ArticleMolecular cell2022
RIF1 acts in DNA repair through phosphopeptide recognition of 53BP1.
Article in Molecular cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- Current status of radionuclide therapy targeting PARP in cancer: challenges and prospects.European journal of nuclear medicine and molecular imaging · 2026Review
- Mechanisms and disease relevance of DNA break repair pathway choice.Nature reviews. Molecular cell biology · 2026Review
- The Host Cell Factor Phosphatase-2A Subunit PR130 Restricts Replication of Herpes Simplex Virus Type-1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Interplay Between Poly(ADP-ribosyl)ation and Specific Inner Cellular Events That Suggest Combination Strategies for Overcoming PARP Inhibitor Resistance.Pharmaceutics · 2026Review
- A busy BOD1-y: the diverse functions of an intracellular signaling regulatory protein family.Biochemical Society transactions · 2025Review
- Recombination junctions from antibody isotype switching classify immune and DNA repair dysfunction.Nature communications · 2025Article
- Implications of DNA damage response and immunotherapy in tumor therapy.Cell communication and signaling : CCS · 2025Review
- PARP inhibitor resistance in IDH1-mutant cancers due to loss of end protection factors, 53BP1 and REV7.NAR cancer · 2025Article
- DNA-damage dependent isoform switching modulates RIF1 DNA repair complex assembly and phase separation.The Journal of biological chemistry · 2025Article
- 53BP1-RIF1 and DNA-PKcs show distinct genetic interactions with diverse chromosomal break repair outcomes.Nature communications · 2025Article
- HMMR has oncoprotein-like properties in neuroblastoma cells and high HMMR expression has independent prognostic potential in neuroblastomas.Scientific reports · 2025Article
- GSK3B directs DNA repair choice and determines tumor response to PARP1 inhibition independent of BRCA1.The Journal of clinical investigation · 2025Article
- C8orf33 dictates DNA double-strand break repair choice by modulating KAT8-mediated H4K16 acetylation.Cell death & disease · 2025Article
- Using the safety scissors: DNA resection regulation at DNA double-strand breaks and telomeres.DNA repair · 2025Review
- Article
- Shieldin and CST co-orchestrate DNA polymerase-dependent tailed-end joining reactions independently of 53BP1-governed repair pathway choice.Nature structural & molecular biology · 2025Article
- 53BP1-the 'Pandora's box' of genome integrity.DNA repair · 2024Review
- PTEN-mediated dephosphorylation of 53BP1 confers cellular resistance to DNA damage in cancer cells.Molecular oncology · 2024Article
- Deciphering the phospho-signature induced by hepatitis B virus in primary human hepatocytes.Frontiers in microbiology · 2024Article
- Shieldin and CST co-orchestrate DNA polymerase-dependent tailed-end joining reactions independently of 53BP1-governed repair pathway choice.bioRxiv : the preprint server for biology · 2023Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
The chromatin-binding protein 53BP1 promotes DNA repair by orchestrating the recruitment of downstream effectors including PTIP, RIF1, and shieldin to DNA double-strand break sites. While we know how PTIP recognizes 53BP1, the molecular details of RIF1 recruitment to DNA-damage sites remains undefined. Here, we report that RIF1 is a phosphopeptide-binding protein that directly interacts with three phosphorylated 53BP1 epitopes. The RIF1-binding sites on 53BP1 share an essential LxL motif followed by two closely apposed phosphorylated residues. Simultaneous mutation of these sites on 53BP1 abrogates RIF1 accumulation into ionizing-radiation-induced foci, but surprisingly, only fully compromises 53BP1-dependent DNA repair when an alternative mode of shieldin recruitment to DNA-damage sites is also disabled. Intriguingly, this alternative mode of recruitment still depends on RIF1 but does not require its interaction with 53BP1. RIF1 therefore employs phosphopeptide recognition to promote DNA repair but also modifies shieldin action independently of 53BP1 binding.
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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.