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β2微球蛋白中的点突变导致表位表达丧失。

A point mutation in beta2-microglobulin results in loss of epitope expression.

作者信息

Dimaano C, Nguyen T, Ahmed A, Abel E, Schultz C S, Nieto M C

机构信息

Department of Biological Sciences, California State University, Hayward 94542, USA.

出版信息

Tissue Antigens. 2000 Nov;56(5):473-5. doi: 10.1034/j.1399-0039.2000.560516.x.

Abstract

A common tool in studying the structure and function of major histocompatibility complex: (MHC) class I is the generation and analysis of beta2-microglobulin (beta2m) mutations. beta2m has been shown to affect proper class I antigen presentation at the level of structural functionality. Many studies characterizing beta2m function in class I presentation have used antibody-based assays. Monitoring the effect of beta2m mutation on antibody epitope expression, therefore, is essential in being able to truly characterize the impact of a mutant interaction between beta2m and class I. Here we describe a mutant beta2m molecule, beta2m #32, that in association with class I loses reactivity with the human beta2m-specific monoclonal antibody, BBM.1. However, the BBM.1 epitope remains intact when beta2m #32 is free from class I association.

摘要

研究主要组织相容性复合体(MHC)I类分子结构和功能的一种常用工具是β2微球蛋白(β2m)突变体的产生与分析。β2m已被证明在结构功能水平上会影响I类抗原的正确呈递。许多表征β2m在I类呈递中功能的研究都使用了基于抗体的检测方法。因此,监测β2m突变对抗体表位表达的影响,对于真正表征β2m与I类分子之间突变相互作用的影响至关重要。在此,我们描述了一种突变型β2m分子β2m #32,它与I类分子结合时会失去与人β2m特异性单克隆抗体BBM.1的反应性。然而,当β2m #32不与I类分子结合时,BBM.1表位保持完整。

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