Michael Tscherner
Medical University of Vienna
27 Papers
75 Citations
Michael Tscherner is an academic researcher from Medical University of Vienna. The author has contributed to research in topics: Candida albicans & Chromatin. The author has an hindex of 11, co-authored 27 publications. Previous affiliations of Michael Tscherner include Wyss Institute for Biologically Inspired Engineering & University of Graz.
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Papers
Systematic phenotyping of a large-scale Candida glabrata deletion collection reveals novel antifungal tolerance genes.
Tobias Schwarzmüller,Biao Ma,Ekkehard Hiller,Fabian Istel,Michael Tscherner,Sascha Brunke,Lauren Ames,Arnaud Firon,Brian Green,Vitor Cabral,Marina Marcet-Houben,Ilse D. Jacobsen,Jessica Quintin,Katja Seider,Ingrid E. Frohner,Walter Glaser,Helmut Jungwirth,Sophie Bachellier-Bassi,Murielle Chauvel,Ute Zeidler,Dominique Ferrandon,Toni Gabaldón,Bernhard Hube,Christophe d'Enfert,Steffen Rupp,Brendan P. Cormack,Ken Haynes,Karl Kuchler +27 more
TL;DR: The results demonstrate the potential of the C. glabrata mutant collection as a valuable resource in functional genomics studies of this important fungal pathogen of humans, and to facilitate the identification of putative novel antifungal drug target and virulence genes.
Positions and Numbers of FKS Mutations in Candida albicans Selectively Influence In Vitro and In Vivo Susceptibilities to Echinocandin Treatment
Michaela Lackner,Michael Tscherner,Martin Schaller,Karl Kuchler,Christian Mair,Bettina Sartori,Fabian Istel,Maiken Cavling Arendrup,Cornelia Lass-Flörl +8 more
TL;DR: It is shown for the first time the caspofungin-mediated in vivo selection of a double mutation within one allele of the FKS1 hot spot 1 in a clinical isolate, and it is demonstrated that echinocandin EUCAST breakpoint definitions correlate with the in vivo response when a standard dosing regimen is used but cannot predict the in vitro response after a dose escalation.
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Pathogenesis and Antifungal Drug Resistance of the Human Fungal Pathogen Candida glabrata
TL;DR: The mechanisms underlying virulence and drug resistance of C. glabrata are emphasized, its ability to escape from the host immune surveillance or persist inside host cells is discussed, and the development of antifungal resistance is diminishing efficacies of therapeutic interventions.
The histone acetyltransferase Hat1 facilitates DNA damage repair and morphogenesis in Candida albicans
TL;DR: It is demonstrated that C. albicans is the first organism known to require histone H4 processing for endogenous DNA damage repair and morphogenesis, and it is proposed that targeting this class of histone acetyltransferases in fungal pathogens may have potential in antifungal therapy.
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The Fungal Histone Acetyl Transferase Gcn5 Controls Virulence of the Human Pathogen Candida albicans through Multiple Pathways
Raju Shivarathri,Michael Tscherner,Florian Zwolanek,Nitesh Kumar Singh,Neeraj Chauhan,Karl Kuchler +5 more
TL;DR: It is reported here that Gcn5, a paradigm lysyl-acetyl transferase modifying both histone and non-histone targets, controls fungal morphogenesis – a key virulence factor of C. albicans.