ライフサイエンスコーパス: ISG

1 ISG expression was confirmed in patient-derived organoid

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

3 ISG signature-positive cancer cells are sensitive to the

4 ISG(high) patients die significantly earlier after hospi

5 ISG-15 mRNA was prominent near infected cells, but not i

6 We identified interactions between 104 ISGs and 1,401 cellular binding partners engaging in 2,7

7 The mRNA of interferon-stimulated gene-15 (ISG-15), also known as ISG15 ubiquitin like modifier (IS

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

9 Moreover, we detected activated ISG-expressing microglia enveloping NA-containing neurit

10 In AD models, activated ISG-expressing microglia exclusively surrounded NA+ amyl

11 and localized to the promoters of activated ISGs.

12 osinic:polycytidylic acid exposure activates ISGs, and this stimulation significantly inhibits HBV in

13 cGAS is primarily responsible for activating ISG responses in biologically relevant cell types infect

14 tes PDAC growth and metastasis by activating ISGs and maintaining Golgi complex integrity.

15 The interferon epigenomic signature affects ISGs and other gene sets, including canonical targets of

16 The amplified ISG profile is then maintained lifelong.

17 that blocking Ifnar1 reverses the amplified ISG transcriptome in adults.

18 ADAR, a dsRNA-editing enzyme that is also an ISG.

19 ession screening, we identified TRIM69 as an ISG that potently inhibits VSIV.

20 demonstrate that dACE2, but not ACE2, is an ISG.

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

22 RNA sequencing and other methods to analyze ISG expression across five time points from fetal develo

23 afish and humans, revealing a core ancestral ISG repertoire that includes most of the known signaling

24 erferon response factor (IRF) activation and ISG responses to vaccinia virus lacking F17 in both macr

25 2',3'-cGAMP and also activated IFN-beta and ISG expression; and (v) UL46 binds to both STING and TBK

26 lterations in MBC, including AR, CHI3L1, and ISG, arise following estrogen-deprivation, and ER-mutant

27 so transcriptionally regulate cell cycle and ISG responses that permit ZIKV to persistently infect hB

28 s ability to block the expression of IFN and ISG mRNA.

29 100 proteins that act as immune response and ISG antagonists, while F17 helps suppress cGAS-mediated

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

31 hway and independently facilitates antiviral ISG expression.

32 5 as critical in the regulation of antiviral ISG and cell cycle responses that permit ZIKV to persist

33 repeats 1 (IFIT1) is the principal antiviral ISG for parainfluenza virus 5.

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

35 e early overexpression of specific antiviral ISGs, but the later response is dominated by an unantici

36 Using arrayed ISG expression screening, we identified TRIM69 as an ISG

37 systemically had exacerbated and arrhythmic ISG/Irf7 expression after IMQ.

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

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

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

41 Immunophenotyping and CD4 T-cell ISG expression analysis revealed marginal differences ac

42 s methodologies to identify and characterize ISG function.

43 We identified 72 orthology groups containing ISGs in both zebrafish and humans, revealing a core ance

44 FN-stimulated response elements that control ISG expression.

45 However, anti-CSFV ISGs are poorly documented.

46 y neutrophils were analyzed for differential ISG expression by PCR, STAT1 phosphorylation and markers

47 types play an important role in the diurnal ISG response to IMQ.

48 Finally, BS patients demonstrate elevated ISG expression in peripheral blood.

49 thies, in which individuals exhibit elevated ISG expression in the absence of pathogenic infection.

50 orcine and rhesus cells demonstrate enhanced ISG expression and protection against vesicular stomatit

51 f the cytoplasmic exonuclease TREX1 enhances ISG expression in BLM-deficient fibroblasts.

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

53 Gs) in the absence of IRF-7, with only a few ISGs showing attenuated expression in IRF-7-deficient pe

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

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

56 RF9 (key transcription factors necessary for ISG transcription) to ISG promoters.

57 at mitochondrial respiration is required for ISG expression in CD4(+) T cells and provides a novel me

58 quimod (IMQ) to activate IFN-sensitive gene (ISG) pathways and induce psoriasiform inflammation.

59 ogens, and interferon (IFN)-stimulated gene (ISG) activation is a central feature.

60 r JQ1 suppressed interferon-stimulated gene (ISG) expression and in combination with MEK inhibitors d

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

62 ramatically hyperinduce IFN stimulated gene (ISG) expression following M. tuberculosis infection, cyt

63 s and quantified interferon-stimulated gene (ISG) expression in CD4 T cells.

64 , as measured by interferon-stimulated gene (ISG) expression, and decreased HBV transcription and rep

65 of inflammatory interferon-stimulated gene (ISG) expression, which is mediated by the cGAS-STING-IRF

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

67 mediated by the interferon-stimulated gene (ISG) family.

68 ACE2 is a human interferon-stimulated gene (ISG) in vitro using airway epithelial cells and extend o

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

70 s of specific antiviral IFN-stimulated gene (ISG) products, such as RIG-I and IFITM3, in human and mo

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

72 rferon (IFN) and interferon-stimulated gene (ISG) responses, including the HIV-1 restriction factor I

73 TOR) to suppress interferon-stimulated gene (ISG) responses.

74 led intrahepatic interferon stimulated gene (ISG) responses.

75 ibited higher levels of IFN-stimulated gene (ISG) RNA, the transcriptional end point of IFN activatio

76 An IFN-stimulated gene (ISG) signature was detected in the brains of multiple mu

77 signaling, specifically IFN-stimulated gene (ISG) signatures, in primary tumors from The Cancer Genom

78 1 (SLFN11) is an interferon-stimulated gene (ISG) that we previously have demonstrated to ablate tran

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

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

81 n proposed as an interferon-stimulated gene (ISG).

82 l expression of interferon stimulated genes (ISG(high)) and cytokines, high viral loads and limited p

83 ression of IFNbeta and IFN-stimulated genes (ISG) in breast cancer cells in vitro and tumors in vivo.

84 to identify two interferon-stimulated genes (ISG) with poorly characterized function, interferon-indu

85 ranscription of interferon-stimulated genes (ISG).

86 iptional activation of IFN-stimulated genes (ISG).

87 rotein 1 (CHI3L1), and IFN-stimulated genes (ISG).

88 ects on the expression of IFN-induced genes (ISGs) in the absence of IRF-7, with only a few ISGs show

89 is.IMPORTANCE The role of IFN-induced genes (ISGs) in viral infection remains incompletely understood

90 sion of antiviral interferon response genes (ISGs) and positive correlation with integrin alpha(v) (I

91 s the transcription of IFN-stimulated genes (ISGs) after IFN-alpha treatment.

92 y of nearly 400 interferon-stimulated genes (ISGs) against a biologically contained Ebola virus and i

93 feron (IFN) and interferon stimulated genes (ISGs) and causes blunted interferon responses to mycobac

94 Interferon (IFN)-stimulated genes (ISGs) and extracellular matrix remodeling genes were sup

95 ecreased expression of IFN-stimulated genes (ISGs) and gamma interferon (IFN-gamma), likely secondary

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

97 ubsequent induction of IFN-stimulated genes (ISGs) are highly effective innate strategies utilized by

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

99 ession of interferon (IFN) stimulated genes (ISGs) associated with decreased capacity of neutrophils

100 pregulation of several IFN-stimulated genes (ISGs) at both the mRNA and protein levels.

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

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

103 d expression of interferon-stimulated genes (ISGs) distinguished cells from children with SLE from he

104 ', of canonical interferon-stimulated genes (ISGs) encoding molecules important for antiviral respons

105 tion of several interferon-stimulated genes (ISGs) following WNV infection or IFN-beta treatment.

106 Interferon-stimulated genes (ISGs) form the backbone of the innate immune system and

107 aling decreases interferon-stimulated genes (ISGs) in cancer cells, it increases ISGs in immune cells

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

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

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

111 and the expression of IFN-stimulated genes (ISGs) IRF1, IRF7, and MxA.

112 iption of these interferon-stimulated genes (ISGs) occurs upon activation of the canonical Janus kina

113 creening of individual IFN-stimulated genes (ISGs) on hepadnaviral mRNAs transcribed from cccDNA, we

114 a short list of interferon-stimulated genes (ISGs) previously reported to have antiviral activity.

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

116 interferons (IFN) and IFN-stimulated genes (ISGs) provided important insights into the contributions

117 -28A/B) and the interferon-stimulated genes (ISGs) such as myxovirus resistance 1 (Mx1), oligoadenyla

118 the expression of many IFN-stimulated genes (ISGs) that encode host-protective proteins.

119 to induction of interferon-stimulated genes (ISGs) through JAK/STAT signaling.

120 e expression of interferon-stimulated genes (ISGs) upon alpha interferon (IFN-alpha) stimulation in c

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

122 y, increased levels of IFN-stimulated genes (ISGs) were described in COPA syndrome.

123 induction of a set of IFN stimulated genes (ISGs) with regulatory or antiviral function, resulting i

124 that one of the interferon-stimulated genes (ISGs), cholesterol 25-hydroxylase (CH25H), is induced by

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 f interferon (IFN) and IFN-stimulated genes (ISGs), including, among others, the ubiquitin-like prote

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

129 e expression of interferon-stimulated genes (ISGs), many of which are responsible for the cellular an

130 by a family of interferon-stimulated genes (ISGs), providing cell-intrinsic immunity.

131 enes as well as interferon-stimulated genes (ISGs), such as ISG15 and bone marrow stromal cell antige

132 ntiviral type I interferon-stimulated genes (ISGs), we hypothesized that STING N153S knock-in mice ma

133 bits the expression of IFN-stimulated genes (ISGs), which are necessary for KLF7-mediated PDAC tumor

134 of hundreds of interferon-stimulated genes (ISGs), which can inhibit viral replication at different

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

136 ling and expression of IFN-stimulated genes (ISGs), which mediate antiviral activity.

137 activate expression of IFN-stimulated genes (ISGs), which protect hosts from infection.

138 riptional induction of IFN-stimulated genes (ISGs).

139 f which are encoded by IFN-stimulated genes (ISGs).

140 upregulation of interferon-stimulated genes (ISGs).

141 e production of interferon-stimulated genes (ISGs).

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

143 lation of type I IFN (IFN)-stimulated genes (ISGs).

144 cation by upregulating IFN-stimulated genes (ISGs).

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

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

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

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

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

150 ility to induce interferon stimulated genes (ISGs).

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

152 T (roIFNT) induced the IFN-stimulated genes (ISGs; MX2, ISG15, and OAS1Y).

153 timulate genes (interferon-stimulated genes [ISGs]) that are integral to antiviral host defense.

154 cellular life of insulin secretory granules (ISGs) from biogenesis to secretion depends on their stru

155 ansporter in the insulin-secretory granules (ISGs) of pancreatic beta-cells.

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

157 he Cancer Cell Line Encyclopedia that harbor ISG signatures demonstrate that this is a by-product of

158 sults could have implications for harnessing ISG responses to reduce transmission or control pathogen

159 The high ISG expression signature (ISG(hi)) derived from a small

160 d from day 18 pregnant cows comprised higher ISGs together with elevated FGF2, PDGFB, and XIAP, compa

161 data contribute to our understanding of how ISGs prevent viral infections.

162 ic and vaccine strategies, understanding how ISGs restrict VSIV not only helps in understanding VSIV-

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

164 ly to WT, infection with W105A inhibited IFN/ISG expression despite displaying an attenuated phenotyp

165 eview is the antiviral activities of the IFN/ISG system.

166 omprehensive understanding of this important ISG.

167 f IEC organoids with type III IFN results in ISG expression that mirrors the in vivo type III IFN res

168 pansion of unique subpopulations enriched in ISGs and/or in monogenic lupus-associated genes classifi

169 heir human orthologs were highly enriched in ISGs, particularly for highly inducible genes.

170 role of the innate immune system, including ISGs, in controlling retroviral infections is currently

171 d genes (ISGs) in cancer cells, it increases ISGs in immune cells by enhancing IFNG produced by exhau

172 How the majority of individual ISGs inhibit the replication of particular viruses is un

173 xplore the molecular functions of individual ISGs.

174 , reverses the diurnal rhythm of IMQ-induced ISG expression in the skin.

175 sion results in a reduction of the inducible ISG response.

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

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

178 on of IFN, while vIRF1 and vIRF2 can inhibit ISG induction downstream of the IFN receptor.

179 ade PML, reduce STAT2 expression, or inhibit ISG induction.

180 t is not known whether any RRV vIRFs inhibit ISG induction following IFN receptor signaling.

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

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

183 tern shows severely damaged lungs, low ISGs (ISG(low)), low viral loads and abundant infiltrating act

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

185 after IMQ treatment, ISGs, including the key ISG transcription factor IFN regulatory factor 7 (Irf7),

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

187 These results reveal that BLM limits ISG induction, thus connecting DNA damage to cellular in

188 er pattern shows severely damaged lungs, low ISGs (ISG(low)), low viral loads and abundant infiltrati

189 they have exacerbated inflammation and lower ISG expression in the lungs.

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

191 quantitatively dramatic upregulation of many ISGs, which confers broad viral infection resistance.

192 to trigger constitutive upregulation of many ISGs.

193 In contrast, type I IFN elicits a marginal ISG response in neonatal mouse IECs and does not inhibit

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

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

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

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

198 While most ISGs are antiviral, some ISGs have been shown to promote

199 h-specific gene families containing multiple ISGs, including finTRIMs.

200 Specifically, the expression of multiple ISGs was lower in infected than in bystander cells.

201 Notably, LTRs nearby ISGs are derepressed likely rendering these genes more r

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

203 Despite this, ablation of ISG responses through cGAS or STING knockout did not res

204 d in immune-deficient mice shows evidence of ISG-positive tumors that correlates with expression of h

205 hed by numerous human and murine examples of ISG hyperactivation, including constitutive MDA5 activat

206 ure in some primary tumors, the existence of ISG signature-positive tumors without evident infiltrati

207 t phosphorylation of STAT1 and expression of ISG proteins, while SARS-CoV is able to suppress both.

208 This includes general paradigms of ISG function, supported by specific examples in the lite

209 y to high-throughput cell-based screening of ISG structure and dynamics under various physiological a

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

211 ression of 60% of ISGs and upregulates 3% of ISGs.

212 y represses IFN-induced expression of 60% of ISGs and upregulates 3% of ISGs.

213 Despite a complete absence of ISGs induction, the GS2 cell line has a remarkable abili

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

215 was due to the direct antiviral activity of ISGs or whether cells were nonpermissive because of tran

216 Assessment of ISGs and neutrophil maturation genes in Klinefelter synd

217 ge diffusivity, and anomalous coefficient of ISGs, without the need to extract individual trajectorie

218 ciated with altered neutrophil expression of ISGs and neutrophil extracellular trap release is not kn

219 Moreover, the high expression of ISGs was associated with significantly reduced survival

220 uding IRF3 phosphorylation and expression of ISGs.

221 ts crucial to tightly regulate expression of ISGs.

222 pulse also demonstrated robust expression of ISGs.

223 One family of ISGs with antiviral function is the interferon-inducible

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

225 In this cell line, the induction of ISGs by stimulation with a recombinant type I IFN is com

226 BeAg(+) patients exhibit weaker induction of ISGs in their livers than do HBeAg(-) patients upon IFN-

227 We observed elevated levels of ISGs and IFN-alpha in blood of symptomatic COPA patients

228 quencing to generate a comprehensive list of ISGs of zebrafish, taking advantage of the high-quality

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

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

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

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

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

234 -1 infection highlights the complex roles of ISGs in viral infection and viral pathogenesis.

235 Thus, these results highlight a set of ISGs directly relevant for rescuing cells from ZIKV infe

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

237 illuminates a far wider activity spectrum of ISGs than is currently known.

238 n the IFN responsiveness of major subsets of ISGs depending on the presence of butyrate in the cell e

239 bsequently required for the transcription of ISGs and for IFN-driven antiproliferative responses in b

240 ded PR alone could decrease transcription of ISGs.

241 responded to plasmid DNA by upregulation of ISGs and release of bioactive interferon.

242 One ISG located at the plasma membrane is interferon-inducib

243 A comprehensive study of one ISG (CCDC92) that shows anti-Ebola activity in our scree

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

245 sult in preferential induction of peripheral ISG responses.

246 more careful interpretation of many previous ISG-based reports in living beta-cells.

247 ANCE Interferon and its downstream products, ISGs, are essential in defending against pathogen invasi

248 to respond to dsRNA accumulation, rendering ISG-positive tumors susceptible to ADAR loss.

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

250 osphorylation of STAT3 at Ser727 and resolve ISG expression.

251 Integration of the resulting ISG-interaction network with published datasets and func

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

253 tion of PML-NBs and the inhibition of robust ISG transcription.IMPORTANCE KSHV and RRV encode a uniqu

254 eas splenic cells show a reduction in select ISGs in response to IFN.

255 Cs to type III IFN in vivo enables selective ISG expression during infection that confers antiviral p

256 n factors IRF3, IRF7, and STAT1, and several ISG including RIG-I, IRF7, STAT1, and ADAR-p150.

257 y contained Ebola virus and identify several ISGs not previously known to affect Ebola virus infectio

258 The high ISG expression signature (ISG(hi)) derived from a small number of transcriptionall

259 Some ISGs have specific antiviral activity, whereas others re

260 While most ISGs are antiviral, some ISGs have been shown to promote viral infection, includi

261 Human specific ISG transcript levels in mouse liver increased significa

262 ducible GTPase 1 (IIGP1) is a mouse-specific ISG and belongs to the immunity-related GTPases (IRGs) f

263 ght into the function of this mouse-specific ISG.IMPORTANCE Interferon and its downstream products, I

264 reas the expanded set of type I IFN-specific ISGs, including proapoptotic genes, have weak ISRE motif

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

266 nate immunity and to determine how sustained ISG upregulation can be compatible with robust health.

267 fter, we investigate the effect of FP-tagged ISG protein markers on the structural and dynamic proper

268 Overexpression of the top ten ISGs attenuates virus titers by up to 1000-fold.

269 ificantly earlier after hospitalization than ISG(low) patients.

270 rray of antiviral genes, particularly in the ISG family, the mechanism of which is poorly understood.

271 Intriguingly, baseline serum levels of the ISG CXCL10 predicted HBV reactivation in a cohort of coi

272 A large proportion of the ISG repertoire is lineage specific; around 40% of protei

273 ven by BMAL1, as a negative regulator of the ISG response, and highlight the finding that feeding tim

274 Our results suggest that the ISG-type induction of dACE2 in IFN-high conditions creat

275 hile immune infiltration correlates with the ISG signature in some primary tumors, the existence of I

276 The ISGs stimulated in common by type I and III IFNs have st

277 e is a need to identify and characterize the ISGs that possess anti-VSIV activity.

278 ultidimensional parametric space defines the ISGs' properties for different conditions.

279 One of the ISGs, IIGP1, has been found to constrain intracellular p

280 These ISGs can constrain viral replication, limit tissue tropi

281 These ISGs were otherwise induced in primary respiratory epith

282 any of the protein products encoded by these ISGs work alone or in concert to achieve one or more cel

283 n, the increased expression of both of these ISGs and the global enhancement in protein ISGylation we

284 robustness of the innate immune system, this ISG network may serve as a blueprint for therapeutic tar

285 oss 398 cancer cell lines, we show that this ISG transcriptional state creates a novel genetic vulner

286 Mechanistic studies demonstrate that three ISGs interfere with virus entry, six affect viral transc

287 ChIP analysis showed HDAC4 was recruited to ISG promoters following IFN stimulation and was needed f

288 factors necessary for ISG transcription) to ISG promoters.

289 The T-PLL International Study group (TPLL-ISG) set out to define standardized criteria for diagnos

290 Although transient ISG upregulation is essential for effective innate immun

291 In mouse skin 1 d after IMQ treatment, ISGs, including the key ISG transcription factor IFN reg

292 III IFN treatment elicits robust and uniform ISG expression in neonatal mouse IECs and inhibits the r

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

294 In conclusion, the upregulated ISG profile of RdRP mice is mostly triggered early postn

295 In RdRP mice, the proportion of upregulated ISGs increased during development, with the most dramati

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

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

298 umors, ZMYND8 was negatively correlated with ISGs, CD4, CD8A, CD8B, and the tumor-lymphocyte infiltra

299 We identified more than 400 zebrafish ISGs, defined as being either directly induced by IFN or

300 ific; around 40% of protein-coding zebrafish ISGs had no human ortholog.