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RNF126 and BRAP safeguard genome integrity after DNA damage in late mitosis
Jessel Ayra-Plasencia1, Inmaculada Jorge2, Jesús Vázquez2
1Unidad de Investigación, Hospital Universitario de Canarias, Instituto de Investigación Sanitaria de Canarias (IISC)/FIISC, La Laguna, Santa Cruz de Tenerife, Spain; Instituto de Tecnologías Biomédicas, Universidad de La Laguna, La Laguna, Santa Cruz de Tenerife, Spain.
Cell Reports
|April 17, 2026
Summary
Late mitotic DNA damage is partially repaired by E3 ubiquitin ligases RNF126 and BRAP. These proteins aid cell survival and lesion resolution, offering potential cancer therapy targets.
Area of Science:
- Molecular Biology
- Cell Biology
- Cancer Research
Background:
- DNA double-strand breaks during mitosis are poorly repaired.
- Cellular responses to late mitotic damage are not well understood.
Purpose of the Study:
- Investigate cellular responses to DNA damage in late mitosis.
- Identify key regulators of DNA damage repair in late mitosis.
Main Methods:
- Cell synchronization in anaphase/telophase followed by irradiation.
- Proteomic analysis to identify E3 ubiquitin ligases.
- Functional assays for DNA damage signaling and repair markers.
Main Results:
- Irradiation in late mitosis induced partial DNA damage signaling (H2AX phosphorylation, MDC1 accumulation).
- RNF126 and BRAP were identified as ATM-dependent regulators accumulating in damaged late mitotic cells.
- RNF126 and BRAP are crucial for DNA damage marker formation, lesion resolution, and cell survival.
- E3 ligases RNF126 and BRAP are overexpressed in some tumors and linked to chromosomal instability.
Conclusions:
- RNF126 and BRAP facilitate tolerance of late mitotic DNA damage.
- These E3 ligases represent potential therapeutic targets for genotoxic cancer therapies.
Keywords:
BRAPCP: genomicsDNA damage responseRNF126cell cycle checkpointchromosomal instabilitydouble-strand breakionizing radiationlate mitosisreplication stressubiquitin ligaseMore Related Videos
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