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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | He, D. M. Reeves, W. Hendrickson, E. A. Lee, S. E. Pulaski, C. R. Boubnov, N. V. Wills, Z. Band, H. Hall, K. T. Benjamin, D. M. |
| Description | Author Affiliation: Boubnov NV ( Division of Tumor Immunology, Dana-Farber Cancer Institute, Boston, MA 02115.); |
| Abstract | Two ionizing radiation-sensitive (IRs) and DNA double-strand break (DSB) mutants, sxi-3 and sxi-2, were shown to be severely deficient in a DNA end binding activity, similar to a previously described activity of the Ku autoantigen, correlating with the xrs (XRCC5) mutations. Cell fusions with xrs-6, another IRs, DSB repair-deficient cell line, defined these sxi mutants in the XRCC5 group. sxi-3 cells have low expression levels of the p86Ku mRNA. Introduction of the Ku p86 gene, but not the p70 Ku gene, complemented the IRs, DNA end binding, and variable (diversity) joining [V(D)J] recombination signal and coding junction deficiencies of sxi-3. Thus, the p86 Ku gene product is essential for DSB repair and V(D)J recombination. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 3 |
| Volume Number | 92 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 1995-03-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Antigens, Nuclear DNA Helicases DNA Repair DNA-Binding Proteins Physiology Genetic Complementation Test Mutation Nuclear Proteins Recombination, Genetic Genetics Animals CHO Cells Cell Fusion Cell Line Cricetinae DNA Metabolism DNA Damage RNA, Messenger Biosynthesis Radiation Tolerance Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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