Mdm2 Widens Its Repertoire.
From: Laboratory of Cancer Biology, Division of Medical Sciences, University of Oxford, Oxford, UK.
Cell cycle (Georgetown, Tex.)
- Publish Date: Apr 2007
- ISSN: 1551-4005
- Volume: 6
- Issue: 7
- Pages: 827-9
- Medium: Internet
- Language: English
- Citation (JAMA): Coutts Amanda S, La Thangue Nicholas B, et al. Mdm2 Widens Its Repertoire.. Cell Cycle Apr 2007;6:827-9
Abstract
The p53 tumor suppressor protein is a DNA damage responsive transcription factor that affects diverse cellular processes which include transcription, DNA synthesis and repair, cell cycle arrest, senescence and apoptosis. The Mdm2 oncoprotein is a primary regulator of p53, mediating p53 control via ubiquitin-dependent proteasomal degradation. During DNA damage, the interaction between p53 and Mdm2 is reduced, which allows p53 levels to accumulate. p53 activity is tightly controlled and regulated at a multiplicity of levels, and the importance of co-factors that influence p53 activity is becoming increasingly evident. Recent studies have highlighted the role of Mdm2 in the control of p53 co-factors. Thus, Mdm2 targets JMY, a p53 co-factor, for ubiquitin-dependent Mdm2 targets JMY, a p53 co-factor, for ubiquitin-dependent proteasomal degradation and in doing so overcomes the ability of JMY to augment the p53 response. These results define a new functional relationship between control of p53 activity and Mdm2, and suggest that transcription co-factors which facilitate the p53 response are important targets through which Mdm2 mediates its oncogenic activity.
Mesh Headings (Keywords): Animals, Cell Transformation, Neoplastic, DNA Damage, Gene Expression Regulation, Neoplastic, Humans, Nuclear Proteins, Proteasome Endopeptidase Complex, Proto-Oncogene Proteins c-mdm2, Regulatory Elements, Transcriptional, Trans-Activators, Tumor Suppressor Protein p53
Check for Full Text / PubMed Unique Identifier (PMID): 17377491
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