ライフサイエンスコーパス: IRES

1 IRES activity was dependent on upstream MAPK (mitogen-ac

2 Binding of miR-134 to Sabin-1 IRES caused degradation of the IRES transcript in a miR-

3 nesis of the miR-134 binding site in Sabin-1 IRES relieved miR-134-mediated repression indicating tha

4 PK activity is a major determinant of type 1 IRES competency, host cell cytotoxicity, and viral proli

5 e roles of PCBP2 and the tetraloop in Type 1 IRES function are unknown.

6 SRPK activity to enhance picornavirus type 1 IRES translation and favor PVSRIPO tumor cell toxicity a

7 diverges structurally from canonical Type 1 IRESs (e.g. poliovirus) but nevertheless also contains a

8 Initiation on Type 1 IRESs also requires IRES trans-acting factors (ITAFs), a

9 Picornavirus Type 1 IRESs comprise five principal domains (dII-dVI).

10 o corresponding elements in canonical Type 1 IRESs, and non-canonical flanking domains (d8, d9 and d1

11 reconstitution of initiation on three Type 1 IRESs: poliovirus (PV), enterovirus 71 (EV71), and bovin

12 134 binding to Sabin-1 and 3 but not Sabin-2 IRES.

13 Studies with IL-4-IRES-eGFP (4get) reporter mice showed eosinophils were t

14 ons are labeled by expression of the or111-7:IRES:GAL4 transgene whose axons terminate in the central

15 K1 mediates adaptive responses by activating IRES-dependent translation, and the impairments in trans

16 ovirus 2A protease generates a high-affinity IRES binding truncation of eIF4G that stimulates eIF4A d

17 gs from AgRP neurons in awake, behaving AgRP-IRES-Cre mice.

18 We created an Alpi-IRES-CreERT2 (Alpi(CreER)) knockin allele for lineage tr

19 indings are consistent with NCL acting as an IRES trans-acting factor (ITAF) for ORF2 translation and

20 s nuclear ribonucleoprotein, hnRNP A1, is an IRES transacting factor (ITAF) that regulates the IRES-d

21 KH2 and KH3 bind adjacently to an IRES subdomain (d10b) that is unrelated to dIV, with KH3

22 Using an IRES-dependent reporter system, we established that PRMT

23 are required for 80S ribosomes assembly and IRES activity.

24 Mechanistic studies with C11 and IRES-J007 revealed binding of the inhibitors within the

25 cells, as well as that of cap-dependent and IRES-dependent reporters.

26 nctional link between tRNA modification- and IRES-dependent translation during tumor cell invasion an

27 inaccessibility of the pyrimidine tract and IRES activity, as determined in both in vitro and in viv

28 screen identified hnRNP A1 (A1) and RPS25 as IRES-binding trans-acting factors required for ER stress

29 1, which can program increased initiation at IRES motifs on mRNA by the translational initiation comp

30 biquitous CAG promoter (namely pCAG-miR200-b-IRES-eGFP).

31 the deletion of IIId2 from the CSFV and BDV IRES elements impairs initiation of translation by inhib

32 However, the connection between IRES-mediated p53 translation and p53's tumor suppressiv

33 The following events can differ between IRESs, depending on the stability of dVI.

34 omains, facilitating head swivel and biasing IRES translocation via hitherto-elusive intermediates wi

35 nd 3) the retarding effect of ribosome-bound IRES on protein synthesis is largely overcome following

36 Suppression of CACNA1A IRES function in SCA6 may be a potential therapeutic str

37 The cadicivirus IRES diverges structurally from canonical Type 1 IRESs (

38 How PCBP2 binds the cadicivirus IRES, and the roles of PCBP2 and the tetraloop in Type 1

39 e canonical Type 1 and divergent cadicivirus IRESs require the same IRES trans-acting factor, poly(C)

40 hosphorylation of La protein regulates CCND1 IRES-mediated translation.

41 well as T389 is required to stimulate CCND1 IRES-mediated translation in cells.

42 cular mechanism by which La stimulates CCND1 IRES-mediated translation, and we propose that its RNA c

43 On the other hand, the CDV IRES forms a 40S/eIF3/IRES ternary complex, with multipl

44 suggesting that this viral IRES and cellular IRES may have similar strategies for internal translatio

45 designer drugs (DREADD)' approach, and ChAT-IRES-Cre mice.

46 ellow fluorescent protein expression in ChAT-IRES-Cre mice, we tested the hypothesis that there is a

47 These CHIKV/IRES vaccine candidates appear to be safe and efficaciou

48 We confirmed IRES activity by both peptide sequencing and ribosome pr

49 The CP IRES is A-rich, independent of orientation, and strongly

50 reERLacZ (Prom1C-L) mice, in which a CreERT2-IRES-nuclear LacZ cassette is knocked into the first ATG

51 sults distinguished two pathways of 80S:CrPV IRES complex assembly that produce elongation-competent

52 itiation factor nor initiator tRNA, the CrPV IRES jumpstarts translation in the elongation phase from

53 We directly tracked the CrPV IRES, 40S and 60S ribosomal subunits, and tRNA using sin

54 sites (IRESs) to minimize or, like the CrPV IRES, eliminate the need for initiation factors.

55 Here, by exploiting the CrPV IRES, we observed the entire process of initiation and t

56 Once the 60S is recruited, the binary CrPV-IRES/80S complex oscillates between canonical and rotate

57 oscopy, we have solved the structure of CrPV-IRES bound to the ribosome of the yeast Kluyveromyces la

58 is Virus Internal Ribosomal Entry Site (CrPV-IRES) binds the small ribosomal subunit (40S) and the tr

59 sis virus internal ribosome entry site (CrPV-IRES) is a folded structure in a viral mRNA that allows

60 ompanying factor-binding data show that CrPV-IRES binding mimics a pretranslocation rather than initi

61 both states, the pseudoknot PKI of the CrPV-IRES mimics a tRNA/mRNA interaction in the decoding cent

62 The CrPV-IRES restricts tvhe otherwise flexible 40S head to a con

63 interact with pseudoknot I (PKI) of the CrPV-IRES stabilizing it in a conformation reminiscent of a h

64 rgenic IRES of Cricket Paralysis Virus (CrPV-IRES) forms a tight complex with 80S ribosomes capable o

65 e demonstrate that C11 also blocks cyclin D1 IRES-dependent initiation and demonstrates synergistic a

66 tream of the pyrimidine-tract also decreases IRES activity.

67 A subset of dicistrovirus IRESs directs translation in the 0 and +1 frames to prod

68 ubset of mutations that are known to disrupt IRES activity failed to produce virus, demonstrating the

69 eotides in either RNA dramatically disrupted IRES activity.

70 es insight into how conformationally dynamic IRESs operate.

71 a scaffold for the RNA to fold for efficient IRES activity.

72 ell as Apc(+/Min) and Apc(CKO/CKO)/Lgr5-EGFP-IRES-CreERT2 mice, were analyzed by immunohistochemistry

73 ble knockout (Cbl/Cbl-b DKO) using Lgr5-EGFP-IRES-CreERT2, to demonstrate a mammary epithelial cell-a

74 r 5-positive (Lgr5(+)) stem cells (Lgr5-eGFP-IRES-CreERT2/Rosa26-TdTomato mice) and in situ hybridiza

75 he other hand, the CDV IRES forms a 40S/eIF3/IRES ternary complex, with multiple points of contact.

76 We are targeting unfettered enterovirus IRES activity in cancer with PVSRIPO, the type 1 live-at

77 s work provides key details into how an EV71 IRES structure adapts to hijack a cellular protein, and

78 which highlights the importance of examining IRES activity in its physiological context.

79 Domain 3 in FMDV IRES is phylogenetically conserved and highly structured

80 egion of domain 3, thought to be crucial for IRES function.

81 us (SVV), a picornavirus, is dispensable for IRES activity, while the IIId2 sub-domains of two pestiv

82 ck of structure was an important feature for IRES activity.

83 and RNA-protein interactions, important for IRES activity.

84 RNA synthesis and growth of SVV, but not for IRES function.

85 demonstrated experimentally, is suitable for IRES activity.

86 tagenesis, we demonstrate that the HIV-1 gag IRES does not use pre-folded RNA structure to drive func

87 a bicistronic reporter construct, HIV-1 gag IRES' activity is cell type-specific, with higher activi

88 devoid of extensive secondary structure has IRES activity and produces low levels of viral coat prot

89 Here we demonstrate that eIF4E regulates HAV IRES-mediated translation by two distinct mechanisms.

90 Remarkably, the hepatitis A virus (HAV) IRES requires eIF4E for its translation, but no mechanis

91 These findings show that 40S:HCV IRES complex formation is accompanied by dynamic conform

92 demonstrated that after binding, the 40S:HCV IRES complex is conformationally dynamic, undergoing slo

93 ovide an overview of approaches to block HCV IRES function by nucleic acid, peptide, and small molecu

94 wn of PKR or IMPDH prevented RBV induced HCV IRES-GFP translation.

95 Our data support a single-step model of HCV IRES recruitment to 40S subunits, irreversible on the in

96 pecifically contributes to activation of HCV IRES-driven translation by miR-122, but not to other act

97 ed the inhibitory effect of IFN-alpha on HCV IRES-GFP expression.

98 is C virus internal ribosome entry site (HCV IRES) RNA.

99 ce of the rRNA interaction and show that HCV IRES activity requires a 3-nt Watson-Crick base-pairing

100 rokaryotes, the rRNA-binding site in the HCV IRES functions as an essential component of a more compl

101 the rates of 40S subunit arrival to the HCV IRES.

102 rt translation mediated by the wild-type HCV IRES, but did not block translation mediated by the cap

103 The activities of the mutated HCV IRESs could be restored by compensatory mutations in the

104 ed binding specificity to domain IIId of HCV-IRES.

105 ion in the 3' NTR and domain IIId of the HCV-IRES in the 5' NTR, and promoted HCV replication and tra

106 containing a human rhinovirus type 2 (HRV2) IRES, is demonstrating early promise in clinical trials

107 containing a human rhinovirus type 2 (HRV2) IRES.

108 Type I IRES elements require auxiliary host proteins to organiz

109 , nts 341-950) constitute a divergent Type I IRES.

110 ution revealed that as with canonical Type I IRESs, 48S complex formation requires eukaryotic initiat

111 However, in contrast to canonical Type I IRESs, subsequent recruitment of 43S ribosomal complexes

112 oach reveals that the PKI domain of the IAPV IRES adopts an RNA structure that resembles a complete t

113 rovirus Israeli acute paralysis virus (IAPV) IRES PKI domain can uncouple 0 and +1 frame translation,

114 ned the role of previously characterized IGR IRES mutations on viral yield and translation in CrPV-in

115 This is the first study to examine IGR IRES translation in its native context during virus infe

116 g the key IRES-ribosome interactions for IGR IRES translation in infected cells, which highlights the

117 s have provided mechanistic details into IGR IRES translation, these studies have been limited to in

118 al for translation in different types of IGR IRESs and from diverse viruses.

119 The intergenic region (IGR) IRES adopts an unusual structure that directly recruits

120 The intergenic region (IGR) IRESs from the Dicistroviridae family of viruses are str

121 Importantly, IRES mutations that delete the bulge impair viral transl

122 ation of IRES-J007, which displayed improved IRES-dependent initiation blockade and synergistic anti-

123 rkedly reduces an equol-mediated increase in IRES-dependent mRNA translation and the expression of sp

124 esting that ribosome dynamics play a role in IRES translocation.

125 ne-tract within a stable hairpin inactivates IRES activity, since the stronger the stability of the h

126 e ribosome that are necessary for initiating IRES translation in a specific reading frame.

127 The intergenic IRES of Cricket Paralysis Virus (CrPV-IRES) forms a tigh

128 to the family of Dicistroviridae intergenic IRESs.

129 neous nuclear ribonucleoprotein A1, with its IRES.

130 Viral mRNA sequences with a type IV IRES are able to initiate translation without any host i

131 to virus production, thus revealing the key IRES-ribosome interactions for IGR IRES translation in i

132 om HeLa cells to examine their effects on L1 IRES-mediated translation and L1 retrotransposition.

133 Within hepatitis C virus (HCV)-like IRES elements, the sub-domain IIId(1) is crucial for rec

134 However, some HCV-like IRES elements possess an additional sub-domain, termed I

135 Initiation on HCV-like IRESs relies on their specific interaction with the 40S

136 ole for the specific interaction of HCV-like IRESs with eIF3 in preventing ribosomal association of e

137 demonstrate that adjacent mutations modulate IRES activity, independently of protein-coding sequence

138 Cellular mRNA IRES also lack extensive RNA structures or sequence cons

139 findings may be applicable to cellular mRNA IRES that also have little or no sequences/structures in

140 , we show that ribosomes assembled on mutant IRESs that direct exclusive 0 or +1 frame translation la

141 ikingly, PCBP2 enhanced initiation on mutant IRESs that retained consensus GNRA tetraloops, whereas m

142 d in the epicardium and EPDCs using the mWt1/IRES/GFP-Cre (Wt1(Cre)) mouse.

143 Myc IRES activity was upregulated in MM cells during ER stre

144 locking the interaction of a requisite c-MYC IRES trans-acting factor, heterogeneous nuclear ribonucl

145 a small molecule capable of inhibiting c-MYC IRES translation as a consequence of blocking the intera

146 the myc IRES and specifically inhibited myc IRES activity in MM cells.

147 the potential for targeting A1-mediated myc IRES activity in MM cells during ER stress.

148 ain how c-myc was maintained, we studied myc IRES (internal ribosome entry site) function, which does

149 ound that prevented binding of A1 to the myc IRES and specifically inhibited myc IRES activity in MM

150 es the question of what effect the necessary IRES dissociation from the tRNA binding sites, and ultim

151 del with mice that overexpress the ErbB2/Neu-IRES-Cre transgene (NIC) specifically in the mammary epi

152 rates of reaction for the initial cycles of IRES-dependent elongation.

153 p53 inactivation that links deregulation of IRES-mediated p53 translation with tumorigenesis.

154 igated and resulted in the identification of IRES-J007, which displayed improved IRES-dependent initi

155 re knockin mice with a targeted insertion of IRES-Cre at the Ins2 locus and demonstrated with a cell

156 o studies revealed slowed growth kinetics of IRES-controlled VSVs in most of the cell lines tested.

157 This specialized mode of IRES-dependent translation is enabled by an additional r

158 5 facilitates the translation of a subset of IRES-containing genes.

159 The structures suggest a trajectory of IRES translocation, required for translation initiation,

160 x and Hsp90 to upregulate the translation of IRES-containing transcripts such as HIF1a, Myc and VEGF,

161 These data support the combined use of IRES-J007 and PP242 to achieve synergistic antitumor res

162 ounts for 15 gene-targeted strains of the OR-IRES-marker design coexpressing a fluorescent protein.

163 icase A (RHA), which positively regulate p53 IRES activity.

164 s required to significantly increase the p53 IRES activity in these cells.

165 In this study, we identified two p53 IRES trans-acting factors, translational control protein

166 TN-mut) was inserted in frame into the pEF1a-IRES-DsRed-Express2 vector and transfected into bovine f

167 usion, the studies have shown that the pEF1a-IRES-DsRed-Express2-bMSTN-mut recombinant plasmid could

168 itiation codon in type I and II picornavirus IRES.

169 sought to determine whether the picornavirus IRES could be engineered into VSV to attenuate its neuro

170 Therefore, our data reveal how picornavirus IRESs use eIF4E-dependent and -independent mechanisms to

171 P2 has three KH domains and binds poliovirus IRES domain dIV in the vicinity of the tetraloop.

172 S) trans-acting factor (ITAF) for poliovirus IRES-mediated translation; however, it is not known whet

173 raction of hnRNP A1 with IRES RNA to promote IRES-dependent translation.

174 ell lines, we were able to identify putative IRES activity (nucleotides 442-637) in the coding region

175 This provides a mechanism to explain why PV IRES-mediated translation is stimulated by eIF4E availab

176 rate of restructuring of the poliovirus (PV) IRES.

177 Initiation on Type 1 IRESs also requires IRES trans-acting factors (ITAFs), and several candidate

178 ed in the development of insulin resistance (IRES) in mice.

179 F2 with a GTP analog stabilizes the ribosome-IRES complex in a rotated state with an extra ~3 degrees

180 anINs) in p48Cre; TetO-KrasG12D; Rosa26(rtTa-IRES-EGFP) (iKras*) mice and LSL-KrasG12D mice bred with

181 divergent cadicivirus IRESs require the same IRES trans-acting factor, poly(C)-binding protein 2 (PCB

182 anslation and internal ribosomal entry site (IRES) activity in infected cells.

183 The internal ribosomal entry site (IRES) activity varied in different cell types, suggestin

184 cross-kingdom internal ribosome entry site (IRES) activity.

185 ergenic region internal ribosome entry site (IRES) adopts a triple-pseudoknotted RNA structure and oc

186 discovered an internal ribosome entry site (IRES) at the 5' untranslated region of the p53 mRNA.

187 s virus (EMCV) internal ribosome entry site (IRES) at the same sites as linear molecules with the IRE

188 Viral internal ribosomes entry site (IRES) elements coordinate the recruitment of the host tr

189 he function of Internal Ribosome Entry Site (IRES) elements is intimately linked to their RNA structu

190 NAs containing internal ribosome entry site (IRES) elements such as those encoding for the tumor supp

191 The internal ribosome entry site (IRES) in the 5' untranslated region (UTR) of the hepatit

192 presence of an internal ribosome entry site (IRES) in the 5' UTR of VEGF-D mRNA.

193 An internal ribosome entry site (IRES) initiates protein synthesis in RNA viruses, includ

194 iation routes, internal ribosome entry site (IRES) initiation and ribosome shunting, rely on ribosoma

195 Internal ribosome entry site (IRES) RNAs are important regulators of gene expression,

196 ugh structured internal ribosome entry site (IRES) RNAs can manipulate ribosomes to initiate translat

197 e tests on the internal ribosome entry site (IRES) segments yield satisfiable results with experiment

198 a picornavirus internal ribosome entry site (IRES) sequence into the genome of CHIKV.

199 s use a type I Internal Ribosome Entry Site (IRES) structure to facilitate protein synthesis and prom

200 ilitated by an internal ribosome entry site (IRES) that can autonomously bind a 40S ribosomal subunit

201 CrPV) uses an internal ribosomal entry site (IRES) to hijack the ribosome.

202 s an important internal ribosome entry site (IRES) trans-acting factor (ITAF) for poliovirus IRES-med

203 We define an internal ribosome entry site (IRES) within ELANE and demonstrate that adjacent mutatio

204 om usage of an internal ribosome entry site (IRES) within exon 5 that is glucocorticoid inducible.

205 ion, including internal ribosome entry site (IRES), ribosome shunting, and eIF4G enhancers.

206 C virus (HCV) internal ribosome entry site (IRES), we measured the rates of 40S subunit arrival to t

207 vation of this internal ribosome entry site (IRES)-dependent mRNA translation initiation pathway resu

208 the ratio of internal ribosomal entry site (IRES)-dependent to cap-dependent translation.

209 ivation of HCV internal ribosome entry site (IRES)-driven translation by miR-122.

210 Picornavirus internal ribosomal entry site (IRES)-mediated translation and cytopathogenic effects ar

211 eplication or internal ribosomal entry site (IRES)-mediated translation.

212 ion through an internal ribosome entry site (IRES).

213 ing a cryptic internal ribosomal entry site (IRES).

214 containing an internal ribosome entry site (IRES).

215 y virtue of an internal ribosome entry site (IRES).

216 disease virus internal ribosome entry site (IRES); this junction contains highly conserved motifs fo

217 iral genomes, internal ribosome entry sites (IRES) can be used to bypass the traditional requirement

218 n by distinct internal ribosome entry sites (IRES).

219 Internal ribosome entry sites (IRESs) are powerful model systems to understand how the

220 Internal ribosome entry sites (IRESs) mediate cap-independent translation of viral mRNA

221 genome with internal ribosomal entry sites (IRESs) preceding both open reading frames.

222 Internal ribosome entry sites (IRESs) promote translation of mRNAs in a cap-independent

223 Viruses use internal ribosome entry sites (IRESs) to minimize or, like the CrPV IRES, eliminate the

224 naviruses use internal ribosome entry sites (IRESs) to translate their genomes into protein.

225 embling viral internal ribosome entry sites (IRESs), are found in subsets of Hox mRNAs.

226 virus type 1 internal ribosomal entry sites (IRESs).

227 isms, such as internal ribosome entry sites (IRESs).

228 n mediated by internal ribosome entry sites (IRESs).

229 ic interactions with its stem loop II (SLII) IRES domain.

230 SST-IRES-Cre mice were injected in FC (prelimbic/precingulat

231 in slice preparation of transgenic adult Sst-IRES-Cre mice expressing tdTomato fluorescence, channelr

232 e shown that the human La protein stimulates IRES-mediated translation of the cooperative oncogene CC

233 ic ductal epithelial cells in Prrx1creER(T2)-IRES-GFP mice.

234 e investigated initiation on the 5'-terminal IRES.

235 The IRES rearranges from extended to bent to extended confor

236 The IRES was dependent on eIF4G, but not eIF4E, for activity

237 poses: relieving the competition between the IRES and eIF3 for a common binding site on the 40S subun

238 These studies show that PCBP2 enables the IRES to exploit the GNRA tetraloop to enhance initiation

239 During this unusual translocation event, the IRES undergoes a pronounced conformational change to a m

240 ng conformation of the eIF4F complex for the IRES.

241 Our results show how the IRES directs multiple steps after 80S ribosome placement

242 een the apical loop of subdomain IIId in the IRES and helix 26 in 18S rRNA.

243 ete elongation factor-dependent steps in the IRES initiation mechanism.

244 ing a previously unseen binding state of the IRES and directly rationalizing that an eEF2-dependent t

245 Translocation of the IRES by elongation factor 2 (eEF2) is required to bring

246 ed a truncated reading frame upstream of the IRES by exon skipping, which led to synthesis of a funct

247 the tRNA-mRNA-like pseudoknot I (PKI) of the IRES from the decoding center.

248 that an eEF2-dependent translocation of the IRES is required to allow the first A-site occupation.

249 Pseudoknot I of the IRES occupies the ribosomal decoding center at the amino

250 Analysis of the IRES region in vitro by use of both the TCV gRNA and rep

251 d eukaryotes depends on the structure of the IRES RNA, but in bacteria this RNA uses a different mech

252 ated region and inhibits the activity of the IRES through this sequence-specific targeting.

253 34 to Sabin-1 IRES caused degradation of the IRES transcript in a miR-134 and sequence specific manne

254 Specifically, the ORF of the IRES-driven mRNA is established by the placement of the

255 the rate of duplex unwinding by eIF4A on the IRES.

256 As a result, DEK promotes the IRES-dependent translation of the proinvasive transcript

257 transacting factor (ITAF) that regulates the IRES-dependent translation of Cyclin D1 and c-Myc.

258 quence conservation of the 5' UTR render the IRES RNA a potential target for the development of selec

259 d CTU1-dependent regulation and restores the IRES-dependent LEF1 expression.

260 slation: generating a vsRNA that targets the IRES.

261 ubgenomic RNAs, strongly suggesting that the IRES was active in the gRNA invivo Since the TCV CP also

262 Binding of MDM2 RING protein to the IRES region on XIAP mRNA results in MDM2 protein stabili

263 Emphasis will be given to the IRES subdomain IIa, which currently is the most advanced

264 teraction of their eIF3 constituent with the IRES-bound eIF4G.

265 the same sites as linear molecules with the IRES.

266 e of specific structural elements within the IRES for virus infection.

267 ociates from these mRNAs de-repressing their IRES-mediated translation.

268 ly computational design of functional thermo-IRES elements.

269 osensor internal ribosome entry site (thermo-IRES) elements, whose normalized cap-independent transla

270 that miR-134 may regulate function of these IRES sequences in circulation.

271 umerous layers of Hox gene regulation, these IRES elements are essential for converting Hox transcrip

272 These IRESs require an RNA pseudoknot that mimics a codon-anti

273 little is known about the behavior of these IRESs during infection.

274 A typical feature of these IRESs is their ability to bind directly to the eukaryoti

275 This IRES RNA bridges billions of years of evolutionary diver

276 We solved the crystal structure of this IRES bound to a bacterial ribosome to 3.8 A resolution,

277 ween bacterial and eukaryotic ribosomes this IRES binds directly to both and occupies the space norma

278 KH3 is critical for PCBP2's binding to this IRES whereas KH1 is essential for PCBP2's function in pr

279 light a process of noncanonical translation, IRES-mediated translation, that is a growing source for

280 The structures reveal that the TSV IRES initiates translation by a previously unseen mechan

281 he ribosome-bound Taura syndrome virus (TSV) IRES belonging to the family of Dicistroviridae intergen

282 ficiency is lower than that of the wild-type IRES element, which on the other hand is fully resistant

283 We have used IRES elements from human rhinovirus type 2 (HRV2) and fo

284 VEGF IRES-mediated initiation of translation requires the mod

285 translation following heat shock stress via IRES activation.

286 Viral IRES elements are organized in modular domains consistin

287 Viral IRES, in general, contain extensive secondary structure

288 Although viral IRES typically contain higher-order RNA structure, an un

289 Rather, MNK catalytic activity enabled viral IRES-mediated translation/host cell cytotoxicity through

290 report our discovery that a eukaryotic viral IRES can initiate translation in live bacteria.

291 -responsive conformational switches in viral IRES elements.

292 ionally conserved switches involved in viral IRES-driven translation and may be captured by identical

293 tion of Raf-MEK-ERK1/2 signals induced viral IRES-mediated translation in a manner dependent on MNK1/

294 The tRNA shape-mimicry enables the viral IRES to gain access to the ribosome tRNA-binding sites a

295 nce conservation, suggesting that this viral IRES and cellular IRES may have similar strategies for i

296 In contrast to most viral IRESs, it does not depend on structural integrity and sp

297 mediated by the cap structure or other viral IRESs.

298 Because foot-and-mouth disease virus IRES structure depends on long-range interactions involv

299 uctures formed with the Taura syndrome virus IRES and translocase eEF2*GTP bound with sordarin.

300 facilitates the interaction of hnRNP A1 with IRES RNA to promote IRES-dependent translation.

301 We further demonstrate that co-therapy with IRES-J007 and PP242 significantly reduces tumor growth o