Increased neutrophil respiratory burst in bcr-null mutants.
Increased neutrophil respiratory burst in bcr-null mutants.
复制标题
bcr 缺失突变体中中性粒细胞呼吸爆发增加。
DOI：
10.1016/0092-8674(95)90350-x
复制
发表时间：
1995
期刊：
影响因子：
64.5
通讯作者：
Groffen,J
中科院分区：
文献类型：
--
作者：
Voncken,JW;vanSchaick,H;Kaartinen,V;Deemer,K;Coates,T;Landing,B;Pattengale,P;Dorseuil,O;Bokoch,GM;Groffen,J
费城（Ph）阳性白血病总是含有融合BCR和ABL的染色体易位。BCR-ABL蛋白是白血病发生的原因。在这里，我们表明，暴露于革兰氏阴性内毒素的bcr基因缺失突变小鼠导致严重的脓毒性休克和增加中性粒细胞的组织损伤。bcr（-/-）小鼠的中性粒细胞在激活时表现出活性氧代谢产物的显著增加，并且对引发刺激更敏感。与（+/+）中性粒细胞相比，活化的（-/-）中性粒细胞显示出3倍增加的p21'ac-膜易位。这些结果将Bcr在体内与白细胞的NADPH氧化酶系统调节Rac介导的超氧化物产生联系起来，并表明Bcr功能与Ph阳性白血病受影响的细胞类型之间存在联系。
Philadelphia (Ph)-positive leukemias invariably contain a chromosomal translocation fusing BCR to ABL. The BCR-ABL protein is responsible for leukemogenesis. Here we show that exposure of bcr-null mutant mice to gram-negative endotoxin led to severe septic shock and increased tissue injury by neutrophils. Neutrophils of bcr (-/-) mice showed a pronounced increase in reactive oxygen metabolite production upon activation and were more sensitive to priming stimuli. Activated (-/-) neutrophils displayed a 3-fold increased p21'ac~ membrane translocation compared with (+/+) neutrophils. These results connect Bcr in vivo with the regulation of Rac-mediated superoxide production by the NADPH-oxidase system of leukocytes and suggest a link between Bcr function and the cell type affected in Ph-positive leukemia.