Suppr超能文献

C57BL小鼠中bm1基因转换事件的一个潜在供体基因。

A potential donor gene for the bm1 gene conversion event in the C57BL mouse.

作者信息

Mellor A L, Weiss E H, Ramachandran K, Flavell R A

出版信息

Nature. 1983;306(5945):792-5. doi: 10.1038/306792a0.

Abstract

The mammalian major histocompatibility complex (MHC; H-2 complex in mouse) is a large multigene complex which encodes cell-surface antigens involved in the cellular immune response to foreign antigens. Class I polypeptides expressed at the H-2K and H-2D loci of numerous mouse strains exhibit an unusually high degree of genetic polymorphism, which is assumed to be related to their function as primary recognition elements in the immune response. We suggested that this H-2 polymorphism may arise by gene conversion-like events between non-allelic class I genes. This is supported by our recent comparison of the DNA sequences of the normal H-2Kb gene sequence, from the C57BL/10 mouse, and a mutant form of this gene called H-2Kbm1: the mutant allele differs from the H-2Kb gene in seven bases out of a region of 13 bases in exon 3 of the class I gene (which encodes alpha 2 (C1) the second highly polymorphic protein domain), suggesting that this region of new sequence had been introduced into the H-2Kb sequence following unequal pairing of two class I genes in the genome of the C57BL mouse. Schulze et al. have obtained similar results. Here we report work identifying a potential donor gene in our library of 26 class I genes cloned from the C57BL/10 mouse.

摘要

哺乳动物主要组织相容性复合体(MHC;小鼠中的H-2复合体)是一个大型多基因复合体,它编码参与对外源抗原的细胞免疫反应的细胞表面抗原。在众多小鼠品系的H-2K和H-2D位点表达的I类多肽表现出异常高程度的遗传多态性,这被认为与其作为免疫反应中主要识别元件的功能有关。我们提出这种H-2多态性可能通过非等位I类基因之间类似基因转换的事件产生。这得到了我们最近对来自C57BL/10小鼠的正常H-2Kb基因序列与该基因的一种突变形式H-2Kbm1的DNA序列比较的支持:该突变等位基因在I类基因外显子3的13个碱基区域中的7个碱基上与H-2Kb基因不同(该区域编码α2(C1)第二个高度多态的蛋白质结构域),这表明新序列的这个区域是在C57BL小鼠基因组中两个I类基因不等位配对后引入到H-2Kb序列中的。舒尔茨等人也得到了类似的结果。在此我们报告在从C57BL/10小鼠克隆的26个I类基因文库中鉴定出一个潜在供体基因的工作。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验