ライフサイエンスコーパス: C. albicans

1 C. albicans adjusted its cytosolic SODs accordingly and

2 C. albicans and S. oralis decreased epithelial E-cadheri

3 C. albicans biofilms are intrinsically resistant to conv

4 C. albicans biofilms are not static structures; rather t

5 C. albicans budding mother cells were found to be nonadh

6 C. albicans cells phagocytosed by macrophages undergo a

7 C. albicans induced the release of IL-1beta, IL-6, and I

8 C. albicans is able to induce mucosal defenses through a

9 C. albicans is also a predominantly opportunistic fungal

10 C. albicans opaque cells do not secrete this chemoattrac

11 C. albicans sap6 deletion mutants failed to accumulate i

12 C. albicans secreted aspartic protease Sap6 is important

13 C. albicans strains lacking this toxin do not activate o

14 C. albicans strains were constructed in which Hog1 was e

15 C. albicans Zfs1 bound to the ideal mammalian TTP bindin

16 lood culture isolates of 5 Candida spp. (120 C. albicans, 38 C. glabrata, 10 C. parapsilosis, 12 C. t

17 olates of four Candida species, including 16 C. albicans and 11 C. glabrata isolates with defined FKS

18 cultures with different Candida species (28% C. albicans, 27% C. parapsilosis, 26% C. tropicalis, etc

19 d with clinical isolates (40 C. glabrata, 46 C. albicans, 36 C. parapsilosis, 19 C. tropicalis, and 2

20 evaluated using a double-blinded panel of 50 C. albicans strains.

21 of 258 clinical samples (89 C. glabrata, 79 C. albicans, 23 C. parapsilosis, 18 C. tropicalis, and 4

22 ction was due to: Candida spp. in 267 (90%), C. albicans in 128 (48%), and other Candida spp. in 145

23 By screening a C. albicans SN152 mutant library and a panel of F. nucle

24 Despite these abnormalities, C. albicans SOD5 can disproportionate superoxide at rate

25 saliva contains various proteins that affect C. albicans growth positively by promoting mucosal adher

26 n source or temperature, are known to affect C. albicans stress adaptation.

27 Importantly, CHI3L1 administered after C. albicans inoculation also had strong protection again

28 In this model, PMN activation 10 min after C. albicans infection was largely dependent on the anaph

29 93.7%), and posaconazole (EA, 94.8%) against C. albicans, but its error rate for this species was hig

30 unifying host innate immune defenses against C. albicans as a communicating medium and how C. albican

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

32 ed with PMMA microspheres and probed against C. albicans cells immobilized onto biopolymer-coated sub

33 et of cell types for skin protection against C. albicans invasion.

34 ls that selectively detect Candida albicans (C. albicans).

35 hibited synergistic growth inhibition of all C. albicans strains, except C. albicans MYA-2876 by ITC.

36 mediator of the metabolic changes that allow C. albicans to overcome the macrophage innate immunity b

37 Although C. albicans could directly stimulate IL-17 production by

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

39 ion between wild-type F. nucleatum 23726 and C. albicans SN152 in an in vitro assay could be greatly

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

41 cell effector responses against E. coli and C. albicans displayed differential MR1 dependency and TC

42 triggers marked fluctuations in host Cu and C. albicans readily adapts by modulating Cu uptake and b

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

44 king to beta-1,3 glucan-, A. fumigatus-, and C. albicans-containing phagosomes.

45 L-17 affords protection against both HIV and C. albicans, and because Vdelta1 T cells are not deplete

46 (NAC) species with various morphologies and C. albicans transcription factor mutants (efg1/efg1 and

47 xplain the mutualistic role of S. mutans and C. albicans in cariogenic biofilms.

48 f respiratory yeasts such as P. pastoris and C. albicans, and it may have novel moonlighting function

49 cing of individual host cell populations and C. albicans revealed that dermal invasion is directly im

50 ompartmentalization of Th cell responses and C. albicans pathogenesis and have critical implications

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

52 are unable to form hyphae are as virulent as C. albicans during polymicrobial IAI.

53 on, we demonstrated that S. oralis augmented C. albicans invasion through epithelial junctions.

54 omeostasis (PHO) to TORC1 may differ between C. albicans and S. cerevisiae The converse direction of

55 This sensor distinguishes between C. albicans and those microbes devoid of cell-surface ma

56 nism underlying physical interaction between C. albicans and F. nucleatum and for the first time reve

57 study suggests that the interaction between C. albicans and F. nucleatum leads to a mutual attenuati

58 icated that the physical interaction between C. albicans and F. nucleatum was mediated by the carbohy

59 signaling pathways at the interface between C. albicans and host cells in various contexts of infect

60 l trend, in mixed- Candida species biofilms, C. albicans lost dominance in the presence of antifungal

61 q to characterize the transcriptomes of both C. albicans and human endothelial cells or oral epitheli

62 Four species cause >90% of Candida BSI: C. albicans, C. glabrata, C. parapsilosis, and C. tropic

63 t sensory neurons were directly activated by C. albicans.

64 This review focuses on diseases caused by C. albicans, the role of IL-17-mediated immunity in cand

65 our current knowledge of biofilms formed by C. albicans and closely related fungal species.

66 profound resistance to systemic infection by C. albicans, such that greater than 80% of mice lacking

67 In many host niches inhabited by C. albicans, glucose is scarce, with protein being avail

68 .1 nM are completely resistant to killing by C. albicans The peptide also protects macrophages and au

69 crease in the level of macrophage killing by C. albicans.

70 rotecting macrophages from lysis mediated by C. albicans hyphae.

71 gen in humans, and most diseases produced by C. albicans are associated with biofilms.

72 typic analyses were performed on 21 clinical C. albicans isolates.

73 Using mating-competent C. albicans haploids, each carrying a different gene dri

74 In contrast, C. albicans isolates could be correctly identified as su

75 In laboratory cultures with abundant Cu, C. albicans expresses a Cu-requiring form of superoxide

76 gnostics for identifying and differentiating C. albicans from other Candida species are critical for

77 Similarly, diploid C. albicans also showed enhanced biofilm formation in th

78 ls were the dominant source of IL-17A during C. albicans infection and were required for pathogen res

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

80 is a critical mediator in human blood during C. albicans infection.

81 This response to Cu is initiated during C. albicans invasion of the host where the yeast is expo

82 ctivity promotes phagosome maturation during C. albicans infection but is dysregulated on the phagoso

83 s MDSCs to comparable levels observed during C. albicans infection.

84 genera were typically associated with either C. albicans colonization or altered cytokine expression

85 ing-deficient DeltalasR mutant also enhances C. albicans pathogenicity in coinfection and induces ext

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

87 against planktonic C. albicans and excellent C. albicans versus mammalian cell selectivity.

88 nhibition of all C. albicans strains, except C. albicans MYA-2876 by ITC.

89 endritic cells (DCs) were required to expand C. albicans-responsive Vdelta1 T cells to generate suffi

90 Moreover, the IL-17A-expressing C. albicans strains showed significantly reduced pathoge

91 lper cell responses to yeast and filamentous C. albicans.

92 ught to depend on recognition of filamentous C. albicans.

93 nsitivity of 92.3% (95% CI, 85.4%-96.6%) for C. albicans/C. tropicalis, 94.2% (95% CI, 84.1%-98.8%) f

94 and exhibited similar binding affinities for C. albicans yeast and purified mannan.

95 CaTAF12, but not CaTAF12L, is essential for C. albicans growth.

96 broth microdilution was slightly higher for C. albicans (87%) than for other species (85.8%).

97 t the creation of systematic identifiers for C. albicans genes and sequence features using a system s

98 or C. tropicalis and C. krusei, 2 CFU/mL for C. albicans and C. glabrata, and 3 CFU/mL for C. parapsi

99 as a detection limit of around 32 CFU/mL for C. albicans.

100 to 5.5-fold-higher discriminatory power for C. albicans than P-CalB2208.

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

102 temic inflammation without a requirement for C. albicans morphogenesis.

103 al effect against three C. albicans and four C. albicans strains, respectively.

104 help to protect the epithelial barrier from C. albicans breach.

105 ion significantly protected the corneal from C. albicans and induced CHI3L1 expression in C57BL/6 mou

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

107 phosphorylation-mimicking Mep2 variants from C. albicans show large conformational changes in a conse

108 ognition of the clinically important fungus, C. albicans.

109 trength and binding dynamics modulating GtfB-C. albicans adhesive interactions in situ.

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

111 We find that high C. albicans burden, fungal epithelial invasion, swimblad

112 . albicans as a communicating medium and how C. albicans overgrowth in the oral cavity may be a resul

113 ccordingly, we found that a hyperfilamentous C. albicans strain breaches the epithelial barrier more

114 a rapid and accurate method for identifying C. albicans, C. glabrata, and C. parapsilosis, the three

115 In C. albicans, exposure to GlcNAc activates cell signallin

116 arker for TOR-dependent anabolic activity in C. albicans.

117 y to perform genetic interaction analysis in C. albicans and is readily extended to other fungal path

118 to facilitate efficient genetic analysis in C. albicans.

119 needed to observe a full metabolic cycle in C. albicans, metabolic profiling provides an avenue for

120 pecies genetic and phenotypic differences in C. albicans and delineates a natural mutation that alter

121 exity of the processes influenced by Dig1 in C. albicans, and the observation that Dig1 is one of the

122 anizes chromosomes at the spindle equator in C. albicans to overcome fundamental noisiness in microtu

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

124 dance of IL-17-controlled gene expression in C. albicans-infected human oral epithelial cells (OECs)

125 uingly, even though loss of Dig1 function in C. albicans enhances filamentous growth and biofilm form

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

127 nderlies the epigenetic control of mating in C. albicans We also discuss how fitness advantages could

128 ey regulators of cell fate and morphology in C. albicans.

129 uncovers a mechanism of azole resistance in C. albicans, involving increased membrane rigidity and T

130 s regulating genome stability are rewired in C. albicans.

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

132 ing unknown components of TORC1 signaling in C. albicans revealed that the phosphate transporter Pho8

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

134 Thus in C. albicans, differential chromatin states controls gene

135 ock genes and genes involved in virulence in C. albicans.

136 la, which was associated with both increased C. albicans colonization and reduced IL-21 expression.

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

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

139 bilitated and immunocompromised individuals, C. albicans may spread to cause life-threatening systemi

140 To understand how antibiotics influence C. albicans colonization, we treated mice orally with va

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

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

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

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

145 owed increased killing activity against live C. albicans that was dependent on Dectin-1, Syk, and NAD

146 M treated with heat-killed C. albicans, live C. albicans, or the specific Dectin-1 agonists curdlan o

147 Phagosomes containing live C. albicans cells became transiently Rab14 positive with

148 genital mucosae with Candida species, mainly C. albicans.

149 issue from moribund animals revealed massive C. albicans hyphal invasion coupled with S. aureus deep

150 e the contribution of each factor to mating, C. albicans white cells were reverse-engineered to expre

151 Moreover, C. albicans hyphal growth factor HWP1 as well as ALS1 an

152 transporters are repressed in MTLa/MTLalpha C. albicans.

153 er CX3CR1 confers protection against mucosal C. albicans infection has not been investigated.

154 Importantly, impeding development of mucosal C. albicans infection by administering antifungal flucon

155 tans restored the biofilm-forming ability of C. albicans bcr1Delta mutant and bcr1Delta/Delta mutant,

156 lled by Efg1 are critical for the ability of C. albicans to induce mortality from an intra-abdominal

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

158 le technique to characterize the adhesion of C. albicans to acrylic surfaces.

159 troscopy results showed that the adhesion of C. albicans to PMMA is morphology dependent, as hyphal t

160 Here we perform a genome-scale analysis of C. albicans morphogenesis and identify 102 negative morp

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

162 impacts the macrophage-killing capability of C. albicans.

163 1-->3)-beta-D-glucan levels and clearance of C. albicans from liver, spleen, kidney, brain, lung, vit

164 ng showed that mortality is a consequence of C. albicans breaching the epithelial barrier and invadin

165 Deletion of C. albicans genes that control zinc acquisition in the Z

166 Detection of C. albicans by Dectin-1, a C-type signaling lectin speci

167 me were much more consistent determinants of C. albicans colonization than either the GI fungal micro

168 Moreover, it allowed distinction of C. albicans from other related Candida spp. and could th

169 mice lacking Sts-1 and -2 survive a dose of C. albicans (2.5 x 10(5) CFU/mouse) that is uniformly le

170 rom systemic infection with a lethal dose of C. albicans, and deficiency of dectin-1, dectin-2, or bo

171 phage phagosomes following the engulfment of C. albicans cells.

172 combined with azoles, with the exception of C. albicans 64124 and MYA-2876 by FLC and VOR.

173 hologies is an important virulence factor of C. albicans.

174 ss filamentation, a key virulence feature of C. albicans, through the production of lactic acid and o

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

176 ybridization assay for the identification of C. albicans (green fluorescence), C. glabrata (red fluor

177 for the rapid and specific identification of C. albicans in clinical and related applications, especi

178 electron microscopy (SEM) and AFM imaging of C. albicans confirmed the polymorphic behavior of both s

179 ion cultures; however, the medical impact of C. albicans (like that of many other microorganisms) dep

180 tes to the differences in the interaction of C. albicans white and opaque cells with macrophages.

181 laboratory strain and a clinical isolate of C. albicans were used for SCFS experiments.

182 s fluconazole-resistant clinical isolates of C. albicans and non-albicans species, and it exhibited p

183 ition of biofilm formation and by killing of C. albicans in mature biofilms.

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

185 ative adhesin-like cell wall mannoprotein of C. albicans and radD, an arginine-inhibitable adhesin-en

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

187 inhibits growth and hyphal morphogenesis of C. albicans SN152 in a contact-dependent manner.

188 the first farnesol hypersensitive mutant of C. albicans.

189 nd discriminative ability against a panel of C. albicans and various nontarget Candida spp.

190 ings offer insights into the pathogenesis of C. albicans and suggest therapeutic avenues for candidia

191 In contrast, phagocytosis of C. albicans by PMN 60 min postinfection occurred almost

192 o mediate the engulfment and phagocytosis of C. albicans cells by human immune cells in biologically

193 The presence of C. albicans enhances S. mutans growth within biofilms, y

194 this has on the innate immune recognition of C. albicans.

195 ecessary and sufficient for the reduction of C. albicans virulence and biofilm formation through the

196 n factor Pho4 is vital for the resistance of C. albicans to these diverse stresses.

197 This cell type-specific response of C. albicans to different environmental conditions reflec

198 echanisms underlie the stress sensitivity of C. albicans sfp1 cells during growth on glucose, and rtg

199 us here on human and mouse skin as a site of C. albicans infection, and we review established and new

200 ering host susceptibilities for the sites of C. albicans infection have revealed tissue compartmental

201 model setup with a drug-resistant strain of C. albicans.

202 ch was transformed into the DAY286 strain of C. albicans.

203 ) against laboratory and clinical strains of C. albicans, C. glabrata and C. tropicalis were evaluate

204 We determined the X-ray structures of C. albicans CYP51 complexes with posaconazole and VT-116

205 To date, most studies of C. albicans have been carried out in suspension cultures

206 dition of these cytokines or supernatants of C. albicans-treated DCs to Vdelta1 T cells was not suffi

207 attern (PAMP) located at the cell surface of C. albicans and other pathogenic Candida species, is mod

208 he carbohydrate components on the surface of C. albicans and the protein components on the Fusobateri

209 fB adhered heterogeneously on the surface of C. albicans, showing a higher frequency of adhesion fail

210 ogen interaction by regulating the uptake of C. albicans by host cells.

211 s been suggested to enhance the virulence of C. albicans, indicating that it may exert detrimental ef

212 ggest that IL-17A mitigates the virulence of C. albicans.

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

214 profound effects, EntV(68) has no effect on C. albicans viability, even in the presence of significa

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

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

217 mune response and their collective impact on C. albicans colonization.

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

219 ffects of a Bdf1 BD-inactivating mutation on C. albicans viability.

220 s showed that IL-23 was required for optimal C. albicans-induced IL-17 production.

221 in response to either fungal beta-glucan or C. albicans hyphae and fibronectin, with VLA3 inducing h

222 hogenetic conversions in the fungal pathogen C. albicans.

223 s, as well as against human fungal pathogens C. albicans and C. grubii.

224 y used by successful human fungal pathogens, C. albicans provokes recognition by host immune cells le

225 mers with potent activity against planktonic C. albicans and excellent C. albicans versus mammalian c

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

227 cosyltransferase B (GtfB) itself can promote C. albicans biofilm development.

228 ducing innate immune mechanisms, may promote C. albicans colonization and likely subsequent sensitiza

229 n that elevated CO(2) concentration promotes C. albicans cells to undergo a phenotypic switch from wh

230 ion of Candida hyphal morphogenesis promotes C. albicans survival and negatively impacts the macropha

231 ortance of metabolic adaptation in promoting C. albicans survival in the host.

232 Remarkably, C. albicans infections can fit into all six DRF classifi

233 n the fluconazole-susceptible and -resistant C. albicans.

234 nd selective activity against drug-resistant C. albicans in biofilms, as manifested by inhibition of

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

236 e in vivo protects mice from lethal systemic C. albicans infection.

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

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

239 We conclude that C. albicans and S. oralis synergize to activate host enz

240 pressing SUR7 These results demonstrate that C. albicans eisosomes promote the ability of Sur7 to reg

241 We demonstrate that C. albicans filamentation is not required for escape fro

242 e Cu-sensing regulator Mac1 and ensures that C. albicans maintains constant SOD activity for cytosoli

243 in the face of assembly noise and find that C. albicans operates very close to this limit, which may

244 Here we report that C. albicans cells switch between two heritable cell type

245 ost phagocytic defenses, we also report that C. albicans pho4Delta cells are acutely sensitive to mac

246 and genome-wide RNA sequencing reveals that C. albicans heterochromatin represses expression of repe

247 o model mucosal lung infection and show that C. albicans and P. aeruginosa are synergistically virule

248 We show that C. albicans may evade immune detection by presenting a m

249 These data show that C. albicans stimulates proliferation and IL-17 productio

250 Altogether, we show that C. albicans-driven neutralization of the phagosome promo

251 We have shown that C. albicans co-opts amino acid catabolism to generate an

252 The data suggest that C. albicans exploits environmentally contingent regulato

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

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

255 at a bacterial exoenzyme (GtfB) augments the C. albicans counterpart in mixed-species biofilms throug

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

257 mosome-level, phased diploid assembly of the C. albicans genome, coupled with improvements that we ha

258 lently and selectively bind to mannan on the C. albicans cell surface to form crosslinks.

259 We discover that the C. albicans transcription factor Cas5 is crucial for pro

260 enzyme binds with remarkable strength to the C. albicans cell surface (~2 nN) and showed a low dissoc

261 a narrower range of binding forces (vs. the C. albicans surface).

262 To accomplish this, C. albicans white cells secrete a low-molecular-weight c

263 synergistic antifungal effect against three C. albicans and four C. albicans strains, respectively.

264 Thus, C. albicans morphology drives distinct T helper cell res

265 d binding (10-fold reduction) of Fe-Hst 5 to C. albicans cells.

266 e sequence properties influencing binding to C. albicans cells.

267 The strong and highly stable GtfB binding to C. albicans could explain, at least in part, why this ba

268 C is essential for mucocutaneous immunity to C. albicans but is otherwise largely redundant.

269 Immunity to C. albicans involves various immune parameters, but the

270 Mucocutaneous immunity to C. albicans requires T helper 17 (Th17) cell differentia

271 Immunity to C. albicans, the most frequent species to be isolated in

272 nt microbiota, and other factors can lead to C. albicans overgrowth, causing a wide range of infectio

273 ther to immobilized fungal beta-glucan or to C. albicans hyphae without ECM.

274 Flagellin applied topically 24 h prior to C. albicans inoculation significantly protected the corn

275 dermal gammadelta T cells and resistance to C. albicans required IL-23 production from CD301b(+) der

276 typic aggregation and NETosis in response to C. albicans mediated by the beta2 integrin, complement r

277 escence quantitative analysis in response to C. albicans vaginal infection in the presence of hormone

278 the maximal mucosal inflammatory response to C. albicans.

279 ntial components of the mucosal responses to C. albicans.

280 evels and were more frequently sensitized to C. albicans than controls.

281 C. tropicalis was highly lethal, similar to C. albicans, while S. aureus-C. dubliniensis, S. aureus-

282 sensory neurons increased susceptibility to C. albicans infection, which could be rescued by exogeno

283 t affect the migration of macrophages toward C. albicans cells, the rate of engulfment, the overall u

284 hanges in iron uptake genes in Hst 5-treated C. albicans cells.

285 or the two TAF12 variants in the unicellular C. albicans genome.

286 Unlike C. albicans, IL-17 responses were induced normally in CA

287 Nanoscopic imaging of caspofungin-unmasked C. albicans cell walls revealed that the increase in glu

288 nscriptome analysis of treated and untreated C. albicans using Gene Ontology (GO) revealed a large cl

289 The new decamer peptide FBP4 stained viable C. albicans cells more efficiently in their mature hypha

290 In vitro, C. albicans and P. aeruginosa have a bidirectional and l

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

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

293 we underscore select oral diseases in which C. albicans is a contributory microorganism in immune-co

294 at F. nucleatum ATCC 23726 coaggregates with C. albicans SN152, a process mainly mediated by fusobact

295 Coinoculation with C. albicans strains deficient in the transcription facto

296 n sustained, high-level GI colonization with C. albicans.

297 rter (renamed CDR6/ROA1 for consistency with C. albicans nomenclature) could efflux xenobiotics such

298 in both mouse and human cells infected with C. albicans, indicating that JNK1 may be a therapeutic t

299 properties governing GtfB interactions with C. albicans.

300 ntamicin (PSG) and then inoculated them with C. albicans by gavage.