PHOSPHORYLATION AND INACTIVATION OF HMG-COA REDUCTASE AT THE AMP-ACTIVATED PROTEIN-KINASE SITE IN RESPONSE TO FRUCTOSE TREATMENT OF ISOLATED RAT HEPATOCYTES

被引：65

作者：

GILLESPIE, JG ^{[1
]}

HARDIE, DG ^{[1
]}

机构：

[1] UNIV DUNDEE,DEPT BIOCHEM,DUNDEE DD1 4HN,SCOTLAND

来源：

FEBS LETTERS | 1992年 / 306卷 / 01期

基金：

英国惠康基金;

关键词：

HMG-COA REDUCTASE; CHOLESTEROL SYNTHESIS; PROTEIN KINASE; PHOSPHORYLATION SITE; PROTEIN PHOSPHORYLATION; HEPATOCYTE;

D O I：

10.1016/0014-5793(92)80837-7

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

We have previously shown that incubation of isolated hepatocytes with fructose leads to elevation of AMP and activation of the AMP-activated protein kinase. We now show that this treatment causes marked inactivation of HMG-CoA reductase. Using immunoprecipitation from the microsomal fraction of P-32-labelled cells, we also show that this treatment leads to a 2.6-fold increase in the phosphorylation of the 100 kDa subunit of HMG-CoA reductase. Successive digestion of this P-32-labelled subunit with cyanogen bromide and endoproteinase Lys-C confirmed that Ser-871, the site phosphorylated in cell-free assays by the AMP-activated protein kinase, was the only site phosphorylated under these conditions.

引用

页码：59 / 62

页数：4

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