Journal
TRENDS IN CELL BIOLOGY
Volume 10, Issue 3, Pages 98-105Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/S0962-8924(99)01711-0
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Funding
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R37GM025874, R01GM025874] Funding Source: NIH RePORTER
- NIGMS NIH HHS [GM025874] Funding Source: Medline
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Recent work suggests that two unrelated phenotypes, [PSI+] and [URE3], in the yeast Saccharomyces cerevisiae are transmitted by non-covalent changes in the physical states of their protein determinants, Sup35p and Ure2p, rather than by changes in the genes that encode these proteins. The mechanism by which alternative protein states are self-propagating is the key to understanding how proteins function as elements of epigenetic inheritance. Here, we fonts on recent molecular-genetic analysis of the inheritance of the [PSI+] factor of S. cerevisiae. Insights into this process might be extendable to a group of mammalian diseases (the amyloidoses), which are also believed to be a manifestation of self-perpetuating changes in protein conformation.
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