ライフサイエンスコーパス: IRES

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

2 IRES are characterized by periods of flow cessation, dur

3 IRES usually function when 5' cap-dependent translation

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

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

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

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

10 134 binding to Sabin-1 and 3 but not Sabin-2 IRES.

11 ms collected during the dry phase across 205 IRES from five major climate zones.

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

13 CrPV IGR IRES activity either decreased 40S-IRES complex formation, or increased the rate of the con

14 hange that was required to form a stable 40S-IRES complex.

15 region (CrPV IGR) IRES to form a stable 40S-IRES complex.

16 he conformational change stabilizing the 40S-IRES complex does not occur prematurely.

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

18 ansduction and growth, but it did not affect IRES-driven translation.

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

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

21 t provides a publicly available tool for all IRES researchers, and can be used in other genomics appl

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

23 They are incorporated into an IRES classifier based on XGBoost.

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

25 ry, our findings suggest the existence of an IRES in the 5' coding sequence of TDP2 that translationa

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

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

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

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

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

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

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

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

34 1, which can program increased initiation at IRES motifs on mRNA by the translational initiation comp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

49 However, a limited number of confirmed IRES have been reported due to the requirement for highl

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

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

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

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

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

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

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

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

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

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

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

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

62 the full-length eIF4GI, is required for CVB3 IRES activity for translation of input viral RNA.

63 but DAP5 exhibits a lower affinity for CVB3 IRES compared with the C-terminal eIF4GI fragment.

64 nslation by sustaining a basal level of CVB3 IRES activity.

65 on of 2A protease and consequent robust CVB3 IRES-mediated translation by the C-terminal eIF4GI fragm

66 AP5 and C-terminal eIF4GI interact with CVB3 IRES in the same region, but DAP5 exhibits a lower affin

67 Using the Coxsackievirus B3 (CVB3) IRES as a model system, here we demonstrate that DAP5, b

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

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

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

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

72 y examines the features that can distinguish IRES from non-IRES sequences.

73 red by functionally and structurally diverse IRESs, impacts both steps of the complex formation.

74 nly Cre alleles (Villin-Cre(ERT2), Lgr5-EGFP-IRES-Cre(ERT2), Hnf4alpha(+/+), and Hnf4gamma(+/+)) or m

75 rmed studies with Villin-Cre(ERT2);Lgr5-EGFP-IRES-Cre(ERT2);Hnf4alpha(f/f);Hnf4gamma(Crispr/Crispr) m

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

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

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

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

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

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

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

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

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

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

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

89 fect was not observed with the bona fide HCV IRES.

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

91 sis of eIF3 subunits associated with the HCV IRES disclosed similar effects and that the a subunit is

92 a subunit is critical for binding to the HCV IRES.

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

94 ith SLII which may further stabilize the HCV IRES.

95 5' terminus and promote formation of the HCV IRES.

96 The hepatitis C virus (HCV) IRES binds eukaryotic translation initiation factor 3 (e

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

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

99 that DAP5 is specifically required by type I IRES but not by type II or type III IRES, in which cleav

100 Type I IRES elements require auxiliary host proteins to organiz

101 a model for enteroviral 5' UTRs with type I IRES elements that links structure to function during th

102 The poliovirus type I IRES is able to recruit ribosomal machinery only in the

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

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

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

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

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

108 ese, we reconstructed the trajectory of IAPV-IRES from the early small subunit recruitment to the fin

109 n and a post-translocation state of the IAPV-IRES in the ribosome, allowing us to identify six struct

110 ed toward fighting CCD by targeting the IAPV-IRES using RNA-interference technology are underway, and

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

112 Mutations in eS25 that reduced CrPV IGR IRES activity either decreased 40S-IRES complex formatio

113 facilitates initial binding of the CrPV IGR IRES to the 40S while ensuring that the conformational c

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

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

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

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

118 paralysis virus intergenic region (CrPV IGR) IRES to form a stable 40S-IRES complex.

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 y type I IRES but not by type II or type III IRES, in which cleavage of eIF4GI has not been observed.

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

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

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

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 neous nuclear ribonucleoprotein A1, with its IRES.

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

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

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

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

133 motifs found in hepatitis C virus (HCV)-like IRESs, suggesting mechanistic similarities.

134 5'UTR of various cellular genes and HCV-like IRESs.

135 live-attenuated MAYV vaccine candidate (MAYV/IRES).

136 Moreover, MAYV/IRES vaccination of immunocompetent and interferon recep

137 Inoculation of MAYV/IRES in BALB/c mice induced strong specific cellular and

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

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

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

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

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

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 Cre(tg/wt) mice were crossed to Rosa26(N1ICD-IRES-GFP) to enhance Notch signaling in HEC (NICD(OE-HEC

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

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

153 features that can distinguish IRES from non-IRES sequences.

154 ive components, we characterized how a novel IRES at the 5'-UTR of a viral RNA assembles a functional

155 We show that bursts of IRES translation are shorter and rarer than bursts of ca

156 An early commitment of IRES/ribosome complexes for global pre-translocation mim

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

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

159 ey are well-studied in bulk, the dynamics of IRES-mediated translation remain unexplored at the singl

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

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

162 roup II intron RNAs, and the tRNA mimicry of IRES RNAs.

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

164 preferred initiation site from a plethora of IRES-encoded AUG triplets.

165 cal cycles, especially because prevalence of IRES will increase due to increasing severity of drying

166 These results show that the role of IRES should be accounted for in global biogeochemical cy

167 5 facilitates the translation of a subset of IRES-containing genes.

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

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

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

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

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

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

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

175 in DYN+ neurons was confirmed in CeA of Pdyn-IRES-Cre mice and functionality of an inhibitory (hM4Di)

176 Picornaviral IRES elements are essential for initiating the cap-indep

177 itiation codon in type I and II picornavirus IRES.

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

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

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

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

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

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

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

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

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

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

188 atitis C virus internal ribosome entry site (IRES) and the flavin-mononucleotide riboswitch.

189 uses encode an internal ribosome entry site (IRES) at the 5' end of their RNA, which, unlike most cel

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

191 s virus (EMCV) internal ribosome entry site (IRES) between NS2 and NS3 to separate the two proteins i

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

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

194 d by the viral internal ribosome entry site (IRES) for efficient translation of the viral RNA.

195 te functional internal ribosomal entry site (IRES) formation.

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

197 H2 bound to an internal ribosome entry site (IRES) in the 5'UTR of p53 mRNA and enhanced p53 protein

198 aralysis virus internal ribosome entry site (IRES) RNA, which shows that it is nonfunctional because

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

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

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

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

203 l level via an internal ribosome entry site (IRES) that initiates translation at codon 54, the second

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

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

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

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

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

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

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

211 ining a type I internal ribosome entry site (IRES).

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

213 containing an internal ribosome entry site (IRES).

214 Internal ribosome entry sites (IRES) are segments of mRNA found in untranslated regions

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

216 Viruses use internal ribosome entry sites (IRES) to hijack host ribosomes and promote cap-independe

217 nces, called Internal Ribosomal Entry Sites (IRES), in viral RNAs is a widespread strategy for the ex

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

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

220 e presence of internal ribosome entry sites (IRESs) in the viral RNAs, using different sets of host t

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

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

223 anism for how internal ribosome entry sites (IRESs) recruit ribosomes to initiate translation of an m

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

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

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

227 Similar to internal ribosome entry sites (IRESs), specialized translation initiation requires the

228 nces, called internal ribosomal entry sites (IRESs), to precisely exploit the host machinery for vira

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

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

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

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

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

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

235 f intermittent rivers and ephemeral streams (IRES), which comprise half of the global river network a

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

237 The IRES features a novel extended, multi-domain architectur

238 The IRES rearranges from extended to bent to extended confor

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

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

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

242 ng conformation of the eIF4F complex for the IRES.

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

244 opy (cryo-EM), we have characterized how the IRES of Israeli acute paralysis virus (IAPV) intergenic

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

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

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

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

249 ukaryotic ribosome, we took advantage of the IRES from the intergenic region (IGR) of the Cricket Par

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

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

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

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

254 o-steps: an initial fast binding step of the IRES to the 40S ribosomal subunit, followed by a slow un

255 34 to Sabin-1 IRES caused degradation of the IRES transcript in a miR-134 and sequence specific manne

256 ctor PCBP2 that binds to stem-loop IV of the IRES.

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

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

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

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

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 well as hAgo2:miR-122 interactions with the IRES-40S complex that suggest hAgo2 is likely to form ad

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

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

266 ly computational design of functional thermo-IRES elements.

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

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

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

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

271 opological conservation observed among these IRESs and other viral domains implicates a structured th

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

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

274 This IRES RNA bridges billions of years of evolutionary diver

275 plains the high efficiency observed for this IRES.

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 We observed that this IRES drives expression of a shorter, N-terminally trunca

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

280 IRESpy is a fast, reliable, high-throughput IRES online prediction tool.

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

282 arity to the 18S rRNA markedly reduced TriMV IRES activity, as did the delivery of antisense oligonuc

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

284 easured the kinetics of cap-dependent versus IRES-mediated translation in living human cells.

285 out mice with either VGluT2-IRES-cre or Vgat-IRES-cre mice and used both male and female mice to conf

286 onditional knock-out mice with either VGluT2-IRES-cre or Vgat-IRES-cre mice and used both male and fe

287 translation following heat shock stress via IRES activation.

288 Viral IRES elements are organized in modular domains consistin

289 Viral IRES, in general, contain extensive secondary structure

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

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

292 e, this is the first report of a plant viral IRES YX-AUG motif, and our findings suggest that a conse

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

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

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

296 relevance of the untapped diversity of viral IRESs.

297 ution crystal structure of hepatitis A virus IRES domain V (dV) in complex with a synthetic antibody

298 he other from the encephalomyocarditis virus IRES.

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