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NKG2D配体调控的综合观点。

An integrated view of the regulation of NKG2D ligands.

作者信息

Stern-Ginossar Noam, Mandelboim Ofer

机构信息

Lautenberg Center for General and Tumor Immunology, The Hebrew University, The BioMedical Research Institute, Hadassah Medical School, Jerusalem, Israel.

出版信息

Immunology. 2009 Sep;128(1):1-6. doi: 10.1111/j.1365-2567.2009.03147.x.

DOI:10.1111/j.1365-2567.2009.03147.x
PMID:19689730
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2747133/
Abstract

NKG2D is one of the best characterized activating receptors and is expressed on natural killer cells and on various T-cell subsets. This receptor recognizes several different ligands that are induced by cellular stresses. In this review, we described the mechanisms controlling the expression of NKG2D ligands, with the emphasis on post-transcriptional and post-translational regulation.

摘要

NKG2D是特征最为明确的激活受体之一,表达于自然杀伤细胞和多种T细胞亚群上。该受体识别由细胞应激诱导产生的几种不同配体。在本综述中,我们描述了控制NKG2D配体表达的机制,重点是转录后和翻译后调控。

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本文引用的文献

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Diverse herpesvirus microRNAs target the stress-induced immune ligand MICB to escape recognition by natural killer cells.多种疱疹病毒微小RNA靶向应激诱导的免疫配体MICB,以逃避自然杀伤细胞的识别。
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Posttranslational regulation of the NKG2D ligand Mult1 in response to cell stress.NKG2D配体Mult1在细胞应激反应中的翻译后调控。
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Interferon-gamma down-regulates NKG2D ligand expression and impairs the NKG2D-mediated cytolysis of MHC class I-deficient melanoma by natural killer cells.干扰素-γ下调NKG2D配体的表达,并损害自然杀伤细胞对MHC I类缺陷型黑色素瘤的NKG2D介导的细胞溶解作用。
Int J Cancer. 2009 Apr 1;124(7):1594-604. doi: 10.1002/ijc.24098.
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Human microRNAs regulate stress-induced immune responses mediated by the receptor NKG2D.人类微小RNA调控由NKG2D受体介导的应激诱导免疫反应。
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Proliferating cells express mRNAs with shortened 3' untranslated regions and fewer microRNA target sites.增殖细胞表达的信使核糖核酸(mRNA)具有缩短的3'非翻译区和较少的微小RNA靶位点。
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