田邊　賢司    Department   Research Institutes and Facilities, Research Institutes and Facilities    Position   Associate Professor
Article types	Original article
Language	English
Peer review	Peer reviewed
Title	PtdIns4KIIα generates endosomal PtdIns(4)P and is required for receptor sorting at early endosomes.
Journal	Formal name：Molecular biology of the cell Abbreviation：Mol Biol Cell ISSN code：(1939-4586)1059-1524(Linking)
Domestic / Foregin	Foregin
Volume, Issue, Page	27(6),pp.990-1001
Author and coauthor	Henmi Yuji, Morikawa Yoshiaki, Oe Natsuko, Ikeda Narumi, Fujita Akikazu, Takei Kohji, Minogue Shane, Tanabe Kenji
Authorship	Last author,Corresponding author
Publication date	2016/03
Summary	Phosphatidylinositol 4-kinase IIα (PtdIns4KIIα) localizes to the trans-Golgi network and endosomal compartments and has been implicated in the regulation of endosomal traffic, but the role of both its enzymatic activity and the site of its action have not been elucidated. This study shows that PtdIns4KIIα is required for production of endosomal phosphatidylinositol 4-phosphate (PtdIns(4)P) on early endosomes and for the sorting of transferrin and epidermal growth factor receptor into recycling and degradative pathways. Depletion of PtdIns4KIIα with siRNA significantly reduced the amount of vesicular PtdIns(4)P on early endosomes but not on Golgi membranes. Cells depleted of PtdIns4KIIα had an impaired ability to sort molecules destined for recycling from early endosomes. We further identify the Eps15 homology domain-containing protein EHD3 as a possible endosomal effector of PtdIns4KIIα. Tubular endosomes containing EHD3 were shortened and became more vesicular in PtdIns4KIIα-depleted cells. Endosomal PtdIns(4,5)P2 was also significantly reduced in PtdIns4KIIα-depleted cells. These results show that PtdIns4KIIα regulates receptor sorting at early endosomes through a PtdIns(4)P-dependent pathway and contributes substrate for the synthesis of endosomal PtdIns(4,5)P2.
DOI	10.1091/mbc.E15-08-0564
PMID	26823017