ライフサイエンスコーパス: glabrata

1 y to amphotericin B for C. tropicalis and C. glabrata.

2 xation of constraint specifically in Candida glabrata.

3 3p and Dur31p that are uncharacterized in C. glabrata.

4 pathway mutant flies succumb to injected C. glabrata.

5 expression of C. albicans Dur proteins in C. glabrata.

6 of mice infected intravenously with Candida glabrata.

7 t for reduced Hst 5 uptake and killing in C. glabrata.

8 vigation between genes of C. albicans and C. glabrata.

9 onferred a CRS-MIS phenotype on wild-type C. glabrata.

10 bloodstream infections (BSI) due to Candida glabrata.

11 dida including the distantly related Candida glabrata.

12 and echinocandins in clinical isolates of C. glabrata.

13 us system (CNS) and peripheral tissues of B. glabrata.

14 ed Candida albicans, C. parapsilosis, and C. glabrata.

15 ous levels of effectiveness in recovering C. glabrata.

16 ession of RPs in the fungal pathogen Candida glabrata.

17 f persisters in Candida albicans and Candida glabrata.

18 otic FMNAT from the pathogenic yeast Candida glabrata.

19 he primary sensor of niacin limitation in C. glabrata.

20 into the mechanism of GM-CSF induction by C. glabrata.

21 sinistral (left-handed) species Biomphalaria glabrata.

22 clinically important human pathogen Candida glabrata.

23 ong some Candida species, especially Candida glabrata.

24 and multi-drug resistance associated with C. glabrata.

25 ion in the life cycle and pathobiology of C. glabrata.

26 88.1% (95% CI, 80.2%-93.7%) for C. krusei/C. glabrata.

27 CI, 99.7%-100.0%) for Candida krusei/Candida glabrata.

28 sing purified complexes derived from Candida glabrata.

29 onazole (from 6.1% to 18.4%) against Candida glabrata.

30 ment for invasive candidiasis due to Candida glabrata.

31 C. albicans, 2 (96.2) and 0.5 (90.4%) for C. glabrata, 0.25 (99.3) and 0.12 (97.9) for C. parapsilosi

32 ws: for C. albicans, 0.016 and 0.007; for C. glabrata, 0.5 and 0.06; for C. parapsilosis, 0.06 and 0.

33 : for C. albicans, 0.3, 0.1, and 2.1; for C. glabrata, 0.8, 1.3, and 1.6; for C. parapsilosis, 0.0, 1

34 9.4%), 0.12 (98.5%), and 0.03 (98.2%) for C. glabrata; 0.12 (98.9%), 0.12 (99.4%), and 0.12 (99.1%) f

35 of Candida spp. (4,283 C. albicans, 1,236 C. glabrata, 1,238 C. parapsilosis, 996 C. tropicalis, 270

36 ows: C. albicans, 2,567 (43.5%) isolates; C. glabrata, 1,464 (24.8%) isolates; C. parapsilosis, 1,048

37 lation of the common non-albicans species C. glabrata (10.2% to 11.7%), C. tropicalis (5.4% to 8.0%),

38 as active against all Candida spp. except C. glabrata (10.5% non-WT), whereas posaconazole showed dec

39 es of 5 Candida spp. (120 C. albicans, 38 C. glabrata, 10 C. parapsilosis, 12 C. tropicalis, and 7 C.

40 With the exception of C. glabrata (11.9% resistant), resistance to fluconazole wa

41 (52%), Candida parapsilosis (23.7%), Candida glabrata (12.7%), Candida tropicalis (5.8%), Candida kru

42 All C. albicans (15) and C. glabrata (16) isolates, alone or mixed, were identified

43 luded 560 isolates of C. albicans, 175 of C. glabrata, 162 of C. parapsilosis, 124 of C. tropicalis,

44 lbicans predominated (48.4%), followed by C. glabrata (18.0%), C. parapsilosis (17.2%), C. tropicalis

45 es of Candida albicans, 2,352 isolates of C. glabrata, 2,195 isolates of C. parapsilosis, 1,841 isola

46 es of Candida albicans, 2,415 isolates of C. glabrata, 2,278 isolates of C. parapsilosis, 1,895 isola

47 .0)/0.5 (97.5), and 2 (95.2)/4 (93.5) for C. glabrata; 2 (99.7)/2 (97.3), 0.5 (98.7)/0.5 (97.8), and

48 0.03 for C. albicans; 32, 2, and 0.5 for C. glabrata; 2, 0.25, and 0.12 for C. parapsilosis; 2, 0.12

49 of Candida (42 Candida albicans, 25 Candida glabrata, 22 Candida parapsilosis, 14 Candida tropicalis

50 andida albicans (52.7%), followed by Candida glabrata (25.6%) and Candida tropicalis (16.3%).

51 isolated species (38%), followed by Candida glabrata (29%), Candida parapsilosis (17%), and Candida

52 hest proportion of BSI isolates that were C. glabrata (32%) and the lowest rate of fluconazole resist

53 ene mutations and included 34 isolates of C. glabrata (4 mutant strains), 32 of C. albicans (1 mutant

54 ere observed for Candida albicans (2.7%), C. glabrata (4.1%), C. tropicalis (9.7%), and other less co

55 ate wild-type (WT) from non-WT strains of C. glabrata, 42 of the 55 (76.4%) C. glabrata mutants were

56 (5 isolates), C. krusei (2 isolates), and C. glabrata (44 isolates) that were nonsusceptible (either

57 les inoculated with clinical isolates (40 C. glabrata, 46 C. albicans, 36 C. parapsilosis, 19 C. trop

58 (4 isolates), C. kefyr (2 isolates), and C. glabrata (47 isolates) that were nonsusceptible (NS; eit

59 ts), Candida krusei (3 mutants), and Candida glabrata (55 mutants).

60 d, consisting of 258 clinical samples (89 C. glabrata, 79 C. albicans, 23 C. parapsilosis, 18 C. trop

61 ate wild-type (WT) from non-WT strains of C. glabrata, 80% of the C. glabrata mutants were non-WT for

62 C. albicans; 96.0%, 98.9%, and 93.7% for C. glabrata; 90.8%, 98.1%, and 98.1% for C. parapsilosis; 9

63 , we characterize the genome of Biomphalaria glabrata, a lophotrochozoan protostome, and provide time

64 glabrata granulin (BgGRN)] from the snail B. glabrata, a natural host for the human blood fluke Schis

65 gously expressed C. albicans ALS3 in Candida glabrata, a yeast that lacks a close ALS3 ortholog and h

66 e delineated the fungal ligands to be the C. glabrata adhesins Epa1, Epa6, and Epa7 and demonstrated

67 those in the 1998 trial to have IC due to C. glabrata (adjusted OR: 1.93, 95% CI: 0.20-18.98), while

68 ization or in the proportion of IC due to C. glabrata after a 3-year period of routine fluconazole pr

69 ntially multidrug-resistant pathogen Candida glabrata against anidulafungin and fluconazole.

70 nd that the Ure2p of Candida albicans and C. glabrata also regulate nitrogen catabolism.

71 Little is known about how C. glabrata, an emerging pathogen, resists attack by phagoc

72 Adherence of Candida glabrata, an opportunistic yeast pathogen, to host cells

73 d: FKS hot-spot mutations were found in 5 C. glabrata and 2 C. tropicalis isolates; of these, 5 (incl

74 resent the structures of Atp11p from Candida glabrata and Atp12p from Paracoccus denitrificans, and w

75 The two species examined, Biomphalaria glabrata and Biomphalaria alexandrina, are the major int

76 was low (1%), but the high percentage of C. glabrata and C. krusei isolates within this group of pat

77 that seen with the resistant (R) species C. glabrata and C. krusei.

78 Biochemically, C. glabrata and C. nivariensis are distinguished by their d

79 tory and clinical strains of C. albicans, C. glabrata and C. tropicalis were evaluated.

80 s, fluconazole exposure favored growth of C. glabrata and C. tropicalis, while caspofungin generally

81 T and CLSI results with the exceptions of C. glabrata and caspofungin (85.3%) and C. krusei and caspo

82 hat reduced dependence on Pho2 evolved in C. glabrata and closely related species.

83 ing the human pathogens Candida albicans, C. glabrata and Cryptococcus neoformans, the food spoilage

84 Fluconazole (FLC) resistance is common in C. glabrata and echinocandins are often used as first-line

85 odstream infection (BSI) isolates of Candida glabrata and grouped the isolates by patient age and geo

86 everal Candida species, most notably Candida glabrata and more recently Candida auris.

87 ain how Epa-like adhesins have evolved in C. glabrata and related fungal species.

88 Comparative genomic analyses of Candida glabrata and Saccharomyces cerevisiae suggest many signa

89 that were infected intraperitoneally with C. glabrata and sterile feces.

90 d C. krusei, 2 CFU/mL for C. albicans and C. glabrata, and 3 CFU/mL for C. parapsilosis.

91 26 isolates, including 58 C. albicans, 62 C. glabrata, and 53 C. krusei isolates), 35 Cryptococcus ne

92 urate method for identifying C. albicans, C. glabrata, and C. parapsilosis, the three most common Can

93 Candida albicans, Candida glabrata, and Candida parapsilosis endophthalmitis isola

94 ring interaction of epithelial cells with C. glabrata, and pre-treatment with an NF-kappaB inhibitor

95 goencephalitis and colitis caused by Candida glabrata, and Q295* for the patient with Candida albican

96 gion of epithelial adhesin (Epa1) of Candida glabrata, and the carboxyl region of the cell wall prote

97 of the Tom40 protein from the yeast Candida glabrata, and truncated constructs lacking the N- and/or

98 C. glabrata anp1 and mnn2 mutants showed increased virulenc

99 d polysaccharide structural analyses that C. glabrata ANP1, MNN2, and MNN11 encode functional ortholo

100 Furthermore, we show that deletion of the C. glabrata Anp1, Mnn2, and Mnn11 mannosyltransferases dire

101 ions with the azole-refractory yeast Candida glabrata are now commonly treated with the echinocandins

102 Candida albicans and Candida glabrata are predominant fungi associated with oral cand

103 inst C. albicans, however many strains of C. glabrata are resistant.

104 Both Candida albicans and C. glabrata are restrained by the Toll pathway, yet the com

105 albicans and with increasing prevalence, C. glabrata, are responsible for the majority of fungal blo

106 e requires the freshwater snail Biomphalaria glabrata as its primary intermediate host.

107 nformation and the reference sequence for C. glabrata, as well as orthology relationships that interc

108 C. glabrata BG2 (5 x 10(8) CFU) caused a 100% mortality rat

109 C. albicans SC5314 was more virulent than C. glabrata BG2 during IAC, causing a 100% mortality rate f

110 The diminished NET response to C. glabrata biofilms likely contributes to the resilience o

111 When exposed to C. glabrata biofilms, neutrophils also release NETs, but si

112 Patients with C. glabrata bloodstream infection admitted to a large, tert

113 We reviewed records of all patients with C. glabrata bloodstream infection at Duke Hospital over the

114 d ninety-three episodes (313 isolates) of C. glabrata bloodstream infection were analyzed.

115 Mice receiving C. glabrata bmt2-6 mutant strains had normal body weight an

116 The results show that C. glabrata bmt2-6 strains had a significant reduction in b

117 Lower numbers of colonies of C. glabrata bmt2-6 were recovered from stools and different

118 ssion by diverse microbes, including Candida glabrata, Bordetella pertussis, Escherichia coli, and L.

119 l structures of DHFR from C. albicans and C. glabrata bound to lead compounds, 13 new para-linked com

120 ation and of fluconazole resistance among C. glabrata BSI isolates were higher in the present study (

121 tion of an emerging fungal pathogen, Candida glabrata, by the human NK cytotoxic receptor NKp46 and i

122 non- albicans Candida species, including C. glabrata, C. dubliniensis, and C. tropicalis, which are

123 s cause >90% of Candida BSI: C. albicans, C. glabrata, C. parapsilosis, and C. tropicalis.

124 pathogenic Candida species (C. albicans, C. glabrata, C. parapsilosis, C. tropicalis, C. krusei, C.

125 common Candida spp., such as C. albicans, C. glabrata, C. tropicalis, and the C. parapsilosis group.

126 Five Candida species (C. albicans, C. glabrata, C. tropicalis, C. parapsilosis, and C. krusei)

127 of fluconazole-R isolates of C. albicans, C. glabrata, C. tropicalis, C. rugosa, C. lipolytica, C. pe

128 (Candida albicans/C. parapsilosis, 100%; C. glabrata/C. krusei, 92.3%; C. tropicalis, 100%) and spec

129 icity (C. albicans/C. parapsilosis, 100%; C. glabrata/C. krusei, 94.8%; C. tropicalis, 100%).

130 assay detecting Candida albicans and Candida glabrata (CAN-PCR) was compared with the Affirm VPIII Ca

131 dida 7-plex panel (Candida albicans, Candida glabrata, Candida tropicalis, Candida parapsilosis, Cand

132 Echinocandins are recommended for Candia glabrata candidemia.

133 ere identified in 18% of 72 patients with C. glabrata candidemia.

134 evisiae, but Ure2p of Candida glabrata (Ure2(glabrata)) cannot, even though the Ure2(glabrata) N-term

135 Emerging resistance patterns among C. glabrata cases in NAM require focused surveillance.

136 he crystal structure of the OB4 domain of C. glabrata Cdc13, which revealed a novel mechanism of OB f

137 Thus, neither C. glabrata cell surface or biofilm matrix beta-1,3-glucan

138 By mixing defined numbers of C. glabrata cells (the calibration genome) with S. cerevisi

139 also report that macrophage-internalized C. glabrata cells express CgFtr1 on the cell membrane indic

140 e, we demonstrate for the first time that C. glabrata cells respond to iron limitation by expressing

141 thogenic Candida albicans CaUpc2 and Candida glabrata CgUpc2 to AR1b and SRE/AR1c elements.

142 There is a strong association between C. glabrata chorioamnionitis and assisted fertility techniq

143 Candida glabrata chorioamnionitis presents unique management cha

144 We hypothesized that species of the Candida glabrata clade and species with phenotypic traits that o

145 a mismatch repair defect is prevalent in C. glabrata clinical isolates.

146 S. aureus-C. parapsilosis, and S. aureus-C. glabrata coinoculations resulted in little to no mortali

147 C. glabrata colonization and IC prevalence among patients i

148 lso present in C. glabrata, their role in C. glabrata colonization and virulence was investigated in

149 There was no increase in C. glabrata colonization or in the proportion of IC due to

150 C. glabrata colonization was not significantly more common

151 Similarly, the biofilm matrix of C. glabrata contained significantly higher levels of beta-1

152 eloped a 2053 element cDNA microarray for B. glabrata containing clones from ORESTES (Open Reading fr

153 A C. glabrata Deltaplb1-2 mutant (phospholipase B genes disru

154 C. glabrata differed from C. albicans during IAC by being l

155 rast, the N/Q-rich N-terminal domain of Ure2(glabrata) does not readily form amyloid, and that formed

156 icating the transporters in the growth of C. glabrata during infection.

157 Five clustered genes of C. glabrata encoding beta-mannosyltransferases, BMT2-BMT6,

158 nctionally identified as adhesins in Candida glabrata (Epa1, Epa6 and Epa7) bind to ligands containin

159 The fungal pathogen Candida glabrata expresses a protein homologous to Ybp1 called C

160 Following this lead, C. glabrata fen1Delta and cka2Delta deletants were construc

161 Four crystal structures of C. glabrata FMNAT in different complexed forms were determi

162 Expression microarray analysis of Candida glabrata following phagocytosis by human neutrophils was

163 004) to 1.8% (2009) for anidulafungin and C. glabrata, from 2.4% (2004) to 5.7% (2009) for micafungin

164 Determining the NMR structure of the C. glabrata Gal11A KIX domain provides a detailed understan

165 glabrata Pdr1 activation domain with the C. glabrata Gal11A KIX domain.

166 ole use in the 3 months prior to the IFI, C. glabrata, ganciclovir use in the 3 months prior to the I

167 Screening a C. glabrata genomic library, we identified CgPMU2, a member

168 lly characterize a progranulin [Biomphalaria glabrata granulin (BgGRN)] from the snail B. glabrata, a

169 s not abundant in mammalian tissues where C. glabrata grows.

170 The human pathogenic yeast Candida glabrata harbors more than 20 surface-exposed, epithelia

171 These results showed that C. glabrata has a high pathogenic potential in DSS-induced

172 The fungal pathogen Candida glabrata has emerged as a major health threat since it r

173 C. glabrata has higher surface levels of beta-1,3-glucans a

174 trate that BgGRN induces proliferation of B. glabrata hemocytes, and specifically drives the producti

175 nd virulence in the pathogenic yeast Candida glabrata Here, we demonstrate PI3-kinase (CgVps34) to be

176 ting the fungal enzymes and the growth of C. glabrata; however, the inhibition of the growth of C. al

177 n encounter with planktonic (non-biofilm) C. glabrata, human neutrophils initially phagocytose the ye

178 In conclusion, a mouse model of C. glabrata IAC mimics disease in humans and distinguishes

179 involves changes in global SUMOylation in C. glabrata Importantly, loss of the deSUMOylating enzyme C

180 Imaging of the host response to C. glabrata in a rat vascular model of infection supports a

181 xpression that support the persistence of B. glabrata in the field and may define this species as a s

182 and yapsins are required for virulence of C. glabrata in this model.

183 single species, the fungal pathogen Candida glabrata, in which a trans mutation has occurred very re

184 Whereas the frequency of C. glabrata increased with patient age, the rate of flucona

185 and results were compared with those from C. glabrata incubated under conditions of carbohydrate or n

186 We found that C. glabrata-induced GM-CSF synthesis was adhesion-dependent

187 g organism virulence using ace2Delta Candida glabrata infection in neutropenic mice.

188 d recognition was crucial for controlling C. glabrata infection in vitro and in vivo.

189 models for disseminated and urinary tract C. glabrata infection.

190 d demonstrated that clearance of systemic C. glabrata infections in vivo depends on their recognition

191 The pathogenesis of Candida glabrata infections is poorly understood.

192 C. glabrata is a NAD(+) auxotroph, and its growth depends o

193 The fungus Candida glabrata is an important and increasingly common pathoge

194 The yeast Candida glabrata is an opportunistic pathogen of humans.

195 interaction of oral epithelial cells with C. glabrata is granulocyte monocyte colony-stimulating fact

196 onization, the human fungal pathogen Candida glabrata is known to utilize a large family of highly re

197 We demonstrated that C. glabrata is limited from an environment where phytic aci

198 Echinocandin failure in C. glabrata is linked exclusively to Fks1p and Fks2p amino

199 The prevalence of C. glabrata is rising, partly owing to its low intrinsic su

200 common with other fungi, the cell wall of C. glabrata is the initial point of contact between the hos

201 a rapid and cost-effective way to screen C. glabrata isolates for echinocandin resistance.

202 We analyzed 1,598 Candida glabrata isolates for the presence of the cryptic specie

203 Among echinocandin-resistant C. glabrata isolates from 2011, 38% were fluconazole resist

204 All C. glabrata isolates had caspofungin MICs of >/=0.5 mug/ml,

205 C. glabrata isolates in spleens of gp91(phox-/-) knockout m

206 isolates decreased, and the proportion of C. glabrata isolates increased, while the proportion of C.

207 C. glabrata isolates were more common in NAM (23.5%), and C

208 ida parapsilosis (2.1%); however, 8.8% of C. glabrata isolates were resistant to fluconazole.

209 species, including 16 C. albicans and 11 C. glabrata isolates with defined FKS mutations.

210 itro antifungal exposure failed to detect C. glabrata isolates with echinocandin resistance-associate

211 alis isolates; of these, 5 (including all C. glabrata isolates) had micafungin MICs of >2 microg/ml,

212 in 1.2% of C. albicans isolates, 5.9% of C. glabrata isolates, 0.3% of C. parapsilosis isolates, and

213 es (3.5 to 5.6%) was most prevalent among C. glabrata isolates, as determined using recently establis

214 riginal published findings, we found that C. glabrata isolates, but not C. nivariensis isolates, are

215 s low (1% of isolates) but was higher for C. glabrata isolates, ranging from 2.1% isolates resistant

216 ortant cues about the in vitro fitness of C. glabrata isolates, which may lead to genotypic or phenot

217 esistance was 3% overall but was 8% among C. glabrata isolates.

218 onfer in vitro echinocandin resistance in C. glabrata isolates.

219 In C. glabrata, its Pho4 binds to more locations and induces t

220 Candida glabrata, like Candida albicans, is an opportunistic yea

221 We observed that the yeast Candida glabrata lost the gene encoding a phosphate-repressible

222 r translocation, reduced Hst 5 binding to C. glabrata may be the reason for its insensitivity.

223 structures of the Vik1 ortholog from Candida glabrata may provide insight into this mechanism by show

224 Drug-resistant clinical isolates of C. glabrata most commonly contain point mutations in Pdr1 t

225 tivation pathway represents a linchpin in C. glabrata multidrug resistance.

226 ains of C. glabrata, 42 of the 55 (76.4%) C. glabrata mutants were non-WT and 8 of the 55 (14.5%) wer

227 non-WT strains of C. glabrata, 80% of the C. glabrata mutants were non-WT for both agents (96% concor

228 An additional 10 C. glabrata mutants, two C. albicans mutants, and one mutan

229 s contained a single fungal species, with C. glabrata (n = 129; 30.8%) being the most common isolate,

230 fied were Candida albicans (n = 85), Candida glabrata (n = 63), and Candida parapsilosis (n = 44).

231 Ure2(glabrata)) cannot, even though the Ure2(glabrata) N-terminal domain is more similar to that of t

232 for the ancestral PHO5 was lost and that C. glabrata neofunctionalized a weak phosphatase to replace

233 ibility was independently associated with C. glabrata, non-Hodgkin's lymphoma, cytomegalovirus (CMV)

234 e required for Toll pathway activation by C. glabrata, only GNBP3, and not psh mutants, are susceptib

235 f VT-1161 against Candida krusei and Candida glabrata, pathogens that are intrinsically resistant to

236 cule inhibitors of the interaction of the C. glabrata Pdr1 activation domain with the C. glabrata Gal

237 In the related human commensal C. glabrata, Pho4 is required but Pho2 is dispensable for s

238 previously noted that the snail Biomphalaria glabrata produces a secreted lectin, fibrinogen-related

239 in Drosophila, the Toll pathway restrains C. glabrata proliferation.

240 are recovered at a high rate (55% of all C. glabrata recovered) from patients.

241 tion of C. albicans (green fluorescence), C. glabrata (red fluorescence), and C. parapsilosis (yellow

242 starvation-inducible acid phosphatase in C. glabrata relative to most yeast species provides an exam

243 , heterologous expression of HYR1 in Candida glabrata rendered the organism more resistant to neutrop

244 Recent reports of BSI due to strains of C. glabrata resistant to both fluconazole and the echinocan

245 We report a case of Candida glabrata sepsis associated with chorioamnionitis in an i

246 s and the higher echinocandin resistance, C. glabrata should be closely monitored in future surveilla

247 These and other meiotic proteins in C. glabrata showed marked rate acceleration, likely due to

248 Six yeast isolates (all Candida glabrata) showing caspofungin MIC values of >or=0.5 micr

249 Unlike S. cerevisiae, C. glabrata shows little dependence on the transcription fa

250 tionally, we demonstrate that susceptible B. glabrata snails can be made resistant to infection with

251 nsoni (trematode) infections in Biomphalaria glabrata snails, we competed these three models against

252 te acquisition of resistance mutations in C. glabrata specifically.

253 However, C. glabrata still had phosphate starvation-inducible phosph

254 Three clinical C. glabrata strains (5 x 10(8) CFU) caused 80 to 100% morta

255 breakpoints differentiate wild-type from C. glabrata strains bearing clinically significant FKS1/FKS

256 C. glabrata strains expressing CaDur3 and CaDur31 had two-f

257 inical echinocandin resistance among Candida glabrata strains is increasing, especially in the United

258 azole and echinocandin coresistance among C. glabrata strains warrants continued close surveillance.

259 s assessed using a blind collection of 50 C. glabrata strains, including 16 FKS1 and/or FKS2 mutants.

260 mined in mice receiving DSS and different C. glabrata strains.

261 on of this quality control system in Candida glabrata suggests that many pathogenic species of fungi

262 ed for high-throughput screening of 1,032 C. glabrata surveillance isolates.

263 s in vertebrates, wild-type flies contain C. glabrata systemic infections yet are unable to kill the

264 ong 110 fluconazole-resistant isolates of C. glabrata tested in 2001 to 2004.

265 elevant for pathogenic fungi such as Candida glabrata that are closely related to S. cerevisiae and c

266 Candida albicans and Candida glabrata that were resistant to anidulafungin, caspofung

267 ltispecies episodes, with C. albicans and C. glabrata the most frequently encountered combination.

268 Because beta-Mans are also present in C. glabrata, their role in C. glabrata colonization and vir

269 n about potential sources of serotonin in B. glabrata tissues.

270 tivation and re-sensitizes drug-resistant C. glabrata to azole antifungals in vitro and in animal mod

271 nderstanding of the attributes that allow C. glabrata to cause disease will provide insights that can

272 We conclude that exposure of C. glabrata to commonly used preservatives can alter the ex

273 Susceptibility of C. glabrata to fluconazole was lowest in the northeast regi

274 susceptibilities of 1,669 BSI isolates of C. glabrata to fluconazole, voriconazole, anidulafungin, ca

275 sceptibility testing of echinocandins for C. glabrata to guide therapeutic decision making.

276 egulated in three models of resistance of B. glabrata to infection with Schistosoma mansoni or Echino

277 The pathogenicity of Candida glabrata to patients remains poorly understood for lack

278 hypothesized that interaction with viable C. glabrata triggers GM-CSF synthesis via NF-kappaB activat

279 Taken together, these findings show that C. glabrata triggers NET release.

280 Eight mutants of C. glabrata, two of C. albicans, and one each of C. tropica

281 ccharomyces cerevisiae, but Ure2p of Candida glabrata (Ure2(glabrata)) cannot, even though the Ure2(g

282 a [URE3] prion in S. cerevisiae, but the C. glabrata Ure2p, which does have the conserved sequence,

283 Growth of C albicans and C glabrata was observed in all voriconazole-supplemented v

284 tion between Saccharomyces cerevisiae and C. glabrata We demonstrate that SUMOylation is an essential

285 f SUMOylation in the human pathogen, Candida glabrata We identified the enzymes involved in small ubi

286 hate signal transduction (PHO) pathway of C. glabrata, we demonstrate that components of the pathway

287 ncentrations of Candida albicans and Candida glabrata were each added to a set of vials.

288 d 0.5x MIC on day 2, when viable counts of C glabrata were reduced by 99% and 96%, respectively.

289 ere echinocandin-resistant, and 9 (8 Candida glabrata) were multidrug resistant to both fluconazole a

290 remaining 7 mutants (2 C. albicans and 5 C. glabrata) were susceptible to one of the agents and eith

291 e proportion of infections caused by Candida glabrata, which has reduced susceptibility to fluconazol

292 l resistance has been reported among Candida glabrata, which is also frequently resistant to azole dr

293 eins in Saccharomyces cerevisiae and Candida glabrata, whose sequences have diverged to a degree that

294 A single gavage of C. glabrata wild-type strain in mice with DSS-induced colit

295 Culture of C. glabrata with a variety of vaginal products induced expr

296 The majority of cases were due to C. glabrata with an FKS mutation or wild-type C. parapsilos

297 utant strains from wild type, but testing C. glabrata with caspofungin should be approached cautiousl

298 mechanisms of echinocandin resistance in C. glabrata within 4 h.

299 h phenotypic traits that overlap those of C. glabrata would produce white colonies on CHROMagar Candi

300 Persistent C. glabrata yeasts in wild-type flies do not appear to be a