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脱氧胞苷不仅被挽救进入DNA,还被挽救进入磷脂前体。III. 扁桃体淋巴细胞中dCOP-二酰基甘油的形成。

Deoxycytidine is salvaged not only into DNA but also into phospholipid precursors. III. dCOP-diacylglycerol formation in tonsillar lymphocytes.

作者信息

Spasokukotskaja T, Taljanidisz J, Sasvári-Székely M, Staub M

机构信息

1st Institute of Biochemistry, Semmelweis University Medical School, Budapest, Hungary.

出版信息

Biochem Biophys Res Commun. 1991 Jan 31;174(2):680-7. doi: 10.1016/0006-291x(91)91471-n.

Abstract

In addition to the water-soluble deoxyliponucleotides (Spasokukotskaja et al. (1988), Biochem. Biophys. Res. Commun. 155, 923), a lipid compound was shown to be labeled from external 3H-deoxycytidine (5-3H-CdR) in infant tonsillar lymphocytes. Chlorpromazine enhanced the labeling of this compound, identified by TLC as 3H-dCDP-diacylglycerol (3H-dCOP-DAG). The deoxynucleotide salvage pathway seems to be the main source for dCDP-DAG synthesis, as hydroxyurea increased its labeling from CdR. myo-Inositol induced the disappearance of 5-3H-dCOP-DAG, suggesting its utilization for phosphatidylinositol synthesis. 3H-Arabinosyl-Cytosine (araC) is also incorporated into the lipidic fraction at a rate comparable to its incorporation into DNA, supporting the effect of araC on membrane functions.

摘要

除了水溶性脱氧脂核苷酸(斯帕索库科茨卡娅等人(1988年),《生物化学与生物物理研究通讯》155卷,923页)外,在婴儿扁桃体淋巴细胞中,一种脂质化合物被证明可从外部的3H-脱氧胞苷(5-3H-CdR)进行标记。氯丙嗪增强了这种经薄层层析鉴定为3H-dCDP-二酰甘油(3H-dCOP-DAG)的化合物的标记。脱氧核苷酸补救途径似乎是dCDP-DAG合成的主要来源,因为羟基脲增加了其从CdR的标记。肌醇诱导5-3H-dCOP-DAG消失,表明其用于磷脂酰肌醇合成。3H-阿拉伯糖基胞嘧啶(araC)也以与其掺入DNA相当的速率掺入脂质部分,支持了araC对膜功能的作用。

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