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大鼠肝细胞核中的磷酸肌醇3激酶

Phosphoinositide 3-kinase in rat liver nuclei.

作者信息

Lu P J, Hsu A L, Wang D S, Yan H Y, Yin H L, Chen C S

机构信息

Division of Medicinal Chemistry and Pharmaceutics, College of Pharmacy, University of Kentucky, Lexington 40536, USA.

出版信息

Biochemistry. 1998 Apr 21;37(16):5738-45. doi: 10.1021/bi972551g.

Abstract

Biochemical and immunochemical data from the present investigation reveal the existence of a p85/p110 phosphoinositide 3-kinase (PI 3-kinase) in rat liver nuclei. 32P-Labeling of membrane phosphoinositides by incubating intact nuclei with [gamma-32P]ATP results in the formation of [32P]phosphatidyl-inositol 3,4, 5-trisphosphate [PtdIns(3,4,5)P3], accompanied by small quantities of [32P]phosphatidylinositol 3-phosphate [PtdIns(3)P]. Studies with subnuclear fractions indicate that the PI 3-kinase is not confined to nuclear membranes. The nuclear soluble fraction also contains PI 3-kinase and an array of inositide-metabolizing enzymes, including phospholipase C (PLC), phosphoinositide phosphatase, and diacylglycerol (DAG) kinase. As a result, exposure of phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2] to the nuclear extract in the presence of [gamma-32P]ATP generates a series of 32P-labeled D-3 phosphoinositides and phosphatidic acid (PA) in an interdependent manner. On the basis of the immunological reactivity and kinetic behavior, the nuclear PI 3-kinase is analogous, if not identical, to PI 3-kinase alpha, and constitutes about 5% of the total PI 3-kinase in the cell. Moreover, we test the premise that nuclear PI 3-kinase may, in part, be regulated through the control of substrate availability by PtdIns(4,5)P2-binding proteins. Effect of CapG, a nuclear actin-regulatory protein, on PI 3-kinase activity is examined in view of its unique Ca2+-dependent PtdIns(4, 5)P2-binding capability. In vitro data show that the CapG-mediated inhibition of nuclear PI 3-kinase is prompted by PKC phosphorylation of CapG and elevated [Ca2+]. This CapG-dependent regulation provides a plausible link between nuclear PLC and PI 3-kinase pathways for cross-communications. Taken together, these findings provide definite data concerning the presence of an autonomous PI 3-kinase cycle in rat liver nuclei. The nuclear location of PI 3-kinase may lead to a better understanding regarding its functional role in transducing signals from the plasma membrane to the nucleus in response to diverse physiological stimuli.

摘要

本研究的生化和免疫化学数据表明,大鼠肝细胞核中存在p85/p110磷酸肌醇3激酶(PI 3激酶)。完整细胞核与[γ-32P]ATP孵育后,膜磷酸肌醇的32P标记导致[32P]磷脂酰肌醇3,4,5-三磷酸[PtdIns(3,4,5)P3]形成,同时伴有少量[32P]磷脂酰肌醇3-磷酸[PtdIns(3)P]。对亚核组分的研究表明,PI 3激酶并不局限于核膜。核可溶性组分中也含有PI 3激酶以及一系列肌醇代谢酶,包括磷脂酶C(PLC)、磷酸肌醇磷酸酶和二酰基甘油(DAG)激酶。因此,在[γ-32P]ATP存在的情况下,将磷脂酰肌醇4,5-二磷酸[PtdIns(4,5)P2]暴露于核提取物会以相互依赖的方式产生一系列32P标记的D-3磷酸肌醇和磷脂酸(PA)。基于免疫反应性和动力学行为,核PI 3激酶即便不完全相同,也与PI 3激酶α类似,并且占细胞中总PI 3激酶的约5%。此外,我们检验了这样一个前提,即核PI 3激酶可能部分通过PtdIns(4,5)P2结合蛋白对底物可用性的控制来进行调节。鉴于核肌动蛋白调节蛋白CapG独特的Ca2+依赖性PtdIns(4,5)P2结合能力,研究了其对PI 3激酶活性的影响。体外数据表明,CapG介导的核PI 3激酶抑制是由CapG的PKC磷酸化和升高的[Ca2+]引发的。这种CapG依赖性调节为核PLC和PI 3激酶途径之间的交叉通讯提供了一个合理的联系。综上所述,这些发现提供了关于大鼠肝细胞核中存在自主PI 3激酶循环的确切数据。PI 3激酶的核定位可能有助于更好地理解其在响应各种生理刺激时将信号从质膜转导至细胞核中的功能作用。

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