ライフサイエンスコーパス: ribosome binding

1 ed for an alternative function that requires ribosome binding.

2 to the Shine-Dalgarno sequence and blocking ribosome binding.

3 formation of an RNA structure that inhibits ribosome binding.

4 effect on codon-anticodon interaction during ribosome binding.

5 of basic residues within either loop abolish ribosome binding.

6 hibition assays showed that the TE increases ribosome binding.

7 g to their leader transcripts and preventing ribosome binding.

8 bits Hfq synthesis by competitively blocking ribosome binding.

9 pG Shine-Dalgarno sequence, thereby blocking ribosome binding.

10 ponsible for nucleocytoplasmic shuttling and ribosome binding.

11 nd TRAP regulates YcbK synthesis by blocking ribosome binding.

12 of pabA, trpP and ycbK by directly blocking ribosome binding.

13 AP regulates translation of trpP by blocking ribosome binding.

14 formation of an RNA structure that prevents ribosome binding.

15 ation of cstA by sterically interfering with ribosome binding.

16 oncentration dependence as the inhibition of ribosome binding.

17 , whereas loop C2 appeared to be involved in ribosome binding.

18 ify the Gib2 amino acid residues involved in ribosome binding.

19 release from the mRNA peripherally, allowing ribosome binding.

20 ecause deletion does not completely abrogate ribosome binding.

21 n and the conformational state of Sec61 upon ribosome binding.

22 esting a possible interplay between sRNA and ribosome binding.

23 of RTB to determine if they are critical for ribosome binding.

24 gulatory proteins (IRP) proteins, inhibiting ribosome binding.

25 virus-like translational enhancer (PTE) and ribosome-binding 3' T-shaped structure (TSS) have been f

26 Pea Enation Mosaic Virus possesses a ribosome-binding 3'CITE that can connect to the 5' end t

27 Although both ribosome-binding 3'CITEs are critical for virus accumula

28 )U34 stabilizes anticodon structure, confers ribosome binding ability to tRNA and improves reading fr

29 The chimeric 5'NTR retained ribosome binding activity and was competent in directing

30 The ribosome binding activity of Sec61beta(c), like that of

31 he PRT1 RRM is crucial for the integrity and ribosome-binding activity of eIF3.

32 Ribosome-binding activity was increased or decreased by

33 slocation without significantly reducing the ribosome-binding activity, indicating that the L6 and L8

34 se-deficient mutant in yeast by lowering the ribosome binding affinity of eIF5B.

35 Ribosome binding also makes the mccA RNA exceptionally s

36 re L7Ae motif required for SECIS binding and ribosome binding and (ii) an auxiliary motif involved in

37 G start codon is an important determinant of ribosome binding and expression of leaderless mRNAs in E

38 der sequence are strong determinants of both ribosome binding and expression.

39 Here, we have used 70S ribosome binding and GTP hydrolysis assays to study the

40 similar to other translational GTPases, the ribosome binding and GTPase activities of BipA are tight

41 mutant versions of RACK1 to assess roles in ribosome binding and in vivo function.

42 A second promotes ribosome binding and is conserved between all eukaryotes

43 polypeptides within the translocon requires ribosome binding and is mediated by an acidic residue, A

44 conserved three-dimensional RNA fold governs ribosome binding and manipulation.

45 pairing with these targets directly occludes ribosome binding and prevents translation initiation.

46 have shown that Sec61beta is inessential for ribosome binding and protein translocation, but transloc

47 , the natural fepB GUG start codon decreased ribosome binding and reduced fepB expression 2.5-fold co

48 he data are consistent with a model in which ribosome binding and the formation of the ternary comple

49 spacing, and the initiation region to model ribosome binding and to identify gene starts that do not

50 as a secondary mechanism to further improve ribosome binding and translation control.

51 ) sequence, thus freeing the SD sequence for ribosome binding and translation initiation.

52 rRNA and mRNA serve as the primary mode for ribosome binding and translational initiation, the algor

53 These findings indicate that ribosome binding and translocation can have a major impa

54 Here we report the influence of ribosome binding and translocation on each pathway, usin

55 ns of the Sec61 complex that are involved in ribosome binding and translocation promotion, ribosome-s

56 pression post-transcriptionally by affecting ribosome binding and/or mRNA stability.

57 TSS is required in cis to function, and both ribosome-binding and RNA interaction activities of the k

58 Thus, the OB-fold is crucial for ribosome-binding and the C-terminal domain of eIF1A has

59 conformational rearrangement of the RBD upon ribosome binding, and an increase in rigidity within TF

60 ces the bound protein directly competes with ribosome binding, and in other instances the bound prote

61 Further implications about dimerization, ribosome binding, and other functions of trigger factor

62 nent of the degradosome, also contributes to ribosome binding, and this is favoured through an activa

63 By contrast, we found that geneticin, a ribosome-binding antibiotic with translational 'read-thr

64 Mechanisms of GTPase function and ribosome binding are discussed.

65 FLP-22), or D92 (FLP-23) also showed reduced ribosome binding as well as reduced L3 binding, further

66 Ribosome binding assays in vitro revealed that the hASL(

67 ng GTPase assays, biosensor experiments, and ribosome binding assays.

68 equence conservation, both trigger factor, a ribosome-binding bacterial chaperone, and SurA, a peripl

69 richia coli YidC plays a significant role in ribosome binding but is not the sole determinant because

70 These findings provide strong evidence that ribosome binding by GCN1 is required for its role as a p

71 ed GCN2 activation much more than it reduced ribosome binding by GCN1.

72 tion likely plays a role in the differential ribosome binding by the protein.

73 nd eIF5 from eIF3 in vivo, and destroyed 40S ribosome binding by the residual PRT1-TIF34-TIF35 subcom

74 From these results, we conclude that ribosome binding cannot simply be an induced fit of the

75 nds to T3SS transcripts where it may prevent ribosome binding causing accelerated mRNA degradation.

76 This process requires the tmRNA-binding and ribosome-binding cofactor SmpB, a beta-barrel protein wi

77 e, along with the associated changes in tRNA ribosome-binding configuration.

78 The ribosome-binding determinant located in the NTR was iden

79 se mutations also bypass the requirement for ribosome binding, dimerization, and association with the

80 to direct competition between repressor and ribosome binding ("displacement").

81 The three-dimensional architecture of the ribosome binding domain from these IRESes is organized a

82 to paromomycin in a manner dependent on its ribosome binding domain, supporting the idea that GCN1 b

83 temperature sensitivity are mediated by the ribosome binding domain.

84 TF binds via its N-terminal ribosome-binding domain (RBD) mainly to ribosomal protei

85 ere we present the crystal structures of the ribosome-binding domain from a Dicistroviridae intergeni

86 Part of the ribosome-binding domain in Gcn1 has homology to one of t

87 odular organization for eIF1A wherein a core ribosome-binding domain is flanked by flexible segments

88 rial translation; similarly, deletion of the ribosome-binding domain of Oxa1 prevents an enrichment o

89 ng domain in Gcn1 has homology to one of the ribosome-binding domains in eEF3, suggesting that these

90 Although the ribosome-binding face of eIF1 was identified, interfaces

91 ic surface area termed KH, distinct from the ribosome-binding face.

92 Ribosome binding factor A (RbfA) is a bacterial cold sho

93 Ribosome-binding factor A (RbfA) from Escherichia coli i

94 putative homolog of the bacterial RbfA (for ribosome-binding factor A) protein that was identified a

95 RbfA, a 30S ribosome-binding factor, is a multicopy suppressor of a

96 of 5' end-independent decay is greater, poor ribosome binding favours degradation by that pathway.

97 adenines to in vivo expression and in vitro ribosome binding from mRNAs with different SD-containing

98 PTE, suggesting that the PTE may support the ribosome-binding function of the kl-TSS.

99 BipA is a novel member of the ribosome binding GTPase superfamily and is widely distri

100 Finally, we show that non-cognate tRNA-ribosome binding has an important weight in translation,

101 ve in SAM binding and showed no reduction of ribosome binding in the presence of SAM, whereas a compe

102 s, it may be responsible for Met-tRNA(i)-40S ribosome binding in vivo, possibly together with the TC.

103 M, respectively, indicating that much of the ribosome binding interactions are mediated by the C-doma

104 or the RNA-RNA interaction, suggesting that ribosome binding is important for function.

105 um (ER), isolated for its ability to mediate ribosome binding, is capable of inducing new membrane bi

106 cleotide 3' untranslated region (3'UTR), the ribosome-binding, kissing-loop T-shaped structure (kl-TS

107 nd in viruses of different genera, while the ribosome-binding kl-TSS that provides a long-distance in

108 ns that confer moderate to strong defects in ribosome binding mimic some phenotypes of a RACK1 deleti

109 aeal genomes feature a strong Shine-Dalgarno ribosome-binding motif more pronounced in Euryarchaea co

110 s, study translational regulation, and probe ribosome binding of noncoding RNAs.

111 we present the molecular details underlying ribosome binding of Ssb in Saccharomyces cerevisiae.

112 Strikingly, ribosome binding of Ssb is not essential.

113 tivity of YidC in vivo but did not influence ribosome binding or substrate insertion, whereas loop C2

114 t that suppressed translation reduced either ribosome binding or the RNA-RNA interaction, suggesting

115 fects are not due to reduced protein levels, ribosome binding, or GTP hydrolysis.

116 annel in its closed state, and indicate that ribosome binding per se causes only minor changes.

117 g at any stage during translation, including ribosome binding, polypeptide elongation, or translation

118 s were designed and their GTP hydrolysis and ribosome binding properties assessed.

119 ng assays were used to assess the GTPase and ribosome-binding properties of S. enterica BipA.

120 function of these factors, we identified the ribosome binding protein Stm1 as a multicopy suppressor

121 A novel bacterial ribosome binding protein, protein Y (also known as YfiA)

122 noprecipitation-mass spectrometry identified ribosome-binding protein 1 (RRBP1) as SYNJ2BP's ERM bind

123 Elongation factor P (EF-P) is a conserved ribosome-binding protein that structurally mimics tRNA t

124 anslation elongation is modulated by various ribosome-binding proteins.

125 The restrictocin-ribosome binding rate constant was observed to exceed 10

126 plex theory to dissect the high restrictocin-ribosome binding rate constant.

127 haracterizing mRNAs with rationally designed ribosome binding rates, folding kinetics, and folding en

128 id residues between the insertase domain and ribosome-binding region of Oxa1 of Saccharomyces cerevis

129 N-terminal insertase domain and a C-terminal ribosome-binding region.

130 firmed the interaction between PsrR1 and the ribosome binding regions of the psaL, psaJ, chlN, and cp

131 ent, which are critical for dimerization and ribosome binding, respectively.

132 Deletion of SSH1, which encodes a ribosome-binding Sec61p homologue in the ER, had no effe

133 Mutant proteins were analyzed for ribosome binding, SECIS element binding, and Sec incorpo

134 Unexpectedly, the C-terminal ribosome binding segment of GCN2 (C-term) was required i

135 The effect of the downstream coat gene ribosome binding sequence on maturation gene expression

136 on binding SAM (OFF state) by encrypting the ribosome binding sequence.

137 sed different levels of RfaH by altering the ribosome-binding sequence and start codon.

138 A1 in high Mg(2+), subsequently opening the ribosome-binding sequence for mgtL translation.

139 ted domain but is largely independent of the ribosome binding sequences of Gcn2p.

140 Disruption of SD2 so as to weaken ribosome binding significantly reduces the concentration

141 The stem-loop structure interferes with ribosome binding, silencing gene expression.

142 epress translation by binding in between the ribosome binding site (RBS) and the start codon (in Esch

143 tensive secondary structure sequestering the ribosome binding site (RBS).

144 open reading frame consisting of a consensus ribosome binding site and an ATG initiation codon, follo

145 rfere with internal initiation on the gene X ribosome binding site and limit gene X translation.

146 of the transcript, one of which occludes the ribosome binding site and start codon.

147 anslated regions that include a T7 promoter, ribosome binding site and T7 terminator.

148 repression operates through occlusion of the ribosome binding site and that SAM binding requires the

149 producer) revealed polymorphisms in the tcdR ribosome binding site and the tcdR-tcdB intergenic regio

150 te that a specific mRNA fold forms the split ribosome binding site at the gene 26-25 intercistronic j

151 Hp8 contains the ribosome binding site for tetQ.

152 plex secondary structure that sequesters the ribosome binding site for the tet gene.

153 se-pairing with DsrA, however, made the rpoS ribosome binding site fully accessible, as predicted by

154 We conclude that this ribosome binding site has evolved after T-even diverged

155 sequences, and function by sequestering the ribosome binding site in a hairpin structure at lower te

156 In Qbeta RNA, sequestering the coat gene ribosome binding site in a putatively strong hairpin ste

157 entary cis sequence directly upstream of the ribosome binding site in a target gene.

158 eveals that a stem-loop sequestering the Fst ribosome binding site is required for translational repr

159 nkage between a sensor and output gene using ribosome binding site libraries and genetic selection.

160 ced by the presence or absence of a stronger ribosome binding site located elsewhere on the same RNA

161 ntify gene starts that do not conform to the ribosome binding site model.

162 We used sequence conservation and ribosome binding site models to predict genes encoding s

163 or easily constructing biologically sensible ribosome binding site models.

164 tified a region of sstT mRNA upstream of the ribosome binding site needed for negative regulation by

165 re predicted to pair with sequences near the ribosome binding site of each of these targets; mutation

166 t upon binding RsmA, the region spanning the ribosome binding site of psl mRNA folds into a secondary

167 tion of the Hp1-Hp8 structure, releasing the ribosome binding site of tetQ.

168 ult from an unusual mutation in the putative ribosome binding site of the cbs gene, encoding cystathi

169 The ribosome binding site of the flgD gene was found to be i

170 Though it lacks the canonical ribosome binding site present upstream of both prcA and

171 gion of a putative norM promoter or a likely ribosome binding site resulted in an increased resistanc

172 o correctly predicted that reusing identical ribosome binding site sequences in different genetic con

173 mbination of transcriptional termination and ribosome binding site sequestration increases repression

174 t the isocost line rotates when changing the ribosome binding site strength of the inducible gene and

175 assembly with randomization of gene order or ribosome binding site strength; and (iii) modify an asse

176 ional rearrangements at the 3' border of the ribosome binding site that required ATP and active eIF4A

177 and structure probing experiments reveal the ribosome binding site to be an important determinant of

178 tration, and activates aphA by revealing the ribosome binding site while the sRNA itself is degraded.

179 mains together comprising by far the largest ribosome binding site yet discovered.

180 sters the Shine-Dalgarno sequence (i.e., the ribosome binding site) via base-pairing, thus preventing

181 lated region of the mtlA mRNA, occluding the ribosome binding site, and inhibits the synthesis of the

182 n of the hly 5' UTR, while retaining the hly ribosome binding site, had a moderate effect on LLO prod

183 Systematic changes to the ribosome binding site, plasmid sequence, E. coli strain,

184 One mutant contained a mutation in the glnA ribosome binding site, while the other mutant synthesize

185 repeats embedded in the spacer region of the ribosome binding site.

186 age mRNAs tend to be unstructured around the ribosome binding site.

187 allow progressively increased access to the ribosome binding site.

188 bsence of leader translation, expose the tet ribosome binding site.

189 o provide the tet gene with a nonsequestered ribosome binding site.

190 a 5'-untranslated region and Shine-Dalgarno ribosome binding site.

191 ance between the secondary structure and the ribosome binding site.

192 hat would prevent access of ribosomes to the ribosome binding site.

193 achieved with the araBAD promoter lacking a ribosome binding site.

194 e likely -10 polymerase binding site and the ribosome binding site.

195 a nested pseudoknot structure that spans the ribosome binding site.

196 itory structure in vca0939 that occludes the ribosome binding site.

197 substitution or deletion) extended the fabK ribosome binding site.

198 immediate effect on cleavage upstream of the ribosome binding site.

199 DeltaermC mRNA features a strong ribosome-binding site (RBS) and a 62-amino-acid-encoding

200 we now show that 24 nucleotides of the rpoS ribosome-binding site (RBS) are necessary and sufficient

201 ct mapped to the region upstream of the rpoS ribosome-binding site (RBS) that contains a cis-acting a

202 knot that does not appear to incorporate its ribosome-binding site (RBS).

203 in their mRNAs and thus appear not to use a ribosome-binding site (Shine-Dalgarno)-based mechanism f

204 al efficiency of RpoS mRNA, we examined both ribosome-binding site accessibility and the binding of R

205 The ribosome-binding site accessibility correlates with the

206 We find that that ribosome-binding site accessibility is modulated as a fu

207 ted region of its target mRNA and making the ribosome-binding site accessible.

208 at the distal end of DIVa that contains the ribosome-binding site and initiation codon of the LtrA o

209 pts a distinct structure that sequesters the ribosome-binding site and leads to a reduction in gene e

210 ne had all 7 bp deleted between the putative ribosome-binding site and the start codon, ATG, causing

211 The ribosome-binding site falls squarely within the LtrA-bin

212 and (iii) remodels the structure of the atpH ribosome-binding site in a manner that can account for P

213 vitro RNase E assay when the AU box and the ribosome-binding site in the 5' untranslated region of p

214 in the mature virus, protecting a conserved ribosome-binding site in the capsid protein from exposur

215 At elevated temperatures, the ribosome-binding site is exposed to promote translation

216 The ribosome-binding site is partially sequestered in double

217 odon engineered just upstream of a predicted ribosome-binding site near codon M164 abolished formatio

218 n structure, which lies outside the putative ribosome-binding site of the mRNA.

219 regulated binding of PyrR occludes the first ribosome-binding site of the pyr operon.

220 ribDEAHT operon and precluding access to the ribosome-binding site of ypaA mRNA.

221 he structure offers insight into the mode of ribosome-binding site sequestration by a minimal RNA fol

222 ts and predicts the impact of the receptor's ribosome-binding site strength, as a tunable parameter t

223 uences to a lacZ gene that retained the lacZ ribosome-binding site were not regulated by PyrR plus ur

224 Such sequences include the Shine- Dalgarno ribosome-binding site, as well as other motifs surroundi

225 C9 of the decaloop and the first base of the ribosome-binding site, G33.

226 stem and for comparison, we altered the lacI ribosome-binding site, start codon, and/or codon content

227 le simultaneously increasing exposure of the ribosome-binding site.

228 te, an RNase III-sensitive hairpin and the N ribosome-binding site.

229 h contained a putative promoter region and a ribosome-binding site.

230 ene was shown to be preceded by a functional ribosome-binding site.

231 r, and the RpoN-dependent transcript lacks a ribosome-binding site.

232 ted by double-stranded RNA that occludes the ribosome-binding site.

233 em to construct and clone libraries of yeast ribosome binding sites and bacterial Azurine, which were

234 odels of individual parts such as promoters, ribosome binding sites and coding sequences.

235 Ribosome binding sites and noncoding RNAs tend to be und

236 12,563 combinations of common promoters and ribosome binding sites and simultaneously measured DNA,

237 upled with the observation that high quality ribosome binding sites are found to occur within E. coli

238 onsistent with a mechanism in which multiple ribosome binding sites compete in cis for translational

239 iency of an mRNA can be tuned by varying the ribosome binding sites controlling the recruitment of th

240 rotein translation efficiency by customizing ribosome binding sites for both the upstream acetyl coen

241 Never before have the ribosome binding sites of any IRES domains, cellular or

242 ced alternative fold that controls access to ribosome binding sites or other regulatory sites in RNA.

243 mperature dependent manner via non-canonical ribosome binding sites positioned >120 bp upstream of dn

244 ent TSS selection and a stem-loop masking of ribosome binding sites was predicted from the longer 5'

245 r the control of synthetic parts (promoters, ribosome binding sites, and terminators) that are functi

246 orthogonal promoter sequences, Streptomyces ribosome binding sites, and yeast selectable marker gene

247 e strategy to achieve assembly of promoters, ribosome binding sites, cis-regulatory elements, and rib

248 a predictive method for designing synthetic ribosome binding sites, enabling a rational control over

249 ressors, activators, promoters, terminators, ribosome binding sites, signaling devices, and measureme

250 eins, and the majority upstream and proximal ribosome binding sites, suggesting a regulatory role of

251 omic model allowed us to identify the Tet(O)-ribosome binding sites, which involve three characterist

252 frameshifting and the existence of multiple ribosome binding sites.

253 ction of gene products that have inefficient ribosome binding sites.

254 inhibitory stem-loop containing the sRNA and ribosome binding sites.

255 itiated at two positions, with two predicted ribosome-binding sites and translation start codons, pot

256 ntinuous editing of small DNA parts, such as ribosome-binding sites, as well as efficient manipulatio

257 Examples of BioBricks include promoters, ribosome-binding sites, coding sequences and transcripti

258 s, putative palindromic sites, and predicted ribosome-binding sites.

259 ikely transcription factor binding sites and ribosome-binding sites.

260 sequences of complementarity, blocking their ribosome-binding sites.

261 G initiation codon showed a greater in vitro ribosome binding strength and a higher level of full-len

262 tiation codon is an important determinant of ribosome binding strength and translational efficiency f

263 correlated closely with changes in in vitro ribosome binding strength.

264 translation element (CITE), which includes a ribosome-binding structural element (RBSE) that particip

265 is the smallest 5' mRNA leader necessary for ribosome binding, suggesting that selective pressure min

266 d the active site cleft, indicating that the ribosome binding surface of RTA is on the opposite side

267 S complex, and instead interacts through its ribosome-binding surface exclusively with the apical reg

268 h a reduced affinity for peptide and altered ribosome binding that is unable to substitute for Ssb in

269 eprint) and filter binding assays to measure ribosome binding, the changes in in vivo expression corr

270 The dimethylallyl modification may enhance ribosome binding through multiple mechanisms including d

271 the biogenesis of membrane proteins require ribosome binding to a membrane channel formed by the Sec

272 terestingly, this stability depended also on ribosome binding to a nearby Shine-Dalgarno sequence but

273 n of some viral and cellular mRNAs occurs by ribosome binding to an internal ribosome entry site (IRE

274 sembling the initiation complex required for ribosome binding to an mRNA.

275 Ribosome binding to btuB RNA was inhibited by Ado-Cbl bu

276 Ribosome binding to btuB RNA was much less efficient tha

277 CsrA regulates CstA synthesis by inhibiting ribosome binding to cstA transcripts.

278 imary transcript and concomitantly enhancing ribosome binding to increase expression of the transport

279 n of translation initiation factors affected ribosome binding to leaderless mRNAs.

280 To examine ribosome binding to mammalian mitochondria, we used ribo

281 Removal of this structure resulted in better ribosome binding to RNA I and a 300-fold increase in pro

282 ted that purified RNA II was able to inhibit ribosome binding to RNA I.

283 This assay allowed the study of ribosome binding to streptomycete leaderless and leadere

284 In current views, translation-coupled ribosome binding to the endoplasmic reticulum (ER) membr

285 to the ribosome and is sufficient to prevent ribosome binding to the endoplasmic reticulum membrane.

286 xperiments indicate that bound CsrA prevents ribosome binding to the glgC Shine-Dalgarno sequence and

287 studies demonstrate that bound CsrA prevents ribosome binding to the hag transcript, thereby inhibiti

288 Cytoplasmic ZBP1 and ribosome binding to the mRNA were anti-correlated depend

289 MicC was also shown to inhibit ribosome binding to the ompC mRNA leader in vitro and to

290 the trpE S-D blocking hairpin, and blocking ribosome binding to the pabA and trpP transcripts.

291 Here, we show that ribosome binding to the resting SecYEG channel triggers

292 Ribosome binding to the SecYEG complex is strongly stimu

293 ation via a mechanism that is facilitated by ribosome binding to the Shine-Dalgarno sequence.

294 Ribosome binding to the translation initiation site impe

295 Turnip crinkle virus contains a T-shaped, ribosome-binding, translation enhancer (TSS) in its 3'UT

296 orming a highly interactive structure with a ribosome-binding tRNA-shaped structure (TSS) acting as a

297 rm a T-shaped structure (TSS) similar to the ribosome-binding TSS of Turnip crinkle virus (TCV).

298 ction in toxicity, depurination activity and ribosome binding was observed when R235A was combined wi

299 by terminating transcription or by blocking ribosome binding, whereas most eukaryotic TPP riboswitch

300 sights into the three-dimensional layout for ribosome binding, which may serve as a structural basis