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Genetic and environmental effects in paroxysmal nocturnal hemoglobinuria: this little PIG-A goes "Why? Why? Why?".

作者信息

Young N S, Maciejewski J P

机构信息

Hematology Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland, USA.

出版信息

J Clin Invest. 2000 Sep;106(5):637-41. doi: 10.1172/JCI11002.

DOI:10.1172/JCI11002
PMID:10974016
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC381297/
Abstract
摘要

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Genetic and environmental effects in paroxysmal nocturnal hemoglobinuria: this little PIG-A goes "Why? Why? Why?".阵发性睡眠性血红蛋白尿症中的遗传和环境影响:这只小小的PIG-A基因在问“为什么?为什么?为什么?”
J Clin Invest. 2000 Sep;106(5):637-41. doi: 10.1172/JCI11002.
2
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3
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6
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本文引用的文献

1
Impaired growth and elevated fas receptor expression in PIGA(+) stem cells in primary paroxysmal nocturnal hemoglobinuria.原发性阵发性夜间血红蛋白尿症中PIGA(+)干细胞生长受损及Fas受体表达升高
J Clin Invest. 2000 Sep;106(5):689-96. doi: 10.1172/JCI8328.
2
HSP70 stimulates cytokine production through a CD14-dependant pathway, demonstrating its dual role as a chaperone and cytokine.热休克蛋白70(HSP70)通过一种依赖于CD14的途径刺激细胞因子的产生,这表明了它作为伴侣蛋白和细胞因子的双重作用。
Nat Med. 2000 Apr;6(4):435-42. doi: 10.1038/74697.
3
Immunosuppressive treatment of aplastic anemia with antithymocyte globulin and cyclosporine.使用抗胸腺细胞球蛋白和环孢素对再生障碍性贫血进行免疫抑制治疗。
Semin Hematol. 2000 Jan;37(1):56-68. doi: 10.1016/s0037-1963(00)90030-1.
4
Cytotoxicity against lymphoblastoid cells mediated by a T-cell clone from an aplastic anaemia patient: role of CD59 on target cells.再生障碍性贫血患者T细胞克隆介导的对淋巴母细胞的细胞毒性:CD59在靶细胞上的作用。
Br J Haematol. 1999 Dec;107(4):791-6. doi: 10.1046/j.1365-2141.1999.01790.x.
5
Paroxysmal nocturnal hemoglobinuria cells in patients with bone marrow failure syndromes.骨髓衰竭综合征患者中的阵发性睡眠性血红蛋白尿细胞
Ann Intern Med. 1999 Sep 21;131(6):401-8. doi: 10.7326/0003-4819-131-6-199909210-00002.
6
High incidence of transiently appearing complement-sensitive bone marrow precursor cells in patients with severe aplastic anemia--A possible role of high endogenous IL-2 in their suppression.重型再生障碍性贫血患者中短暂出现的补体敏感骨髓前体细胞的高发生率——内源性白细胞介素-2升高在其抑制中的可能作用
Acta Haematol. 1999;101(4):165-72. doi: 10.1159/000040948.
7
The PIG-A mutation and absence of glycosylphosphatidylinositol-linked proteins do not confer resistance to apoptosis in paroxysmal nocturnal hemoglobinuria.阵发性睡眠性血红蛋白尿症中的PIG-A突变及糖基磷脂酰肌醇连接蛋白缺失并不赋予细胞对凋亡的抗性。
Blood. 1998 Oct 1;92(7):2541-50.
8
The pathophysiology of acquired aplastic anemia.获得性再生障碍性贫血的病理生理学。
N Engl J Med. 1997 May 8;336(19):1365-72. doi: 10.1056/NEJM199705083361906.
9
Impaired hematopoiesis in paroxysmal nocturnal hemoglobinuria/aplastic anemia is not associated with a selective proliferative defect in the glycosylphosphatidylinositol-anchored protein-deficient clone.阵发性睡眠性血红蛋白尿/再生障碍性贫血中造血功能受损与糖基磷脂酰肌醇锚定蛋白缺陷克隆中的选择性增殖缺陷无关。
Blood. 1997 Feb 15;89(4):1173-81.
10
Somatic mutations in paroxysmal nocturnal hemoglobinuria: a blessing in disguise?阵发性夜间血红蛋白尿中的体细胞突变:因祸得福?
Cell. 1997 Jan 10;88(1):1-4. doi: 10.1016/s0092-8674(00)81850-4.