The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Tor, a Phosphatidylinositol Kinase Homologue, Controls Autophagy in Yeast
Open accessAbstract
Autophagy is a bulk protein degradation process that is induced by starvation. The control mechanism for induction of autophagy is not well understood. We found that Tor, a phosphatidylinositol kinase homologue, is involved in the control of autophagy in the yeast, Saccharomyces cerevisiae. When rapamycin, an inhibitor of Tor function, is added, autophagy is induced even in cells growing in nutrient-rich medium. A temperature-sensitive tor mutant also leads to induction of autophagy at a nonpermissive temperature. These results indicate that Tor negatively regulates the induction of autophagy. Tor is the first molecule that is identified as a pivotal player in the starvation-signaling pathway of autophagy. Furthermore, we found that a high concentration of cAMP is inhibitory for induction of autophagy. APG gene products are involved in autophagy induced by starvation. Autophagy was not induced in apg mutants in the presence of rapamycin, indicating that the site of action of Tor is upstream of those of Apg proteins. In nutrient-rich medium, Apg proteins are involved also in the transport of aminopeptidase I from the cytosol to the vacuole. Tor may act to switch Apg function between autophagy and transport of aminopeptidase I.
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Cites
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RAPT1, a mammalian homolog of yeast Tor, interacts with the FKBP12/rapamycin complex.
Chiu, M. I., Katz, H., & Berlin, V (1994) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.91.26.12574 · Cited by 481
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Metadata
- Authors
- Noda, T., & Ohsumi, Y.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 1998-02
- Volume
- 273
- Issue
- 7
- Pages
- 3963-3966
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2057764483
- Cited by
- 1,309
- References
- 2
- FWCI
- 22.47
- Type
- journal article
- Language
- en
- Open access
- hybrid
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