Regulation of p53 in response to DNA damage View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

1999-12

AUTHORS

N D Lakin, S P Jackson

ABSTRACT

Activation of p53 can occur in response to a number of cellular stresses, including DNA damage, hypoxia and nucleotide deprivation. Several forms of DNA damage have been shown to activate p53, including those generated by ionising radiation (IR), radio-mimetic drugs, ultraviolet light (UV) and chemicals such as methyl methane sulfonate (MMS). Under normal conditions, p53 levels are maintained at a low state by virtue of the extremely short-half life of the polypeptide. In addition to this, p53 normally exists in an largely inactive state that is relatively inefficient at binding to DNA and activating transcription. Activation of p53 in response to DNA damage is associated with a rapid increase in its levels and with an increased ability of p53 to bind DNA and mediate transcriptional activation. This then leads to the activation of a number of genes whose products trigger cell-cycle arrest, apoptosis, or DNA repair. Recent work has suggested that this regulation is brought about largely through DNA damage triggering a series of phosphorylation, de-phosphorylation and acetylation events on the p53 polypeptide. Here, we discuss the nature of these modifications, the enzymes that bring them about, and how changes in p53 modification lead to p53 activation. More... »

PAGES

7644-7655

References to SciGraph publications

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/sj.onc.1203015

    DOI

    http://dx.doi.org/10.1038/sj.onc.1203015

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1033036291

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/10618704


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