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10.1080/15548627.2015.1093718

http://scihub22266oqcxt.onion/10.1080/15548627.2015.1093718
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C4824573!4824573!26391226
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suck abstract from ncbi


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pmid26391226      Autophagy 2015 ; 11 (11): 2127-9
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  • GABARAP-mediated targeting of PI4K2A/PI4KII? to autophagosomes regulates PtdIns4P-dependent autophagosome-lysosome fusion #MMPMID26391226
  • Albanesi J; Wang H; Sun HQ; Levine B; Yin H
  • Autophagy 2015[Nov]; 11 (11): 2127-9 PMID26391226show ga
  • For decades, phosphatidylinositol 4-phosphate (PtdIns4P) was considered primarily as a precursor in the synthesis of phosphatidylinositol(4,5)bisphosphate (PtdIns(4,5)P2). More recently, specific functions for PtdIns4P itself have been identified, particularly in the regulation of intracellular membrane trafficking. PI4K2A/PI4KII? (phosphatidylinositol 4-kinase type 2 ?), one of the 4 enzymes that catalyze PtdIns4P production in mammalian cells, promotes vesicle formation from the trans-Golgi network (TGN) and endosomes. We recently identified a novel function for PI4K2A-derived PtdIns4P, as a facilitator of autophagosome-lysosome (A-L) fusion. We further showed that that this function requires the presence of the autophagic adaptor protein GABARAP (GABA[A] receptor-associated protein), which binds to PI4K2A and recruits it to autophagosomes. The mechanism whereby GABARAP-PI4K2A-PtdIns4P promotes A-L fusion remains to be defined. Based on other examples of phosphoinositide involvement in membrane trafficking, we speculate that it acts by recruiting elements of the membrane docking and fusion machinery.
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