ライフサイエンスコーパス: IRF

1 IRF also caused vagus nerve, esophageal, and lung injury

2 IRF and PFA deliveries were randomized in 8 dogs with 2

3 IRF energy (25-30 W) or PFA was delivered (16 pulse trai

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

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

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

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

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

9 IRF-3, HIF-1, and CASP1 were exclusively upregulated in

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

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

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

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

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

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

16 -suppressive interferon regulatory factor 1 (IRF-1) selectively promotes the murine gammaherpesvirus

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 roreceptor to endow IFN regulatory factor 1 (IRF-1) with apoptotic functions, which redirect murine n

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

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

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

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

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

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

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

27 ranscription factor IFN regulatory factor 3 (IRF-3), inhibiting its phosphorylation and downstream be

28 or molecule, interferon regulatory factor 3 (IRF-3), receptor-interacting protein 1, IFNbeta-1, and n

29 P5 decreased interferon regulatory factor 3 (IRF-3)-mediated and nuclear factor kappa-B (NF-kappaB) i

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

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

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

33 Interferon regulatory factor 7 (IRF-7) is a transcription factor with many target genes,

34 Interferon regulatory factor 7 (IRF-7) is an innate immune transcription factor that res

35 xpression of interferon regulatory factor 8 (IRF-8)/aldehyde dehydrogenase 1 family member A2 (Aldh1a

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

37 ared with irrigated radiofrequency ablation (IRF).

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

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

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

41 confined and often incomplete lesions after IRF.

42 was noted in 3 left superior PV lobes after IRF.

43 ve arm: SRF intolerant) or resolution of all IRF only (relaxed arm: SRF tolerant except for SRF >200

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

45 foveal center pathology (all P < 0.001) and IRF (P < 0.05) were independently associated with worse

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

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

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

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

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

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

52 or motifs and overexpression of the bZIP and IRF transcription factors that have been implicated in m

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

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

55 ion factors (TFs) - particularly the ETS and IRF families - in regulating MZB and FOB lineage selecti

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

57 species (ROS) levels are elevated, mTOR and IRF/IFN-beta signaling pathways are enhanced, leading to

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

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

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

61 alysis reveals enrichment of ETS-IRF and AP1-IRF composite regulatory elements in antigen-presentatio

62 IRF4 can each interact with TF BATF3 at AP1-IRF composite elements (AICEs) and with TF PU.1 at Ets-I

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

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

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

66 In first-treated eyes, the majority had both IRF and SRF (54.7%).

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

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

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

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

71 hrough inhibitory interactions with cellular IRFs and other mediators of antiviral signaling, the vIR

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

73 ntrinsic, we generated mice with conditional IRF-1 deficiency.

74 In contrast, IRF-7 expression restricted latent gammaherpesvirus infe

75 mentation are convolved by the corresponding IRFs, which can complicate quantitative analyses.

76 In the cytoplasm, IRF-1 can no longer serve as an anti-viral transcription

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

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

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

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

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

82 ology.IMPORTANCE Human herpesvirus 8-encoded IRF homologues were the first to be identified in a viru

83 uced STAT6 phosphorylation serves to enhance IRF-1 transcription and promotes its egress from the nuc

84 ite elements (AICEs) and with TF PU.1 at Ets-IRF composite elements (EICEs), it is unclear how these

85 Chromatin analysis reveals enrichment of ETS-IRF and AP1-IRF composite regulatory elements in antigen

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

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

88 The host transcription factor IRF-1, a well-established tumor suppressor, selectively

89 (encoding PD-L1) by the transcription factor IRF-1, which induced the acetylation of Histone H3 at CD

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

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

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

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

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

95 activation of interferon regulatory factor (IRF) 3.

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

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

98 ption (STAT)-1, IL-6, IFN regulatory factor (IRF) 5, and TLR4 and suppressed c-Jun N-terminal kinase

99 tly demonstrated that IFN regulatory factor (IRF) 8 was dispensable for caspase-11-mediated NLRP3 inf

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

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

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

103 member of the interferon regulatory factor (IRF) family of transcription factors, was essential for

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

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

106 B (NF-kappaB), interferon regulatory factor (IRF), and the signal transducer and activator of transcr

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

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

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

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

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

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

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

114 nts identified interferon regulatory factor (IRF)7, a driver of type I IFN, as a potential target for

115 nsor RIG-I and interferon regulatory factor (IRF)7.

116 or that mediates interferon response factor (IRF) activation and ISG responses to vaccinia virus lack

117 es highlight the interferon response factor (IRF) pathway as a putative novel hallmark with frequent

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

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

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

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

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

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

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

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

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

127 activation of interferon regulatory factors (IRFs) 3 and 7, type I interferon, and interferon-stimula

128 upregulating interferon regulatory factors (IRFs) and downregulating an inhibitor of IFN signalling,

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

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

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

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

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

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

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

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

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

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

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

140 tream through interferon regulatory factors (IRFs), transcription factors that induce synthesis of ty

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

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

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

144 5 years, 60% of eyes had intraretinal fluid (IRF), 38% had subretinal fluid (SRF), 36% had subretinal

145 ubretinal fluid (SRF) or intraretinal fluid (IRF), and on-study events (atrophy status, fibrosis, ret

146 volumes (nanoliters) for intraretinal fluid (IRF), subretinal fluid (SRF), and pigment epithelial det

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

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

149 ry retina (NSR), drusen, intraretinal fluid (IRF), subretinal fluid (SRF), subretinal hyperreflective

150 te resolution of SRF and intraretinal fluid (IRF; intensive arm: SRF intolerant) or resolution of all

151 ubfield thickness [CST], intraretinal fluid [IRF], or subretinal fluid [SRF]) versus aflibercept (q8-

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

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

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

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

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

157 al GA, foveal scar, foveal CNV, SHRM, foveal IRF, retinal thinning, CNV lesion area, and GA area) bet

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

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

160 nd the instrument impulse response function (IRF).

161 o a Lorentzian instrument response function (IRF).

162 Further, IRF-7 expression was dispensable for the induction of a

163 unveiled in MHV68-infected mice with global IRF-1 deficiency are mediated via IRF-1 expression by no

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

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

166 ICE-dependent enhancers, which required high IRF concentrations, but were activated by either IRF4 or

167 Less attention has been paid to how IRFs maintain basal levels of protection against viruses

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

169 a few ISGs showing attenuated expression in IRF-7-deficient peritoneal cells.

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

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

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

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

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

175 This cytokine-induced, IRF-1-mediated developmental death network weakens neona

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

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

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

179 In contrast, in testing, B cell-intrinsic IRF-1 expression promoted the MHV68-driven germinal cent

180 n the IFNB1 enhanceosome that overlaps a key IRF site.

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

182 imated through convolution of the Lorentzian IRF with a step function representing the ideal junction

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

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

185 1, IFN-gamma, TRIF-related adapter molecule, IRF-3, HIF-1, nucleotide-binding oligomerization domain,

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

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

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

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

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

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

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

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

194 f IFN-induced genes (ISGs) in the absence of IRF-7, with only a few ISGs showing attenuated expressio

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

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

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

198 own pathway of transcriptional activation of IRF-3.

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

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

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

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

203 ine the extent to which antiviral effects of IRF-1 are B cell intrinsic, we generated mice with condi

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

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

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

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

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

209 The new pivotal function of IRF-1 in the death of neonatal Th1 cells stems from the

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

211 udy indicate that the antiviral functions of IRF-1 unveiled in MHV68-infected mice with global IRF-1

212 showed a volume-dependent negative impact of IRF on vision and weak positive prognostic effect of SRF

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

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

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

216 ng to FKBP5 decreased the phosphorylation of IRF-3 and IkappaBalpha mediated by IKKepsilon and IKKbet

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

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

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

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

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

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

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

224 ts the underappreciated multifaceted role of IRF-1 in MHV68 infection and pathogenesis.

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

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

227 Despite the classical role of IRF-7 as a stimulator of type I interferon (IFN) transcr

228 is study, we show that the antiviral role of IRF-7 continues into the chronic phase of gammaherpesvir

229 ntly, very little is known about the role of IRF-7 during chronic virus infections.

230 first demonstration of the antiviral role of IRF-7 during the chronic stage of gammaherpesvirus infec

231 r knowledge, the first to define the role of IRF-7 in chronic virus infection.

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

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

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

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

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

237 At the distal PV sites, only IRF ablations were grossly identified based on focal fib

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

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

240 n patient characteristics, persistent SRF or IRF, or on-study events to account for the observed diff

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

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

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

244 Phosphorylated IRF-3 translocates to the nucleus and initiates the expr

245 ional area at 4-weeks was -46.1+/-45.1% post-IRF compared with -5.5+/-20.5% for PFA (P<=0.001).

246 factor 3 (IRF3) and IRF7 are closely related IRF members and the major factors for the induction of i

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

248 and reovirus infection both induce a similar IRF-dependent gene expression program, gene expression d

249 Surprisingly, B cell-specific IRF-1 deficiency attenuated the establishment of chronic

250 Further, we found that B cell-specific IRF-1 deficiency led to reduced levels of active tyrosin

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

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

253 Conversely, activating STAT5 suppressed IRF-8 transcription.

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

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

256 of type I interferons through the STING-TBK1-IRF-3 signalling axis(13-15).

257 In this study, we demonstrate that IRF-7 attenuates chronic infection by restricting establ

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

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

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

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

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

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

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

265 The IRF and Ets families of transcription factors regulate t

266 The IRF-3 transcription factor is then recruited to the sign

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

268 the deconvolved photon arrival times and the IRF.

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

270 Using random initial guesses for the IRF, the NMF filter simultaneously recovered both the de

271 a polydimethylsiloxane (PDMS) membrane, the IRF derived from fitting the experimental profile was sl

272 Regulatory Factor-1) is the prototype of the IRF family of DNA binding transcription factors.

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

274 tightly regulated like other members of the IRF family.

275 specifically impaired the activation of the IRF pathway without affecting NF-kappaB and MAPK signall

276 ton events require advanced knowledge of the IRF, which is not generally trivial to obtain.

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

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

279 arding the evolution and adaptation of those IRFs to the environments.

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

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

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

283 V68 may, in a B cell-intrinsic manner, usurp IRF-1 to promote the germinal center response and expans

284 ith global IRF-1 deficiency are mediated via IRF-1 expression by non-B cell populations.IMPORTANCE Ga

285 Viral IRFs 1, 2, and 3 are also expressed during latency in pr

286 Viral IRFs 1, 3, and 4 are known to interact with ubiquitin-sp

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

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

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

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

291 phase of gammaherpesvirus infection, wherein IRF-7 restricts the establishment of viral latency and v

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

293 s dilation occurred at sites associated with IRF.

294 ntly fewer vessel restrictions compared with IRF (P<=0.023).

295 ly reduced risk of PV stenosis compared with IRF postprocedure in a canine model.

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

297 2 years of follow-up compared with eyes with IRF without CME (43.8%) and eyes with neither CME nor IR

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

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

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