Abstract
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.
Original language | English |
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Pages (from-to) | 221-223 |
Number of pages | 3 |
Journal | Genomics |
Volume | 56 |
Publication status | Published - 1 Mar 1999 |
Keywords
- SACCHAROMYCES-CEREVISIAE
- ATAXIA-TELANGIECTASIA
- GENE
- MUTATION
- HOMOLOG
- TEL1