急性肾损伤介导磷脂酰肌醇-4-羟基激酶-β的募集，并刺激高尔基体复合物上磷脂酰肌醇-4,5-二磷酸的合成。

ARF mediates recruitment of PtdIns-4-OH kinase-beta and stimulates synthesis of PtdIns(4,5)P2 on the Golgi complex.

作者信息

Godi A, Pertile P, Meyers R, Marra P, Di Tullio G, Iurisci C, Luini A, Corda D, De Matteis M A

机构信息

Department of Cell Biology and Oncology, Istituto di Ricerche Farmacologiche Mario Negri, Santa Maria Imbaro, Italy.

出版信息

Nat Cell Biol. 1999 Sep;1(5):280-7. doi: 10.1038/12993.

DOI:10.1038/12993

PMID:10559940

Abstract

The small GTPase ADP-ribosylation factor (ARF) regulates the structure and function of the Golgi complex through mechanisms that are understood only in part, and which include an ability to control the assembly of coat complexes and phospholipase D (PLD). Here we describe a new property of ARF, the ability to recruit phosphatidylinositol-4-OH kinase-beta and a still unidentified phosphatidylinositol-4-phosphate-5-OH kinase to the Golgi complex, resulting in a potent stimulation of synthesis of phosphatidylinositol-4-phosphate and phosphatidylinositol-4,5-bisphosphate; this ability is independent of its activities on coat proteins and PLD. Phosphatidylinositol-4-OH kinase-beta is required for the structural integrity of the Golgi complex: transfection of a dominant-negative mutant of the kinase markedly alters the organization of the organelle.

摘要

小GTP酶ADP核糖基化因子（ARF）通过部分已知的机制调节高尔基体复合体的结构和功能，这些机制包括控制衣被复合体和磷脂酶D（PLD）组装的能力。在此，我们描述了ARF的一种新特性，即它能够将磷脂酰肌醇-4-OH激酶β和一种尚未鉴定的磷脂酰肌醇-4-磷酸-5-OH激酶募集到高尔基体复合体，从而有力地刺激磷脂酰肌醇-4-磷酸和磷脂酰肌醇-4,5-二磷酸的合成；这种能力与其对衣被蛋白和PLD的活性无关。磷脂酰肌醇-4-OH激酶β是高尔基体复合体结构完整性所必需的：转染该激酶的显性负性突变体可显著改变细胞器的组织结构。