| Literature DB >> 19249672 |
Christine M Eischen1, Guillermina Lozano.
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.Entities:
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Year: 2009 PMID： 19249672 DOI： 10.1016/j.ccr.2009.02.004
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743