Nucleoplasm
--
--
--
csml-variable:Double
m56
0
infinite
0
--
--
e57
cso30:c:EntityBiologicalCompartment
cso30:i:CC_NuclearBody
--
--
--
csml-variable:Double
m57
0
infinite
0
--
--
e58
cso30:c:EntityBiologicalCompartment
cso30:i:CC_Nucleolus
--
--
--
csml-variable:Double
m58
0
infinite
0
--
--
e59
cso30:c:EntityBiologicalCompartment
cso30:i:CC_NuclearEnvelope
--
--
--
csml-variable:Double
m59
0
infinite
0
--
ERK2
--
e6
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
--
csml-variable:Double
m6
0
infinite
0
--
--
e60
cso30:c:EntityBiologicalCompartment
cso30:i:CC_Chromatin
--
--
--
csml-variable:Double
m60
0
infinite
0
--
--
e61
cso30:c:EntityBiologicalCompartment
cso30:i:CC_NuclearChromosome
--
--
--
csml-variable:Double
m61
0
infinite
0
--
--
e62
cso30:c:EntityBiologicalCompartment
cso30:i:CC_NuclearCentromere
--
--
--
csml-variable:Double
m62
0
infinite
0
--
ERK
--
e63
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m63
0
infinite
0
--
ERK{p}
--
e64
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m64
0
infinite
0
--
ERK{active}
--
e65
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m65
0
infinite
0
--
Fcepsilon RI
--
e66
cso30:c:Complex
cso30:i:CC_Cytoplasm
--
--
csml-variable:Double
m66
0
infinite
0
--
DUSP2
--
e67
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m67
0
infinite
0
--
DUSP2:ERK
--
e68
cso30:c:Complex
cso30:i:CC_Cytoplasm
--
--
csml-variable:Double
m68
0
infinite
0
--
DUSP2:JNK
--
e69
cso30:c:Complex
cso30:i:CC_Cytoplasm
--
--
csml-variable:Double
m69
0
infinite
0
--
DUSP6:ERK2
--
e7
cso30:c:Complex
cso30:i:CC_Cytoplasm
--
--
csml-variable:Double
m7
0
infinite
0
--
DUSP2:p38
--
e70
cso30:c:Complex
cso30:i:CC_Cytoplasm
--
--
csml-variable:Double
m70
0
infinite
0
--
IL-10
--
e71
cso30:c:mRNA
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m71
0
infinite
0
--
p38{active}
--
e72
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m72
0
infinite
0
--
TLR5
--
e73
cso30:c:Complex
cso30:i:CC_PlasmaMembrane_IntegralToPlasmaMembrane_
--
--
csml-variable:Double
m73
0
infinite
0
--
TLR9
--
e74
cso30:c:Complex
cso30:i:CC_PlasmaMembrane_IntegralToPlasmaMembrane_
--
csml-variable:Double
m74
0
infinite
0
--
TLR2:Ligand
--
e75
cso30:c:Complex
cso30:i:CC_PlasmaMembrane_IntegralToPlasmaMembrane_
--
--
csml-variable:Double
m75
0
infinite
0
--
TLR9
--
e76
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
--
csml-variable:Double
m76
0
infinite
0
--
csml-variable:Double
m77
0
infinite
0
--
JNK{p}
--
e78
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m78
0
infinite
0
--
csml-variable:Double
m79
0
infinite
0
--
--
e8
cso30:c:EntityBiologicalCompartment
cso30:i:CC_Cell_WithoutCellWall_
--
--
--
csml-variable:Double
m8
0
infinite
0
--
MAP3K
--
e80
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
--
csml-variable:Double
m80
0
infinite
0
--
MAP3K{active}
--
e81
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m81
0
infinite
0
--
TCR
--
e82
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
--
csml-variable:Double
m82
0
infinite
0
--
Ligand
--
e83
cso30:c:Protein
cso30:i:CC_Cytoplasm
--
--
csml-variable:Double
m83
0
infinite
0
--
Ligand:TCR
--
e84
cso30:c:Complex
cso30:i:CC_Cytoplasm
--
csml-variable:Double
m84
0
infinite
0
--
DUSP10
--
e85
cso30:c:mRNA
cso30:i:CC_Nucleoplasm
--
--
csml-variable:Double
m85
0
infinite
0
--
--
e9
cso30:c:EntityBiologicalCompartment
cso30:i:CC_Cytoplasm
--
--
--
csml-variable:Double
m9
0
infinite
0
--
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c1 : 1
stoichiometry:c2 : 1
stoichiometry:c3 : 1
m6*m5*0.1
nodelay
--
0
PMID:17114416,9596579 As shown for DUSP6, binding to the substrate ERK2 MAPK then strongly increases the catalytic activity
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c22 : 1
stoichiometry:c38 : 1
stoichiometry:c48 : 1
stoichiometry:c23 : 1
m20*m32*0.1
nodelay
--
0
PMID: 17114416,16184516,12193690 Mining of transcriptome datasets from primary mouse macrophages stimulated with LPS or the RAW 264.7 macrophage cell line after activation with a set of TLR ligands, our laboratory identified DUSP1, DUSP2, and DUSP16 as the most strongly induced MKP; thus, there is substantial overlap between these studies in the human and mouse system PMID: 17114416,12444149 However, the role of ERK signaling in DUSP1 mRNA expression is not entirely clear, because the MEK-1 inhibitor U0126 was reported to block LPS-induced increases of DUSP1 at the mRNA and protein level PMID: 17114416,10604989,10452980 Celada and colleagues then showed that DUSP1 is induced by signaling through the M-CSF receptor as well as in response to LPS, and additionally demonstrated the involvement of PKC in this process.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c24 : 1
stoichiometry:c25 : 1
m20*0.1
nodelay
--
0
PMID: 17114416,16184516,12193690 Mining of transcriptome datasets from primary mouse macrophages stimulated with LPS or the RAW 264.7 macrophage cell line after activation with a set of TLR ligands, our laboratory identified DUSP1, DUSP2, and DUSP16 as the most strongly induced MKP; thus, there is substantial overlap between these studies in the human and mouse system
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c26 : 1
stoichiometry:c27 : 1
m20*0.1
nodelay
--
0
PMID: 17114416,16184516,12193690 Mining of transcriptome datasets from primary mouse macrophages stimulated with LPS or the RAW 264.7 macrophage cell line after activation with a set of TLR ligands, our laboratory identified DUSP1, DUSP2, and DUSP16 as the most strongly induced MKP; thus, there is substantial overlap between these studies in the human and mouse system
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c28 : 1
stoichiometry:c29 : 1
m24*0.1
nodelay
--
0
PMID: 17114416,16184516,12193690 Mining of transcriptome datasets from primary mouse macrophages stimulated with LPS or the RAW 264.7 macrophage cell line after activation with a set of TLR ligands, our laboratory identified DUSP1, DUSP2, and DUSP16 as the most strongly induced MKP; thus, there is substantial overlap between these studies in the human and mouse system
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c30 : 1
stoichiometry:c31 : 1
m24*0.1
nodelay
--
0
PMID: 17114416,16184516,12193690 Mining of transcriptome datasets from primary mouse macrophages stimulated with LPS or the RAW 264.7 macrophage cell line after activation with a set of TLR ligands, our laboratory identified DUSP1, DUSP2, and DUSP16 as the most strongly induced MKP; thus, there is substantial overlap between these studies in the human and mouse system
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c32 : 1
stoichiometry:c33 : 1
m24*0.1
nodelay
--
0
PMID: 17114416,16184516,12193690 Mining of transcriptome datasets from primary mouse macrophages stimulated with LPS or the RAW 264.7 macrophage cell line after activation with a set of TLR ligands, our laboratory identified DUSP1, DUSP2, and DUSP16 as the most strongly induced MKP; thus, there is substantial overlap between these studies in the human and mouse system
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c34 : 1
stoichiometry:c49 : 1
stoichiometry:c35 : 1
m25*m32*0.1
nodelay
--
0
PMID: 17114416,10604989,10452980 Celada and colleagues then showed that DUSP1 is induced by signaling through the M-CSF receptor as well as in response to LPS, and additionally demonstrated the involvement of PKC in this process.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c36 : 1
stoichiometry:c37 : 1
m21*0.1
nodelay
--
0
PMID: 17114416,12444149 However, the role of ERK signaling in DUSP1 mRNA expression is not entirely clear, because the MEK-1 inhibitor U0126 was reported to block LPS-induced increases of DUSP1 at the mRNA and protein level PMID: 17114416,10604989,10452980 Celada and colleagues then showed that DUSP1 is induced by signaling through the M-CSF receptor as well as in response to LPS, and additionally demonstrated the involvement of PKC in this process. PMID: 17114416,16184516,12356755,15590669,11742987 Consistent with a negative regulatory function for DUSP1 in macrophage activation, anti-inflammatory glucocorticoids increase DUSP1 expression in macrophages, and mast cells at the mRNA and protein level
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c39 : 1
stoichiometry:c41 : 1
stoichiometry:c40 : 1
m29*m11*0.1
nodelay
--
0
PMID: 17114416,10570180,16375603 Serine phosphorylation of STAT1 mediated by p38 MAPK represents another example of cross-talk that may be indirectly controlled by DUSP proteins and contribute to the shaping of the transcriptional responses
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c42 : 1
stoichiometry:c43 : 1
stoichiometry:c44 : 1
m26*m28*0.1
nodelay
--
0
PMID: 17114416,12459177,9804857 Curiously, there are reports from two different groups suggesting that DUSP1 dephosphorylates STAT1 at tyrosine residues in hepatocytes and vascular smooth muscle cells, which would imply a more direct interaction with the JAK-STAT pathway
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c4 : 1
stoichiometry:c5 : 1
stoichiometry:c6 : 1
m10*m11*0.1
nodelay
--
0
PMID: 17114416 In contrast to DUSP6, the catalytic activity of DUSP10 is not increased by binding to p38 or JNK
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c45 : 1
stoichiometry:c46 : 1
stoichiometry:c47 : 1
m30*m31*0.1
nodelay
--
0
PMID: 17114416,11861597,7914033,9799232,9794373 All three MAPK are phosphorylated on the threonine and tyrosine residues of the shared TxY motif within minutes after TLR stimulation of macrophages and dendritic cells (DC) , as shown early on for the TLR4 ligand LPS
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c50 : 1
stoichiometry:c51 : 1
m33*0.1
nodelay
--
0
PMID: 17114416,16461893 TLR stimuli increase DUSP1 expression through MyD88- or, in the case of poly(I:C), TRIF-dependent signaling
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c52 : 1
stoichiometry:c53 : 1
m34*0.1
nodelay
--
0
PMID: 17114416,16461893 TLR stimuli increase DUSP1 expression through MyD88- or, in the case of poly(I:C), TRIF-dependent signaling
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c54 : 1
stoichiometry:c55 : 1
m13*0.1
nodelay
--
0
PMID: 17114416,8557667 MAPK signaling controls DUSP1 expression at various levels. In fibroblasts, activation of the JNK pathway, but not of ERK, resulted in increased DUSP1 mRNA
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c56 : 1
stoichiometry:c57 : 1
m36*0.1
nodelay
--
0
PMID: 17114416,16184516,12356755,15590669,11742987 Consistent with a negative regulatory function for DUSP1 in macrophage activation, anti-inflammatory glucocorticoids increase DUSP1 expression in macrophages, and mast cells at the mRNA and protein level
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c58 : 1
stoichiometry:c60 : 1
stoichiometry:c61 : 1
stoichiometry:c59 : 1
m37*m38*m39*0.1
nodelay
--
0
PMID: 17114416,16184516 Recently, we found that the immunosuppressive cytokine IL-10 enhanced and prolonged DUSP1 expression in TLR-stimulated macrophages, acting in synergy with dexamethasone.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c63 : 1
stoichiometry:c66 : 1
stoichiometry:c64 : 1
m41*0.1
nodelay
--
0
PMID: 17114416,16387640 Finally, the anti-inflammatory effects of the endocannabinoid anandamide on microglia have recently been correlated to up-regulation of DUSP1 protein levels, suggesting that signaling through the CB2 receptor is another pathway that leads to dampened MAPK activation through increased DUSP1 levels
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c62 : 1
stoichiometry:c65 : 1
m40*0.1
nodelay
--
0
PMID: 17114416,16387640 Finally, the anti-inflammatory effects of the endocannabinoid anandamide on microglia have recently been correlated to up-regulation of DUSP1 protein levels, suggesting that signaling through the CB2 receptor is another pathway that leads to dampened MAPK activation through increased DUSP1 levels
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c68 : 1
stoichiometry:c67 : 1
stoichiometry:c69 : 1
m41*0.1
nodelay
--
0
PMID: 17114416,12444149,15590669,15485842 A negative effect of DUSP1 on macrophage activation was suggested by overexpression of DUSP1, which was shown in a number of studies to inhibit phosphorylation of MAPK and the production of the cytokines TNF-{alpha} and IL-6 in response to diverse TLR stimuli
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c70 : 1
stoichiometry:c72 : 1
stoichiometry:c73 : 1
stoichiometry:c71 : 1
m44*m38*0.1
nodelay
--
0
--
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c7 : 1
stoichiometry:c8 : 1
stoichiometry:c9 : 1
m10*m13*0.1
nodelay
--
0
PMID: 17114416 In contrast to DUSP6, the catalytic activity of DUSP10 is not increased by binding to p38 or JNK
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c74 : 1
stoichiometry:c75 : 1
m47*0.1
nodelay
--
0
--
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c76 : 1
stoichiometry:c77 : 1
stoichiometry:c78 : 1
m48*m49*0.1
nodelay
--
0
PMID: 17114416, 8626452 Cloned in 1993 as an immediate early gene from TCR-activated T cells, DUSP2/PAC-1 localizes to the nucleus and primarily inactivates p38 MAPK and ERK in vitro PMID: 17114416, 8626452 From overexpression studies in vitro, DUSP2 appeared to dephosphorylate p38 and ERK
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c81 : 1
stoichiometry:c91 : 1
stoichiometry:c92 : 1
m67*m63*0.1
nodelay
--
0
PMID: 17114416 Figure 1 PMID: 17114416 Finally, the authors also showed that DUSP2 physically interacts with p38, JNK, and ERK, providing a basis for the cross-talk between MAPK that is suggested by the data
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c82 : 1
stoichiometry:c83 : 1
m63*0.1
nodelay
--
0
PMID: 17114416,8649402 In another study, DUSP2 expression was found to be controlled by ERK activation
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c84 : 1
stoichiometry:c85 : 1
m65*0.1
nodelay
--
0
PMID: 17114416,8649402 In another study, DUSP2 expression was found to be controlled by ERK activation
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c86 : 1
stoichiometry:c87 : 1
m38*0.1
nodelay
--
0
PMID: 17114416, DUSP2 is induced in macrophages by TLR ligands and in mast cells by Fc{epsilon}RI ligation.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c88 : 1
stoichiometry:c89 : 1
m66*0.1
nodelay
--
0
PMID: 17114416, DUSP2 is induced in macrophages by TLR ligands and in mast cells by Fc{epsilon}RI ligation.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c90 : 1
stoichiometry:c79 : 1
stoichiometry:c80 : 1
m48*m64*0.1
nodelay
--
0
PMID: 17114416, 8626452 Cloned in 1993 as an immediate early gene from TCR-activated T cells, DUSP2/PAC-1 localizes to the nucleus and primarily inactivates p38 MAPK and ERK in vitro PMID: 17114416, 8626452 From overexpression studies in vitro, DUSP2 appeared to dephosphorylate p38 and ERK
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c93 : 1
stoichiometry:c94 : 1
stoichiometry:c95 : 1
m67*m13*0.1
nodelay
--
0
PMID: 17114416 Figure 1 PMID: 17114416 Finally, the authors also showed that DUSP2 physically interacts with p38, JNK, and ERK, providing a basis for the cross-talk between MAPK that is suggested by the data
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c96 : 1
stoichiometry:c97 : 1
stoichiometry:c98 : 1
m11*m67*0.1
nodelay
--
0
PMID: 17114416 Figure 1 PMID: 17114416 Finally, the authors also showed that DUSP2 physically interacts with p38, JNK, and ERK, providing a basis for the cross-talk between MAPK that is suggested by the data
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c10 : 1
stoichiometry:c11 : 1
m15*0.1
nodelay
--
0
PMID: 17114416,15980098,12435740 Kovanen et al. analyzed T cell transcriptional responses to cytokine signaling through the common {gamma}-chain and identified DUSP5/VH3 and DUSP6/MKP-3 as up-regulated by IL-2, IL-7, and IL-15.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c99 : 1
stoichiometry:c101 : 1
stoichiometry:c100 : 1
m71*0.1
nodelay
--
0
PMID: 17114416,11971021,16713974,15107845 For example, IL-10 production was inhibited by the Map2k1/MEK1 inhibitor U0126, whereas IL-12 expression was suppressed by inhibition of p38 with SB203580
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c102 : 1
stoichiometry:c103 : 1
stoichiometry:c104 : 1
m20*m11*0.1
nodelay
--
0
PMID: 17114416,15067049,14607893 High levels of IL-10 along with low IL-12 production in response to TLR2 stimulation were shown to correlate with strong ERK activation, whereas TLR4, TLR5, or TLR9 ligands preferentially activated p38 and induced more IL-12
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c105 : 1
stoichiometry:c106 : 1
stoichiometry:c107 : 1
m73*m11*0.1
nodelay
--
0
PMID: 17114416,15067049,14607893 High levels of IL-10 along with low IL-12 production in response to TLR2 stimulation were shown to correlate with strong ERK activation, whereas TLR4, TLR5, or TLR9 ligands preferentially activated p38 and induced more IL-12
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c108 : 1
stoichiometry:c109 : 1
stoichiometry:c110 : 1
m74*m11*0.1
nodelay
--
0
PMID: 17114416,15067049,14607893 High levels of IL-10 along with low IL-12 production in response to TLR2 stimulation were shown to correlate with strong ERK activation, whereas TLR4, TLR5, or TLR9 ligands preferentially activated p38 and induced more IL-12
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c111 : 1
stoichiometry:c112 : 1
m72*0.1
nodelay
--
0
PMID: 17114416,15067049,14607893 High levels of IL-10 along with low IL-12 production in response to TLR2 stimulation were shown to correlate with strong ERK activation, whereas TLR4, TLR5, or TLR9 ligands preferentially activated p38 and induced more IL-12
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c113 : 1
stoichiometry:c114 : 1
stoichiometry:c115 : 1
m75*m63*0.1
nodelay
--
0
PMID: 17114416,15067049,14607893 High levels of IL-10 along with low IL-12 production in response to TLR2 stimulation were shown to correlate with strong ERK activation, whereas TLR4, TLR5, or TLR9 ligands preferentially activated p38 and induced more IL-12
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c116 : 1
stoichiometry:c117 : 1
m65*0.1
nodelay
--
0
PMID: 17114416,15067049,14607893 High levels of IL-10 along with low IL-12 production in response to TLR2 stimulation were shown to correlate with strong ERK activation, whereas TLR4, TLR5, or TLR9 ligands preferentially activated p38 and induced more IL-12
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c118 : 1
stoichiometry:c119 : 1
m65*0.1
nodelay
--
0
PMID: 17114416,15067049,14607893 High levels of IL-10 along with low IL-12 production in response to TLR2 stimulation were shown to correlate with strong ERK activation, whereas TLR4, TLR5, or TLR9 ligands preferentially activated p38 and induced more IL-12
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c120 : 1
stoichiometry:c121 : 1
stoichiometry:c122 : 1
m76*m77*0.1
nodelay
--
0
PMID: 17114416,11861597,7914033,9799232,9794373 All three MAPK are phosphorylated on the threonine and tyrosine residues of the shared TxY motif within minutes after TLR stimulation of macrophages and dendritic cells (DC) , as shown early on for the TLR4 ligand LPS
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c123 : 1
stoichiometry:c124 : 1
stoichiometry:c125 : 1
m20*m11*0.1
nodelay
--
0
PMID: 17114416,11861597,7914033,9799232,9794373 All three MAPK are phosphorylated on the threonine and tyrosine residues of the shared TxY motif within minutes after TLR stimulation of macrophages and dendritic cells (DC) , as shown early on for the TLR4 ligand LPS
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c12 : 1
stoichiometry:c13 : 1
m17*0.1
nodelay
--
0
PMID: 17114416,15980098,12435740 Kovanen et al. analyzed T cell transcriptional responses to cytokine signaling through the common {gamma}-chain and identified DUSP5/VH3 and DUSP6/MKP-3 as up-regulated by IL-2, IL-7, and IL-15.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c126 : 1
stoichiometry:c127 : 1
stoichiometry:c128 : 1
m20*m13*0.1
nodelay
--
0
PMID: 17114416,11861597,7914033,9799232,9794373 All three MAPK are phosphorylated on the threonine and tyrosine residues of the shared TxY motif within minutes after TLR stimulation of macrophages and dendritic cells (DC) , as shown early on for the TLR4 ligand LPS
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c129 : 1
stoichiometry:c130 : 1
stoichiometry:c131 : 1
m20*m63*0.1
nodelay
--
0
PMID: 17114416,11861597,7914033,9799232,9794373 All three MAPK are phosphorylated on the threonine and tyrosine residues of the shared TxY motif within minutes after TLR stimulation of macrophages and dendritic cells (DC) , as shown early on for the TLR4 ligand LPS
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c132 : 1
stoichiometry:c133 : 1
stoichiometry:c134 : 1
m74*m11*0.1
nodelay
--
0
PMID: 17114416,11861597,7914033,9799232,9794373 All three MAPK are phosphorylated on the threonine and tyrosine residues of the shared TxY motif within minutes after TLR stimulation of macrophages and dendritic cells (DC) , as shown early on for the TLR4 ligand LPS
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c135 : 1
stoichiometry:c136 : 1
stoichiometry:c137 : 1
m74*m13*0.1
nodelay
--
0
PMID: 17114416,11861597,7914033,9799232,9794373 All three MAPK are phosphorylated on the threonine and tyrosine residues of the shared TxY motif within minutes after TLR stimulation of macrophages and dendritic cells (DC) , as shown early on for the TLR4 ligand LPS
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c138 : 1
stoichiometry:c139 : 1
stoichiometry:c140 : 1
m74*m63*0.1
nodelay
--
0
PMID: 17114416,11861597,7914033,9799232,9794373 All three MAPK are phosphorylated on the threonine and tyrosine residues of the shared TxY motif within minutes after TLR stimulation of macrophages and dendritic cells (DC) , as shown early on for the TLR4 ligand LPS
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c141 : 1
stoichiometry:c142 : 1
stoichiometry:c143 : 1
m79*m80*0.1
nodelay
--
0
PMID: 17114416,11861597 Rapid transduction of the signal from TNFR-associated factor 6 to the MAPK is achieved through the sequential activation of upstream MAP3K and MAPK kinases
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c144 : 1
stoichiometry:c145 : 1
stoichiometry:c146 : 1
m81*m41*0.1
nodelay
--
0
PMID: 17114416,11861597 Rapid transduction of the signal from TNFR-associated factor 6 to the MAPK is achieved through the sequential activation of upstream MAP3K and MAPK kinases
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c147 : 1
stoichiometry:c148 : 1
stoichiometry:c149 : 1
m83*m82*0.1
nodelay
--
0
PMID: 17114416 In CD4+ T cells, DUSP10 is constitutively expressed but down-regulated 24 h after TCR activation.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c150 : 1
stoichiometry:c151 : 1
m84*0.1
nodelay
--
0
PMID: 17114416 In CD4+ T cells, DUSP10 is constitutively expressed but down-regulated 24 h after TCR activation.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c14 : 1
stoichiometry:c15 : 1
m18*0.1
nodelay
--
0
PMID: 17114416,15980098,12435740 Kovanen et al. analyzed T cell transcriptional responses to cytokine signaling through the common {gamma}-chain and identified DUSP5/VH3 and DUSP6/MKP-3 as up-regulated by IL-2, IL-7, and IL-15.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c16 : 1
stoichiometry:c17 : 1
m15*0.1
nodelay
--
0
PMID: 17114416,15980098,12435740 Kovanen et al. analyzed T cell transcriptional responses to cytokine signaling through the common {gamma}-chain and identified DUSP5/VH3 and DUSP6/MKP-3 as up-regulated by IL-2, IL-7, and IL-15.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c18 : 1
stoichiometry:c19 : 1
m17*0.1
nodelay
--
0
PMID: 17114416,15980098,12435740 Kovanen et al. analyzed T cell transcriptional responses to cytokine signaling through the common {gamma}-chain and identified DUSP5/VH3 and DUSP6/MKP-3 as up-regulated by IL-2, IL-7, and IL-15.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c20 : 1
stoichiometry:c21 : 1
m18*0.1
nodelay
--
0
PMID: 17114416,15980098,12435740 Kovanen et al. analyzed T cell transcriptional responses to cytokine signaling through the common {gamma}-chain and identified DUSP5/VH3 and DUSP6/MKP-3 as up-regulated by IL-2, IL-7, and IL-15.
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