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1 foreign DNA elements increases resistance to bicyclomycin.
2 region as the functional domain inhibited by bicyclomycin.
3 f a gram-positive organism can be blocked by bicyclomycin.
4 ts sensitivity to the Rho-specific inhibitor bicyclomycin.
5                                              Bicyclomycin (1) is a commercial antibiotic whose primar
6                                              Bicyclomycin (1) is a commercial antibiotic whose primar
7                                              Bicyclomycin (1) is a commercially available antibiotic
8                                              Bicyclomycin (1) is a novel antibiotic that targets rho
9 growth and survival of Escherichia coli, and bicyclomycin (1) is its only known selective inhibitor.
10                                              Bicyclomycin (1) is the only natural product inhibitor o
11                                              Bicyclomycin (1), a commercial antibiotic that inhibits
12                                  Addition of bicyclomycin, a specific inhibitor of Rho factor action,
13                                              Bicyclomycin, a specific inhibitor of Rho, increased the
14               We show that Rho inhibition by bicyclomycin allows for the expression of prophage genes
15 positive phylogenetic group, is prevented by bicyclomycin, an antibiotic that inhibits the activity o
16                                  Addition of bicyclomycin, an inhibitor of Rho, to these UAG construc
17 mation with rho to enhance the affinity of a bicyclomycin analogue and determine the binding stoichio
18 icyclomycin has a Rho that is insensitive to bicyclomycin and has the single amino acid residue chang
19  action of two Rho effectors, the antibiotic bicyclomycin and nucleic acids that bind to Rho's primar
20 seen on Scatchard analysis in the absence of bicyclomycin and poly(C).
21 factors nusA and nusG were hypersensitive to bicyclomycin, and had extensive chromosome fragmentation
22                       This study establishes bicyclomycin as a conformational inhibitor of Rho ring d
23 air (recB and ruvC) increased sensitivity to bicyclomycin, as did loss of the replication fork reload
24 sceptibility or resistance to the antibiotic bicyclomycin (BCM), a potent inhibitor of the transcript
25 ent adaptation of the BGC for the antibiotic bicyclomycin (BCM), facilitating improved production in
26 AP in response to the Rho-specific inhibitor bicyclomycin (BCM).
27 shown to confer resistance to the antibiotic bicyclomycin (BCM).
28 weak) imposed on the rho hexamer, the nearby bicyclomycin binding pocket is not affected, and both 1
29 specific species and novel variations in the bicyclomycin binding pocket.
30 d 3 per rho hexamer indicating the number of bicyclomycin binding sites for the rho hexamer is betwee
31 ure of the Rho model has enabled a candidate bicyclomycin-binding pocket to be delineated.
32             Previous studies have shown that bicyclomycin binds near the ATP hydrolysis pocket on rho
33                     This report examines the bicyclomycin C(5)-C(5a) structural constraints necessary
34                                          The bicyclomycin derivative 5a-formylbicyclomycin, an inhibi
35 activities for the C(5a)-extended conjugated bicyclomycin derivatives and the (5E) and (5Z) isomers w
36                                  None of the bicyclomycin derivatives exhibited antibiotic activity a
37  bond with unsaturated substituents provides bicyclomycin derivatives with excellent inhibitory activ
38                                              Bicyclomycin did not inhibit poly(C) binding to Rho.
39                   The Rho-specific inhibitor bicyclomycin enabled transcription of the coding regions
40 involved, because the Rho-specific inhibitor bicyclomycin failed to show synergism with either aza-C
41 nthesis, and characterization of a series of bicyclomycin fluorescent probes (BFP) constructed to sen
42             A mutant that can grow in 0.3 mM bicyclomycin has a Rho that is insensitive to bicyclomyc
43         Three classes of C(5)-C(5a)-modified bicyclomycins have been prepared and their inhibitory ac
44 f Rho-dependent transcription termination by bicyclomycin in Escherichia coli induced double-strand b
45 aining these mutations are very resistant to bicyclomycin in vitro.
46 nd L208R Rho mutations are very resistant to bicyclomycin in vivo.
47                         Addition of the drug bicyclomycin increases basal operon expression of all mu
48 as a different structure and is inhibited by bicyclomycin, indicating that T2 is probably Rho depende
49  assays, limited tryptic digestions, and the bicyclomycin inhibition kinetics of ATPase activity in t
50 ntibiotic concentrations near the I50 value, bicyclomycin inhibition of Rho-dependent transcripts was
51            The approximate I50 value for the bicyclomycin inhibition of transcription termination at
52                               The antibiotic bicyclomycin inhibits rho-dependent termination processe
53                                        A new bicyclomycin irreversible inactivator, 5a-formylbicyclom
54                                 Our designed bicyclomycin ligand, 5a-(3-formyl-phenylsulfanyl)-dihydr
55 file and increased counts of aminoglycoside, bicyclomycin, phenicol, triclosan, and multidrug resista
56 on that destabilizes TEC (rpoB*35) increased bicyclomycin resistance >40-fold.
57  rac prophage in wild-type E. coli increases bicyclomycin resistance and permits deletion of nusG.
58 r-mediated repression, as well as a putative bicyclomycin resistance gene (so2280) and cation efflux
59 taining the G337S Rho mutation also has high bicyclomycin resistance, and the proximity of L208, S266
60                                A total of 38 bicyclomycin-resistant mutants of Escherichia coli trans
61                        The utility of BFP in bicyclomycin-rho binding studies was documented through
62 epared to provide information concerning the bicyclomycin-rho inactivation process and the drug's bin
63                              As a whole, the bicyclomycin sensitivities of the mutants are consistent
64                 In the presence of poly(dC), bicyclomycin showed a reversible mixed inhibition of the
65                           In the presence of bicyclomycin, the K(d)(1) changed from 3.0 to 1.4 microm
66 ed-ring (RNA-translocation) states, we found bicyclomycin to be a direct antagonist of ring closure.
67 pondingly, the Km(app) for ribo(C)10 without bicyclomycin was 0.8 microM and with bicyclomycin was 5
68                      The extrapolated Ki for bicyclomycin was 2.8 microM without ribo(C)10 and increa
69 without bicyclomycin was 0.8 microM and with bicyclomycin was 5 microM at infinite inhibitor concentr
70    The interaction of Rho and the antibiotic bicyclomycin was probed using in vitro transcription ter
71 rmylbicyclomycin, an inhibitor comparable to bicyclomycin, was previously shown to form a stable imin
72                       We used the antibiotic bicyclomycin, which inhibits Rho, to assess its role on