The sensitivity of Cockayne's syndrome cells to DNA-damaging agents is not due to defective transcription-coupled repair of active genes.
Two of the hallmarks of Cockayne's syndrome (CS) are the hypersensitivity of cells to UV light and the lack of recovery of the ability to synthesize RNA following exposure of cells to UV light, in spite of the normal repair capacity at the overall genome level. The prolonged repressed RNA synthesis...
Guardat en:
| Publicat a: | Mol Cell Biol |
|---|---|
| Autors principals: | , , , , |
| Format: | Artigo |
| Idioma: | Inglês |
| Publicat: |
Taylor & Francis
1996
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| Matèries: | |
| Accés en línia: | https://ncbi.nlm.nih.govhttps://pmc.ncbi.nlm.nih.gov/articles/PMC231442/ https://ncbi.nlm.nih.govhttps://pubmed.ncbi.nlm.nih.gov/8754844/ https://ncbi.nlm.nih.govhttps://doi.org/10.1128/mcb.16.8.4436 |
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