ArticleNucleic acids research2019
The nuclear structural protein NuMA is a negative regulator of 53BP1 in DNA double-strand break repair.
Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- DDX17 is required for efficient DSB repair at DNA:RNA hybrid deficient loci.Nucleic acids research · 2022Pooled it
- Article
- The nuclear structural protein NuMA is required for efficient DNA replication by ensuring association of core replication factors to replication forks.bioRxiv : the preprint server for biology · 2026Article
- Closing the loops: chromatin loop dynamics after DNA damage.Nucleus (Austin, Tex.) · 2025Review
- ADP-ribosylation of NuMA promotes DNA single-strand break repair and transcription.Cell reports · 2025Article
- An ATM-PPM1D Circuit Controls the Processing and Restart of DNA Replication Forks.bioRxiv : the preprint server for biology · 2025Article
- Whole‑exome sequencing insights into synchronous bilateral breast cancer with discordant molecular subtypes.Oncology letters · 2024Article
- Growth hormone and radiation therapy: friend, foe, or both?Endocrine-related cancer · 2024Review
- Discovery and Characterization of ZL-2201, a Potent, Highly Selective, and Orally Bioavailable Small-molecule DNA-PK Inhibitor.Cancer research communications · 2023Article
- NUMA1 modulates apoptosis of esophageal squamous cell carcinoma cells through regulating ASK1-JNK signaling pathway.Cellular and molecular life sciences : CMLS · 2023Article
- Review
- Article
- Cancer Cells Haploinsufficient for ATM Are Sensitized to PARP Inhibitors byInternational journal of molecular sciences · 2022Article
- A guide for single-particle chromatin tracking in live cell nuclei.Cell biology international · 2022Review
- ZMYM2 restricts 53BP1 at DNA double-strand breaks to favor BRCA1 loading and homologous recombination.Nucleic acids research · 2022Article
- Nuclear IGF1R interacts with NuMA and regulates 53BP1‑dependent DNA double‑strand break repair in colorectal cancer.Oncology reports · 2021Article
- TSHZ2 is an EGF-regulated tumor suppressor that binds to the cytokinesis regulator PRC1 and inhibits metastasis.Science signaling · 2021Article
- Monitoring Dark-State Dynamics of a Single Nitrogen-Vacancy Center in Nanodiamond by Auto-Correlation Spectroscopy: Photonionization and Recharging.Nanomaterials (Basel, Switzerland) · 2021Article
- Targeted exome sequencing for the identification of common mutational signatures and potential driver mutations for brain metastases and prognosis.Oncology letters · 2021Article
- Phosphoproteomics reveals novel modes of function and inter-relationships among PIKKs in response to genotoxic stress.The EMBO journal · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 6 institutions in 1 country.
Funding
Abstract
P53-binding protein 1 (53BP1) mediates DNA repair pathway choice and promotes checkpoint activation. Chromatin marks induced by DNA double-strand breaks and recognized by 53BP1 enable focal accumulation of this multifunctional repair factor at damaged chromatin. Here, we unveil an additional level of regulation of 53BP1 outside repair foci. 53BP1 movements are constrained throughout the nucleoplasm and increase in response to DNA damage. 53BP1 interacts with the structural protein NuMA, which controls 53BP1 diffusion. This interaction, and colocalization between the two proteins in vitro and in breast tissues, is reduced after DNA damage. In cell lines and breast carcinoma NuMA prevents 53BP1 accumulation at DNA breaks, and high NuMA expression predicts better patient outcomes. Manipulating NuMA expression alters PARP inhibitor sensitivity of BRCA1-null cells, end-joining activity, and immunoglobulin class switching that rely on 53BP1. We propose a mechanism involving the sequestration of 53BP1 by NuMA in the absence of DNA damage. Such a mechanism may have evolved to disable repair functions and may be a decisive factor for tumor responses to genotoxic treatments.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.