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| Content Provider | PubMed Central |
|---|---|
| Author | Rosner, Margit Fuchs, Christiane Siegel, Nicol Valli, Alessandro Markus, Hengstschläger |
| Abstract | Dysregulation of the mammalian target of rapamycin (mTOR) kinase pathway is centrally involved in a wide variety of cancers and human genetic diseases. In mammalian cells, mTOR is part of two different kinase complexes: mTORC1 composed of mTOR, raptor and mLST8, and mTORC2 containing mTOR, rictor, sin1 and mLST8. Whereas, mTORC1 is known to be a pivotal regulator of cell size and cell cycle control, the question whether the recently discovered mTORC2 complex is involved in these processes remains elusive. We report here that the mTORC1-mediated consequences on cell cycle and cell size are separable and do not involve effects on mTORC2 activity. However, we show that mTORC2 itself is a potent regulator of mammalian cell size and cell cycle via a mechanism involving the Akt/TSC2/Rheb cascade. Our data are of relevance for the understanding of the molecular development of the many human diseases caused by deregulation of upstream and downstream effectors of mTOR. |
| Related Links | http://dx.doi.org/10.1093/hmg/ddp271 |
| Ending Page | 3310 |
| Page Count | 13 |
| Starting Page | 3298 |
| File Format | |
| ISSN | 09646906 |
| e-ISSN | 14602083 |
| Journal | Human Molecular Genetics |
| Issue Number | 17 |
| Volume Number | 18 |
| Language | English |
| Publisher | Oxford University Press |
| Publisher Date | 2009-09-01 |
| Access Restriction | Open |
| Rights Holder | Oxford University Press |
| Subject Keyword | Genetics(clinical) Genetics Molecular Biology Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Genetics Molecular Biology Genetics (clinical) |
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