Platelet GPIIb-IIIa: Molecular Variations and Alloantigens

Platelet GPIIb-IIIa: Molecular Variations and Alloantigens
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血小板 GPIIb-IIIa:分子变异和同种抗原

DOI:
--
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发表时间:
1991
影响因子:
6.7
通讯作者:
P. Newman
P. Newman
中科院分区:
医学2区
文献类型:
--
作者:
P. Newman

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分子和细胞生物学的最新进展使得在先前糖蛋白IIb和IIIa的血清学和生化研究的基础上,以重要和令人兴奋的方式建立起来成为可能。除了提供对导致Glanzmann血栓减少症的多态性的详细基本了解,以及在其他情况下引发同种免疫反应,血小板膜糖蛋白多态性的分子表征预计将具有越来越大的临床影响。随着剩下的血小板抗原系统的分子基础逐渐为人所知,我们为PTP和NATP患者的护理和管理设计新的诊断和治疗方法的能力应该得到提高。对于格兰兹曼氏病,未来有希望通过基因治疗来纠正血小板异常。GT动物模型的建立将是这一方向重要的第一步。
Recent advances in molecular and cellular biology have made it possible to build upon previous serologic and biochemical studies of glycoproteins IIb and IIIa in important and exciting ways. In addition to providing a detailed basic understanding of the polymorphisms that are responsible for Glanzmann's thrombasthenia, and in other cases for eliciting an alloimmune response, the molecular characterization of platelet membrane glycoprotein polymorphisms is expected to have an increasingly large clinical impact. As the molecular basis of the remaining platelet antigen systems becomes known, our ability to design novel diagnostic and therapeutic approaches for the care and management of patients with PTP and NATP should improve. For Glanzmann's disease, the future holds the promise of gene therapy to correct the platelet abnormality. Establishment of animal models for GT will be an important first step in this direction.
以色列格兰兹曼血小板无力症患者糖蛋白 IIb 和 IIIa 基因的结构完整性。
DOI: --
发表时间: 1988
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影响因子: 20.3
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发表时间: 1987-10-23
期刊: SCIENCE
影响因子: 56.9
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