ライフサイエンスコーパス: ISG

1 ISG mRNAs were readily detected in HCV-infected cells, c

2 ISG ranks third and LFGTE fourth on all four soil-qualit

3 ISGs constitute over 300 antiviral effectors, which coop

4 Here we screened 20 ISGs that are commonly induced by type I IFNs against CS

5 s approach revealed a conserved 'core' of 62 ISGs, including genes not previously associated with IFN

6 ile tripartite motif-56 (TRIM56) accentuates ISG induction by IFNalpha and inhibits the expression of

7 and localized to the promoters of activated ISGs.

8 Although ISGs mediate a protective state against many pathogens,

9 Among ISGs, the genes encoding interferon-induced transmembran

10 Recently, Mx2 was identified as an ISG that contributes to the inhibition of HIV-1 replicat

11 esent work therefore identifies PARP12 as an ISG with a potential role in cellular defenses against v

12 rate that IFN regulatory factor 2 (IRF2), an ISG and a negative regulator of IFN signaling, influence

13 -dependent endoribonuclease, which is not an ISG in humans, is highly IFN inducible in black flying f

14 2',3'-cGAMP and also activated IFN-beta and ISG expression; and (v) UL46 binds to both STING and TBK

15 This IFN-beta and ISG induction is dependent on ataxia-telangiectasia muta

16 n ISG factor 3 (ISGF3) complex formation and ISG expression.

17 inhibition of interferon (IFN) induction and ISG messenger RNA (mRNA) translation.

18 HCV RNA and ISG mRNA using HCV isolate- and ISG mRNA-specific probes in liver biopsy sections from 1

19 dization (ISH) system capable of HCV RNA and ISG mRNA detection in human liver biopsies and applied i

20 We simultaneously monitored HCV RNA and ISG mRNA using HCV isolate- and ISG mRNA-specific probes

21 ciated with a change in apoptosis, sCD14 and ISG expression showed an association with increasing vir

22 in IFN regulatory factor 1 stabilization and ISG expression.

23 xpression of IFN-beta, IFN-lambda1/IL-29 and ISGs in their sputum cells that may reflect ongoing inna

24 induce DDR also does not induce IFN-beta and ISGs.

25 Detailed analyses of two antiretroviral ISGs indicate that indoleamine 2,3-dioxygenase 1 (IDO1)

26 5-hydroxylase (CH25H) as a broadly antiviral ISG.

27 identified Ifi27l2a as a candidate antiviral ISG within neuronal subsets of the central nervous syste

28 hway and independently facilitates antiviral ISG expression.

29 SNPs may be associated with higher antiviral ISG expression, which results in better replication cont

30 However, antiviral ISG specificity across multiple distinct classes of viru

31 nding protein 1 (GBP1) as a potent antiviral ISG against CSFV.

32 on of IFN-lambda1, TLR3, RIG-I and antiviral ISGs in hepatocytes.

33 forts to identify and characterize antiviral ISGs, and we provide a forward-looking perspective on th

34 gulation of several protein-coding antiviral ISGs.

35 FN-lambda stimulates expression of antiviral ISGs preferentially in cells of epithelial origin, recen

36 g infection with CMV, but higher "antiviral" ISG expression (eg, OAS1).

37 Moreover, RA augments ISG induction in response to viral infection or exposure

38 N-lambda (1 to 4) in C/C cells induced basal ISG expression and prevented IFN-alpha antiviral activit

39 expressed in hepatocytes and maintains basal ISG expression.

40 g IFN-lambda1 in T/T cell line reduced basal ISG expression and improved antiviral activity.

41 In IFN-stimulated cells, bat ISGs comprise two unique temporal subclusters with simil

42 Notably, in unstimulated cells, bat ISGs were expressed more highly than their human counter

43 nt screening studies have begun to catalogue ISGs with antiviral activity against several RNA and DNA

44 licing to activate IRF3 and induce classical ISG expression independent of the JAT-STAT signaling pat

45 , causing IFN-beta production and consequent ISG expression in human cells.

46 our findings together, GBP1 is an anti-CSFV ISG whose action depends on its GTPase activity.

47 nding protein 1 (GBP1) as a potent anti-CSFV ISG.

48 However, anti-CSFV ISGs are poorly documented.

49 d promoted induction of IKKepsilon-dependent ISGs.

50 These distinguished ISGs by cell-type specificity, kinetics, and sensitivity

51 ese results advance our knowledge of diverse ISG proteins functioning as antivirals and may provide n

52 cantly reduced IFN-alpha/beta and downstream ISG mRNAs Ifit1, Isg15, and Pkr, while expression of pro

53 els, demonstrating that the stimulus driving ISG expression originates from HCV-infected hepatocytes.

54 ave been associated with persistent elevated ISG expression in individuals chronically infected with

55 f high IFN-lambdaR1 expression with elevated ISG expression, with IFN-lambda3 minor alleles, and with

56 a quantitative PCR array, 23 of 84 examined ISGs were found to be overexpressed by at least fivefold

57 tantly, we show that intrinsically expressed ISGs protect stem cells against viral infection.

58 There were significantly fewer ISGs in the absence of STAT1 or STAT2 versus in the abse

59 cle, we demonstrate that BAFF is a bona fide ISG and that IFN regulatory factors (IRFs) control the e

60 nized energy impacts range from -0.32 MJ for ISG to 1.14 MJ for AC.

61 1 (LILRB1) to inhibit FcgammaR signaling for ISG expression.

62 revealed a typical pattern of expression for ISGs in the liver, gut, and blood vessels with both viru

63 = 0.001); a 2-fold reduction in a four-gene ISG signature predicted an increase in DeltaHCVIFN,72 of

64 .05) and increased expression of a nine-gene ISG signature (P < 0.001) predicted the eventual decreas

65 transferases, as an interferon-induced gene (ISG), whose function remains incompletely characterized.

66 (MX2/MXB) is an interferon-stimulated gene (ISG) and was recently identified as a late postentry sup

67 (MAVS)/TBK1/IRF3/interferon-stimulated gene (ISG) axis, causing either an upregulation or a downregul

68 hibited impaired interferon-stimulated gene (ISG) expression and, in the case of mice deficient in IR

69 antiviral interferon (IFN)-stimulated gene (ISG) expression in uninfected remote regions of the brai

70 se livers type I interferon-stimulated gene (ISG) expression is strongly induced.

71 enotypes on IL-28B, and IFN-stimulated gene (ISG) expression, and CMV replication in human foreskin f

72 B, IL-29), preactivated IFN-stimulated gene (ISG) expression, and impaired Stat phosphorylation when

73 iviral defenses through IFN-stimulated gene (ISG) expression.

74 se (CH25H) as an interferon-stimulated gene (ISG) has recently been shown to exert broad antiviral ac

75 n their level of interferon-stimulated gene (ISG) induction with a clearly detectable hierarchy (IFN-

76 er despite interferon (IFN)-stimulated gene (ISG) induction; robust induction actually predicts treat

77 Interferon-stimulated gene (ISG) products take on a number of diverse roles.

78 ucing a large number of IFN-stimulated gene (ISG) proteins, several of which have been shown to have

79 , collectively known as IFN-stimulated gene (ISG) proteins, which act as antivirals.

80 uced a transient interferon stimulated gene (ISG) response in mice and cynomolgus monkeys.

81 led intrahepatic interferon stimulated gene (ISG) responses.

82 ying significant interferon-stimulated gene (ISG) transcript upregulation that recapitulates theISGsi

83 did not activate interferon-stimulated gene (ISG) transcription following treatment with the noncanon

84 ts 2 (Ifit2), an interferon-stimulated gene (ISG) with possible RNA-binding capacity, is an important

85 dicated that cGAS is an IFN-stimulated gene (ISG), and two adjacent IFN-sensitive response elements (

86 able IFN-beta or interferon-stimulated gene (ISG; MX1, oligoadenylate synthetase [OAS], IFIT-1) respo

87 ession of interferon (IFN)-responsive genes (ISG) following stimulation by lipopolysaccharide (LPS) o

88 sting that a subset of IFN-stimulated genes (ISG) may play a role in the control of WHV replication.

89 nscription of numerous IFN-stimulated genes (ISG), which in turn protect these cells by inhibiting vi

90 xpression of interferon (IFN)-induced genes (ISGs).

91 Interferon-stimulated genes (ISGs) act in concert to provide a tight barrier against

92 cing the expression of IFN-stimulated genes (ISGs) and mediating signals downstream of IFN-gamma.

93 upregulate an array of IFN-stimulated genes (ISGs) and potently suppress Human immunodeficiency virus

94 Interferon (IFN) and IFN-stimulated genes (ISGs) are amplified during HCV infection but fail to eli

95 ns, hundreds of interferon-stimulated genes (ISGs) are induced.

96 e whether interferon (IFN)-stimulated genes (ISGs) are overexpressed in human T1D islets affected wit

97 d expression of type 1 IFN-stimulated genes (ISGs) as the predominant transcriptomal feature of H/H-N

98 type III IFN genes and IFN-stimulated genes (ISGs) at 37 degrees C.

99 sified as interferon (IFN) stimulated genes (ISGs) but that expression is intrinsic, as stem cells ar

100 ession of interferon (IFN)-stimulated genes (ISGs) by biogenesis of RA.

101 ibit the production of IFN-stimulated genes (ISGs) by blocking Jak-STAT signaling; however, this occu

102 Interestingly, interferon-stimulated genes (ISGs) encoding proteins such as IFIT1, IFIT2, and IFIT3,

103 and several antiviral IFN-stimulated genes (ISGs) expression.

104 ription of a subset of IFN-stimulated genes (ISGs) in an IRF3-dependent, IFN-independent fashion.

105 nduce antiviral interferon-stimulated genes (ISGs) in epithelia, while the effect of IFN-lambda in no

106 on of the interferon (IFN)-stimulated genes (ISGs) in Huh7 cells.

107 ts in the induction of IFN-stimulated genes (ISGs) in human fibroblasts and confers an antiviral stat

108 V-induced interferon (IFN)-stimulated genes (ISGs) in infected monocytes remained unclear.

109 apid downregulation of IFN-stimulated genes (ISGs) in liver and blood, regardless of treatment outcom

110 lation of interferon (IFN)-stimulated genes (ISGs) in patients with SAVI.

111 uction of interferon (IFN)-stimulated genes (ISGs) in the liver of patients with chronic hepatitis C

112 g expression of interferon stimulated genes (ISGs) in the liver.

113 of hundreds of interferon-stimulated genes (ISGs) provide an immediate barrier to virus infection.

114 -28A/B) and the interferon-stimulated genes (ISGs) such as myxovirus resistance 1 (Mx1), oligoadenyla

115 o repurpose the interferon-stimulated genes (ISGs) viperin and tetherin to facilitate its replication

116 A typical signature of IFN-stimulated genes (ISGs) was observed with both viruses, but was stronger f

117 he expression of IFN-alpha-stimulated genes (ISGs) was reduced in number and magnitude in MGCs that l

118 nd 16 antiviral interferon-stimulated genes (ISGs) were upregulated 3.1- to 48.2-fold at 8 h postchal

119 type I IFNs and interferon-stimulated genes (ISGs), a strong activation of the inflammasome, and upre

120 hundreds of different IFN-stimulated genes (ISGs), but it is often unclear which ISGs are responsibl

121 CSFV, including interferon-stimulated genes (ISGs), have been characterized.

122 wnstream expression of IFN-stimulated genes (ISGs), including chemokines CXCL9 and CXCL10 that are ch

123 ltiple critical interferon-stimulated genes (ISGs), including IFITM3 and MxA, by affecting histone mo

124 IFN-beta and multiple IFN stimulated genes (ISGs), including Myxovirus resistance protein 2 (Mx2), 2

125 ng type I interferon (IFN)-stimulated genes (ISGs), including Stat1, in adipocytes in vitro and in vi

126 tion of several interferon-stimulated genes (ISGs), including those involved in cholesterol pathway,

127 e show that two interferon-stimulated genes (ISGs), ISG20 and tetherin, restrict HBV spread in NTCP-e

128 ilar to protein-coding IFN-stimulated genes (ISGs), its induction was dependent on JAK-STAT signaling

129 sion of Rb1 and interferon-stimulated genes (ISGs), plasma soluble CD163 (sCD163) concentration, and

130 ing hundreds of interferon-stimulated genes (ISGs), some of which encode direct antiviral effectors.

131 latory factors (IRFs), IFN-stimulated genes (ISGs), transforming growth factor-beta1 (TGFbeta1), and

132 host induces over 300 IFN-stimulated genes (ISGs), which are the central component of intracellular

133 of hundreds of interferon-stimulated genes (ISGs), which define the antiviral state of the host.

134 ion of selected interferon-stimulated genes (ISGs).

135 ading to expression of IFN-stimulated genes (ISGs).

136 nd 16 antiviral interferon-stimulated genes (ISGs).

137 interferons (IFNs) and IFN-stimulated genes (ISGs).

138 tor 3 (IRF3)-dependent IFN-stimulated genes (ISGs).

139 s on the expression of IFN-stimulated genes (ISGs).

140 ) via the induction of IFN-stimulated genes (ISGs).

141 anscription of IFN and IFN-stimulated genes (ISGs).

142 of hundreds of interferon-stimulated genes (ISGs).

143 ty and upregulation of IFN-stimulated genes (ISGs).

144 erted action of interferon-stimulated genes (ISGs).

145 duction of hundreds of IFN-stimulated genes (ISGs).

146 to the IRF3-dependent IFN-stimulated genes (ISGs).

147 tion to measure interferon stimulated genes (ISGs).

148 ed induction of interferon-stimulated genes (ISGs).

149 ation of hundreds of IFN-I-stimulated genes (ISGs).

150 by inducing the type-I IFN-stimulated genes (ISGs).

151 stimulation for interferon stimulated genes (ISGs).

152 (IFN-beta) and interferon-stimulated genes (ISGs).

153 duction of hundreds of IFN-stimulated genes (ISGs).

154 ivation of a subset of IFN-stimulated genes (ISGs).

155 ression of hundreds of IFN-stimulated genes (ISGs).

156 of hundreds of interferon-stimulated genes (ISGs).

157 eins encoded by interferon-stimulated genes (ISGs); among these are the interferon-induced proteins w

158 n expression of interferon-stimulated genes (ISGs; MX1 and IFIT5) and increased viral yield in respon

159 nnate immune pathways (IFN-stimulated genes [ISGs]) of increasing magnitude with NYVAC-C-DeltaB19R an

160 demonstrate herein that PARP12 is a genuine ISG, whose expressed protein displays at least two disti

161 d composition of insulin secretory granules (ISG) has never previously been thoroughly characterized.

162 recent study of insulin secretory granules (ISG) suggested that phosphatidylserine and other phospho

163 In-sink grinding (ISG) via a food-waste disposer and flushing for manageme

164 Internet support group (ISG) members benefit from receiving social support and,

165 Thus, IFITM1 is an anti-HCV ISG whose actions impart control of HCV infection throug

166 and that change is linked to reduced hepatic ISG expression.

167 re, further understanding of the hepatocytic ISG regulation machinery will guide us to an improved ma

168 We further compared the zebrafish and human ISG repertoires and made a genomic and phylogenic charac

169 y to screen a library of more than 350 human ISGs for effects on 14 viruses representing 7 families a

170 of hundreds of individual macaque and human ISGs to inhibit early and late replication steps for 11

171 In contrast, human ISGs lack this decline phase and remained elevated for l

172 Recently, we and others identified ISG myxovirus resistance 2 (MX2) as an inhibitor of HIV-

173 we applied an image-based screen to identify ISGs inhibiting late stages of influenza A virus (IAV) i

174 cGAS DNA sensor directs a dominant IRF3/IFN/ISG antiviral response to adenovirus in human cell lines

175 The magnitude of the IRF3/IFN/ISG antiviral response was strongly influenced by seroty

176 ng pathway to highlight features that impact ISG production.

177 In ISG phosphatidylserine, phosphatidylinositol, phosphatid

178 are consistent with the idea that changes in ISG phospholipids facilitate fusion of ISG with the plas

179 TP8B1 and CDC50A were highly concentrated in ISG.

180 ining unsaturated fatty acids were higher in ISG than in whole cells and in mitochondria.

181 STAT1 phosphorylation, which is involved in ISG factor 3 (ISGF3) complex formation and ISG expressio

182 lipids, such as phosphatidylethanolamine, in ISG could play important roles in docking and fusion of

183 sphatidylserine, and phosphatidylinositol in ISG were 5-fold higher than in the whole cell.

184 ological and molecular phenotypes, including ISG induction, autoantibody production, aberrant T-cell

185 cells and neighboring cells showed increased ISG mRNA levels, demonstrating that the stimulus driving

186 in IA patients and pointed toward increased (ISG) transcript levels in IT patients, compared to subse

187 shed light on the contribution of individual ISG effectors to the antiviral state, but most have exam

188 The inhibitory activity of individual ISGs varies depending on the specific cell type and vira

189 s with Dhx15 as a viral RNA sensor to induce ISGs, and this effect is especially important in the int

190 IL-28B pretreatment induced ISG expression in noninfected fibroblasts, but a relativ

191 f monocytes inhibited TLR3- and TLR4-induced ISG expression by 50 to 90% depending on the genes, wher

192 We describe a core set of well-induced ISGs conserved across vertebrates, as well as multigenic

193 We found that in addition to inducing ISG transcription, IFN-lambda (but not IFN-beta) specifi

194 the absence of neurotropic virus infection, ISGs are induced in the posterior regions of the brain,

195 and mouse datasets to computationally infer ISG modules and their regulators, validated by genetic a

196 at intracellular RA levels greatly influence ISG expression under basal conditions.

197 onstrate the in vivo importance of intrinsic ISG expression for protecting stem cells and their diffe

198 This intrinsic ISG expression varies in a cell-type-specific manner, an

199 enhanced expression and activation of a key ISG transcriptional regulator, signal transducer and act

200 The activity of known ISGs is insufficient to account for the antiretroviral e

201 N-lambdas resulted in a similar long-lasting ISG induction, IFN-alpha signaling peaked early after st

202 ), blunt host antiviral defenses by limiting ISG expression, the overall abundance of ISG15 monomer a

203 ucose stimulation, the concentration of many ISG phosphatidylserines and phosphatidylinositols increa

204 ies in a cell-type-specific manner, and many ISGs decrease upon differentiation, at which time cells

205 While the functional significance of many ISGs has yet to be determined, their cell type and tempo

206 In conclusion, 1) IFN-I can mediate ISG expression in MGCs via ISGF3-independent signaling p

207 plays a critical role in type I IFN-mediated ISG induction.

208 or IRF9 play a minor role only in mediating ISG expression in MGCs.

209 vivo ischemia/reperfusion-induced microglial ISG responses by quantitative real-time PCR and demonstr

210 Finally, we demonstrated that the microglial ISG chemokine responses to TLR4 agonists were dependent

211 CD16(+) frequencies, sCD14, sCD163, and most ISG expression were not directly associated with a chang

212 No ISG induction was observed in untreated HEV gt3 and gt1

213 on of IFN-beta transcription and of numerous ISGs, acting at the point of transcriptional complex ass

214 These screens uncovered numerous ISGs with antiretroviral activity at both the early and

215 The full breadth of ISG induction demands activation of a number of cellular

216 demonstrated that TNK1 governs a cluster of ISG expression that defines the TNK1 pathway effector ge

217 haracterized the phospholipid composition of ISG and mitochondria in pancreatic beta cells without an

218 cted fibroblasts, but a relative decrease of ISG expression could be observed in CMV-infected fibrobl

219 rane to facilitate the docking and fusion of ISG to the plasma membrane during insulin exocytosis.

220 lay important roles in docking and fusion of ISG to the plasma membrane in the pancreatic beta cell d

221 es in ISG phospholipids facilitate fusion of ISG with the plasma membrane-enhancing glucose-stimulate

222 f IL-28 signaling resulted in an increase of ISG expression and 3-log reduction of CMV-replication (P

223 Viral expression and inhibition of ISG transcription was, however, rescued by restoration o

224 sphatidylserine to the cytosolic leaflets of ISG and the plasma membrane to facilitate the docking an

225 te that IL-28B may act as a key regulator of ISG expression during primary CMV infection.

226 IFN-beta induces dose-dependent secretion of ISG chemokines in cultured microglia and robust ISG expr

227 In further screening a set of ISG proteins we discovered that several other such prote

228 s and new insights into the specificities of ISG actions.

229 mily proteins constitute a major subclass of ISG proteins and are characterized by multiple tetratric

230 nduction, IFN signaling, or transcription of ISG mRNA.

231 This delayed activation of ISGs required IRF3 and coincided with an approximately 1

232 the robust production of type I IFNs and of ISGs, whose expression was inhibited by anti-type I IFN

233 The conservation of ISGs involved in antiviral signaling indicates conservat

234 mRNA expression of ISGs was higher in EOT liver biopsies of patients who ac

235 s revealed that EFTUD2-induced expression of ISGs was mediated through interaction of the EFTUD2 down

236 pulse also demonstrated robust expression of ISGs.

237 ly, knockdown of SOCS1 enhanced induction of ISGs and reduced viral yield in chIFN-alpha-stimulated D

238 to a sustained increase in the induction of ISGs at 37 degrees C relative to 33 degrees C.

239 IFN also stimulated more robust induction of ISGs at 37 degrees C than at 33 degrees C.

240 Inefficient induction of ISGs contributes to poor control and persistence of hepa

241 We constructed an arrayed library of ISGs from rhesus macaques and tested the ability of hund

242 The majority of ISGs regulated in the STAT1-, STAT2-, or IRF9-deficient

243 However, only a minor number of ISGs were common to WT and STAT1-, STAT2-, and IRF9-defi

244 ged and correlated with increased numbers of ISGs expressed at 12 h versus 4 h of IFN-alpha exposure

245 nt-onset T1D subjects show overexpression of ISGs, with an expression pattern similar to that seen in

246 pression and tissue distribution patterns of ISGs that segregated with treatment outcome.

247 Our results expand the range of ISGs that can be exploited by HCMV for its replication.

248 edly, we observed only mild up-regulation of ISGs in STING N153S fibroblasts and splenocytes and STIN

249 each mammal possesses a unique repertoire of ISGs, including genes common to all mammals and others u

250 e, allowing induction of a broad spectrum of ISGs by IFN signaling.

251 rex1 regulated the activation of a subset of ISGs independently of interferon.

252 with p12/p8 did not demonstrate an effect on ISG expression.

253 ith viral load, but not with HCV genotype or ISG expression.

254 No difference in interferon or ISG expression was observed according to clinical asthma

255 FN regulatory factor 3 (IRF3) to IFN-beta or ISGs promoters and sharply reduced gene activation.

256 Most of the overexpressed ISGs, including GBP1, TLR3, OAS1, EIF2AK2, HLA-E, IFI6,

257 ccess to an asynchronous discussion board; P-ISG also included structured opportunities to help and e

258 ISG (S-ISG) and an enhanced prosocial ISG (P-ISG).

259 e randomly assigned to either the S-ISG or P-ISG condition.

260 Relative to the S-ISG, participants in the P-ISG condition exhibited more supportive behaviors (emoti

261 Relative to the S-ISG, participants in the P-ISG condition had a higher level of depression and anxie

262 manipulation of supportive behaviors, the P-ISG did not produce better mental health outcomes in dis

263 Using a minilibrary of porcine ISGs, we identify porcine guanylate-binding protein 1 (G

264 andard ISG (S-ISG) and an enhanced prosocial ISG (P-ISG).

265 aling, LILRB1 coligation resulted in reduced ISG expression for enhanced DENV replication.

266 roughput cDNA screening for genes regulating ISG expression identified a tyrosine kinase nonreceptor

267 Mechanistically, PRDM16 represses ISGs through binding to promoter regions of these genes

268 chemokines in cultured microglia and robust ISG expression in microglia both in vitro and in vivo Fi

269 survivors of breast cancer relative to an S-ISG.

270 l compared the efficacy of a standard ISG (S-ISG) and an enhanced prosocial ISG (P-ISG).

271 Women were randomly assigned to either the S-ISG or P-ISG condition.

272 Relative to the S-ISG, participants in the P-ISG condition exhibited more

273 Relative to the S-ISG, participants in the P-ISG condition had a higher le

274 mparative analysis reveals that the screened ISGs target positive-sense single-stranded RNA viruses m

275 roteins of PVM lowered the levels of several ISG (IFN-stimulated gene) proteins as well.

276 In this article, we report several ISG proteins that strongly inhibit PIV3 growth, the use

277 Several ISGs that directly inhibit virus infection are described

278 with decreased hepatic expression of several ISGs (r = -0.68; P = 0.001); a 2-fold reduction in a fou

279 First, lack of a single ISG in mice, Ifit2, resulted in high mortality after SeV

280 Some ISGs are controlled by Stat1/2 and Irf9 and the ISRE DNA

281 e in subsets of cells and that at least some ISGs have specific inhibitory functions in restricted ti

282 Human specific ISG transcript levels in mouse liver increased significa

283 The protective roles of specific ISGs against the mouse hepatitis virus (MHV) members of

284 is trial compared the efficacy of a standard ISG (S-ISG) and an enhanced prosocial ISG (P-ISG).

285 ISG15, one such ISG, can form covalent conjugates to many cellular prote

286 ntrast, eVP24 and mVP40, despite suppressing ISG production upon RIG-I activation, failed to block up

287 The results indicate that ISG phospholipids are in a dynamic state and are consist

288 tiretroviral effects of IFN, suggesting that ISGs with antiretroviral activity are yet to be describe

289 nreceptor 1 (TNK1) as a unique player in the ISG induction pathway.

290 study demonstrates a protective role of the ISG Ifit2 in encephalitis induced by the dual hepato- an

291 provide a forward-looking perspective on the ISG landscape.

292 ions from gene expression changes within the ISG and Bcl2 gene families.

293 ks exist upstream of nuclear import, but the ISGs that suppress infection, e.g., prior to (or during)

294 These ISGs were otherwise induced in primary respiratory epith

295 IFITM3 is a small transmembrane ISG that restricts a broad range of viruses, including o

296 pus alecto) consists of conserved and unique ISG expression profiles.

297 Next, we describe ways in which ISGs both enhance innate pathogen-sensing capabilities a

298 genes (ISGs), but it is often unclear which ISGs are responsible for inhibition of a given virus.

299 r which forms of HCV RNA are associated with ISG induction and IFN resistance during natural infectio

300 anded RNA (ssRNA) correlated positively with ISG induction.