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中国仓鼠卵巢细胞热敏和耐热性缺陷突变体中的蛋白质糖基化

Protein glycosylation in heat-sensitive and thermotolerance-deficient mutants of Chinese hamster ovary cells.

作者信息

Henle K J, Nagle W A, Bedford J S, Harvey W F

机构信息

Department of Medicine, University of Arkansas for Medical Sciences, Little Rock 72205.

出版信息

J Cell Sci. 1990 Apr;95 ( Pt 4):555-61. doi: 10.1242/jcs.95.4.555.

DOI:10.1242/jcs.95.4.555
PMID:2117015
Abstract

Chinese hamster ovary (CHO) cells are capable of developing a high degree of thermotolerance in response to appropriate heat conditioning. In this study we examined the relationship between thermotolerance development and protein glycosylation using four sublines of CHO cells. Two of these CHO sublines are characterized by an increased heat sensitivity and impaired cellular capacity for thermotolerance development. The data show that thermotolerance development after heat conditioning in the heat-sensitive, thermotolerance-deficient mutants was accompanied by reduced labeling of a Mr 50,000 glycoprotein (GP50), in both soluble and insoluble cell fractions. Similarly, activation of UDP-N-acetylgalactosaminyltransferase (Gal-NAcT) after hyperthermia was almost completely abolished in these cell lines. Both of these endpoints have been correlated previously with thermotolerance expression. The data are consistent with the glycosylation hypothesis that attributes increased heat resistance of thermotolerant cells, at least in part, to enhanced glycosylation and accumulation of endogenous glycoproteins, such as GP50.

摘要

中国仓鼠卵巢(CHO)细胞能够在适当的热预处理后产生高度的耐热性。在本研究中,我们使用四个CHO细胞亚系研究了耐热性发展与蛋白质糖基化之间的关系。其中两个CHO亚系的特点是热敏感性增加和耐热性发展的细胞能力受损。数据表明,在热敏感、耐热性缺陷的突变体中,热预处理后的耐热性发展伴随着Mr 50,000糖蛋白(GP50)在可溶性和不可溶性细胞组分中的标记减少。同样,在这些细胞系中,热疗后UDP-N-乙酰半乳糖胺基转移酶(Gal-NAcT)的激活几乎完全被消除。这两个终点之前都与耐热性表达相关。这些数据与糖基化假说一致,该假说认为耐热细胞的耐热性增加至少部分归因于内源性糖蛋白(如GP50)的糖基化增强和积累。

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Protein glycosylation in heat-sensitive and thermotolerance-deficient mutants of Chinese hamster ovary cells.中国仓鼠卵巢细胞热敏和耐热性缺陷突变体中的蛋白质糖基化
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