5TDQ
Crystal Structure of the GOLD domain of ACBD3
5TDQ の概要
| エントリーDOI | 10.2210/pdb5tdq/pdb |
| 分子名称 | Golgi resident protein GCP60 (1 entity in total) |
| 機能のキーワード | beta barrel, gold domain, transport protein |
| 由来する生物種 | Homo sapiens (Human) |
| タンパク質・核酸の鎖数 | 1 |
| 化学式量合計 | 19214.14 |
| 構造登録者 | |
| 主引用文献 | McPhail, J.A.,Ottosen, E.H.,Jenkins, M.L.,Burke, J.E. The Molecular Basis of Aichi Virus 3A Protein Activation of Phosphatidylinositol 4 Kinase III beta , PI4KB, through ACBD3. Structure, 25:121-131, 2017 Cited by PubMed Abstract: Phosphatidylinositol 4-kinase III beta (PI4KIIIβ) is an essential enzyme in mediating membrane transport, and plays key roles in facilitating viral infection. Many pathogenic positive-sense single-stranded RNA viruses activate PI4KIIIβ to generate phosphatidylinositol 4-phosphate (PI4P)-enriched organelles for viral replication. The molecular basis for PI4KIIIβ activation during viral infection has remained largely unclear. We describe the biochemical reconstitution and characterization of the complex of PI4KIIIβ with the Golgi protein Acyl-coenzyme A binding domain containing protein 3 (ACBD3) and Aichi virus 3A protein on membranes. We find that 3A directly activates PI4KIIIβ, and this activation is sensitized by ACBD3. The interfaces between PI4KIIIβ-ACBD3 and ACBD3-3A were mapped with hydrogen-deuterium exchange mass spectrometry (HDX-MS). Determination of the crystal structure of the ACBD3 GOLD domain revealed a unique N terminus that mediates the interaction with 3A. Rationally designed complex-disrupting mutations in both ACBD3 and PI4KIIIβ completely abrogated the sensitization of 3A activation by ACBD3. PubMed: 27989622DOI: 10.1016/j.str.2016.11.016 主引用文献が同じPDBエントリー |
| 実験手法 | X-RAY DIFFRACTION (2.493 Å) |
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