title: Protein folding diseases and neurodegeneration: lessons learned from yeast.
abstract: Budding yeast Saccharomyces cerevisiae has proven to be a valuable model organism for studying fundamental cellular processes across the eukaryotic kingdom including man. In this respect, complementation assays, in which the yeast protein is replaced by a homologous protein from another organism, have been very instructive. A newer trend is to use the yeast cell factory as a toolbox to understand cellular processes controlled by proteins for which the yeast lacks functional counterparts. An increasing number of studies have indicated that S. cerevisiae is a suitable model system to decipher molecular mechanisms involved in a variety of neurodegenerative disorders caused by aberrant protein folding. Here we review the current knowledge gained by the use of so-called humanized yeasts in the field of Huntington's, Parkinson's and Alzheimer's diseases.
authors.affiliation: Functional Biology, Katholieke Universiteit Leuven, Kasteelpark Arenberg 31, Leuven-Heverlee, Belgium. joris.winderickx@bio.kuleuven.be
authors.forename: Joris
authors.initials: J
authors.lastname: Winderickx
authors.forename: Charlotte
authors.initials: C
authors.lastname: Delay
authors.forename: Ann
authors.initials: A
authors.lastname: De Vos
authors.forename: Harald
authors.initials: H
authors.lastname: Klinger
authors.forename: Klaartje
authors.initials: K
authors.lastname: Pellens
authors.forename: Thomas
authors.initials: T
authors.lastname: Vanhelmont
authors.forename: Fred
authors.initials: F
authors.lastname: Van Leuven
authors.forename: Piotr
authors.initials: P
authors.lastname: Zabrocki
mesh_terms: D000544:Alzheimer Disease / Q000378:metabolism* / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000378:metabolism; D017209:Apoptosis / Q000502:physiology; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism*; D006360:Heat-Shock Proteins / Q000378:metabolism; D006801:Humans; D000071058:Huntingtin Protein; D006816:Huntington Disease / Q000378:metabolism* / Q000503:physiopathology; D008954:Models, Biological; D009410:Nerve Degeneration / Q000378:metabolism*; D009419:Nerve Tissue Proteins / Q000737:chemistry / Q000378:metabolism; D009687:Nuclear Proteins / Q000737:chemistry / Q000378:metabolism; D010300:Parkinson Disease / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D010455:Peptides / Q000378:metabolism; D017510:Protein Folding; D012441:Saccharomyces cerevisiae / Q000378:metabolism*; D015003:Yeasts; D051844:alpha-Synuclein / Q000737:chemistry / Q000378:metabolism; D016875:tau Proteins / Q000737:chemistry / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D051017:Apoptosis Regulatory Proteins; C086055:HTT protein, human; D006360:Heat-Shock Proteins; D000071058:Huntingtin Protein; D009419:Nerve Tissue Proteins; D009687:Nuclear Proteins; D010455:Peptides; D051844:alpha-Synuclein; D016875:tau Proteins; C097188:polyglutamine