Different regulation of p53 stability in UV-irradiated normal and DNA repair deficient human cells.
The stabilization of p53 protein was studied after UV exposure of normal human skin fibroblasts and cells derived from patients suffering from xeroderma pigmentosum (XP) and trichothiodystrophy (TTD). The data show that p53 is transiently stabilized both in UV-irradiated normal and repair deficient cells. However, particularly at later times after UV irradiation, stabilization of p53 persists much longer in repair deficient XP and TTD cells than in normal cells. The stabilization of p53 was found to be dose-dependent in normal and XP cells. These results indicate that unremoved DNA damage could possibly be responsible for the induction of transient stabilization of p53.
Abrahams
P J
PJ
Laboratory for Molecular Carcinogenesis, Sylvius Laboratory, Leiden University, The Netherlands.
Schouten
R
R
van Laar
T
T
Houweling
A
A
Terleth
C
C
van der Eb
A J
AJ
D016475:3T3 Cells; D000818:Animals; D002478:Cells, Cultured; D004260:DNA Repair / Q000235:genetics / Q000502:physiology*; D004307:Dose-Response Relationship, Radiation; D005347:Fibroblasts; D006197:Hair / Q000002:abnormalities / Q000378:metabolism; D006801:Humans; D051379:Mice; D016159:Tumor Suppressor Protein p53 / Q000502:physiology*; D014466:Ultraviolet Rays / Q000009:adverse effects*; D014983:Xeroderma Pigmentosum / Q000378:metabolism
D016159:Tumor Suppressor Protein p53