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1 tance among some Candida species, especially Candida glabrata.
2 are conserved in the distantly related yeast Candida glabrata.
3 dida krusei, Candida tropicalis, and perhaps Candida glabrata.
4 tes of Candida, including Candida krusei and Candida glabrata.
5 ans, Candida tropicalis, Candida krusei, and Candida glabrata.
6 e MTI and MTII genes of the pathogenic yeast Candida glabrata.
7 9% (95% CI, 99.7%-100.0%) for Candida krusei/Candida glabrata.
8 by CST using purified complexes derived from Candida glabrata.
9 nd voriconazole (from 6.1% to 18.4%) against Candida glabrata.
10 ed treatment for invasive candidiasis due to Candida glabrata.
11 rom relaxation of constraint specifically in Candida glabrata.
12 spleens of mice infected intravenously with Candida glabrata.
13 tment of bloodstream infections (BSI) due to Candida glabrata.
14 s of Candida including the distantly related Candida glabrata.
15 ortion of persisters in Candida albicans and Candida glabrata.
16 ent repression of RPs in the fungal pathogen Candida glabrata.
17 a eukaryotic FMNAT from the pathogenic yeast Candida glabrata.
18 attributed to trailing growth observed with Candida glabrata.
19 d in the clinically important human pathogen Candida glabrata.
20 (DB) > white (W), similar to the result for Candida glabrata.
21 g 74 yeast isolates (14 Candida albicans, 10 Candida glabrata, 10 Candida tropicalis, 10 Candida krus
22 albicans, 14.4% Candida parapsilosis, 13.4% Candida glabrata, 10.1% Candida tropicalis, 2.4% Candida
23 lbicans (52%), Candida parapsilosis (23.7%), Candida glabrata (12.7%), Candida tropicalis (5.8%), Can
24 5 isolates of Candida krusei, 3 isolates of Candida glabrata, 2 isolates of Saccharomyces cerevisiae
25 here were a total of 41 Candida albicans, 23 Candida glabrata, 20 Candida parapsilosis, 9 Candida tro
26 isolates of Candida (42 Candida albicans, 25 Candida glabrata, 22 Candida parapsilosis, 14 Candida tr
27 sed by Candida albicans (52.7%), followed by Candida glabrata (25.6%) and Candida tropicalis (16.3%).
28 equently isolated species (38%), followed by Candida glabrata (29%), Candida parapsilosis (17%), and
29 he most frequently misidentified species was Candida glabrata (37% of all discrepant identifications)
32 the characterization of the SNF1 homolog of Candida glabrata, a pathogenic yeast phylogenetically re
33 heterologously expressed C. albicans ALS3 in Candida glabrata, a yeast that lacks a close ALS3 orthol
34 thogenic yeasts such as Candida albicans and Candida glabrata adhere to medical devices and form drug
37 the potentially multidrug-resistant pathogen Candida glabrata against anidulafungin and fluconazole.
38 Rapid transcriptional autoactivation of the Candida glabrata AMT1 copper metalloregulatory transcrip
40 ere we present the structures of Atp11p from Candida glabrata and Atp12p from Paracoccus denitrifican
42 potentially fluconazole-resistant organisms (Candida glabrata and Candida krusei) to those with other
43 Is were due to Candida albicans, followed by Candida glabrata and Candida parapsilosis (15%), Candida
45 and caspofungin of 601 invasive isolates of Candida glabrata and grouped the isolates by geographic
46 ole of 559 bloodstream infection isolates of Candida glabrata and grouped the isolates by patient age
47 642 bloodstream infection (BSI) isolates of Candida glabrata and grouped the isolates by patient age
48 plies most directly to fluconazole-resistant Candida glabrata and is variable among other species of
50 between four yeast strains from two species, Candida glabrata and Saccharomyces cerevisiae (haploid s
52 da albicans, 26 of Candida tropicalis, 23 of Candida glabrata, and 27 of other yeasts, were tested by
56 icans, Candida krusei, Candida parapsilosis, Candida glabrata, and Candida tropicalis as well as othe
57 da albicans, one Histoplasma capsulatum, one Candida glabrata, and one Fusarium species isolate); thr
58 es were found in CPT for Candida tropicalis, Candida glabrata, and other common pathogenic fungi.
59 th meningoencephalitis and colitis caused by Candida glabrata, and Q295* for the patient with Candida
60 -rich region of epithelial adhesin (Epa1) of Candida glabrata, and the carboxyl region of the cell wa
61 nt forms of the Tom40 protein from the yeast Candida glabrata, and truncated constructs lacking the N
62 PS on YPD-CuSO(4) is also similar to that in Candida glabrata, and we hypothesize that this is due to
63 icans, 27 Candida tropicalis, 22 Torulopsis (Candida) glabrata, and 29 other yeast isolates were test
64 Infections with the azole-refractory yeast Candida glabrata are now commonly treated with the echin
66 r modifying genes from the pathogenic fungus Candida glabrata as well as a companion vector for compl
67 the established pathogens Candida krusei and Candida glabrata, as a species of Candida with reduced s
69 plant recipients that developed breakthrough Candida glabrata bloodstream infections while receiving
70 ne expression by diverse microbes, including Candida glabrata, Bordetella pertussis, Escherichia coli
72 recognition of an emerging fungal pathogen, Candida glabrata, by the human NK cytotoxic receptor NKp
74 xed PCR assay detecting Candida albicans and Candida glabrata (CAN-PCR) was compared with the Affirm
75 ccharomyces from each other, as well as from Candida glabrata, Candida albicans, and Blastomyces derm
76 mplemented by the Ure2p of Candida albicans, Candida glabrata, Candida kefyr, Candida maltosa, Saccha
77 ve isolates per species of Candida albicans, Candida glabrata, Candida parapsilosis, Aspergillus fumi
78 the rRNA gene to identify Candida albicans, Candida glabrata, Candida parapsilosis, Candida tropical
79 er a Candida 7-plex panel (Candida albicans, Candida glabrata, Candida tropicalis, Candida parapsilos
81 2 and pathogenic Candida albicans CaUpc2 and Candida glabrata CgUpc2 to AR1b and SRE/AR1c elements.
86 charomyces cerevisiae and the human pathogen Candida glabrata directly bind to structurally diverse d
88 mbers functionally identified as adhesins in Candida glabrata (Epa1, Epa6 and Epa7) bind to ligands c
91 e divergence of Saccharomyces cerevisiae and Candida glabrata, followed by massive gene loss that res
93 impact of the treatment of fungemias due to Candida glabrata from a hospital perspective using three
94 he presumptive identification of Torulopsis (Candida) glabrata from other common clinical isolates of
101 vival, and virulence in the pathogenic yeast Candida glabrata Here, we demonstrate PI3-kinase (CgVps3
102 npoint a single species, the fungal pathogen Candida glabrata, in which a trans mutation has occurred
105 o protect against neurological degeneration, Candida glabrata infection, and possibly to enhance reve
116 ctor from the opportunistic pathogenic yeast Candida glabrata is dependent on rapid metal-induced DNA
117 host colonization, the human fungal pathogen Candida glabrata is known to utilize a large family of h
119 rs ACE1 (Saccharomyces cerevisiae) and AMT1 (Candida glabrata) is present in the promoters of three m
120 invasive candidiasis and candidemia due to a Candida glabrata isolate that developed resistance to al
122 The antifungal susceptibilities of 79 oral Candida glabrata isolates to fluconazole and voriconazol
123 s for testing of the susceptibilities of 235 Candida glabrata isolates to fluconazole and voriconazol
124 ) and included 303 C. albicans isolates, 153 Candida glabrata isolates, 70 Candida tropicalis isolate
125 p to six missed episodes of candidemia (four Candida glabrata isolates, one C. albicans isolate, and
128 crystal structures of the Vik1 ortholog from Candida glabrata may provide insight into this mechanism
129 st isolates were Candida albicans (n = 420), Candida glabrata (n = 112), Candida parapsilosis (n = 30
130 solates included Candida albicans (n = 161), Candida glabrata (n = 41), Candida tropicalis (n = 35),
131 s identified were Candida albicans (n = 85), Candida glabrata (n = 63), and Candida parapsilosis (n =
132 solates included Candida albicans (n = 486), Candida glabrata (n = 96), Candida tropicalis (n = 51),
133 tivity of VT-1161 against Candida krusei and Candida glabrata, pathogens that are intrinsically resis
134 ated the performance of the Candida albicans/Candida glabrata peptide nucleic acid fluorescent in sit
136 albicans, heterologous expression of HYR1 in Candida glabrata rendered the organism more resistant to
137 creen assay to accurately detect isolates of Candida glabrata resistant to the azole antifungal agent
144 nservation of this quality control system in Candida glabrata suggests that many pathogenic species o
147 cer or fungemia caused by the DA nonproducer Candida glabrata than in patients with cancer or fungemi
148 ularly relevant for pathogenic fungi such as Candida glabrata that are closely related to S. cerevisi
150 identified only 102 (82%) of 124 isolates of Candida glabrata, the predictive value of an MIS identif
155 on in Saccharomyces cerevisiae, but Ure2p of Candida glabrata (Ure2(glabrata)) cannot, even though th
156 nsertional mutagenesis of the yeast pathogen Candida glabrata using the bacterial transposon Tn7.
158 e CBF1 (centromere binding factor 1) gene of Candida glabrata was cloned by functional complementatio
159 dentified throughout the reading period, but Candida glabrata was difficult to differentiate from oth
161 nsis, a yeast species genetically related to Candida glabrata, was described following its isolation
162 rtance of SUMOylation in the human pathogen, Candida glabrata We identified the enzymes involved in s
163 d decrease the cost of the identification of Candida glabrata, we evaluated four methods for the dete
164 Known concentrations of Candida albicans and Candida glabrata were each added to a set of vials.
165 a albicans and Candida tropicalis (those for Candida glabrata were unchanged) within the 4-year span.
166 olates were echinocandin-resistant, and 9 (8 Candida glabrata) were multidrug resistant to both fluco
168 relative proportion of infections caused by Candida glabrata, which has reduced susceptibility to fl
169 her-level resistance has been reported among Candida glabrata, which is also frequently resistant to
170 ous proteins in Saccharomyces cerevisiae and Candida glabrata, whose sequences have diverged to a deg
171 C), and posaconazole (PSZ) in 24 isolates of Candida glabrata with decreased susceptibility to azoles
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