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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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Detalles Bibliográficos
Autores principales: Ozaki, Toshinori, Nakagawara, Akira
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2011
Materias:
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.
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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
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