ライフサイエンスコーパス: shine

1 teric control of proteins provides a tool to shine a light on the complex cascades of cellular proces

2 e parallel epidemics of obesity and diabetes shine a spotlight on the potential for therapeutic manip

3 e scale research in marine biology, but also shines a new light on big biology, suggesting new ways t

4 compatible with statistical decision theory, shining a new light on the old questions of how such jud

5 nano-bioreplicated surfaces were verified by shining a white laser on the decoys in a dark room and p

6 the southern hemisphere illuminated by Pluto-shine and also images taken during the approach phase th

7 A mechanism proposed by Shine and Dalgarno (SD), focused on the base pairing of

8 riophage T4 gene 25 contains three potential Shine and Dalgarno sequences: SD1, SD2 and SD3.

9 is(p-tolyl)-1,2-dioxin (1g) was suggested by Shine and Zhao as a product in an electron-transfer (ET)

10 th cases the crystals take the form of black shining blades and are indistinguishable by optical micr

11 nous x-ray sources (ULXs) in nearby galaxies shine brighter than any x-ray source in our Galaxy.

12 kable rates and active galactic nuclei (AGN) shone brightly as a result of accretion onto black holes

13 ralis and its specialist brood parasite, the shining bronze-cuckoo Chalcites lucidus in New Caledonia

14 in MYH6 accounting for approximately 11% of Shone complex, and dominant FLT4 mutations accounting fo

15 These include a Shine Dalgarno (SD)-like sequence, a slippery sequence o

16 Such sequences include the Shine- Dalgarno ribosome-binding site, as well as other

17 erved helix/loop 70 of 23S rRNA and the anti-Shine-Dalgarno (aSD) sequence of 16S rRNA.

18 one AAG) that surround and overlap the trpP Shine-Dalgarno (S-D) sequence and translation start codo

19 leading to extended interaction between the Shine-Dalgarno (SD) and anti-SD sequences compensate for

20 d downstream of the initiation codon, called Shine-Dalgarno (SD) and downstream box (DB) sequences, r

21 tif in the 5' UTR of toxT, with a fourU anti-Shine-Dalgarno (SD) element that base pairs with the SD

22 like 70S ribosome complex containing an 8-bp Shine-Dalgarno (SD) helix was determined at 3.8-A resolu

23 The relationship between this Shine-Dalgarno (SD) region and the binding of ribosomes

24 ndent RNA structure that sequesters the trpE Shine-Dalgarno (SD) sequence (the SD blocking hairpin).

25 not bind mRNA with the wild-type, canonical Shine-Dalgarno (SD) sequence and (iii) minimally interac

26 signals: a slippery sequence (A AAA AAG), a Shine-Dalgarno (SD) sequence and a downstream hairpin.

27 karyotic genomes between the presence of the Shine-Dalgarno (SD) sequence and other gene features, in

28 rearrangement in the RNA that sequesters the Shine-Dalgarno (SD) sequence by pairing with a complemen

29 structural rearrangement that sequesters the Shine-Dalgarno (SD) sequence by pairing with an anti-SD

30 DNA sequencing uncovered a mutation in the Shine-Dalgarno (SD) sequence for gIIp, a protein involve

31 (5'-GAGGAGG-3') that resemble the consensus Shine-Dalgarno (SD) sequence found at translation initia

32 ventionally leadered lacZ with and without a Shine-Dalgarno (SD) sequence in Escherichia coli and fou

33 regulation originates from occlusion of the Shine-Dalgarno (SD) sequence upon ligand binding; howeve

34 bosome to a translational start site are the Shine-Dalgarno (SD) sequence within the untranslated lea

35 reason for inefficient translation is a weak Shine-Dalgarno (SD) sequence, AGG(G).

36 onstrate that, in the absence of an upstream Shine-Dalgarno (SD) sequence, PoTC breakdown proceeds in

37 t sequesters a sequence complementary to the Shine-Dalgarno (SD) sequence, thus freeing the SD sequen

38 sembled on an mRNA with and without a strong Shine-Dalgarno (SD) sequence-a sequence found just upstr

39 n the RF2 gene (prfB) involves an intragenic Shine-Dalgarno (SD) sequence.

40 upstream of the initiation codon, called the Shine-Dalgarno (SD) sequence.

41 spI, and is located 11 bases upstream of the Shine-Dalgarno (SD) sequence.

42 uctures with various stabilities and contain Shine-Dalgarno (SD) sequences of different strengths.

43 y RNAs would be predicted to occlude the rot Shine-Dalgarno (SD) site and to block rot translation.

44 frameshifting in translation of dnaX mRNA: a Shine-Dalgarno (SD)-like sequence, a double-shift site,

45 (stem-loop) and two others mapped just 5' to Shine-Dalgarno (SD)-like sequences located immediately u

46 ound E-site tRNA and the Shine-Dalgarno-anti-Shine-Dalgarno (SD-aSD) interaction on A-site tRNA inter

47 The role of the Shine-Dalgarno blocking hairpin in controlling translati

48 R, including the terminator 5'-stem-loop and Shine-Dalgarno blocking hairpins, demonstrated 5'-tripho

49 NA (mRNA/rRNA elements forming the bacterial Shine-Dalgarno duplex) also resembles elements of the ba

50 und in yeast, calling into question the anti-Shine-Dalgarno effect's role in ribosome pausing.

51 t the espADB leader region contains a strong Shine-Dalgarno element (SD2) and a translatable mini-ORF

52 mRNA translation not only by binding to the Shine-Dalgarno element but also by base pairing anywhere

53 mobilities of features interacting with the Shine-Dalgarno helix are decreased in the presence of th

54 ting the proposal that that formation of the Shine-Dalgarno helix during initiation may contribute to

55 The Shine-Dalgarno helix is bound in a large cleft between t

56 o helix are decreased in the presence of the Shine-Dalgarno helix, supporting the proposal that that

57 s an untranslated leader with a conventional Shine-Dalgarno homology.

58 less stringent in the RF2 context, as if the Shine-Dalgarno interaction can help stabilize a quasi-st

59 Increasing the strength of the Shine-Dalgarno interaction with 16S rRNA at the gene VII

60 540 and 1541 (E. coli numbering) in the anti-Shine-Dalgarno mRNA binding sequence.

61 ons because they terminate either within the Shine-Dalgarno or coding sequence of the next gene on th

62 signal extracted by computer analysis was a Shine-Dalgarno pattern matching the complementary sequen

63 epA on ARD is related to the sequence of the Shine-Dalgarno region.

64 nscript lacking a 5'-untranslated region and Shine-Dalgarno ribosome binding site.

65 site shows little homology to the canonical Shine-Dalgarno ribosome recognition sequence, but the re

66 Archaeal genomes feature a strong Shine-Dalgarno ribosome-binding motif more pronounced in

67 nism to compensate for the lack of a classic Shine-Dalgarno rRNA interaction in the translation of so

68 ely), followed by stop codon context and the Shine-Dalgarno sequence (3.7-5.1% and 1.9-3.8%, respecti

69 tiary KL interaction directly sequesters the Shine-Dalgarno sequence (i.e., the ribosome binding site

70 sequence in the 3' end of the 16S rRNA (anti-Shine-Dalgarno sequence [aSD]).

71 nce element upstream of the start codon (the Shine-Dalgarno sequence [SD]) and a complementary sequen

72 ion by CsrA involves binding directly to the Shine-Dalgarno sequence and blocking ribosome binding.

73 ture is achieved in the presence of both the Shine-Dalgarno sequence and DB.

74 ations in CsrA binding sites overlapping the Shine-Dalgarno sequence and initiation codon partially r

75 ocessing occurs just upstream of a consensus Shine-Dalgarno sequence and results in the removal of 54

76 a stem-loop structure upstream of the CC3461 Shine-Dalgarno sequence and stabilizes the transcript.

77 d charged-tRNA(Trp) deficiency to expose the Shine-Dalgarno sequence and start codon for the AT prote

78 d two dipeptide coding minigenes between the Shine-Dalgarno sequence and start codon of ycbK.

79 and stimulates translation by releasing the Shine-Dalgarno sequence and start site from a stable sec

80 d CsrA prevents ribosome binding to the glgC Shine-Dalgarno sequence and that this reduces GlgC synth

81 omes were identified, the "AGGA" core of the Shine-Dalgarno sequence and the "A-rich" sequence locate

82 tain fragmented operator sites such that the Shine-Dalgarno sequence and the initiation codon of the

83 inding to a 19 nt RNA hairpin containing the Shine-Dalgarno sequence and the initiation codon of the

84 sumptive TRAP binding site overlaps the yhaG Shine-Dalgarno sequence and translation initiation regio

85 d a hairpin structure that can sequester the Shine-Dalgarno sequence are necessary for cobalamin-depe

86 the leader nucleotides just upstream of the Shine-Dalgarno sequence but is conflicted on the questio

87 epended also on ribosome binding to a nearby Shine-Dalgarno sequence but was independent of downstrea

88 get site of glgC that lies upstream from the Shine-Dalgarno sequence did not affect regulation by HD-

89 anslation as independent elements, e.g., the Shine-Dalgarno sequence in prokaryotes, the rRNA-binding

90 ort that three-base substitutions around the Shine-Dalgarno sequence in the 159-base 5'-untranslated

91 ed expression in the absence of a leader and Shine-Dalgarno sequence indicated that stimulation by CA

92 target (translational operator), but that a Shine-Dalgarno sequence is not required for specificity.

93 A operator sites, including one in which the Shine-Dalgarno sequence is positioned 4 nt outside the c

94 otes refolding of the RNA such that the trpE Shine-Dalgarno sequence is sequestered in a hairpin, thu

95 proximal to regulatory features such as the Shine-Dalgarno sequence is sufficient to enable regulati

96 t abolish the structure without altering the Shine-Dalgarno sequence itself.

97 d TUP resulting from a G-->A mutation in the Shine-Dalgarno sequence of gene II.

98 otential CsrA binding site that overlaps the Shine-Dalgarno sequence of hfq, a gene that encodes an R

99 o analyzed the 350-bp region upstream of the Shine-Dalgarno sequence of norA by gel mobility shift ex

100 of 3-methyl-3-buten-1-ol by engineering the Shine-Dalgarno sequence of nudB, which increased protein

101 pseudoknot, occur to sequester the putative Shine-Dalgarno sequence of the RNA only after metabolite

102 tion regulates the accessibility of the secA Shine-Dalgarno sequence on secM secA mRNA.

103 bstantial number of genes overlap either the Shine-Dalgarno sequence or the coding sequence of the ne

104 By mutating either the Shine-Dalgarno sequence or the start codon, we find that

105 The trpG Shine-Dalgarno sequence overlaps the stop codon of the u

106 ether with the contribution of 16S rRNA anti-Shine-Dalgarno sequence pairing with GAG, facilitates pe

107 , different segments of the single consensus Shine-Dalgarno sequence serve the two translational star

108 -terminal region immediately upstream of the Shine-Dalgarno sequence that contributes to formation of

109 Addition of an untranslated lac leader and Shine-Dalgarno sequence to cI increased expression but s

110 Addition of an untranslated leader and Shine-Dalgarno sequence to the cat coding sequence incre

111 tends to be compensated by mutations in the Shine-Dalgarno sequence towards a stronger translation i

112 mRNA) contained the frameshifting signals: a Shine-Dalgarno sequence, a slippery sequence, and a down

113 ted region of the psbA mRNA that disrupt the Shine-Dalgarno sequence, acting as a ribosome binding si

114 inding sites, one of which overlaps the cstA Shine-Dalgarno sequence, as predicted.

115 modimer to the 5'UTR of an mRNA occludes the Shine-Dalgarno sequence, blocking ribosome access for tr

116 e found either in or upstream of the gene II Shine-Dalgarno sequence, but still within the mRNA trans

117 des of the mRNA, immediately upstream of the Shine-Dalgarno sequence, explains the protein's role in

118 close to the AUG, including over a potential Shine-Dalgarno sequence, have little effect on Fis prote

119 n RNA hairpin at a distance of 9 nt from the Shine-Dalgarno sequence, implying that a discrete region

120 its stop codon, it blocks the adjacent rtpA Shine-Dalgarno sequence, inhibiting AT synthesis.

121 ryotes, whereas the CCUCC, known as the anti-Shine-Dalgarno sequence, is conserved in noneukaryotes o

122 otes refolding of the RNA such that the trpE Shine-Dalgarno sequence, located more than 100 nucleotid

123 re resistant to viomycin indicating that the Shine-Dalgarno sequence, or other features contained wit

124 Because the recJ gene lacks a canonical Shine-Dalgarno sequence, other unknown features of the m

125 This stalling exposes the rtpA Shine-Dalgarno sequence, permitting AT synthesis.

126 econdary stem-loop structure that blocks the Shine-Dalgarno sequence, preventing ribosome access and

127 in the absence of an untranslated leader and Shine-Dalgarno sequence, the streptomycete cat mRNA is t

128 by binding to a site that overlaps the trpG Shine-Dalgarno sequence, thereby blocking ribosome bindi

129 airing with a short sequence overlapping the Shine-Dalgarno sequence, thereby blocking ribosome bindi

130 One of these sites overlaps the glgC Shine-Dalgarno sequence, whereas the other CsrA target i

131 erlaps with that of the messenger RNA (mRNA) Shine-Dalgarno sequence, which prevents the interaction

132 d segment of nhaR, one of which overlaps the Shine-Dalgarno sequence.

133 nitiation codon, one of which overlapped its Shine-Dalgarno sequence.

134 tes, with one of these sites overlapping the Shine-Dalgarno sequence.

135 er transcript, one of which overlaps the hag Shine-Dalgarno sequence.

136 ranslational enhancer (TE) located 5' to the Shine-Dalgarno sequence.

137 egion located immediately preceding the rtpA Shine-Dalgarno sequence.

138 thereby blocking ribosome access to the glgC Shine-Dalgarno sequence.

139 contained an exact match that overlapped its Shine-Dalgarno sequence.

140 at is facilitated by ribosome binding to the Shine-Dalgarno sequence.

141 acent RNA to the 3' side, which contains the Shine-Dalgarno sequence.

142 tential RNA secondary structure overlaps the Shine-Dalgarno sequence.

143 , the latter of which would occlude the secA Shine-Dalgarno sequence.

144 not formation and, in turn, sequestering the Shine-Dalgarno sequence.

145 faster rate than phage bearing the wild-type Shine-Dalgarno sequence.

146 rocessed equally by RegB; those found at the Shine-Dalgarno sequences and in intercistronic regions a

147 utation of 27 rare codons and five secondary Shine-Dalgarno sequences in the cDNA.

148 Loss of good Shine-Dalgarno sequences might then have fixed the fusio

149 SgrS binding sites overlapping the Shine-Dalgarno sequences of adiY and folE mRNAs suggest

150 and targets mostly (but not exclusively) the Shine-Dalgarno sequences of early genes.

151 e 3' end of the 16S ribosomal rRNA (internal Shine-Dalgarno sequences), there is an increased probabi

152 s with structured standby sites, upstream of Shine-Dalgarno sequences, and show that these interactio

153 ferent translational stages: (i) initiation, Shine-Dalgarno sequences, start codon identity, and star

154 with structured 5'-ends, or with no or weak Shine-Dalgarno sequences.

155 genes are positively correlated with strong Shine-Dalgarno signal sequences.

156 secondary structure: a loop with projecting Shine-Dalgarno site and well-defined stem that interacts

157 y of a hairpin stem comprising the coat gene Shine-Dalgarno site was incrementally increased, there w

158 /G-any nucleotide) often associated with the Shine-Dalgarno translation initiation sequence in mRNAs.

159 e pair with the 3'end of 16 S rRNA (the anti-Shine-Dalgarno) to enhance frameshifting.

160 iple sources, sequence motifs (promoters and Shine-Dalgarno), microarray data, multi-genome alignment

161 s appear not to use a ribosome-binding site (Shine-Dalgarno)-based mechanism for translation initiati

162 Instead, Shine-Dalgarno-(SD)-like features within coding sequence

163 sed on the role of bound E-site tRNA and the Shine-Dalgarno-anti-Shine-Dalgarno (SD-aSD) interaction

164 The RNA exit tunnel of RNAP aligns with the Shine-Dalgarno-binding site of the 30S subunit.

165 y programmed into the coding sequence, where Shine-Dalgarno-like elements trigger elongation pauses a

166 It is suggested that the Shine-Dalgarno-like interaction elevates frameshifting s

167 In this issue of Neuron, Shine et al. (2016) describe a possible mechanism respon

168 In the 1970s China was a shining example of health development, but no longer.

169 n the premature aging disorder Progeria is a shining example of the impact that studies of rare disea

170 As a result, the nanoparticle shines >30 times brighter than state-of-the-art organic

171 d integrated longitudinal intervention for a SHINE household as it expects (during pregnancy) and the

172 connection between the points of light that shine in the night sky and the diffuse and abundant cell

173 Information visualization shines in this type of exploratory analysis, motivating

174 We hypothesize that the impact of SHINE interventions on child stunting and anemia will be

175 will increase understanding of the impact of SHINE interventions, and the generalizability of our fin

176 SHINE is a proof-of-concept, 2 x 2 factorial, cluster-ra

177 By shining laser light through a nanomechanical beam, we me

178 s approaches that we and others have used to shine light into these previously dark corners of the hu

179 Herein, we shine light on CPs and MOFs as optical media for state-o

180 e studies of the Btbd9 mutant mice will help shine light on its role in the pathophysiology of RLS.

181 functional genomic technology have begun to shine light on such gene network problems at both transc

182 NEXAFS measurements shine light on the action of the functional groups and e

183 ll-defined heparan sulfate structures helped shine light on the fine substrate specificities of biosy

184 ization of chromosome fragmentation may also shine light on the mechanism of chromosomal pulverizatio

185 the existence of secondary binding sites and shine light on the preference for intramolecular rather

186 Our findings shine light on the robustness of single-mode operation a

187 second crystallography (SFX) can potentially shine light on these conformational changes.

188 In this issue of JCI, Rokavec and colleagues shine light on this murky aspect of tumor biology by foc

189 This study also shines light on the motility of flagellated bacteria in

190 The study of photon-induced materials growth shines light on the rational design of complex nanostruc

191 This remarkable observation shines light onto the preferred binding mode of auristat

192 Shining light on Zeise: In a study of Zeise's anion, [Pt

193 peech and audio, whereas recurrent nets have shone light on sequential data such as text and speech.

194 ) antineutrinos radiate to space from Earth, shining like a faint antineutrino star.

195 These results shine new light onto stereoselective molecular recogniti

196 neoformans glucosylceramide (GlcCer) mutant shines new light on the initiation of cryptococcal infec

197 This work shines new light onto this powerful C-H oxidation method

198 anslucent protective shell ensures the vivid shine of the blue stripes, which can be perceived under

199 When light from above is shone on a dye-doped LCE sample floating on water, the L

200 Then the spotlight is shone on the sophisticated fabrication methods that have

201 In this article, we present the SHINE PIP including definitions and measurements of key

202 photosensitizer (PS) with the photoCORM and shining red light, energy transfer occurs from triplet e

203 l (hazard ratio 4.76, 95% CI 1.59 to 14.30), Shone's syndrome (hazard ratio 3.68, 95% CI 1.14 to 11.8

204 Jude prosthesis and more likely to have Shone's syndrome.

205 (Arabidopsis thaliana) transcription factor, SHINE (SHN), in rice (Oryza sativa), a model for the gra

206 s and ribosomes in functional binding states shine some light on this fundamental life-sustaining pro

207 Whereas most of the literature on this topic shines the spotlight toward melanocytes, the focus of th

208 SHINE therefore provides an opportunity to longitudinall

209 Let the light shine through: A transparent film of copper nanowires wa

210 The shine-through activity could reach 46% of the reconstruc

211 The ratio between the activity of the shine-through and the activity reconstructed in the orig

212 For the radioactive paper, shine-through artifacts appeared in the location of the

213 etic field, the axial resolution worsens and shine-through artifacts may appear.

214 n air, was scanned, and the magnitude of the shine-through was quantified from the PET images for var

215 g gratings with a larger number of elements (shine-through).

216 The SHINE trial infant feeding intervention led to significa

217 a constrained randomization technique in the SHINE trial.

218 ationale, design, and methods underlying the SHINE trial.

219 n, and our approach to evaluating EED in the SHINE trial.

220 anitation Hygiene Infant Nutrition Efficacy (SHINE) trial in Zimbabwe is evaluating the independent a

221 anitation Hygiene Infant Nutrition Efficacy (SHINE) trial is designed to measure the independent and

222 anitation Hygiene Infant Nutrition Efficacy (SHINE) trial is motivated by the premise that environmen

223 anitation Hygiene Infant Nutrition Efficacy (SHINE) trial, we utilize the concept of maternal capabil

224 ation Hygiene and Infant Nutrition Efficacy (SHINE) Trial, we utilize the program impact pathway (PIP

225 anitation Hygiene Infant Nutrition Efficacy (SHINE) trial.

226 rowth was detected by fluorescence caused by shining UV light (lambda = 365 nm) onto the indicator on

227 We demonstrate that by shining UV light for an hour on a frozen pure endogenous

228 Within SHINE we will measure 2 causal pathways.

229 t twenty-three known satellite galaxies that shine with luminosities ranging from about a thousand to