ライフサイエンスコーパス: Candida albicans

1 was immunized (Mycobacterium tuberculosis or Candida albicans).

2 mmune responses to Aspergillus fumigatus and Candida albicans.

3 peptide toxin in the opportunistic pathogen Candida albicans.

4 equired for clearance of the fungal pathogen Candida albicans.

5 ose residues that cap the glycan produced by Candida albicans.

6 a transition in the human pathogenic fungus Candida albicans.

7 lysins have weak antifungal activity against Candida albicans.

8 lity and provided partial protection against Candida albicans.

9 ion to Cu taken by the human fungal pathogen Candida albicans.

10 li) bacteria, as well as on pathogenic fungi Candida albicans.

11 e to NLRP3 stimuli, including infection with Candida albicans.

12 helper T cells in controlling infection with Candida albicans.

13 toward aneuploidy-based azole resistance in Candida albicans.

14 al infection caused by the commensal microbe Candida albicans.

15 ndependent phagolysosomal mechanisms to kill Candida albicans.

16 ureus, and Micrococcus luteus and the yeast, Candida albicans.

17 cellular functions in the pathogenic fungus Candida albicans.

18 ittle was known about their interaction with Candida albicans.

19 an opportunistic fungal infection caused by Candida albicans.

20 tic infection caused by the commensal fungus Candida albicans.

21 nnerella forsythia, Treponema denticola, and Candida albicans.

22 lidin variants that exhibit activity against Candida albicans.

23 onas aeruginosa, Streptococcus pyogenes, and Candida albicans.

24 s have received less attention than those of Candida albicans.

25 ing NETs were determined for the response to Candida albicans.

26 itor FK506 against the human fungal pathogen Candida albicans.

27 d no significant effect after challenge with Candida albicans.

28 ingle Dig1 orthologue in the fungal pathogen Candida albicans.

29 lucans on the surface of the fungal pathogen Candida albicans.

30 s to cell wall stress in the fungal pathogen Candida albicans.

31 irulence factor of the human fungal pathogen Candida albicans.

32 antarum and the opportunistic human pathogen Candida albicans.

33 rium oxysporum, Saccharomyces cerevisiae and Candida albicans.

34 athogenesis of many fungal pathogens such as Candida albicans.

35 ith DNA repeats in the human fungal pathogen Candida albicans.

36 of temperature stress in the fungal pathogen Candida albicans.

37 Mice were intraperitoneally infected with Candida albicans (1 x 10(6) colony-forming units) and st

38 heir ability to detect fks mutant strains of Candida albicans (11 mutants), Candida tropicalis (4 mut

39 Among the 62 isolates of Candida albicans (4 isolates), C. tropicalis (5 isolates

40 nk order of Candida isolates was as follows: Candida albicans (52%), Candida parapsilosis (23.7%), Ca

41 Most CUTS cases were caused by Candida albicans (52.7%), followed by Candida glabrata (

42 mpt to generate a protective vaccine against Candida albicans, a beta-mannan tetanus toxoid conjugate

43 is essential for GlcNAc signalling (NGS1) in Candida albicans, a commensal and pathogenic yeast of hu

44 e for IL-17 in protection against the fungus Candida albicans, a commensal microbe of the human oral

45 In Candida albicans, a fungal pathogen, the small G-protein

46 cus faecalis, a Gram-positive bacterium, and Candida albicans, a fungus, occupy overlapping niches as

47 tabolism is integral to the pathogenicity of Candida albicans, a major fungal pathogen of humans.

48 Candida albicans, a major human fungal pathogen, can swi

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

50 revisit this concept from the perspective of Candida albicans, a microbial pathogen uniquely adapted

51 7 cells were detected after stimulation with Candida albicans, a pathogen that has been linked to dis

52 the N-terminal domain of Tps2 (Tps2NTD) from Candida albicans, a transition-state complex of the Tps2

53 Vulvovaginal candidiasis (VVC), caused by Candida albicans, affects women worldwide.

54 e Oma1 ortholog in the human fungal pathogen Candida albicans also alters TOR signaling and, unexpect

55 Phagosomes containing Candida albicans also require Dectin-1-dependent Syk act

56 trated that medically relevant fungi such as Candida albicans and Aspergillus fumigatus also form bio

57 Both Candida albicans and Aspergillus fumigatus sun proteins

58 we compared the cytokine responses evoked by Candida albicans and C. parapsilosis.

59 Candida albicans and Candida glabrata are predominant fu

60 Candida albicans and Candida glabrata that were resistan

61 Known concentrations of Candida albicans and Candida glabrata were each added to

62 so increased the proportion of persisters in Candida albicans and Candida glabrata.

63 Candida albicans and Candida tropicalis are opportunisti

64 Candida albicans and cross-reactive plant allergen compo

65 y against the opportunistic fungal pathogens Candida albicans and Cryptococcus neoformans However, th

66 Candida albicans and Fusobacterium nucleatum are well-st

67 iroscytalin showed moderate activity against Candida albicans and good activity against an export-def

68 MA, the calcium ionophore A23187, nigericin, Candida albicans and Group B Streptococcus.

69 d mannan biosynthesis in the fungal pathogen Candida albicans and highlights new insights gained from

70 The human fungal pathogens Candida albicans and Histoplasma capsulatum have been re

71 The opportunistic fungal pathogen Candida albicans and lactic acid bacteria (LAB) are comm

72 The secondary outcome was the rate of Candida albicans and nonalbicans strains after treatment

73 cacy of blocking the host cell receptors for Candida albicans and Rhizopus oryzae has been demonstrat

74 us neoformans) to labeling at the bud sites (Candida albicans and Saccharomyces cerevisiae).

75 rthologues from Saccharomyces cerevisiae and Candida albicans and show that under nitrogen-sufficient

76 had recurrent mucocutaneous infections with Candida albicans and Staphylococcus aureus and chronic i

77 (Listeria monocytogenes) and extracellular (Candida albicans and Staphylococcus aureus) pathogens.

78 tin-1, mannose, and Toll-like receptors with Candida albicans and Staphylococcus epidermidis was 2.5-

79 sensitivity to early systemic infection with Candida albicans and T cell-mediated colitis.

80 The fungus Candida albicans and the bacterium Pseudomonas aeruginos

81 Although the dimorphic fungal species Candida albicans and the bacterium Staphylococcus aureus

82 s, whereas Th17 cells are protective against Candida albicans and to a lesser degree Staphylococcus a

83 nt antifungal activity (MIC = 3.1 mug/mL for Candida albicans ) and favorable selectivity (IC10 > 400

84 (methicillin-resistant S. aureus (MRSA) and Candida albicans) and standard (Pseudomonas aeruginosa 1

85 module subunits of Saccharomyces cerevisiae, Candida albicans, and Candida dubliniensis Mediator, whi

86 aphylococcus aureus, Listeria monocytogenes, Candida albicans, and Candida parapsilosis isolates were

87 ease in phagocytosis of complement-opsonized Candida albicans, and decreased production of TNF-alpha

88 major fungal species of the gut microbiome, Candida albicans, and each of five prevalent bacterial g

89 togenes, Neisseria meningitidis serogroup B, Candida albicans, and P. berghei ANKA, and against colon

90 ey pattern-recognition receptors for sensing Candida albicans, and their downstream kinase SYK, thus

91 gal models such as Saccharomyces cerevisiae, Candida albicans, and Ustilago maydis.

92 cterium Enterococcus faecalis and the fungus Candida albicans are both found as commensals in many of

93 hylococcus aureus, Bacteroides fragilis, and Candida albicans are investigated.

94 responses to opportunistic pathogens such as Candida albicans are lost early, but CMV-specific CD4 re

95 pid detection methods for the human pathogen Candida albicans are still missing.

96 ospora crassa, Saccharomyces cerevisiae, and Candida albicans, are highly sensitized to fluoride (>20

97 Using the opportunistic fungal pathogen Candida albicans as a model, we identified a highly spec

98 Sequencing the genome of Candida albicans as it evolves in a patient reveals the

99 t fungal infections, caused most commonly by Candida albicans, Aspergillus fumigatus and Cryptococcus

100 se may support morphologic transformation of Candida albicans at a wide range of ambient temperatures

101 Here we measured ASE in the diploid yeast Candida albicans at both the transcriptional and transla

102 of the expression product was detected using Candida albicans (ATCC10231) as the indicator.

103 is study evaluated the antifungal effects on Candida albicans ATCC90028, the cytotoxicity toward huma

104 hown that if the gene for AHAS is deleted in Candida albicans , attenuation of virulence is achieved,

105 substrate and metal ions reveal that, unlike Candida albicans, binding of substrate to vDHBPS induces

106 Candida albicans biofilm formation is an important virul

107 for the study of urinary catheter-associated Candida albicans biofilm infection that mimics this comm

108 Candida albicans biofilms are composed of highly adheren

109 proteins associated with several in vivo rat Candida albicans biofilms, including those from vascular

110 s after intravenous inoculation of 1 x 10(3) Candida albicans blastoconidia.

111 s) that are toxic toward the fungal pathogen Candida albicans but exert little effect on mammalian ce

112 alized to the nucleus of Pichia pastoris and Candida albicans but is cytoplasmic in Saccharomyces cer

113 tly lost in the Metschnikowiaceae, including Candida albicans, but became more complex in the Sacchar

114 C) sensing materials that selectively detect Candida albicans (C. albicans).

115 rine infection with microorganisms including Candida albicans (C.albicans).

116 combinations, including the human pathogens Candida albicans, C. glabrata and Cryptococcus neoforman

117 rom Schizosaccharomyces pombe (Sp-Hsp104) or Candida albicans (Ca-Hsp104) also trimmed and cured the

118 The fungal pathogen Candida albicans can transition from budding to hyphal g

119 Candida albicans, Candida glabrata, and Candida parapsil

120 ecificity of 98.9% (95% CI, 98.3%-99.4%) for Candida albicans/Candida tropicalis, 99.3% (95% CI, 98.7

121 xpressed S. cerevisiae ScUpc2 and pathogenic Candida albicans CaUpc2 and Candida glabrata CgUpc2 to A

122 The human fungal pathogen Candida albicans causes invasive candidiasis, characteri

123 The polymorphic commensal fungus Candida albicans causes life-threatening disease via blo

124 profiles of human monocytes trained with the Candida albicans cell wall constituent beta-glucan, toge

125 S. mutans may not act alone; Candida albicans cells are frequently detected along wit

126 Candida albicans cells are often detected with Streptoco

127 his research was to evaluate the adhesion of Candida albicans cells onto PMMA surfaces by employing a

128 nt in wild type Saccharomyces cerevisiae and Candida albicans cells.

129 lla pneumophila, Streptococcus pneumonia and Candida albicans cleaved the N-terminus of immunoglobuli

130 ceipt of broad-spectrum antibiotics enhances Candida albicans colonization of the GI tract, a risk fa

131 The fungal pathogen Candida albicans colonizes basically all human epithelia

132 enhanced in patients with CF colonized with Candida albicans compared with that in noncolonized pati

133 human vaginal epithelium, and to the fungus Candida albicans Complementary crystallographic and biop

134 nous SHIP-1 relocated to live or heat-killed Candida albicans-containing phagosomes in a Dectin-1-dep

135 Candida albicans contains four ORFs (GIT1,2,3,4) predict

136 that the hyphae of the human fungal pathogen Candida albicans continue to extend throughout the whole

137 The adhesive phenotype of Candida albicans contributes to its ability to colonize

138 The fungal pathogens Candida albicans, Cryptococcus neoformans, and Aspergill

139 In the human pathogen Candida albicans, deep sequencing of mutants lacking the

140 is is not the case for the pathogenic fungus Candida albicans despite its ability to use propionate a

141 cell responses against Escherichia coli and Candida albicans displayed microbe-specific polyfunction

142 Infection with Candida albicans, disseminated disease, pneumonia, and c

143 prevented the death of the pathogenic yeast Candida albicans during exposure to fluconazole plus a c

144 sponses to host cells in the fungal pathogen Candida albicans Eukaryotic Target of Rapamycin complex

145 Candida albicans excretes E,E-farnesol as a virulence fa

146 cently, we reported that the fungal pathogen Candida albicans expresses a novel copper-only SOD, know

147 redundancy of signaling pathways controlling Candida albicans filamentation and pathogenicity.

148 For the leading human fungal pathogen Candida albicans, filamentation is thought to be require

149 lecular-based assay for the detection of the Candida albicans FKS1 gene mutations responsible for res

150 The plasma membrane of the fungal pathogen Candida albicans forms a protective barrier that also me

151 nsition of the opportunistic fungal pathogen Candida albicans from budding to hyphal growth has been

152 e was also increased for fluconazole against Candida albicans (from 2.1% to 5.7%).

153 l cells in response to the vaginal pathogens Candida albicans, Gardnerella vaginalis, and Neisseria g

154 e capacity of peach DMSO extracts to inhibit Candida albicans growth was more pronounced, especially,

155 ce of opportunistic fungal pathogens such as Candida albicans has increased.

156 fection, and opportunistic pathogens such as Candida albicans have evolved complex circuitry to sense

157 The secreted aspartyl proteinases of Candida albicans have long been implicated in virulence

158 organisms in the oral cavity, while TM7x and Candida albicans have served as crucial paradigms for CP

159 artificial promoters (potef, pthiA) and the Candida albicans hsp90 promoter resulted in hypersensiti

160 ETs) in response to large pathogens, such as Candida albicans hyphae and extracellular aggregates of

161 Candida albicans hyphae grow in a highly polarized fashi

162 d NETs in response to fungal beta-glucan and Candida albicans hyphae when presented with extracellula

163 elicited via Mycobacterium tuberculosis and Candida albicans immunization, respectively.

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

165 48), Staphylococcus aureus in 7.8% (35/448), Candida albicans in 5.8% (26/443), other coagulase-negat

166 The virulence of Candida albicans in a mouse model of invasive candidiasi

167 shown that S. mutans is often detected with Candida albicans in early childhood caries.

168 ons of amphotericin B after inoculation with Candida albicans in light-exposed and light-protected co

169 Innate resistance to Candida albicans in mucosal tissues requires the product

170 ether the recently observed sensitization to Candida albicans in patients with EoE is owing to pre-ex

171 ns in the most common human fungal pathogen: Candida albicans In this organism, the histone deacetyla

172 ells expand and produce IL-17 in response to Candida albicans in vitro.

173 ida glabrata, and Q295* for the patient with Candida albicans-induced colitis.

174 eles: R70W and Q289* for the 3 patients with Candida albicans-induced meningoencephalitis, R35Q for t

175 n pathogenic fungi Aspergillus fumigatus and Candida albicans induces a distinct subset of neutrophil

176 In Candida albicans-infected resident peritoneal macrophage

177 epithelial gene transcriptional responses to Candida albicans infection by microarray.

178 Systemic Candida albicans infection causes high morbidity and mor

179 myeloid cells show higher susceptibility to Candida albicans infection due to impairment in neutroph

180 enting the corneal innate immune response to Candida albicans infection in an animal model of fungal

181 ive pathogen gene regulation during invasive Candida albicans infection of a mammalian host.

182 Candida albicans infection produces elongated hyphae res

183 o demonstrated in a murine model of systemic Candida albicans infection with a significant fungal loa

184 e than wild-type control mice in response to Candida albicans infection, and the expression of JNK1 i

185 e showed enhanced resistance to disseminated Candida albicans infection, which was reversed in an Il1

186 crucial role in the defense against systemic Candida albicans infection.

187 on and resistance to fungal dissemination in Candida albicans infection.

188 , Xiap(-/-) mice became highly vulnerable on Candida albicans infection.

189 or clusters of miRNAs in countering systemic Candida albicans infection.

190 The oral cavity is a unique niche where Candida albicans infections occur in immunocompetent as

191 onal replacement therapy predispose women to Candida albicans infections.

192 imental mouse model of Staphylococcus aureus-Candida albicans intra-abdominal infection results in ap

193 genously disseminated infection, blood-borne Candida albicans invades the endothelial cell lining of

194 The fungus Candida albicans is a benign member of the mucosal micro

195 Candida albicans is a commensal fungus of the human gast

196 Candida albicans is a commensal fungus that can cause sy

197 Candida albicans is a dimorphic commensal fungus that co

198 Candida albicans is a dimorphic fungus responsible for c

199 Candida albicans is a leading cause of fungal infections

200 The commensal yeast Candida albicans is a major cause of invasive fungal inf

201 Candida albicans is a ubiquitous mucosal commensal that

202 Candida albicans is a well-tolerated resident of human m

203 Candida albicans is a yeast-like pathogen and can cause

204 mmune response, and yet the commensal fungus Candida albicans is able to colonize immuno competent in

205 Candida albicans is able to undergo reversible morpholog

206 Candida albicans is among the most common human fungal p

207 Candida albicans is an important cause of systemic funga

208 Candida albicans is an opportunistic fungal pathogen col

209 Candida albicans is an opportunistic fungal pathogen fou

210 Candida albicans is an opportunistic fungal pathogen of

211 Candida albicans is an opportunistic human fungal pathog

212 Candida albicans is an opportunistic pathogen that lives

213 Candida albicans is an opportunistic pathogen, typically

214 invasive infection with the fungal pathogen Candida albicans is associated with high morbidity and m

215 Candida albicans is both a member of the healthy human m

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

217 ith its mammalian host, the pathogenic yeast Candida albicans is exposed to a range of stresses such

218 Candida albicans is frequently detected with heavy infec

219 Candida albicans is normally a commensal fungus of the h

220 Candida albicans is part of the normal commensal microbi

221 The Hog1 SAPK in Candida albicans is robustly phosphorylated in response

222 DJ-1 superfamily member ORF 19.251/GLX3 from Candida albicans is shown to possess glyoxalase activity

223 Candida albicans is the leading cause of fungal infectio

224 Candida albicans is the leading cause of systemic candid

225 Candida albicans is the most common cause of invasive fu

226 Candida albicans is the most common fungal pathogen in h

227 Candida albicans is the most common fungal pathogen resp

228 Candida albicans is the most common human fungal pathoge

229 Candida albicans is the most prevalent fungal species of

230 Although Candida albicans is the predominant organism found in pa

231 Candida albicans is the single most prevalent cause of f

232 diasis (OPC), caused by the commensal fungus Candida albicans, is an opportunistic infection associat

233 ogenicity of the clinically important yeast, Candida albicans, is dependent on robust responses to ho

234 balamin-independent methionine synthase from Candida albicans, known as Met6p, is a 90-kDa enzyme tha

235 In the fungal commensal and pathogen, Candida albicans, little is known of how these pathways

236 Candida albicans maintains both commensal and pathogenic

237 It is not enriched for vaccinia virus and Candida albicans-MP65 (immunodominant protein), typical

238 Notably, experiments against Candida albicans mutants lacking those genes showed resi

239 NOPE1 encodes a functional homologue of the Candida albicans N-acetylglucosamine (GlcNAc) transporte

240 e most common fungal species identified were Candida albicans (n = 85), Candida glabrata (n = 63), an

241 e ability of these cells to kill/phagocytose Candida albicans or Escherichia coli cells both ex vivo

242 tears and protected the eye from pathogenic Candida albicans or Pseudomonas aeruginosa infection.

243 overturned by mono-colonization with either Candida albicans or Saccharomyces cerevisiae.

244 monstrated that monomicrobial infection with Candida albicans or Staphylococcus aureus is nonlethal.

245 d with lipopolysaccharide (LPS), heat-killed Candida albicans, or anti-CD3/anti-CD28 antibodies.

246 an be extended to other systems such as e.g. Candida albicans, or selected plant cells.

247 e in which the loss of an ABC transporter in Candida albicans, orf19.4531 (previously named ROA1), in

248 To dissect their separate roles in Candida albicans pathogenicity we generated knock-out st

249 ative (Acinetobacter baumannii), and fungal (Candida albicans) pathogens by sequestering iron and dis

250 ulvovaginal candidiasis, caused primarily by Candida albicans, presents significant health issues for

251 re-establishing intestinal colonization with Candida albicans primes expansion of Th17 cells with com

252 Biofilms of the fungus Candida albicans produce extracellular matrix that confe

253 Systemic infection by the pathogenic yeast Candida albicans produces high mortality in immune-compr

254 the probiotic methanol cell extracts against Candida albicans ranged between 1.25 and 5mg/ml after 48

255 tes (Fusarium solani, Aspergillus fumigatus, Candida albicans) recovered from patients with confirmed

256 ha-mannoside, found in Saccharopolyspora and Candida albicans, respectively, induced the activation o

257 Candida albicans reversibly switches between yeast and h

258 a, Klebsiella pneumoniae, Salmonellae typhi, Candida albicans, Rhizopus stolonifer, Aspergillus niger

259 viously proposed as a new species within the Candida albicans species complex, together with C. albic

260 clusively on immune stimulation, including a Candida albicans-specific master regulator at the CR1 lo

261 An experimental mouse model of Candida albicans-Staphylococcus aureus intra-abdominal i

262 increased cytokine production in response to Candida albicans stimulation.

263 riconazole (VOR), was examined against seven Candida albicans strains.

264 y (EIS) that allows multiplexed detection of Candida albicans, Streptococcus agalactiae and Chlamydia

265 nal regulator from the human fungal pathogen Candida albicans that binds DNA specifically but has no

266 us oralis forms robust mucosal biofilms with Candida albicans that have increased pathogenic potentia

267 tein histatin 5 (Hst 5) is fungicidal toward Candida albicans, the causative agent of oropharyngeal c

268 Candida albicans, the leading fungal pathogen of humans,

269 Candida albicans, the major invasive fungal pathogen of

270 Candida albicans, the most common cause of human fungal

271 While virulence properties of Candida albicans, the most commonly isolated human funga

272 Candida albicans, the most prevalent human fungal pathog

273 Candida albicans, the most prevalent human fungal pathog

274 Surprisingly, we found that the genome of Candida albicans, the predominant human fungal pathogen,

275 In the fungus Candida albicans, the Rho-family small GTPase, Cdc42, is

276 e circuitry that enables the fungal pathogen Candida albicans to couple cell cycle dynamics with resp

277 el role for beta-1, 3- glucanase in inducing Candida albicans to form filaments at 22 degrees C and e

278 able the human opportunistic fungal pathogen Candida albicans to proliferate in two different niches.

279 osamine (GlcNAc), induce the fungal pathogen Candida albicans to switch from budding to hyphal growth

280 and long-lasting antifungal effects against Candida albicans to the PMMA resin, and it has low toxic

281 Here we show that four Candida albicans transcription regulators that arose by

282 The fungal pathogen Candida albicans undergoes morphogenetic switching from

283 The human fungal pathogen Candida albicans undergoes white-opaque phenotypic switc

284 s, and rewired transcription subnetworks for Candida albicans versus Saccharomyces cerevisiae, agains

285 IgE sensitization to Candida albicans was found in 43% of EoE patients.

286 gal polyketide with in vivo efficacy against Candida albicans, was discovered using LCMS-based metabo

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

288 a model of intradermal footpad injection of Candida albicans, we observed that inflammation as measu

289 ntage of the minimal MT nucleation system of Candida albicans, we reconstituted the interactions of M

290 as the major source of IL-17 in response to Candida albicans, we show that fungal control is mediate

291 ive (Escherichia coli) bacteria and a fungi (Candida albicans) were examined; which showed good antib

292 In the human pathogen Candida albicans (which last shared a common ancestor wi

293 analysis of the polymorphic fungal pathogen Candida albicans, which contains one of the smallest kno

294 We recently showed that in Candida albicans, which has circular mapping mtDNA, reco

295 epigenetic states, "white" and "opaque." In Candida albicans, white cells are essentially sterile, w

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

297 e exhibited 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 ke

299 rofoundly resistant to systemic infection by Candida albicans, with resistance characterized by enhan

300 nate immune system differentially recognizes Candida albicans yeast and hyphae.