ライフサイエンスコーパス: IRF-7

1 ith cellular interferon-regulatory factor 7 (IRF-7).

2 xpression of interferon regulatory factor 7 (IRF-7).

3 e of degradation of IFN regulatory factor 7 (IRF-7).

4 transactivation and that repression involves IRF-7.

5 ty of a constitutively active mutant form of IRF-7.

6 had no effect on the nuclear localization of IRF-7.

7 ivation of IFN regulatory factor (IRF)-3 and IRF-7.

8 of IRF-3, and it regulates the expression of IRF-7.

9 promoters via its interaction with IRF-3 and IRF-7.

10 or on genes controlled by cellular IRF-3 and IRF-7.

11 n LMP-1 and TRAFs abolished the induction of IRF-7.

12 (LMP-DM), the LMP-1 mutant failed to induce IRF-7.

13 p65 plus p50) could induce the expression of IRF-7.

14 n, NF-kappaB is involved in the induction of IRF-7.

15 f interferon regulatory factor 3 (IRF-3) and IRF-7.

16 LMP-1 independently induce the expression of IRF-7.

17 TRAFs) is needed to induce the expression of IRF-7.

18 , a modifier of chromatin structure, induces IRF-7.

19 ypes in human cells required the presence of IRF-7.

20 AR-2 are also important for the induction of IRF-7.

21 tent with the ability of IFN-alpha to induce IRF-7.

22 phosphorylation and nuclear translocation of IRF-7.

23 isordered in apo IRF-3 but is ordered in apo IRF-7.

24 RF45 interacts with the inhibitory domain of IRF-7.

25 nderlying the ORF45-mediated inactivation of IRF-7.

26 tners, including their substrates, IRF-3 and IRF-7.

27 dsRNA-activated signaling events upstream of IRF-7.

28 ivity of the transcription factors IRF-3 and IRF-7.

29 erferon production by blocking activation of IRF-7.

30 on, the constitutively active IRF-3 (5D) and IRF-7 (2D) mutants activate the endogenous IFNA genes in

31 n the expression of IFN regulatory factor 7 (IRF-7), a strong transactivator of the IFN-alpha promote

32 together, these data indicate that IRF-5 and IRF-7 act primarily as transcriptional activators and th

33 This analysis shows that IRF-5 and IRF-7 activate a broad profile of heterologous genes enc

34 TRIF-induced IRF-3 and IRF-7 activation was mediated by TBK1 and its downstream

35 IRF-7 activity in cell lines during cytolytic viral repl

36 e interference with Smad3 function decreased IRF-7 activity.

37 promoter can be activated by either IRF-3 or IRF-7 alone, whereas the P31 element of the interferon-b

38 and reovirus-induced expression of IFN-beta, IRF-7 (an interferon-stimulated gene [ISG] that further

39 lar effectors, the Smads, on the function of IRF-7, an essential transcription factor for IFN-alpha a

40 iac fibroblasts but equivalent expression of IRF-7 and 561 in the two cell types (though fold inducti

41 he two cell types (though fold induction for IRF-7 and 561 was higher in fibroblasts than in myocytes

42 LMP-1 both induces the expression of IRF-7 and activates the IRF-7 protein by phosphorylation

43 Both endogenous and transiently expressed IRF-7 and EBV BZLF-1 proteins physically associate in ce

44 follows: LMP-1 stimulates the expression of IRF-7 and facilitates its phosphorylation and nuclear tr

45 a dominant-negative mutant of both IRF-3 and IRF-7 and inhibited virus-mediated transcriptional activ

46 tegument protein of virions, interacts with IRF-7 and inhibits virus-mediated type I interferon indu

47 The binding of recombinant IRF-7 and IRF-3 to these VREs correlated with their tran

48 we demonstrate that TRIF interacts with both IRF-7 and IRF-3.

49 ression but impairs nuclear translocation of IRF-7 and its downstream molecules.

50 The induction of Tap-2 by IRF-7 and LMP-1 may have an important implication for th

51 c-Jun, interferon regulatory factor (IRF)-3, IRF-7 and NF-kappaB, and the coactivators p300/CBP play

52 ) expressed in type III latency might induce IRF-7 and repress Qp.

53 /-) mice post-DENV infection, whereas in the Irf-7(-/-) and Irf-3(-/-)7(-/-) mice, significantly low

54 xpression of interferon regulatory factor 7 (IRF-7) and activates IRF-7 protein by phosphorylation an

55 teracts with interferon regulatory factor 7 (IRF-7) and inhibits virus-induced type I interferon prod

56 xpressed less interferon regulator factor 7 (IRF-7) and produced significantly less IFN-alpha upon To

57 erferon regulatory factor 3 and 7 (IRF-3 and IRF-7) and STAT-1, suggesting that neuronal maturation m

58 virus, while both viruses activate IRF-3 and IRF-7, and 2) NDV infection of IRF-5-overexpressing cell

59 Basal IFN-beta, IRF-7, and 561 expression was higher in cardiac myocytes

60 e IFNA promoters increases binding of IRF-3, IRF-7, and acetylated histone H3 to this promoter region

61 dominant protective role for MAVS, IRF-3 and IRF-7, and IFNAR in restricting OROV infection and tissu

62 ression impairs IKKepsilon-IRF-3, IKKepsilon-IRF-7, and IKKepsilon-IPS-1 interactions.

63 with nuclear translocation of IRF-1, IRF-3, IRF-7, and NF-kappaB p65.

64 ivates interferon regulatory factor (IRF)-3, IRF-7, and NF-kappaB-dependent signaling pathways.

65 ructure of the DNA-binding domains of IRF-3, IRF-7, and NFkappaB, bound to one half of the enhancer,

66 n enhanceosome containing ATF-2/c-Jun, IRF-3/IRF-7, and NFkappaB.

67 gene is robustly activated only when IRF-3, IRF-7, and the p300/CBP coactivators are all present.

68 ar interferon regulatory factor (IRF) IRF-3, IRF-7, and the transcriptional co-activator CBP/p300.

69 as the 2'5'-oligoadenylate synthetase, MX1, IRF-7, and toll-like receptor TLR-7 genes was lower in p

70 NF-kappa B (p50/p65), ATF-2/c-jun, IRF-3 and IRF-7, architectural protein HMGI(Y), and the coactivato

71 However, both IRF-3 and IRF-7 are critical for the production of type I and type

72 In this study, we demonstrate that IRF-3 and IRF-7 are functionally redundant, but lack of both facto

73 porter gene expression but IRF-1, IRF-3, and IRF-7 are more potent activators of the H4 promoter than

74 onse; only the combined actions of IRF-3 and IRF-7 are necessary for efficient control of early DENV

75 ly, these results demonstrate that IRF-3 and IRF-7 are redundant, albeit IRF-7 plays a more important

76 Interferon regulatory factors IRF-3 and IRF-7 are transcription factors essential in the activat

77 The identification of IRF-7 as a key regulator in monocyte differentiation sug

78 These data point to the role of IRF-7 as a secondary mediator of LMP-1-activated signal

79 3 as an adjuvant than for immunizations with IRF-7 as an adjuvant.

80 ear interferon regulatory factor (IRF)-3 and IRF-7 as well as IRF-1 bind to IFNA1 virus-responsive el

81 m regulatory transcription factors (IRF-3 or IRF-7), beta interferon (IFN-beta), or the receptor for

82 pitation strongly suggest that the IRF-3 and IRF-7 bind to IFNA1 promoter as a dimer.

83 As a correlate, a deficiency of IRF-7 blunted the systemic type I IFN response in mice.

84 Maximal synergy required IRF-3 and IRF-7 but not IRF-1, and was strongly dependent on the p

85 s that ectopic expression of either IRF-3 or IRF-7, but not IRF-1, was sufficient to allow virus-depe

86 IRF-7 interacted with Smads, and IRF-7, but not IRF-3, cooperated with Smad3 to activate

87 te the intrinsic transcriptional activity of IRF-7, but they are also indispensable for its ability t

88 Negative regulation of IRF-7 by BZLF-1 required the activation domain but not t

89 mutants of TRAFs inhibited the induction of IRF-7 by CTAR-1.

90 ssion of BZLF-1 also inhibited activation of IRF-7 by double-stranded RNA, as well as the activity of

91 amate efficiently inhibited the induction of IRF-7 by HSV or LPS, and also down-regulated the constit

92 The induction of IRF-7 by LMP-1 may be relevant to the silencing of Qp in

93 aB (sr-IkappaB) could block the induction of IRF-7 by LMP-1, and overexpression of NF-kappaB (p65 plu

94 Whether silencing of IRF-7 by methylation is instrumental for the process of

95 egulation of the transactivation activity of IRF-7 by Smad3, and dominant-negative interference with

96 Also, LMP-DM blocked the induction of IRF-7 by wild-type LMP-1.

97 sults indicate that IRF-1, IRF-2, IRF-3, and IRF-7 can all regulate histone H4 gene expression.

98 Also, IRF-7 can bind to the Tap-2 promoter under physiological

99 erived from Qp only in type I cells in which IRF-7 could be induced.

100 endogenous Tap-2, and ectopic expression of IRF-7 could enhance the induction.

101 nclusive of IFN-stimulated genes (STAT-1 and IRF-7), cytokines, chemokines, and innate immune effecto

102 ave solved the X-ray structures of IRF-3 and IRF-7 DBDs in the absence of DNA.

103 IRF-7 deficiency exacerbates arthritis and replacement t

104 on by Smad3, the transcriptional activity of IRF-7 depended on and was regulated by TGF-beta signalin

105 However, IRF-7-dependent activity of the IFN-alpha4, IFN-beta, an

106 's antiviral activity involves regulation of IRF-7-dependent production of IFN-alpha subtypes and con

107 alpha response against WNV occurs through an IRF-7-dependent transcriptional signal.

108 The stability of loop L1 in IRF-7 derives from a unique combination of hydrophobic r

109 vitro methylation of IRF-7 promoter silenced IRF-7 directed expression of luciferase gene in HeLa cel

110 tion, and a constitutively active variant of IRF-7 displayed normal activity in Fadd(-/-) murine embr

111 The X-ray structures of IRF-3 and IRF-7 DNA binding domains (DBDs) bound to IFN-beta promo

112 at the same conserved amino acid residue in IRF-7 drastically reduced its ability to bind to DNA and

113 llular genes that are modulated by IRF-5 and IRF-7 during the innate response to viral infection.

114 An appreciable amount of the IRF-7 expressed in lymphoma cells was localized in the n

115 uclear proteins from infected and uninfected IRF-7 expressing 2FTGH cells formed multiple DNA-protein

116 ubtype, while IFNA1 was primarily induced in IRF-7 expressing cells.

117 IRF-7-expressing NIH 3T3 cells formed tumors in athymic

118 Here we report the stimulation of IRF-7 expression by 12-O-tetradecanoylphorbol-13-acetate

119 We report the induction of IRF-7 expression by 12-O-tetradecanoylphorbol-13-acetate

120 bone marrow chimeras indicated that IRF-3 or IRF-7 expression in either hematopoietic or nonhemotopoi

121 ecently reported high constitutive levels of IRF-7 expression in PDC as compared with other PBMC.

122 availability of high constitutive levels of IRF-7 expression in PDC, and suggests an activation requ

123 o the nucleus was observed beginning at 8 h, IRF-7 expression was detected by 12 h, but IRF-1 express

124 Furthermore, IRF-7 expression was restricted in the HCV replicon cell

125 dependent on interferon regulatory factor 7 (IRF-7) expression but not on IRF-3 expression.

126 -3 dependent activation, but does not affect IRF-7 function.

127 mer and is required for the induction of the IRF-7 gene by TPA and TNFalpha.

128 In addition, we report stimulation of IRF-7 gene expression by topoisomerase II (TOPII) inhibi

129 his was associated with the up-regulation of IRF-7 gene expression, a known positive feedback molecul

130 This suggests that the IRF-7 gene is localized in the condensed area of the chr

131 mine the factors that regulate expression of IRF-7 gene, as well as its inducibility by type I IFNs,

132 of acetylated histone 3 with the promoter of IRF-7 gene, indicating that TOPII-mediated changes in ch

133 e gene in HeLa cells that express endogenous IRF-7 gene.

134 d the promoter and first intron of the human IRF-7 gene.

135 iments, IRF-3 had good activity for T cells, IRF-7 had good activity for both antibody and T cells, a

136 Thus, IRF-7 has oncogenic properties and, along with LMP-1, ma

137 eron regulatory factor 1 (IRF-1), IRF-3, and IRF-7 have been tested as genetic adjuvants for influenz

138 e regulatory transcription factors IRF-3 and IRF-7, have key protective roles during OROV infection.

139 The formation of the IRF-5/IRF-7 heterodimer is dependent on IRF-7 phosphorylation,

140 derlying the formation and function of IRF-5/IRF-7 heterodimers in infected cells.

141 tion domain revealed that formation of IRF-5/IRF-7 heterodimers occurs through the amino terminus res

142 he previously observed lack of expression of IRF-7 in 2fTGH fibrosarcoma cell line, correlated with h

143 examine the effect of genetic deficiency of IRF-7 in a passive K/BxN serum-transfer model of arthrit

144 ted with a marked depletion of IRF-3 but not IRF-7 in HIV-1-infected cells, which supported robust vi

145 e roles of IFN regulatory factor (IRF)-3 and IRF-7 in innate antiviral immunity against dengue virus

146 differentiation suggests a novel function of IRF-7 in innate immunity.

147 In this paper, the involvement of IRF-7 in monocyte differentiation was examined in U937,

148 own-regulated the constitutive expression of IRF-7 in PDC and blocked the HSV-induced production of I

149 th LPS and HSV up-regulate the expression of IRF-7 in PDC, and that this enhancement of IRF-7 is depe

150 ur data highlight a pivotal role of CCL7 and IRF-7 in RV-induced inflammation and IFN responses and l

151 helices and sheets to the autoinhibition of IRF-7 in the absence of viral signal.

152 NB genes and can replace the requirement for IRF-7 in the induction of IFNA genes.

153 Given the significance of IRF-7 in the induction of immune responses, many viruses

154 idly induced independently of both IRF-3 and IRF-7 in the Irf-3(-/-)7(-/-) mice with DENV infection.

155 ylation is inhibited and the accumulation of IRF-7 in the nucleus in response to viral infection is b

156 First, we detected significant levels of IRF-7 in the nucleus, as well as in the cytoplasm, of ce

157 and that LMP-1 stimulates the expression of IRF-7 in type III latency in which Qp is inactive.

158 Cotransfection of HA with IRF-3 and IRF-7 increased CD4 T-cell responses by 2- to 4-fold and

159 Interestingly, overexpression of IRF-7 increased the otherwise weak binding of both IRF-3

160 rly DENV infection; and the late, IRF-3- and IRF-7-independent pathway contributes to anti-DENV immun

161 t3, and Mx2 can be induced via an IRF-3- and IRF-7-independent pathway that does not involve IFN-gamm

162 anism of HCV action on IFN-alpha showed that IRF-7-induced IFN-alpha promoter activation was inhibite

163 ranscriptional activators and that IRF-5-and IRF-7-induced innate antiviral response results in a bro

164 le in infected BJAB/IRF-5 cells, whereas the IRF-7-induced transcripts were enriched for the group of

165 ses, through interferon regulatory factor 7 (IRF-7) induction.

166 The most striking feature in the IRF-7 inhibitory domain is two alpha-helices H3 and H4 t

167 IRF-7 interacted with Smads, and IRF-7, but not IRF-3, c

168 Furthermore, we find that IRF-7 interacts with four distinct regions of p300/CBP.

169 amma-interferon-activated sequence (GAS) and IRF-7 interferon-stimulated responsive element (ISRE).

170 recently determined that, besides IRF-3 and IRF-7, IRF-5 serves as a direct transducer of virus-medi

171 These studies suggest that IRF-7 is a critical determinant for the induction of IFN

172 tio between the relative levels of IRF-3 and IRF-7 is a critical determinant for the induction of the

173 In addition, we have found that human IRF-7 is a stable protein, and sodium butyrate, a modifi

174 IRF-7 is a transcription regulator that is responsible f

175 The mechanism by which IRF-7 is activated and cooperates with other transcripti

176 Expression of IRF-7 is associated with EBV type III latency, where Qp

177 f IRF-7 in PDC, and that this enhancement of IRF-7 is dependent on NF-kappa B activation.

178 Here we report that the expression of IRF-7 is increased in EBV-immortalized B lymphocytes com

179 The interaction between IRF-5 and IRF-7 is not cooperative and results in a repression rat

180 ition, we demonstrate that overexpression of IRF-7 is sufficient to trigger monocyte differentiation

181 IRF-7 is the master regulator of type I interferon-depen

182 Interferon regulatory factor 7 (IRF-7) is expressed predominantly in lymphoid tissues an

183 Interferon regulatory factor 7 (IRF-7) is implicated in the regulation of Epstein-Barr v

184 Although IFN regulatory factor-7 (IRF-7) is known to play an essential role in virus-activ

185 shown previously that IRF-5, like IRF-3 and IRF-7, is a direct transducer of virus-mediated signalin

186 and dendritic cells, as well as of IRF-3 and IRF-7, is critical for innate immune responses to NoV in

187 A similar switch in IRF-7 isoforms also occurred in the brains of maturing C

188 duced STAT binding to both the IRF-1 GAS and IRF-7 ISRE by inhibition of inducible STAT1 and STAT3 ty

189 whereas STAT1, STAT2, IRF-1, and IRF-9 bind IRF-7 ISRE.

190 e binding of ORF45 to the critical domain of IRF-7 leads to a hypothesis that ORF45 may maintain the

191 expression by interferon regulatory factor (IRF-7) led to the inhibition of HCV replicon expression,

192 Cross-linking did not affect IRF-7 levels in PDC, however, cross-linking BDCA-2, BDCA

193 Here we show that activation of IRF-7, like that of IRF-3, is dependent on modifications

194 acrophage- and synoviocyte-specific roles of IRF-7 likely contribute to the increased arthritis.

195 Neutralizing CCL7 or inhibiting IRF-7 limited neutrophil and macrophage influx and IFN r

196 ta BL cells, in which LMP-1 could not induce IRF-7, LMP-1 could not induce Tap-2.

197 ls, in which LMP-1 induces the expression of IRF-7, LMP-1 induced endogenous Tap-2, and ectopic expre

198 Thus, IRF-7 may mediate repression of Qp by LMP-1.

199 nsequently, vIRF-3 stimulates the IRF-3- and IRF-7-mediated activation of type I interferon (IFNA and

200 lpha receptor antibody could partially block IRF-7-mediated HCV replicon inhibition.

201 rscore a role of TGF-beta/Smad3 signaling in IRF-7-mediated induction of IFN-beta expression.

202 eptor signaling and Smad3 function decreased IRF-7-mediated transcription.

203 uclear translocation, and then the activated IRF-7 mediates the activation of the cellular Tap-2 gene

204 itis severity was significantly increased in IRF-7(-/-) mice compared with wild-type (WT) mice.

205 IRF-7(-/-) mice injected with replacement IFNbeta had a

206 n of fibroblast-like synoviocytes (FLS) from IRF-7(-/-) mice resulted in increased induction of proin

207 Compared to congenic wild-type mice, IRF-7(-/-) mice showed increased lethality after WNV inf

208 In contrast, peritoneal macrophages from IRF-7(-/-) mice showed significantly less induction of I

209 Passive-transfer arthritis was induced in IRF-7(-/-) mice, and additional groups were treated with

210 Poly(I-C) treatment diminished arthritis in IRF-7(-/-) mice, restored synovial IFNbeta gene expressi

211 evaluated IFN induction and virus control in IRF-7(-/-) mice.

212 IRF-7 might play an antiinflammatory role in passive-tra

213 egulatory factors (IRF) IRF-1, IRF-3, IRF-5, IRF-7, mitochondrial antiviral signaling molecule [MAVS]

214 The number of IRF-5- and IRF-7-modulated genes was significantly higher in infect

215 to a hypothesis that ORF45 may maintain the IRF-7 molecule in the closed form and prevent it from be

216 ctor 7 (IRF-7), revealed an increase in both IRF-7 mRNA and protein in Dcp2(beta/beta) cells.

217 enuating the antiviral response by promoting IRF-7 mRNA degradation.

218 RNA, suggesting that Dcp2 normally modulates IRF-7 mRNA stability.

219 pecificity of Dcp2 in targeting the decay of IRF-7 mRNA suggest that Dcp2 may negatively contribute t

220 IRF-7 mRNA was induced under conditions of IFN-alpha/bet

221 Importantly, the increase in IRF-7 mRNA within the background of reduced Dcp2 levels

222 els was attributed to a stabilization of the IRF-7 mRNA, suggesting that Dcp2 normally modulates IRF-

223 ited in cells expressing a dominant negative IRF-7 mutant, as evidenced by decreased expression of tw

224 hat cellular interferon regulatory factor 7 (IRF-7) negatively regulates this process by competing wi

225 the transcription factors ATF-2/c-Jun, IRF-3/IRF-7, NF-kappaB and HMGI(Y).

226 nscription factor (ATF)-2 (nt -571 to -568), IRF-7 (nt -533 to-525), and NF-kappaB (nt -215 to -209)

227 controls type I IFN production by regulating IRF-7 nuclear translocation in human pDCs and could serv

228 Interestingly, HCV infection blocked IRF-7 nuclear translocation upon poly(I-C) or IFN-alpha

229 tion, we found that nuclear translocation of IRF-7 occurred rapidly in response to HSV stimulation, b

230 gnaling, the transcription factors IRF-3 and IRF-7, or IFNAR than in wild-type (WT) cells.

231 phosphorylation and nuclear translocation of IRF-7, ORF45 efficiently inhibits the activation of inte

232 IRF-1/IRF-3 and IRF-1/IRF-7 pairs each mediate the highest levels of site II-d

233 Ectopic overexpression of IRF-7 partially rescued dsRNA responsiveness and IFN-alp

234 induced by IFN-alpha, especially through the IRF-7 pathway.

235 ated type I interferon induction by blocking IRF-7 phosphorylation and nuclear translocation.

236 In consequence, IRF-7 phosphorylation is inhibited and the accumulation

237 the IRF-5/IRF-7 heterodimer is dependent on IRF-7 phosphorylation, as shown by the glutathione S-tra

238 Two of these factors, IRF-5 and IRF-7, play a critical role in the induction of interfer

239 e that IRF-3 and IRF-7 are redundant, albeit IRF-7 plays a more important role than IRF-3 in inducing

240 Interferon regulatory factor 7 (IRF-7) plays an important role in innate immunity, where

241 strongly affected by promoter context, with IRF-7 preferentially being recruited to the natural inte

242 e reduced and viral titers were increased in IRF-7(-/-) primary macrophages, fibroblasts, dendritic c

243 IRF-7 produced by undifferentiated AP-7 neurons was excl

244 Furthermore, IRF-7 promoted the anchorage-independent growth of NIH 3

245 Previously, we characterized human IRF-7 promoter and showed that an interferon-stimulated

246 In vitro methylation of IRF-7 promoter silenced IRF-7 directed expression of luc

247 ermethylation of the CpG island in the human IRF-7 promoter.

248 es the expression of IRF-7 and activates the IRF-7 protein by phosphorylation and nuclear translocati

249 on regulatory factor 7 (IRF-7) and activates IRF-7 protein by phosphorylation and nuclear translocati

250 We initiated these studies by examining IRF-7 protein expression in vivo in lesions of hairy leu

251 ral replication was examined by assay of the IRF-7-responsive promoters, IFN-alpha4, IFN-beta, and Ta

252 IRF-3 and IRF-7 restrict MNV replication in both cultured macropha

253 mice, deletion of IFNAR, MAVS, or IRF-3 and IRF-7 resulted in uncontrolled OROV replication, hypercy

254 Activation of IRF-7 results from a conformational change triggered by

255 Here, detailed analysis of the expression of IRF-7 revealed that it is associated with the expression

256 anscription factor, IFN regulatory factor 7 (IRF-7), revealed an increase in both IRF-7 mRNA and prot

257 Two of these proteins, IRF-3 and IRF-7, serve as direct transducers of virus-mediated sig

258 LMP-1 and IRF-7 showed additive effects on the growth transformati

259 -3, SMAD-3, ATF-2, or NF-kappaB, but not the IRF-7, sites significantly reduced promoter activity.

260 The IRF-7-Smad3 cooperativity resulted from the regulation o

261 IRF-7 small interfering RNA primarily suppressed IFN-alp

262 Furthermore, LMP-1 and IRF-7A but not other IRF-7 splicing variants could activate endogenous Tap-2.

263 he amplification of the IFN response such as IRF-7, STAT1, STAT2, IFN-beta, and the IFNARs in vitro a

264 Although IRF-5 and IRF-7 stimulated a large number of common genes, a disti

265 Reconstitution of IRF-7 synthesis in these cells resulted, upon virus infe

266 their roles we employed anti-CCL7 Abs and an IRF-7-targeting small interfering RNA in vivo.

267 ly EBV protein BZLF-1 counteracts effects of IRF-7 that are central to host antiviral responses.

268 PDC, and suggests an activation required for IRF-7 that contributes to IFN-alpha production in virus-

269 d that vIRF-3 associates with both IRF-3 and IRF-7 through its C-terminal region.

270 vation of IFN-alpha4, IFN-beta, and Tap-2 by IRF-7 through the medium of BZLF-1 as a negative regulat

271 Furthermore, binding of IRF-3 and IRF-7 to IFNA VRE is associated with the presence of ace

272 the otherwise weak binding of both IRF-3 and IRF-7 to IFNA2 VRE.

273 ered together with virus-activated IRF-3 and IRF-7 to the IFNA1 promoter.

274 of lytic gene expression through binding of IRF-7 to the lytic viral gene promoter.

275 feron regulatory factors (IRF)-1, IRF-3, and IRF-7 to the RANTES independently of myeloid differentia

276 CD4, but not CD123, inhibited the ability of IRF-7 to translocate to the nucleus.

277 al contributions of IRF-1, IRF-2, IRF-3, and IRF-7 using transient transfection assays with H4 promot

278 lls selectively activated IFNA1 VRE, whereas IRF-7 was able to activate IFNA1, A2, and A4.

279 Interestingly, redundancy of IRF-3 and IRF-7 was age dependent, as neonatal animals lacking eit

280 The expression of IRF-7 was detected in 19 of 27 specimens of primary lymp

281 ly, IRF-3 and IRF-7, where the expression of IRF-7 was found to be indispensable for the induction of

282 IRF-7 was identified as the only gene exclusively induce

283 However, nuclear translocation of IRF-7 was impaired following HCV infection.

284 IRF-7 was phosphorylated and predominantly localized in

285 The association between LMP-1 and IRF-7 was statistically highly significant for these spe

286 Moreover, the activity of IRF-3 and IRF-7 was strongly affected by promoter context, with IR

287 Interferon (IFN) regulatory factor 7 (IRF-7) was identified first as a negative regulator of Q

288 as well as Ab to the IFN regulatory factor, IRF-7, was used in intracellular flow cytometry to eluci

289 two unique DNA-protein complexes containing IRF-7 were detected.

290 infected BJAB cells overexpressing IRF-5 or IRF-7 were determined by using oligonucleotide arrays wi

291 (IRF-3), and interferon regulatory factor 7 (IRF-7) were not required.

292 oth IFN regulatory factor 3 and 7 (IRF-3 and IRF-7) were suggested to play positive roles in these ge

293 ription factors of the IRF family, IRF-3 and IRF-7, were shown to play a role in their activation.

294 FN regulatory factor (IRF) family, IRF-3 and IRF-7, where the expression of IRF-7 was found to be ind

295 nd activates interferon regulatory factor 7 (IRF-7), which is essential for production of alpha/beta

296 Addition of IRF-7, which complements the defect in Akata cells, coul

297 results suggest that by targeting IRF-3 and IRF-7, which play a critical role in the activation of a

298 gulates IFN-alpha production at the level of IRF-7, while the decrease in IFN-alpha production after

299 he requisite interferon regulatory factor 7 (IRF-7), whose gene expression in turn was limited as a c

300 how that the transcription factors IRF-3 and IRF-7 work in concert to initiate unique and overlapping