Panasyuk, G and Nemazanyy, I and Zhyvoloup, A and Filonenko, V and Davies, D and Robson, M and Pedley, RB and Waterfield, M and Gout, I (2009) mTORbeta splicing isoform promotes cell proliferation and tumorigenesis. J.Biol.Chem. , 284 (45) 30807 - 30814.
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The mTOR (mammalian target of rapamycin) promotes growth in response to nutrients and growth factors and is deregulated in numerous pathologies, including cancer. The mechanisms by which mTOR senses and regulates energy metabolism and cell growth are relatively well understood, whereas the molecular events underlining how it mediates survival and proliferation remain to be elucidated. Here, we describe the existence of the mTOR splicing isoform, TOR beta, which, in contrast to the full-length protein (mTOR alpha), has the potential to regulate the G(1) phase of the cell cycle and to stimulate cell proliferation. mTOR beta is an active protein kinase that mediates downstream signaling through complexing with Rictor and Raptor proteins. Remarkably, overexpression of mTOR beta transforms immortal cells and is tumorigenic in nude mice and therefore could be a proto-oncogene
|Title:||mTORbeta splicing isoform promotes cell proliferation and tumorigenesis|
|Additional information:||DA - 20091102 IS - 1083-351X (Electronic) IS - 0021-9258 (Linking) LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't RN - 0 (Protein Isoforms) RN - EC 2.7.- (Protein Kinases) RN - EC 2.7.1.- (mTOR protein) SB - IM|
|Keywords:||Animals, Cell Cycle, Cell Line, Cell Proliferation, Cell Transformation,Neoplastic, Humans, Mice, Mice,Nude, Protein Isoforms, genetics, metabolism, Protein Kinases, Protein Transport, RNA Splicing|
|UCL classification:||UCL > School of Life and Medical Sciences > Faculty of Life Sciences > Biosciences (Division of) > Structural and Molecular Biology|
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