Hande P, Slijepcevic P, Silver A, Bouffler S, van Buul P, Bryant P, Lansdorp P
The Terry Fox Laboratory, British Columbia Cancer Research Center, 601 West 10th Avenue, Vancouver, British Columbia, V5Z 1L3, Canada.
Genomics. 1999 Mar 1;56(2):221-3. doi: 10.1006/geno.1998.5668.
Severe combined immunodeficiency (scid) mice are deficient in the enzyme DNA-PK (DNA-dependent protein kinase) as a result of the mutation in the gene encoding the catalytic subunit (DNA-PKcs) of this enzyme. DNA-PKcs is a member of the phosphatidylinositol 3-kinase superfamily, which includes the human protein ATM (ataxia telangiectasia mutated) and the yeast protein Tel1. Using Q-FISH (quantitative fluorescence in situ hybridization), we show here that scid mice from four different genetic backgrounds have, on average, 1.5-2 times longer telomeres than those of corresponding wild-type mice. Our results point to the possibility that DNA-PKcs may, directly or indirectly, be involved in telomere length regulation in mammalian cells.
严重联合免疫缺陷（scid）小鼠由于编码该酶催化亚基（DNA-PKcs）的基因突变，导致其缺乏DNA-PK（DNA依赖性蛋白激酶）酶。DNA-PKcs是磷脂酰肌醇3激酶超家族的成员，该家族包括人类蛋白ATM（共济失调毛细血管扩张突变）和酵母蛋白Tel1。通过定量荧光原位杂交（Q-FISH），我们在此表明，来自四种不同遗传背景的scid小鼠的端粒平均比相应野生型小鼠的端粒长1.5至2倍。我们的结果表明，DNA-PKcs可能直接或间接参与哺乳动物细胞中端粒长度的调节。
