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Article

A cancer persistent DNA repair circuit driven by MDM2, MDM4 (MDMX), and mutant p53 for recruitment of MDC1 and 53BP1 on chromatin.

Nucleic acids research - 8 Jul 2025

Ellison Viola, Polotskaia Alla, Xiao Gu, Leybengrub Pamella, Lee Rusia, Qiu Weigang, Hendrickson Ronald C, Hu Wenwei, Bargonetti Jill

Abstract excerpt

DNA damage signaling requires functional interactions between 53BP1 and the wild-type p53 tumor suppressor. Cancer cells often express elevated levels of transcriptionally inactive mutant p53 (mtp53) that maintains MDM2 and MDMX (MDM4) binding partners. The ability of mtp53 to functionally interact with additional proteins in the context of a dynamic equilibrium with MDM2-MDMX heterodimers has not been described....

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Source

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Identifiers

PMID: 40626562
DOI: 10.1093/nar/gkaf627
PMCID: PMC12235508

Genes

MDM2
MDC1
MDM4
ATM

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

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