ライフサイエンスコーパス: rifamycin

1 in patients also receiving ethambutol and a rifamycin.

2 of complex lipids, including the antibiotic rifamycin.

3 on initiation inhibitors myxopyronin and the rifamycins.

4 luding antibiotics, such as erythromycin and rifamycins.

5 in Mg2+ concentration confers resistance to rifamycins.

6 ions confer resistance to some but not other rifamycins.

7 TB was defined as resistance to isoniazid, a rifamycin, a fluoroquinolone, and at least 1 of amikacin

8 t has 71% identity (80% similarity) with the rifamycin AHBA synthase from Amycolatopsis mediterranei,

9 rapAT2) of A. mediterranei S699 produced new rifamycin analogs, 24-desmethylrifamycin B and 24-desmet

10 rates of mutation may reflect the choice of rifamycin analogs.

11 (AHBA), the unique biosynthetic precursor of rifamycin and related ansamycins, a series of target-dir

12 arding drug interactions, chiefly related to rifamycins and antiretroviral drugs; and 5) revised reco

13 linked to other antibacterial agents such as rifamycins and oxazolidinones are designed to overcome b

14 rate proof of principle for this subclass of rifamycins and support further expansion of structure-ac

15 m Amycolatopsis mediterranei, which produces rifamycin, and Actinosynnema pretiosum, which produces a

16 KSs harboring modules from the erythromycin, rifamycin, and rapamycin synthases.

17 Ansamycins such as rifamycin, ansamitocin, and geldanamycin are an importan

18 Rifamycin antibacterial agents inhibit bacterial RNA pol

19 aliniketals and the ansa chain of the potent rifamycin antibiotics, which co-occur in the fermentatio

20 l resistance to a variety of clinically used rifamycin antibiotics.

21 elapse were higher with shorter durations of rifamycins (aOR 2 vs >/=8 months = 5.0 [1.9, 13.2]; 6 vs

22 ll, our results suggest that doxycycline and rifamycin are general inhibitors of Cu(II)-induced beta2

23 Mutants of the rifH and -J genes produced rifamycin B at 1% and 10%, respectively, of the yields o

24 Inactivation of rifF gives a rifamycin B nonproducing mutant that still accumulates a

25 The assembly of the polyketide backbone of rifamycin B on the type I rifamycin polyketide synthase

26 Rifamycin B, a product of Amycolatopsis mediterranei S69

27 biosynthesis of ansamycin antibiotics, like rifamycin B, involves formation of 3-amino-5-hydroxybenz

28 Among many semisynthetic rifamycins, benzoxazinorifamycins have great potential f

29 site on RNAP is immediately adjacent to the rifamycin binding site.

30 E binding site on RNAP is different from the rifamycin binding site.

31 n regulatory functions in AHBA formation for rifamycin biosynthesis by A. mediterranei.

32 adieno ic acid (P8/1-OG), an intermediate in rifamycin biosynthesis, in an extensively manipulated st

33 omal peptide synthetases/polyketide synthase rifamycin biosynthetic cluster of Amycolatopsis mediterr

34 RifN, product of one of three genes from the rifamycin biosynthetic gene cluster known to be essentia

35 that the saliniketals are byproducts of the rifamycin biosynthetic pathway diverging at the stage of

36 f three-dimensional structure information of rifamycins bound to RNA polymerase (RNAP) and the human

37 o not exhibit cross-resistance, and GE and a rifamycin can bind simultaneously to RNAP.

38 azid/rifapentine group had monoresistance to rifamycin, compared with none of three in the rifampin g

39 ng sites of other antibiotics, including two rifamycin derivatives, rifabutin and rifapentine, and st

40 omplete cross-resistance among the different rifamycin derivatives.

41 Here, we show that rifamycins do not affect the affinity of binding of Mg(2

42 Accordingly, GE and rifamycins do not exhibit cross-resistance, and GE and a

43 We conclude that rifamycins do not function by allosteric modulation of b

44 ith ART demonstrated no associations between rifamycin duration, dosing schedule, and outcomes.

45 es the chemical backbone that members of the rifamycin family of antibiotics have in common.

46 Use of rifamycins for >/=8 months and daily dosing in the inten

47 ens showed that various therapies containing rifamycins for 3 months or more were efficacious at prev

48 he A. mediterranei genome results in loss of rifamycin formation; production of the antibiotic is res

49 Recently, Artsimovitch et al. proposed that rifamycins function by allosteric modulation of binding

50 Mycobacterium tuberculosis monoresistant to rifamycin had very low concentrations of isoniazid.

51 Since 1967, Rifampin (RMP, a Rifamycin) has been used as a first line antibiotic trea

52 (levofloxacin, ethambutol, azithromycin, and rifamycin) has shown some promise in preliminary studies

53 We propose that a rifamycin-induced signal is transmitted over approximate

54 RNA polymerase at a site distinct from where rifamycins interact.

55 Rifampin, a semisynthetic rifamycin, is the cornerstone of current tuberculosis tr

56 Of the agents tested, rifamycins led to DD Mtb generation, an effect lacking i

57 Regimens containing rifamycins may be effective alternatives to isoniazid mo

58 Patients who relapsed with rifamycin monoresistance were younger (median age 29 vs

59 No rifamycin monoresistant relapse has occurred among 1004

60 Relapse with rifamycin monoresistant tuberculosis occurred among HIV-

61 No rifamycin pharmacokinetic parameter was consistently and

62 sequence; and RifKR10 from module 10 of the rifamycin PKS, whose specificity is unclear from both th

63 oduct structure; RifKR7 from module 7 of the rifamycin PKS, whose stereospecificity cannot be predict

64 ketide backbone of rifamycin B on the type I rifamycin polyketide synthase (PKS), encoded by the rifA

65 ed the acyltransferase domain of module 6 of rifamycin polyketide synthase with that of module 2 of r

66 inactivation of the rifG gene did not affect rifamycin production significantly.

67 ts of the genomic rifG-N and -J mutations on rifamycin production, indicating that all these genes en

68 Accordingly, covalent linkage of GE to a rifamycin provides a bipartite inhibitor having very hig

69 Decarboxylation of rifamycin provides salinisporamycin, which upon truncati

70 f treatment failure or relapse with acquired rifamycin resistance among patients with low CD4 lymphoc

71 e PCR ribotypes present and the emergence of rifamycin resistance during the infection cycle.

72 malabsorption of anti-TB drugs and acquired rifamycin resistance.

73 nine (89%) cases had isolates with acquired rifamycin resistance.

74 Increased occurrence of Rifamycin-resistant (RIF(R) ) TB, approximately 41% of w

75 antibiotics has resulted in the emergence of rifamycin-resistant strains of Mycobacterium tuberculosi

76 synthase (PKS) genes, rifA-rifE, involved in rifamycin (Rf) biosynthesis in Amycolatopsis mediterrane

77 The mycothiol S-conjugate of rifamycin S was produced under physiologically relevant

78 he C(15)-C(27) fragments of chaxamycins A/D, rifamycin S, and the C(12)-C(24) fragment of salinispora

79 metabolite from a biosynthetic precursor to rifamycin S.

80 nalysis assessing the effects of duration of rifamycins, schedule of dosing, and antiretroviral thera

81 A potent rifamycin-sparing regimen could revolutionize the treatm

82 A proposed mechanism in which rifamycins sterically block the extension of nascent RNA

83 rifamyin W to yield both the saliniketal and rifamycin structural classes.

84 all-molecule inhibitors rifampicin (Rif) and rifamycin SV (Rif SV).

85 ied small molecule amyloid inhibitors (i.e., rifamycin SV and doxycycline), we demonstrate that coval

86 monomer stage, we found that doxycycline and rifamycin SV exert their effect by binding to oligomeric

87 We found that two molecules, doxycycline and rifamycin SV, can inhibit beta2m amyloid formation in vi

88 ed together to pinpoint the binding sites of rifamycin SV, doxycycline, and another molecule, suramin

89 In the presence of the antibiotic rifamycin SV, which inhibits amyloid growth of wild-type

90 erated in situ by DEBS KR1, DEBS KR6, or the rifamycin synthase KR7 (RIFS KR7), respectively.

91 Rifamycin synthetase assembles the chemical backbone tha

92 four-module RifA protein (530 kDa) from the rifamycin synthetase could not be efficiently produced i

93 The rifamycin synthetase is primed with a 3-amino-5-hydroxyb

94 he loading and initial elongation modules of rifamycin synthetase reveal that this bimodular protein

95 substrate tolerance of the loading module of rifamycin synthetase suggests that the module has potent

96 Rifamycins, the clinically important antibiotics, target

97 Concomitant use of rifamycins to treat or prevent tuberculosis can result i

98 of our effort to generate better analogs of rifamycin, we substituted the acyltransferase domain of

99 Rifapentine is a cyclopentyl-substituted rifamycin whose serum half-life is five times that of ri