Cells from ERCC1-deficient mice show increased genome instability and a reduced frequency of S-phase-dependent illegitimate chromosome exchange but a normal frequency of homologous recombination.

@article{Melton1998CellsFE,
  title={Cells from ERCC1-deficient mice show increased genome instability and a reduced frequency of S-phase-dependent illegitimate chromosome exchange but a normal frequency of homologous recombination.},
  author={David W. Melton and A M Ketchen and Felipe N{\'u}{\~n}ez and S Bonatti-Abbondandolo and Angelo Abbondandolo and Shoshana Squires and Robert T. Johnson},
  journal={Journal of cell science},
  year={1998},
  volume={111 ( Pt 3)},
  pages={395-404}
}
The ERCC1 protein is essential for nucleotide excision repair in mammalian cells and is also believed to be involved in mitotic recombination. ERCC1-deficient mice, with their extreme runting and polyploid hepatocyte nuclei, have a phenotype that is more reminiscent of a cell cycle arrest/premature ageing disorder than the classic DNA repair deficiency disease, xeroderma pigmentosum. To understand the role of ERCC1 and the link between ERCC1-deficiency and cell cycle arrest, we have studied… CONTINUE READING
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