N-连接糖基化在3-羟基-3-甲基戊二酰辅酶A还原酶活性调节及SV40转化的3T3细胞增殖中的作用。
The role of N-linked glycosylation in the regulation of activity of 3-hydroxy-3-methylglutaryl-coenzyme A reductase and proliferation of SV40-transformed 3T3 cells.
作者信息
Larsson O, Engström W
机构信息
Department of Tumour Pathology, Karolinska Hospital, Stockholm, Sweden.
出版信息
Biochem J. 1989 Jun 1;260(2):597-600. doi: 10.1042/bj2600597.
The effects of glycosylation inhibitors on the proliferation of SV40-transformed 3T3 cells (SV-3T3) were examined in vitro. Whereas swainsonine and castanospermine, which inhibit distal steps in the glycosylational processing, exerted marginal or no effects on cell proliferation, a proximal inhibitor, tunicamycin, efficiently decreased the rate of DNA synthesis and also inhibited the activity of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase. The inhibitory effects of tunicamycin on cell proliferation could be partially reversed by addition of dolichol, a metabolite in the pathway regulated by HMG-CoA reductase. This finding suggests that tunicamycin exerts at least one of its effects on cell proliferation by modulating the activity of HMG-CoA reductase.
在体外研究了糖基化抑制剂对猿猴病毒40（SV40）转化的3T3细胞（SV - 3T3）增殖的影响。抑制糖基化加工远端步骤的苦马豆素和野靛碱对细胞增殖影响甚微或没有影响，而一种近端抑制剂衣霉素能有效降低DNA合成速率，还能抑制3 - 羟基 - 3 - 甲基戊二酰辅酶A（HMG - CoA）还原酶的活性。通过添加法尼基醇（一种受HMG - CoA还原酶调节的途径中的代谢物），衣霉素对细胞增殖的抑制作用可部分逆转。这一发现表明，衣霉素通过调节HMG - CoA还原酶的活性，至少对细胞增殖发挥了一种作用。
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