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1 factor interferon-stimulated gene factor 3 (ISGF3).
2 ated the IFN-alpha-stimulated gene factor 3 (ISGF3).
3 iption factor, IFN-stimulated gene factor 3 (ISGF3).
4 inly driven by IFN-stimulated gene factor 3 (ISGF3).
5 K2, as well of IFN-stimulated gene factor 3 (ISGF3).
6 ation is required for complete activation of ISGF3.
7 amma, forms the transcription factor complex ISGF3.
8 rferon (IFN)-regulated transcription factor, ISGF3.
9 eric transcription complex with Stat1 termed ISGF3.
10 leus and associate on the DNA target site as ISGF3.
11 nteraction, implying contact that stabilizes ISGF3.
12 ediated by both STAT1-STAT2 heterodimers and ISGF3.
13 ch is known to mediate the nuclear import of ISGF3.
14 r of transcription 1 (STAT1), a component of ISGF3.
15 tial transcriptional activation function for ISGF3.
16 he assembly of IFN-stimulated gene factor 3 (ISGF3), a multimeric transcriptional activation complex
17 tivated via IFN beta-stimulated formation of ISGF3, a heterotrimeric DNA binding complex consisting o
19 ormation of complexes consisting of Stat1 or ISGF3 and DNA sequences containing the interferon-stimul
21 gamma, as assessed by STAT1 phosphorylation, ISGF3 and GAF-mediated binding to IFN-stimulated respons
23 sary for maintaining prolonged activation of ISGF3 and of Janus kinases, an activity that was blocked
24 C-like properties is due to high levels of U-ISGF3 and that treatment with IFN-beta reduces CSC prope
25 n indispensable component of a heterotrimer (ISGF3) and a STAT1 homodimer (GAF) that function as tran
26 vation, interferon-stimulated gene factor 3 (ISGF3) and c-sis-inducible factor (SIF) complex formatio
28 mplex known as IFN-stimulated gene factor 3 (ISGF3) and the subsequent production of CXCL10 and addit
30 Stat2 tyrosine phosphorylation, induction of ISGF3, and an antiviral effect always required the proxi
33 IMP1) binds the ISRE sites and competes with ISGF3 binding in a virus inducible manner to inhibit Vip
35 duction of IFN-stimulated gene factor three (ISGF3) by IFN-alpha, is blocked by cPLA2 inhibitors in c
36 expressing wild-type STAT2 contain much less ISGF3 capable of binding to an interferon-stimulated res
37 ) of both IRF9 and STAT2 is critical for the ISGF3 complex activation and its associated antiviral ge
38 s, we have demonstrated that this ISRE binds ISGF3 complex and IRF-1 from the extract of IFN-treated
39 NA immunoprecipitation assays identified the ISGF3 complex as the key regulator of Viperin gene expre
41 d into 5637 cells was sufficient to form the ISGF3 complex by IFN-alpha treatment, suggesting the def
43 infection does not degrade components of the ISGF3 complex or interfere with STAT1 or STAT2 nuclear t
45 osphorylated STAT1 and STAT2 and that of the ISGF3 complex were markedly reduced in IFN-beta-treated
48 via the interferon-stimulated gene factor 3 (ISGF3) complex consisting of STAT1, STAT2, and IRF9, IFN
54 ple of a nuclear localization signal for any ISGF3 component and assigns a second function to the IRF
55 N-beta or subjected to gene silencing of the ISGF3 component Stat1 exhibited decreased CXCL10 respons
61 ady-state increased expression of only the U-ISGF3-dependent proteins, with no sustained increase in
63 between transcription factors NF-kappaB and ISGF3 divides the task of transcription by recruiting an
64 , the tyrosine kinases Jak1 or Tyk2, nor the ISGF3 DNA-binding subunit, IFN regulatory factor 9 (IRF9
65 that DRIP150 binds to the mature, activated ISGF3-DNA complex and is recruited to target gene promot
66 interferon-stimulated gene factor 3 complex (ISGF3) does not bind to promoter elements of the affecte
67 t also signaling through antagonism with the ISGF3 effector function, revealing a novel facet of the
68 cific inhibitor of p38, was found to inhibit ISGF3 formation but had no apparent effects on signal tr
71 able to block IFN-stimulated gene factor 3 (ISGF3) formation and inhibit the antiviral cytopathic ef
72 ible gene, and IFN-stimulated gene factor 3 (ISGF3) formation was normal in primary human urothelial
73 he related factor un-phosphorylated ISGF3 (U-ISGF3), formed by IFNbeta-induced high levels of IRF9 an
77 nduction and antiviral activity, implicating ISGF3(II) formation as a significant component of the ce
78 factor 3 containing unphosphorylated STAT2 (ISGF3(II)) also plays a role in IFN-gamma-mediated antiv
80 pha treatment formed extremely low levels of ISGF3 in electrophoretic mobility shift assays in these
83 Here we determined the role of IFN-I-driven, ISGF3-independent signaling in regulating global gene ex
84 IFN-I can mediate ISG expression in MGCs via ISGF3-independent signaling pathways but with reduced ef
86 accessory signaling pathway that supplements ISGF3/interferon-stimulated response element signaling f
87 s relies on activation of a protein complex, ISGF3, involving two signal transducers and activators o
90 through interferon-stimulated gene factor 3 (ISGF3)] is surprisingly not essential for host defense a
91 uction and transcription activation complex, ISGF3, is assembled from three proteins, STAT1, STAT2, a
92 to be studied, the alpha-interferon-induced ISGF3, is composed of a Stat1:2 heterodimer and a weak D
93 oding p48, a subunit of transcription factor ISGF3, is transcriptionally induced by interferon gamma
95 readily converted to a constitutively active ISGF3-like activator by fusion with the C-terminal trans
96 FN beta weakly stimulates the assembly of an ISGF3-like complex that lacks Stat1, even though ISG54 m
98 transcription is enhanced at the expense of ISGF3-mediated transcription, rendering cells less resis
99 ide the STAT2 interaction region, suppressed ISGF3-mediated transcriptional activity in a dominant-ne
101 These results indicate that Nsp1beta blocks ISGF3 nuclear translocation by inducing KPNA1 degradatio
106 lpha in human endothelial cells though a JAK-ISGF3 pathway under normoxic conditions, and that this r
107 , or depletion by GC-activated GR attenuated ISGF3 promoter occupancy, preinitiation complex assembly
109 es thus establish that NOD1 can activate the ISGF3 signaling pathway that is usually associated with
110 through tonic IFN-stimulated gene factor 3 (ISGF3) signaling, which leads to persistent expression o
111 ha) and interferon-stimulated gene factor 3 (ISGF3)-specific transcriptional activation in transient
115 IFN-alpha/beta-induced transcription complex ISGF3 such that the DNA-binding component of this comple
116 dies identify Viperin as a tightly regulated ISGF3 target gene, which is counter-regulated by PRDI-BF
117 The IRF9 hybrids are targeted to endogenous ISGF3 target loci and can activate their transcription.
118 IFN-dependent recruitment of DRIP130 to an ISGF3 target promoter and SRB10-STAT2 coprecipitation su
119 r dependent on the transcriptional activator ISGF3 that led to altered cytokine production, cell prol
120 duction pathway leading to activation of the ISGF3 transcription complex and subsequent antiviral res
121 tase (PTP) is required for activation of the ISGF3 transcription complex by IFNalpha/beta, but the sp
122 ese findings indicate that the IFN-activated ISGF3 transcription factor regulates transcription throu
123 ISGF3 transcriptional activity or to enhance ISGF3 transcription without binding STAT2, but only DRIP
124 heterotrimeric IFN-stimulated gene factor 3 (ISGF3) transcription complex for induction of IFN-stimul
125 bition, the heterotrimeric STAT1-STAT2-IRF9 (ISGF3) transcription complex, utilized the GR cofactor G
126 ound either to bind STAT2 without augmenting ISGF3 transcriptional activity or to enhance ISGF3 trans
127 bility to induce STAT1 and STAT2 activation, ISGF3 transcriptional complex formation, gene expression
130 phase, the related factor un-phosphorylated ISGF3 (U-ISGF3), formed by IFNbeta-induced high levels o
131 he activation of gamma-activating factor and ISGF3 was impaired only at early time points in the vari
132 factor interferon-stimulated gene factor 3 (ISGF3) was necessary but not sufficient for beta-R1 indu
133 otein, to form IFN-stimulated gene factor 3 (ISGF3), which binds to IFN-stimulated response elements
134 osphorylated IFN-stimulated gene factor 3 (U-ISGF3), which was previously linked to resistance to DNA
135 rimers (interferon-stimulated gene factor 3 [ISGF3]) with interferon regulatory factor 9 (IRF9) and t
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