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糖基化对心肌细胞中脂蛋白脂肪酶的激活需要在内质网中修剪葡萄糖残基。

Activation of lipoprotein lipase in cardiac myocytes by glycosylation requires trimming of glucose residues in the endoplasmic reticulum.

作者信息

Carroll R, Ben-Zeev O, Doolittle M H, Severson D L

机构信息

MRC Signal Transduction Group, Faculty of Medicine, University of Calgary, Alberta, Canada.

出版信息

Biochem J. 1992 Aug 1;285 ( Pt 3)(Pt 3):693-6. doi: 10.1042/bj2850693.

Abstract

Incubation of cycloheximide-treated cardiac myocytes results in a time-dependent increase in cellular and heparin-releasable lipoprotein lipase (LPL) activities. N-Methyldeoxynojirimycin (1 mM) and castanospermine (100 micrograms/ml), inhibitors of glucosidases in the endoplasmic reticulum (ER), prevented the increase in cellular LPL activity. The glucosidase inhibitors did not influence the synthesis or turnover of LPL protein. Therefore activation of LPL by glycosylation in cardiac myocytes requires the trimming of glucose residues in oligosaccharide chains by glucosidases of the ER.

摘要

用环己酰亚胺处理心肌细胞后,细胞内及可从肝素中释放的脂蛋白脂肪酶(LPL)活性随时间增加。内质网(ER)中葡糖苷酶的抑制剂N-甲基脱氧野尻霉素(1 mM)和栗精胺(100微克/毫升)可阻止细胞LPL活性的增加。葡糖苷酶抑制剂不影响LPL蛋白的合成或周转。因此,心肌细胞中LPL通过糖基化的激活需要内质网葡糖苷酶对寡糖链中葡萄糖残基进行修剪。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb84/1132848/bd7d3760a524/biochemj00130-0025-a.jpg

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