TREX1 D18N mice fail to process erythroblast DNA resulting in inflammation and dysfunctional
erythropoiesis
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期刊名称： Autoimmunity
作者： Stephen L. Rego,Scott Harvey,Sean R. Simpson,Wayne O. Hemphill,Fred W.柔的词语
Perrino
年份： 2018年
杜的组词期号： 第7期历史名人故事
教育叙事范文关键词： Exonuclea;anaemia;autoimmunity;lupus;erythropoiesis
摘要：Anaemia is commonly obrved in chronic inflammatory conditions, including systemic lupus erythematosus (SLE), where 50% of patients display clinical signs of anaemia. Mutation at the aspartate residue 18 of the three prime repair exonuclea 1 (TREX1) gene caus a monogenic form
of cutaneous lupus in humans and the genetically preci TREX1 D18N mice recapitulate a lupus-like dia. TREX1 degrades single- and double-stranded DNA (dsDNA), and the link between failed DNA degradation by nucleas, including nucleoside-diphosphate kinas (NM23H1/H2) and Deoxyribonuclea II (DNa II), and anaemia prompted our studies to investigate whether TREX1 dysfunction contributes to anaemia. Utilizing the TREX1 D18N mice we demonstrate that (1) TREX1 mutant mice develop normocytic normochromic anaemia and (2) TREX1 exonuclea participates
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