ライフサイエンスコーパス: antifungal drug

1 s inhibited by ketoconazole, a commonly used antifungal drug.

2 on glucose utilization in the presence of an antifungal drug.

3 a fitness advantage in fluconazole, a common antifungal drug.

4 ria, and flucytosine (5-FC), an FDA-approved antifungal drug.

5 itraconazole, a triazole that is used as an antifungal drug.

6 hesis enzymes represent potential targets of antifungal drugs.

7 approach to enhance the activity of current antifungal drugs.

8 ion and may be targeted for developing novel antifungal drugs.

9 fferent ways to detect potential targets for antifungal drugs.

10 ments have increased susceptibility to azole antifungal drugs.

11 H3 gene dosage affects resistance to polyene antifungal drugs.

12 MD) for the determination of MICs of various antifungal drugs.

13 in growth and virulence and as a target for antifungal drugs.

14 h species had high in vitro MICs to multiple antifungal drugs.

15 e presence of sterol biosynthesis-inhibiting antifungal drugs.

16 ubingensis isolates had low in vitro MICs to antifungal drugs.

17 ertain Archaea and is a potential target for antifungal drugs.

18 ant roles in cell growth and as a target for antifungal drugs.

19 fungal enzymes may provide a new target for antifungal drugs.

20 l synthesis is a primary pathway targeted by antifungal drugs.

21 f C. glabrata to develop resistance to azole antifungal drugs.

22 tress, including the response to azole-class antifungal drugs.

23 ave many complex mechanisms of resistance to antifungal drugs.

24 genic fungi and promotes resistance to azole antifungal drugs.

25 therefore be targeted for the design of new antifungal drugs.

26 rate utilization by fungi in the presence of antifungal drugs.

27 ation of potential protein targets for novel antifungal drugs.

28 in its endemic regions, and discovery of new antifungal drugs.

29 copy number CNVs during adaptation to azole antifungal drugs.

30 hylogeny and corresponding susceptibility to antifungal drugs.

31 ncluding species innately resistant to azole antifungal drugs.

32 This step should be an effective target for antifungal drugs.

33 evolving resistance to all licensed systemic antifungal drugs.

34 mphotericin B (AmB) is the gold standard for antifungal drugs.

35 that are resistant to almost all classes of antifungal drugs.

36 nd steadily increasing resistance to current antifungal drugs.

37 ne exhibited profound resistance to multiple antifungal drugs.

38 ant S. cerevisiae mutants and C. glabrata to antifungal drugs.

39 ses challenges to the host immune system and antifungal drugs.

40 sp110s as targets for the development of new antifungal drugs.

41 e increasingly resistant to first-line azole antifungal drugs.

42 is an important target in the development of antifungal drugs.

43 didiasis, and for potentiating resistance to antifungal drugs.

44 esistance to environmental stress, including antifungal drugs.

45 ed as a valuable target for developing novel antifungal drugs.

46 BM3 enzyme binds inefficiently to many azole antifungal drugs.

47 be due at least in part to excessive use of antifungal drugs.

48 the primary target of the most commonly used antifungal drugs.

49 that PS synthase may be a useful target for antifungal drugs.

50 ead to the identification of new targets for antifungal drugs.

51 uced by echinocandins, a front-line class of antifungal drugs.

52 itro antifungal susceptibility against eight antifungal drugs.

53 dulates cell cycle dynamics and responses to antifungal drugs.

54 y high mortality despite the availability of antifungal drugs.

55 athways commonly targeted by clinically used antifungal drugs.

56 ibility to all three classes of contemporary antifungal drugs.

57 d according to CLSI document M38-A2 for nine antifungal drugs.

58 ltidrug transporter and hence sensitivity to antifungal drugs.

59 cells resistant to host defenses and certain antifungal drugs.

60 Resistance to the antifungal drug 5-fluorocytosine was not deleterious and

61 on of UDP-GlcUA and confer resistance to the antifungal drug 5-fluorocytosine.

62 ungal pathogens makes the development of new antifungal drugs a medical imperative that in recent yea

63 tral role for calcineurin B in virulence and antifungal drug action in the human fungal pathogen C. n

64 and may potentiate both innate immunity and antifungal drug activity against A. fumigatus.

65 ge-scale studies of virulence mechanisms and antifungal drug activity in candidiasis.

66 ive conformation of PalH, which might act as antifungal drugs against ascomycetes.

67 ons between the immunosuppressive agents and antifungal drugs against many pathogenic fungi, includin

68 n vitro antifungal susceptibilities of eight antifungal drugs against the Ochroconis isolates reveale

69 resulted in increased susceptibility to the antifungal drug amphotericin B.

70 exemplified by a different tolerance to the antifungal drug amphotericin B.

71 l meningitis relies on three old, off-patent antifungal drugs: amphotericin B deoxycholate, flucytosi

72 as increased sensitivity to a wide range of antifungal drugs and cell wall inhibitors, and impaired

73 entives to facilitate development of inhaled antifungal drugs and combination inhalational devices, l

74 riod, and efficacy with different classes of antifungal drugs and different yeast isolates.

75 Over the last 3 decades, advances in antifungal drugs and early diagnosis have improved IFD o

76 llenge, and is leading to the empiric use of antifungal drugs and emergence of azole resistance.

77 alytic properties and inhibition by clinical antifungal drugs and experimental substituted azoles wit

78 state in which they are highly resistant to antifungal drugs and express the drug efflux determinant

79 osome missegregation to acquire tolerance to antifungal drugs and for nonmeiotic ploidy reduction aft

80 y adult patients who received systemic azole antifungal drugs and had a recorded diagnosis of toxic l

81 s associated with identifying broad-spectrum antifungal drugs and highlight novel targets that could

82 d profound effects both on susceptibility to antifungal drugs and on the levels of secreted proteinas

83 cts that include important antibacterial and antifungal drugs and some of the most-powerful known bio

84 , melanization, protease production, MICs of antifungal drugs, and growth rates in vitro.

85 uction, increased susceptibility to triazole antifungal drugs, and is avirulent in a murine model of

86 action, which is distinct from that of other antifungal drugs, and its efficacy make herbicolin A a p

87 nterest as a potential target for developing antifungal drugs, and the genes encoding glucan and chit

88 Although there was a flurry of new antifungal drugs approved in the early part of the last

89 Only a few classes of antifungal drugs are available, so the emergence of resi

90 timely diagnosis and early intervention with antifungal drugs are key factors in the successful treat

91 Among the most recently developed antifungal drugs are the echinocandins, which noncompeti

92 of these genomic changes in the presence of antifungal drugs are unknown.

93 New antifungal drugs are urgently needed to address the emer

94 n shown previously to give resistance to the antifungal drug aureobasidin A, leading us to predict th

95 d asking about laboratory infrastructure and antifungal drug availability.

96 ent ligand, thereby extending the library of antifungal drugs available to medical professionals for

97 at, particularly given the limited number of antifungal drugs available to treat invasive infections.

98 ere using topical steroids and antiviral and antifungal drugs before randomization.

99 wth defect when grown in the presence of the antifungal drug Brefeldin A (BFA), indicating that H3K4

100 Subsequent removal of the antifungal drug can lead to a dramatic loss of the CNV a

101 tunicamycin, dithiothreitol, and azole-class antifungal drugs can induce nonapoptotic cell death in y

102 Limited antifungal drug choices and emergence of drug-resistant

103 The antifungal drug, clotrimazole, demonstrated ability to i

104 The limited number of antifungal drugs combined with the isolation of Candida

105 growth of cells in the presence of supra-MIC antifungal drug concentrations.

106 This long antifungal drug coordinates the P450 heme iron with the

107 ts because of toxicity and resistance to the antifungal drugs currently in use.

108 ssible exploitation of this vulnerability in antifungal drug design are discussed.

109 gal growth, and we currently pursue it as an antifungal drug design target.

110 gi, HCS has been proposed as a candidate for antifungal drug design.

111 ng Cu-only SODs a possible target for future antifungal drug design.

112 l pathogens, and represent novel targets for antifungal drug design.

113 have access to certain diagnostic tools and antifungal drugs, despite most being considered essentia

114 dating a URA3-disrupted gene as a target for antifungal drug development could be devised, it is clea

115 Antifungal drug development lags far behind in compariso

116 ntifungal agents will be of great use in the antifungal drug development process.

117 An equally important aspect of modern antifungal drug development takes a balanced look at the

118 Despite some recent advances in antifungal drug development, complementary therapeutic s

119 geting the calcineurin signaling cascade for antifungal drug development, we examined the activity of

120 tial utility of gene expression profiling in antifungal drug development.

121 sents an attractive target for antiprotozoal/antifungal drug development.

122 malian host and thus an excellent target for antifungal drug development.

123 important implications for pathogenesis and antifungal drug development.

124 in C. albicans and forms a basis for further antifungal drug development.

125 host environment and suggest new avenues for antifungal drug development.

126 dent processes at the host-pathogen axis for antifungal drug development.

127 nd there are a limited number of targets for antifungal drug development; as a result the antifungal

128 ngal pathogens and are promising targets for antifungal drug discovery because their domain compositi

129 ole carboxylase enzyme as a novel target for antifungal drug discovery is discussed.

130 nism, it represents an unexplored target for antifungal drug discovery.

131 inesin may offer promise as cidal agents for antifungal drug discovery.

132 for cell division, cell wall remodeling, and antifungal drug discovery.

133 This study suggests two new targets for antifungal drug discovery.

134 presents an ideal target for structure-based antifungal drug discovery.

135 an fungal pathogens are untapped targets for antifungal drug discovery.

136 AmB was selected as a model antifungal drug due to the complexity of its supramolecu

137 both innate and acquired resistance against antifungal drugs, due to its ability to modify ergostero

138 cular bases of human TRPV6 inhibition by the antifungal drug econazole and the universal ion channel

139 Fungal-mediated disease progression and antifungal drug efficacy are significantly impacted by t

140 nical breakpoints are available to delineate antifungal drug efficacy in non-Aspergillus invasive mol

141 is disease, as well as for the evaluation of antifungal drug efficacy.

142 oides develops spontaneous resistance to the antifungal drug FK506 (tacrolimus) via two distinct mech

143 h encodes the target of the immunosuppresive antifungal drugs FK506 and rapamycin.

144 n-3 polymer (poly-betaNM) is superior to the antifungal drug fluconazole for all three strains examin

145 combination of either CsA or FK506 with the antifungal drug fluconazole that perturbs synthesis of t

146 (5b, 6i) were fungicidal, unlike a standard antifungal drug fluconazole, which was fungistatic.

147 , and many compounds that synergize with the antifungal drug fluconazole.

148 assessed by assays for sequestration of the antifungal drug fluconazole.

149 ins of C. albicans that are resistant to the antifungal drugs fluconazole and amphotericin B.

150 oints for the most commonly prescribed azole antifungal drug, fluconazole, can be difficult to determ

151 e modification of one of the most well-known antifungal drugs, fluconazole, with organometallic moiet

152 WP1 is a promising target for development of antifungal drugs for treatment of oroesophageal candidia

153 pplicable to the determination MICs of other antifungal drugs for yeasts.

154 of membrane-embedded transporters to efflux antifungal drugs from the cells.

155 Ciclopirox (CPX), an FDA-approved antifungal drug, has exhibited promising antitumor activ

156 y of infection, and new diagnostic tests and antifungal drugs have become available.

157 Some antifungal drugs have been reformulated to reduce toxici

158 New classes of antifungal drugs have only been partly successful in imp

159 Antifungal drugs have their own toxicities and interact

160 Itraconazole and posaconazole, widely used antifungal drugs, have been shown to stabilize misfolded

161 a novel class of drug, the orotomides, is an antifungal drug in clinical development that demonstrate

162 ding that thiabendazole, an orally available antifungal drug in clinical use for 40 years, also poten

163 The strategy of combining antifungal drugs in a treatment regimen may improve the

164 esults indicate that combinations of BRI and antifungal drugs in clinical use are likely to improve t

165 in Malawi, assessed the ability of different antifungal drugs in selective agar to reduce contaminati

166 We investigated the mechanism of action of antifungal drugs in the human pathogen Acanthamoeba cast

167 Susceptibilities of the isolates to eight antifungal drugs in vitro showed mostly high MICs, excep

168 at differs greatly from that of the parental antifungal drug, including targets involved in biosynthe

169 Additionally, antifungal drugs, including amphotericin B, liposomal am

170 ergosterol synthesis, and the azole class of antifungal drugs inhibits Erg11.

171 , a US Food and Drug Administration-approved antifungal drug, inhibits the Hedgehog (HH) signaling pa

172 esistance to the limited number of available antifungal drugs is a serious problem in the treatment o

173 ucomatous conditions, while voriconazole, an antifungal drug, is retinotoxic.

174 Using a sordarin derivative, an antifungal drug, it was possible to determine the struct

175 y hepatic stellate cells that identified the antifungal drug itraconazole (ITA) as an inhibitor of MF

176 elial cell proliferation identified the oral antifungal drug itraconazole as a novel agent with poten

177 14alpha-demethylase (CYP51) is a target for antifungal drugs known as conazoles.

178 photericin B (AmB) is an effective but toxic antifungal drug, known to increase the permeability of t

179 al drugs make turbinmicin a highly promising antifungal drug lead to help address devastating global

180 id assay may aid in the selection of initial antifungal drugs, leading to improved patient outcomes.

181 fety, and mode of action distinct from other antifungal drugs make turbinmicin a highly promising ant

182 strains of Candida are becoming resistant to antifungal drugs, making the treatment of candidiasis di

183 and necrosis, and for this, administering an antifungal drug may be of benefit.

184 peculate that this lengthy exposure to azole antifungal drugs may have caused or promoted the atypica

185 d not metabolize lanosterol, and the topical antifungal drug miconazole was the strongest inhibitor t

186 rturbations of cell wall biosynthesis by the antifungal drugs nikkomycin Z (a chitin synthase inhibit

187 evolving in parallel in the presence of the antifungal drug nystatin are frequently incompatible wit

188 Here we report that nystatin (NYT), an antifungal drug of the family of polyene macrolide antib

189 to recapitulate the exacerbating effects of antifungal drugs on allergic airway disease.

190 Current antifungal drugs only demonstrate partial success in imp

191 fungal strains that are less susceptible to antifungal drugs or that rapidly evolve drug resistance

192 s a growing concern due to its resistance to antifungal drugs, particularly amphotericin B (AMB), det

193 of the key intermediate of an orally active antifungal drug posaconazole (Noxafil).

194 The antifungal drug posaconazole that blocks sterol biosynth

195 1) were proven effective against Chagas, and antifungal drugs posaconazole and ravuconazole have ente

196 ural settings and often during adaptation to antifungal drugs, posing significant challenges to human

197 The use of antifungal drugs, primarily azoles and polyenes, has inc

198 nant resistance to the immunosuppressive and antifungal drug rapamycin (Rm).

199 f mutagenesis and resistance to 5FOA and the antifungal drugs rapamycin/FK506 (rap/FK506) and 5-fluor

200 hospitalization, and no patients experienced antifungal drug-related toxicity or IFD-associated morta

201 an also be advantageous and in fungi confers antifungal drug resistance and enables rapid adaptive ev

202 i) and/or chromatin modifications can confer antifungal drug resistance and may impact virulence trai

203 novel mechanism for the rapid acquisition of antifungal drug resistance and provide genomic evidence

204 omic copy number changes are associated with antifungal drug resistance and virulence across diverse

205 By tackling antifungal drug resistance as an evolutionary problem, t

206 We calculated candidemia incidence and antifungal drug resistance compared with prior surveilla

207 current knowledge of the mechanisms by which antifungal drug resistance evolves in experimental popul

208 on, emergence and expansion of fungicide and antifungal drug resistance globally.

209 ding of the mechanistic principles governing antifungal drug resistance is fundamental for the develo

210 Treatment options are limited, and antifungal drug resistance is increasing.

211 e diagnosis, epidemiology, and mechanisms of antifungal drug resistance of pathogenic fungi.

212 es of filamentous fungal biofilms that drive antifungal drug resistance remain largely unknown.

213 We also identified the induction of an antifungal drug resistance response upon the treatment o

214 Due to emerging antifungal drug resistance, novel strategies are urgentl

215 of Candida bloodstream infections (BSI) and antifungal drug resistance, population-based active labo

216 g proteins that regulate fungal virulence or antifungal drug resistance, such as regulators of fungal

217 n of non-albicans Candida species and rising antifungal drug resistance, the Infectious Diseases Soci

218 , CNV and LOH confer increased virulence and antifungal drug resistance, yet the mechanisms driving t

219 that proper ergosterol levels are needed for antifungal drug resistance.

220 is due to relapse rather than reinfection or antifungal drug resistance.

221 identify novel solutions for the increase in antifungal drug resistance.

222 play reduced biofilm matrix accumulation and antifungal drug resistance.

223 health concern, with a growing prevalence of antifungal drug resistance.

224 the base of A. fumigatus biofilms increases antifungal drug resistance.

225 erstand the molecular mechanisms that govern antifungal drug resistance.

226 s fungal biofilm physiology and contemporary antifungal drug resistance.

227 regulation, and uncover circuitry governing antifungal drug resistance.Cas5 is a transcriptional reg

228 lular, and molecular factors contributing to antifungal-drug resistance continues to accumulate.

229 Prolonged oral treatment of mice with antifungal drugs resulted in increased disease severity

230 ines why cells lacking H3K4 methylation have antifungal drug sensitivity.

231 s, launched biotech companies to develop new antifungal drugs, served as an unofficial advisor to two

232 tibility testing of 92 isolates against nine antifungal drugs showed a variety of results but high ac

233 A survey of azole antifungal drugs showed that CYP126A1 is inhibited stron

234 first analysis of the Hsp90 interactome upon antifungal drug stress and demonstrated that Hsp90 stabi

235 Antifungal drugs such as amphotericin B (AmB) interact w

236 ced test), as well as access to mould-active antifungal drugs such as amphotericin B deoxycholate (av

237 The PMAA resins bound cationic antifungal drugs such as miconazole and chlorhexidine di

238 vitro and in vivo, and to act together with antifungal drugs, suggesting Adh proteins could be inter

239 ence of antagonism in combination with other antifungal drugs suggests that combination antifungal th

240 ioselective synthesis of the clinically used antifungal drug sulconazole.

241 Antifungal drug susceptibility can vary with molecular t

242 A rapid flow cytometric assay for in vitro antifungal drug susceptibility testing was developed by

243 anin synthesis, carbon assimilation pattern, antifungal drug susceptibility, colony morphology, growt

244 therapeutic strategy and identify Bdf1 as an antifungal drug target that can be selectively inhibited

245 uggest that CaEss1 might constitute a useful antifungal drug target, and that structural differences

246 h direction to uncover a new fungal specific antifungal drug target.

247 virulence is achieved, suggesting AHAS as an antifungal drug target.

248 , so fungal PS synthase is a potential novel antifungal drug target.

249 ey enzyme in this pathway, is an exploitable antifungal drug target.

250 ic fungi, suggesting a promising new type of antifungal drug target.

251 ll, our results validate ATIC as a promising antifungal drug target.

252 se genes were those previously identified as antifungal drug targets (i.e., FKS1, ERG1, and ERG11), v

253 growing public health threat, and yet viable antifungal drug targets are limited as fungi share a sim

254 sm could lead to the identification of novel antifungal drug targets.

255 These findings may expand the range of antifungal drug targets.

256 odel organisms and thus constitute candidate antifungal drug targets.

257 self-splicing introns with great promise as antifungal drug targets.

258 and identifies potential anticryptococcal or antifungal drug targets.

259 zes that of the ergosterol pathway-targeting antifungal drug terbinafine.

260 In general, of the eight antifungal drugs tested, voriconazole had the greatest i

261 g and were far more resistant to a number of antifungal drugs than commensal isolates from healthy in

262 d mice and mice treated with caspofungin, an antifungal drug that inhibits beta-1,3-glucan synthase.

263 Griseofulvin is an antifungal drug that inhibits FECH as an off-target effe

264 Itraconazole is a safe and widely used antifungal drug that was recently found to possess poten

265 eveal constrained interactions with triazole antifungal drugs that are important for drug design and

266 ic activity of C. albicans CYP51 by clinical antifungal drugs that are used systemically (fluconazole

267 The echinocandins are relatively new antifungal drugs that represent, together with the older

268 iscovery of broad spectrum antiprotozoal and antifungal drugs that selectively block the capping of p

269 stems should facilitate rational screens for antifungal drugs that target cap formation in vivo.

270 This reinforces the view that antifungal drugs that target fungal Icl1 have potential

271 egrity pathway would enhance the activity of antifungal drugs that target the cell wall.

272 tructures will facilitate the development of antifungal drugs that target this essential protein.

273 on of conidia with various concentrations of antifungal drug, the percentage of residual glucose in t

274 of C. albicans to host-imposed stresses and antifungal drugs, the expression of key virulence factor

275 s species of dermatophytes respond to common antifungal drugs, the recently identified Trichophyton i

276 rgets for the development of next-generation antifungal drugs, the structures of Sec14 bound to SMIs

277 Current antifungal drug therapies are limited and suffer from to

278 of virulence, host-pathogen interactions and antifungal drug therapies in both the clinic and agricul

279 g pathogenesis, immunological effectors, and antifungal drug therapy for invasive pulmonary aspergill

280 may influence the management of patients on antifungal drug therapy.

281 d its efficacy make herbicolin A a promising antifungal drug to combat devastating fungal pathogens,

282 logical activities of the most commonly used antifungal drug to promote DC maturation.

283 lts support the development of this class of antifungal drug to treat invasive candidiasis.

284 he development of drug combinations or novel antifungal drugs to address emerging drug resistance is

285 it was applied in a concise synthesis of the antifungal drug Tolciclate.

286 ce in a murine systemic infection model, and antifungal drug tolerance in C. lusitaniae.

287 f clinical resistance may be attributable to antifungal drug tolerance.

288 vo ergosterol biosynthesis, brought about by antifungal drug treatment.

289 re important adverse effects associated with antifungal drug treatment.

290 Certain nutrients, stresses and antifungal drugs trigger beta-glucan masking, whereas ot

291 Amphotericin B (AmB) is the standard antifungal drug used on SSCC plates at a concentration o

292 We review the antifungal drugs used to treat cryptococcal meningitis w

293 Azoles are antifungal drugs used to treat fungal infections such as

294 and the rate of acquisition of tolerance to antifungal drugs via aneuploidy.

295 39 NAIMI episodes, the MIC of the first-line antifungal drug was the most important predictor of ther

296 The affinity of the enzyme for antifungal drugs was characterized to investigate its po

297 e presence of a panel of chemotherapeutic or antifungal drugs, we found that some aneuploid strains g

298 Melanin and protease production and MICs of antifungal drugs were comparable for serial isolates.

299 Multiple antifungal drugs were used (consecutively or in combinat

300 rystal structures of P450 BM3 bound to azole antifungal drugs - with the BM3 DM heme domain bound to