Targeted deletion of mouse Rad1 leads to deficient cellular DNA damage responses.
作者： Chunbo Zhang , Yuheng Liu , Zhishang Hu , Lili An , Yikun He
DOI: 10.1007/S13238-011-1049-7
关键词:
摘要: The Rad1 gene is evolutionarily conserved from yeast to human. fission Schizosaccharomyces pombe ortholog promotes cell survival against DNA damage and required for G2/M checkpoint activation. In this study, mouse embryonic stem (ES) cells with a targeted deletion of Mrad1, the gene, were created evaluate its function in mammalian cells. Mrad1−/− ES highly sensitive ultraviolet-light (UV light), hydroxyurea (HU) gamma rays, defective as well S/M checkpoints. These data indicate that Mrad1 repairing lesions induced by UV-light, HU mediating controls. We further demonstrated plays an important role homologous recombination repair (HRR) cells, but minor HRR differentiated
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