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黑色素瘤细胞中的核鞘磷脂合酶和蛋白激酶Cδ

Nuclear sphingomyelin-synthase and protein kinase C delta in melanoma cells.

作者信息

Albi Elisabetta, La Porta Caterina A M, Cataldi Samuela, Magni Mariapia Viola

机构信息

Department of Clinical and Experimental Medicine, Physiopathology, Policlinico Monteluce, University of Perugia, Italy.

出版信息

Arch Biochem Biophys. 2005 Jun 15;438(2):156-61. doi: 10.1016/j.abb.2005.04.004. Epub 2005 Apr 25.

DOI:10.1016/j.abb.2005.04.004
PMID:15907783
Abstract

The aim of this research is to study the influence of protein kinase C delta on the nuclear phospholipids metabolism. Murine and human melanoma cells, in which overexpression of protein kinase delta was induced, were used. After purification of the nuclei, the phosphatidylcholine-dependent phospholipase C, sphingomyelin-synthase, and sphingomyelinase activities were measured. The results showed that the nuclear sphingomyelin-synthase activity increased and sphingomyelinase activity decreased in the protein kinase C delta overexpressive cells with respect to the controls. As a consequence, the ceramide pool decreased and diacylglycerol pool increased; this effect was not due to the phosphatidylcholine-dependent phospholipase C activity that did not change. The inhibition of sphingomyelinase could be due to protein kinase C delta as well as to existence of a sort of nuclear self-regulation between sphingomyelin-synthase and sphingomyelinase. The possible role of nuclear sphingomyelin-synthase in cell proliferation is discussed.

摘要

本研究的目的是探讨蛋白激酶Cδ对核磷脂代谢的影响。使用诱导了蛋白激酶δ过表达的小鼠和人黑色素瘤细胞。纯化细胞核后,测定磷脂酰胆碱依赖性磷脂酶C、鞘磷脂合酶和鞘磷脂酶的活性。结果表明,与对照组相比,蛋白激酶Cδ过表达细胞中核鞘磷脂合酶活性增加,鞘磷脂酶活性降低。因此,神经酰胺池减少,二酰基甘油池增加;这种效应不是由于磷脂酰胆碱依赖性磷脂酶C活性未发生变化所致。鞘磷脂酶的抑制可能归因于蛋白激酶Cδ以及鞘磷脂合酶和鞘磷脂酶之间存在的一种核自我调节。文中讨论了核鞘磷脂合酶在细胞增殖中的可能作用。

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