Suppressing mTORC1 on the lysosome |
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Authors: | Camilla Raiborg Kay O Schink Harald Stenmark |
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Institution: | 1. Centre for Cancer Biomedicine, Faculty of Medicine, University of Oslo, Montebello, Oslo, Norway;2. Department of Molecular Cell Biology, Institute for Cancer Research, Oslo University Hospital, Montebello, Oslo, Norway;3. Centre of Molecular Inflammation Research, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway |
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Abstract: | The mechanistic target of rapamycin, mTOR, is a protein kinase that integrates environmental and nutritional inputs into regulation of cell growth and metabolism. Key outputs of mTOR signalling occur from the lysosome membrane in the form of the multi‐subunit mTOR complex 1 (mTORC1), which phosphorylates multiple targets. While class I phosphoinositide kinase (PI3K‐I) is a well‐known activator of mTORC1, a recent paper (Marat et al, 2017) shows that a class II PI3K with a different substrate specificity, PI3K‐C2β, serves to inhibit mTORC1 on lysosomes under conditions of growth factor deprivation. |
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