血小板无力症中血小板的糖蛋白IIb-IIIa缺陷。 - Suppr

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超能文献

The GPIIb-IIIa defect of platelets in Glanzmann thrombasthenia.

作者信息

Nurden Alan T

机构信息

Institut Hospitalo-Universitaire LIRYC, Pessac.

出版信息

Haematologica. 2023 Apr 1;108(4):937-938. doi: 10.3324/haematol.2023.282836.

DOI:10.3324/haematol.2023.282836

PMID:37002607

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10073873/

Abstract

摘要

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f37/10073873/1962ed77de24/108937.fig1.jpg

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The GPIIb-IIIa defect of platelets in Glanzmann thrombasthenia.血小板无力症中血小板的糖蛋白IIb-IIIa缺陷。

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Glycoprotein IIb Leu214Pro mutation produces glanzmann thrombasthenia with both quantitative and qualitative abnormalities in GPIIb/IIIa.糖蛋白IIb亮氨酸214脯氨酸突变导致血小板无力症，伴有糖蛋白IIb/IIIa的数量和质量异常。

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A point mutation in the cysteine-rich domain of glycoprotein (GP) IIIa results in the expression of a GPIIb-IIIa (alphaIIbbeta3) integrin receptor locked in a high-affinity state and a Glanzmann thrombasthenia-like phenotype.糖蛋白（GP）IIIa富含半胱氨酸结构域中的一个点突变导致表达一种锁定在高亲和力状态的GPIIb-IIIa（αIIbβ3）整合素受体以及类似血小板无力症的表型。

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A frameshift mutation at Gly975 in the transmembrane domain of GPIIb prevents GPIIb-IIIa expression--analysis of two novel mutations in a kindred with type I glanzmann thrombasthenia.

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Type I Glanzmann thrombasthenia: most common subtypes in North Indians.I型Glanzmann血小板无力症：北印度人最常见的亚型。

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A novel homozygous mutation (1619delC) in GPIIb gene associated with Glanzmann thrombasthenia, the decay of GPIIb-mRNA and the synthesis of a truncated GPIIb unable to form complex with GPIIIa.与Glanzmann血小板无力症相关的GPIIb基因中的一种新型纯合突变（1619delC），GPIIb-mRNA的衰减以及无法与GPIIIa形成复合物的截短型GPIIb的合成。

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Identification of one novel pathogenic mutation and two known mutations in two Chinese pedigrees with hereditary Glanzmann thrombasthenia.鉴定两个中国家系遗传性血小板无力症中一个新的致病性突变和两个已知突变。

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Glanzmann thrombasthenia secondary to a Gly273-->Asp mutation adjacent to the first calcium-binding domain of platelet glycoprotein IIb.

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Mutations in the alphaIIb and beta3 genes that cause Glanzmann thrombasthenia can be distinguished by a simple procedure using transformed B-lymphocytes.导致Glanzmann血小板无力症的αIIb和β3基因突变可通过使用转化B淋巴细胞的简单程序加以区分。

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Management challenge of a rare concomitant platelet glycoprotein IV/CD36 and IIb/IIIa deficiencies: Case illustration.罕见的血小板糖蛋白IV/CD36和IIb/IIIa联合缺乏症的管理挑战：病例说明

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本文引用的文献

The GPIIb/IIIa (integrin alphaIIbbeta3) odyssey: a technology-driven saga of a receptor with twists, turns, and even a bend.血小板糖蛋白IIb/IIIa（整合素αIIbβ3）的历程：一个受体由技术驱动的曲折传奇，甚至还有一个转折。

Blood. 2008 Oct 15;112(8):3011-25. doi: 10.1182/blood-2008-06-077891.

An abnormal platelet glycoprotein pattern in three cases of Glanzmann's thrombasthenia.三例Glanzmann血小板无力症的异常血小板糖蛋白模式。

Br J Haematol. 1974 Oct;28(2):253-60. doi: 10.1111/j.1365-2141.1974.tb06660.x.

Molecular differences of exposed surface proteins on thrombasthenic platelet plasma membranes.血小板无力症患者血小板质膜上暴露表面蛋白的分子差异

Nature. 1975 Oct 16;257(5527):599-600. doi: 10.1038/257599a0.

Specific roles for platelet surface glycoproteins in platelet function.血小板表面糖蛋白在血小板功能中的特定作用。

Nature. 1975 Jun 26;255(5511):720-2. doi: 10.1038/255720a0.

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