Transcriptional Regulation of the p53 Tumor Suppressor Gene in S-Phase of the Cell-Cycle and the Cellular Response to DNA Damage

The p53 tumor suppressor induces the transcription of genes that negatively regulate progression of the cell cycle in response to DNA damage or other cellular stressors and thus participates in maintaining genome stability. Numerous studies have demonstrated that p53 transcription is activated befor...

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Main Authors: David Reisman, Paula Takahashi, Amanda Polson, Kristy Boggs
Format: Article
Language:English
Published: Wiley 2012-01-01
Series:Biochemistry Research International
Online Access:http://dx.doi.org/10.1155/2012/808934
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author David Reisman
Paula Takahashi
Amanda Polson
Kristy Boggs
author_facet David Reisman
Paula Takahashi
Amanda Polson
Kristy Boggs
author_sort David Reisman
collection DOAJ
description The p53 tumor suppressor induces the transcription of genes that negatively regulate progression of the cell cycle in response to DNA damage or other cellular stressors and thus participates in maintaining genome stability. Numerous studies have demonstrated that p53 transcription is activated before or during early S-phase in cells progressing from G0/G1 into S-phase through the combined action of two DNA-binding factors RBP-Jκ and C/EBPβ-2. Here, we review evidence that this induction occurs to provide available p53 mRNA in order to prepare the cell for DNA damage in S-phase, this ensuring a rapid response to DNA damage before exiting this stage of the cell cycle.
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institution Kabale University
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spelling doaj-art-0e5d590edc224652bfd2a253b02bf6392025-02-03T05:44:52ZengWileyBiochemistry Research International2090-22472090-22552012-01-01201210.1155/2012/808934808934Transcriptional Regulation of the p53 Tumor Suppressor Gene in S-Phase of the Cell-Cycle and the Cellular Response to DNA DamageDavid Reisman0Paula Takahashi1Amanda Polson2Kristy Boggs3Department of Biological Sciences, University of South Carolina, Columbia, SC 29208, USADepartamento de Genética, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, BrazilDepartment of Biological Sciences, University of South Carolina, Columbia, SC 29208, USADepartment of Hematology-Oncology, St. Jude Children's Research Hospital, Memphis, TN 38105, USAThe p53 tumor suppressor induces the transcription of genes that negatively regulate progression of the cell cycle in response to DNA damage or other cellular stressors and thus participates in maintaining genome stability. Numerous studies have demonstrated that p53 transcription is activated before or during early S-phase in cells progressing from G0/G1 into S-phase through the combined action of two DNA-binding factors RBP-Jκ and C/EBPβ-2. Here, we review evidence that this induction occurs to provide available p53 mRNA in order to prepare the cell for DNA damage in S-phase, this ensuring a rapid response to DNA damage before exiting this stage of the cell cycle.http://dx.doi.org/10.1155/2012/808934
spellingShingle David Reisman
Paula Takahashi
Amanda Polson
Kristy Boggs
Transcriptional Regulation of the p53 Tumor Suppressor Gene in S-Phase of the Cell-Cycle and the Cellular Response to DNA Damage
Biochemistry Research International
title Transcriptional Regulation of the p53 Tumor Suppressor Gene in S-Phase of the Cell-Cycle and the Cellular Response to DNA Damage
title_full Transcriptional Regulation of the p53 Tumor Suppressor Gene in S-Phase of the Cell-Cycle and the Cellular Response to DNA Damage
title_fullStr Transcriptional Regulation of the p53 Tumor Suppressor Gene in S-Phase of the Cell-Cycle and the Cellular Response to DNA Damage
title_full_unstemmed Transcriptional Regulation of the p53 Tumor Suppressor Gene in S-Phase of the Cell-Cycle and the Cellular Response to DNA Damage
title_short Transcriptional Regulation of the p53 Tumor Suppressor Gene in S-Phase of the Cell-Cycle and the Cellular Response to DNA Damage
title_sort transcriptional regulation of the p53 tumor suppressor gene in s phase of the cell cycle and the cellular response to dna damage
url http://dx.doi.org/10.1155/2012/808934
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