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p53 and MDM2: antagonists or partners in crime?

Abstract
Therapeutics that disrupt the p53-MDM2 interaction show promise for cancer treatment but surprisingly have different biological outcomes. A study by Enge et al. in this issue of Cancer Cell shows that the ability of MDM2 to target hnRNP K for degradation contributes to the decision to induce apoptosis rather than cell-cycle arrest.
AuthorsChristine M Eischen, Guillermina Lozano
JournalCancer cell (Cancer Cell) Vol. 15 Issue 3 Pg. 161-2 (Mar 03 2009) ISSN: 1878-3686 [Electronic] United States
PMID19249672 (Publication Type: Journal Article, Review, Comment)
Chemical References
  • Antineoplastic Agents
  • Tumor Suppressor Protein p53
  • Proto-Oncogene Proteins c-mdm2
Topics
  • Animals
  • Antineoplastic Agents (pharmacology)
  • Apoptosis (physiology)
  • Cell Cycle (drug effects)
  • Gene Expression Regulation
  • Humans
  • Neoplasms (drug therapy, metabolism)
  • Proto-Oncogene Proteins c-mdm2 (metabolism)
  • Tumor Suppressor Protein p53 (metabolism)

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