Defining the proximal interaction networks of Arf GTPases reveals a mechanism for the regulation of PLD1 and PI4KB.

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第一作者： Fu-Long,Li

第一单位： Department of Pharmacology and Moores Cancer Center, University of California San Diego, La Jolla, CA, USA.

作者： Fu-Long,Li ^[1] ; Zhengming,Wu ^[1] ; Yong-Qi,Gao ^[2] ; Forrest Z,Bowling ^[3] ; J Matthew,Franklin ^[1] ; Chongze,Hu ^[4] ; Raymond T,Suhandynata ^[2] ; Michael A,Frohman ^[5] ; Michael V,Airola ^[3] ; Huilin,Zhou ^[2] ; Kun-Liang,Guan ^[1]

作者单位： Department of Pharmacology and Moores Cancer Center, University of California San Diego, La Jolla, CA, USA. ^[1] Department of Cellular and Molecular Medicine, University of California San Diego, La Jolla, CA, USA. ^[2] Department of Biochemistry and Cell Biology, Stony Brook University, Stony Brook, NY, USA. ^[3] Department of Nanoengineering, Program of Materials Science and Engineering, University of California San Diego, La Jolla, CA, USA. ^[4] Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY, USA. ^[5]

关键词 ARL11 ARL5 PI4KB PLD1 Phagocytosis

主题词 1-磷脂酰肌醇4-激酶(1-Phosphatidylinositol 4-Kinase);GTP磷酸水解酶类(GTP Phosphohydrolases);高尔基体(Golgi Apparatus);磷脂酶D(Phospholipase D)

DOI 10.15252/embj.2022110698

PMID 35844135

发布时间 2023-12-01

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