Fungal cytoskeleton dysfunction or immune activation triggered by beta-glucan synthase inhibitors: potential mechanisms for the prolonged antifungal activity of echinocandins.
Department of Infectious Diseases, Infection Control, and Employee Health, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA. asafdar@mdanderson.org
Amar
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Safdar
D000818:Animals; D000935:Antifungal Agents / Q000494:pharmacology*; D002473:Cell Wall / Q000187:drug effects; D003599:Cytoskeleton / Q000187:drug effects*; D054714:Echinocandins / Q000494:pharmacology*; D005656:Fungal Proteins / Q000276:immunology / Q000378:metabolism*; D005964:Glucosyltransferases / Q000037:antagonists & inhibitors*; D006801:Humans; D007113:Immunity, Innate / Q000187:drug effects*; D008954:Models, Biological; D047071:beta-Glucans / Q000276:immunology* / Q000378:metabolism
D000935:Antifungal Agents; D054714:Echinocandins; D005656:Fungal Proteins; D047071:beta-Glucans; D005964:Glucosyltransferases; C020570:1,3-beta-glucan synthase