ライフサイエンスコーパス: albicans

1 nized (Mycobacterium tuberculosis or Candida albicans).

2 microorganisms including Candida albicans (C.albicans).

3 enetic conversions in the fungal pathogen C. albicans.

4 facilitate efficient genetic analysis in C. albicans.

5 n the surface of the fungal pathogen Candida albicans.

6 he fluconazole-susceptible and -resistant C. albicans.

7 e first farnesol hypersensitive mutant of C. albicans.

8 l wall stress in the fungal pathogen Candida albicans.

9 maximal mucosal inflammatory response to C. albicans.

10 factor of the human fungal pathogen Candida albicans.

11 ogies is an important virulence factor of C. albicans.

12 and the opportunistic human pathogen Candida albicans.

13 sporum, Saccharomyces cerevisiae and Candida albicans.

14 sis of many fungal pathogens such as Candida albicans.

15 egulating genome stability are rewired in C. albicans.

16 del setup with a drug-resistant strain of C. albicans.

17 repeats in the human fungal pathogen Candida albicans.

18 rature stress in the fungal pathogen Candida albicans.

19 ays after intra-amniotic administration of C.albicans.

20 sponses to Aspergillus fumigatus and Candida albicans.

21 acts the macrophage-killing capability of C. albicans.

22 toxin in the opportunistic pathogen Candida albicans.

23 genes and genes involved in virulence in C. albicans.

24 ition of the clinically important fungus, C. albicans.

25 for clearance of the fungal pathogen Candida albicans.

26 ansporters are repressed in MTLa/MTLalpha C. albicans.

27 nificant effect after challenge with Candida albicans.

28 g1 orthologue in the fungal pathogen Candida albicans.

29 tures with different Candida species (28% C. albicans, 27% C. parapsilosis, 26% C. tropicalis, etc.)

30 Most CUTS cases were caused by Candida albicans (52.7%), followed by Candida glabrata (25.6%) a

31 tial for GlcNAc signalling (NGS1) in Candida albicans, a commensal and pathogenic yeast of humans.

32 alis, a Gram-positive bacterium, and Candida albicans, a fungus, occupy overlapping niches as ubiquit

33 as a potential antifungal target in Candida albicans, a major human fungal pathogen.

34 this concept from the perspective of Candida albicans, a microbial pathogen uniquely adapted to its h

35 rminal domain of Tps2 (Tps2NTD) from Candida albicans, a transition-state complex of the Tps2 C-termi

36 we found that S. mutans augmented haploid C. albicans accumulation in mixed-species biofilms.

37 rtholog in the human fungal pathogen Candida albicans also alters TOR signaling and, unexpectedly, le

38 Similarly, diploid C. albicans also showed enhanced biofilm formation in the p

39 tes of four Candida species, including 16 C. albicans and 11 C. glabrata isolates with defined FKS mu

40 hat medically relevant fungi such as Candida albicans and Aspergillus fumigatus also form biofilms du

41 C. tropicalis and C. krusei, 2 CFU/mL for C. albicans and C. glabrata, and 3 CFU/mL for C. parapsilos

42 Members of the genus Candida, such as C. albicans and C. parapsilosis, are important human pathog

43 ased the proportion of persisters in Candida albicans and Candida glabrata.

44 t the opportunistic fungal pathogens Candida albicans and Cryptococcus neoformans However, the molecu

45 udy suggests that the interaction between C. albicans and F. nucleatum leads to a mutual attenuation

46 Candida albicans and Fusobacterium nucleatum are well-studied or

47 We show that PMA, C. albicans and GBS use a related pathway for NET induction

48 lin showed moderate activity against Candida albicans and good activity against an export-deficient m

49 calcium ionophore A23187, nigericin, Candida albicans and Group B Streptococcus.

50 o characterize the transcriptomes of both C. albicans and human endothelial cells or oral epithelial

51 o perform genetic interaction analysis in C. albicans and is readily extended to other fungal pathoge

52 The opportunistic fungal pathogen Candida albicans and lactic acid bacteria (LAB) are common membe

53 luconazole-resistant clinical isolates of C. albicans and non-albicans species, and it exhibited pote

54 he secondary outcome was the rate of Candida albicans and nonalbicans strains after treatment.

55 ern (PAMP) located at the cell surface of C. albicans and other pathogenic Candida species, is modula

56 odel mucosal lung infection and show that C. albicans and P. aeruginosa are synergistically virulent.

57 In vitro, C. albicans and P. aeruginosa have a bidirectional and larg

58 ostasis (PHO) to TORC1 may differ between C. albicans and S. cerevisiae The converse direction of sig

59 C. albicans and S. oralis decreased epithelial E-cadherin l

60 We conclude that C. albicans and S. oralis synergize to activate host enzyme

61 rmans) to labeling at the bud sites (Candida albicans and Saccharomyces cerevisiae).

62 es from Saccharomyces cerevisiae and Candida albicans and show that under nitrogen-sufficient conditi

63 urrent mucocutaneous infections with Candida albicans and Staphylococcus aureus and chronic inflammat

64 annose, and Toll-like receptors with Candida albicans and Staphylococcus epidermidis was 2.5- and 2.9

65 ity to early systemic infection with Candida albicans and T cell-mediated colitis.

66 that the BET protein Bdf1 is essential in C. albicans and that mutations inactivating its two BDs res

67 The fungus Candida albicans and the bacterium Pseudomonas aeruginosa are co

68 illin-resistant S. aureus (MRSA) and Candida albicans) and standard (Pseudomonas aeruginosa 15692) pa

69 systemic infection with a lethal dose of C. albicans, and deficiency of dectin-1, dectin-2, or both

70 espiratory yeasts such as P. pastoris and C. albicans, and it may have novel moonlighting functions i

71 ty of the processes influenced by Dig1 in C. albicans, and the observation that Dig1 is one of the fe

72 rn-recognition receptors for sensing Candida albicans, and their downstream kinase SYK, thus inhibiti

73 fying host innate immune defenses against C. albicans as a communicating medium and how C. albicans o

74 ng the opportunistic fungal pathogen Candida albicans as a model, we identified a highly specific bif

75 infections, caused most commonly by Candida albicans, Aspergillus fumigatus and Cryptococcus neoform

76 evaluated the antifungal effects on Candida albicans ATCC90028, the cytotoxicity toward human dental

77 We found that zinc specifically increased C. albicans autoaggregation induced by Sap6; and that Sap6

78 s restored the biofilm-forming ability of C. albicans bcr1Delta mutant and bcr1Delta/Delta mutant, wh

79 ort small-molecule compounds that inhibit C. albicans Bdf1 with high selectivity over human BDs.

80 how the presence of S. mutans influences C. albicans biofilm development and coexistence.

81 yltransferase B (GtfB) itself can promote C. albicans biofilm development.

82 Candida albicans biofilm formation is an important virulence fac

83 lp to protect the epithelial barrier from C. albicans breach.

84 showed that mortality is a consequence of C. albicans breaching the epithelial barrier and invading s

85 C. albicans budding mother cells were found to be nonadhere

86 We find that high C. albicans burden, fungal epithelial invasion, swimbladder

87 o the nucleus of Pichia pastoris and Candida albicans but is cytoplasmic in Saccharomyces cerevisiae

88 in the Metschnikowiaceae, including Candida albicans, but became more complex in the Saccharomycetac

89 Detection of C. albicans by Dectin-1, a C-type signaling lectin specific

90 ection with microorganisms including Candida albicans (C.albicans).

91 gainst laboratory and clinical strains of C. albicans, C. glabrata and C. tropicalis were evaluated.

92 detects seven pathogenic Candida species (C. albicans, C. glabrata, C. parapsilosis, C. tropicalis, C

93 zosaccharomyces pombe (Sp-Hsp104) or Candida albicans (Ca-Hsp104) also trimmed and cured the weak var

94 The fungal pathogen Candida albicans can transition from budding to hyphal growth, w

95 itory concentration (MIC) values against non-albicans Candida and Aspergillus strains.

96 treatment favors the growth of specific non- albicans Candida species in mixed- Candida species biofi

97 l colonization and infections caused by non- albicans Candida species, including C. glabrata, C. dubl

98 Candida albicans, Candida glabrata, and Candida parapsilosis end

99 Intra-amniotic C.albicans caused intestinal colonization and invasive gro

100 Intra-amniotic C.albicans caused intestinal infection, injury and inflamm

101 Using affinity purifications from C. albicans cell extracts, we demonstrate that CaTAF12L uni

102 fine structure of beta-glucan exposed on C. albicans cell walls before and after treatment with the

103 anoscopic imaging of caspofungin-unmasked C. albicans cell walls revealed that the increase in glucan

104 de influx assay demonstrated the lysis of C. albicans cells by carvacrol and its 2,3-unsaturated 1-O-

105 ediate the engulfment and phagocytosis of C. albicans cells by human immune cells in biologically rel

106 with PMMA microspheres and probed against C. albicans cells immobilized onto biopolymer-coated substr

107 arch was to evaluate the adhesion of Candida albicans cells onto PMMA surfaces by employing an atomic

108 Here we report that C. albicans cells switch between two heritable cell types,

109 mophila, Streptococcus pneumonia and Candida albicans cleaved the N-terminus of immunoglobulins.

110 We have shown that C. albicans co-opts amino acid catabolism to generate and e

111 ing innate immune mechanisms, may promote C. albicans colonization and likely subsequent sensitizatio

112 c chitinase deficiency was associated with C albicans colonization in patients with CF.

113 le treatment in utero decreased intestinal C.albicans colonization, mucosal injury but failed to atte

114 anced chitinase activation associated with C albicans colonization.

115 The fungal pathogen Candida albicans colonizes basically all human epithelial surfac

116 d in patients with CF colonized with Candida albicans compared with that in noncolonized patients.

117 aginal epithelium, and to the fungus Candida albicans Complementary crystallographic and biophysical

118 ctron microscopy (SEM) and AFM imaging of C. albicans confirmed the polymorphic behavior of both stra

119 g to beta-1,3 glucan-, A. fumigatus-, and C. albicans-containing phagosomes.

120 a bacterial exoenzyme (GtfB) augments the C. albicans counterpart in mixed-species biofilms through a

121 The fungal pathogens Candida albicans, Cryptococcus neoformans, and Aspergillus fumig

122 , and inhibition of enzymatic activity of C. albicans CYP51 by clinical antifungal drugs that are use

123 We determined the X-ray structures of C. albicans CYP51 complexes with posaconazole and VT-1161,

124 Thus in C. albicans, differential chromatin states controls gene ex

125 sion of HWP1, ALS1, and ALS3 genes in the C. albicans diploid wild-type SC5314 and bcr1Delta/Delta, l

126 We propose a homeostatic model where C. albicans disease pressure is balanced by neutrophil-medi

127 ll effector responses against E. coli and C. albicans displayed differential MR1 dependency and TCR b

128 sponses against Escherichia coli and Candida albicans displayed microbe-specific polyfunctional respo

129 Infection with Candida albicans, disseminated disease, pneumonia, and cardiovas

130 Altogether, we show that C. albicans-driven neutralization of the phagosome promotes

131 ssing SUR7 These results demonstrate that C. albicans eisosomes promote the ability of Sur7 to regula

132 gly, even though loss of Dig1 function in C. albicans enhances filamentous growth and biofilm formati

133 The presence of C. albicans enhances S. mutans growth within biofilms, yet

134 to host cells in the fungal pathogen Candida albicans Eukaryotic Target of Rapamycin complex 1 (TORC1

135 Candida albicans excretes E,E-farnesol as a virulence factor and

136 The data suggest that C. albicans exploits environmentally contingent regulatory

137 In C. albicans, exposure to GlcNAc activates cell signalling a

138 we reported that the fungal pathogen Candida albicans expresses a novel copper-only SOD, known as SOD

139 asma membrane of the fungal pathogen Candida albicans forms a protective barrier that also mediates m

140 of the opportunistic fungal pathogen Candida albicans from budding to hyphal growth has been implicat

141 >3)-beta-D-glucan levels and clearance of C. albicans from liver, spleen, kidney, brain, lung, vitreo

142 he creation of systematic identifiers for C. albicans genes and sequence features using a system simi

143 Deletion of C. albicans genes that control zinc acquisition in the ZAP1

144 ome-level, phased diploid assembly of the C. albicans genome, coupled with improvements that we have

145 the two TAF12 variants in the unicellular C. albicans genome.

146 iva contains various proteins that affect C. albicans growth positively by promoting mucosal adherenc

147 ty of peach DMSO extracts to inhibit Candida albicans growth was more pronounced, especially, in the

148 TAF12, but not CaTAF12L, is essential for C. albicans growth.

149 Using mating-competent C. albicans haploids, each carrying a different gene drive

150 portunistic fungal pathogens such as Candida albicans has increased.

151 and opportunistic pathogens such as Candida albicans have evolved complex circuitry to sense and res

152 The secreted aspartyl proteinases of Candida albicans have long been implicated in virulence at the m

153 s in the oral cavity, while TM7x and Candida albicans have served as crucial paradigms for CPR specie

154 Saccharomyces cerevisiae and C. albicans have transporters for farnesylated peptides, li

155 d genome-wide RNA sequencing reveals that C. albicans heterochromatin represses expression of repeat-

156 Consequently, heat shock increases C. albicans host cell adhesion, damage and virulence.

157 response to either fungal beta-glucan or C. albicans hyphae and fibronectin, with VLA3 inducing homo

158 n response to fungal beta-glucan and Candida albicans hyphae when presented with extracellular matrix

159 r to immobilized fungal beta-glucan or to C. albicans hyphae without ECM.

160 Moreover, C. albicans hyphal growth factor HWP1 as well as ALS1 and A

161 most commonly isolated pathogen was Candida albicans in 20% of the patients.

162 ain the mutualistic role of S. mutans and C. albicans in cariogenic biofilms.

163 hat S. mutans is often detected with Candida albicans in early childhood caries.

164 mphotericin B after inoculation with Candida albicans in light-exposed and light-protected conditions

165 e recently observed sensitization to Candida albicans in patients with EoE is owing to pre-existing d

166 is known about defense mechanisms against C. albicans in subepithelial layers such as the dermis.

167 e most common human fungal pathogen: Candida albicans In this organism, the histone deacetylase Sir2,

168 both mouse and human cells infected with C. albicans, indicating that JNK1 may be a therapeutic targ

169 InC. albicans-infected cPLA2alpha(+/+)macrophages, COX-2 expr

170 InC. albicans-infected cPLA2alpha(-/-)or COX-1(-/-)macrophage

171 ce of IL-17-controlled gene expression in C. albicans-infected human oral epithelial cells (OECs) and

172 albicans-infected macrophages plays a dual role by promo

173 In Candida albicans-infected resident peritoneal macrophages, activ

174 ated by cAMP/PKA because it was similar inC. albicans-infected wild type and cPLA2alpha(-/-)or COX-1(

175 erlying mechanisms by which intra-amniotic C.albicans infection adversely affects the fetal gut remai

176 ortantly, impeding development of mucosal C. albicans infection by administering antifungal fluconazo

177 Finally, we demonstrate that systemic C. albicans infection contributes to a reduction in the tot

178 ng host susceptibilities for the sites of C. albicans infection have revealed tissue compartmentaliza

179 that are required for PMN activity during C. albicans infection in a situation similar to in vivo, we

180 Candida albicans infection produces elongated hyphae resistant t

181 refore, we assessed whether intra-amniotic C.albicans infection would cause intestinal inflammation a

182 ild-type control mice in response to Candida albicans infection, and the expression of JNK1 in hemato

183 here on human and mouse skin as a site of C. albicans infection, and we review established and newly

184 that MDSCs are protective during invasive C. albicans infection, but not A. fumigatus infection.

185 ers of miRNAs in countering systemic Candida albicans infection.

186 n vivo protects mice from lethal systemic C. albicans infection.

187 verse intestinal outcome of intra-amniotic C.albicans infection.

188 Remarkably, C. albicans infections can fit into all six DRF classificat

189 oral cavity is a unique niche where Candida albicans infections occur in immunocompetent as well as

190 lacement therapy predispose women to Candida albicans infections.

191 mug/mL; the remaining 2 vials received no C albicans inoculation and no antifungal supplementation (

192 we demonstrated that S. oralis augmented C. albicans invasion through epithelial junctions.

193 of cell types for skin protection against C. albicans invasion.

194 covers a mechanism of azole resistance in C. albicans, involving increased membrane rigidity and TOR

195 underscore select oral diseases in which C. albicans is a contributory microorganism in immune-compe

196 Candida albicans is a dimorphic commensal fungus that colonizes

197 Candida albicans is a ubiquitous mucosal commensal that is norma

198 sponse, and yet the commensal fungus Candida albicans is able to colonize immuno competent individual

199 C. albicans is able to induce mucosal defenses through acti

200 C. albicans is also a predominantly opportunistic fungal pa

201 Candida albicans is among the most common human fungal pathogens

202 Candida albicans is an opportunistic fungal pathogen colonizing

203 Candida albicans is an opportunistic human fungal pathogen that

204 Candida albicans is an opportunistic pathogen, typically found a

205 The cell wall of Candida albicans is composed largely of polysaccharides.

206 mammalian host, the pathogenic yeast Candida albicans is exposed to a range of stresses such as super

207 Candida albicans is frequently detected with heavy infection of

208 The Hog1 SAPK in Candida albicans is robustly phosphorylated in response to a num

209 The cell wall of C. albicans is the interface between the fungus and the inn

210 Candida albicans is the leading cause of fungal infections; yet,

211 Although Candida albicans is the predominant organism found in patients w

212 Candida albicans is the single most prevalent cause of fungal bl

213 y of the clinically important yeast, Candida albicans, is dependent on robust responses to host-impos

214 In contrast, C. albicans isolates could be correctly identified as susce

215 -deficient GM-BM treated with heat-killed C. albicans, live C. albicans, or the specific Dectin-1 ago

216 rend, in mixed- Candida species biofilms, C. albicans lost dominance in the presence of antifungals.

217 We show that C. albicans may evade immune detection by presenting a movi

218 itated and immunocompromised individuals, C. albicans may spread to cause life-threatening systemic i

219 Finally, we demonstrate that, in C. albicans, mechanisms regulating genome stability are pla

220 ic aggregation and NETosis in response to C. albicans mediated by the beta2 integrin, complement rece

221 ed mucosal injury but failed to ameliorate C.albicans-mediated mucosal inflammation emphasizing the n

222 eded to observe a full metabolic cycle in C. albicans, metabolic profiling provides an avenue for rap

223 Notably, experiments against Candida albicans mutants lacking those genes showed resistance t

224 ncodes a functional homologue of the Candida albicans N-acetylglucosamine (GlcNAc) transporter NGT1,

225 r (renamed CDR6/ROA1 for consistency with C. albicans nomenclature) could efflux xenobiotics such as

226 y of these cells to kill/phagocytose Candida albicans or Escherichia coli cells both ex vivo and in v

227 nd protected the eye from pathogenic Candida albicans or Pseudomonas aeruginosa infection.

228 ned by mono-colonization with either Candida albicans or Saccharomyces cerevisiae.

229 injections with 10(7) colony-forming units C.albicans or saline at 3 or 5 days before preterm deliver

230 tended to other systems such as e.g. Candida albicans, or selected plant cells.

231 reated with heat-killed C. albicans, live C. albicans, or the specific Dectin-1 agonists curdlan or w

232 ch the loss of an ABC transporter in Candida albicans, orf19.4531 (previously named ROA1), increases

233 lbicans as a communicating medium and how C. albicans overgrowth in the oral cavity may be a result o

234 Together, these observations suggest that C. albicans-P. aeruginosa cross talk in vivo can benefit bo

235 morbidity is associated with exacerbated C. albicans pathogenesis and elevated inflammation.

236 artmentalization of Th cell responses and C. albicans pathogenesis and have critical implications for

237 -deficient DeltalasR mutant also enhances C. albicans pathogenicity in coinfection and induces extrus

238 ntact with serum and at body temperature, C. albicans performs a regulated switch to filamentous morp

239 Trafficking of TLR9 to A. fumigatus and C. albicans phagosomes requires Dectin-1 recognition.

240 phagocytic defenses, we also report that C. albicans pho4Delta cells are acutely sensitive to macrop

241 Although the C. albicans presence has been shown to enhance bacterial ac

242 Furthermore, the yeast form of C. albicans repressed F. nucleatum-induced MCP-1 and TNFalp

243 side, found in Saccharopolyspora and Candida albicans, respectively, induced the activation of iNKT c

244 Thus, we describe a mechanism by which C. albicans responds to temperature via Hsf1 and Hsp90 to o

245 g of individual host cell populations and C. albicans revealed that dermal invasion is directly imped

246 unknown components of TORC1 signaling in C. albicans revealed that the phosphate transporter Pho84 i

247 C. albicans sap6 deletion mutants failed to accumulate intr

248 C. albicans secreted aspartic protease Sap6 is important fo

249 anisms underlie the stress sensitivity of C. albicans sfp1 cells during growth on glucose, and rtg3 c

250 sphorylation-mimicking Mep2 variants from C. albicans show large conformational changes in a conserve

251 Contrary to any other systems analysed, C. albicans Sir2 is largely dispensable for repressing reco

252 hibits growth and hyphal morphogenesis of C. albicans SN152 in a contact-dependent manner.

253 F. nucleatum ATCC 23726 coaggregates with C. albicans SN152, a process mainly mediated by fusobacteri

254 Despite these abnormalities, C. albicans SOD5 can disproportionate superoxide at rates l

255 ant clinical isolates of C. albicans and non-albicans species, and it exhibited potent, dose-dependen

256 y on immune stimulation, including a Candida albicans-specific master regulator at the CR1 locus.

257 rdingly, we found that a hyperfilamentous C. albicans strain breaches the epithelial barrier more fre

258 C. albicans strains lacking this toxin do not activate or d

259 C. albicans strains were constructed in which Hog1 was eith

260 that allows multiplexed detection of Candida albicans, Streptococcus agalactiae and Chlamydia trachom

261 ource or temperature, are known to affect C. albicans stress adaptation.

262 of Candida hyphal morphogenesis promotes C. albicans survival and negatively impacts the macrophage-

263 ance of metabolic adaptation in promoting C. albicans survival in the host.

264 ls and were more frequently sensitized to C. albicans than controls.

265 s forms robust mucosal biofilms with Candida albicans that have increased pathogenic potential.

266 nM are completely resistant to killing by C. albicans The peptide also protects macrophages and augme

267 isingly, we found that the genome of Candida albicans, the predominant human fungal pathogen, contain

268 filamentation, a key virulence feature of C. albicans, through the production of lactic acid and othe

269 technique to characterize the adhesion of C. albicans to acrylic surfaces.

270 An evolutionary pressure for C. albicans to become diploid could derive from its use of

271 try that enables the fungal pathogen Candida albicans to couple cell cycle dynamics with responses to

272 This cell type-specific response of C. albicans to different environmental conditions reflects

273 Binding of C. albicans to EphA2 on oral epithelial cells activates sig

274 scopy results showed that the adhesion of C. albicans to PMMA is morphology dependent, as hyphal tube

275 g-lasting antifungal effects against Candida albicans to the PMMA resin, and it has low toxicity towa

276 actor Pho4 is vital for the resistance of C. albicans to these diverse stresses.

277 We discover that the C. albicans transcription factor Cas5 is crucial for proper

278 The fungal pathogen Candida albicans undergoes morphogenetic switching from the yeas

279 in S. cerevisiae was genetically shown in C. albicans using conditional TOR1 alleles.

280 riptome analysis of treated and untreated C. albicans using Gene Ontology (GO) revealed a large clust

281 ence quantitative analysis in response to C. albicans vaginal infection in the presence of hormones.O

282 to lactate induces beta-glucan masking in C. albicans via a signalling pathway that has recruited an

283 ofound effects, EntV(68) has no effect on C. albicans viability, even in the presence of significant

284 cts of a Bdf1 BD-inactivating mutation on C. albicans viability.

285 ssary and sufficient for the reduction of C. albicans virulence and biofilm formation through the inh

286 ear accumulation of Hog1 had no impact on C. albicans virulence in two distinct models of systemic in

287 model of KD (induced by a cell wall Candida albicans water-soluble fraction [CAWS]), we identify an

288 rlies the epigenetic control of mating in C. albicans We also discuss how fitness advantages could ha

289 ewly established haploid biofilm model of C. albicans, we found that S. mutans augmented haploid C. a

290 the minimal MT nucleation system of Candida albicans, we reconstituted the interactions of Mzt1, gam

291 boratory strain and a clinical isolate of C. albicans were used for SCFS experiments.

292 herichia coli) bacteria and a fungi (Candida albicans) were examined; which showed good antibacterial

293 In the human pathogen Candida albicans (which last shared a common ancestor with S. ce

294 he contribution of each factor to mating, C. albicans white cells were reverse-engineered to express

295 tic states, "white" and "opaque." In Candida albicans, white cells are essentially sterile, whereas o

296 ain of Trl1 from the fungal pathogen Candida albicans with GDP and Mg2+ in the active site.

297 ted good antifungal activity against Candida albicans with MIC of 15.6mug/mL.

298 The interaction of Candida albicans with the innate immune system is the key determ

299 y resistant to systemic infection by Candida albicans, with resistance characterized by enhanced surv

300 Most surface-accessible glucan on C. albicans yeast and hyphae is limited to isolated Dectin-