ライフサイエンスコーパス: fosfomycin

1 amydial MurA was resistant to high levels of fosfomycin.

2 owth of C. trachomatis was also resistant to fosfomycin.

3 s of host cells, and increased resistance to fosfomycin.

4 li O157:H7 and given either ciprofloxacin or fosfomycin.

5 d they were both inhibited by the antibiotic fosfomycin.

6 the primary site of action of the antibiotic fosfomycin.

7 e dependent on the presence of the substrate fosfomycin.

8 bserved reversible competitive inhibition by fosfomycin.

9 ly resistant to time-dependent inhibition by fosfomycin.

10 sphate (G3P), glucose-6-phosphate (G6P), and fosfomycin.

11 a coli host for responding to the antibiotic fosfomycin.

12 t step in the biosynthesis of the antibiotic fosfomycin.

13 -2-HPP in the biosynthesis of the antibiotic fosfomycin.

14 alcohol of (S)-2-HPP to the epoxide ring of fosfomycin.

15 ynthesis of the clinically useful antibiotic fosfomycin.

16 )-HPP) in the biosynthesis of the antibiotic fosfomycin.

17 bout inhibition/alkylation by the antibiotic fosfomycin.

18 S-HPP) in the biosynthesis of the antibiotic fosfomycin.

19 s115, the molecular target of the antibiotic fosfomycin.

20 egio- and enantiomerically specific epoxide, fosfomycin.

21 turally occurring, broad-spectrum antibiotic fosfomycin.

22 and by exogenous ligands, such as substrate fosfomycin.

23 ber of bacteria have developed resistance to fosfomycin.

24 mydia rendering these organisms resistant to fosfomycin.

25 nthesis and is the target for the antibiotic fosfomycin.

26 (S)-2-hydroxypropylphosphonic acid (HPP) to fosfomycin.

27 The fosfomycin (1) resistance proteins FosA and FosX in path

28 zyme conferring resistance to the antibiotic fosfomycin [(1R,2S)-1,2-epoxypropylphosphonic acid] orig

29 opyl-1-phosphonate (S-HPP) to the antibiotic fosfomycin [(1R,2S)-epoxypropylphosphonate] in an unusua

30 Fosfomycin [(1R,2S)-epoxypropylphosphonic acid] is a sim

31 nt addition of glutathione to the antibiotic fosfomycin, (1R,2S)-epoxypropylphosphonic acid, renderin

32 resistance to the broad-spectrum antibiotic fosfomycin, (1R,2S)-epoxypropylphosphonic acid.

33 X, catalyzes the hydration of the antibiotic fosfomycin, (1R,2S)-epoxypropylphosphonic acid.

34 Treatment with fosfomycin (2 g/6 hours IV) plus imipenem (1 g/6 hours I

35 hanges due to treatment with the antibiotics fosfomycin (a cell-wall biosynthesis inhibitor) and chlo

36 Treatment with fosfomycin (a PG synthesis inhibitor) leads to lower inf

37 The last step of the biosynthesis of fosfomycin, a clinically useful antibiotic, is the conve

38 the epoxide ring closure of (S)-HPP to form fosfomycin, a clinically useful antibiotic.

39 previously been shown to cause resistance to fosfomycin, a potent antibiotic that specifically target

40 closed enzyme conformation, with the Cys115-fosfomycin adduct buried in the active site.

41 Fosfomycin, an epoxide, is a relatively poor drug becaus

42 r, cells lacking BSH are highly sensitive to fosfomycin, an epoxide-containing antibiotic detoxified

43 Several of these compounds, such as fosfomycin and bialaphos, figure prominently in human he

44 As a result, fosfomycin and D-cycloserine were added to the group of

45 al efficacy and safety of the combination of fosfomycin and imipenem as rescue therapy for MRSA infec

46 is the active site nucleophile alkylated by fosfomycin and implicated this residue in the formation

47 sed on available literature, the activity of fosfomycin and nitrofurantoin remain high for most cases

48 We report two cases cured with oral fosfomycin and provide a pharmacokinetic analysis of fos

49 as used to methylate the clinical antibiotic fosfomycin and the antimalaria clinical candidate fosmid

50 d to catalyze the epoxidation of ( S)-HPP to fosfomycin and the oxidation of ( R)-HPP to 2-oxopropylp

51 esis of the antibiotics nisin, lacticin 481, fosfomycin, and bialaphos.

52 ound to be associated with susceptibility to fosfomycin, and loss of this system or general inhibitio

53 (+), residues that furnish hydrogen bonds to fosfomycin, and residues located in a putative glutathio

54 Fosfomycin appears to achieve reasonable intraprostatic

55 ent) will determine the clinical efficacy of fosfomycin as step-down oral therapy to treat complicate

56 ma-imido)-triphosphate (AMPPNP), Mg(II), and fosfomycin, at 1.53 and 2.2 angstroms resolution, respec

57 d residues located in a putative glutathione/fosfomycin-binding site.

58 the enzyme that catalyzes the second step of fosfomycin biosynthesis in Streptomyces wedmorensis.

59 eport the crystal structure of FomA from the fosfomycin biosynthetic gene cluster of Streptomyces wed

60 n orientation that is different than that of fosfomycin bound to the related enzyme, FosA.

61 for substrate-free enzyme to 0.23 cm(-1) for fosfomycin-bound enzyme, 0.28 (1) cm(-1) for FosA with p

62 -lactams, including cefuroxime (CEF), and to fosfomycin but that resistant mutants arise due to gain-

63 (S)-2-hydroxypropylphosphonic acid (HPP) to fosfomycin by HPP epoxidase (HppE), which is a mononucle

64 sfomycin resistance protein FomA inactivates fosfomycin by phosphorylation of the phosphonate group o

65 accelerated by bound substrate and produces fosfomycin catalytically with a stoichiometry of unity.

66 age demonstrated that ciprofloxacin, but not fosfomycin, caused enhanced intraintestinal transfer of

67 Ciprofloxacin but not fosfomycin causes Shiga toxin-encoding bacteriophage ind

68 Thus, the cyclization of HPP to fosfomycin clearly represents an intriguing conversion b

69 The MurA-fosfomycin complex exists in the closed enzyme conformat

70 Only 1 patient had a mean prostatic fosfomycin concentration of <1 microg/g, whereas the maj

71 ansition zone [TZ] and peripheral zone [PZ]) fosfomycin concentrations using liquid chromatography-ta

72 eus (0.3mg dry weight analyzed) treated with fosfomycin, D-boroAla, D-cycloserine, and vancomycin.

73 lysis when exposed to low concentrations of fosfomycin, d-cycloserine, vancomycin, and nisin, indica

74 ith death in two-thirds of the mice, whereas fosfomycin did not.

75 ies within the zone of inhibition around the fosfomycin disk is occasionally observed upon susceptibi

76 ss spectrometry, following a single 3-g oral fosfomycin dose within 17 hours of surgery.

77 EPR spectrum of oxidized iron-reconstituted fosfomycin epoxidase reveals resonances typical of S = (

78 Whole cells treated with fosfomycin exhibited decreased peptidoglycan contributio

79 xpression of the glpTQ genes, which leads to fosfomycin (FOS) resistance.

80 s (penicillin, cephalosporins, streptomycin, fosfomycin, gramicidin S, rapamycin, indolmycin, microci

81 Since the ring oxygen in fosfomycin has been shown in earlier feeding experiments

82 Fosfomycin has reasonable in vitro and urinary activity

83 Although the addition of the substrate, fosfomycin, has no appreciable effect on the association

84 t success was achieved after commencement of fosfomycin in conjunction with high-dose meropenem.

85 rulence factor, Hpt, also mediates uptake of fosfomycin in Listeria monocytogenes.

86 The final step in the biosynthesis of fosfomycin in Streptomyces wedmorensis is catalyzed by (

87 These bacteria therefore seem resistant to fosfomycin in vitro, although they are in fact susceptib

88 resistance of the C115D and C115E mutants to fosfomycin inactivation.

89 The antibiotic fosfomycin inhibits bacterial cell wall biosynthesis by

90 the mechanisms of inactivation are similar, fosfomycin is approximately 50 times more potent than te

91 thoprim-sulfamethoxazole, nitrofurantoin, or fosfomycin is indicated for acute cystitis in adult wome

92 The last step of the biosynthesis of fosfomycin is the conversion of (S)-2-hydroxypropylphosp

93 off) = 5 s(-1)) that is slower than that for fosfomycin (k(off) = 30 s(-1)).

94 r that interacts strongly with the substrate fosfomycin (Kd = 17 microM) more weakly with the product

95 the 26 participants, mean plasma and urinary fosfomycin levels were 11.4 +/- 7.6 microg/mL and 571 +/

96 Mean overall prostate fosfomycin levels were 6.5 +/- 4.9 microg/g (range, 0.7-

97 Fosfomycin maintains activity against most Escherichia c

98 In conclusion, fosfomycin-nonsusceptible inner colony mutants can occur

99 ed to cycloserine and bacitracin, but not to fosfomycin or valinomycin; these drugs, like beta-lactam

100 involved in biosynthesis of the antibiotics fosfomycin, phosphinothricin tripeptide, and dehydrophos

101 Fosfomycin plus imipenem was an effective and safe combi

102 in and provide a pharmacokinetic analysis of fosfomycin predose concentrations during treatment.

103 ics of MurA inactivation by terreic acid and fosfomycin reflect the importance of noncovalent binding

104 of glutathione to carbon-1 of the antibiotic fosfomycin, rendering it ineffective as an antibacterial

105 and encoded for blaACT-15 beta-lactamase and fosfomycin resistance (fosA).

106 or bshA caused a 16- to 60-fold reduction in fosfomycin resistance in these S. aureus strains.

107 The fosfomycin resistance protein FomA inactivates fosfomyci

108 amily of amino acid kinases that include the fosfomycin resistance protein fomA, which deactivates th

109 The fosfomycin resistance protein FosA is a member of a dist

110 The fosfomycin resistance protein, FosA, catalyzes the Mn(2+

111 The fosfomycin resistance protein, FosX, catalyzes the hydra

112 Bacillus subtilis fosB(yndN) gene encodes a fosfomycin resistance protein.

113 te-binding site are conserved in the related fosfomycin resistance proteins FosB and FosX, whereas no

114 ioxygenase), and nucleophilic substitutions (fosfomycin resistance proteins).

115 or the ability of resulting clones to confer fosfomycin resistance to Escherichia coli were used to i

116 Moreover, fosfomycin resistance was imparted to the E. coli strain

117 ich encodes a BSH-S-transferase that confers fosfomycin resistance, in several S. aureus strains, inc

118 B. anthracis prophage, encoding demonstrable fosfomycin resistance.

119 A fosfomycin-resistant C115E mutant with -1% activity of t

120 and 2 inhibited not only wild-type but also fosfomycin-resistant MurA in an unprecedented way.

121 ted that 2 is a potent inhibitor of MRSA and fosfomycin-resistant MurA, laying the foundation for the

122 nce to the oxirane or phosphonate oxygens of fosfomycin resulted in variants with very low or no acti

123 sigma(W), and both fosB and sigW mutants are fosfomycin sensitive.

124 s the excision of all, and ciprofloxacin and fosfomycin significantly promote the excision of a subse

125 Fosfomycin still bound to the active site of C115D MurA,

126 Fosfomycin still bound to the active site of C115D MurA,

127 carry high biological costs, we suggest that fosfomycin susceptibility of strains that generate inner

128 products, including the approved antibiotic fosfomycin, the widely used herbicide phosphinothricin (

129 sistance against the Streptomyces antibiotic fosfomycin, these studies support the notion that sigma(

130 y FosA involves the attack by glutathione on fosfomycin to yield the product 1-(S-glutathionyl)-2-hyd

131 novel ways of using an existing antibiotic, fosfomycin, to treat ESBL-producing Enterobacteriaceae (

132 stals (100 mg twice daily for 5-7 days), and fosfomycin trometamol (3 g in a single dose) are all app

133 thway of the clinically important antibiotic fosfomycin uses enzymes that catalyse reactions without

134 e retention of the hydroxyl oxygen of HPP in fosfomycin was demonstrated.

135 Disk diffusion testing of fosfomycin was performed on 649 multidrug-resistant E. c

136 resistance to the broad-spectrum antibiotic fosfomycin, which contains a phosphonate group.

137 target of the naturally occurring antibiotic fosfomycin, which covalently attaches to Cys115 in the a

138 Although fosfomycin, which is the only clinically used MurA-targe

139 hed antibiotic target since the discovery of fosfomycin, which specifically inhibits MurA by covalent

140 high intrinsic resistance to the antibiotic fosfomycin, which targets UDP-MurNAc de novo biosynthesi