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金属硫蛋白基因启动子控制下主要组织相容性抗原的表达。

The expression of major histocompatibility antigens under metallothionein gene promoter control.

作者信息

Weis J H, Seidman J G

出版信息

J Immunol. 1985 Mar;134(3):1999-2003.

PMID:3918115
Abstract

A model system has been developed that provides insights into the mechanisms that control the amount of H-2 antigen on the cell surface. Hybrid genes have been constructed by using the metallothionein gene promoter to replace the H-2 gene promoter. The hybrid genes have been introduced into murine L cells and their expression has been studied. Cells containing the hybrid genes contain 20- to 60-fold more H-2 mRNA than nontransfected L cells, since the metallothionein gene promoter is much more active than the H-2 promoter. However, the total amount of H-2 antigen on the surface of the transfected L cell is similar to the amount of H-2 antigen on the normal L cell. Even after transcription from the metallothionein promoter is induced by the addition of cadmium to the cell culture medium, the amount of H-2 antigen on the surface of cells containing the hybrid genes does not increase. We conclude that the amount of H-2 antigen is controlled by events that occur after gene transcription. Evidence is presented that suggests that these post-transcriptional mechanisms may cause the expression of threefold more H-2Dd than H-2Ld on the surface of BALB/c cells. Furthermore, we suggest that the 5' untranslated portion of the H-2 mRNA is not important for directing the growing H-2 polypeptide to the cell surface.

摘要

已经开发出一种模型系统,该系统能深入了解控制细胞表面H-2抗原数量的机制。通过使用金属硫蛋白基因启动子取代H-2基因启动子构建了杂种基因。这些杂种基因已被导入小鼠L细胞并对其表达进行了研究。含有杂种基因的细胞所含的H-2 mRNA比未转染的L细胞多20至60倍,因为金属硫蛋白基因启动子比H-2启动子活性高得多。然而,转染的L细胞表面H-2抗原的总量与正常L细胞表面H-2抗原的量相似。即使在向细胞培养基中添加镉诱导金属硫蛋白启动子转录后,含有杂种基因的细胞表面H-2抗原的量也没有增加。我们得出结论,H-2抗原的量是由基因转录后发生的事件控制的。有证据表明,这些转录后机制可能导致BALB/c细胞表面H-2Dd的表达比H-2Ld多三倍。此外,我们认为H-2 mRNA的5'非翻译部分对于将正在生长的H-2多肽导向细胞表面并不重要。

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The expression of major histocompatibility antigens under metallothionein gene promoter control.金属硫蛋白基因启动子控制下主要组织相容性抗原的表达。
J Immunol. 1985 Mar;134(3):1999-2003.
2
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