ライフサイエンスコーパス: glabrata

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

2 sing purified complexes derived from Candida glabrata.

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

4 ment for invasive candidiasis due to Candida glabrata.

5 xation of constraint specifically in Candida glabrata.

6 3p and Dur31p that are uncharacterized in C. glabrata.

7 pathway mutant flies succumb to injected C. glabrata.

8 n and its importance for the virulence of C. glabrata.

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

10 of mice infected intravenously with Candida glabrata.

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

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

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

14 bloodstream infections (BSI) due to Candida glabrata.

15 dida including the distantly related Candida glabrata.

16 and echinocandins in clinical isolates of C. glabrata.

17 hways, but its role is less understood in C. glabrata.

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

19 pport the growth and survival of engulfed C. glabrata.

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

21 ous levels of effectiveness in recovering C. glabrata.

22 ession of RPs in the fungal pathogen Candida glabrata.

23 otic FMNAT from the pathogenic yeast Candida glabrata.

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

25 ong some Candida species, especially Candida glabrata.

26 ctivator for isolated human NK cells than C. glabrata.

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

28 f persisters in Candida albicans and Candida glabrata.

29 clinically important human pathogen Candida glabrata.

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

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

32 88.1% (95% CI, 80.2%-93.7%) for C. krusei/C. glabrata.

33 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

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

35 : 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

36 rales [2], Fusarium species [2], and Candida glabrata [1]) occurred, representing 8.3% of patients an

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

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

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

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

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

42 (52%), Candida parapsilosis (23.7%), Candida glabrata (12.7%), Candida tropicalis (5.8%), Candida kru

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 proven infectious endophthalmitis (2 Candida glabrata, 2 coagulase-negative Staphylococcus, 1 Strepto

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

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

48 .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

49 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

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

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

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

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

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

55 (5 isolates), C. krusei (2 isolates), and C. glabrata (44 isolates) that were nonsusceptible (either

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

57 (4 isolates), C. kefyr (2 isolates), and C. glabrata (47 isolates) that were nonsusceptible (NS; eit

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

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

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

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

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

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

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

65 e investigate the molecular mechanisms of C. glabrata adaptation to heat stress via adaptive laborato

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

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

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

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

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

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

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

75 simultaneous identification of C. auris, C. glabrata and C. krusei, at species-level as well as of s

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

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

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

79 by recovering two species of Candida (Cornus glabrata and Candida albicans) from Candida-spiked blood

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

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

82 o clinically relevant yeast species (Candida glabrata and Cryptococcus neoformans), is shown.

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 s in macrophages upon infection with Candida glabrata and exacerbate infection.

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

87 m six different laboratory populations of B. glabrata and one population of B. alexandrina.

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

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

90 ida species group, 4% for VVC due to Candida glabrata, and 10% for T. vaginalis Sensitivity and speci

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

92 26 isolates, including 58 C. albicans, 62 C. glabrata, and 53 C. krusei isolates), 35 Cryptococcus ne

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

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

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 andida species group; 84.7% and 99.1% for C. glabrata; and 96.5% and 95.1% for T. vaginalis Sensitivi

99 C. glabrata anp1 and mnn2 mutants showed increased virulenc

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

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

102 The human fungal pathogen Candida glabrata appears to utilise unique stealth, evasion and

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

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

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

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

107 Candida albicans and Candida glabrata are the 2 most prevalent Candida species causin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

124 eral other low-virulence Candida species (C. glabrata, C. auris, and C. albicans efg1Delta/Delta cph1

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

126 ns, C. auris, C. dubliniensis, C. famata, C. glabrata, C. guilliermondii, C. kefyr, C. krusei, C. lus

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

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

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

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

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

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

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

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

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

136 Echinocandins are recommended for Candia glabrata candidemia.

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

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

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

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

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

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

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

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

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

146 Candida glabrata chorioamnionitis presents unique management cha

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

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

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

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

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

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

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

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

155 Compared with S. cerevisiae, C. glabrata exhibits higher innate tolerance to various env

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

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

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

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

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

161 t species, such as Candida auris and Candida glabrata, further threatens the limited armamentarium of

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

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

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

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

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

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

168 teraction, the human fungal pathogen Candida glabrata harbors a large family of more than 20 cell wal

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

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

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

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

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

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

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

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

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

178 In addition, C. glabrata icl1Delta cells displayed significantly reduced

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 -talks between MAPK signaling pathways in C. glabrata in response to environmental challenges.

182 that ICL1 is crucial for the survival of C. glabrata in response to macrophage engulfment.

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

184 a severe attenuation in the virulence of C. glabrata in the mouse model of invasive candidiasis.

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

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

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

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

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

190 ma) secretion, was more pronounced during C. glabrata infection.

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

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

193 The pathogenesis of Candida glabrata infections is poorly understood.

194 Candida glabrata is a human commensal and an opportunistic human

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

229 ainst 18 isolates of C. albicans (n = 9), C. glabrata (n = 4), and C. auris (n = 5).

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 Candida glabrata's ability to adhere to host tissue is mediated

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

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

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

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

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 enome-wide association study of Biomphalaria glabrata snails, we identify genomic region PTC2 which e

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 ere, developmental exposures of Biomphalaria glabrata to selective pharmaceutical 5alpha-reductase in

279 ctional glyoxylate cycle is essential for C. glabrata to utilise certain alternative carbon sources i

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

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

282 e, we performed a de novo assembly of the C. glabrata type strain CBS138 using long single-molecule r

283 a showed that disruption of ICL1 rendered C. glabrata unable to utilise acetate, ethanol or oleic aci

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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