Cellular UV damage responses--functions of tumor suppressor p53.
DNA damage, provoked by ultraviolet (UV) radiation, evokes a cellular damage response composed of activation of stress signaling and DNA checkpoint functions. These are translated to responses of replicative arrest, damage repair, and apoptosis aimed at cellular recovery from the damage. p53 tumor suppressor is a central stress response protein, activated by multiple endogenous and environmental insults, including UV radiation. The significance of p53 in the DNA damage responses has frequently been reviewed in the context of ionizing radiation or other double strand break (DSB)-inducing agents. Despite partly similar patterns, the molecular events following UV radiation are, however, distinct from the responses induced by DSBs and are profoundly coupled with transcriptional stress. These are illustrated, e.g., by the UV damage-specific translocations of Mdm2, promyelocytic leukemia protein, and nucleophosmin and their interactions with p53. In this review, we discuss UV damage-provoked cellular responses and the functions of p53 in damage recovery and cell death.
Latonen
Leena
L
Molecular and Cancer Biology Program and Haartman Institute, University of Helsinki, PO Box 63, FIN-00014 Helsinki, Finland.
Laiho
Marikki
M
D000818:Animals; D004260:DNA Repair / Q000528:radiation effects; D006801:Humans; D018384:Oxidative Stress / Q000528:radiation effects; D012878:Skin Neoplasms / Q000235:genetics; D014158:Transcription, Genetic / Q000528:radiation effects; D016159:Tumor Suppressor Protein p53 / Q000235:genetics* / Q000528:radiation effects; D014466:Ultraviolet Rays / Q000009:adverse effects*
D016159:Tumor Suppressor Protein p53