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系统性红斑狼疮中紫外线损伤DNA的修复

Repair of UV damaged DNA in systemic lupus erythematosus.

作者信息

Beighlie D J, Teplitz R L

出版信息

J Rheumatol. 1975 Jun;2(2):149-60.

PMID:1151952
Abstract

The NZB/NZW hybrid mouse is an animal model of human systemic lupus erythematosus (SLE). Two breeding schemes were devised using NZB, NZW, B/W, and CBA mice, which permit definitive decisions regarding genetic and/or viral origin of the disease. It is proposed that at least two factors must be involved: (1) a genetic abnormality producing hyper-responsiveness to nucleic acid antigens, and (2) a DNA repair defect which results in liberation of DNA and RNA when cells are lethally injured. Evidence is presented for a DNA repair deficit in human SLE lymphocytes following in vitro irradiation with ultraviolet (UV) light. Lymphocytes from adult New Zealand and control mice were found to lack normal amounts of endonuclease necessary for repairing UV damage.

摘要

NZB/NZW杂交小鼠是人类系统性红斑狼疮(SLE)的动物模型。使用NZB、NZW、B/W和CBA小鼠设计了两种育种方案,这有助于对该疾病的遗传和/或病毒起源做出明确判断。有人提出,至少必须涉及两个因素:(1)一种导致对核酸抗原有高反应性的基因异常,以及(2)一种DNA修复缺陷,当细胞受到致死性损伤时会导致DNA和RNA的释放。有证据表明,体外紫外线(UV)照射后的人类SLE淋巴细胞存在DNA修复缺陷。发现成年新西兰小鼠和对照小鼠的淋巴细胞缺乏修复紫外线损伤所需的正常量的内切核酸酶。

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