Related Experiment Videos
A novel cofactor for p300 that regulates the p53 response
1Division of Biochemistry and Molecular Biology, University of Glasgow, United Kingdom.
Molecular Cell
|October 13, 1999
Summary
A newly discovered protein, JMY, works with p300 to enhance the p53 protein's role in cellular stress response. This p300/JMY complex boosts p53-driven gene activation and apoptosis, crucial for cell survival.
Area of Science:
- Molecular Biology
- Cellular Biology
- Biochemistry
Background:
- The p53 protein is a critical transcription factor in cellular stress response.
- p300/CBP proteins are known coactivators that regulate transcription factors, including p53.
Purpose of the Study:
- To identify novel cofactors that modulate the p53 response.
- To investigate the role of JMY as a cofactor for p300 in the context of p53 activity.
Main Methods:
- Co-immunoprecipitation assays to demonstrate JMY and p300 association.
- Analysis of p53-dependent gene activation (e.g., bax gene).
- Investigation of alternative splicing in JMY isoforms and their functional impact.
Main Results:
- JMY was identified as a novel cofactor that associates with p300 under physiological conditions.
- The p300/JMY complex is recruited to activated p53 during cellular stress.
- JMY enhances p53-dependent transcription of target genes like bax.
- Alternative splicing of JMY affects the outcome of the p53 response.
Conclusions:
- The p300/JMY coactivator complex plays a significant role in facilitating the p53-mediated cellular stress response.
- JMY acts as a crucial mediator, augmenting p53-dependent transcription and apoptosis.