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第二信使参与低密度脂蛋白受体基因的调控。

Involvement of second messengers in regulation of the low-density lipoprotein receptor gene.

作者信息

Auwerx J H, Chait A, Wolfbauer G, Deeb S S

机构信息

Department of Medicine, University of Washington, Seattle 98195.

出版信息

Mol Cell Biol. 1989 Jun;9(6):2298-302. doi: 10.1128/mcb.9.6.2298-2302.1989.

Abstract

Transcription of the low-density lipoprotein receptor (LDL-R) gene in the human monocytic leukemic cell line THP-1 and in the human hepatocarcinoma cell line Hep-G2 is regulated by second messengers of the diacylglycerol-protein kinase C (DAG-PKC), inositol 1,4,5-triphosphate-Ca2+, and cyclic AMP pathways. Exogenous phospholipase C (which releases DAG and inositol 1,4,5-triphosphate), PKC activators (phorbol esters and DAG), Ca2+ ionophores, and a cyclic AMP analog all transiently induced accumulation of LDL-R mRNA. The effects of these three signal-transducing pathways were to a large extent additive. Furthermore, PKC stimulation effected an increase in LDL binding, which suggested that the increase in LDL-R mRNA resulted in an increase in functional cell surface receptor activity. These results suggest that uptake of cholesterol by these cells is under control of both intracellular cholesterol levels and external signals.

摘要

人单核细胞白血病细胞系THP - 1和人肝癌细胞系Hep - G2中低密度脂蛋白受体(LDL - R)基因的转录受二酰基甘油 - 蛋白激酶C(DAG - PKC)、肌醇1,4,5 - 三磷酸 - Ca2 +和环磷酸腺苷途径的第二信使调控。外源性磷脂酶C(释放DAG和肌醇1,4,5 - 三磷酸)、PKC激活剂(佛波酯和DAG)、Ca2 +离子载体和环磷酸腺苷类似物均能瞬时诱导LDL - R mRNA的积累。这三条信号转导途径的作用在很大程度上是累加的。此外,PKC刺激导致LDL结合增加,这表明LDL - R mRNA的增加导致功能性细胞表面受体活性增加。这些结果表明,这些细胞对胆固醇的摄取受细胞内胆固醇水平和外部信号的控制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b67/362302/b9e704f709ad/molcellb00054-0019-a.jpg

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