TY - JOUR
T1 - Cellular UV damage responses - Functions of tumor suppressor p53
AU - Latonen, Leena
AU - Laiho, Marikki
N1 - Funding Information:
Original work in the authors laboratory has been supported by the Academy of Finland (grant no. 44885), University of Helsinki, Biocentrum Helsinki, and the Finnish Cancer Organization.
Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2005/7/25
Y1 - 2005/7/25
N2 - 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.
AB - 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.
KW - Apoptosis
KW - Cell cycle arrest
KW - DNA damage
KW - Nucleotide excision repair
KW - UV radiation
KW - p53 tumor suppressor
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U2 - 10.1016/j.bbcan.2005.04.003
DO - 10.1016/j.bbcan.2005.04.003
M3 - Review article
C2 - 15921859
AN - SCOPUS:22144460207
SN - 0304-419X
VL - 1755
SP - 71
EP - 89
JO - Biochimica et Biophysica Acta - Reviews on Cancer
JF - Biochimica et Biophysica Acta - Reviews on Cancer
IS - 2
ER -