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PMID: 18249132, 17217339
IRAK-4 was shown to phosphorylate NADPH oxidase p47phox and contribute to cellular oxidative response in neutrophils.</csml:comment>
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PMID: 18249132
Figure 1</csml:comment>
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PMID: 18249132
From fig.1
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PMID: 18249132
The first step involves the classical pathway causing the activation of IKKα/β complex, which contributes to IκBα phosphorylation and degradation, and subsequent nuclear translocation of p65/RelA.</csml:comment>
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PMID: 18249132
The second step involves IKKε/TBK-1 dependent p65/RelA phosphorylation, which is independent of the classical pathway and IκBα degradation. </csml:comment>
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indirect</csml:comment>
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PMID: 18249132
Figure 1

PMID: 18249132
Recent evidence indicates that IRAK-1 contributes to NFκB activation by facilitating p65/RelA phosphorylation, but not the classical pathway leading to IκBα degradation and p65 nuclear translocation</csml:comment>
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PMID: 18249132
The first step involves the classical pathway causing the activation of IKKα/β complex, which contributes to IκBα phosphorylation and degradation, and subsequent nuclear translocation of p65/RelA.
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PMID: 18249132, 15767370, 15695821
Perhaps one of the major functions of IRAK-1 is to mediate the ligand-stimulated phosphorylation of IRF5/7.</csml:comment>
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PMID: 18249132, 15767370, 15695821
Perhaps one of the major functions of IRAK-1 is to mediate the ligand-stimulated phosphorylation of IRF5/7.
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PMID: 18249132, 15767370
In contrast, NFκB-mediated gene expressions such as TNFα seem to be un-altered in IRAK-1−/− cells upon challenge with agonists for TLR 7/8 as well as TLR9</csml:comment>
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PMID: 18249132
Consequently, interferon alpha4 gene expression is dramatically decreased in IRAK-1−/− cells following the stimulation with TLR7 and TLR9 ligand.</csml:comment>
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PMID: 18249132
Consequently, interferon alpha4 gene expression is dramatically decreased in IRAK-1−/− cells following the stimulation with TLR7 and TLR9 ligand.</csml:comment>
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PMID: 18249132
Consequently, interferon alpha4 gene expression is dramatically decreased in IRAK-1−/− cells following the stimulation with TLR7 and TLR9 ligand.</csml:comment>
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PMID: 18249132, 15767370
In contrast, NFκB-mediated gene expressions such as TNFα seem to be un-altered in IRAK-1−/− cells upon challenge with agonists for TLR 7/8 as well as TLR9.
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PMID: 18249132, 15767370
In contrast, NFκB-mediated gene expressions such as TNFα seem to be un-altered in IRAK-1−/− cells upon challenge with agonists for TLR 7/8 as well as TLR9.
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PMID: 18249132, 15767370
In contrast, NFκB-mediated gene expressions such as TNFα seem to be un-altered in IRAK-1−/− cells upon challenge with agonists for TLR 7/8 as well as TLR9.
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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.</csml:comment>
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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.</csml:comment>
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PMID: 18249132, 17161373
Upstream kinases such as IRAK-4 may contribute to the initial phosphorylation of IRAK-1 at Threonine 381</csml:comment>
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PMID: 18249132
Following such event, IRAK-1 can be quickly activated and exhibit self-phosphorylation within its Pro/Ser rich region</csml:comment>
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PMID: 18249132
This self-phosphorylation may subject the IRAK-1 molecule to subsequent ubiquitination and proteosome-mediated degradation.</csml:comment>
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PMID: 18249132
This self-phosphorylation may subject the IRAK-1 molecule to subsequent ubiquitination and proteosome-mediated degradation.</csml:comment>
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PMID: 18249132, 16690127, 15465816
IRAK-1 also gets sumoylated following either LPS or Pam3CSK4 challenge.</csml:comment>
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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</csml:comment>
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PMID: 18249132, 16690127, 15465816
IRAK-1 also gets sumoylated following either LPS or Pam3CSK4 challenge.
</csml:comment>
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PMID: 18249132, 15465816
Sumoylated IRAK-1 enters the nucleus and contributes to Stat3 activation and selected gene expression</csml:comment>
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PMID: 18249132, 15465816
Sumoylated IRAK-1 enters the nucleus and contributes to Stat3 activation and selected gene expression

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Sumoylated IRAK-1 enters the nucleus and contributes to Stat3 activation and selected gene expression
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PMID: 18249132
Overexpression of IRAK-1c blocks IL-1β induced MAP kinase activation, suggesting that IRAK-1c may serve as a negative regulator of inflammation.</csml:comment>
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PMID: 18249132
Upon overexpression, IRAK-2 can associate with MyD88 as well as TRAF6, and activate NFκB-dependent reporter gene expression.</csml:comment>
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PMID: 18249132
Upon overexpression, IRAK-2 can associate with MyD88 as well as TRAF6, and activate NFκB-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 NFκB activation</csml:comment>
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PMID: 18249132
Upon overexpression, IRAK-2 can associate with MyD88 as well as TRAF6, and activate NFκB-dependent reporter gene expression.</csml:comment>
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PMID: 18249132, 11544529
IRAK-2, instead of IRAK-1 can also interact with another distinct TLR intracellular adaptor molecule Mal/TIRAP</csml:comment>
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PMID: 18249132, 17878161
A recent study further confirmed that indeed IRAK-2 instead of IRAK-1 is primarily involved in TRAF-6 ubiquitination and NFκB activation</csml:comment>
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PMID: 18249132
Upon overexpression, IRAK-2a and IRAK-2b can activate, while IRAK-2c and IRAK-2d inhibit NFκB activation.</csml:comment>
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PMID: 18249132
Upon overexpression, IRAK-2a and IRAK-2b can activate, while IRAK-2c and IRAK-2d inhibit NFκB activation.</csml:comment>
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PMID: 18249132
From fig.2</csml:comment>
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PMID: 18249132
From fig.2
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PMID: 18249132
From fig.2

PMID: 18249132, 17892204
we have observed that IRAK-M primarily affects the alternative NIK-IKKα/IKKα-RelB NFκB pathway, instead of the classical TAK1-IKKα/IKKβ-RelA pathway</csml:comment>
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PMID: 18249132
From fig.2
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PMID: 18249132
From fig.2
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PMID: 18249132
From fig.2
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<csml:comment type="text">
PMID: 18249132
From fig.2
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<csml:comment type="text">
PMID: 18249132
From fig.2
</csml:comment>
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PMID: 18249132
From fig.2
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PMID: 18249132
From fig.2
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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.</csml:comment>
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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.

</csml:comment>
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PMID: 18249132, 16574867
IRAK-4 is also critically involved in T cell receptor (TCR)-induced T cell proliferation through NFκB activation</csml:comment>
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PMID: 18249132, 16574867
IRAK-4 is also critically involved in T cell receptor (TCR)-induced T cell proliferation through NFκB activation</csml:comment>
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