Kirchgessner C U, Patil C K, Evans J W, Cuomo C A, Fried L M, Carter T, Oettinger M A, Brown J M
Department of Radiation Oncology, Stanford University School of Medicine, CA 94305.
Science. 1995 Feb 24;267(5201):1178-83. doi: 10.1126/science.7855601.
Severe combined immunodeficient (SCID) mice are deficient in a recombination process utilized in both DNA double-strand break repair and in V(D)J recombination. The phenotype of these mice involves both cellular hypersensitivity to ionizing radiation and a lack of B and T cell immunity. The catalytic subunit of DNA-dependent protein kinase, p350, was identified as a strong candidate for the murine gene SCID. Both p350 and a gene complementing the SCID defect colocalize to human chromosome 8q11. Chromosomal fragments expressing p350 complement the SCID phenotype, and p350 protein levels are greatly reduced in cells derived from SCID mice compared to cells from wild-type mice.
严重联合免疫缺陷(SCID)小鼠在DNA双链断裂修复和V(D)J重组中所利用的重组过程存在缺陷。这些小鼠的表型包括对电离辐射的细胞超敏反应以及缺乏B细胞和T细胞免疫。DNA依赖性蛋白激酶的催化亚基p350被确定为鼠基因SCID的有力候选者。p350和一个补充SCID缺陷的基因都定位于人类染色体8q11。表达p350的染色体片段可补充SCID表型,并且与野生型小鼠的细胞相比,SCID小鼠来源的细胞中p350蛋白水平大大降低。