| Autor: |
Errami A; Department of Radiation Genetics and Chemical Mutagenesis, MGC, Leiden University-Medical Center, Leiden, The Netherlands., He DM, Friedl AA, Overkamp WJ, Morolli B, Hendrickson EA, Eckardt-Schupp F, Oshimura M, Lohman PH, Jackson SP, Zdzienicka MZ |
| Jazyk: |
angličtina |
| Zdroj: |
Nucleic acids research [Nucleic Acids Res] 1998 Jul 01; Vol. 26 (13), pp. 3146-53. |
| DOI: |
10.1093/nar/26.13.3146 |
| Abstrakt: |
DNA-dependent protein kinase (DNA-PK) plays an important role in DNA double-strand break (DSB) repair and V(D)J recombination. We have isolated a new X-ray-sensitive CHO cell line, XR-C1, which is impaired in DSB repair and which was assigned to complementation group 7, the group that is defective in the XRCC7 / SCID ( Prkdc ) gene encoding the catalytic subunit of DNA-PK (DNA-PKcs). Consistent with this complementation analysis, XR-C1 cells lackeddetectable DNA-PKcs protein, did not display DNA-PK catalytic activity and were complemented by the introduction of a single human chromosome 8 (providing the Prkdc gene). The impact of the XR-C1 mutation on V(D)J recombination was quite different from that found in most rodent cells defective in DNA-PKcs, which are preferentially blocked in coding joint formation, whereas XR-C1 cells were defective in forming both coding and signal joints. These results suggest that DNA-PKcs is required for both coding and signal joint formation during V(D)J recombination and that the XR-C1 mutant cell line may prove to be a useful tool in understanding this pathway. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
|
