p53 and MDM2: Antagonists or Partners in Crime?

Christine M. Eischen; Guillermina Lozano

doi:10.1016/j.ccr.2009.02.004

p53 and MDM2: Antagonists or Partners in Crime?

Christine M. Eischen, Guillermina Lozano

Genetics

Research output: Contribution to journal › Short survey › peer-review

41 Scopus citations

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.

Original language	English (US)
Pages (from-to)	161-162
Number of pages	2
Journal	Cancer cell
Volume	15
Issue number	3
DOIs	https://doi.org/10.1016/j.ccr.2009.02.004
State	Published - Mar 3 2009

ASJC Scopus subject areas

Oncology
Cell Biology
Cancer Research

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10.1016/j.ccr.2009.02.004

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title = "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.",

author = "Eischen, {Christine M.} and Guillermina Lozano",

year = "2009",

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AU - Eischen, Christine M.

AU - Lozano, Guillermina

PY - 2009/3/3

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N2 - 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.

AB - 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.

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M3 - Short survey

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SP - 161

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JO - Cancer cell

JF - Cancer cell

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ER -

p53 and MDM2: Antagonists or Partners in Crime?

Abstract

ASJC Scopus subject areas

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