ライフサイエンスコーパス: PKR

1 PKR activation occurs in a three-step cascade.

2 PKR dimers then autophosphorylate, leading to a conforma

3 PKR inhibits translation initiation through eIF2alpha ph

4 PKR involvement was assessed through pharmacological and

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

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

7 PKR is regulated by the noncoding RNA nc886, which has a

8 PKR mRNA, protein, and phosphorylation are increased in

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

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

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

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

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

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

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

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

17 PKR in C9orf72 BAC transgenic mice using AAV-PKR-K296R or the Food and Drug Administration (FDA)-appr

18 derived from SLE can alleviate the aberrant PKR activation cascade, thus providing a connection betw

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

20 , CAGG, and G(4)C(2) expansion RNAs activate PKR, which leads to increased levels of multiple RAN pro

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

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

23 0.5mM, the trp 5'-UTR continued to activate PKR potently.

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

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

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

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

28 Protein kinase RNA-activated (PKR) is a cytoplasmic receptor for dsRNA, and as such is

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

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

31 However, active PKR has also been found to be involved in the NF-kappaB

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

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

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

35 lation of eIF2alpha via the kinases GCN2 and PKR.

36 to increased sensor levels (MDA5, RIG-I and PKR).

37 and MACV infections, accompanied by IFN and PKR responses.

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

39 t an activated unfolded protein response and PKR and markedly increased DNA damage and apoptosis caus

40 Both TKR and PKR are effective, offer similar clinical outcomes, and

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

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

43 es collectively define VA-I as an archetypal PKR inhibitor made of RNA.

44 Augmented PKR phosphorylation and circRNA reduction are found in p

45 nexpected inhibitor cross-activities between PKR and FGFR2 kinases.

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

47 Blocking PKR using PKR-K296R, the TAR RNA binding protein or PKR-

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

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

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

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

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

53 y of cytokines that is, in part, mediated by PKR-like ER kinase (PERK) and Janus kinase (JAK) 1.

54 f the cellular stress response, monitored by PKR-mediated phosphorylation of eIF2alpha, in fibroblast

55 ing to double-stranded RNA ligand sensing by PKR and MDA5; this results in growth inhibition and tumo

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

62 On binding dsRNA, PKR dimerizes, autophosphorylates, and then phosphorylat

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

64 t ILF3 regulation is the transcript encoding PKR, a crucial player in immune and viral response.

65 ive sweep during passaging, despite enhanced PKR activity.

66 tations employ different mechanisms to evade PKR.

67 ns activates the nucleic acid sensing factor PKR.

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

69 degraded by RNase L, a process required for PKR activation in early cellular innate immune responses

70 PKR activation by dsRNA, it was required for PKR phosphorylation during T cell stimulation, with subs

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

72 and tetra-stems necessary and sufficient for PKR inhibition, and a central domain pseudoknot that res

73 etwork mediated by RBP-J/NFATc1-miR182-FoxO3/PKR (previously identified miR182 targets) towards more

74 rons (IFN-alpha/beta), IFN-stimulated genes (PKR, OAS, Mx1, and ISG15 genes), IFN-induced proteins wi

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

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

77 R) and recruit the antiviral proteins Rig-I, PKR, OAS, and RNase L to avSGs.

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 urons but this does not apparently result in PKR-eIF2alpha activation that normally induces an anti-v

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

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

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

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

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 ies, we found that pTRS1 bound and inhibited PKR.

90 Although nc886 inhibited PKR activation by dsRNA, it was required for PKR phospho

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

92 S/FTD human and mouse brains, and inhibiting PKR in C9orf72 BAC transgenic mice using AAV-PKR-K296R o

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

94 sphorylation of eIF2alpha through inhibiting PKR phosphorylation.

95 MLAV VP35 also inhibits PKR activation.

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 Intriguingly, PKR can also be regulated by PRKRA (protein interferon-i

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

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

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

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

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

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

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

110 lication against the potent antiviral kinase PKR.

111 double-stranded RNA (dsRNA)-dependent kinase PKR.

112 double-stranded RNA (dsRNA)-dependent kinase PKR.

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

114 r, the translation-inhibiting protein kinase PKR.

115 ouble-stranded RNA-activated protein kinase (PKR) also decreased eIF2alpha phosphorylation, the trans

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

117 phorylation of RNA-dependent protein kinase (PKR) or eIF2alpha, indicating that L(pro) does not affec

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

119 randed RNA (dsRNA)-activated protein kinase (PKR) related to innate immunity.

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

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

122 ivation of the RNA-dependent protein kinase (PKR)-mediated stress response, leading to a stop in cell

123 ouble-stranded RNA-dependent protein kinase (PKR).

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

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

126 IFN pathway and the dsRNA-activated kinase, PKR, are required for the lethality induced by ADAR depl

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

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

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

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

131 satisfied general requirements for a medial PKR were randomly assigned (1:1) to receive PKR or TKR b

132 Here we identified PACT-mediated PKR kinase activation as a marker of the termination of

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

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

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

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

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

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

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

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

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

142 dsRNA-activated kinase protein activator of PKR (PACT) mediates many of these tumor-intrinsic respon

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

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

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

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

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

148 Cyp inhibitors, and uncover novel aspects of PKR activity and regulation.

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

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

151 Depletion of PKR prevented eIF2alpha phosphorylation, rescued HCMV re

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

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

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

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

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

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

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

159 g RNAs to accomplish efficient inhibition of PKR.

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

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

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

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

164 rather slightly augmented in the presence of PKR.

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

166 marker of T cell activation and regulator of PKR-dependent signaling.

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

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

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

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

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

172 hosphate and flanking RNA tail dependence on PKR activation.

173 key stress granule protein, G3BP1, with only PKR and Rig-I and not with OAS or RNase L.

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

175 ng PKR-K296R, the TAR RNA binding protein or PKR-KO cells, reduces RAN protein levels.

176 p-PKR is elevated in C9orf72 ALS/FTD human and mouse brain

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

178 We found that high stress-induced PACT-PKR activation inhibits the interaction between NF-kappa

179 Our results suggest that inhibiting PACT-PKR signaling may prove a novel target for alleviating s

180 smotic stress, which is inhibited via a PACT/PKR-dependent dimer redistribution of the Rel family tra

181 osed and raised interest for pharmacological PKR inhibitors.

182 sults demonstrate that targeting of a PI4K2A/PKR lysosome complex may be an effective approach for ca

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

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

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

186 d to PKR in human T cell lysates, preventing PKR phosphorylation by polyinosinic:polycytidylic acid o

187 of host translation, US11 through preventing PKR activation and ICP34.5 through mediating dephosphory

188 es codon-anticodon interactions and prevents PKR activation by VA-I.

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

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

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

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

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

194 The role of RNA-dependent protein kinase R (PKR) and its association with misfolded protein expressi

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

196 nded RNA (dsRNA)-dependent protein kinase R (PKR) and recruit the antiviral proteins Rig-I, PKR, OAS,

197 uble-stranded RNA (dsRNA), protein kinase R (PKR) and ribonuclease L (RNase L) reprogram translation

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

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

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

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

202 anner and readily activate protein kinase R (PKR), a known host double-stranded RNA (dsRNA) sensor.

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

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

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

206 ble-stranded RNA-activated protein kinase R (PKR)-dependent macrophage activation.

207 y response is dependent on protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK) activation

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

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

210 In the cell, the protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK) pathway mo

211 lls upon activation of the protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK), a key com

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

213 dependent on the effector protein kinase R (PKR).

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

215 56 with the host antiviral protein kinase R (PKR).

216 o the innate immune sensor protein kinase R (PKR).

217 increased SG formation and protein kinase R (PKR/EIF2AK2) phosphorylation, we speculate that DHX36 is

218 EIF2AK2 encodes a kinase (protein kinase R [PKR]) that phosphorylates eukaryotic translation initiat

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

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

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

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

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

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

225 Treatment of Pauson-Khand reaction (PKR) products with SeO(2) in the presence or absence of

226 PKR were randomly assigned (1:1) to receive PKR or TKR by surgeons who were either expert in and wil

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

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

229 nc886 also regulated PKR phosphorylation during human monocyte-derived macrop

230 rcular RNAs are globally degraded to release PKR, which becomes activated to aid in the immune respon

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

232 placement (TKR) or partial knee replacement (PKR).

233 Pharmacological inhibition of CypA rescues PKR from antagonism by HCV NS5A, leading to activation o

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

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

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

237 cumulate and can activate ER stress sensors; PKR-like endoplasmic reticulum kinase (PERK), inositol-r

238 ively transposed cyclopentenones from simple PKR products.

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

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

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

242 How VA-I suppresses PKR activation despite its strong dsRNA character, and i

243 In summary, targeting PKR, including by use of metformin, is a promising thera

244 We demonstrated that PKR contributes to the lysosome function and regulates m

245 l cost-effectiveness analysis, we found that PKR was more effective (0.240 additional quality-adjuste

246 We hypothesized that PKR-associated lysosome function is critical for cancer

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

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

249 We observed that PKR and PI4K2A play significant prognostic roles in brea

250 Herein we report that PKR regulates misfolded protein clearance by preventing

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

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

253 ing the 5-year study period, we suggest that PKR should be considered the first choice for patients w

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

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

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

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

258 The PKR-mediated hyperinduction of iNOS decreases cell survi

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

260 Pac 1 binds to PI4K2A and disrupts the PKR/PI4K2A-associated lysosome complex, contributing to

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

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

263 es not affect SG formation by inhibiting the PKR-triggered signaling cascade.

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

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

266 the role of the intrinsic activation of the PKR-like endoplasmic reticulum (ER) kinase (PERK) in the

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

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

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

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

271 ell death in cancer cells depending on their PKR expression status.

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

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

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

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

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

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

278 escribed in other cell types, nc886 bound to PKR in human T cell lysates, preventing PKR phosphorylat

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

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

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

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

283 First, binding to dsRNA triggers PKR homodimerizaton.

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

285 eening a compound library, we identified two PKR-associated compounds 1 and 2 (Pac 1 and 2) did not a

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

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

288 Blocking PKR using PKR-K296R, the TAR RNA binding protein or PKR-KO cells,

289 iveness and cost-effectiveness of TKR versus PKR in patients with medial compartment osteoarthritis o

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

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

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

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

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

295 , and lower follow-up health-care costs with PKR than TKR.

296 wer costs and better cost-effectiveness with PKR during the 5-year study period, we suggest that PKR

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

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

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

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

301 nonical NF-kappaB activation synergizes with PKR to promote SINV replication in differentiated neuron

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