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固醇调节元件结合蛋白-1(SREBP-1)介导胰岛素及胰岛素样生长因子-I对低密度脂蛋白受体启动子的激活作用。

SREBP-1 mediates activation of the low density lipoprotein receptor promoter by insulin and insulin-like growth factor-I.

作者信息

Streicher R, Kotzka J, Müller-Wieland D, Siemeister G, Munck M, Avci H, Krone W

机构信息

Klinik II und Poliklinik für Innere Medizin, University of Cologne, D-50924 Cologne, Germany.

出版信息

J Biol Chem. 1996 Mar 22;271(12):7128-33. doi: 10.1074/jbc.271.12.7128.

Abstract

Transcription of the low density lipoprotein (LDL) receptor gene is regulated by intracellular cholesterol concentration, hormones, and growth factors. We studied the mechanisms by which insulin and estradiol stimulate promoter activity of the LDL receptor gene. Hormonal effects were analyzed in HepG2 cells after transient transfection with promotor reporter gene constructs. Successive 5' deletions of the LDL receptor promoter fragment from -537 to +88 revealed the sterol regulatory element 1 (SRE-1) between -65 and -56 as an insulin- and estradiol-sensitive cis-element. If the SRE-1 is point mutated at position -59 (C to G), which abolishes the binding of the SRE binding proteins (SREBP-1 and SREBP-2), no insulin or estradiol stimulatory effect on reporter gene expression was observed, indicating a role of SRE binding proteins in this regulatory mechanism. The concentration of the 125-kDa membrane-integrated SREBP-1 precursor protein in LDL repressed HepG2 cells is not altered by hormone treatment. Concentrations of SREBP-1 mRNA and precursor protein are reduced significantly by high and stable expression of an SREBP-1 antisense cDNA fragment in HepG2 cells (SREBP1(-) cells). Transfection of SREBP1(-) cells with promoter construct phLDL4 (-105 to +88) reduces induction of reporter gene activity by insulin and insulin-like growth factor-I to 35 and 17%, respectively, compared with HepG2 cells. The stimulatory effect of estradiol remains unchanged, and the inductions by pravastatin are enlarged. We conclude that different regulatory effects converge at SRE-1, but that SREBP-1 is selectively involved in the signal transduction pathway of insulin and insulin-like growth factor-I leading to LDL receptor gene activation.

摘要

低密度脂蛋白(LDL)受体基因的转录受细胞内胆固醇浓度、激素和生长因子的调节。我们研究了胰岛素和雌二醇刺激LDL受体基因启动子活性的机制。在用启动子报告基因构建体进行瞬时转染后,在HepG2细胞中分析了激素效应。将LDL受体启动子片段从-537至+88进行连续的5'缺失,结果显示-65至-56之间的固醇调节元件1(SRE-1)是一个对胰岛素和雌二醇敏感的顺式元件。如果SRE-1在-59位(C突变为G)发生点突变,这会消除SRE结合蛋白(SREBP-1和SREBP-2)的结合,那么就观察不到胰岛素或雌二醇对报告基因表达的刺激作用,这表明SRE结合蛋白在这种调节机制中发挥作用。激素处理不会改变LDL抑制的HepG2细胞中125-kDa膜整合SREBP-1前体蛋白的浓度。通过在HepG2细胞(SREBP1(-)细胞)中高稳定表达SREBP-1反义cDNA片段,SREBP-1 mRNA和前体蛋白的浓度显著降低。与HepG2细胞相比,用启动子构建体phLDL4(-105至+88)转染SREBP1(-)细胞可使胰岛素和胰岛素样生长因子-I对报告基因活性的诱导分别降至35%和17%。雌二醇的刺激作用保持不变,普伐他汀的诱导作用增强。我们得出结论,不同的调节作用在SRE-1处汇聚,但SREBP-1选择性地参与了导致LDL受体基因激活的胰岛素和胰岛素样生长因子-I的信号转导途径。

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