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Signaling to the p53 Tumor Suppressor through Pathways Activated by Genotoxic and Non-genotoxic Stresses.

DE200415006681

Publication Date	2003
Personal Author	Anderson, C. W.; Appella, E.
Page Count	38
Abstract	The p53 tumor suppressor is a tetrameric transcription factor that is post-translational modified at(approx)18 different sites by phosphorylation, acetylation, or sumoylation in response to various cellular stress conditions. Specific posttranslational modifications, or groups of modifications, that result from the activation of different stress-induced signaling pathways are thought to modulate p53 activity to regulate cell fate by inducing cell cycle arrest, apoptosis, or cellular senescence. Here we review the posttranslational modifications to p53 and the pathways that produce them in response to both genotoxic and non-genotoxic stresses.
Keywords	Neoplasms Cell cycle Transcription factors Modifications Phosphorylation Stresses Modification
Source Agency	Technical Information Center Oak Ridge Tennessee
Corporate Authors	Brookhaven National Lab., Upton, NY. Biology Dept.; National Cancer Inst., Bethesda, MD.; Department of Energy, Washington, DC.
Supplemental Notes	Prepared in cooperation with National Cancer Inst., Bethesda, MD. Sponsored by Department of Energy, Washington, DC.
Document Type	Technical Report
NTIS Issue Number	200419

Signaling to the p53 Tumor Suppressor through Pathways Activated by Genotoxic and Non-genotoxic Stresses.

Signaling to the p53 Tumor Suppressor through Pathways Activated by Genotoxic and Non-genotoxic Stresses.
DE200415006681

Publication Date	2003
Personal Author	Anderson, C. W.; Appella, E.
Page Count	38
Abstract	The p53 tumor suppressor is a tetrameric transcription factor that is post-translational modified at(approx)18 different sites by phosphorylation, acetylation, or sumoylation in response to various cellular stress conditions. Specific posttranslational modifications, or groups of modifications, that result from the activation of different stress-induced signaling pathways are thought to modulate p53 activity to regulate cell fate by inducing cell cycle arrest, apoptosis, or cellular senescence. Here we review the posttranslational modifications to p53 and the pathways that produce them in response to both genotoxic and non-genotoxic stresses.
Keywords	Neoplasms Cell cycle Transcription factors Modifications Phosphorylation Stresses Modification
Source Agency	Technical Information Center Oak Ridge Tennessee
Corporate Authors	Brookhaven National Lab., Upton, NY. Biology Dept.; National Cancer Inst., Bethesda, MD.; Department of Energy, Washington, DC.
Supplemental Notes	Prepared in cooperation with National Cancer Inst., Bethesda, MD. Sponsored by Department of Energy, Washington, DC.
Document Type	Technical Report
NTIS Issue Number	200419