Original Literature | Model OverView |
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Publication
Title
The involvement of the interleukin-1 receptor-associated kinases (IRAKs) incellular signaling networks controlling inflammation.
Affiliation
The Laboratory of Innate Immunity and Inflammation, Department of BiologicalSciences, West Campus Drive, Fralin Biotechnology Center, Virginia Tech,Blacksburg, VA 24061, USA.
Abstract
Innate immunity and inflammation plays a key role in host defense and woundhealing. However, Excessive or altered inflammatory processes can contribute tosevere and diverse human diseases including cardiovascular disease, diabetes andcancer. The interleukin-1 receptor-associated kinases (IRAKs) are criticallyinvolved in the regulation of intracellular signaling networks controllinginflammation. Collective studies indicate that IRAKs are present in many celltypes, and can mediate signals from various cell receptors includingtoll-like-receptors (TLRs). Consequently, diverse downstream signaling processescan be elicited following the activation of various IRAKs. Given the criticaland complex roles IRAK proteins play, it is not surprising that geneticvariations in human IRAK genes have been found to be linked with various humaninflammatory diseases. This review intends to summarize the recent advancesregarding the regulations of various IRAK proteins and their cellular functionsin mediating inflammatory signaling processes.
PMID
18249132
|
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LPS:TLR4:MYD88:IRAK4
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--
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0
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Stat3
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--
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IL-1beta
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--
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IRAK-1c
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--
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--
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--
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Mal
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--
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IRAK-2b
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--
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0
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IRAK-2c
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e87
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--
csml-variable:Double
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0
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IRAK-2d
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--
csml-variable:Double
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TAK1{active}
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csml-variable:Double
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--
e9
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--
--
csml-variable:Double
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0
--
IKK complex
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e90
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csml-variable:Double
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0
--
NIK
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e91
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--
csml-variable:Double
m91
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0
--
NIK{active}
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e92
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csml-variable:Double
m92
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0
--
IRAK-M
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e93
cso30:c:Protein
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--
csml-variable:Double
m93
0
infinite
0
--
IkappaB-alpha
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e94
cso30:c:mRNA
cso30:i:CC_Nucleoplasm
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csml-variable:Double
m94
0
infinite
0
--
csml-variable:Double
m95
0
infinite
0
--
csml-variable:Double
m96
0
infinite
0
--
IkappaB-alpha:p50:p65
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e97
cso30:c:Complex
cso30:i:CC_Nucleoplasm
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csml-variable:Double
m97
0
infinite
0
--
inflammatory mediators
--
e98
cso30:c:mRNA
cso30:i:CC_Nucleoplasm
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--
csml-variable:Double
m98
0
infinite
0
--
TCR ligand:TCR
--
e99
cso30:c:Complex
cso30:i:CC_Cytosol
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--
csml-variable:Double
m99
0
infinite
0
--
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c1 : 1
stoichiometry:c3 : 1
stoichiometry:c2 : 1
m5*m47*0.1
nodelay
--
0
PMID: 18249132, 17217339 IRAK-4 was shown to phosphorylate NADPH oxidase p47phox and contribute to cellular oxidative response in neutrophils.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c29 : 1
stoichiometry:c31 : 1
stoichiometry:c30 : 1
m30*m20*0.1
nodelay
--
0
PMID: 18249132, 15767370, 15695821 Perhaps one of the major functions of IRAK-1 is to mediate the ligand-stimulated phosphorylation of IRF5/7.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c32 : 1
stoichiometry:c34 : 1
stoichiometry:c33 : 1
m33*m20*0.1
nodelay
--
0
PMID: 18249132, 15767370, 15695821 Perhaps one of the major functions of IRAK-1 is to mediate the ligand-stimulated phosphorylation of IRF5/7.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c35 : 1
stoichiometry:c36 : 1
m42*0.1
nodelay
--
0
PMID: 18249132, 15767370 In contrast, NF¦ÊB-mediated gene expressions such as TNF¦Á seem to be un-altered in IRAK-1¡Ý/¡Ý cells upon challenge with agonists for TLR 7/8 as well as TLR9
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c44 : 1
stoichiometry:c37 : 1
m37*0.1
nodelay
--
0
PMID: 18249132 Consequently, interferon alpha4 gene expression is dramatically decreased in IRAK-1¡Ý/¡Ý cells following the stimulation with TLR7 and TLR9 ligand.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c38 : 1
stoichiometry:c43 : 1
stoichiometry:c39 : 1
m17*m39*0.1
nodelay
--
0
PMID: 18249132 Consequently, interferon alpha4 gene expression is dramatically decreased in IRAK-1¡Ý/¡Ý cells following the stimulation with TLR7 and TLR9 ligand.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c41 : 1
stoichiometry:c42 : 1
stoichiometry:c40 : 1
m17*m38*0.1
nodelay
--
0
PMID: 18249132 Consequently, interferon alpha4 gene expression is dramatically decreased in IRAK-1¡Ý/¡Ý cells following the stimulation with TLR7 and TLR9 ligand.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c123 : 1
stoichiometry:c125 : 1
stoichiometry:c129 : 1
stoichiometry:c124 : 1
m91*m84*0.1
nodelay
--
0
PMID: 18249132 From fig.2 PMID: 18249132, 17892204 we have observed that IRAK-M primarily affects the alternative NIK-IKK¦Á/IKK¦Á-RelB NF¦ÊB pathway, instead of the classical TAK1-IKK¦Á/IKK¦Â-RelA pathway
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c45 : 1
stoichiometry:c53 : 1
stoichiometry:c50 : 1
m41*m39*0.1
nodelay
--
0
PMID: 18249132, 15767370 In contrast, NF¦ÊB-mediated gene expressions such as TNF¦Á seem to be un-altered in IRAK-1¡Ý/¡Ý cells upon challenge with agonists for TLR 7/8 as well as TLR9.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c46 : 1
stoichiometry:c52 : 1
stoichiometry:c49 : 1
m41*m38*0.1
nodelay
--
0
PMID: 18249132, 15767370 In contrast, NF¦ÊB-mediated gene expressions such as TNF¦Á seem to be un-altered in IRAK-1¡Ý/¡Ý cells upon challenge with agonists for TLR 7/8 as well as TLR9.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c47 : 1
stoichiometry:c51 : 1
stoichiometry:c48 : 1
m41*m40*0.1
nodelay
--
0
PMID: 18249132, 15767370 In contrast, NF¦ÊB-mediated gene expressions such as TNF¦Á seem to be un-altered in IRAK-1¡Ý/¡Ý cells upon challenge with agonists for TLR 7/8 as well as TLR9.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c4 : 1
stoichiometry:c5 : 1
stoichiometry:c6 : 1
m14*m13*0.1
nodelay
--
0
PMID: 18249132 Figure 1
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c54 : 1
stoichiometry:c55 : 1
stoichiometry:c57 : 1
stoichiometry:c56 : 1
m17*m43*m45*0.1
nodelay
--
0
PMID: 18249132, 16107720 T cell co-stimulatory molecule CD26 can trigger the association of IRAK-1 with caveolin on antigen presenting monocytes, which is responsible for the subsequent expression of co-stimulatory molecule CD86.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c59 : 1
stoichiometry:c58 : 1
m44*0.1
nodelay
--
0
PMID: 18249132, 16107720 T cell co-stimulatory molecule CD26 can trigger the association of IRAK-1 with caveolin on antigen presenting monocytes, which is responsible for the subsequent expression of co-stimulatory molecule CD86.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c61 : 1
stoichiometry:c62 : 1
m20*0.1
nodelay
--
0
PMID: 18249132, 17161373 Upstream kinases such as IRAK-4 may contribute to the initial phosphorylation of IRAK-1 at Threonine 381
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c63 : 1
stoichiometry:c64 : 1
m48*0.1
nodelay
--
0
PMID: 18249132 Following such event, IRAK-1 can be quickly activated and exhibit self-phosphorylation within its Pro/Ser rich region
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c65 : 1
stoichiometry:c66 : 1
m63*0.1
nodelay
--
0
PMID: 18249132 This self-phosphorylation may subject the IRAK-1 molecule to subsequent ubiquitination and proteosome-mediated degradation.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c67 : 1
stoichiometry:c68 : 1
stoichiometry:c69 : 1
m64*0.1
nodelay
--
0
PMID: 18249132 This self-phosphorylation may subject the IRAK-1 molecule to subsequent ubiquitination and proteosome-mediated degradation.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c70 : 1
stoichiometry:c72 : 1
stoichiometry:c71 : 1
m66*m67*0.1
nodelay
--
0
PMID: 18249132, 16690127, 15465816 IRAK-1 also gets sumoylated following either LPS or Pam3CSK4 challenge.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c73 : 1
stoichiometry:c74 : 1
stoichiometry:c75 : 1
stoichiometry:c76 : 1
stoichiometry:c77 : 1
m65*m15*m17*m47*0.1
nodelay
--
0
PMID: 18249132, 16690127, 15465816 IRAK-1 also gets sumoylated following either LPS or Pam3CSK4 challenge. PMID: 18249132, 11960013 MyD88 is critically involved in recruiting IRAK-4 into the TLR4 complex
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c78 : 1
stoichiometry:c79 : 1
m68*0.1
nodelay
--
0
PMID: 18249132, 16690127, 15465816 IRAK-1 also gets sumoylated following either LPS or Pam3CSK4 challenge.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c80 : 1
stoichiometry:c81 : 1
stoichiometry:c82 : 1
m69*0.1
nodelay
--
0
PMID: 18249132, 15465816 Sumoylated IRAK-1 enters the nucleus and contributes to Stat3 activation and selected gene expression
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c7 : 1
stoichiometry:c8 : 1
stoichiometry:c9 : 1
m12*m15*0.1
nodelay
--
0
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c83 : 1
stoichiometry:c85 : 1
stoichiometry:c84 : 1
m72*m70*0.1
nodelay
--
0
PMID: 18249132, 15465816 Sumoylated IRAK-1 enters the nucleus and contributes to Stat3 activation and selected gene expression
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c86 : 1
stoichiometry:c87 : 1
m73*0.1
nodelay
--
0
PMID: 18249132, 15465816 Sumoylated IRAK-1 enters the nucleus and contributes to Stat3 activation and selected gene expression
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c88 : 1
stoichiometry:c90 : 1
stoichiometry:c91 : 1
stoichiometry:c89 : 1
m76*m75*0.1
nodelay
--
0
PMID: 18249132 Overexpression of IRAK-1c blocks IL-1¦Â induced MAP kinase activation, suggesting that IRAK-1c may serve as a negative regulator of inflammation.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c92 : 1
stoichiometry:c93 : 1
stoichiometry:c94 : 1
stoichiometry:c95 : 1
stoichiometry:c116 : 1
stoichiometry:c96 : 1
m12*m15*m79*m80*m47*0.1
nodelay
--
0
PMID: 18249132 Upon overexpression, IRAK-2 can associate with MyD88 as well as TRAF6, and activate NF¦ÊB-dependent reporter gene expression.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c97 : 1
stoichiometry:c99 : 1
stoichiometry:c98 : 1
m41*m84*0.1
nodelay
--
0
PMID: 18249132 Upon overexpression, IRAK-2 can associate with MyD88 as well as TRAF6, and activate NF¦ÊB-dependent reporter gene expression. PMID: 18249132, 17878161 A recent study further confirmed that indeed IRAK-2 instead of IRAK-1 is primarily involved in TRAF-6 ubiquitination and NF¦ÊB activation
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c100 : 1
stoichiometry:c101 : 1
m42*0.1
nodelay
--
0
PMID: 18249132 Upon overexpression, IRAK-2 can associate with MyD88 as well as TRAF6, and activate NF¦ÊB-dependent reporter gene expression.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c102 : 1
stoichiometry:c103 : 1
stoichiometry:c104 : 1
stoichiometry:c105 : 1
m12*m79*m82*0.1
nodelay
--
0
PMID: 18249132, 11544529 IRAK-2, instead of IRAK-1 can also interact with another distinct TLR intracellular adaptor molecule Mal/TIRAP
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c106 : 1
stoichiometry:c107 : 1
m81*0.1
nodelay
--
0
PMID: 18249132, 17878161 A recent study further confirmed that indeed IRAK-2 instead of IRAK-1 is primarily involved in TRAF-6 ubiquitination and NF¦ÊB activation
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c110 : 1
stoichiometry:c113 : 1
stoichiometry:c111 : 1
m41*m85*0.1
nodelay
--
0
PMID: 18249132 Upon overexpression, IRAK-2a and IRAK-2b can activate, while IRAK-2c and IRAK-2d inhibit NF¦ÊB activation.
p39
p39
cso30:i:ME_UnknownActivation
cso30:i:CC_Cytosol
--
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c108 : 1
stoichiometry:c112 : 1
stoichiometry:c114 : 1
stoichiometry:c115 : 1
stoichiometry:c109 : 1
m41*m86*0.1
nodelay
--
0
PMID: 18249132 Upon overexpression, IRAK-2a and IRAK-2b can activate, while IRAK-2c and IRAK-2d inhibit NF¦ÊB activation.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c10 : 1
stoichiometry:c12 : 1
stoichiometry:c13 : 1
stoichiometry:c14 : 1
stoichiometry:c60 : 1
stoichiometry:c11 : 1
m16*m18*m19*m17*m47*0.1
nodelay
--
0
PMID: 18249132 From fig.1
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c117 : 1
stoichiometry:c119 : 1
stoichiometry:c118 : 1
m11*m84*0.1
nodelay
--
0
PMID: 18249132 From fig.2
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c120 : 1
stoichiometry:c122 : 1
stoichiometry:c121 : 1
m90*m89*0.1
nodelay
--
0
PMID: 18249132 From fig.2
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c126 : 1
stoichiometry:c128 : 1
stoichiometry:c127 : 1
m90*m92*0.1
nodelay
--
0
PMID: 18249132 From fig.2
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c130 : 1
stoichiometry:c131 : 1
m29*0.1
nodelay
--
0
PMID: 18249132 From fig.2
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c133 : 1
stoichiometry:c132 : 1
m94*0.1
nodelay
--
0
PMID: 18249132 From fig.2
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c134 : 1
stoichiometry:c135 : 1
m95*0.1
nodelay
--
0
PMID: 18249132 From fig.2
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c136 : 1
stoichiometry:c137 : 1
stoichiometry:c138 : 1
m29*m96*0.1
nodelay
--
0
PMID: 18249132 From fig.2
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c139 : 1
stoichiometry:c140 : 1
m97*0.1
nodelay
--
0
PMID: 18249132 From fig.2
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c142 : 1
stoichiometry:c141 : 1
m29*0.1
nodelay
--
0
PMID: 18249132 From fig.2
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c143 : 1
stoichiometry:c144 : 1
stoichiometry:c146 : 1
stoichiometry:c145 : 1
m99*m47*m101*0.1
nodelay
--
0
PMID: 18249132 Upon TCR stimulation, IRAK-4 is recruited to T cell lipid rafts, where it can associate with Zap70 and activate protein kinase C.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c15 : 1
stoichiometry:c17 : 1
stoichiometry:c16 : 1
m21*m23*0.1
nodelay
--
0
PMID: 18249132 The first step involves the classical pathway causing the activation of IKK¦Á/¦Â complex, which contributes to I¦ÊB¦Á phosphorylation and degradation, and subsequent nuclear translocation of p65/RelA.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c147 : 1
stoichiometry:c149 : 1
stoichiometry:c148 : 1
m103*m100*0.1
nodelay
--
0
PMID: 18249132 Upon TCR stimulation, IRAK-4 is recruited to T cell lipid rafts, where it can associate with Zap70 and activate protein kinase C.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c150 : 1
stoichiometry:c152 : 1
stoichiometry:c151 : 1
m41*m100*0.1
nodelay
--
0
PMID: 18249132, 16574867 IRAK-4 is also critically involved in T cell receptor (TCR)-induced T cell proliferation through NF¦ÊB activation
PMID: 18249132, 16574867 IRAK-4 is also critically involved in T cell receptor (TCR)-induced T cell proliferation through NF¦ÊB activation
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c18 : 1
stoichiometry:c19 : 1
stoichiometry:c20 : 1
m22*0.1
nodelay
--
0
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c21 : 1
stoichiometry:c23 : 1
stoichiometry:c22 : 1
m25*m27*0.1
nodelay
--
0
PMID: 18249132 The second step involves IKK¦Å/TBK-1 dependent p65/RelA phosphorylation, which is independent of the classical pathway and I¦ÊB¦Á degradation.
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c24 : 1
stoichiometry:c26 : 1
stoichiometry:c25 : 1
m28*m20*0.1
nodelay
--
0
PMID: 18249132 Figure 1 PMID: 18249132 Recent evidence indicates that IRAK-1 contributes to NF¦ÊB activation by facilitating p65/RelA phosphorylation, but not the classical pathway leading to I¦ÊB¦Á degradation and p65 nuclear translocation
--
and
mass
coefficient1:0.1
coefficient2:1.0
stoichiometry:c27 : 1
stoichiometry:c28 : 1
m26*0.1
nodelay
--
0
PMID: 18249132 The first step involves the classical pathway causing the activation of IKK¦Á/¦Â complex, which contributes to I¦ÊB¦Á phosphorylation and degradation, and subsequent nuclear translocation of p65/RelA.
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputInhibitor
threshold
--
0
1,
--
cso30:c:InputInhibitor
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputInhibitor
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--
cso30:c:InputInhibitor
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:InputAssociation
threshold
--
0
1,
--