作者: Michiel T. van Diepen , Maddy Parsons , C. Peter Downes , Nicholas R. Leslie , Robert Hindges
DOI: 10.1038/NCB1961
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摘要: The tumour suppressor PTEN can inhibit cell proliferation and migration as well control growth, in different types. functions predominately a lipid phosphatase, converting PtdIns(3,4,5)P(3) to PtdIns(4,5)P(2), thereby antagonizing PI(3)K (phosphoinositide 3-kinase) its established downstream effector pathways. However, much is unclear concerning the mechanisms that regulate movement membrane, which necessary for activity towards (Refs 3, 4, 5). Here we show requirement functional motor proteins of PI3K signalling, involving previously unknown association between myosinV. FRET (Forster resonance energy transfer) measurements revealed interacts directly with myosinV, dependent on phosphorylation mediated by CK2 and/or GSK3. Inactivation myosinV-transport function neurons increased size, which, line known attributes PTEN-loss, required mTor. Our data demonstrate myosin-based transport mechanism regulates function, providing new insights into signalling networks regulating growth.