Research Topics
| M NiimiSummaryAffiliation: University of Otago Country: New Zealand Publications
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Detail Information
Publications
Differential profiles of soluble proteins during the initiation of morphogenesis in Candida albicansM Niimi
Experimental Oral Biology Laboratory, Department of Oral Biology and Oral Pathology, School of Dentistry, University of Otago, P O Box 647, Dunedin, New Zealand
Arch Microbiol 166:260-8. 1996..albicans morphogenesis may be differentially synthesised...
Temperature-related expression of the vacuolar aspartic proteinase (APR1) gene and beta-N-acetylglucosaminidase (HEX1) gene during Candida albicans morphogenesisM Niimi
Department of Oral Biology and Oral Pathology, University of Otago, Dunedin, New Zealand
FEMS Microbiol Lett 148:247-54. 1997..The expression of HEX1 mRNA is in part under the control of culture pH and translation of HEX1 mRNA seems to be regulated by glucose...
Candida albicans pathogenicity: a proteomic perspectiveM Niimi
Department of Oral Sciences and Orthodontics, School of Dentistry, University of Otago, Dunedin, New Zealand
Electrophoresis 20:2299-308. 1999..albicans cells. This article describes the potential of applying proteome analysis to C. albicans in order to better understand pathogenicity and identify new antifungal targets...
Functional expression of Candida albicans drug efflux pump Cdr1p in a Saccharomyces cerevisiae strain deficient in membrane transportersK Nakamura
Department of Oral Sciences and Orthodontics, University of Otago, Dunedin, New Zealand
Antimicrob Agents Chemother 45:3366-74. 2001..albicans Cdr1p in an S. cerevisiae background deficient in other pumps allows the functional analysis of pumping specificity and mechanisms of a major ABC transporter involved in drug efflux from an important human pathogen...
Regulation of N-acetylglucosaminidase production in Candida albicansK Niimi
Department of Oral Biology and Oral Pathology, School of Dentistry, University of Otago, Dunedin, New Zealand
Arch Microbiol 168:464-72. 1997..The cellular location of the enzyme and the regulation of production by the carbon source indicate a scavenging role for C. albicans N-acetylglucosaminidase...
Overexpression of Candida albicans CDR1, CDR2, or MDR1 does not produce significant changes in echinocandin susceptibilityK Niimi
Department of Oral Sciences, University of Otago, P.O. Box 647, 310 Great King Street, Dunedin, New Zealand
Antimicrob Agents Chemother 50:1148-55. 2006..The assessment of micafungin and caspofungin potency is therefore assay dependent; the differences seen with agar plate drug resistance assays occur over narrow ranges of echinocandin concentrations and are not of clinical significance...
Clinically significant micafungin resistance in Candida albicans involves modification of a glucan synthase catalytic subunit GSC1 (FKS1) allele followed by loss of heterozygosityK Niimi
Department of Oral Sciences, University of Otago, 310 Great King St, Dunedin 9054, New Zealand
J Antimicrob Chemother 65:842-52. 2010..To determine the mechanism of intermediate- and high-level echinocandin resistance, resulting from heterozygous and homozygous mutations in GSC1 (FKS1), in both laboratory-generated and clinical isolates of Candida albicans...
Chemosensitization of fluconazole resistance in Saccharomyces cerevisiae and pathogenic fungi by a D-octapeptide derivativeK Niimi
Department of Oral Sciences, University of Otago, Dunedin, New Zealand
Antimicrob Agents Chemother 48:1256-71. 2004..KN20 therefore appears to indirectly chemosensitize cells to FLC by a nonlethal permeabilization of the fungal plasma membrane...
Multiple efflux mechanisms are involved in Candida albicans fluconazole resistanceG D Albertson
Department of Oral Biology and Oral Pathology, University of Otago, Dunedin, New Zealand
Antimicrob Agents Chemother 40:2835-41. 1996..These results suggest that fluconazole enters C. albicans cells by facilitated diffusion and that fluconazole resistance may involve energy-dependent drug efflux associated with increased expression of Benr and/or Cdr1...
