ライフサイエンスコーパス: IRF

1 IRF occurred in 31% of the 896 patients meeting eligibil

2 IRF was defined as >/=20% increase and worsening renal f

3 IRF-1 contributed significantly to I/R injury because IR

4 IRF-1 expression limited CHIKV-induced foot swelling in

5 IRF-1 restricts the replication of diverse viruses; howe

6 IRF-1 was induced in liver grafts immediately after repe

7 IRF-1-KO livers had significantly reduced NK, NKT, and C

8 IRF-3(-/-) and select IRF-3/7(-/-) mice were resistant t

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

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

11 ignaling and interferon regulatory factor 1 (IRF-1) expression is required to ensure survival of a ga

12 ption factor interferon regulatory factor 1 (IRF-1) has a demonstrated role in shaping innate and ada

13 Interferon regulatory factor 1 (IRF-1) is a transcription factor that regulates innate a

14 g.IMPORTANCE Interferon regulatory factor 1 (IRF-1) is a transcription factor that regulates the expr

15 Interferon (IFN) regulatory factor 1 (IRF-1) is a tumor suppressor that is also involved in th

16 Interferon regulatory factor 1 (IRF-1) is a tumor suppressor that is also involved in th

17 y identifies interferon-regulatory factor 1 (IRF-1) to be one of such candidate host factors.

18 gnaling, and interferon regulatory factor 1 (IRF-1) transactivation.

19 ocyte expression of IFN regulatory factor 1 (IRF-1), a key transcription factor that regulates apopto

20 e absence of interferon-regulatory factor 1 (IRF-1), a transcription factor with antiviral and tumor

21 IFN regulatory factor-1 (IRF-1) is a nuclear transcription factor that plays a cr

22 in DCs deficient in IFN regulatory factor-1 (IRF-1), a key transcription factor required for IL-12 pr

23 ntraretinal fluid (IRF) status: (1) CME, (2) IRF without CME, (3) neither CME nor IRF.

24 cal MAVS effectors TNFR-associated factor-2, IRF-3/7, or IFN-beta but the physical interaction of MAV

25 ption factor interferon regulatory factor 3 (IRF-3) are often vital for early pathogen control, and e

26 -kappaB) and interferon regulatory factor 3 (IRF-3) at a step subsequent to their nuclear translocati

27 -kappaB) and interferon regulatory factor 3 (IRF-3), classically inducing IFNbeta production.

28 orylation of interferon regulatory factor 3 (IRF-3), which is the key transcription factor for IFN in

29 s pathway is interferon regulatory factor 3 (IRF-3), which upon activation by virus infection binds B

30 The miR-31/IRF-1/CTSS pathway may play a functional role in the pat

31 Interferon (IFN)-regulatory factor 5 (IRF-5) is a transcription factor that induces inflammato

32 luding interferon regulatory factor 3 and 7 (IRF-3 and IRF-7) and STAT-1, suggesting that neuronal ma

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

34 Interferon regulatory factor-8 (IRF-8) is a transcription factor that is essential for m

35 transcriptionally inert; this single-action IRF-3 could protect mice from lethal viral infection.

36 rs (TLR) 3, 7, 8, and 9, which also activate IRFs and NF-kappaB, resulted in more robust production o

37 Activated IRF-3 translocates to the nucleus and initiates the tran

38 We found that WEEV activated IRF-3-mediated neuronal innate immune pathways in a repl

39 equent innate signaling cascades, activating IRF-3 independently of CD14.

40 All IRF proteins share an N-terminal DNA-binding domain (DBD

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

42 l responses, IFN-independent, but IRF-1- and IRF-5-dependent mechanisms, restrict HCV replication in

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

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

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

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

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

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

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

50 GF-beta signaling, NF-kappaB activation, and IRF-1 transactivation pathways.

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

52 f sufficient quality for determining CME and IRF at baseline, 92 (8.1%) had CME, 766 (67.7%) had IRF

53 re, we show that type I interferon (IFN) and IRF-1 cooperate to control acute gammaherpesvirus infect

54 cytes these IFN-independent require MAVS and IRF-1.

55 ultiple cells types (e.g. A549, P388D1), and IRF-3 was not translocated to the nucleus in TCRV-infect

56 Specifically, both type I IFN receptor and IRF-1 expression potentiated antiviral effects of type I

57 divergent effects on TGF-beta signaling and IRF-1 transactivation.

58 TING and mediates the activation of TBK1 and IRF-3.

59 ansducer and activator of transcription) and IRF (IFN-regulatory factor) transcription factors.

60 ancer with multiple transcription factor AP1-IRF composite elements (AICEs) within the Irf8 superenha

61 function, and gene expression profiles; (b) IRF-8 overexpression in mice attenuated MDSC accumulatio

62 tributed significantly to I/R injury because IRF-1-knockout (KO) grafts displayed much less damage as

63 tion of necroptosis in response to IFN-beta, IRF-9-STAT1- or -STAT2-deficient macrophages were highly

64 dies reveal an intriguing cross talk between IRF-1 and type I and II IFNs in the induction of the ant

65 On the basis of its biology, IRF-1 represents a plausible host factor to attenuate ga

66 2 were rapidly induced independently of both IRF-3 and IRF-7 in the Irf-3(-/-)7(-/-) mice with DENV i

67 lyubiquitinating enzyme complex, which bound IRF-3 in signal-dependent fashion.

68 ed antiviral responses, IFN-independent, but IRF-1- and IRF-5-dependent mechanisms, restrict HCV repl

69 and death receptor 5, which are regulated by IRF-1.

70 In RNA-virus infected cells, IRF-3's transcriptional activation is triggered primaril

71 Cellular IRFs are a family of transcription factors that are part

72 our viral homologs (vIRF1 to -4) of cellular IRFs into its genome.

73 ffinity multimerized IRF sites and composite IRF-AP-1 sites, which were not premarked by PU.1 and did

74 active and activated forms of IAD-containing IRF proteins (IRF3 to IRF9), allowing a multipronged att

75 STAT3- and STAT5-dependent pathways; and (d) IRF-8 levels in MDSCs of breast cancer patients declined

76 ot develop in mice with IRF-4-deficient DCs (IRF-4(f/f) CD11c-cre).

77 Additionally, we found decreased IRF-1 expression in cases of human posttransplant lympho

78 Further, we found decreased IRF-1 expression in human gammaherpesvirus-induced B cel

79 ithelial cells with a miR-31 mimic decreased IRF-1 protein levels with concomitant knockdown of CTSS

80 cAIMP analogs induce greater STING-dependent IRF and NF-kappaB pathway signaling than do the referenc

81 Depressed IRF-8 levels are observed in a majority of CML patients

82 Irf-1 mRNA expression, but rather diminished IRF-1 protein levels and nuclear localization.

83 rge repulsions that unmask the IAD, enabling IRF dimerization and subsequent nuclear translocation.

84 to require MyD88 and Mal, whereas endosomal IRF activation by TLR2 requires MyD88.

85 neither mutant was able to regulate the Ets/IRF composite element or interferon-stimulated response

86 ents with heart failure likely to experience IRF with treatment, providing proof of concept that reve

87 nducing factors G-CSF and GM-CSF facilitated IRF-8 downregulation via STAT3- and STAT5-dependent path

88 thermore, levels of the transcription factor IRF-1 correlated with increased levels of its target gen

89 ng TNF induction of the transcription factor IRF-1.

90 t and activation of the transcription factor IRF-3 (IFN regulatory factor 3).

91 The transcription factor IRF-3 mediates cellular antiviral response by inducing t

92 on factors NF-kappaB, IFN regulatory factor (IRF) 1, and IRF5 driving the expression of inflammatory

93 activation suppressed IFN regulatory factor (IRF) 1-induced IFN-lambda production and increased viral

94 I interferons, interferon regulatory factor (IRF) 3 and IRF7, were significantly inhibited in patient

95 phorylation of interferon regulatory factor (IRF) 3 and transcription of type I interferons (IFNs) an

96 IFN regulatory factor (IRF) 3 plays a key role in innate responses against viru

97 stimulator 1 (IPS-1), IFN regulatory factor (IRF) 3, and IRF7.

98 activation of interferon regulatory factor (IRF) 3.

99 The contributions of IFN regulatory factor (IRF) 3/7 and the type I IFNs IFN-alpha/beta to the innat

100 operation with interferon regulatory factor (IRF) 4 along with Stat3 and Stat6 trigger IL-4 productio

101 that basal levels of IFN regulatory factor (IRF) 5 in pDCs were significantly higher in females comp

102 ignaling by silencing IFN regulatory factor (IRF) 7 gene expression, the resting CD4(+) T cells secre

103 y deficient in interferon regulatory factor (IRF) as a model, we show that blood-borne ZIKV administr

104 members of the interferon regulatory factor (IRF) family may also play a role in this process.

105 Interferon regulatory factor (IRF) family members have been implicated as critical tra

106 Members of the interferon regulatory factor (IRF) family of transcription factors are key components

107 member of the interferon regulatory factor (IRF) family playing critical regulatory roles in immune

108 activates the interferon regulatory factor (IRF) pathway with enhanced levels of IFN-beta, elicits i

109 Interferon regulatory factor (IRF) regulation of the type I interferon response has no

110 we discovered interferon regulatory factor (IRF) sites among the top enriched motifs.

111 Notably, interferon regulatory factor (IRF)-3 and -7 are the key transcriptional factors for th

112 stigated the roles of IFN regulatory factor (IRF)-3 and IRF-7 in innate antiviral immunity against de

113 ription factor interferon regulatory factor (IRF)-5 is an important modulator of myeloid function and

114 roup box-1 and interferon regulatory factor (IRF)-5, preventing activation of IRF3 and NF-kappaB, whi

115 d identified CCL7 and IFN regulatory factor (IRF)-7 among the most upregulated mRNA transcripts in th

116 ed CpG-induced interferon regulatory factor (IRF)-7 expression by suppressing histone H3K4 trimethyla

117 ne integral player is IFN regulatory factor (IRF)-8, which promotes monocyte/dendritic cell different

118 of Il6 and Il12b via IFN regulatory factor (IRF)1 (TLR3-TIR domain-containing adaptor inducing IFN-b

119 transcription factors IFN regulatory factor (IRF)4 and Blimp1, and paradoxically also activation-indu

120 transcription factor IFN regulatory factor (IRF)4 was shown to play a crucial role in the protective

121 IFN regulatory factor (IRF)7 is a critical regulator of type I IFN production w

122 rylated IFN regulatory transcription factor (IRF)-3 to the nucleus and a decrease in IFN1-beta expres

123 later at those for the transcription factors IRF and Oct-2 and was coincident with activation and dif

124 cularly the regulatory transcription factors IRF-3 and IRF-7, have key protective roles during OROV i

125 ng MAVS signaling, the transcription factors IRF-3 and IRF-7, or IFNAR than in wild-type (WT) cells.

126 ll as the downstream IFN regulatory factors (IRF) 3 and 7 in type I IFN induction and Ag-specific imm

127 porcine interferon (IFN) regulatory factors (IRF) 7 and 3 [IRF7/3(5D)] strongly induced type I IFN an

128 porcine interferon (IFN) regulatory factors (IRF) 7 and 3 delivered by an adenovirus vector [Ad5-poIR

129 Interferon regulatory factors (IRF) have critical functions in lymphoid development and

130 downstream regulatory transcription factors (IRF-3 or IRF-7), beta interferon (IFN-beta), or the rece

131 thways that activate IFN regulatory factors (IRFs) and nuclear factor kappaB.

132 by inducible interferon regulatory factors (IRFs) and retinoic acid inducible gene (RIG-I).

133 Interferon regulatory factors (IRFs) are mediators of this defense with shared enhancer

134 The interferon regulatory factors (IRFs) are transcription factors that play major roles in

135 e key role of Interferon regulatory factors (IRFs) as controllers of the human Langerhans cell respon

136 na fide ISG and that IFN regulatory factors (IRFs) control the expression of BAFF.

137 Although various IFN-regulatory factors (IRFs) facilitated the induction of necroptosis in respon

138 tokine that requires IFN regulatory factors (IRFs) for its transcription, but the signaling mechanism

139 Interferon (IFN) regulatory factors (IRFs) have crucial roles in immune regulation and oncoge

140 IFN regulatory factors (IRFs) help to shape the immune response to pathogens by

141 pression of selected IFN-regulatory factors (IRFs), IFN-stimulated genes (ISGs), transforming growth

142 iated degradation of IFN-regulatory factors (IRFs), including IRF3, IRF5, and IRF7.

143 s of cellular interferon regulatory factors (IRFs), known as viral IRFs (vIRFs), participate in evasi

144 ellular interferon (IFN) regulatory factors (IRFs), known as viral IRFs (vIRFs).

145 s to cellular interferon regulatory factors (IRFs), known as vIRFs.

146 s to cellular interferon regulatory factors (IRFs), termed viral IRFs (vIRFs).

147 n of type I IFNs via IFN regulatory factors (IRFs).

148 es by ubiquitinating IFN regulatory factors (IRFs).

149 tion of interferon (IFN) regulatory factors (IRFs).

150 we compared inhaler reminders and feedback (IRF) and/or personalized adherence discussions (PADs) wi

151 asis of baseline CME and intraretinal fluid (IRF) status: (1) CME, (2) IRF without CME, (3) neither C

152 CT scans for presence of intraretinal fluid (IRF), subretinal fluid (SRF), and sub-retinal pigment ep

153 At 2 years, intraretinal fluid (IRF), subretinal fluid (SRF), sub-retinal pigment epithe

154 Intraretinal fluid (IRF), subretinal fluid (SRF), subretinal pigment epithel

155 uid (i.e., both SRF and intra-retinal fluid [IRF]) in patients with nAMD.

156 a tetracycline (Tet)-inducible cell line for IRF-3 expression, which enabled us to express various le

157 with the IAD, burying residues necessary for IRF dimerization.

158 f our study define an unappreciated role for IRF-1 in B cell biology and provide insight into the pot

159 ively, these results indicate a key role for IRF-5 in modulating the host antiviral response in perip

160 We demonstrate an important role for IRF-5 in preventing neuroinvasion and the ensuing enceph

161 ts reveal a previously unrecognized role for IRF-8 expression in MDSC subset development, which may p

162 Our study revealed a new role for IRFs in differentially regulating the induction patterns

163 s, eyes with residual IRF, especially foveal IRF, had worse mean VA (9 letters) than those without IR

164 Eyes with foveal IRF, abnormally thin retina, greater thickness of the su

165 as AP1 proteins (FOS, JUN, and JUNB), FOXP3, IRFs, and EGR1, dictates the gene regulatory action of N

166 to experience improvement in renal function (IRF) with treatment.

167 Furthermore, IRF-3-dependent neuronal protection from virus-mediated

168 Furthermore, IRF-8 expression in cell line models was necessary for i

169 baseline, 92 (8.1%) had CME, 766 (67.7%) had IRF without CME, and 273 (24.1%) had neither.

170 Notably, hepatic IRF-1 expression was reduced significantly by neutralizi

171 r pDC to induce liver damage through hepatic IRF-1 up-regulation after I/R injury.

172 as a consequence of induction of hepatocyte IRF-1 expression.

173 ssion BUN/Cr was associated with in-hospital IRF (odds ratio, 1.5 per 10 increase; 95% confidence int

174 However, IRF-1 was required for optimal expression of cholesterol

175 with increasing MDSC frequency, implicating IRF-8 as a negative regulator in human MDSC biology.

176 erence (covertly for non-IRF groups) and, in IRF groups, provided twice-daily reminders for missed do

177 y responses, and exacerbated liver injury in IRF-1-KO graft recipients.

178 s were experienced by 11% of the patients in IRF groups and 28% of the patients in non-IRF groups (P

179 a global type I IFN response was similar in IRF-1-deficient and -proficient macrophages during gamma

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

181 d NF-kappaB and AP-1 signaling and increased IRF and STAT signaling).

182 g a recently discovered antagonist increased IRF-8 expression in patient samples.

183 CR-ABL(+) cell lines with imatinib increased IRF-8 transcription.

184 LR), which can also activate the RLR-induced IRF-3-mediated pathway of apoptosis (RIPA).

185 of STAT5 and that silencing of STAT5 induced IRF-8 expression.

186 anges in the spleens of chronically infected IRF-1-deficient animals.

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

188 ion on IFN-I-responsive macrophages inhibits IRF-1-mediated transactivation of IL-27 gene expression

189 Instead, IRF-4(f/f) CD11c-cre mice have fewer CD11b(+) migrating

190 with RORgammat in the cytoplasm through its IRF interaction domain and limits its ability to bind an

191 production in primary cells and mice lacking IRF-5.

192 infected; although seven out of them had low IRF-3 levels, four did not.

193 tablish a dominant protective role for MAVS, IRF-3 and IRF-7, and IFNAR in restricting OROV infection

194 n reveals that the pLxIS motif also mediates IRF-3 dimerization and activation.

195 l IRF association domain (IAD) that mediates IRF dimerization.

196 regions containing low-affinity multimerized IRF sites and composite IRF-AP-1 sites, which were not p

197 Our data demonstrate that multiple IRFs tightly regulate expression of Trim21 in immune cel

198 lly targeted mouse, which expressed a mutant IRF-3 that was RIPA-competent but transcriptionally iner

199 onate/salmeterol adherence (covertly for non-IRF groups) and, in IRF groups, provided twice-daily rem

200 ficantly higher in the IRF group than in non-IRF groups (73% +/- 26% vs 46% +/- 28% of prescribed dai

201 in IRF groups and 28% of the patients in non-IRF groups (P = .013; after adjustment for exacerbation

202 ut CME (43.8%) and eyes with neither CME nor IRF (32.5%; P < 0.001).

203 RF without CME and eyes with neither CME nor IRF (52 vs. 60 vs. 66 letters, P < 0.001); higher mean t

204 ME, (2) IRF without CME, (3) neither CME nor IRF.

205 lication-dependent manner, and abrogation of IRF-3 function enhanced virus-mediated injury by WEEV an

206 Correspondingly, in the absence of IRF-1, chronic gammaherpesvirus infection induced pathol

207 The antiviral actions of IRF-1 appeared to be independent of the induction of typ

208 The antiviral actions of IRF-1 resulted in decreased local inflammatory responses

209 hanism for the recruitment and activation of IRF-3 that can be subverted by viral proteins to evade i

210 hMPV infection induces activation of IRF-3, and it regulates the expression of IRF-7.

211 own pathway of transcriptional activation of IRF-3.

212 Thus, antagonism of IRF-1 is a novel mechanism that synergizes with the note

213 at a reading centre while the assessment of IRF is physician-determined.

214 ically, we demonstrate that a combination of IRF-1 and type I IFN signaling ensures host survival dur

215 ata obtained in vitro, since a deficiency of IRF-5 resulted in enhanced OROV infection and diminished

216 disrupted signal transduction downstream of IRF-3 activation and was independent of capsid-mediated

217 sms responsible for the antiviral effects of IRF-1 are still poorly understood.

218 ly to contribute to the antiviral effects of IRF-1 in other virus systems.

219 and contributed to the antiviral effects of IRF-1.

220 s was associated with impaired expression of IRF-1 and proapoptotic molecules such as Fas ligand, its

221 Ectopic expression of IRF-1 in epithelial cells relieved P. gingivalis-induced

222 Egg antigens do not induce the expression of IRF-4-related genes.

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

224 d edema may explain the greater frequency of IRF detected with TD OCT.

225 nts have suggested an inhibitory function of IRF-1 against infection of alphaviruses in cell culture,

226 nd assessed the early antiviral functions of IRF-1 prior to induction of adaptive B and T cell respon

227 Specific knockdown of IRF-1 in human primary hepatocytes gave similar results.

228 solated after I/R induced elevated levels of IRF-1 production by hepatocytes compared with liver pDC

229 hich enabled us to express various levels of IRF-3.

230 The underlying mechanisms of IRF-8 loss in CML are unknown.

231 Here, we have reported that the pathway of IRF-3 activation in RIPA was independent of and distinct

232 oma cells led to impaired phosphorylation of IRF-3 and reduced ubiquitination of RIG-I and TBK-1, whi

233 visual acuity, new haemorrhage, presence of IRF and SRF on an optical coherence tomography (OCT) sca

234 nducing IFN-beta) mediate the recruitment of IRF-3 through a conserved pLxIS motif.

235 itination of two specific lysine residues of IRF-3 by LUBAC, the linear polyubiquitinating enzyme com

236 intensive" treatment (complete resolution of IRF and SRF) or ranibizumab "relaxed" treatment (resolut

237 nibizumab "relaxed" treatment (resolution of IRF or >200 mum SRF only at foveal centre).

238 as to determine the immunomodulatory role of IRF-1 during I/R injury following allogeneic LTx.

239 Irf1 (-/-) mice, we investigated the role of IRF-1 in modulating pathogenesis of two related arthrito

240 In spite of the known role of IRF-1 in stimulating type I IFN expression, induction of

241 To define the role of IRF-5 during bunyavirus infection, we evaluated Oropouch

242 Silencing of IRF expression did not improve virus multiplication in d

243 intact IAD for recognition and targeting of IRF proteins.

244 zed that BCR-ABL suppresses transcription of IRF-8 through STAT5, a proximal BCR-ABL target.

245 Activation of IRFs is prerequisite for their functions.

246 Agreement on IRF was 73% (kappa = 0.47; 95% CI, 0.42-0.52), with 6% m

247 The effect on IRF-1 was also observed in DCs infected with the highly

248 atory factor 7 (IRF-7) expression but not on IRF-3 expression.

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

250 In mice, deletion of IFNAR, MAVS, or IRF-3 and IRF-7 resulted in uncontrolled OROV replicatio

251 te for PU.1, and also show that unlike other IRF members, IRF4 has a flexible autoinhibitory region.

252 ulation, increased expression of IRF8, other IRFs, and AP-1 family TFs enabled IRF8 binding to thousa

253 in response to TLR4 ligands HMGB1 and LPS, p-IRF-3 activation and transcription of its target genes a

254 inhibited rhinovirus-induced IFN production, IRF-3 phosphorylation, and IKKepsilon expression and inh

255 IRF5, and IRF7 contain a similar C-proximal IRF association domain (IAD) that mediates IRF dimerizat

256 ch is decreased in the CF airways, regulates IRF-1 in CF epithelial cells.

257 ever, at all time points, eyes with residual IRF, especially foveal IRF, had worse mean VA (9 letters

258 s of disease activity such as intra-retinal (IRF) or sub-retinal fluid (SRF) were evident on SD-OCT,

259 IRF-3(-/-) and select IRF-3/7(-/-) mice were resistant to LP-BM5-induced patho

260 by epidermal cytokine induction of specific IRF-controlled pathways.

261 ed occupancy of transcription factors STAT1, IRF-1, and associated histone acetylation at promoters a

262 veal a previously unrecognized BCR-ABL-STAT5-IRF-8 network, which widens the repertoire of potentiall

263 Conversely, activating STAT5 suppressed IRF-8 transcription.

264 l protein 1) employs a pLxIS motif to target IRF-3 for degradation, but phosphorylation of NSP1 is no

265 Ralpha production and suggest that targeting IRF-1 and IL-15/IL-15Ralpha may be effective in reducing

266 We have demonstrated that IRF-8 is a direct target of STAT5 and that silencing of

267 Specifically, we found that IRF-1 enforces long-term suppression of an inherently mu

268 These results indicate that IRF-1 promotes LTx I/R injury via hepatocyte IL-15/IL-15

269 Our observations indicated that IRF-3-mediated apoptosis of virus-infected cells could b

270 gical and virological analyses revealed that IRF-1 preferentially restricted CHIKV infection in cells

271 Our studies show that IRF-1 controlled alphavirus replication and swelling in

272 Here we show that IRF-1 expression attenuates gammaherpesvirus replication

273 In this study, we show that IRF-1 restricts gammaherpesvirus replication in primary

274 tively, our in vivo experiments suggest that IRF-1 restricts CHIKV and RRV infection in stromal cells

275 to expression of inflammatory genes and the IRF-RIG-I autoamplification pathway and independently fa

276 t of approximately 37 kDa that comprises the IRF dimerization and transactivation domains but lacks t

277 ut only if they can find a way to impair the IRF-3-dependent apoptotic pathway.

278 s, adherence was significantly higher in the IRF group than in non-IRF groups (73% +/- 26% vs 46% +/-

279 egulatory factor 5 (IRF5) is a member of the IRF family of transcription factors.

280 tightly regulated like other members of the IRF family.

281 The structure of the IRF-3 phosphomimetic mutant S386/396E bound to the cAMP

282 we assembled a Petri net-based model of the IRF-GRN which provides molecular pathway predictions for

283 We confirmed this IRF-3 threshold idea by generating a tetracycline (Tet)-

284 In addition to IRF-3- and IFN-mediated antiviral responses, IFN-indepen

285 hosphorylated STING, MAVS, and TRIF binds to IRF-3 in a similar manner, whereas residues upstream of

286 essential for progression from NF-kappaB to IRF signalling, and ultimately for traffic to lysosomes

287 Surprisingly, transferred IRF-4-deficient DCs also effectively prime S. mansoni-sp

288 induce Trim21 expression in immune cells via IRFs and that IFN-alpha and IFN-beta are the most potent

289 on regulatory factors (IRFs), known as viral IRFs (vIRFs), participate in evasion of the host interfe

290 N) regulatory factors (IRFs), known as viral IRFs (vIRFs).

291 eron regulatory factors (IRFs), termed viral IRFs (vIRFs).

292 In vitro, IRF-1 regulated both constitutive and induced expression

293 When IRF-3-knockdown cells were infected with Sendai virus (S

294 response also peaked at 2 dynes/cm(2), where IRF-1-regulated VCAM-1 expression and monocyte recruitme

295 vides an insight into the mechanism by which IRF-1 attenuates gammaherpesvirus replication in primary

296 offer an insight into the mechanism by which IRF-1 attenuates the replication of gammaherpesviruses,

297 Eyes with IRF in the foveal center had worse mean VA than eyes wit

298 2 years of follow-up compared with eyes with IRF without CME (43.8%) and eyes with neither CME nor IR

299 E had worse mean VA (letters) than eyes with IRF without CME and eyes with neither CME nor IRF (52 vs

300 oma mansoni eggs do not develop in mice with IRF-4-deficient DCs (IRF-4(f/f) CD11c-cre).

301 l center had worse mean VA than eyes without IRF (59.9 vs. 70.9 letters; P < 0.0001).

302 worse mean VA (9 letters) than those without IRF.