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1 was immunized (Mycobacterium tuberculosis or Candida albicans).
2 l as with heat-inactivated and viable fungi (Candida albicans).
3 d no significant effect after challenge with Candida albicans.
4 equired for clearance of the fungal pathogen Candida albicans.
5 ingle Dig1 orthologue in the fungal pathogen Candida albicans.
6 lucans on the surface of the fungal pathogen Candida albicans.
7 s to cell wall stress in the fungal pathogen Candida albicans.
8 irulence factor of the human fungal pathogen Candida albicans.
9 antarum and the opportunistic human pathogen Candida albicans.
10 rium oxysporum, Saccharomyces cerevisiae and Candida albicans.
11 athogenesis of many fungal pathogens such as Candida albicans.
12 ith DNA repeats in the human fungal pathogen Candida albicans.
13 of temperature stress in the fungal pathogen Candida albicans.
14 mmune responses to Aspergillus fumigatus and Candida albicans.
15  peptide toxin in the opportunistic pathogen Candida albicans.
16 rived dendritic cells (moDCs) that presented Candida albicans.
17 ose residues that cap the glycan produced by Candida albicans.
18  a transition in the human pathogenic fungus Candida albicans.
19 lysins have weak antifungal activity against Candida albicans.
20 lity and provided partial protection against Candida albicans.
21 ion to Cu taken by the human fungal pathogen Candida albicans.
22 li) bacteria, as well as on pathogenic fungi Candida albicans.
23 e to NLRP3 stimuli, including infection with Candida albicans.
24 helper T cells in controlling infection with Candida albicans.
25  toward aneuploidy-based azole resistance in Candida albicans.
26 al infection caused by the commensal microbe Candida albicans.
27 n mentagrophytes, Aspergillus fumigatus, and Candida albicans.
28 n yeast species identified in all groups was Candida albicans.
29 n different cellular systems stimulated with Candida albicans.
30 il recruitment during invasion of the CNS by Candida albicans.
31 ganisms including the human fungal pathogen, Candida albicans.
32 of Hsp90 in a leading human fungal pathogen, Candida albicans.
33 ning and integration into a neutral locus in Candida albicans.
34  from the most common human fungal pathogen, Candida albicans.
35 e homophilic adhesion in the fungal pathogen Candida albicans.
36  with a lethal dose of the pathogenic fungus Candida albicans.
37               Most CUTS cases were caused by Candida albicans (52.7%), followed by Candida glabrata (
38 is essential for GlcNAc signalling (NGS1) in Candida albicans, a commensal and pathogenic yeast of hu
39 e for IL-17 in protection against the fungus Candida albicans, a commensal microbe of the human oral
40 cus faecalis, a Gram-positive bacterium, and Candida albicans, a fungus, occupy overlapping niches as
41 e in the CTG clade of ascomycetes, including Candida albicans, a human pathogen.
42 roteins, as a potential antifungal target in Candida albicans, a major human fungal pathogen.
43                                              Candida albicans, a major opportunistic fungal pathogen,
44                 A simple example is found in Candida albicans, a member of the human microbiota and a
45 revisit this concept from the perspective of Candida albicans, a microbial pathogen uniquely adapted
46 the N-terminal domain of Tps2 (Tps2NTD) from Candida albicans, a transition-state complex of the Tps2
47                                              Candida albicans, a ubiquitous commensal fungus that col
48                                              Candida albicans-a yeast-like fungus that inhabits mucos
49 ells compared with polyclonal stimulation or Candida albicans Ag exposure.
50 e Oma1 ortholog in the human fungal pathogen Candida albicans also alters TOR signaling and, unexpect
51 e separase homologue Esp1p in the ascomycete Candida albicans, an important pathogen of humans, is es
52 trated that medically relevant fungi such as Candida albicans and Aspergillus fumigatus also form bio
53                                              Candida albicans and Aspergillus fumigatus are dangerous
54                                              Candida albicans and Candida glabrata are the 2 most pre
55 so increased the proportion of persisters in Candida albicans and Candida glabrata.
56 formed stable homotetramers, the mtSSBs from Candida albicans and Candida parapsilosis formed stable
57 y against the opportunistic fungal pathogens Candida albicans and Cryptococcus neoformans However, th
58                                              Candida albicans and Fusobacterium nucleatum are well-st
59 iroscytalin showed moderate activity against Candida albicans and good activity against an export-def
60 MA, the calcium ionophore A23187, nigericin, Candida albicans and Group B Streptococcus.
61            The opportunistic fungal pathogen Candida albicans and lactic acid bacteria (LAB) are comm
62                       Aspergillus fumigatus, Candida albicans and Mycosphaerella tassiana had the hig
63        The secondary outcome was the rate of Candida albicans and nonalbicans strains after treatment
64 erimental whole-genome mutation screening in Candida albicans and Pseudomonas aureginosa genomes, whi
65 us neoformans) to labeling at the bud sites (Candida albicans and Saccharomyces cerevisiae).
66 rthologues from Saccharomyces cerevisiae and Candida albicans and show that under nitrogen-sufficient
67 l IAI and demonstrated that coinfection with Candida albicans and Staphylococcus aureus (C. albicans/
68  had recurrent mucocutaneous infections with Candida albicans and Staphylococcus aureus and chronic i
69 tin-1, mannose, and Toll-like receptors with Candida albicans and Staphylococcus epidermidis was 2.5-
70 sensitivity to early systemic infection with Candida albicans and T cell-mediated colitis.
71                                   The fungus Candida albicans and the bacterium Pseudomonas aeruginos
72        Although the dimorphic fungal species Candida albicans and the bacterium Staphylococcus aureus
73                                   The fungus Candida albicans and the Gram-positive bacterium S. aure
74 s, whereas Th17 cells are protective against Candida albicans and to a lesser degree Staphylococcus a
75                                       CaTOK (Candida albicans) and CnTOK (Cryptococcus neoformans neo
76  (methicillin-resistant S. aureus (MRSA) and Candida albicans) and standard (Pseudomonas aeruginosa 1
77 h responses against Clostridium perfringens, Candida albicans, and Bacteroides vulgatus were also cou
78 module subunits of Saccharomyces cerevisiae, Candida albicans, and Candida dubliniensis Mediator, whi
79 aphylococcus aureus, Listeria monocytogenes, Candida albicans, and Candida parapsilosis isolates were
80 ease in phagocytosis of complement-opsonized Candida albicans, and decreased production of TNF-alpha
81 ey pattern-recognition receptors for sensing Candida albicans, and their downstream kinase SYK, thus
82 gal models such as Saccharomyces cerevisiae, Candida albicans, and Ustilago maydis.
83  efflux in highly azole-resistant strains of Candida albicans, another human fungal pathogen, increas
84                   Bloodborne infections with Candida albicans are an increasingly recognized complica
85 hylococcus aureus, Bacteroides fragilis, and Candida albicans are investigated.
86 y childhood caries, Streptococcus mutans and Candida albicans are often co-isolated from carious lesi
87      Using the opportunistic fungal pathogen Candida albicans as a model, we identified a highly spec
88                     Sequencing the genome of Candida albicans as it evolves in a patient reveals the
89 d by the opportunistic human fungal pathogen Candida albicans Aside from its primary function of bloc
90 t fungal infections, caused most commonly by Candida albicans, Aspergillus fumigatus and Cryptococcus
91    Here we measured ASE in the diploid yeast Candida albicans at both the transcriptional and transla
92 of the expression product was detected using Candida albicans (ATCC10231) as the indicator.
93 is study evaluated the antifungal effects on Candida albicans ATCC90028, the cytotoxicity toward huma
94 substrate and metal ions reveal that, unlike Candida albicans, binding of substrate to vDHBPS induces
95                                              Candida albicans biofilm formation is an important virul
96                                              Candida albicans biofilms are composed of highly adheren
97 proteins associated with several in vivo rat Candida albicans biofilms, including those from vascular
98 s after intravenous inoculation of 1 x 10(3) Candida albicans blastoconidia.
99 alized to the nucleus of Pichia pastoris and Candida albicans but is cytoplasmic in Saccharomyces cer
100 , a stronger cytokine response compared with Candida albicans, but a lower macrophage lysis capacity.
101 tly lost in the Metschnikowiaceae, including Candida albicans, but became more complex in the Sacchar
102 C) sensing materials that selectively detect Candida albicans (C. albicans).
103 rine infection with microorganisms including Candida albicans (C.albicans).
104  combinations, including the human pathogens Candida albicans, C. glabrata and Cryptococcus neoforman
105 ccus (VRE), Pseudomonas aeruginosa (PA), and Candida albicans (CA)].
106 rom Schizosaccharomyces pombe (Sp-Hsp104) or Candida albicans (Ca-Hsp104) also trimmed and cured the
107                                              Candida albicans can cause systemic infection in immunoc
108                          The fungal pathogen Candida albicans can transition from budding to hyphal g
109 ad-spectrum synergistic interactions against Candida albicans, Candida auris, Cryptococcus neoformans
110                                              Candida albicans, Candida glabrata, and Candida parapsil
111 ecificity of 98.9% (95% CI, 98.3%-99.4%) for Candida albicans/Candida tropicalis, 99.3% (95% CI, 98.7
112 ely colonized by pathobiont microbes such as Candida albicans, capable of invasive disseminated infec
113                    The human fungal pathogen Candida albicans causes invasive candidiasis, characteri
114             The polymorphic commensal fungus Candida albicans causes life-threatening disease via blo
115                                              Candida albicans cells are often detected with Streptoco
116 his research was to evaluate the adhesion of Candida albicans cells onto PMMA surfaces by employing a
117 nt in wild type Saccharomyces cerevisiae and Candida albicans cells.
118 hibited markedly increased susceptibility to Candida albicans challenge.
119 lla pneumophila, Streptococcus pneumonia and Candida albicans cleaved the N-terminus of immunoglobuli
120                 In the human fungal pathogen Candida albicans, CNV and LOH confer increased virulence
121 ceipt of broad-spectrum antibiotics enhances Candida albicans colonization of the GI tract, a risk fa
122                          The fungal pathogen Candida albicans colonizes basically all human epithelia
123  enhanced in patients with CF colonized with Candida albicans compared with that in noncolonized pati
124  levels of effector cytokines in response to Candida albicans, compared to CD69(-) T cells.
125  human vaginal epithelium, and to the fungus Candida albicans Complementary crystallographic and biop
126 nous SHIP-1 relocated to live or heat-killed Candida albicans-containing phagosomes in a Dectin-1-dep
127  CD82 and Dectin-1 on the plasma membrane of Candida albicans-containing phagosomes independent of ph
128                    The adhesive phenotype of Candida albicans contributes to its ability to colonize
129 man fungal pathogens (Aspergillus fumigatus, Candida albicans, Cryptococcus neoformans and Coccidioid
130                         The fungal pathogens Candida albicans, Cryptococcus neoformans, and Aspergill
131                        In the human pathogen Candida albicans, deep sequencing of mutants lacking the
132  cell responses against Escherichia coli and Candida albicans displayed microbe-specific polyfunction
133                          The fungal pathogen Candida albicans displays striking genome dynamics durin
134                               Infection with Candida albicans, disseminated disease, pneumonia, and c
135  prevented the death of the pathogenic yeast Candida albicans during exposure to fluconazole plus a c
136 The genome of the meiosis-defective pathogen Candida albicans encodes an Rme1 homolog that is part of
137 sponses to host cells in the fungal pathogen Candida albicans Eukaryotic Target of Rapamycin complex
138                                              Candida albicans excretes E,E-farnesol as a virulence fa
139 polymicrobial biofilms containing the fungus Candida albicans exist.
140 al membrane integrity as the fungal pathogen Candida albicans expands.
141     Here, we reveal that the fungal pathogen Candida albicans exploits diverse host-associated signal
142 cently, we reported that the fungal pathogen Candida albicans expresses a novel copper-only SOD, know
143            The opportunistic fungal pathogen Candida albicans expresses three copper-only SODs, and d
144        For the leading human fungal pathogen Candida albicans, filamentation is thought to be require
145 lecular-based assay for the detection of the Candida albicans FKS1 gene mutations responsible for res
146           Despite a lack of activity against Candida albicans for these early de novo analogs, the sy
147                               Centromeres of Candida albicans form on unique and different DNA sequen
148   The plasma membrane of the fungal pathogen Candida albicans forms a protective barrier that also me
149 nsition of the opportunistic fungal pathogen Candida albicans from budding to hyphal growth has been
150  two species of Candida (Cornus glabrata and Candida albicans) from Candida-spiked blood samples.
151 e capacity of peach DMSO extracts to inhibit Candida albicans growth was more pronounced, especially,
152                              Fungal pathogen Candida albicans has a complex cell wall consisting of a
153 ce of opportunistic fungal pathogens such as Candida albicans has increased.
154 fection, and opportunistic pathogens such as Candida albicans have evolved complex circuitry to sense
155         The secreted aspartyl proteinases of Candida albicans have long been implicated in virulence
156  SOD5 from the opportunistic fungal pathogen Candida albicans have revealed that the active-site stru
157 organisms in the oral cavity, while TM7x and Candida albicans have served as crucial paradigms for CP
158 sin is a cytolytic peptide toxin secreted by Candida albicans hyphae and has significantly advanced o
159 d NETs in response to fungal beta-glucan and Candida albicans hyphae when presented with extracellula
160 e oral mucosa caused by the commensal fungus Candida albicans IL-17R signaling is essential to preven
161      The most commonly isolated pathogen was Candida albicans in 20% of the patients.
162  shown that S. mutans is often detected with Candida albicans in early childhood caries.
163 ons of amphotericin B after inoculation with Candida albicans in light-exposed and light-protected co
164                         Innate resistance to Candida albicans in mucosal tissues requires the product
165 ether the recently observed sensitization to Candida albicans in patients with EoE is owing to pre-ex
166  were evaluated against the pathogenic yeast Candida albicans in the absence or presence of exogenous
167 eptococcus mutans, Streptococcus oralis, and Candida albicans in the saliva from mothers and their in
168 ns in the most common human fungal pathogen: Candida albicans In this organism, the histone deacetyla
169 ells expand and produce IL-17 in response to Candida albicans in vitro.
170 cterium, Pseudomonas aeruginosa and a yeast, Candida albicans, induce the resistance of the latter to
171 ida glabrata, and Q295* for the patient with Candida albicans-induced colitis.
172 eles: R70W and Q289* for the 3 patients with Candida albicans-induced meningoencephalitis, R35Q for t
173 ononuclear cells, these molecules suppressed Candida albicans-induced production of the cancer-promot
174 n pathogenic fungi Aspergillus fumigatus and Candida albicans induces a distinct subset of neutrophil
175                                           In Candida albicans-infected resident peritoneal macrophage
176 uently, dnTCF4 mice were more susceptible to Candida albicans infection and more sensitive to 5-fluor
177 results in enhanced defense against systemic Candida albicans infection and prolonged host survival.
178  myeloid cells show higher susceptibility to Candida albicans infection due to impairment in neutroph
179 enting the corneal innate immune response to Candida albicans infection in an animal model of fungal
180 ive pathogen gene regulation during invasive Candida albicans infection of a mammalian host.
181                                              Candida albicans infection produces elongated hyphae res
182 o demonstrated in a murine model of systemic Candida albicans infection with a significant fungal loa
183 e than wild-type control mice in response to Candida albicans infection, and the expression of JNK1 i
184                                       During Candida albicans infection, mice lacking TAGAP mount def
185 e showed enhanced resistance to disseminated Candida albicans infection, which was reversed in an Il1
186 or clusters of miRNAs in countering systemic Candida albicans infection.
187 crucial role in the defense against systemic Candida albicans infection.
188      The oral cavity is a unique niche where Candida albicans infections occur in immunocompetent as
189 onal replacement therapy predispose women to Candida albicans infections.
190 ns, it is imperative that we investigate how Candida albicans interacts with blood components.
191 imental mouse model of Staphylococcus aureus-Candida albicans intra-abdominal infection results in ap
192                                              Candida albicans is a commensal fungus of human gastroin
193                                              Candida albicans is a commensal fungus of the human gast
194                                              Candida albicans is a commensal fungus of the human gut,
195                                              Candida albicans is a commensal fungus that can cause sy
196                                              Candida albicans is a commensal yeast able to cause life
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 fungal pathobiont, able to cause e
200                                              Candida albicans is a gut commensal and opportunistic pa
201                                              Candida albicans is a leading cause of systemic bloodstr
202                                              Candida albicans is a pervasive commensal fungus that is
203                                              Candida albicans is a ubiquitous mucosal commensal that
204                                              Candida albicans is a well-tolerated resident of human m
205                                              Candida albicans is a yeast-like pathogen and can cause
206 mmune response, and yet the commensal fungus Candida albicans is able to colonize immuno competent in
207                                              Candida albicans is among the most common human fungal p
208                                              Candida albicans is an important cause of systemic funga
209 recent study shows that the commensal fungus Candida albicans is an inducer of differentiation of hum
210                                              Candida albicans is an opportunistic fungal pathogen col
211                                              Candida albicans is an opportunistic fungal pathogen fou
212                                              Candida albicans is an opportunistic fungal pathogen of
213                                              Candida albicans is an opportunistic human fungal pathog
214                                              Candida albicans is an opportunistic pathogen, typically
215                                              Candida albicans is an opportunistic yeast that can caus
216                                              Candida albicans is both a member of the healthy human m
217                             The cell wall of Candida albicans is composed largely of polysaccharides.
218                           The human pathogen Candida albicans is considered an obligate commensal of
219 ith its mammalian host, the pathogenic yeast Candida albicans is exposed to a range of stresses such
220                                              Candida albicans is frequently detected with heavy infec
221                                              Candida albicans is known to form polymicrobial biofilms
222                                              Candida albicans is normally a commensal fungus of the h
223                                              Candida albicans is part of the normal commensal microbi
224 -> 2)-Inositol-1-P-(O -> 1)-phytoceramide of Candida albicans is reported.
225                             The Hog1 SAPK in Candida albicans is robustly phosphorylated in response
226                                              Candida albicans is the fourth most common cause of syst
227                                              Candida albicans is the leading cause of fungal infectio
228                                              Candida albicans is the most common fungal pathogen in h
229                                              Candida albicans is the most common human fungal pathoge
230                                              Candida albicans is the most prevalent fungal species of
231                                    The yeast Candida albicans is the most prevalent opportunistic fun
232                                     Although Candida albicans is the predominant organism found in pa
233                                              Candida albicans is the single most prevalent cause of f
234 some complement of the human fungal pathogen Candida albicans is unusually unstable, suggesting that
235 erant fungi, including filamentous fungi and Candida albicans, is associated with poor lung function
236 ogenicity of the clinically important yeast, Candida albicans, is dependent on robust responses to ho
237        In the fungal commensal and pathogen, Candida albicans, little is known of how these pathways
238                 In the human fungal pathogen Candida albicans, mating of diploid cells generates tetr
239 PE produced from Escherichia coli membranes, Candida albicans mitochondria, or HeLa cell mitochondria
240 sistant Staphylococcus aureus ATCC 43300 and Candida albicans MTCC 227.
241                 Notably, experiments against Candida albicans mutants lacking those genes showed resi
242 te a multivalent recombinant protein against Candida albicans (mvPC).
243  NOPE1 encodes a functional homologue of the Candida albicans N-acetylglucosamine (GlcNAc) transporte
244 e most common fungal species identified were Candida albicans (n = 85), Candida glabrata (n = 63), an
245 ly important differences with human NatA and Candida albicans NatB, resolves key hNatB protein determ
246 e ability of these cells to kill/phagocytose Candida albicans or Escherichia coli cells both ex vivo
247  tears and protected the eye from pathogenic Candida albicans or Pseudomonas aeruginosa infection.
248  overturned by mono-colonization with either Candida albicans or Saccharomyces cerevisiae.
249 d with lipopolysaccharide (LPS), heat-killed Candida albicans, or anti-CD3/anti-CD28 antibodies.
250 an be extended to other systems such as e.g. Candida albicans, or selected plant cells.
251 e in which the loss of an ABC transporter in Candida albicans, orf19.4531 (previously named ROA1), in
252  growth in the opportunistic fungal pathogen Candida albicans Our results suggest that HHK3 regulates
253                       Biofilms of the fungus Candida albicans produce extracellular matrix that confe
254 rials, contains a recombinant version of the Candida albicans rAls3 N-terminus protein (rAls3p-N) in
255 mon causes of invasive mycotic disease, with Candida albicans reigning as the leading cause of invasi
256 ha-mannoside, found in Saccharopolyspora and Candida albicans, respectively, induced the activation o
257                                              Candida albicans scavenges environmental zinc via two pa
258 common disease affecting women; however, how Candida albicans shift from commensalism towards a patho
259 clusively on immune stimulation, including a Candida albicans-specific master regulator at the CR1 lo
260               An experimental mouse model of Candida albicans-Staphylococcus aureus intra-abdominal i
261 riconazole (VOR), was examined against seven Candida albicans strains.
262 y (EIS) that allows multiplexed detection of Candida albicans, Streptococcus agalactiae and Chlamydia
263                                           In Candida albicans, stress triggers adaptive chromosome de
264 us oralis forms robust mucosal biofilms with Candida albicans that have increased pathogenic potentia
265 tein histatin 5 (Hst 5) is fungicidal toward Candida albicans, the causative agent of oropharyngeal c
266       With the opportunistic fungal pathogen Candida albicans, the Cu-sensing transcription factor Ma
267                                              Candida albicans, the major invasive fungal pathogen of
268    Surprisingly, we found that the genome of Candida albicans, the predominant human fungal pathogen,
269 ulates virulence of pathogenic fungi such as Candida albicans, the underlying mechanisms have remaine
270 hin a population of macrophages encountering Candida albicans, there are distinct host-pathogen traje
271 e of circulating Cryptococcus neoformans and Candida albicans, thereby reducing fungal dissemination
272 ability of the fungal opportunistic pathogen Candida albicans to adhere to denture material and invad
273 e circuitry that enables the fungal pathogen Candida albicans to couple cell cycle dynamics with resp
274 lles and stimulated with bacterial toxins or Candida albicans to induce NETosis.
275 osamine (GlcNAc), induce the fungal pathogen Candida albicans to switch from budding to hyphal growth
276 drug library to sensitize an azole-resistant Candida albicans to the effect of fluconazole.
277  and long-lasting antifungal effects against Candida albicans to the PMMA resin, and it has low toxic
278 iverse isolates of the human fungal pathogen Candida albicans (Todd et al., 2019).
279         In the opportunistic fungal pathogen Candida albicans, transcriptional regulatory networks re
280 rms expressed by Cryptococcus neoformans and Candida albicans, two pathogenic fungi of major clinical
281                          The fungal pathogen Candida albicans undergoes morphogenetic switching from
282                    The human fungal pathogen Candida albicans undergoes white-opaque phenotypic switc
283 otocol for CRISPR-Cas9-based manipulation in Candida albicans using a modified gene-drive-based strat
284                      For the fungal pathogen Candida albicans, utilization of amino acids has been sh
285                                              Candida albicans utilizes chromosome missegregation to a
286 s, and rewired transcription subnetworks for Candida albicans versus Saccharomyces cerevisiae, agains
287 gal polyketide with in vivo efficacy against Candida albicans, was discovered using LCMS-based metabo
288  a mouse model of KD (induced by a cell wall Candida albicans water-soluble fraction [CAWS]), we iden
289  a model of intradermal footpad injection of Candida albicans, we observed that inflammation as measu
290 ntage of the minimal MT nucleation system of Candida albicans, we reconstituted the interactions of M
291  injection of the water-soluble component of Candida albicans, we therefore undertook a mechanistic s
292 ive (Escherichia coli) bacteria and a fungi (Candida albicans) were examined; which showed good antib
293                        In the human pathogen Candida albicans (which last shared a common ancestor wi
294 e of Trl1 KIN-CPD from the pathogenic fungus Candida albicans, which adopts an extended conformation
295  analysis of the polymorphic fungal pathogen Candida albicans, which contains one of the smallest kno
296  epigenetic states, "white" and "opaque." In Candida albicans, white cells are essentially sterile, w
297 nase domain of Trl1 from the fungal pathogen Candida albicans with GDP and Mg2+ in the active site.
298 e exhibited good antifungal activity against Candida albicans with MIC of 15.6mug/mL.
299                           The interaction of Candida albicans with the innate immune system is the ke
300 rofoundly resistant to systemic infection by Candida albicans, with resistance characterized by enhan

 
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