ArticleProceedings of the National Academy of Sciences of the United States of America2000
A protein required for prion generation: [URE3] induction requires the Ras-regulated Mks1 protein.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Article
- Proteins with Intrinsically Disordered Domains Are Preferentially Recruited to Polyglutamine Aggregates.PloS one · 2015Article
- Article
- A promiscuous prion: efficient induction of [URE3] prion formation by heterologous prion domains.Genetics · 2009Article
- Article
- Nucleotide exchange factors for Hsp70s are required for [URE3] prion propagation in Saccharomyces cerevisiae.Molecular biology of the cell · 2007Article
- Suppressor analysis of a histone defect identifies a new function for the hda1 complex in chromosome segregation.Genetics · 2006Article
- Primary sequence independence for prion formation.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Role for Hsp70 chaperone in Saccharomyces cerevisiae prion seed replication.Eukaryotic cell · 2005Article
- Scrambled prion domains form prions and amyloid.Molecular and cellular biology · 2004Article
- Ure2, a prion precursor with homology to glutathione S-transferase, protects Saccharomyces cerevisiae cells from heavy metal ion and oxidant toxicity.The Journal of biological chemistry · 2003Article
- Conservation of a portion of the S. cerevisiae Ure2p prion domain that interacts with the full-length protein.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Interactions among prions and prion "strains" in yeast.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Mks1p is required for negative regulation of retrograde gene expression in Saccharomyces cerevisiae but does not affect nitrogen catabolite repression-sensitive gene expression.The Journal of biological chemistry · 2002Article
- Antagonistic interactions between yeast [PSI(+)] and [URE3] prions and curing of [URE3] by Hsp70 protein chaperone Ssa1p but not by Ssa2p.Molecular and cellular biology · 2002Article
- RTG-dependent mitochondria-to-nucleus signaling is regulated by MKS1 and is linked to formation of yeast prion [URE3].Molecular biology of the cell · 2002Article
- A novel Rtg2p activity regulates nitrogen catabolism in yeast.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- Induction of distinct [URE3] yeast prion strains.Molecular and cellular biology · 2001Article
- The crystal structure of the nitrogen regulation fragment of the yeast prion protein Ure2p.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- The level of DAL80 expression down-regulates GATA factor-mediated transcription in Saccharomyces cerevisiae.Journal of bacteriology · 2000Article
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2 authors.
Funding
Abstract
Infectious proteins (prions) can arise de novo as well as by transmission from another individual. De novo prion generation is believed responsible for most cases of Creutzfeldt-Jakob disease and for initiating the mad cow disease epidemic. However, the cellular components needed for prion generation have not been identified in any system. The [URE3] prion of Saccharomyces cerevisiae is an infectious form of Ure2p, apparently a self-propagating amyloid. We now demonstrate a protein required for de novo prion generation. Mks1p negatively regulates Ure2p and is itself negatively regulated by the presence of ammonia and by the Ras-cAMP pathway. We find that in mks1Delta strains, de novo generation of the [URE3] prion is blocked, although [URE3] introduced from another strain is expressed and propagates stably. Ras2(Val19) increases cAMP production and also blocks [URE3] generation. These results emphasize the distinction between prion generation and propagation, and they show that cellular regulatory mechanisms can critically affect prion generation.
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