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First published online February 8, 2006
doi: 10.1242/10.1242/jcs.02855
Commentary |
Department of Biochemistry, Norwegian Radium Hospital and University of Oslo, Montebello, N-0310 Oslo, Norway
* Author for correspondence (e-mail: stenmark{at}ulrik.uio.no)
Accepted 22 December 2005
Phosphoinositide (PI) 3-kinases control essential cellular functions such as cytoskeletal dynamics, signal transduction and membrane trafficking. FYVE, PX and PH domains mediate the binding of effector proteins to the lipid products of PI 3-kinases. Recent studies have provided significant insights into the roles of PI 3-kinases, their catalytic products and their downstream effectors in membrane trafficking. Class I and II PI 3-kinases trigger receptor-induced trafficking processes, such as phagocytosis, macropinocytosis and regulated exocytosis. Class I PI 3-kinases also function to inhibit autophagy. By contrast, class III PI 3-kinases mainly mediate receptor-independent trafficking events, which mostly are related to endocytic membrane traffic, phagosome maturation and autophagy.
Key words: Autophagy, Endocytosis, Exocytosis, Macropinocytosis, Phagocytosis, PI 3-kinase
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