ライフサイエンスコーパス: ISGF3

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 activation of IFN-stimulated gene factor 3 (ISGF3).

6 K2, as well of IFN-stimulated gene factor 3 (ISGF3).

7 ation is required for complete activation of ISGF3.

8 amma, forms the transcription factor complex ISGF3.

9 rferon (IFN)-regulated transcription factor, ISGF3.

10 eric transcription complex with Stat1 termed ISGF3.

11 leus and associate on the DNA target site as ISGF3.

12 nteraction, implying contact that stabilizes ISGF3.

13 ediated by both STAT1-STAT2 heterodimers and ISGF3.

14 d 2 and enhancing the DNA-binding ability of ISGF3.

15 her the formation or nuclear localization of ISGF3.

16 tivating the type I interferon (IFN)-induced ISGF3.

17 the IFN-stimulated gene transcription factor ISGF3.

18 ch is known to mediate the nuclear import of ISGF3.

19 r of transcription 1 (STAT1), a component of ISGF3.

20 tial transcriptional activation function for ISGF3.

21 he assembly of IFN-stimulated gene factor 3 (ISGF3), a multimeric transcriptional activation complex

22 tivated via IFN beta-stimulated formation of ISGF3, a heterotrimeric DNA binding complex consisting o

23 TAT1 is impaired, with subsequent failure of ISGF3 accumulation in the nucleus.

24 ormation of complexes consisting of Stat1 or ISGF3 and DNA sequences containing the interferon-stimul

25 ISGF3 and GAF bind specifically to unique regulatory DNA

26 gamma, as assessed by STAT1 phosphorylation, ISGF3 and GAF-mediated binding to IFN-stimulated respons

27 apid activation of the transcription factors ISGF3 and GAF.

28 sary for maintaining prolonged activation of ISGF3 and of Janus kinases, an activity that was blocked

29 C-like properties is due to high levels of U-ISGF3 and that treatment with IFN-beta reduces CSC prope

30 n indispensable component of a heterotrimer (ISGF3) and a STAT1 homodimer (GAF) that function as tran

31 vation, interferon-stimulated gene factor 3 (ISGF3) and c-sis-inducible factor (SIF) complex formatio

32 n binds interferon-stimulated gene factor 3 (ISGF3) and confers the response to interferon.

33 mplex known as IFN-stimulated gene factor 3 (ISGF3) and the subsequent production of CXCL10 and addit

34 athways involving 1) IRF family proteins and ISGF3, and 2) STAT1.

35 Stat2 tyrosine phosphorylation, induction of ISGF3, and an antiviral effect always required the proxi

36 nd to both the IFN-stimulated gene factor 3 (ISGF3) as well as to IFN response factor 7 (IRF7).

37 Thus, ISGF3 assembly involves p48 functioning as an adaptor pr

38 IMP1) binds the ISRE sites and competes with ISGF3 binding in a virus inducible manner to inhibit Vip

39 s improves the ability to call enrichment of ISGF3 binding motifs from differential acetylation ChIP-

40 Most effector ISGs (81.1%) had at least one ISGF3 binding region proximal to the transcription start

41 Gs (24.3%) was associated with three or more ISGF3 binding regions.

42 In contrast, STAT1 recruitment to ISGF3 binding sites and type 1 interferon-dependent resp

43 duction of IFN-stimulated gene factor three (ISGF3) by IFN-alpha, is blocked by cPLA2 inhibitors in c

44 expressing wild-type STAT2 contain much less ISGF3 capable of binding to an interferon-stimulated res

45 th STAT1, STAT2, and IRF9, components of the ISGF3 complex activated downstream of IFN-alpha receptor

46 ) of both IRF9 and STAT2 is critical for the ISGF3 complex activation and its associated antiviral ge

47 ) in the Oas1a and Oas1b promoters bound the ISGF3 complex after type I IFN treatment.

48 s, we have demonstrated that this ISRE binds ISGF3 complex and IRF-1 from the extract of IFN-treated

49 NA immunoprecipitation assays identified the ISGF3 complex as the key regulator of Viperin gene expre

50 beta blocks the nuclear translocation of the ISGF3 complex by an unknown mechanism.

51 d into 5637 cells was sufficient to form the ISGF3 complex by IFN-alpha treatment, suggesting the def

52 Consequently, the ISGF3 complex formation and 561 gene induction were rest

53 infection does not degrade components of the ISGF3 complex or interfere with STAT1 or STAT2 nuclear t

54 y2 (IH2) domain, leading to formation of the ISGF3 complex that includes IRF9, STAT1, and STAT2.

55 osphorylated STAT1 and STAT2 and that of the ISGF3 complex were markedly reduced in IFN-beta-treated

56 suppressing the nuclear translocation of the ISGF3 complex, resulting in profound and systemic repres

57 responsiveness to IFN through binding of the ISGF3 complex.

58 elements without affecting formation of the ISGF3 complex.

59 via the interferon-stimulated gene factor 3 (ISGF3) complex consisting of STAT1, STAT2, and IRF9, IFN

60 rylation, which is involved in ISG factor 3 (ISGF3) complex formation and ISG expression.

61 induce interferon-stimulated gene factor 3 (ISGF3) complex formation in HUT78R cells.

62 binding of the IFN-stimulated gene factor 3 (ISGF3) complex to the ISRE.

63 nd IRF3 or the IFN-stimulated gene factor-3 (ISGF3) complex.

64 of the interferon stimulated gene factor 3 (ISGF3) complex.

65 ple of a nuclear localization signal for any ISGF3 component and assigns a second function to the IRF

66 N-beta or subjected to gene silencing of the ISGF3 component Stat1 exhibited decreased CXCL10 respons

67 The transcription factor ISGF3, comprised of IRF9 and tyrosine-phosphorylated STA

68 ISGF3 consists of Stat1, Stat2 and p48.

69 lpha response and is selectively involved in ISGF3-dependent gene activation.

70 Conversely, Sin3a is required for ISGF3-dependent gene transcription and for an efficient

71 Additionally, IFN-alpha induction of ISGF3-dependent genes involved in innate immunity (viper

72 ady-state increased expression of only the U-ISGF3-dependent proteins, with no sustained increase in

73 ses GAF-dependent transcription and promotes ISGF3-dependent transcription.

74 between transcription factors NF-kappaB and ISGF3 divides the task of transcription by recruiting an

75 , the tyrosine kinases Jak1 or Tyk2, nor the ISGF3 DNA-binding subunit, IFN regulatory factor 9 (IRF9

76 that DRIP150 binds to the mature, activated ISGF3-DNA complex and is recruited to target gene promot

77 interferon-stimulated gene factor 3 complex (ISGF3) does not bind to promoter elements of the affecte

78 orylated IFN-stimulated gene (ISG) factor 3 (ISGF3) drives acute deleterious responses to IFN-I, wher

79 t also signaling through antagonism with the ISGF3 effector function, revealing a novel facet of the

80 d for the initial opening of chromatin, with ISGF3 extending accessibility and promoting the depositi

81 cific inhibitor of p38, was found to inhibit ISGF3 formation but had no apparent effects on signal tr

82 The specificity of ISGF3 formation is therefore a result of the distinct na

83 d thus assembly of GAF, but does not disrupt ISGF3 formation.

84 able to block IFN-stimulated gene factor 3 (ISGF3) formation and inhibit the antiviral cytopathic ef

85 ible gene, and IFN-stimulated gene factor 3 (ISGF3) formation was normal in primary human urothelial

86 he related factor un-phosphorylated ISGF3 (U-ISGF3), formed by IFNbeta-induced high levels of IRF9 an

87 ulates IRF9 interactions with STATs for both ISGF3 function and nuclear export.

88 nal segment of Stat2, a domain essential for ISGF3 function.

89 other IRF proteins tested (IRF-1, IRF-2, and ISGF3-gamma) were detected in these cells.

90 nduction and antiviral activity, implicating ISGF3(II) formation as a significant component of the ce

91 factor 3 containing unphosphorylated STAT2 (ISGF3(II)) also plays a role in IFN-gamma-mediated antiv

92 Ns, IFN-gamma treatment induced formation of ISGF3(II).

93 pha treatment formed extremely low levels of ISGF3 in electrophoretic mobility shift assays in these

94 complex interferon-stimulated gene factor 3 (ISGF3) in response to interferon-alpha (IFN-alpha).

95 n mediate significant biological effects via ISGF3-independent pathways.

96 Here we determined the role of IFN-I-driven, ISGF3-independent signaling in regulating global gene ex

97 IFN-I can mediate ISG expression in MGCs via ISGF3-independent signaling pathways but with reduced ef

98 The U-ISGF3-induced anti-viral genes that show prolonged expre

99 accessory signaling pathway that supplements ISGF3/interferon-stimulated response element signaling f

100 s relies on activation of a protein complex, ISGF3, involving two signal transducers and activators o

101 While the transcription factor ISGF3 (IRF9 and tyrosine-phosphorylated STATs 1 and 2) d

102 ISGF3 is a unique STAT complex because it also contains

103 through interferon-stimulated gene factor 3 (ISGF3)] is surprisingly not essential for host defense a

104 uction and transcription activation complex, ISGF3, is assembled from three proteins, STAT1, STAT2, a

105 to be studied, the alpha-interferon-induced ISGF3, is composed of a Stat1:2 heterodimer and a weak D

106 oding p48, a subunit of transcription factor ISGF3, is transcriptionally induced by interferon gamma

107 onses to IFN-I, whereas unphosphorylated (U-)ISGF3, lacking tyrosine phosphorylation, drives essentia

108 This suggests that an extremely low ISGF3 level after IFN-alpha treatment may be due to low

109 readily converted to a constitutively active ISGF3-like activator by fusion with the C-terminal trans

110 FN beta weakly stimulates the assembly of an ISGF3-like complex that lacks Stat1, even though ISG54 m

111 In the present study, we show that ISGF3-mediated transcription is dependent on STAT2 inter

112 transcription is enhanced at the expense of ISGF3-mediated transcription, rendering cells less resis

113 ide the STAT2 interaction region, suppressed ISGF3-mediated transcriptional activity in a dominant-ne

114 Neither ISGF3 nor GAF bound DNA cooperatively in the STAT1F77A m

115 These results indicate that Nsp1beta blocks ISGF3 nuclear translocation by inducing KPNA1 degradatio

116 way of type I IFNs by blocking ISG factor 3 (ISGF3) nuclear translocation.

117 reveal how combinatorial logic gates of IRF1-ISGF3 or IRF1-GAF restrict immune epigenomic memory form

118 tat1 and does not impact on the formation of ISGF3 or SIF nuclear binding complexes.

119 Reporter activity mediated by ISGF3 or STAT1 homodimer was diminished by SB203580 and

120 tion of interferon-stimulated gene factor 3 (ISGF3) or an antiviral state.

121 lpha in human endothelial cells though a JAK-ISGF3 pathway under normoxic conditions, and that this r

122 , or depletion by GC-activated GR attenuated ISGF3 promoter occupancy, preinitiation complex assembly

123 sion of IRF9 (the DNA-binding component of U-ISGF3) reduced the migration of mesenchymal/CSCs.

124 es thus establish that NOD1 can activate the ISGF3 signaling pathway that is usually associated with

125 through tonic IFN-stimulated gene factor 3 (ISGF3) signaling, which leads to persistent expression o

126 ha) and interferon-stimulated gene factor 3 (ISGF3)-specific transcriptional activation in transient

127 ave dissected what constitutes IRF-specific, ISGF3-specific, or universal ISREs.

128 Type I IFNs can activate both the ISGF3 (STAT1:STAT2:IRF9) complex and STAT3, but with cel

129 omplex therefore acts as a context-dependent ISGF3/STAT3 transcriptional switch.

130 y elements, the DNA motifs, the occupancy of ISGF3 subunits (IRF9, STAT1, and STAT2) and other transc

131 IFN-alpha/beta-induced transcription complex ISGF3 such that the DNA-binding component of this comple

132 dies identify Viperin as a tightly regulated ISGF3 target gene, which is counter-regulated by PRDI-BF

133 The IRF9 hybrids are targeted to endogenous ISGF3 target loci and can activate their transcription.

134 IFN-dependent recruitment of DRIP130 to an ISGF3 target promoter and SRB10-STAT2 coprecipitation su

135 r dependent on the transcriptional activator ISGF3 that led to altered cytokine production, cell prol

136 duction pathway leading to activation of the ISGF3 transcription complex and subsequent antiviral res

137 tase (PTP) is required for activation of the ISGF3 transcription complex by IFNalpha/beta, but the sp

138 in mammalian cells induces formation of the ISGF3 transcription factor complex, which binds to inter

139 ese findings indicate that the IFN-activated ISGF3 transcription factor regulates transcription throu

140 ISGF3 transcriptional activity or to enhance ISGF3 transcription without binding STAT2, but only DRIP

141 heterotrimeric IFN-stimulated gene factor 3 (ISGF3) transcription complex for induction of IFN-stimul

142 bition, the heterotrimeric STAT1-STAT2-IRF9 (ISGF3) transcription complex, utilized the GR cofactor G

143 ound either to bind STAT2 without augmenting ISGF3 transcriptional activity or to enhance ISGF3 trans

144 bility to induce STAT1 and STAT2 activation, ISGF3 transcriptional complex formation, gene expression

145 l-specific, selective triggering of only the ISGF3 transcriptional program.

146 The transcription factor ISGF3 transduces interferon (IFN)-alpha signals and acti

147 phase, the related factor un-phosphorylated ISGF3 (U-ISGF3), formed by IFNbeta-induced high levels o

148 However, ISGF3 was generally needed to collaborate with IRF1, par

149 he activation of gamma-activating factor and ISGF3 was impaired only at early time points in the vari

150 factor interferon-stimulated gene factor 3 (ISGF3) was necessary but not sufficient for beta-R1 indu

151 otein, to form IFN-stimulated gene factor 3 (ISGF3), which binds to IFN-stimulated response elements

152 nent of interferon-stimulated gene factor 3 (ISGF3), which drives gene expression in response to IFN-

153 osphorylated IFN-stimulated gene factor 3 (U-ISGF3), which was previously linked to resistance to DNA

154 rimers (interferon-stimulated gene factor 3 [ISGF3]) with interferon regulatory factor 9 (IRF9) and t