ライフサイエンスコーパス: eIF4F

1 eIF4F bound the BTE and a translationally inactive mutan

2 eIF4F complex formation after PH occurred without detect

3 eIF4F is composed of eIF4E, which binds to the mRNA cap,

4 eIF4F is comprised of the subunits eIF4G and eIF4E and o

5 eIF4F is pivotal for oncogenic signaling as it integrate

6 eIF4F-mRNA interactions stabilised by stress are predomi

7 to FRT IRE-RNA, so that at 50 microM Mn(2+) eIF4F bound more than 3-times faster than IRP1.

8 the active eukaryotic initiation factor 4F (eIF4F) complex and induces the protein synthesis of a su

9 eukaryotic translation initiation factor 4F (eIF4F) complex offers an appealing strategy to potentiat

10 ns with the Eukaryotic Initiation Factor 4F (eIF4F) complex, made up of eIF4E, which recognizes the 7

11 The eukaryotic initiation factor 4F (eIF4F) is thought to be the first factor to bind mRNA du

12 eukaryotic translation initiation factor 4F (eIF4F) to recruit ribosomes.

13 Eukaryotic translation initiation factor 4F (eIF4F), comprising the cap-binding protein eIF4E, the he

14 eukaryotic translation initiation factor 4F (eIF4F), preferentially impacts short mRNAs with strong c

15 eukaryotic translation initiation factor 4F (eIF4F), the cap-dependent translation initiation apparat

16 hanneled to eukaryotic initiation factor 4F (eIF4F), the key regulator of the mRNA-ribosome recruitme

17 ng complex, eukaryotic initiation factor 4F (eIF4F), to mediate translation initiation.

18 ormation of eukaryotic initiation factor 4F (eIF4F), which promote cap-dependent translation.

19 re thought to enhance formation of activated eIF4F*mRNA*PABP complexes competent to recruit 43S pre-i

20 ) and promotes eIF4E assembly into an active eIF4F complex bound to the cellular polyadenylate-bindin

21 nt RNA helicase) leads to assembly of active eIF4F complex.

22 ssociated factors alters the ratio of active eIF4F complexes in relation to the 4E-BP1 translational

23 IF4E cannot bind to eIF4G to form the active eIF4F complex, an event that is required for the binding

24 pairs simultaneously to the 5'-UTR, allowing eIF4F to recruit the 40S ribosomal subunit to the 5'-end

25 o eIF4G, the forces required to construct an eIF4F complex remain unidentified.

26 omplex formation, suggesting that ICP6 is an eIF4F-assembly chaperone.

27 nd ribosomal protein S6 and studied eIF2 and eIF4F complex.

28 Detailed modeling of eIF3 and eIF4F onto the 40S ribosomal subunit reveals that eIF3 u

29 unit translation initiation factors eIF3 and eIF4F.

30 dependent RNA helicase activity of eIF4A and eIF4F during translation initiation.

31 dependent RNA helicase activity of eIF4A and eIF4F during translation initiation.

32 ays to measure their dependence on eIF4B and eIF4F isoforms.

33 itiation of natural mRNAs, eIF4A, eIF4B, and eIF4F.

34 eIF4G and eIF4F bind TEV1-143 with similar affinity, whereas eIFis

35 tion factor (eIF) 2alpha phosphorylation and eIF4F complex dysfunction.

36 protein 1 (4EBP1), ribosomal protein S6, and eIF4F cap-complex formation, all of which are markers fo

37 How TC and eIF4F assembly are coordinated, however, remains largely

38 on, whereby mTORC1 and CK2 coordinate TC and eIF4F complex assembly to stimulate cell proliferation.

39 Ternary complex (TC) and eIF4F complex assembly are the two major rate-limiting s

40 HCV infection and NS5A expression augmented eIF4F complex assembly, an indicator of cap-dependent tr

41 anning may depend on the interaction between eIF4F (or the eIF4G central domain) and the ribosome bei

42 ts a phosphorylation mark on the cap-binding eIF4F complex that regulates selective mRNA translation

43 r binding assays revealed that the PTE binds eIF4F and its eIF4E subunit with high affinity.

44 tion of eIF2beta and simultaneously bolsters eIF4F complex assembly via the mTORC1/4E-BP pathway.

45 as Arabidopsis HSP21 and AMV RNA 4 used both eIF4F and eIF(iso)4F equally well.

46 ate mRNAs with polysomes was not affected by eIF4F disruption.

47 sults indicate that intrinsic RNA binding by eIF4F depends on a minimal RNA length, rather than on ca

48 , when initiation would be largely driven by eIF4F, but no reinitiation in an eIF4G-depleted lysate.

49 but is resistant to silencing when driven by eIF4F-independent IRESs, demonstrating a critical role f

50 IC) joins the 5' end of mRNA preactivated by eIF4F and poly(A)-binding protein.

51 of cap and poly(A) recognition and bypassing eIF4F complex formation.

52 y cellular and preclinical models of cancer, eIF4F deregulation results in changes in translational e

53 g domains of eIF4G provide the S. cerevisiae eIF4F complex with a second mechanism, in addition to th

54 Here, we show that Saccharomyces cerevisiae eIF4F has a strong preference for unwinding an RNA duple

55 ion mediated by the mRNA cap-binding complex eIF4F contributes to the induction of protein synthesis

56 1 (YB-1) to displace the cap-binding complex eIF4F from capped mRNA, inhibit translation initiation,

57 HCV) IRES RNA and the 5'-cap binding complex eIF4F via the same domain.

58 show that Vhs binds the cap-binding complex eIF4F.

59 a component of the mRNA cap-binding complex eIF4F.

60 of the translation initiation factor complex eIF4F is a hallmark of cancer.

61 = 350 +/- 30 nm), (ii) the helicase complex eIF4F-eIF4A-eIF4B-ATP increases 40S subunit binding (Kd

62 n the availability of the initiation complex eIF4F, because glucose is unable to stimulate eIF4F asse

63 ponent of the translation initiation complex eIF4F, is downregulated by binding the negative-acting f

64 gulates the cellular cap recognition complex eIF4F, a critical component of the cellular translation

65 ic translation initiation factor 4F complex (eIF4F) and initiation of mRNA translation of type II int

66 he 5'-7-methylguanosine cap-binding complex, eIF4F, along with eIF4E, the cap-binding protein, and th

67 f eIFs that include the cap-binding complex, eIF4F.

68 ation of the translation initiation complex, eIF4F.

69 S complex composed of eIF3, ternary complex, eIF4F, and mRNA.

70 ing of eIF4G, eIFiso4G, and their complexes (eIF4F and eIFiso4F, respectively) to the TEV 143-nt 5'-l

71 In contrast, eIF4F inhibition decreased the translation of representa

72 tiRNAs also displace eIF4F, but not eIF4E:4EBP1, from isolated m(7)G cap.

73 la)) is a stable tiRNA analog that displaces eIF4F from capped mRNA, inhibits translation initiation,

74 Dynamic eIF4F-mRNA interaction changes are part of a coordinated

75 onto the eukaryotic initiation factor (eIF) eIF4F complex.

76 ct of p56 on ribosome dissociation, the eIF3.eIF4F interaction, and enhancement of the ternary comple

77 The binding affinity of eIF4G, eIF4F, and eIFiso4G to S1-3 was reduced by 3-5-fold, con

78 of mRNAs particularly responsive to elevated eIF4F activity that typifies tumorigenesis underscores t

79 ch members of the herpesvirus family enhance eIF4F activity during their replicative cycle.

80 which outcompetes IRP binding; (v) exogenous eIF4F rescued metal-dependent IRE-RNA translation in eIF

81 ukaryotic translation initiation factor 4 F (eIF4F).

82 Translation initiation factor eIF4F (eukaryotic initiation factor 4F), composed of eIF

83 mponent of the translation initiation factor eIF4F complex and to engage in an RNA-RNA kissing-loop i

84 he eukaryotic multisubunit initiation factor eIF4F is an essential component of the translational mac

85 ctivity of the translation initiation factor eIF4F is regulated in part by translational repressors (

86 mpete with the translation initiation factor eIF4F to specifically recognize foreign capped mRNAs, wh

87 F4G subunit of translation initiation factor eIF4F with high affinity.

88 o assemble the translation initiation factor eIF4F, promoting viral protein synthesis and replication

89 sembly of the multisubunit initiation factor eIF4F, viral protein production, and replication.

90 multisubunit, cap-binding translation factor eIF4F.

91 he eukaryotic translation initiation factor (eIF4F) complex in infected cells and bound directly to t

92 tiating mRNAs become relatively depleted for eIF4F.

93 kon for eIF4F binding to FRT IRE-RNA in the absence of metal ion

94 and dissociation rate constant (k(off)) for eIF4F binding to IRES were 59 +/- 2.1 micro s(-1) and 12

95 Mn(2+) increased the association rate for eIF4F binding to FRT IRE-RNA, so that at 50 microM Mn(2+

96 of rapamycin (TOR) activity is required for eIF4F assembly in the regenerating liver.

97 the host eIF4F complex, the requirement for eIF4F components in HCMV replication and mRNA translatio

98 ranslation and underscore a dynamic role for eIF4F in remodeling the proteome toward malignancy.

99 Translation factors eIF4E and eIF4G form eIF4F, which interacts with the messenger RNA (mRNA) 5'

100 on factor 4G (eIF4G), subunit of heterodimer eIF4F (plant eIF4F lacks eIF4A), and 3'-BTE-5'-UTR inter

101 S1156A mutant or 4GI, to the heterotrimeric eIF4F (4F) complex that assembles at the 5' cap structur

102 original purification of the heterotrimeric eIF4F was published over 30 years ago.

103 , our data show that the translation of host eIF4F-dependent mRNAs remains dependent on eIF4F activit

104 eased the translation of representative host eIF4F-dependent mRNAs during the late stage of infection

105 eases the abundance and activity of the host eIF4F complex, the requirement for eIF4F components in H

106 e with the abundance or activity of the host eIF4F complex.

107 The host eIF4F translation initiation complex plays a critical ro

108 However, eIF4F preferentially and cooperatively binds to RNAs wit

109 wide ribosome profiling approach to identify eIF4F-driven mRNAs in MDA-MB-231 breast cancer cells.

110 sulated from these stress-induced changes in eIF4F association.

111 s leads to dynamic and unexpected changes in eIF4F-mRNA interactions that are shared among each facto

112 al reprogramming or the moderate decrease in eIF4F complexes at later times.

113 scued metal-dependent IRE-RNA translation in eIF4F-depeleted extracts.

114 ked contrast to many viruses that inactivate eIF4F, HSV-1 stimulates eIF4F complex assembly in quiesc

115 4F, poly(A)-binding protein did not increase eIF4F binding.

116 h affinity to IRE-RNA; (iv) Fe(2+) increased eIF4F/IRE-RNA binding, which outcompetes IRP binding; (v

117 ral pathway, likely as a result of increased eIF4F complex formation and translation initiation.

118 ect corroborated by the finding of increased eIF4F-cap complex formation detected after irradiation i

119 Furthermore, we demonstrate that increasing eIF4F complex availability via the genetic elimination o

120 k1, block eIF4E phosphorylation, and inhibit eIF4F (cap)-dependent cellular mRNA translation.

121 fected these pathways while still inhibiting eIF4F complex formation and melanoma growth, illustratin

122 results indicating that heat shock inhibits eIF4F activity, and that Hsp90 mRNA translation is sensi

123 hibition, providing mechanistic insight into eIF4F pro-oncogenic activity.

124 nhibited the induction of cyclin D1, a known eIF4F-sensitive gene, at the level of protein expression

125 Our screen confirmed several known eIF4F-dependent genes and identified many unrecognized t

126 f MYC and myeloid cell leukemia 1, two known eIF4F-responsive transcripts and key survival factors in

127 scaffold protein, eIF4G, to form the mature eIF4F complex.

128 o translation, indicating that this modified eIF4F complex containing hsp25 has a role to play in rec

129 teracting with eIF4G to assemble a Ded1-mRNA-eIF4F complex, which accumulates in stress granules.

130 s are controlled by the activity of the mTOR-eIF4F pathway.

131 The multipartite eIF4F contains the cap-binding protein eIF4E, and it is

132 y how poxviruses manipulate the multisubunit eIF4F, composed of the cap-binding eIF4E and the RNA hel

133 to mutant BTE but not WT BTE; 3) BTE mutant-eIF4F interactions were found to be both enthalpically a

134 pathways (e.g., Ras, PI3K/AKT/TOR, and MYC), eIF4F serves as a direct link between important steps in

135 ap binding subunits (eIF4E or eIF(iso)4E) of eIF4F or eIF(iso)4F.

136 uces an increase in the overall abundance of eIF4F components and promotes assembly of eIF4F complexe

137 is associated with an increased abundance of eIF4F core components (eIF4E, eIF4G, eIF4A) and the eIF4

138 molecules that target various activities of eIF4F, we observed that cell survival and DEX resistance

139 cap-binding and RNA-unwinding activities of eIF4F.

140 that decreasing the abundance or activity of eIF4F from the start of infection inhibits HCMV replicat

141 is inhibition is reversed by the addition of eIF4F or eIF(iso)4F, and the subunits of eIF4F and eIF(i

142 ibited translation in trans, and addition of eIF4F, but not eIFiso4F, restored translation.

143 nt translation by increasing the affinity of eIF4F for TEV RNA.

144 The binding affinity of eIF4F to TEV RNA correlates with translation efficiency.

145 E as well as 4E-BP1, and promote assembly of eIF4F complexes in infected cells.

146 of eIF4F components and promotes assembly of eIF4F complexes.

147 F4E, two events that lead to the assembly of eIF4F.

148 Variations in the association of eIF4F with individual mRNAs likely contribute to differe

149 ranslation initiation, namely the binding of eIF4F to the 40 S ribosomal subunit.eIF3.ternary complex

150 nthesis typically begins with the binding of eIF4F to the 7-methylguanylate (m(7)G) cap found on the

151 r factors facilitate preferential binding of eIF4F to the m7G cap.

152 ment of cellular mRNAs depends on binding of eIF4F to the mRNA's 5'-terminal 'cap'.

153 essing eIF4E, the rate-limiting component of eIF4F, in primary human mammary epithelial cells (HMECs)

154 d modifies core and associated components of eIF4F and concentrates them within discrete subcellular

155 factor (eIF) 4E and the eIF4G components of eIF4F.

156 phorylation and reduced the concentration of eIF4F complex subunits eIF4G and eIF4E.

157 hypothesis that requires the disassembly of eIF4F during translation initiation to yield free subuni

158 uggests that the subcellular distribution of eIF4F components may potentiate the complex assembly.

159 eIF4G1 have critical functions downstream of eIF4F*mRNA assembly.

160 To examine the effects of eIF4F in BYDV translation initiation, BTE mutants with w

161 tly diminished the translation efficiency of eIF4F-dependent host transcripts.

162 IL-6 and NGF signaling is an enhancement of eIF4F complex formation and an induction of nascent prot

163 een characterized, genome-wide evaluation of eIF4F translational output is incomplete yet critical fo

164 the RNA helicase eIF4A2 as the key factor of eIF4F through which miRNAs function.

165 Plants have an isozyme form of eIF4F (eIFiso4F) with comparable subunits, eIFiso4E and

166 dissociates from eIF4E to allow formation of eIF4F and initiation of cap-dependent translation.

167 mRNA is thought to require the functions of eIF4F and eIF3, with the latter serving as an adaptor be

168 absence of the NTD or when the functions of eIF4F components are compromised.

169 To understand the impact of eIF4F on malignancy, we utilized a genome-wide ribosome

170 y(A)-binding protein, but was independent of eIF4F function.

171 al host translation machinery, inhibition of eIF4F complex, an amalgam of three initiation factors, e

172 Inhibition of eIF4F in MM exerts pleotropic effects unraveling a uniqu

173 nd the mechanism of binding, the kinetics of eIF4F binding to TEV IRES were examined.

174 correlated with a decrease in the levels of eIF4F compounds, the cap-binding protein eIF4E, and eIF4

175 By illustrating the scope and mechanism of eIF4F-independent mRNA translation, these findings resha

176 nd suggest that Ded1p is an integral part of eIF4F, the complex comprising eIF4G, eIF4A, and eIF4E.

177 While the oncogenic properties of eIF4F have been characterized, genome-wide evaluation of

178 ing protein enhanced the association rate of eIF4F approximately 3-fold.

179 morigenesis underscores the critical role of eIF4F in cancer and raises the exciting possibility of d

180 high affinity, thus questioning the role of eIF4F in translation of BYDV.

181 The broad spectrum of eIF4F-resistant translatomes is incompatible with cap-in

182 no impact of the 5'-cap on the stability of eIF4F-RNA complexes.

183 Kinetic studies of eIF4F and eIFiso4F with VPg show approximately 2.6-fold

184 ons by binding to the cap binding subunit of eIF4F (eIF4E).

185 translation by binding the eIF4G subunit of eIF4F in a manner dependent on its RGG domain, thereby f

186 eIF4G is the major adaptor subunit of eIF4F that binds the cap-binding subunit eIF4E and the m

187 ation initiation factors eIF4G, a subunit of eIF4F, and eIF3a, a subunit of eIF3.

188 r between the ribosome and the 4G subunit of eIF4F.

189 of eIF4F or eIF(iso)4F, and the subunits of eIF4F and eIF(iso)4F cross-link to STNV-1 TED, providing

190 t eIF4F-dependent mRNAs remains dependent on eIF4F activity during HCMV infection.

191 he 43S preinitiation complex (PIC) occurs on eIF4F-dependent mRNA recruitment.

192 Convergence of these signals on eIF4F positions this factor as a gatekeeper of malignant

193 hosphorylation, 4E-BP1-eIF4E association, or eIF4F complex assembly concomitant with increased protei

194 ivate Mnk1, as measured with either eIF4E or eIF4F as substrate.

195 Binding of eIF4E or eIF4F to the cap of mRNA is the rate-limiting step for i

196 on: IFIT1 and IFIT1B efficiently outcompeted eIF4F and abrogated initiation on cap0-mRNAs, whereas in

197 rmination kinetics or disruption of the Pab1-eIF4F interaction do not affect recycling, yet the maint

198 (eIF4G), subunit of heterodimer eIF4F (plant eIF4F lacks eIF4A), and 3'-BTE-5'-UTR interaction.

199 cular specificity for the formation of plant eIF4F and eIFiso4F complexes and suggest a role in mRNA

200 ll molecules in wheat germ extract prevented eIF4F binding to mutant BTE but not WT BTE; 3) BTE mutan

201 ng access of eIF4E to the cap and preventing eIF4F assembly.

202 propose that yeIF4B acts in vivo to promote eIF4F assembly by enhancing a conformation of the HEAT d

203 polypeptide associates with eIF4G to promote eIF4F complex assembly.

204 raction with the mRNA-cap appears to promote eIF4F re-acquisition by the re-initiating 40 S subunit.

205 Our data also reveal that eIF4E promotes eIF4F binding and increases the rate of restructuring of

206 able of interacting with eIF4G and promoting eIF4F complex assembly may play important roles in a var

207 IRP) binding and increase activator protein (eIF4F) binding identifies IRE-RNA as a riboregulator.

208 RNA binding domains work together to provide eIF4F with its 5'-end specificity, both by promoting unw

209 have analyzed equilibrium binding of rabbit eIF4F to a series of diverse RNAs and found no impact of

210 We conclude that the PTE recruits eIF4F by binding eIF4E.

211 whereby control of PABP abundance regulates eIF4F assembly.

212 , we identify an eIF3 subunit that regulates eIF4F modification and show that eIF3e is required for i

213 n of 3' directionality additionally required eIF4F.

214 IRE-RNA/IRP1 equilibria and enhanced IRE-RNA/eIF4F equilibria.

215 Notably, increasing the abundance of select eIF4F core components and associated factors alters the

216 gulation in terms of kinetics and stability, eIF4F kinetics with FRT IRE-RNA were determined.

217 y one of several interactions that stabilize eIF4F*mRNA complexes, and emphasize that closed-loop mRN

218 tiation on mRNAs correlates with less stable eIF4F interactions.

219 IF4F, because glucose is unable to stimulate eIF4F assembly or, in the absence of amino acids, modula

220 uses that inactivate eIF4F, HSV-1 stimulates eIF4F complex assembly in quiescent, differentiated cell

221 cal sequence elements in yeIF4B that support eIF4F function in mRNA recruitment by the PIC.

222 G blocks 43S recruitment without suppressing eIF4F complex formation.

223 r with eIF4A and eIF4G into a complex termed eIF4F.

224 roximately 2.9-fold slower for eIFiso4F than eIF4F with VPg.

225 inding protein eIF4E, and it is assumed that eIF4F binds mRNAs primarily at the 5' m7G cap structure.

226 Our results demonstrate that eIF4F complex formation is not required but eIF4G plays

227 uring the late stage of infection found that eIF4F disruption had a minimal impact on the association

228 horter ones, consistent with the notion that eIF4F in its physiological environment preferentially bi

229 The eIF4F cap-binding complex mediates the initiation of cel

230 -binding protein and eIF4B mainly affect the eIF4F/TEV association rate.

231 ore components (eIF4E, eIF4G, eIF4A) and the eIF4F-associated factor poly(A) binding protein (PABP).

232 einitation complex to the 5' mRNA cap by the eIF4F complex (eIF4A, eIF4E, and eIF4G).

233 anine motif that is required to displace the eIF4F complex, inhibit translation, and induce SG assemb

234 hibitor that targets eIF4G1 and disrupts the eIF4F complex.

235 Together with eIF4E, they form the eIF4F complex, which recruits the 40S subunit to the 5'

236 Further, the eIF4F bound to the 3' BTE with higher affinity than for

237 reinitiation was found to occur only if the eIF4F complex, or at a minimum the central one-third fra

238 SBI-756 impaired the eIF4F complex assembly independently of mTOR and attenua

239 t times soon after infection, changes in the eIF4F complex result in the inhibition of host protein s

240 in vivo of only one molecule of eIF4A in the eIF4F complex.

241 TP) and stimulation of eIF4A activity in the eIF4F complex.

242 , the cap binding protein, with eIF4G in the eIF4F translation initiation complex.

243 While eIF4E is the eIF4F cap recognition component, the eIF4G subunit assoc

244 on is suppressed by blocking assembly of the eIF4F and eIF4G complex to the mRNA 5' cap.

245 hat suppression of all three subunits of the eIF4F cap-binding complex synergizes with DEX in MM to i

246 initiation factor (eIF) 4G component of the eIF4F cap-binding complex.

247 not rapamycin, disrupts the assembly of the eIF4F complex and increases the association of the trans

248 mportant role in preventing formation of the eIF4F complex and thus the initiation of protein synthes

249 a crucial role for proper regulation of the eIF4F complex by 4E-BP2 during LTP and learning and memo

250 mechanisms to maintain the integrity of the eIF4F complex even when mTOR signaling is inhibited.

251 a high-affinity binding conformation of the eIF4F complex for the IRES.

252 , which then facilitates the assembly of the eIF4F complex on p53 mRNA.

253 and eIF4B, suggesting that remodeling of the eIF4F complex was required for SG formation.

254 Components of the eIF4F complex were enhanced during recovery as eIF4E ass

255 eIF4G is the scaffold subunit of the eIF4F complex, whose binding domains for eIF4E and poly(

256 at were tested despite the disruption of the eIF4F complex.

257 ends on miRNAs impairing the function of the eIF4F initiation complex.

258 excludes eIF4G and prevents formation of the eIF4F initiation complex.

259 ion step by interfering with assembly of the eIF4F translation complex.

260 -located GPRC5A disturbs the assembly of the eIF4F-mediated translation initiation complex on the mRN

261 eIF4E/eIF4G interaction, thus preventing the eIF4F complex formation, a rate limiting step in the tra

262 ation initiation mechanism by recruiting the eIF4F complex through a direct eIF4E interaction.

263 omplex has a much shorter life-time than the eIF4F/IRE-RNA complex, which suggests that both rate of

264 tion, coupled with earlier findings that the eIF4F complex is modified earlier during VSV infection,

265 osome complex to the mRNA 5' end through the eIF4F initiation complex binding to the 5' m(7)G-mRNA ca

266 the mRNA cap through directly binding to the eIF4F complex with its two middle extracellular loops.

267 oach revealed that VPg binds directly to the eIF4F complex, with a high affinity interaction occurrin

268 The data support the model in which the eIF4F complex binds directly to the BTE which base pairs

269 h a population of hsp25 associating with the eIF4F complex in a p38 mitogen-activated protein kinase-

270 Remarkably, these eIF4F architectural alterations are accompanied by the c

271 Thus, eIF4F is required for accurate AUG selection and re-init

272 e Mnk1 (MAPK signal-integrating kinase 1) to eIF4F depended on eIF3e, and eIF3e was sufficient to pro

273 uent binding of the preinitiation complex to eIF4F bound at the 5'-cap structure of mRNA are necessar

274 , simply tethering an active endonuclease to eIF4F is not sufficient to degrade mRNAs.

275 itates mRNA translation that is resistant to eIF4F inactivation.

276 eplication becomes increasingly resistant to eIF4F inhibition.

277 that Hsp90 mRNA translation is sensitive to eIF4F inactivation.

278 p may either function at steps subsequent to eIF4F-RNA binding, or other factors facilitate preferent

279 d varying responses of the mRNA templates to eIF4F or eIFiso4F, suggesting that some level of mRNA di

280 ll translational output remains robust under eIF4F inhibition.

281 vival and DEX resistance are attenuated upon eIF4F inhibition in MM cell lines and primary human samp

282 ey survival factors in MM, were reduced upon eIF4F inhibition, and their independent suppression also

283 40S ribosomal subunit reveals that eIF3 uses eIF4F or the HCV IRES in structurally similar ways to po

284 nger ribonucleoprotein particles (mRNPs) via eIF4F-poly(A)-binding protein 1 (Pab1) association, sugg

285 When eIF4F is limiting, TEV is preferentially translated comp

286 These results suggest a mechanism where eIF4F initially binds electrostatically, followed by a c

287 ve data presented here suggest a model where eIF4F.VPg interaction enhances cap-independent translati

288 s, we were interested in determining whether eIF4F interactions with individual mRNAs are reprogramme

289 While eIF4F integrates signals to control translation, precise

290 globin mRNA showed the highest activity with eIF4F, whereas Arabidopsis HSP21 and AMV RNA 4 used both

291 NS5A associated with eIF4F complex and polysomes, suggesting its active invol

292 proteins that degrade mRNAs associated with eIF4F.

293 Association with eIF4F correlated with the ability of Vhs to bind eIF4A b

294 RNA increased more than 4-fold compared with eIF4F alone (19.4 and 79.0 nm, respectively).

295 ssociation for eIFiso4F.VPg as compared with eIF4F.VPg.

296 e that eIFiso4F can kinetically compete with eIF4F for VPg binding.

297 the tunnel provide affinity to compete with eIF4F while allowing IFIT1 to select against N1 methylat

298 When VPg formed a complex with eIF4F, the affinity for TEV RNA increased more than 4-fo

299 nternal ribosome entry site interaction with eIF4F, poly(A)-binding protein did not increase eIF4F bi

300 ve characterized the interaction of VPg with eIF4F, eIFiso4F, and a structured RNA derived from tobac