Abstract / Description of output
The role of p53 in DNA repair and cell cycle checkpoint after ultraviolet irradiation was investigated in an embryonic stem cell line homozygous for a targeted deletion of p53, Results indicate that loss of p53 does not alter the capacity of ES cells to respond to DNA damage. wild-type and p53-deficient cells showed similar cessation of DNA synthesis after UV damage and similar ultimate capacity to repair a transiently transfected reporter plasmid, Interestingly, in the absence of DNA damaging treatment, the transit of p53-deficient cells through S phase mas slower than wild-type cells. We suggest that this may result from the absence of a p53-dependent response to endogenous DNA damage: without p53 sensing endogenous damage leading to immediate repair, such damage may persist and thus delay DNA synthesis. (C) 1998 Federation of European Biochemical Societies.
Original language | English |
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Pages (from-to) | 499-504 |
Number of pages | 6 |
Journal | FEBS Letters |
Volume | 425 |
Issue number | 3 |
DOIs | |
Publication status | Published - 3 Apr 1998 |
Keywords / Materials (for Non-textual outputs)
- embryonic stem cell
- p53
- cell cycle
- DNA repair
- UV
- DNA damage
- LI-FRAUMENI SYNDROME
- P53-DEFICIENT MOUSE CELLS
- WILD-TYPE
- ULTRAVIOLET-LIGHT
- EXCISION-REPAIR
- P53 MUTATIONS
- DAMAGE
- MICE
- APOPTOSIS