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1 te RNA in the presence of the aminoglycoside paromomycin.
2 e region of the decoding site RNA with bound paromomycin.
3 o, nip1-1 mutant cells are hypersensitive to paromomycin.
4 s to increased sensitivity to the antibiotic paromomycin.
5 ed for binding the aminoglycoside antibiotic paromomycin.
6 100 microg/mL and inhibited by 400 microg/mL paromomycin.
7 tially resistant to the miscoding effects of paromomycin.
8 72(2AP) yields submicromolar EC50 values for paromomycin (0.5 +/- 0.2 microM) and neomycin B (0.6 +/-
9 shmaniasis to receive a cream containing 15% paromomycin-0.5% gentamicin (called WR 279,396), 15% par
10 D4 cells/microL were treated with open-label paromomycin (1.0 g twice a day) plus azithromycin (600 m
12 ed some 50-fold by growth in the presence of paromomycin, a known translational-error-inducing antibi
16 mycin-gentamicin, 82% (95% CI, 74 to 87) for paromomycin alone, and 58% (95% CI, 50 to 67) for vehicl
17 cin-0.5% gentamicin (called WR 279,396), 15% paromomycin alone, or vehicle control (with the same bas
18 changes (deltaH) for protonation of the five paromomycin amino groups, as well as positive heat capac
19 MR studies provide pK(a) values for the five paromomycin amino groups, as well as the temperature dep
22 its anti-association activity was blocked by paromomycin, an inhibitor for IF3, an essential initiati
24 y, conformationally constrained neomycin and paromomycin analogues designed to mimic the A-site bound
25 action between the aminoglycoside antibiotic paromomycin and a small model oligonucleotide that mimic
27 , and durability of combination therapy with paromomycin and azithromycin for chronic cryptosporidios
28 the pharmacological inhibitor of translation paromomycin and exposure to heat stress and paromomycin
29 ding properties of the 2-DOS aminoglycosides paromomycin and G418 (geneticin) are compared, using bot
31 sitivity to translation fidelity antibiotics paromomycin and geneticin, to high salt and calcium conc
32 in solution and bound to the aminoglycosides paromomycin and gentamicin C1A have been determined.
33 in solution and bound to the aminoglycosides paromomycin and gentamicin C1a were determined previousl
34 vity to other translation inhibitors such as paromomycin and hygromycin B, which affect translation f
35 ates increased sensitivity to the antibiotic paromomycin and increased programmed -1 ribosomal frames
38 be the unsuspected major route of entry for paromomycin and may be of importance in the design and d
41 We show that differences in binding between paromomycin and ribostamycin can be probed by using an M
45 icin bound to an A-site oligonucleotide, and paromomycin and streptomycin complexed to the 30S subuni
46 ere, we demonstrate that the aminoglycosides paromomycin and streptomycin inhibit A-site cleavage of
48 or neomycin B and tobramycin, as compared to paromomycin and streptomycin, indicates differences in t
52 tic rRNA A-site subdomain with ribostamycin, paromomycin, and lividomycin, whereas apramycin preferen
53 des including kanamycin A and B, tobramycin, paromomycin, and neomycin B to the corresponding fully g
55 of the aminoglycoside antibiotics neomycin, paromomycin, and ribostamycin to a RNA oligonucleotide t
56 -deoxystreptamine aminoglycosides, neomycin, paromomycin, and ribostamycin, to two different chimeric
57 f the RNA binding affinities of neomycin and paromomycin are consistent with at least three drug NH(3
58 values associated with the free base form of paromomycin are lower in magnitude than the correspondin
60 ll ribosomal subunit bound to the antibiotic paromomycin at ambient temperature (3.4-A structure).
61 n contrast, the aminoglycoside-based polymer paromomycin-BGDE, enhanced adenoviral gene expression wi
62 veal the following significant features: (i) Paromomycin binding enhances the thermal stabilities of
64 the ribosomal electrostatic potential in the paromomycin binding site provided insight into the elect
69 al titration calorimetry studies reveal that paromomycin binds to the EcWT duplex with a 31-fold high
70 erioribosomal activity comparable to that of paromomycin, but is significantly more selective showing
72 site, and the solution structure of the RNA-paromomycin complex was determined by nuclear magnetic r
73 ide antibiotics and the structure of the RNA-paromomycin complex was previously determined by nuclear
74 change is not observed in the eukaryotic RNA-paromomycin complex, disrupting the binding pocket for r
76 d higher than the estimated intracytoplasmic paromomycin concentration, suggestive of host cell vesic
77 . parvum infection did not lead to increased paromomycin concentrations compared to those in uninfect
78 ent dye labeled derivative of the antibiotic paromomycin (CRP) stoichiometrically with a dissociation
79 family to high concentrations of neomycin or paromomycin decreased to a significant, nearly identical
80 er, preinfection exposure of Caco-2 cells to paromomycin did not result in subsequent inhibition of p
81 te development, indicating that if exogenous paromomycin enters the infected host cell vesicular comp
82 to their specificities of action, with only paromomycin exhibiting a specificity for prokaryotic ver
83 partially inducing these structural changes, paromomycin facilitates binding of near-cognate tRNAs.
84 osides gentamicin, amikacin, tobramycin, and paromomycin for eight premature stop codon mutations ide
88 the apical tip of H69 and the 6'-hydroxyl on paromomycin from within the drug's canonical h44-binding
89 paromomycin and exposure to heat stress and paromomycin functions synergistically to reduce yeast vi
90 ructures of the 80S ribosome in complex with paromomycin, geneticin (G418), gentamicin, and TC007, so
91 s trial provides evidence of the efficacy of paromomycin-gentamicin and paromomycin alone for ulcerat
92 (95% confidence interval [CI], 73 to 87) for paromomycin-gentamicin, 82% (95% CI, 74 to 87) for parom
94 except in five patients, one in each of the paromomycin groups and three in the vehicle-control grou
95 ion-site reactions were more frequent in the paromomycin groups than in the vehicle-control group.
98 oding region A-site oligonucleotide bound to paromomycin has been determined using NMR spectroscopy a
99 n the presence and absence of the antibiotic paromomycin, have been solved at between 3.1 and 3.3 ang
100 icin, streptomycin, kanamycin, amikacin, and paromomycin, have no effect on angiogenin-induced cell p
101 omplemented the nip7-1 ts growth defect, the paromomycin hypersensitivity, and the halfmer defect.
102 of its amino groups, with the RNA binding of paromomycin I and neomycin B being linked to the protona
103 By contrast, at pH 9.0, the RNA binding of paromomycin I and neomycin B is coupled to the uptake of
105 a) values of the amino groups in neomycin B, paromomycin I, and lividomycin A sulfate, with the resul
107 GCN1 expression conferred sensitivity to paromomycin in a manner dependent on its ribosome bindin
109 second, fidelity-modulating binding site for paromomycin in the 16S ribosomal RNA that facilitates cl
110 n15 makes yeast cells extremely sensitive to paromomycin, indicating that the natural high resistance
113 rporation at Ala195 GCU was not increased by paromomycin, inferring that this error did not result fr
116 the aminoglycoside antibiotics neomycin and paromomycin is described in which ring I, involved in cr
118 ral high resistance of the yeast ribosome to paromomycin is, in large part, due to the absence of the
120 inity for neomycin B and tobramycin than for paromomycin (K(d)s = 0.3 +/- 0.1, 0.2 +/- 0.2 and 5.4 +/
121 o 100 microg/ml chloramphenicol, gentamycin, paromomycin, lincomycin, hygromycin, and tetracycline, a
125 study of interaction of the aminoglycosides paromomycin, neomycin, ribostamycin, and neamine with th
129 nced affinity of neomycin relative to either paromomycin or ribostamycin is primarily, if not entirel
131 e of the Leishmania ribosome in complex with paromomycin (PAR), a highly potent compound recently app
132 s < or = 45 microM reveal that the extent of paromomycin protonation linked to the binding of the dru
138 icking the bound side chains of neomycin and paromomycin, respectively, show excellent activity and,
139 Further characterization of the compromised paromomycin response identified a probable second, fidel
142 mpetition ESI-MS with a known A-site binder (paromomycin) revealed that peptide binding occurs near t
143 By solving the crystal structure of the paromomycin-ribosome complex, we observe specific contac
145 he different complexes formed with neomycin, paromomycin, ribostamycin and neamine suggest similar st
146 inoglycosides chemically related to neomycin-paromomycin, ribostamycin and neamine-each bind to sites
147 hydroxymethyl side chain of the neomycin or paromomycin ring I, as part of the dioxabicyclooctane ri
149 on how the bacterial ribosome-targeting drug paromomycin selectively inhibits the eukaryotic L. donov
152 In particular, 4'-O-beta-d-xylopyranosyl paromomycin shows antibacterioribosomal activity compara
153 gly, we found that growth in the presence of paromomycin stimulated luciferase activity for only a sm
154 e 30S subunit complexed with the antibiotics paromomycin, streptomycin and spectinomycin, which inter
156 yotic rRNA sequences show reduced binding of paromomycin, suggesting a physical origin for the specie
157 e sensitive to the aminoglycoside antibiotic paromomycin than a upf1 delta strain, and frameshifting
160 accompany the binding of the aminoglycoside paromomycin to both prokaryotic and eukaryotic rRNA A-si
162 pacity change (DeltaC(p)) for the binding of paromomycin to each rRNA A-site is near zero, with the n
165 e approximately 25-50-fold weaker binding of paromomycin to the eukaryotic decoding-site oligonucleot
167 d contrast the binding of the aminoglycoside paromomycin to three octamer nucleic acid duplexes of id
168 ystallographic information from complexes of paromomycin, tobramycin, and Geneticin bound to an A-sit
170 estimated intracytoplasmic concentrations of paromomycin, using an intracellular bacterial killing as
171 t of cryptosporidiosis with azithromycin and paromomycin was associated with significant reduction in
173 he presence/absence of high concentration of paromomycin was observed in symptomatic or asymptomatic
174 is, respectively, occurred in North America; paromomycin was shown to be ineffective treatment for cr
175 ucleotides that are important for binding of paromomycin were identified by performing quantitative f
176 -glycosides of the aminoglycoside antibiotic paromomycin were synthesized and evaluated for their abi
177 had reduced affinity for the aminoglycoside paromomycin, whereas no discernible reduction in affinit
180 contrast, the aminoglycosides gentamicin and paromomycin, which interact with the decoding region of
181 inical strains of MRSA that are resistant to paromomycin, which is demonstrated to be a consequence o
183 slation rates in the presence and absence of paromomycin, which reflected the effect of the drug on m
184 t readthrough with two drugs, gentamicin and paromomycin, which was confirmed by western blot and in
185 and binding stoichiometry for tobramycin and paromomycin with a 27-nucleotide RNA construct represent
186 ystallographic information from a complex of paromomycin with the 30S subunit was used as a framework
187 3 trial of topical treatments containing 15% paromomycin, with and without 0.5% gentamicin, for cutan
188 A sites with a markedly lower affinity than paromomycin, with the affinities of both drugs for the h
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