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PMID: 17502370
Following IFN-receptor interaction, a latent cytoplasmic IRF-9 complexes with Stat1 and Stat2 through the activation of the JAK/STAT pathway, binds to the IFN-stimulated response element (ISRE), and stimulates transcription of a large set of IFN-stimulated genes.</csml:comment>
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PMID: 17502370
Following IFN-receptor interaction, a latent cytoplasmic IRF-9 complexes with Stat1 and Stat2 through the activation of the JAK/STAT pathway, binds to the IFN-stimulated response element (ISRE), and stimulates transcription of a large set of IFN-stimulated genes.
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PMID: 17502370
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PMID: 17502370
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PMID: 17502370
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PMID: 17502370
Following IFN-receptor interaction, a latent cytoplasmic IRF-9 complexes with Stat1 and Stat2 through the activation of the JAK/STAT pathway, binds to the IFN-stimulated response element (ISRE), and stimulates transcription of a large set of IFN-stimulated genes.
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PMID: 17502370
Following IFN-receptor interaction, a latent cytoplasmic IRF-9 complexes with Stat1 and Stat2 through the activation of the JAK/STAT pathway, binds to the IFN-stimulated response element (ISRE), and stimulates transcription of a large set of IFN-stimulated genes.
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PMID: 17502370, 15947094, 12453417, 11846986
They not only bind the ISRE, the binding site for all IRF factors, but also bind various Ets/IRF composite elements through their interaction with PU.1, an Ets family transcription factor</csml:comment>
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PMID: 17502370, 15947094, 12453417, 11846986
They not only bind the ISRE, the binding site for all IRF factors, but also bind various Ets/IRF composite elements through their interaction with PU.1, an Ets family transcription factor</csml:comment>
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PMID: 17502370, 15947094, 12453417, 11846986
They not only bind the ISRE, the binding site for all IRF factors, but also bind various Ets/IRF composite elements through their interaction with PU.1, an Ets family transcription factor</csml:comment>
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PMID: 17502370, 15947094, 12453417, 11846986
They not only bind the ISRE, the binding site for all IRF factors, but also bind various Ets/IRF composite elements through their interaction with PU.1, an Ets family transcription factor</csml:comment>
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PMID: 17502370, 11846985
IRF-8 coordinates myeloid cell growth and differentiation.

PMID: 17502370
IRF-8 promotes macrophage differentiation while inhibiting granulocyte development.</csml:comment>
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PMID: 17502370, 11846985
IRF-8 coordinates myeloid cell growth and differentiation</csml:comment>
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PMID: 17502370, 15947094
It directly stimulates the expression of genes active in macrophages including those for lysosomal and endosomal proteases.</csml:comment>
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PMID: 17502370, 15947094
It directly stimulates the expression of genes active in macrophages including those for lysosomal and endosomal proteases.
</csml:comment>
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PMID: 17502370
In myeloid cells IRF-8 negatively regulates cell growth as it inhibits c-myc and stimulates expression of tumor suppressor/inhibitor of cyclin-dependent kinase (INK4).</csml:comment>
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PMID: 17502370, 11846985
This growth regulation is relevant to CML in humans, where IRF-8 expression is down-regulated by the Bcr/Abl oncoprotein resulting in abnormal growth promotion.</csml:comment>
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PMID: 17502370, 15728463, 10861061
IRF-8, but not IRF-4, is required for the expression of proinflammatory cytokines including type I IFN and IL-12p40, indicating that IRF-8 is critically required for cytokine gene expression.

PMID: 17502370, 16236719
IRF-4, on the other hand, inhibits expression of proinflammatory cytokine genes.</csml:comment>
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PMID: 17502370, 15728463, 10861061
IRF-8, but not IRF-4, is required for the expression of proinflammatory cytokines including type I IFN and IL-12p40, indicating that IRF-8 is critically required for cytokine gene expression.

PMID: 17502370, 16236719
IRF-4, on the other hand, inhibits expression of proinflammatory cytokine genes.
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PMID: 17502370
Upon activation, IRF-3 and IRF-7 are phosphorylated through the I{kappa}B kinase (IKK) family of kinases, dimerized, and translocated into the nucleus to stimulate IFNbeta and IFN{alpha} transcription.
</csml:comment>
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indirect</csml:comment>
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PMID: 17502370
RF-3 and IRF-7 are early IRFs activated by Toll-like receptor (TLR)and other types of signaling that play a pivotal role in the initial induction of type I IFNs.

PMID: 17502370
Upon activation, IRF-3 and IRF-7 are phosphorylated through the I{kappa}B kinase (IKK) family of kinases, dimerized, and translocated into the nucleus to stimulate IFNbeta and IFN{alpha} transcription.</csml:comment>
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PMID: 17502370
Upon activation, IRF-3 and IRF-7 are phosphorylated through the I{kappa}B kinase (IKK) family of kinases, dimerized, and translocated into the nucleus to stimulate IFNbeta and IFN{alpha} transcription.
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PMID: 17502370
Upon activation, IRF-3 and IRF-7 are phosphorylated through the I{kappa}B kinase (IKK) family of kinases, dimerized, and translocated into the nucleus to stimulate IFNbeta and IFN{alpha} transcription.
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PMID: 17502370
Upon activation, IRF-3 and IRF-7 are phosphorylated through the I{kappa}B kinase (IKK) family of kinases, dimerized, and translocated into the nucleus to stimulate IFNbeta and IFN{alpha} transcription.
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PMID: 17502370
Upon activation, IRF-3 and IRF-7 are phosphorylated through the I{kappa}B kinase (IKK) family of kinases, dimerized, and translocated into the nucleus to stimulate IFNbeta and IFN{alpha} transcription.
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PMID: 17502370
Upon activation, IRF-3 and IRF-7 are phosphorylated through the I{kappa}B kinase (IKK) family of kinases, dimerized, and translocated into the nucleus to stimulate IFNbeta and IFN{alpha} transcription.
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PMID: 17502370
Upon activation, IRF-3 and IRF-7 are phosphorylated through the I{kappa}B kinase (IKK) family of kinases, dimerized, and translocated into the nucleus to stimulate IFNbeta and IFN{alpha} transcription.
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PMID: 17502370, 15741273
the rotavirus regulatory protein NSP1 binds to and degrades IRF-3 to disable IFN induction.</csml:comment>
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PMID: 17502370, 15741273
the rotavirus regulatory protein NSP1 binds to and degrades IRF-3 to disable IFN induction.
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PMID: 17502370
ICP0 interacts with PML and affects SUMO (small ubiquitin-related modifier) modification of PML, thereby counteracting PML inhibition of viral replication.</csml:comment>
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PMID: 17502370
ICP0 interacts with PML and affects SUMO (small ubiquitin-related modifier) modification of PML, thereby counteracting PML inhibition of viral replication.</csml:comment>
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PMID: 17502370, 16689655
Additionally, infection with rabies virus, an RNA virus, also alters PML distribution through the interaction of the viral P protein with PML</csml:comment>
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PMID: 17502370, 16914719
IRF-8 is phosphorylated at the tyrosine residues in the DBD, which is inhibited by the protein tyrosine phosphatases SHP1 and SHP2.</csml:comment>
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PMID: 17502370, 16979567, 16932750
TLR- and retinoic acid inducible gene-I (RIG-I)-mediated phosphorylation of IRF-3 and IRF-7 by IKKi/{epsilon} and Tank-binding kinase-1 (TBK-1) is a prerequisite of IFN induction.</csml:comment>
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PMID: 17502370, 16979567, 16932750
TLR- and retinoic acid inducible gene-I (RIG-I)-mediated phosphorylation of IRF-3 and IRF-7 by IKKi/{epsilon} and Tank-binding kinase-1 (TBK-1) is a prerequisite of IFN induction.</csml:comment>
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indirect</csml:comment>
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PMID: 17502370, 16979567, 16932750
TLR- and retinoic acid inducible gene-I (RIG-I)-mediated phosphorylation of IRF-3 and IRF-7 by IKKi/{epsilon} and Tank-binding kinase-1 (TBK-1) is a prerequisite of IFN induction.

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PMID: 17502370, 16979567, 16932750
TLR- and retinoic acid inducible gene-I (RIG-I)-mediated phosphorylation of IRF-3 and IRF-7 by IKKi/{epsilon} and Tank-binding kinase-1 (TBK-1) is a prerequisite of IFN induction.
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PMID: 17502370, 16979567, 16932750
TLR- and retinoic acid inducible gene-I (RIG-I)-mediated phosphorylation of IRF-3 and IRF-7 by IKKi/{epsilon} and Tank-binding kinase-1 (TBK-1) is a prerequisite of IFN induction.
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PMID: 17502370, 16979567, 16932750
TLR- and retinoic acid inducible gene-I (RIG-I)-mediated phosphorylation of IRF-3 and IRF-7 by IKKi/{epsilon} and Tank-binding kinase-1 (TBK-1) is a prerequisite of IFN induction.
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PMID: 17502370, 16979567, 16932750
TLR- and retinoic acid inducible gene-I (RIG-I)-mediated phosphorylation of IRF-3 and IRF-7 by IKKi/{epsilon} and Tank-binding kinase-1 (TBK-1) is a prerequisite of IFN induction.
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PMID: 17502370, 16979567, 16932750
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PMID: 17502370, 12374802, 12738767
IRF-1, -2, and -7 are acetylated by histone acetylases GCN/PCAF and CBP/p300.</csml:comment>
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PMID: 17502370, 12374802, 12738767
IRF-1, -2, and -7 are acetylated by histone acetylases GCN/PCAF and CBP/p300.
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PMID: 17502370, 12374802, 12738767
IRF-1, -2, and -7 are acetylated by histone acetylases GCN/PCAF and CBP/p300.
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PMID: 17502370, 12374802, 12738767
IRF-1, -2, and -7 are acetylated by histone acetylases GCN/PCAF and CBP/p300.
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PMID: 17502370, 12374802, 12738767
IRF-1, -2, and -7 are acetylated by histone acetylases GCN/PCAF and CBP/p300.

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PMID: 17502370, 12374802, 12738767
IRF-1, -2, and -7 are acetylated by histone acetylases GCN/PCAF and CBP/p300.
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PMID: 17502370, 12374802, 12738767
IRF-1, -2, and -7 are acetylated by histone acetylases GCN/PCAF and CBP/p300.
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PMID: 17502370, 12374802, 12738767
IRF-1, -2, and -7 are acetylated by histone acetylases GCN/PCAF and CBP/p300.
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PMID: 17502370, 12374802, 12738767
IRF-1, -2, and -7 are acetylated by histone acetylases GCN/PCAF and CBP/p300.
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PMID: 17502370, 16699525
The peptidylprolyl isomerase Pin1 interacts with IRF-3 and changes the isomerization status in a phosphorylation-dependent manner, leading to rapid destabilization of IRF-3.</csml:comment>
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PMID: 17502370, 16484229
In a separate study, TRAF6 was shown to associate with IRF-8 in TLR-stimulated macrophages, consistent with the involvement of IRF-8 in ubiquitination-coupled transcription.</csml:comment>
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PMID: 17502370, 16484229
In a separate study, TRAF6 was shown to associate with IRF-8 in TLR-stimulated macrophages, consistent with the involvement of IRF-8 in ubiquitination-coupled transcription.
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PMID: 17502370, 15361868
IRF-7 is ubiquitinated upon TLR stimulation through an E3 ubiquitin ligase, TRAF6.</csml:comment>
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PMID: 17502370, 11846985
This growth regulation is relevant to CML in humans, where IRF-8 expression is down-regulated by the Bcr/Abl oncoprotein resulting in abnormal growth promotion.</csml:comment>
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