Elongated telomeres in scid mice

被引:70
作者
Hande, P
Slijepcevic, P
Silver, A
Bouffler, S
van Buul, P
Bryant, P
Lansdorp, P
机构
[1] British Columbia Canc Res Ctr, Terry Fox Lab, Vancouver, BC V5Z 1L3, Canada
[2] Univ St Andrews, Sch Biomed Sci, St Andrews KY16 9TS, Fife, Scotland
[3] Natl Radiol Protect Board, Radiat Effects Dept, Didcot OX11 0RQ, Oxon, England
[4] Leiden Univ, Dept Radiat Genet & Chem Mutagenesis, MGC, NL-2300 RA Leiden, Netherlands
关键词
D O I
10.1006/geno.1998.5668
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
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 Tell. Using Q-PISH (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. (C) 1999 Academic Press.
引用
收藏
页码:221 / 223
页数:3
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