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Updated: Aug 9, 2026

Two- and Three-Dimensional Live Cell Imaging of DNA Damage Response Proteins
Published on: September 28, 2012
The p53 response during DNA damage: impact of transcriptional cofactors
Amanda S Coutts1, Nicholas La Thangue
1Laboratory of Cancer Biology, Division of Medical Sciences, University of Oxford, Oxford OX3 9DU, UK.
Abstract:
Defects in the DNA damage response pathways can lead to tumour development. The tumour suppressor p53 is a key player in the DNA damage response, and the precise regulation of p53 is critical for the suppression of tumorigenesis. DNA damage induces the activity of p53, via damage sensors such as ATM (ataxia telangiectasia mutated) and ATR (ataxia telangiectasia-related), which leads to the transcriptional regulation of a variety of genes involved in cell cycle control and apoptosis. p53 is therefore tightly controlled, and its activity is regulated at a multiplicity of levels. An increasing array of cofactors are now known to influence p53 activity. Here we will discuss several of the cofactors that impact on p53 activity, specifically those involved in the function of the two novel p53 cofactors JMY (junction-mediating and regulatory protein) and Strap (serine/threonine-kinase-receptor-associated protein).
Insights
Defects in DNA damage response pathways can cause tumors. This study explores how novel cofactors, JMY and Strap, regulate the tumor suppressor p53, crucial for preventing cancer by controlling cell cycle and apoptosis.
Area of Science:
- Molecular Biology
- Cancer Research
- Genetics
Background:
- Tumor suppressor p53 is vital for DNA damage response and preventing tumorigenesis.
- p53 activity is tightly regulated at multiple levels, influenced by various cofactors.
- Damage sensors like ATM and ATR activate p53 following DNA damage.
Purpose of the Study:
- To investigate the role of novel p53 cofactors, JMY and Strap, in regulating p53 activity.
- To understand how these cofactors impact the DNA damage response pathway.
Main Methods:
- Literature review and discussion of existing research on p53 cofactors.
- Focus on the functional mechanisms of JMY (junction-mediating and regulatory protein) and Strap (serine/threonine-kinase-receptor-associated protein).
Main Results:
- Identified JMY and Strap as key cofactors influencing p53 activity.
- Highlighted their involvement in the transcriptional regulation of genes controlling cell cycle and apoptosis.
- Emphasized the importance of cofactor-mediated regulation for tumor suppression.
Conclusions:
- Precise regulation of p53 by cofactors like JMY and Strap is critical for suppressing tumor development.
- Further research into these novel cofactors can reveal new therapeutic targets for cancer.
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