ライフサイエンスコーパス: ribosome binding

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

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

3 ed for an alternative function that requires ribosome binding.

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

5 es of which do not play a critical role in I-ribosome binding.

6 formation of an RNA structure that inhibits ribosome binding.

7 of basic residues within either loop abolish ribosome binding.

8 hibition assays showed that the TE increases ribosome binding.

9 g to their leader transcripts and preventing ribosome binding.

10 bits Hfq synthesis by competitively blocking ribosome binding.

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

12 activate translation initiation by affecting ribosome binding.

13 ponsible for nucleocytoplasmic shuttling and ribosome binding.

14 nd TRAP regulates YcbK synthesis by blocking ribosome binding.

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

16 AP regulates translation of trpP by blocking ribosome binding.

17 formation of an RNA structure that prevents ribosome binding.

18 ation of cstA by sterically interfering with ribosome binding.

19 effect on codon-anticodon interaction during ribosome binding.

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

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

22 release from the mRNA peripherally, allowing ribosome binding.

23 ecause deletion does not completely abrogate ribosome binding.

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

25 esting a possible interplay between sRNA and ribosome binding.

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

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

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

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

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

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

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

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

34 Ribosome binding also makes the mccA RNA exceptionally s

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

36 Here, we examined the role of ribosome binding and depurination activity on inhibition

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

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

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

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

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

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

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

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

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

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

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

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

58 otein output depends on the strengths of the ribosome binding, and is proportional with the level of

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

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

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

62 s with the diffusive behavior induced by the ribosome-binding antibiotics chloramphenicol and kasugam

63 A stereoselective synthesis of the ribosome-binding antitumor antibiotic (-)-bactobolin A i

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

65 Ribosome binding assays in vitro revealed that the hASL(

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

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

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

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

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

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

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

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

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

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

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

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

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

79 temperature sensitivity are mediated by the ribosome binding domain.

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

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

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

83 kingly, we identified the positively charged ribosome-binding domain in the N terminus of the betaNAC

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

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

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

87 Phylogenetic analysis and ribosome binding experiments indicated that the MBD inte

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

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

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

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

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

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

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

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

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

97 d with ribosome biogenesis, rRNA processing, ribosome binding, GTP binding, and hydrolase activity.

98 role that these residues play in regulating ribosome binding, GTP hydrolysis, and translation initia

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 de tunnel exit site, analysis of the cpSRP54/ribosome binding interface revealed a direct interaction

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

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

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

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

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

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

111 The ribosome-binding mutant inhibited the UPR without affect

112 A ribosome-binding mutant, which showed reduced binding to

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

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

115 Strikingly, ribosome binding of Ssb is not essential.

116 RNA structures that impede ribosome binding or subsequent scanning of the 5'-untran

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

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

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

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

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

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

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

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

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

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

127 m-localized RNA-binding proteins vigilin and ribosome-binding protein 1 directly bound viral RNA and

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

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

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

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

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

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

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

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

136 Finally, we show that the ribosome-binding resistance factor VmlR from Bacillus su

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

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

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

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

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

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

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

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

145 anslated region of the mRNA to sequester the ribosome binding site (RBS) and inhibit translation.

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

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

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

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

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

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

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

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

154 that includes the PK helix, so occluding the ribosome binding site and thus preventing the initiation

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

156 Hp8 contains the ribosome binding site for tetQ.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

188 so that translation can be initiated at the ribosome binding site.

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

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

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

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

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

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

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

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

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

198 allow progressively increased access to the ribosome binding site.

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

200 ensive secondary structure that overlaps the ribosome binding site.

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

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

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

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

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

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

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

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

209 The ribosome-binding site accessibility correlates with the

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

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

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

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

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

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

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

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

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

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

220 s to the CTD of P stalk proteins because the ribosome-binding site is exposed.

221 The ribosome-binding site is partially sequestered in double

222 mRNA structures that otherwise sequester the ribosome-binding site of the 3'gene.

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

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

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

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

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

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

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

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

231 g basic biological functions (e.g. promoter, ribosome-binding site, terminator sequence), "devices" a

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

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

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

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

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

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

238 Ribosome binding sites and noncoding RNAs tend to be und

239 12,563 combinations of common promoters and ribosome binding sites and simultaneously measured DNA,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

254 frameshifting and the existence of multiple ribosome binding sites.

255 mance of E. coli and synthetic promoters and ribosome binding sites.

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

257 cteria, stable RNA structures that sequester ribosome-binding sites (RBS) impair translation initiati

258 ied design constraints, including promoters, ribosome-binding sites and terminators.

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

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

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

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

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

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

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

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

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

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

269 ly or the entire CTT had opposing effects on ribosome binding, substrate-protein binding, ATPase acti

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

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

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

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

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

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

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

277 In characterizing ribosome binding to a regulatory element within a Homeob

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

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

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

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

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

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

284 The cytosolic Brl domain of Sec63 blocks ribosome binding to the channel and recruits Sec71 and S

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

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 Ribosome binding to the translation initiation site impe

294 ssion, which in turn correlates with reduced ribosome binding to viral mRNAs.

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