La Thangue, N. and Coutts, A.S. (2007) Mdm2 widens its repertoire. Cell Cycle, 6(7), pp. 827-829.
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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.
Item Type: | Articles |
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Status: | Published |
Refereed: | Yes |
Glasgow Author(s) Enlighten ID: | UNSPECIFIED |
Authors: | La Thangue, N., and Coutts, A.S. |
College/School: | College of Medical Veterinary and Life Sciences |
Journal Name: | Cell Cycle |
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