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1 oded by 25t and the first adenine within the Shine-Dalgarno sequence.
2 not formation and, in turn, sequestering the Shine-Dalgarno sequence.
3 faster rate than phage bearing the wild-type Shine-Dalgarno sequence.
4 d segment of nhaR, one of which overlaps the Shine-Dalgarno sequence.
5 nitiation codon, one of which overlapped its Shine-Dalgarno sequence.
6 tes, with one of these sites overlapping the Shine-Dalgarno sequence.
7 er transcript, one of which overlaps the hag Shine-Dalgarno sequence.
8 ranslational enhancer (TE) located 5' to the Shine-Dalgarno sequence.
9 egion located immediately preceding the rtpA Shine-Dalgarno sequence.
10 thereby blocking ribosome access to the glgC Shine-Dalgarno sequence.
11 contained an exact match that overlapped its Shine-Dalgarno sequence.
12 at is facilitated by ribosome binding to the Shine-Dalgarno sequence.
13 acent RNA to the 3' side, which contains the Shine-Dalgarno sequence.
14 tential RNA secondary structure overlaps the Shine-Dalgarno sequence.
15 zing stem-loop structures that sequester the Shine-Dalgarno sequence.
16 , the latter of which would occlude the secA Shine-Dalgarno sequence.
17 of >50 codons or the presence of an upstream Shine-Dalgarno sequence.
18 with structured 5'-ends, or with no or weak Shine-Dalgarno sequences.
19 mitochondrial mRNAs, which lack typical anti-Shine-Dalgarno sequences.
20 ely), followed by stop codon context and the Shine-Dalgarno sequence (3.7-5.1% and 1.9-3.8%, respecti
21 mRNA) contained the frameshifting signals: a Shine-Dalgarno sequence, a slippery sequence, and a down
22 ted region of the psbA mRNA that disrupt the Shine-Dalgarno sequence, acting as a ribosome binding si
23 ion by CsrA involves binding directly to the Shine-Dalgarno sequence and blocking ribosome binding.
25 ations in CsrA binding sites overlapping the Shine-Dalgarno sequence and initiation codon partially r
26 that this translation initiates from a weak Shine-Dalgarno sequence and is facilitated by a putative
27 ocessing occurs just upstream of a consensus Shine-Dalgarno sequence and results in the removal of 54
28 a stem-loop structure upstream of the CC3461 Shine-Dalgarno sequence and stabilizes the transcript.
29 d charged-tRNA(Trp) deficiency to expose the Shine-Dalgarno sequence and start codon for the AT prote
31 and stimulates translation by releasing the Shine-Dalgarno sequence and start site from a stable sec
32 d CsrA prevents ribosome binding to the glgC Shine-Dalgarno sequence and that this reduces GlgC synth
33 omes were identified, the "AGGA" core of the Shine-Dalgarno sequence and the "A-rich" sequence locate
34 gradation of the functionally important anti-Shine-Dalgarno sequence and the decoding-site helix 44.
35 tain fragmented operator sites such that the Shine-Dalgarno sequence and the initiation codon of the
36 inding to a 19 nt RNA hairpin containing the Shine-Dalgarno sequence and the initiation codon of the
37 sumptive TRAP binding site overlaps the yhaG Shine-Dalgarno sequence and translation initiation regio
38 rocessed equally by RegB; those found at the Shine-Dalgarno sequences and in intercistronic regions a
39 s with structured standby sites, upstream of Shine-Dalgarno sequences, and show that these interactio
40 d a hairpin structure that can sequester the Shine-Dalgarno sequence are necessary for cobalamin-depe
44 modimer to the 5'UTR of an mRNA occludes the Shine-Dalgarno sequence, blocking ribosome access for tr
45 the leader nucleotides just upstream of the Shine-Dalgarno sequence but is conflicted on the questio
46 epended also on ribosome binding to a nearby Shine-Dalgarno sequence but was independent of downstrea
47 e found either in or upstream of the gene II Shine-Dalgarno sequence, but still within the mRNA trans
49 t the deep learning models learn to identify Shine-Dalgarno sequences, deprioritize the wobble positi
50 get site of glgC that lies upstream from the Shine-Dalgarno sequence did not affect regulation by HD-
51 des of the mRNA, immediately upstream of the Shine-Dalgarno sequence, explains the protein's role in
52 close to the AUG, including over a potential Shine-Dalgarno sequence, have little effect on Fis prote
53 tiary KL interaction directly sequesters the Shine-Dalgarno sequence (i.e., the ribosome binding site
54 n RNA hairpin at a distance of 9 nt from the Shine-Dalgarno sequence, implying that a discrete region
55 anslation as independent elements, e.g., the Shine-Dalgarno sequence in prokaryotes, the rRNA-binding
56 ort that three-base substitutions around the Shine-Dalgarno sequence in the 159-base 5'-untranslated
58 ed expression in the absence of a leader and Shine-Dalgarno sequence indicated that stimulation by CA
60 target (translational operator), but that a Shine-Dalgarno sequence is not required for specificity.
61 A operator sites, including one in which the Shine-Dalgarno sequence is positioned 4 nt outside the c
62 otes refolding of the RNA such that the trpE Shine-Dalgarno sequence is sequestered in a hairpin, thu
63 proximal to regulatory features such as the Shine-Dalgarno sequence is sufficient to enable regulati
64 ryotes, whereas the CCUCC, known as the anti-Shine-Dalgarno sequence, is conserved in noneukaryotes o
66 otes refolding of the RNA such that the trpE Shine-Dalgarno sequence, located more than 100 nucleotid
69 otential CsrA binding site that overlaps the Shine-Dalgarno sequence of hfq, a gene that encodes an R
70 o analyzed the 350-bp region upstream of the Shine-Dalgarno sequence of norA by gel mobility shift ex
71 of 3-methyl-3-buten-1-ol by engineering the Shine-Dalgarno sequence of nudB, which increased protein
72 pseudoknot, occur to sequester the putative Shine-Dalgarno sequence of the RNA only after metabolite
75 ferential translation of specific mRNAs, the Shine-Dalgarno sequences of which do not play a critical
77 bstantial number of genes overlap either the Shine-Dalgarno sequence or the coding sequence of the ne
79 hia coli mRNAs, particularly those with weak Shine-Dalgarno sequences or structured 5' UTRs, in addit
80 re resistant to viomycin indicating that the Shine-Dalgarno sequence, or other features contained wit
83 ether with the contribution of 16S rRNA anti-Shine-Dalgarno sequence pairing with GAG, facilitates pe
85 econdary stem-loop structure that blocks the Shine-Dalgarno sequence, preventing ribosome access and
86 We describe in detail programs for finding Shine-Dalgarno sequences, resources used for confident i
88 nce element upstream of the start codon (the Shine-Dalgarno sequence [SD]) and a complementary sequen
89 preQ(1)-binding pocket through the adjoining Shine-Dalgarno sequence (SDS) and include A-minor motifs
91 t to be mediated by the accessibility of the Shine-Dalgarno sequence (SDS) ribosome-binding site.
92 om partial occlusion of the ribosome-binding Shine-Dalgarno sequence (SDS), SDS sequestration driven
93 , different segments of the single consensus Shine-Dalgarno sequence serve the two translational star
94 ferent translational stages: (i) initiation, Shine-Dalgarno sequences, start codon identity, and star
95 -terminal region immediately upstream of the Shine-Dalgarno sequence that contributes to formation of
96 in the absence of an untranslated leader and Shine-Dalgarno sequence, the streptomycete cat mRNA is t
97 e 3' end of the 16S ribosomal rRNA (internal Shine-Dalgarno sequences), there is an increased probabi
98 by binding to a site that overlaps the trpG Shine-Dalgarno sequence, thereby blocking ribosome bindi
99 airing with a short sequence overlapping the Shine-Dalgarno sequence, thereby blocking ribosome bindi
100 Addition of an untranslated lac leader and Shine-Dalgarno sequence to cI increased expression but s
102 tends to be compensated by mutations in the Shine-Dalgarno sequence towards a stronger translation i
103 ing profiling on ribosomes with altered anti-Shine-Dalgarno sequences, we reveal a genome-wide correl
105 erlaps with that of the messenger RNA (mRNA) Shine-Dalgarno sequence, which prevents the interaction