ライフサイエンスコーパス: Shine-Dalgarno sequence

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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