ライフサイエンスコーパス: PKR

1 PKR activation leads to phosphorylation of translation i

2 PKR activation occurs in a three-step cascade.

3 PKR autophosphorylates in the presence of double-strande

4 PKR dimers then autophosphorylate, leading to a conforma

5 PKR inactivates the translation initiation factor eIF2al

6 PKR involvement was assessed through pharmacological and

7 PKR is a cellular kinase involved in the regulation of t

8 PKR is a well-known antiviral protein; however, its regu

9 PKR is known to be activated by interferons and dsRNAs,

10 PKR mRNA, protein, and phosphorylation are increased in

11 PKR transgenic but not PKR null mice demonstrate a mutat

12 PKR, which is induced by both inflammation signals and c

13 ; double cash (DC), a cash transfer of 3,000 PKR; or a fresh food voucher (FFV) of 1,500 PKR; the cas

14 sehold income for the study sample was 8,075 PKR (approximately US$77) at baseline.

15 kistani rupees (PKR) (approximately US$14; 1 PKR = US$0.009543); double cash (DC), a cash transfer of

16 PKR; or a fresh food voucher (FFV) of 1,500 PKR; the cash or voucher amount was given every month ov

17 C1-regulated eIF2alpha phosphorylation and a PKR-eIF2alpha pathway in cell apoptosis may be an import

18 ted that ORFV's two OV20.0 isoforms act as a PKR antagonist via sequestering the PKR activator, dsRNA

19 TMC inhibits apoptosis of HEK293T cells in a PKR-eIF2alpha-dependent manner, with concurrent up- and

20 creased activation of the inflammasome, in a PKR-independent manner.

21 significantly elevated by co-expression of a PKR transgene, whereas knockout of PKR expression or pha

22 Single-stranded RNAs also activate PKR constructs lacking the double-stranded RNA binding d

23 bset of identified snoRNAs bind and activate PKR in vitro; the presence of a 5'-triphosphate enhanced

24 f mutant P222L to interact with and activate PKR.

25 hich are typical of bacterial RNAs, activate PKR in TRAP-free and TRAP/l-Trp-bound forms.

26 the features of bacterial RNA that activate PKR are unknown.

27 NAs containing limited structure to activate PKR by enhancing binding affinity and thereby increasing

28 0.5mM, the trp 5'-UTR continued to activate PKR potently.

29 ichia coli, depleted of rRNA, also activated PKR under these ionic conditions.

30 we show that JNK mediates ceramide-activated PKR inhibitory action on IRS1.

31 es JUNV and MACV, but not OW LASV, activated PKR, concomitant with elevated phosphorylation of the tr

32 owever, JUNV prevents this pool of activated PKR from phosphorylating eIF2alpha, even following expos

33 Here, we have shown that TBI-activated PKR-like ER kinase (PERK) is responsible for memory defi

34 Protein kinase RNA-activated (PKR) has long been known to be activated by viral double

35 ay transducers-protein kinase RNA-activated (PKR)-like ER kinase (PERK), inositol-requiring enzyme-1a

36 that the substitution mutant P222L activates PKR more robustly and for longer duration albeit with sl

37 e-paired regions in bacterial RNA activating PKR.

38 the pTRS1 RNA binding domain did not affect PKR binding or inhibition.

39 to be relevant for the action of NSs against PKR.

40 by palmitate, but not oleate, required AMPK, PKR and JNK1 and involved the activation of the BECN1/PI

41 s chemical inhibitors, we found that AKT and PKR pathways contributed to the transcriptional activati

42 ated in triple-KO cells in which RNase L and PKR were also inactivated.

43 Interestingly, silencing of PK (PKM2 and PKR) inhibited PMA-induced megakaryocytic differentiatio

44 The HCMV pTRS1 and pIRS1 proteins antagonize PKR to promote HCMV protein synthesis and replication; h

45 R ablated the ability of pTRS1 to antagonize PKR activation by dsRNA.

46 OV20.0 is able to bind PKR and its two activators, dsRNA and PACT.

47 pTRS1 did not block PKR dimerization and could bind and inhibit a constituti

48 inase R (PKR) vary in their ability to block PKR-mediated inhibition of viral replication, in part du

49 the PKR eIF2alpha binding site and blocking PKR kinase activity.IMPORTANCE The antiviral kinase PKR

50 In addition, both PKR and eIF2alpha were phosphorylated during infection w

51 ble to restrict MYXV infection, whereas both PKRs were able to restrict replication of a vaccinia vir

52 host dsRNA-responsive defenses controlled by PKR and 2'-5' oligoadenylate synthetase (OAS), which res

53 SGs, for eIF2alpha phosphorylation driven by PKR, and for nucleating SGs of normal composition.

54 derstanding of how HCMV evades inhibition by PKR and identified new strategies for how PKR activity m

55 the binding of either dsRNA or the cellular PKR activator, the PACT protein.

56 l mechanism by which some viruses circumvent PKR-mediated innate immunity.

57 thereby offering a mechanism for the delayed PKR activation in response to stress.

58 enavirus LASV, activated the dsRNA-dependent PKR, another host non-self RNA sensor, during infection.

59 (Skp1, Cul1, F-box protein) type to destroy PKR.

60 bind and inhibit a constitutively dimerized PKR kinase domain.

61 The presence of OV20.0 diminishes PKR phosphorylation when this is stimulated by PACT.

62 g IFITM1, IDO (indoleamine 2,3-dioxygenase), PKR (protein kinase, RNA activated), and viperin (virus

63 mal titration calorimetry, we show that each PKR protein is properly folded with similar domain bound

64 Deletion of a GPCMV genome-encoded PKR inhibitor results in a highly attenuated virus that

65 This proceeds despite VacV-encoded PKR and RNase L antagonists being present.

66 ive sweep during passaging, despite enhanced PKR activity.

67 ; the presence of a 5'-triphosphate enhanced PKR activity compared with the activity with a 5'-monoph

68 tations employ different mechanisms to evade PKR.

69 es have evolved multiple strategies to evade PKR.

70 ns activates the nucleic acid sensing factor PKR.

71 Despite the antiviral activity known for PKR against many other viruses, the replication of JUNV

72 rmation or domain interactions necessary for PKR regulation by RNA.

73 R dimerization, a critical step required for PKR autophosphorylation to attain activity.

74 A role for PKR and PACT in inflammatory processes linked to neurode

75 Infection assays with human HeLa PKR knock-down cells, which were stably transfected with

76 Now, our results indicate that high PKR expression in CD34(+) cells of acute myeloid leukemi

77 by PKR and identified new strategies for how PKR activity might be restored during infection to limit

78 in an early, robust induction of type I IFN, PKR-mediated apoptosis, and RNA degradation.

79 hese genes has previously been implicated in PKR antagonism.

80 proteins and found FBXW11 to be involved in PKR degradation.

81 The E3 mutant replicated in PKR knockout (KO) HAP1 cells in which RNase L is intrins

82 ing the pTRS1 PKR binding domain resulted in PKR activation, suggesting that pTRS1 inhibits PKR throu

83 otein level, but this effect was not seen in PKR-like ER kinase knockout (PERK-KO) or phosphodeficien

84 for the conserved eIF2alpha contact site in PKR binding, pTRS1 bound an additional eIF2alpha kinase,

85 in wild-type (wt) cells compared to that in PKR-deficient cells, suggesting that PKR or PKR activati

86 Increased PKR promotes genomic instability and is associated with

87 irst time that Andes virus infection induced PKR overexpression.

88 anced IFN response in JUNV- or MACV-infected PKR-deficient cells, which was inversely correlated with

89 that attenuate translation during infection, PKR and type I IFN signaling.

90 ded by the OV20.0L gene, are able to inhibit PKR activation both by sequestering dsRNA and by physica

91 ies, we found that pTRS1 bound and inhibited PKR.

92 In addition, pTRS1 binding to PKR inhibited PKR kinase activity.

93 t Andes virus nucleocapsid protein inhibited PKR dimerization, a critical step required for PKR autop

94 cts the PKR antiviral response by inhibiting PKR dimerization, which is required for its activation.

95 sphorylation of eIF2alpha through inhibiting PKR phosphorylation.

96 Luteolin inhibits PKR phosphorylation, the ISR and the induction of pro-in

97 ogether our data suggest that pTRS1 inhibits PKR by binding to conserved amino acids in the PKR eIF2a

98 wever, the mechanism by which pTRS1 inhibits PKR is unclear.

99 R activation, suggesting that pTRS1 inhibits PKR through a direct interaction.

100 Stau1 binds to PKR and strongly inhibits PKR-autophosphorylation.

101 lymphoblasts, thereby leading to intensified PKR activation and enhanced cellular death.

102 double-stranded RNA (dsRNA)-activated kinase PKR and thereby allowed virus-induced increases in the a

103 Thus, NSs eliminates the antiviral kinase PKR by recruitment of SCF-type E3 ubiquitin ligases cont

104 teasomal degradation of the antiviral kinase PKR by the viral protein NSs.

105 dentified inhibition of the antiviral kinase PKR by the viral proteins TRS1 and IRS1 and shown that t

106 ere found to antagonize the antiviral kinase PKR outside the context of HCMV infection, and the expre

107 ase activity.IMPORTANCE The antiviral kinase PKR plays a critical role in controlling HCMV replicatio

108 Although the antiviral kinase PKR was originally characterized as a double-stranded RN

109 lication against the potent antiviral kinase PKR.

110 cided with activation of another eIF2 kinase PKR-like endoplasmic reticulum kinase (PERK), a major IS

111 r, the translation-inhibiting protein kinase PKR.

112 ouble-stranded RNA-activated protein kinase (PKR) has been reported in acute leukemia and solid tumor

113 ouble-stranded RNA-activated protein kinase (PKR) in the pathogenesis of acute myeloid leukemia (AML)

114 randed RNA (dsRNA)-activated protein kinase (PKR) is an important component of the innate immune syst

115 ouble-stranded RNA-dependent protein kinase (PKR) is involved in the long-term effects of saturated f

116 independent of RNA-activated protein kinase (PKR) regulation.

117 randed RNA (dsRNA)-activated protein kinase (PKR), a major component of the cellular antiviral system

118 randed RNA (dsRNA)-activated protein kinase (PKR), a well-characterized antiviral protein that inhibi

119 ouble-stranded RNA-dependent protein kinase (PKR), which has been recently implicated in inflammasome

120 ouble-stranded RNA-activated protein kinase (PKR)-like ER kinase (PERK) blocked the mitochondrial tra

121 randed RNA (dsRNA)-activated protein kinase (PKR).

122 ouble-stranded RNA-activated protein kinase (PKR).

123 racts with RNA in the context of full length PKR.

124 g confirmed the production of: LFN-GAL4, LFn-PKR and PA which were detected at ~45.9 kDa, ~37 kDa, an

125 y confirmed the detection of LFn-GAL4 or LFn-PKR in the cytosol.

126 toxicity of both PA:LFn-GAL4:ASO and PA:LFn-PKR:siRNA complexes was low (IC50>100 mug/mL in HeLa and

127 6 +/- 6.1% whereas treatment with the PA:LFn-PKR:siRNA resulted in 8.5 +/- 3.4% Synt5 expression afte

128 a catalysis-deficient nsp15, activated MDA5, PKR, and the OAS/RNase L system, resulting in an early,

129 d to be essential for reducing PACT-mediated PKR phosphorylation.

130 However, in mice PKR is also activated by metabolic stress in the absence

131 w concepts in relation to how ORFV modulates PKR activation.

132 We report the discovery of a new PKR inhibitor whose expression in hantavirus-infected ce

133 h a hantavirus nucleocapsid protein as a new PKR inhibitor.

134 says, M156 only inhibited rabbit PKR but not PKR from other tested mammalian species.

135 PKR transgenic but not PKR null mice demonstrate a mutator phenotype characteri

136 MA treatment also translocated PKM2, but not PKR, into nucleus.

137 Nuclear PKR antagonizes ataxia-telangiectasia mutated (ATM) acti

138 Thus, nuclear PKR has an oncogenic function and can be a novel therape

139 cellular stress granules with activation of PKR and other innate immune pathways through the activit

140 ication through repressing the activation of PKR and the subsequent antiviral interferon response.

141 h affinity, thereby inhibiting activation of PKR by viral dsRNA.

142 eby snoRNAs play a role in the activation of PKR under metabolic stress.

143 omains (DRBD) are required for activation of PKR, by interaction with either dsRNA or PACT, another c

144 strated significantly stronger activation of PKR, NF-kappaB, and JNK and higher expression of pro-inf

145 nding protein (TRBP) or protein activator of PKR (PACT), while Drosophila Dicer-1 associates with Loq

146 Classical activators of PKR are long viral double-stranded RNAs, but recently, P

147 lity to antagonize the antiviral activity of PKR appears to be complete, as silencing of PKR expressi

148 Together our results show that antagonism of PKR by HCMV pTRS1 and pIRS1 is critical for viral protei

149 This antagonism of PKR by NSs is essential for efficient RVFV replication i

150 during HCMV infection and that antagonism of PKR is critical for efficient viral replication.

151 dulatory functions, including attenuation of PKR phosphorylation, activation of G-protein signaling,

152 This blockade of PKR function is highly specific, as LCMV is unable to si

153 Depletion of PKR prevented eIF2alpha phosphorylation, rescued HCMV re

154 ive but only with a double knockout (DKO) of PKR and RNase L in A549 cells, indicating that both path

155 in the conserved eIF2alpha binding domain of PKR disrupted pTRS1 binding and rendered PKR resistant t

156 r occupies the RBD2 and the kinase domain of PKR, which then prevents PACT binding to PKR.

157 V infection leads to increased expression of PKR as well as its redistribution to viral replication a

158 om these results we conclude that the IDL of PKR is not required for RNA binding or mediating changes

159 vely, these data delineate the importance of PKR in the inflammation process to the ISR and induction

160 We also document the importance of PKR, TRIF, and TBK1 in cytokine secretion during L. pneu

161 er, the mechanism underlying inactivation of PKR by in fl uenza A virus (IAV) remains elusive.

162 viruses and involved in the inactivation of PKR signaling by these viruses.

163 ation of these viral genes is independent of PKR activation, but their expression is dependent on the

164 acting with PKR, leading to an inhibition of PKR activation.

165 KR expression or pharmacologic inhibition of PKR activity reduced the frequency of spontaneous mutati

166 Thus, inhibition of PKR expression or activity promotes ATM activation, gamm

167 rain function and suggest that inhibition of PKR is a way to restore memory impairment in early stage

168 g RNAs to accomplish efficient inhibition of PKR.

169 Pharmacological inhibitors of PKR should be used in combination with drugs targeting d

170 sion of a PKR transgene, whereas knockout of PKR expression or pharmacologic inhibition of PKR activi

171 Since KO of PKR and RNase L was sufficient to enable VACV replicatio

172 n)-type E3 ubiquitin ligases as mediators of PKR destruction by NSs.

173 age of ribosomal RNA, and phosphorylation of PKR and eIF2alpha that correlated with a approximately 1

174 Further, phosphorylation of PKR, which is a prerequisite for its ability to phosphor

175 rather slightly augmented in the presence of PKR.

176 irectly to the RNA binding domains (RBDs) of PKR, and this interaction does not require dsRNA.

177 in G3BP1 is essential for the recruitment of PKR to SGs, for eIF2alpha phosphorylation driven by PKR,

178 e leukemia and solid tumors, but the role of PKR has been unclear.

179 However, the role of PKR in inflammation is subject to controversy.

180 PKR appears to be complete, as silencing of PKR expression has no impact on viral propagation.

181 The partial stabilization of PKR by FBXW11 depletion upregulated PKR autophosphorylat

182 The suppression of PKR activation is one of the main strategies that viruse

183 As was required for efficient suppression of PKR by NS1 during IAV infection.

184 sms that include AKT-mediated suppression of PKR-like kinase (PERK) and increased expression of CReP

185 hosphate and flanking RNA tail dependence on PKR activation.

186 PKR-deficient cells, suggesting that PKR or PKR activation did not negatively affect JUNV and MACV i

187 st cells expressing wild-type PKR (PKRWT) or PKR with a point mutation in each dsRNA-binding motif (P

188 However, the overexpressed PKR was not active due to a significant inhibition of au

189 addition, the affinity of PACT-PACT and PACT-PKR interactions is enhanced in dystonia patient lymphob

190 rtially reversed by short-term pharmacologic PKR inhibition.

191 osed and raised interest for pharmacological PKR inhibitors.

192 e to the synthetic dsRNA poly(I.C), a potent PKR agonist.

193 ither pTRS1 or pIRS1 is necessary to prevent PKR activation during HCMV infection and that antagonism

194 ppropriate Stau1 to its advantage to prevent PKR-mediated inhibition of eIF2alpha, which is required

195 To maximally protect PKR from the action of NSs, knockdown of structurally an

196 nst the conserved SCF subunit Skp1 protected PKR from NSs-mediated degradation.

197 ral antagonist of the host antiviral protein PKR, enabled a recombinant vaccinia virus to replicate i

198 ection with an HCMV mutant lacking the pTRS1 PKR binding domain resulted in PKR activation, suggestin

199 E3 deletion mutant induced protein kinase R (PKR) and eukaryotic translation initiation factor alpha

200 ate the phosphorylation of protein kinase R (PKR) and its substrate eukaryotic translation initiation

201 Protein kinase R (PKR) and RNase L are host cell components that function

202 ion-mediated activation of protein kinase R (PKR) and stimulating 2'5'-oligoadenylate synthetase (OAS

203 motic stress activates the protein kinase R (PKR) independently of its RNA-binding domain.

204 ignated Delta145), a viral protein kinase R (PKR) inhibitor, was generated.

205 Protein kinase R (PKR) is a vital component of host innate immunity agains

206 Protein kinase R (PKR) is activated by dsRNA produced during virus replica

207 nded-RNA (dsRNA)-activated protein kinase R (PKR) is another host non-self RNA sensor classically kno

208 mple, viral antagonists of protein kinase R (PKR) vary in their ability to block PKR-mediated inhibit

209 Protein kinase R (PKR), a classical interferon-stimulated gene product, ph

210 Protein kinase R (PKR), a versatile antiviral host factor, shuts down the

211 se is the antiviral kinase protein kinase R (PKR), which inactivates the eukaryotic initiation factor

212 CV NS5B and a cell factor, protein kinase R (PKR), which is critical for interferon-induced cellular

213 ivate the antiviral kinase protein kinase R (PKR), which potently inhibits virus replication.

214 ts are consistent with the protein kinase R (PKR)-ADAR1 balancing model of innate immunity activation

215 e found that local reduced protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK) expression

216 Protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK) is one of

217 mic reticulum (ER) kinase, protein kinase R (PKR)-like ER kinase (PERK), is a pro-adaptive protein ki

218 56 with the host antiviral protein kinase R (PKR).

219 on of the antiviral factor protein kinase R (PKR).

220 iant that lost its ability to inhibit rabbit PKR and led to virus attenuation.

221 nsfection assays, M156 only inhibited rabbit PKR but not PKR from other tested mammalian species.

222 PKR, revealed that only human but not rabbit PKR was able to restrict MYXV infection, whereas both PK

223 The species-specific inhibition of rabbit PKR by M156 and the M156 loss-of-function in Australian

224 were stably transfected with human or rabbit PKR, revealed that only human but not rabbit PKR was abl

225 se domain, present in hPKR but absent in rat PKR, are exploited by viral non-coding RNAs to accomplis

226 In contrast, inhibition of rat PKR by VA RNAI and TAR RNA was found to be weaker than f

227 ng viral double-stranded RNAs, but recently, PKR has been found to be activated by bacterial RNA.

228 A (dsRNA)-dependent protein kinase receptor (PKR), or TIR domain-containing adaptor inducing interfer

229 The G3BP1-induced SGs also recruit PKR and other antiviral proteins.

230 s, which in multiple copies strongly reduced PKR activation.

231 of PKR disrupted pTRS1 binding and rendered PKR resistant to inhibition by pTRS1.

232 esolved using a parallel kinetic resolution (PKR) strategy upon reaction with a pseudoenantiomeric mi

233 biting pTRS1 and pIRS1 function or restoring PKR activity during infection may be a successful strate

234 , a cash transfer of 1,500 Pakistani rupees (PKR) (approximately US$14; 1 PKR = US$0.009543); double

235 omyces cerevisiae GAL4 or Homo sapien sapien PKR (respectively) to a truncation of Atx lethal factor

236 that functions as an RNA decoy to sequester PKR in an inactive state.

237 lex that is precisely tuned to bind a single PKR monomer with high affinity, thereby inhibiting activ

238 Pretreatment with specific PKR inhibitor or overexpression of p58(IPK) largely abol

239 Like Stau1, PKR displayed binding specificity to domain IIId of HCV-

240 te eIF2alpha dephosphorylation, and suppress PKR toxicity in yeast.

241 This study demonstrates that PKR can signal the presence of bacterial RNAs under phys

242 Significantly, we find that PKR has a novel and previously unrecognized nuclear func

243 o Collectively, these findings indicate that PKR activation is an essential part of the molecular swi

244 These findings indicate that PKR sequence or structural elements in the kinase domain

245 Our results also show that PKR and OAS1 play important roles in the ISG15-mediated

246 Furthermore, we showed that PKR and OAS1 played important roles in the ISG15-mediate

247 that in PKR-deficient cells, suggesting that PKR or PKR activation did not negatively affect JUNV and

248 The PKR-induced translational shutdown helps host cells to e

249 The PKR-like endoplasmic reticulum kinase (PERK) arm of the

250 The PKR-like endoplasmic reticulum kinase (PERK) pathway of

251 The PKR-like ER kinase (PERK), a transmembrane protein, resi

252 The PKR-mediated hyperinduction of iNOS decreases cell survi

253 ing the ability to counter autophagy and the PKR-driven antiviral state had near-wild-type virulence

254 tavirus nucleocapsid protein counteracts the PKR antiviral response by inhibiting PKR dimerization, w

255 ionary pressure on hantaviruses to evade the PKR antiviral response for survival.

256 shift that exposes the binding site for the PKR substrate eIF2alpha.

257 R by binding to conserved amino acids in the PKR eIF2alpha binding site and blocking PKR kinase activ

258 vaccinia virus (VACV) strain that lacks the PKR inhibitors E3 and K3.

259 We envision that evasion of the PKR antiviral response by NP has likely helped hantaviru

260 tophosphorylation and phosphorylation of the PKR substrate eIF2alpha and caused a shutoff of host cel

261 ucing cells revealed early activation of the PKR-like ER kinase/activating transcription factor 4 (PE

262 he flavonoid luteolin as an inhibitor of the PKR/PACT interaction at the level of their DRBDs using h

263 on in hantavirus-infected cells prevents the PKR-induced host translational shutdown to ensure the co

264 act as a PKR antagonist via sequestering the PKR activator, dsRNA, and by interacting with PKR, leadi

265 Moreover, we demonstrate that the PKR inhibitor C16 ameliorates both iNOS amplification an

266 Thus, PKR inhibition may be a therapeutically useful strategy

267 These findings tie PKR activation to its recruitment to SGs by G3BP1 and in

268 sensing innate immune receptors (RLRs, TLRs, PKR), or the cytokines type I interferons and TNF-alpha.

269 The intact TAR molecule was able to bind to PKR and TLR3 effectively, whereas the 5' and 3' stems (T

270 emonstrate that single-stranded RNAs bind to PKR with micromolar dissociation constants and can induc

271 In addition, pTRS1 binding to PKR inhibited PKR kinase activity.

272 pTRS1 binding to PKR was not mediated by an RNA intermediate, and mutatio

273 of PKR, which then prevents PACT binding to PKR.

274 Stau1 binds to PKR and strongly inhibits PKR-autophosphorylation.

275 ibition of viral replication, in part due to PKR allelic variation between species.

276 l for PACT's association with PKR leading to PKR activation.

277 ed neuronal damage and ER stress, leading to PKR-like ER kinase-dependent phosphorylation of the euka

278 enous cellular RNA that potentially leads to PKR activation during metabolic stress is unknown.

279 oRNAs) bound best to TLR7 and -8 and none to PKR.

280 The sensitivity of hantavirus replication to PKR has likely imposed a selective evolutionary pressure

281 Binding of TAR to PKR did not result in its phosphorylation, and therefore

282 First, binding to dsRNA triggers PKR homodimerizaton.

283 In turn, PKR stimulates nuclear accumulation of nuclear factor ka

284 ation of productive complexes containing two PKRs bound to a single RNA.

285 ryonic fibroblast cells expressing wild-type PKR (PKRWT) or PKR with a point mutation in each dsRNA-b

286 ation of PKR by FBXW11 depletion upregulated PKR autophosphorylation and phosphorylation of the PKR s

287 When PKR activity is reduced (siRNA or a pharmacological inhi

288 severely reduced in Skp1-depleted cells when PKR was present.

289 Nevertheless, the association of OV20.0 with PKR, rather than with PACT, was found to be essential fo

290 hin OV20.0 that interact with dsRNA and with PKR have been mapped.

291 d that PC1 truncation mutants associate with PKR, or with PKR and its activator PACT.

292 ACT is essential for PACT's association with PKR leading to PKR activation.

293 ApoE4 mice injected with PKR inhibitor (PKRi) demonstrate a significant reduction

294 ing dsRNA and by physically interacting with PKR in vitro.

295 KR activator, dsRNA, and by interacting with PKR, leading to an inhibition of PKR activation.

296 ns that disrupted the pTRS1 interaction with PKR ablated the ability of pTRS1 to antagonize PKR activ

297 dentified endogenous RNA that interacts with PKR after induction of metabolic stress by palmitic acid

298 assay confirmed the binding of p58(IPK) with PKR, but not other TLR4 downstream signaling molecules.

299 uncation mutants associate with PKR, or with PKR and its activator PACT.

300 ity of enriched RNAs that interacted with WT PKR (>/=twofold, false discovery rate </= 5%) were small