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p53: The Attractive Tumor Suppressor in the Cancer Research Field
p53 is one of the most studied tumor suppressors in the cancer research field. Of note, over 50% of human tumors carry loss of function mutations, and thus p53 has been considered to be a classical Knudson-type tumor suppressor. From the functional point of view, p53 is a nuclear transcription facto...
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Formato: | Texto |
Lenguaje: | English |
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Hindawi Publishing Corporation
2011
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3004423/ https://www.ncbi.nlm.nih.gov/pubmed/21188172 http://dx.doi.org/10.1155/2011/603925 |
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author | Ozaki, Toshinori Nakagawara, Akira |
author_facet | Ozaki, Toshinori Nakagawara, Akira |
author_sort | Ozaki, Toshinori |
collection | PubMed |
description | p53 is one of the most studied tumor suppressors in the cancer research field. Of note, over 50% of human tumors carry loss of function mutations, and thus p53 has been considered to be a classical Knudson-type tumor suppressor. From the functional point of view, p53 is a nuclear transcription factor to transactivate a variety of its target genes implicated in the induction of cell cycle arrest, DNA repair, and apoptotic cell death. In response to cellular stresses such as DNA damage, p53 is activated and promotes cell cycle arrest followed by the replacement of DNA lesions and/or apoptotic cell death. Therefore, p53 is able to maintain the genomic integrity to prevent the accumulation of genetic alterations, and thus stands at a crossroad between cell survival and cell death. In this paper, we describe a variety of molecular mechanisms behind the regulation of p53. |
format | Text |
id | pubmed-3004423 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-30044232010-12-23 p53: The Attractive Tumor Suppressor in the Cancer Research Field Ozaki, Toshinori Nakagawara, Akira J Biomed Biotechnol Review Article p53 is one of the most studied tumor suppressors in the cancer research field. Of note, over 50% of human tumors carry loss of function mutations, and thus p53 has been considered to be a classical Knudson-type tumor suppressor. From the functional point of view, p53 is a nuclear transcription factor to transactivate a variety of its target genes implicated in the induction of cell cycle arrest, DNA repair, and apoptotic cell death. In response to cellular stresses such as DNA damage, p53 is activated and promotes cell cycle arrest followed by the replacement of DNA lesions and/or apoptotic cell death. Therefore, p53 is able to maintain the genomic integrity to prevent the accumulation of genetic alterations, and thus stands at a crossroad between cell survival and cell death. In this paper, we describe a variety of molecular mechanisms behind the regulation of p53. Hindawi Publishing Corporation 2011 2010-12-06 /pmc/articles/PMC3004423/ /pubmed/21188172 http://dx.doi.org/10.1155/2011/603925 Text en Copyright © 2011 T. Ozaki and A. Nakagawara. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Ozaki, Toshinori Nakagawara, Akira p53: The Attractive Tumor Suppressor in the Cancer Research Field |
title | p53: The Attractive Tumor Suppressor in the Cancer Research Field |
title_full | p53: The Attractive Tumor Suppressor in the Cancer Research Field |
title_fullStr | p53: The Attractive Tumor Suppressor in the Cancer Research Field |
title_full_unstemmed | p53: The Attractive Tumor Suppressor in the Cancer Research Field |
title_short | p53: The Attractive Tumor Suppressor in the Cancer Research Field |
title_sort | p53: the attractive tumor suppressor in the cancer research field |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3004423/ https://www.ncbi.nlm.nih.gov/pubmed/21188172 http://dx.doi.org/10.1155/2011/603925 |
work_keys_str_mv | AT ozakitoshinori p53theattractivetumorsuppressorinthecancerresearchfield AT nakagawaraakira p53theattractivetumorsuppressorinthecancerresearchfield |