ライフサイエンスコーパス: albicans

1 h heat-inactivated and viable fungi (Candida albicans).

2 ted with drug-sensitive or MDR strains of C. albicans.

3 rophytes, Aspergillus fumigatus, and Candida albicans.

4 species identified in all groups was Candida albicans.

5 of evolutionary new centromeres (ENCs) in C. albicans.

6 ent cellular systems stimulated with Candida albicans.

7 ntifungal activity against drug-resistant C. albicans.

8 itment during invasion of the CNS by Candida albicans.

9 including the human fungal pathogen, Candida albicans.

10 in a leading human fungal pathogen, Candida albicans.

11 integration into a neutral locus in Candida albicans.

12 e most common human fungal pathogen, Candida albicans.

13 nhances the growth and GI colonization of C. albicans.

14 th, morphogenesis, and GI colonization of C. albicans.

15 ns that physically interact with Cdc14 in C. albicans.

16 ctin-1 signaling machinery in response to C. albicans.

17 ilic adhesion in the fungal pathogen Candida albicans.

18 lethal dose of the pathogenic fungus Candida albicans.

19 al activity against all four fungi except C. albicans.

20 morphogenesis - a key virulence factor of C. albicans.

21 nificant effect after challenge with Candida albicans.

22 facilitate efficient genetic analysis in C. albicans.

23 for clearance of the fungal pathogen Candida albicans.

24 of the role of CaWss1 in DPC tolerance in C. albicans.

25 ndritic cells (moDCs) that presented Candida albicans.

26 didiasis, C. auris was less virulent than C. albicans.

27 o dissect complex genetic interactions in C. albicans, a CRISPR-Cas9-based Gene Drive Array (GDA) was

28 CTG clade of ascomycetes, including Candida albicans, a human pathogen.

29 Candida albicans, a major opportunistic fungal pathogen, is freq

30 A simple example is found in Candida albicans, a member of the human microbiota and also the

31 Candida albicans, a ubiquitous commensal fungus that colonizes h

32 Candida albicans-a yeast-like fungus that inhabits mucosal surfa

33 i-rAls3p-N antibodies that interfere with C. albicans ability to adhere to and invade endothelial cel

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

35 We then investigated C. albicans actions on platelet activation, granule release

36 on epithelial tissue, facilitated by the C. albicans adhesin encoded by ALS3 While a bacterium-fungu

37 pared with polyclonal stimulation or Candida albicans Ag exposure.

38 the Ca37 monoclonal antibody against the C. albicans alcohol dehydrogenase (Adh) 1.

39 C. albicans also expresses a Cu-only SOD4 that is highly si

40 cells subsets and potentially conferring C. albicans, an advantage in overcoming DC-mediated immunit

41 se homologue Esp1p in the ascomycete Candida albicans, an important pathogen of humans, is essential

42 We discovered that the ancestor of C. albicans and 2 related pathogens evolved a variant of hi

43 Overall, our results demonstrate that C. albicans and A. fumigatus induce PANoptosis and that ZBP

44 Here, we report that C. albicans and A. fumigatus infection induced inflammatory

45 s associated with genetic manipulation in C. albicans and advances researchers' ability to perform ge

46 Candida albicans and Aspergillus fumigatus are dangerous fungal

47 ngicidal activity, reducing the burden of C. albicans and C. auris below the limit of detection withi

48 ducing the metabolic activity of adherent C. albicans and C. auris biofilms by more than 66% and 50%,

49 ost potent molecule, inhibiting growth of C. albicans and C. auris strains at concentrations ranging

50 the isolation of Candida species, namely C. albicans and C. auris, exhibiting resistance to current

51 habditis elegans infected with strains of C. albicans and C. auris, relative to the untreated control

52 translocations in the common ancestor of C. albicans and C. tropicalis.

53 Candida albicans and Candida glabrata are the 2 most prevalent C

54 table homotetramers, the mtSSBs from Candida albicans and Candida parapsilosis formed stable homodime

55 We find that both C. albicans and candidalysin activate human epithelial EGFR

56 e expectations set by baseline methods in C. albicans and D. melanogaster, it leaves considerable roo

57 Aspergillus fumigatus, Candida albicans and Mycosphaerella tassiana had the highest rel

58 t species-level as well as of six additional albicans and non-albicans pathogenic Candida at genus le

59 e of multidrug resistant (MDR) strains of C. albicans and other Candida spp., highlighting the urgent

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

61 l whole-genome mutation screening in Candida albicans and Pseudomonas aureginosa genomes, which provi

62 e response that augmented host defense to C. albicans and S. aureus.

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

64 ic and glucan-dependent synergism between C. albicans and S. mutans contribute to enhanced pathogenes

65 d demonstrated that coinfection with Candida albicans and Staphylococcus aureus (C. albicans/S. aureu

66 The fungus Candida albicans and the Gram-positive bacterium S. aureus can f

67 CaTOK (Candida albicans) and CnTOK (Cryptococcus neoformans neoformans)

68 ses against Clostridium perfringens, Candida albicans, and Bacteroides vulgatus were also coupled wit

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

70 in highly azole-resistant strains of Candida albicans, another human fungal pathogen, increasing thei

71 Bloodborne infections with Candida albicans are an increasingly recognized complication of

72 ood caries, Streptococcus mutans and Candida albicans are often co-isolated from carious lesions and

73 H3VCTG null (hht1/hht1) cells of C. albicans are viable but produce more robust biofilms tha

74 hich may explain evolutionary benefits of C. albicans as a commensal microbe.

75 82 knockout mice were more susceptible to C. albicans as compared with wild-type mice.

76 opportunistic human fungal pathogen Candida albicans Aside from its primary function of blocking the

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

78 t S. parasanguinis disrupts S. mutans and C. albicans biofilm synergy in a contact and H(2)O(2)-indep

79 rains, and was active against established C. albicans biofilms in vitro.

80 C cells and inhibition and eradication of C. albicans biofilms.

81 iofilm initiation compared to S. gordonii-C. albicans biofilms.

82 l antibody proved to be effective against C. albicans, both in vitro and in vivo, and to act together

83 nger cytokine response compared with Candida albicans, but a lower macrophage lysis capacity.

84 at modulation of the Th1 response against C. albicans by platelets is dependent on PGs.

85 cificity of detection of Candida species (C. albicans, C. auris, C. dubliniensis, C. famata, C. glabr

86 E), Pseudomonas aeruginosa (PA), and Candida albicans (CA)].

87 Additionally, C. albicans can also exert inhibitory effects on platelet a

88 Candida albicans can cause systemic infection in immunocompromis

89 rum synergistic interactions against Candida albicans, Candida auris, Cryptococcus neoformans, and As

90 nized by pathobiont microbes such as Candida albicans, capable of invasive disseminated infection.

91 mechanism mediated by GtfB that enhances C. albicans carbohydrate utilization.

92 Healthy women, asymptomatic C. albicans carriers, and symptomatic patients with vaginal

93 ntified Wss1 (weak suppressor of Smt3) in C. albicans (CaWss1) using bioinformatics, genetic compleme

94 These results indicate that C. albicans CCL represents a 'parameiosis' that blurs the c

95 in live cells, as well as its function in C. albicans cell fate determination.

96 forces are dramatically enhanced when the C. albicans cell surface is locally coated with extracellul

97 iron changes the composition of all major C. albicans cell wall components.

98 show that intravenous injection of 25,000 C. albicans cells causes a highly localized cerebritis mark

99 enhanced antifungal resistance, high iron C. albicans cells had reduced survival upon phagocytosis by

100 data showed that Ca37 was able to detect C. albicans cells, and it bound to Adh1 in yeast and Adh2 i

101 regulates cell differentiation in diploid C. albicans cells, as EFG1 hemizygous cells undergo a pheno

102 o trigger genome instability in polyploid C. albicans cells.

103 o extended to a lethal intravenous (i.v.) C. albicans challenge but had no effect in the C. albicans

104 markedly increased susceptibility to Candida albicans challenge.

105 Of note, pathogenic and drug-resistant C. albicans clones were similarly sensitive to 5-FUrd, and

106 In the human fungal pathogen Candida albicans, CNV and LOH confer increased virulence and ant

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

108 e novel formulation for the prevention of C. albicans colonization on denture material and developmen

109 provide insights into the determinants of C. albicans commensal fitness within the mammalian gut.

110 of effector cytokines in response to Candida albicans, compared to CD69(-) T cells.

111 d Dectin-1 on the plasma membrane of Candida albicans-containing phagosomes independent of phagocytic

112 al pathogens (Aspergillus fumigatus, Candida albicans, Cryptococcus neoformans and Coccidioides immit

113 In C. albicans cultures, SOD4 and SOD5 were predominantly cell

114 Mice infected with C. albicans display mild memory impairment that resolves wi

115 gle infected macrophages and phagocytosed C. albicans displayed a tightly coordinated shift in gene e

116 The fungal pathogen Candida albicans displays striking genome dynamics during its pa

117 to placebo, NDV-3A vaccination inhibited C. albicans dissemination to kidneys and prevented coloniza

118 While C. albicans does not appear to affect alpha or dense granul

119 However, commensal C. albicans does not protect against intracellular influenz

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

121 We show that intestinal colonization with C. albicans drives systemic expansion of fungal-specific Th

122 ance mechanisms including upregulation of C. albicans drug-efflux, regulation of oxidative stress res

123 favor S. mutans binding interactions with C. albicans during cariogenic biofilm development.

124 ndida species (C. glabrata, C. auris, and C. albicans efg1Delta/Delta cph1Delta/Delta) and Saccharomy

125 me of the meiosis-defective pathogen Candida albicans encodes an Rme1 homolog that is part of a trans

126 uctose that can be readily metabolized by C. albicans, enhancing growth and acid production.

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

128 to affect alpha or dense granule release, C. albicans exerts a significant attenuation of platelet ag

129 obial biofilms containing the fungus Candida albicans exist.

130 ane integrity as the fungal pathogen Candida albicans expands.

131 Our data reveal that C. albicans exploits a diverse range of specific host signa

132 , we reveal that the fungal pathogen Candida albicans exploits diverse host-associated signals to pro

133 ytosis and proinflammatory response after C. albicans exposure that declined during later time points

134 The opportunistic fungal pathogen Candida albicans expresses three copper-only SODs, and deletion

135 C. albicans faces both low and high zinc bottlenecks in viv

136 Despite a lack of activity against Candida albicans for these early de novo analogs, the synthetic

137 Centromeres of Candida albicans form on unique and different DNA sequences but

138 The high genetic diversity of C. albicans from old oaks shows that they can live in this

139 and single macrophage cells infected with C. albicans from uninfected cells and assessed transcriptio

140 cies of Candida (Cornus glabrata and Candida albicans) from Candida-spiked blood samples.

141 CNS-localized C. albicans further activate the transcription factor NF-ka

142 sed quantitative proteomics revealed that C. albicans genes and proteins associated with carbohydrate

143 Other C. albicans genes and proteins directly and indirectly rela

144 C. albicans grows both as single yeast cells and hyphal fil

145 . albicans PSD mitochondrial activity and C. albicans growth, with an MIC(50) of 22.5 and 15 mug/ml w

146 n efficient transformation protocol using C. albicans haploids, and an optimized mating strategy to g

147 Fungal pathogen Candida albicans has a complex cell wall consisting of an outer

148 During infections, C. albicans has to cope with genotoxic stresses generated b

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

150 om the opportunistic fungal pathogen Candida albicans have revealed that the active-site structure an

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

152 However, competitive infections of C. albicans homozygous gene disruption mutants revealed an

153 cytolytic peptide toxin secreted by Candida albicans hyphae and has significantly advanced our under

154 is study, we show that highly immunogenic C. albicans hyphae attract phagocytic cells, which rapidly

155 s group) has been shown to bind avidly to C. albicans hyphae via direct cell-to-cell interaction, whi

156 TNF-alpha production in response to C. albicans hyphae was significantly higher in patients tha

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

158 ucosa caused by the commensal fungus Candida albicans IL-17R signaling is essential to prevent OPC in

159 ponsive to tonic stimulation by commensal C. albicans improves host defense against extracellular pat

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

161 hat CaTMPK is essential for the growth of C. albicans In conclusion, these findings not only identifi

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

163 strains from oak are similar to clinical C. albicans in that they are predominantly diploid and can

164 aluated against the pathogenic yeast Candida albicans in the absence or presence of exogenous ethanol

165 ether, we identified key pathways used by C. albicans in the mixed biofilm, indicating an active fung

166 es between S. mutans (or S. gordonii) and C. albicans in the presence and absence of in situ glucans

167 MCs were stimulated with heat-killed (HK) C. albicans in the presence or absence of isolated washed p

168 us mutans, Streptococcus oralis, and Candida albicans in the saliva from mothers and their infants, c

169 ngicidal against clinical isolates of MDR C. albicans in vitro.

170 m tube, hyphae and biofilm development of C. albicans in vitro.

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

172 Pseudomonas aeruginosa and a yeast, Candida albicans, induce the resistance of the latter to a widel

173 Furthermore, patient C. albicans-induced cytokine production was influenced by t

174 ar cells, these molecules suppressed Candida albicans-induced production of the cancer-promoting cyto

175 n, the antibody prolonged the survival of C. albicans infected-Galleria mellonella larvae, when C. al

176 dnTCF4 mice were more susceptible to Candida albicans infection and more sensitive to 5-fluorouracil-

177 in enhanced defense against systemic Candida albicans infection and prolonged host survival.

178 cefoperazone-treated mice susceptible to C. albicans infection had significantly decreased levels of

179 Candida albicans infection produces elongated hyphae resistant t

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

181 Upon C. albicans infection, Gsr(-/-) mice exhibited dramatically

182 During Candida albicans infection, mice lacking TAGAP mount defective i

183 Candidalysin is critical for mucosal C albicans infections and is known to activate epithelial

184 As the majority of systemic C. albicans infections stem from endogenous gastrointestina

185 ve potential utility as drug for managing C. albicans infections.

186 gal virulence during disseminated systemic C albicans infections.

187 tential drug target for the management of C. albicans infections.

188 s imperative that we investigate how Candida albicans interacts with blood components.

189 ls, which synergistically protect against C. albicans invasive infection.

190 Candida albicans is a commensal fungus of human gastrointestinal

191 Candida albicans is a commensal fungus of the human gut, but als

192 Candida albicans is a commensal yeast able to cause life threate

193 Candida albicans is a fungal pathobiont, able to cause epithelia

194 Candida albicans is a gut commensal and opportunistic pathogen.

195 Candida albicans is a leading cause of systemic bloodstream infe

196 Candida albicans is a pervasive commensal fungus that is the mos

197 tudy shows that the commensal fungus Candida albicans is an inducer of differentiation of human CD4(+

198 Candida albicans is an opportunistic yeast that can cause life-t

199 ed that the toxicity of the releasates on C. albicans is concentration dependent.

200 The human pathogen Candida albicans is considered an obligate commensal of animals,

201 Candida albicans is known to form polymicrobial biofilms with va

202 ositol-1-P-(O -> 1)-phytoceramide of Candida albicans is reported.

203 Candida albicans is the fourth most common cause of systemic nos

204 The yeast Candida albicans is the most prevalent opportunistic fungal path

205 plement of the human fungal pathogen Candida albicans is unusually unstable, suggesting that the proc

206 ngi, including filamentous fungi and Candida albicans, is associated with poor lung function in adult

207 Drug resistance among C. albicans isolates poses a common challenge, and overcomi

208 CytoD was able to abrogate C. albicans killing.

209 However, C. albicans lacks a sequence homologue of securins found in

210 We show here that C. albicans Mac1p is essential for virulence in a mouse mod

211 development and GtfB-mediated binding to C. albicans mannan.

212 In the human fungal pathogen Candida albicans, mating of diploid cells generates tetraploid p

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

214 ced from Escherichia coli membranes, Candida albicans mitochondria, or HeLa cell mitochondria.

215 lyses to study a possible role of Rme1 in C. albicans morphogenesis.

216 Staphylococcus aureus ATCC 43300 and Candida albicans MTCC 227.

217 tivalent recombinant protein against Candida albicans (mvPC).

218 further evaluated against 18 isolates of C. albicans (n = 9), C. glabrata (n = 4), and C. auris (n =

219 tant differences with human NatA and Candida albicans NatB, resolves key hNatB protein determinants f

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

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

222 y been identified as Cdc14 interactors in C. albicans or S. cerevisiae.

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

224 in the opportunistic fungal pathogen Candida albicans Our results suggest that HHK3 regulates fungal

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

226 s well as of six additional albicans and non-albicans pathogenic Candida at genus level.

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

228 telets in antifungal host defense against C. albicans PBMCs were stimulated with heat-killed (HK) C.

229 were identified as inhibiting both native C. albicans PSD mitochondrial activity and C. albicans grow

230 ontains a recombinant version of the Candida albicans rAls3 N-terminus protein (rAls3p-N) in aluminum

231 es of invasive mycotic disease, with Candida albicans reigning as the leading cause of invasive candi

232 e development of novel methods to prevent C. albicans-related mortality.

233 act of this cross-kingdom relationship on C. albicans remains largely uncharacterized.

234 Protection conferred by commensal C. albicans requires persistent fungal colonization and ext

235 ng affinity of S. mutans to glucan-coated C. albicans resulted in a larger structure during early bio

236 ISPR-mediated deletion of this Ca-loop in C. albicans revealed that the Ca-loop is critical for funga

237 lity, and rechallenge of mice with lethal C. albicans/S. aureus conferred >90% protection up to 60 da

238 days, and also following multiple lethal C. albicans/S. aureus rechallenges.

239 ndida albicans and Staphylococcus aureus (C. albicans/S. aureus) results in 80 to 90% mortality in 48

240 Candida albicans scavenges environmental zinc via two pathways.

241 isease affecting women; however, how Candida albicans shift from commensalism towards a pathogenic st

242 Phagocytosed C. albicans shifted expression programs to survive the nutr

243 ysical, and cell biological properties of C. albicans SOD4 and SOD5.

244 hione zinc (PZ), that effectively inhibit C. albicans SOD5 but not mammalian Cu,Zn-SOD1.

245 e found that unlike mammalian Cu,Zn-SOD1, C. albicans SOD5 indeed rapidly loses its copper to metal c

246 Moreover, upon C. albicans stimulation, Gsr (-/-) macrophages produced inc

247 C. albicans strains from oak are similar to clinical C. alb

248 ores of fluconazole/caspofungin resistant C. albicans strains, and was active against established C.

249 lable annotated reference sequences of 22 C. albicans strains, thus offering a higher coverage and gr

250 lysin-producing and candidalysin-deficient C albicans strains, we show that candidalysin activates mi

251 In Candida albicans, stress triggers adaptive chromosome destabiliz

252 how that S. gordonii binding force to the C. albicans surface is significantly higher than that ofS.

253 hrombin, we saw a significant decrease in C. albicans survival.

254 pact of S. parasanguinis on S. mutans and C. albicans synergy.

255 Here, we reveal that C. albicans tetraploid cells are metabolically hyperactive

256 underlies a key phenotypic transition in C. albicans that enables adaptation to host niches.

257 genome sequence data for three strains of C. albicans that we isolated from oak trees in an ancient w

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

259 th the opportunistic fungal pathogen Candida albicans, the Cu-sensing transcription factor Mac1p gove

260 irulence of pathogenic fungi such as Candida albicans, the underlying mechanisms have remained largel

261 pulation of macrophages encountering Candida albicans, there are distinct host-pathogen trajectories;

262 ways that alter cell wall architecture in C. albicans, thereby affecting its survival upon exposure t

263 culating Cryptococcus neoformans and Candida albicans, thereby reducing fungal dissemination to targe

264 d less IFN-gamma upon stimulation with HK C. albicans This effect was dependent on the direct contact

265 rst time that platelets can directly kill C. albicans through release of their granular contents.

266 mino acids 106-123, namely the Ca-loop of C. albicans TMPK (CaTMPK), contributes to the hyperactivity

267 of the fungal opportunistic pathogen Candida albicans to adhere to denture material and invade palata

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

269 These changes increased the resistance of C. albicans to cell wall-perturbing antifungals.

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

271 ose that it represents a strategy used by C. albicans to efficiently colonize different niches of its

272 stimulated with bacterial toxins or Candida albicans to induce NETosis.

273 or a DPC repair pathway is essential for C. albicans to maintain genomic stability and survive in th

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

275 rary to sensitize an azole-resistant Candida albicans to the effect of fluconazole.

276 solates of the human fungal pathogen Candida albicans (Todd et al., 2019).

277 In the opportunistic fungal pathogen Candida albicans, transcriptional regulatory networks regulate e

278 essed by Cryptococcus neoformans and Candida albicans, two pathogenic fungi of major clinical importa

279 or CRISPR-Cas9-based manipulation in Candida albicans using a modified gene-drive-based strategy that

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

281 For the fungal pathogen Candida albicans, utilization of amino acids has been shown to b

282 Candida albicans utilizes chromosome missegregation to acquire t

283 bicans challenge but had no effect in the C. albicans vaginitis model.

284 diminished fungicidal activity, increased C. albicans viability within macrophages, and decreased cyt

285 rticularly as our previous work has shown C. albicans virulence factor modulation by oral bacteria.

286 ric acid is used in various regimens for non-albicans VVC and recurrent BV.

287 C. albicans was a stronger activator for isolated human NK

288 infected-Galleria mellonella larvae, when C. albicans was exposed to antibody prior to inoculating G.

289 ve extensive acute inflammation following C. albicans water-soluble complex challenge, they do not de

290 Crz1 to induce beta-1,3-glucan masking in C. albicans We show here that iron-induced changes in beta-

291 order to understand the role of Cdc14 in C. albicans we used quantitative proteomics to identify pro

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

293 on of the water-soluble component of Candida albicans, we therefore undertook a mechanistic study to

294 Candida species (predominantly C. albicans) were more often present in the subgingival OB

295 rofiling to unravel molecular pathways of C. albicans when cocultured with S. mutans in mixed biofilm

296 tracellular glucans (~6-fold vs. uncoated C. albicans), which vastly exceeds the forces between S. go

297 1 KIN-CPD from the pathogenic fungus Candida albicans, which adopts an extended conformation in which

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

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

300 In C. albicans Zrc1 plays an important role in the generation