ライフサイエンスコーパス: OAS

1 OAS may also have an important deterministic role in the

2 OAS produces a unique oligonucleotide second messenger,

3 OASs are IFN-induced enzymes that synthesize the RNase L

4 al gene, 2',5'-oligoadenylate synthetase 1a (OAS), were determined by real-time reverse-transcriptase

5 d expression of IFN-beta, IFN-lambda1/IL-29, OAS and viperin in asthmatics compared with healthy subj

6 We show that the induction of 2,5 OAS in response to IFN-gamma is BRCA1 and STAT1 dependen

7 -gamma-induced apoptosis is dependent on 2,5 OAS induction.

8 proliferation, transient transfection of 2,5 OAS into breast cancer cell lines results in decreased c

9 2,5 OAS is the only known upstream regulator of RNaseL, a re

10 targets, 2,5 oligoadenylate synthetase (2,5 OAS), is a mediator of BRCA1/IFN-gamma-induced apoptosis

11 IFN-gamma to transcriptionally activate 2,5 OAS, leading to the downstream activation of RNaseL and

12 ion, the expression of the IFN-inducible 2-5 OAS gene was significantly reduced in HUT78R cells, sugg

13 sis, we characterize the activation of 2'-5' OAS in lungs from mice exposed to CS and viral pathogen-

14 -5' oligoadenylate synthetase (OAS), a 2'-5' OAS-like (OASL) gene, galectin-9, myxovirus protein A (M

15 cells is to sequester dsRNA away from 2'-5' OAS.

16 ) and 2',5'-oligoadenylate synthetase (2',5'-OAS) were down-regulated in IFN-alpha-treated HEV-A549 c

17 N-alpha-stimulated genes encoding PKR, 2',5'-OAS, and myxovirus resistance A.

18 cells and induction of PD-1, PD-L1, and 2,5-OAS-1 in the liver.

19 levels of intrahepatic PD-1, PD-L1, and 2,5-OAS-1 messenger RNAs correlated with peak titers of HCV.

20 In children (N = 670), OAS (2.26 [2.09-2.44]) and AR comorbidity (1.47 [CI 1.39

21 SG-15, ISG-54, ISG-56, ISG-60, STAT1, IRF-9, OAS, and Mx1.

22 eins, of which the major isoforms, OAS-TL A, OAS-TL B, and OAS-TL C, catalyze the formation of Cys by

23 e that sulfate reduction and O-acetylserine (OAS) production together limit cysteine synthesis.

24 utilizes L-homocysteine and O-acetylserine (OAS) to produce cystathionine.

25 present in PC3 cells that bind and activate OAS.

26 in 2 (PCBP2) that bind and potently activate OAS.

27 ion, as well as to provide dsRNA to activate OAS.

28 NA containing modified nucleosides activates OAS less efficiently and induces limited rRNA cleavage.

29 vitro transcribed, unmodified RNA activates OAS, induces RNase L-mediated ribosomal RNA (rRNA) cleav

30 actions capable of binding to and activating OAS.

31 Active OAS proteins detect cytoplasmic dsRNA and synthesize sho

32 We sequenced each exon within all OAS and RNASEL genes in 33 individuals hospitalized with

33 ed through importers and exporters, allowing OAS to remotely activate RNase L and protect neighboring

34 Our results indicate that higher IFN-alpha, OAS, CXCL9, and CXCL10 mRNA expression in LN was associa

35 e activation of endogenous p69-OAS and of an OAS-Luc reporter and a synergistic activation of a GAS-L

36 s, but our study shows that the OAS-TL A and OAS-TL B of both halophytes are enzymes that also degrad

37 ch pollen is a common sensitizing agent, and OAS results when patients consume certain fruits, vegeta

38 the major isoforms, OAS-TL A, OAS-TL B, and OAS-TL C, catalyze the formation of Cys by combining O-a

39 Furthermore, higher expression of CXCL10 and OAS in peripheral blood could potentially serve as a dia

40 d (v) 'no-panallergen PFS': mild disease and OAS triggered by kiwifruit.

41 d to 129 SvEv mice, while prolactin mRNA and OAS mRNA levels were suppressed.

42 interferon-stimulated gene produces MxA and OAS.

43 The immunologic surrogates, neopterin and OAS, were induced at all doses with a sustained concentr

44 NA and can prevent activation of the PKR and OAS pathways.

45 ons of host defense proteins such as PKR and OAS that have been previously synthesized and merely awa

46 emical analyses of recombinant plant SAT and OAS-TL indicate that the reversible association of the p

47 e interaction between mitochondrial SAT3 and OAS-TL C in planta by FRET and establish the role of the

48 s regulated by the CysE-dependent signal and OAS were identified in P. stuartii and E. coli.

49 inetic parameters for cysteine synthesis and OAS: acetate lyase activity yield, within error, identic

50 ons, deletions, or nonsense mutations in any OAS or RNASEL gene.

51 ar complex, which is the origin of assembly (OAS) in RCNMV that selectively recruits and orients CP s

52 ch pollen rhinoconjunctivitis and associated OAS to apple were included in an open, randomized, contr

53 ufficient to compensate for inadequate basal OAS levels.

54 that the Us11 protein is sufficient to block OAS activation in extracts from uninfected, interferon-t

55 malian cells depleted 2-5A levels induced by OAS activation with poly(rI):poly(rC), preventing RNase

56 the result of high l-Cys degradation rate by OAS-TLs, whereas the greater organic-S and biomass accum

57 to Bet v 1 and/or Bet v 2, and foods causing OAS were similar in the two groups.

58 efficient Cys synthesis than total cellular OAS-TL activity in leaves.

59 intravascular drug delivery, and controlled OAS treatment of calcific plaques resulted in greater dr

60 Compared to controls, OAS-treated femoropopliteal segments exhibited 180mum th

61 ed by pretreatment at pH 8.5, which converts OAS to NAS.

62 regulation of interferon-inducible cytokines OAS and CXCL10/IP-10 compared with control mice treated

63 mutation previously hypothesized to disrupt OAS self-association had only a minor effect on OAS2 act

64 A sequences of the rat, cattle, pig, and dog OAS genes were amplified, sequenced and compared with ea

65 Upon binding dsRNA, OAS undergoes a conformational change and is activated t

66 While two tandemly duplicated OAS-like (OASL) genes were identified in the dog genome,

67 Products of the CysE enzyme (OAS, N-acetyl-L-serine [NAS], O-acetyl-L-threonine, and

68 ntitumor drug bleomycin produces exclusively OAS in the form of C-4-keto-C-1-aldehydes in unbroken DN

69 nes were detected in the pig genome and five OAS genes were found in both the cattle and dog genomes.

70 s compensated by an increase in affinity for OAS, leading to the observed second-order rate constant,

71 emained an independent prognostic factor for OAS (P = .013; hazard ratio [HR], 1.893).

72 s not a statistically significant factor for OAS or EFS in the total cohort or in pediatric patients.

73 e to the WT and loss-of-function mutants for OAS-TLs in the cytosol, plastids, and mitochondria.

74 tegy based on stringent affinity of RNAs for OAS.

75 Four OAS genes were detected in the pig genome and five OAS g

76 e OASS-catalyzed elimination of acetate from OAS.

77 The elimination of acetic acid from OAS is thought to proceed via an anti-E2 mechanism, and

78 Furthermore, in the absence of a functional OAS pathway, corneal HSV-1 Ag expression was more widesp

79 wild-type mice or mice lacking a functional OAS pathway, these results suggest that PKR is the domin

80 that the presence of at least one functional OAS-TL isoform is essential for the proper function of t

81 ptional upregulation of IFN-responsive genes OAS and ISG54 (encoding 2'-5' oligoadenylate synthetase

82 red with CSC-bound SAT and explains the high OAS export rate of WT mitochondria in the presence of cy

83 -acetyl-serine(thiol)lyase (OASTL) homologs, OAS-B, which is an authentic OASTL, and CS26, which has

84 Three forms of human OAS have been described corresponding to proteins of 40/

85 of the gene encoding the large form of human OAS.

86 izing 2-5As and differs from the other human OAS family members by having two C-terminal ubiquitin-li

87 ed among the different isoforms of the human OAS family, reflecting the evolutionary link among them.

88 The human OAS-like (OASL) protein, however, does not harbor the ca

89 r prostate cancer, we sought to determine if OAS activators are present in prostate cancer cells.

90 immune regulatory genes (e.g., IFI27, IFI44, OAS, and BST2) was increased.

91 representative IFN-stimulated genes (IFIT3, OAS, LMP2, TGTP, and USP18) in both neonatal and adult b

92 clease domain is preferentially conserved in OAS derivatives that lack an active nucleotidyltransfera

93 fluorescent paclitaxel penetrated deeper in OAS-treated femoropopliteal segments compared to control

94 wever, participants with larger increases in OAS level exhibited greater decreases in plasma viral lo

95 and mice; the functions of these inactivated OAS derivatives remain unknown.

96 In peripheral blood, increased OAS and CXCL10 expression were elevated in SIV(+) monkey

97 So far, the significance of individual OAS-TL-like enzymes is unresolved.

98 occurrence of PF to correlate with inferior OAS expectancies in adult but not in pediatric patients.

99 propose that OAS1D suppresses the interferon/OAS/RNase L-mediated cellular destruction by interacting

100 -like proteins, of which the major isoforms, OAS-TL A, OAS-TL B, and OAS-TL C, catalyze the formation

101 ; (iii) 'LTP PFS': living in Southern Italy, OAS triggered by hazelnut and peanut; (iv) 'PR-10 PFS':

102 in RNA reduce 2-5A pathway activation joins OAS and RNase L to the list of RNA sensors and effectors

103 rine)E(t), V/K(AcCoA)E(t), V(2)/E(t), V(2)/K(OAS)E(t), and V/K(CoA)E(t) are 3300 +/- 180 s(-1), (9.6

104 rections, as well as the V/K(serine) and V/K(OAS), decrease at low pH, exhibiting a pK of approximate

105 The V/K(OAS), which reflects the first half-reaction, is identic

106 virus antagonize the oligoadenylate-RNase L (OAS-RNase L) pathway.

107 the host oligoadenylate synthetase-RNase L (OAS-RNase L) system, a potent antiviral pathway effectiv

108 rase (SAT) and O-acetylserine (thiol) lyase (OAS-TL) in the cytosol, plastids, and mitochondria of pl

109 ajor function of O-acetyl-Ser-(thiol) lyase (OAS-TL; EC 2.5.1.47) is the formation of l-Cys, but our

110 genes encode for O-acetylserine(thiol)lyase (OAS-TL)-like proteins, of which the major isoforms, OAS-

111 Generation of all major OAS-TL double loss-of-function mutants in combination wi

112 sis was not affected by the absence of major OAS-TLs, indicating significant transport of Cys into th

113 siveness of Cys synthesis by the three major OAS-TLs and ruled out alternative sulfur fixation by oth

114 her two human DNA repair enzymes can mediate OAS excision in vitro: Ape1 protein (the main human abas

115 The predominant role of mitochondrial OAS synthesis was validated in planta by feeding [(3)H]s

116 of episodic positive selection in the mouse OAS-like proteins with inactivated nucleotidyltransferas

117 uced mRNA expression of antiviral genes MX1, OAS, and ISG56 but not IFN-beta.

118 The ability of OAS to activate the cma37::lacZ fusion was abolished by

119 abidopsis was found to cause accumulation of OAS, Cys, and glutathione, mimicking the biochemical cha

120 roduct is able to counteract the activity of OAS, a third cellular protein critical for host defense.

121 ha-aminoacrylate intermediate on addition of OAS, suggesting that K42 is involved in the abstraction

122 ha-aminoacrylate intermediate on addition of OAS.

123 Comparative sequence analysis of OAS, poly(A)-polymerases, TRF4/sigma-family polymerases,

124 bstituted enzyme suggest that the binding of OAS as it forms the external Schiff base is such that th

125 In the 7 cases of OAS, detection rate of allergen-specific IgE to shrimp w

126 an a similar linear sequence is the cause of OAS.

127 nse revealed that the high concentrations of OAS, Cys, and GSH observed in this hyperaccumulator coin

128 The first half-reaction, conversion of OAS to the alpha-aminoacrylate intermediate and acetate,

129 rases, suggest that the C-terminal domain of OAS and their homologs might have nuclease activity.

130 To better understand these drivers of OAS activation, we tested the impact of defined sequence

131 We compared the effect of OAS gene family variants on 2 DENV serotypes in cell cul

132 dditionally, our studies provide evidence of OAS in the acute-phase dengue virus immune response, pro

133 -C plants showed the SAT-dependent export of OAS.

134 with relatively high levels of expression of OAS genes, which are necessary but not sufficient for in

135 Feeding of OAS to the PaAPR-expressing plants caused cysteine and g

136 he oligomerization and catalytic function of OAS enzymes.

137 asis for future work examining the impact of OAS phenotype antibodies on protective immunity and dise

138 L following infection, despite induction of OAS expression.

139 Inhibition of OAS specifically requires the Us11 dsRNA-binding domain,

140 interferon and the consequent high levels of OAS mRNA induced in these cell types.

141 express significantly higher basal levels of OAS transcripts than nonmyeloid cells.

142 relates with high basal expression levels of OAS, as found in myeloid cells.

143 relates with high basal expression levels of OAS, as found in myeloid cells.

144 es revealed that subcellular localization of OAS-TL proteins is more important for efficient Cys synt

145 In addition, oligomerization of OAS isozymes, potentially OAS1 and OAS2, is hypothesized

146 servations help define mammalian pathways of OAS repair, point to interactions that might coordinate

147 possibly involved in the physiopathology of OAS and (ii) CD68+ macrophages likely critical in allerg

148 cleaves 2',5'-oligoadenylate, the product of OAS, to prevent activation of the cellular endoribonucle

149 plotype in the transcriptional regulation of OAS genes at baseline and infected conditions.

150 en from the general population, reporting of OAS and of AR comorbidity appear to be the strongest pre

151 article, we review how the understanding of OAS has progressed from its initial description and high

152 , hepatocytes express undetectable levels of OASs and RNase L, which likely explains the lack of RNas

153 r regular apple consumption has an effect on OAS and immune parameters of Mal d 1 or Bet v 1 allergy.

154 Only OAS was capable of activating the cma37::lacZ fusion.

155 led out alternative sulfur fixation by other OAS-TL-like proteins.

156 ced an additive activation of endogenous p69-OAS and of an OAS-Luc reporter and a synergistic activat

157 In the decades that have passed, OAS-like responses have been shown to play an integral r

158 In pediatric patients, OAS and EFS did not differ significantly between patient

159 ed by hazelnut and peanut; (iv) 'PR-10 PFS': OAS triggered by Rosaceae; and (v) 'no-panallergen PFS':

160 (IFN-alpha/beta), IFN-stimulated genes (PKR, OAS, Mx1, and ISG15 genes), IFN-induced proteins with te

161 d recruit the antiviral proteins Rig-I, PKR, OAS, and RNase L to avSGs.

162 es known to encode antagonists of the potent OAS-RNase L antiviral pathway, highlighting its importan

163 which the wild-type virus blocks the potent OAS-RNase L antiviral pathway.

164 atalyzes the acetylation of l-Ser to produce OAS, which acts as both a key positive regulator of sulf

165 ermediate collapses, generating the products OAS and CoASH.

166 The presence of cysteine resulted in reduced OAS export in mitochondria of oastl-C mutants but not in

167 In addition, the reduced OAS expression may result in modulation of prolactin rec

168 does not consistently improve apple related OAS symptoms, we evaluated whether regular apple consump

169 ity with the substrate L-serine and required OAS exclusively.

170 Upon sensing double-stranded RNA, OAS produces 2',5'-oligoadenylates (2-5A), which activat

171 Upon binding target RNA, OAS is activated to produce 2'-5'-linked oligoadenylates

172 manner to stimulate the production of select OAS moieties.

173 , synthesizes cysteine from O-acetyl serine (OAS) and sulfur in bacteria and plants.

174 thesis of l-cysteine from O-acetyl-l-serine (OAS) and inorganic bisulfide.

175 cysteine and acetate from O-acetyl-L-serine (OAS) and sulfide.

176 the beta-acetoxy group of O-acetyl-L-serine (OAS) by a thiol to give L-cysteine.

177 replacement of acetate in O-acetyl-L-serine (OAS) by sulfide to give L-cysteine.

178 ubstitution of acetate in O-acetyl-L-serine (OAS) by sulfide via a ping-pong kinetic mechanism .

179 the beta-acetoxy group of O-acetyl-L-serine (OAS) is replaced by bisulfide to give L-cysteine and ace

180 on of the acetyl group of O-acetyl-L-serine (OAS) to form the alpha-aminoacrylate intermediate.

181 the beta-acetoxy group of O-acetyl-l-serine (OAS) with inorganic bisulfide.

182 of glutathione, Cys, and O-acetyl-l-serine (OAS), in shoot tissue, are strongly correlated with the

183 e conversion of serine to O-acetyl-L-serine (OAS).

184 mvent the effects of original antigenic sin (OAS) in certain circumstances.

185 s are reminiscent of original antigenic sin (OAS), given that the patients had prior dengue virus exp

186 address the issue of original antigenic sin (OAS): the phenomenon where the induced antibody shows hi

187 The term "original antigenic sin" (OAS) was first used in the 1960s to describe how one's f

188 deoxyribose generates oxidized abasic sites (OAS) that may constitute one-third of ionizing radiation

189 as compared with its affinity for substrate, OAS.

190 ivariable analysis, 5-year overall survival (OAS) of patients with and without PF was 63% versus 71%,

191 [95% CI 1.29-1.41]), oral allergy symptoms (OAS) (4.46 [4.19-4.75]), allergic rhinitis (AR) comorbid

192 ols with a history of oral allergy syndrome (OAS) induced by the same foods.

193 e often an associated oral allergy syndrome (OAS) to apple, which contains the cross-reactive allerge

194 (ii) 'profilin PFS': oral allergy syndrome (OAS) triggered by Cucurbitaceae; (iii) 'LTP PFS': living

195 e diagnosed as having oral allergy syndrome (OAS), and only few cases of FDEIA are reported.

196 patients with/without oral allergy syndrome (OAS), at baseline and after 5 months of sublingual aller

197 to be responsible for oral allergy syndrome (OAS), in which sensitization to airborne allergens cause

198 genes p56- and p69-oligoadenylate synthase (OAS).

199 The 2',5'-oligoadenylate (2-5A) synthetase (OAS)-RNase L system is a mechanism for restricting viral

200 NA activation of 2'-5' oligo (A) synthetase (OAS), it is likely that the primary role of dsRNA bindin

201 (NOS2) and 2', 5' oligoadenylate synthetase (OAS) 1 induction in response to virus or IFNgamma.

202 urements of 2',5'-oligoadenylate synthetase (OAS) activity, and induction levels of interferon-induci

203 d equivalent 2'5' oligoadenylate synthetase (OAS) and MX1 gene expression in this cell type.

204 ced enzymes 2'-5'-oligoadenylate synthetase (OAS) and RNase L are key components of innate immunity i

205 )-inducible 2'-5'-oligoadenylate synthetase (OAS) and RNase L pathway effectively suppresses the repl

206 sistance 1 (Mx1), oligoadenylate synthetase (OAS) and viperin in unstimulated sputum cells in 57 asth

207 PKR and the 2'-5' oligoadenylate synthetase (OAS) are both activated by double-stranded RNA (dsRNA) p

208 2',5'-Oligoadenylate synthetase (OAS) enzymes and RNase-L constitute a major effector arm

209 The oligoadenylate synthetase (OAS) enzymes are cytoplasmic dsRNA sensors belonging to

210 < 0.01); and 2'5'-oligoadenylate synthetase (OAS) had a 163 (+/-120.6) pmol/dl increase (P < 0.01).

211 The 2'-5' oligoadenylate synthetase (OAS) locus encodes for three OAS enzymes (OAS1-3) involv

212 e Mx(+) and 2'-5' oligoadenylate synthetase (OAS) proteins was not regulated, whereas expression of d

213 poptosis-1, 2'-5' oligoadenylate synthetase (OAS), a 2'-5' OAS-like (OASL) gene, galectin-9, myxoviru

214 isoform of 2'-5'-oligoadenylate synthetase (OAS), a member of the OAS/RNase L system of innate viral

215 m levels of 2'-5' oligoadenylate synthetase (OAS), a validated interferon response marker.

216 ene product 2'-5' oligoadenylate synthetase (OAS), and the chemokines CXCL9 and CXCL10 in the slow pr

217 olymerases, 2'-5' oligoadenylate synthetase (OAS), and yeast Trf4p .

218 eron (IFN-alpha), oligoadenylate synthetase (OAS), CXCL9, and CXCL10-was positively associated with d

219 ies such as 2'-5' oligoadenylate synthetase (OAS), stimulated trans-acting factor of 50 kDa (STAF-50)

220 by PKR and 2'-5' oligoadenylate synthetase (OAS), which respectively inactivate the translation init

221 o block the 2',5'-oligoadenylate synthetase (OAS)-RNase L (RNase L) antiviral pathway.

222 The oligoadenylate synthetase (OAS)-RNase L pathway is a potent antiviral activity.

223 The oligoadenylate synthetase (OAS)-RNase L pathway is a potent interferon (IFN)-induce

224 n inducible 2',5'-oligoadenylate synthetase (OAS)-RNase L pathway to facilitate hepatitis development

225 nterferon-induced oligoadenylate synthetase (OAS)-RNase L pathway.

226 through the 2',5'-oligoadenylate synthetase (OAS)-RNase L pathway.

227 stimulating 2'5'-oligoadenylate synthetase (OAS).

228 R (PKR) and 2'-5' oligoadenylate synthetase (OAS).

229 opterin and 2'-5' oligoadenylate synthetase (OAS).

230 ance of the 2'-5' oligoadenylate synthetase (OAS)/RNase L and double-stranded RNA (dsRNA)-dependent p

231 ed that the 2'-5' oligoadenylate synthetase (OAS)/RNase L system, an innate immune antiviral pathway,

232 sed expression of oligoadenylate synthetase (OAS)1a mRNA in the eye.

233 in 2 (Mx2), 2',5'-oligoadenylate synthetase (OAS-1), Virus inhibitory protein (viperin), ISG15 and IS

234 d gene (ISG; MX1, oligoadenylate synthetase [OAS], IFIT-1) response in the same cell types.

235 s the 2',5'-oligoadenylate (2-5A) synthetase(OAS)/RNase L system, a component of the interferon-induc

236 2'-5' Oligoadenylate synthetases (OAS) are a family of enzymes, which are best known for t

237 2'-5'-Oligoadenylate synthetases (OAS) are innate immune sensors of cytosolic double-stran

238 CL-10, CXCL-11), oligoadenylate synthetases (OAS) genes, and selectively activated activating transcr

239 The 2'-5' oligoadenylate synthetases (OAS) represent a family of interferon (IFN)-induced prot

240 -inducible 2',5'-oligoadenylate synthetases (OAS) upon activation by viral double-stranded RNA (dsRNA

241 ), but not 2',5'-oligoadenylate synthetases (OAS), in vaginal tissue.

242 dsRNA-activated oligoadenylate synthetases (OAS), which produce signaling 2',5'-linked RNA molecules

243 ble 2',5'-oligoadenylate (2-5A) synthetases (OASs) and ribonuclease (RNase) L are components of a pot

244 Oligoadenylate synthetases (OASs) are a family of interferon-inducible enzymes that

245 wed by addition of RNA-1 to form a synthetic OAS to direct the virion-like assembly by RCNMV CP.

246 treated using an orbital atherectomy system (OAS) under simulated blood flow and fluoroscopy.

247 counteract PKR, HSV-1 functions that target OAS have not been described.

248 DNA polymerase beta excised the 5'-terminal OAS formed by Ape1 incision at a rate similar to its rem

249 merase beta-mediated excision of 5'-terminal OAS was stimulated by Ape1 as it is for unmodified abasi

250 Fpg (MutM) protein also excised 5'-terminal OAS, but in our hands, the RecJ protein did not.

251 Examination of phylogenetic trees shows that OAS inactivation in mammals occurred on several independ

252 Results suggest that OAS activation may occur in prostate cancer cells in viv

253 The OAS family consists of several isozymes, with unique dom

254 The OAS-inhibiting activity is generated late in the virus'

255 eficient nsp15, activated MDA5, PKR, and the OAS/RNase L system, resulting in an early, robust induct

256 diesterases (2',5'-PDEs) that antagonize the OAS-RNase L pathway, and we report here that these prote

257 evidence that a Neandertal haplotype at the OAS locus was subjected to positive selection in the hum

258 te a signal of adaptive introgression at the OAS locus.

259 ulation of dsRNA in HCMV-infected cells, the OAS pathway remains inactive, even in HCMV[DeltaI/DeltaT

260 Upon binding to viral dsRNA, the OAS enzymes synthesize 2'-5' linked oligoadenylates (2-5

261 re, we investigated a potential role for the OAS-RNase L system in the restriction of retrotransposon

262 Different receptors from the OAS family contain one, two, or three copies of the 2-5A

263 strong evidence of positive selection in the OAS region is still lacking.

264 enzyme, while decreases of > 200-fold in the OAS: acetate lyase activity and a 30-fold decrease in V

265 mutant exhibits a > 50-fold increase in the OAS:acetate lyase activity and a 17-fold decrease in V f

266 The dramatic change in the OAS:acetate lyase activity of OASS-A in the C42S and C42

267 t in the downstream effector molecule of the OAS pathway, RNase L, were no more sensitive to ocular H

268 his Article, an oligonucleotide mimic of the OAS sequence was attached to Au, CoFe2O4, and CdSe nanop

269 Covalent linkage of the OAS to nanoparticles directs RNA-dependent encapsidation

270 However, the role of the OAS-like domain of OASL remains unclear.

271 Furthermore, the structure of the OAS-like domain shows that OASL has a dsRNA binding groo

272 Here we present the crystal structure of the OAS-like domain, which shows a striking similarity with

273 challenge the notion that activation of the OAS-RNase L pathway requires virus to induce type I IFN,

274 oadenylate synthetase (OAS), a member of the OAS/RNase L system of innate viral resistance.

275 Inhibition of PDE12 may up-regulate the OAS/RNase-L pathway in response to viral infection resul

276 commitment to catalysis, indicating that the OAS external Schiff base preferentially partitions towar

277 We demonstrate that the OAS-like domain can bind dsRNA and that mutating key res

278 ation of l-Cys, but our study shows that the OAS-TL A and OAS-TL B of both halophytes are enzymes tha

279 in the absence of exogenous IFN, whereas the OAS pathway appears to respond to exogenous IFN, contrib

280 tectable levels of RNase L as well as by the OASs expressed in hepatocytes.

281 ate synthetase (OAS) locus encodes for three OAS enzymes (OAS1-3) involved in innate immune response.

282 Thus, OAS does not seem to be a common occurrence in normal, h

283 Thus, OAS is sticky, and a value of 1.5 is calculated for the

284 alpha-aminoacrylate intermediate compared to OAS being released from enzyme.

285 ues from patients with OAS, when compared to OAS- patients (P < 0.05).

286 slightly lower rate (70-100 s-1) compared to OAS.

287 lated sulfite and thiosulfate in response to OAS feeding.

288 induce type I IFN, which in turn upregulates OAS gene expression, as well as to provide dsRNA to acti

289 e compared to a value of 1.81 +/- 0.04 using OAS-3,3-d2 for alpha-DKeq for the first half-reaction.

290 ndary deuterium kinetic isotope effect using OAS-3,3-d2 is 1.11 +/- 0.06 obtained by direct compariso

291 The value of D(V/KOAS) using OAS-2-d is dependent on pH from 5.8 to 7.0 with independ

292 factor eIF2alpha via phosphorylation, while OAS induces the endonuclease RNase L to degrade RNA.

293 te L-serine, however, did show activity with OAS.

294 In contrast with OAS-B, the loss of CS26 function resulted in dramatic ph

295 The anti-HIV-1 effect correlated with OAS protein levels (weeks 1 and 2) and IFIG induction le

296 G3BP1, with only PKR and Rig-I and not with OAS or RNase L.

297 In patients with OAS to apple, tolerance can be safely induced with slowl

298 LCs found in oral tissues from patients with OAS, when compared to OAS- patients (P < 0.05).

299 ells were identical in patients with/without OAS, except lower numbers of CD207+ LCs found in oral ti

300 In adults, 5-year OAS in patients with and without PF was 46% versus 69% (