ライフサイエンスコーパス: C. albicans

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

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

3 C. albicans faces both low and high zinc bottlenecks in

4 C. albicans grows both as single yeast cells and hyphal

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

6 C. albicans is also a predominantly opportunistic fungal

7 C. albicans sap6 deletion mutants failed to accumulate i

8 C. albicans secreted aspartic protease Sap6 is important

9 C. albicans strains from oak are similar to clinical C.

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

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

12 C. albicans was a stronger activator for isolated human

13 We show that intravenous injection of 25,000 C. albicans cells causes a highly localized cerebritis m

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

15 vailable annotated reference sequences of 22 C. albicans strains, thus offering a higher coverage and

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

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

18 CytoD was able to abrogate C. albicans killing.

19 Additionally, C. albicans can also exert inhibitory effects on platele

20 reducing the metabolic activity of adherent C. albicans and C. auris biofilms by more than 66% and 5

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

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

23 gocytosis and proinflammatory response after C. albicans exposure that declined during later time poi

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

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

26 onal antibody proved to be effective against C. albicans, both in vitro and in vivo, and to act toget

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

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

29 phils, which synergistically protect against C. albicans invasive infection.

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

31 that modulation of the Th1 response against C. albicans by platelets is dependent on PGs.

32 Drug resistance among C. albicans isolates poses a common challenge, and overc

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

34 e C. albicans PSD mitochondrial activity and C. albicans growth, with an MIC(50) of 22.5 and 15 mug/m

35 Candida species (C. glabrata, C. auris, and C. albicans efg1Delta/Delta cph1Delta/Delta) and Sacchar

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

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

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

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

40 orces between S. mutans (or S. gordonii) and C. albicans in the presence and absence of in situ gluca

41 that S. parasanguinis disrupts S. mutans and C. albicans biofilm synergy in a contact and H(2)O(2)-in

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

43 impact of S. parasanguinis on S. mutans and C. albicans synergy.

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

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

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

47 Healthy women, asymptomatic C. albicans carriers, and symptomatic patients with vagi

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

49 Candida albicans and Staphylococcus aureus (C. albicans/S. aureus) results in 80 to 90% mortality in

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

51 bolic and glucan-dependent synergism between C. albicans and S. mutans contribute to enhanced pathoge

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

53 We find that both C. albicans and candidalysin activate human epithelial E

54 .1 nM are completely resistant to killing by C. albicans The peptide also protects macrophages and au

55 fructose that can be readily metabolized by C. albicans, enhancing growth and acid production.

56 together, we identified key pathways used by C. albicans in the mixed biofilm, indicating an active f

57 ropose that it represents a strategy used by C. albicans to efficiently colonize different niches of

58 ans strains from oak are similar to clinical C. albicans in that they are predominantly diploid and c

59 nding affinity of S. mutans to glucan-coated C. albicans resulted in a larger structure during early

60 responsive to tonic stimulation by commensal C. albicans improves host defense against extracellular

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

62 However, commensal C. albicans does not protect against intracellular influ

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

64 l T cells subsets and potentially conferring C. albicans, an advantage in overcoming DC-mediated immu

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

66 Our data showed that Ca37 was able to detect C. albicans cells, and it bound to Adh1 in yeast and Adh

67 or regulates cell differentiation in diploid C. albicans cells, as EFG1 hemizygous cells undergo a ph

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

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

70 ing mechanism mediated by GtfB that enhances C. albicans carbohydrate utilization.

71 strains, and was active against established C. albicans biofilms in vitro.

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

73 ungal activity against all four fungi except C. albicans.

74 have extensive acute inflammation following C. albicans water-soluble complex challenge, they do not

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

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

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

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

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

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

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

82 y biofilm initiation compared to S. gordonii-C. albicans biofilms.

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

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

85 uced less IFN-gamma upon stimulation with HK C. albicans This effect was dependent on the direct cont

86 PBMCs were stimulated with heat-killed (HK) C. albicans in the presence or absence of isolated washe

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

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

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

90 this study, we show that highly immunogenic C. albicans hyphae attract phagocytic cells, which rapid

91 In C. albicans cultures, SOD4 and SOD5 were predominantly c

92 In C. albicans Zrc1 plays an important role in the generati

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

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

95 to facilitate efficient genetic analysis in C. albicans.

96 athways that alter cell wall architecture in C. albicans, thereby affecting its survival upon exposur

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

98 teins that physically interact with Cdc14 in C. albicans.

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

100 h thrombin, we saw a significant decrease in C. albicans survival.

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

102 nt of evolutionary new centromeres (ENCs) in C. albicans.

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

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

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

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

107 "To dissect complex genetic interactions in C. albicans, a CRISPR-Cas9-based Gene Drive Array (GDA)

108 usly been identified as Cdc14 interactors in C. albicans or S. cerevisiae.

109 CRISPR-mediated deletion of this Ca-loop in C. albicans revealed that the Ca-loop is critical for fu

110 ions associated with genetic manipulation in C. albicans and advances researchers' ability to perform

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

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

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

114 the expectations set by baseline methods in C. albicans and D. melanogaster, it leaves considerable

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

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

117 analyses to study a possible role of Rme1 in C. albicans morphogenesis.

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

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

120 identified Wss1 (weak suppressor of Smt3) in C. albicans (CaWss1) using bioinformatics, genetic compl

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

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

123 on of the role of CaWss1 in DPC tolerance in C. albicans.

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

125 in diminished fungicidal activity, increased C. albicans viability within macrophages, and decreased

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

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

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

129 During infections, C. albicans has to cope with genotoxic stresses generate

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

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

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

133 red to placebo, NDV-3A vaccination inhibited C. albicans dissemination to kidneys and prevented colon

134 We then investigated C. albicans actions on platelet activation, granule rele

135 ng enhanced antifungal resistance, high iron C. albicans cells had reduced survival upon phagocytosis

136 first time that platelets can directly kill C. albicans through release of their granular contents.

137 120 days, and also following multiple lethal C. albicans/S. aureus rechallenges.

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

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

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

141 have potential utility as drug for managing C. albicans infections.

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

143 fungicidal against clinical isolates of MDR C. albicans in vitro.

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

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

146 ith the isolation of Candida species, namely C. albicans and C. auris, exhibiting resistance to curre

147 03 were identified as inhibiting both native C. albicans PSD mitochondrial activity and C. albicans g

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

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

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

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

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

153 ric translocations in the common ancestor of C. albicans and C. tropicalis.

154 , which may explain evolutionary benefits of C. albicans as a commensal microbe.

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

156 fungicidal activity, reducing the burden of C. albicans and C. auris below the limit of detection wi

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

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

159 m enhances the growth and GI colonization of C. albicans.

160 rowth, morphogenesis, and GI colonization of C. albicans.

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

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

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

164 8) provide insights into the determinants of C. albicans commensal fitness within the mammalian gut.

165 germ tube, hyphae and biofilm development of C. albicans in vitro.

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

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

168 2)-C cells and inhibition and eradication of C. albicans biofilms.

169 al morphogenesis - a key virulence factor of C. albicans.

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

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

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

173 e most potent molecule, inhibiting growth of C. albicans and C. auris strains at concentrations rangi

174 d that CaTMPK is essential for the growth of C. albicans In conclusion, these findings not only ident

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

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

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

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

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

180 g amino acids 106-123, namely the Ca-loop of C. albicans TMPK (CaTMPK), contributes to the hyperactiv

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

182 potential drug target for the management of C. albicans infections.

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

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

185 the first farnesol hypersensitive mutant of C. albicans.

186 c profiling to unravel molecular pathways of C. albicans when cocultured with S. mutans in mixed biof

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

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

189 the novel formulation for the prevention of C. albicans colonization on denture material and develop

190 ophysical, and cell biological properties of C. albicans SOD4 and SOD5.

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

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

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

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

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

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

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

198 norhabditis elegans infected with strains of C. albicans and C. auris, relative to the untreated cont

199 ence of multidrug resistant (MDR) strains of C. albicans and other Candida spp., highlighting the urg

200 ed genome sequence data for three strains of C. albicans that we isolated from oak trees in an ancien

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

202 fected with drug-sensitive or MDR strains of C. albicans.

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

204 tion, the antibody prolonged the survival of C. albicans infected-Galleria mellonella larvae, when C.

205 istance mechanisms including upregulation of C. albicans drug-efflux, regulation of oxidative stress

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

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

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

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

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

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

212 impact of this cross-kingdom relationship on C. albicans remains largely uncharacterized.

213 howed that the toxicity of the releasates on C. albicans is concentration dependent.

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

215 Other C. albicans genes and proteins directly and indirectly r

216 hogenetic conversions in the fungal pathogen C. albicans.

217 Furthermore, patient C. albicans-induced cytokine production was influenced b

218 Phagocytosed C. albicans shifted expression programs to survive the n

219 single infected macrophages and phagocytosed C. albicans displayed a tightly coordinated shift in gen

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

221 S to trigger genome instability in polyploid C. albicans cells.

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

223 the development of novel methods to prevent C. albicans-related mortality.

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

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

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

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

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

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

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

231 ospores of fluconazole/caspofungin resistant C. albicans strains, and was active against established

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

233 r antifungal activity against drug-resistant C. albicans.

234 particularly as our previous work has shown C. albicans virulence factor modulation by oral bacteria

235 We found that unlike mammalian Cu,Zn-SOD1, C. albicans SOD5 indeed rapidly loses its copper to meta

236 specificity of detection of Candida species (C. albicans, C. auris, C. dubliniensis, C. famata, C. gl

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

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

239 As the majority of systemic C. albicans infections stem from endogenous gastrointest

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

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

242 candidiasis, C. auris was less virulent than C. albicans.

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

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

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

246 These results indicate that C. albicans CCL represents a 'parameiosis' that blurs th

247 Here, we report that C. albicans and A. fumigatus infection induced inflammat

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

249 Our data reveal that C. albicans exploits a diverse range of specific host si

250 Here, we reveal that C. albicans tetraploid cells are metabolically hyperacti

251 -based quantitative proteomics revealed that C. albicans genes and proteins associated with carbohydr

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

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

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

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

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

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

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

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

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

261 lms on epithelial tissue, facilitated by the C. albicans adhesin encoded by ALS3 While a bacterium-fu

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

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

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

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

266 a show that S. gordonii binding force to the C. albicans surface is significantly higher than that of

267 ng forces are dramatically enhanced when the C. albicans cell surface is locally coated with extracel

268 itis group) has been shown to bind avidly to C. albicans hyphae via direct cell-to-cell interaction,

269 rix development and GtfB-mediated binding to C. albicans mannan.

270 mune response that augmented host defense to C. albicans and S. aureus.

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

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

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

274 Dectin-1 signaling machinery in response to C. albicans.

275 the maximal mucosal inflammatory response to C. albicans.

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

277 CD82 knockout mice were more susceptible to C. albicans as compared with wild-type mice.

278 hat cefoperazone-treated mice susceptible to C. albicans infection had significantly decreased levels

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

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

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

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

283 Upon C. albicans infection, Gsr(-/-) mice exhibited dramatica

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

285 , an efficient transformation protocol using C. albicans haploids, and an optimized mating strategy t

286 also extended to a lethal intravenous (i.v.) C. albicans challenge but had no effect in the C. albica

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

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

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

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

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

292 While C. albicans does not appear to affect alpha or dense gra

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

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

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

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

297 es and single macrophage cells infected with C. albicans from uninfected cells and assessed transcrip

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

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

300 anti-rAls3p-N antibodies that interfere with C. albicans ability to adhere to and invade endothelial