ArticleNature structural & molecular biology2018
Mechanism of 53BP1 activity regulation by RNA-binding TIRR and a designer protein.
Article in Nature structural & molecular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 48 citations in OpenAlex.
- RNA-binding proteins in the mouse lens: Functional classifications, expression profiling, and interaction studies of Carhsp1 with crystallin mRNAs.Developmental biology · 2026Article
- A framework for the exploration of subcellular compartmentalization of RNA-binding proteins.Nature communications · 2026Article
- DTX3L-mediated TIRR nuclear export and degradation regulates DNA repair pathway choice and PARP inhibitor sensitivity.Nature communications · 2024Article
- 53BP1-the 'Pandora's box' of genome integrity.DNA repair · 2024Review
- TIRR regulates mRNA export and association with P-bodies in response to DNA damage.Nucleic acids research · 2024Article
- 53BP1 deficiency leads to hyperrecombination using break-induced replication (BIR).Nature communications · 2024Article
- NEAT1 modulates the TIRR/53BP1 complex to maintain genome integrity.Nature communications · 2024Article
- 53BP1 deficiency leads to hyperrecombination using break-induced replication (BIR).bioRxiv : the preprint server for biology · 2024Article
- Endogenous p53 inhibitor TIRR dissociates systemic metabolic health from oncogenic activity.Cell reports · 2024Article
- Regulation of p53 by the mitotic surveillance/stopwatch pathway: implications in neurodevelopment and cancer.Frontiers in cell and developmental biology · 2024Review
- An autoinhibited state of 53BP1 revealed by small molecule antagonists and protein engineering.Nature communications · 2023Article
- TRABID overexpression enables synthetic lethality to PARP inhibitor via prolonging 53BP1 retention at double-strand breaks.Nature communications · 2023Article
- HDGFRP3 interaction with 53BP1 promotes DNA double-strand break repair.Nucleic acids research · 2023Article
- DNA double-strand break-derived RNA drives TIRR/53BP1 complex dissociation.Cell reports · 2022Article
- Multifaceted regulation and functions of 53BP1 in NHEJ‑mediated DSB repair (Review).International journal of molecular medicine · 2022Review
- Biosensor for deconvolution of individual cell fate in response to ion beam irradiation.Cell reports methods · 2022Article
- TIRR inhibits the 53BP1-p53 complex to alter cell-fate programs.Molecular cell · 2021Article
- ATM-phosphorylated SPOP contributes to 53BP1 exclusion from chromatin during DNA replication.Science advances · 2021Article
- Mass spectrometry-based protein‒protein interaction techniques and their applications in studies of DNA damage repair.Journal of Zhejiang University. Science. B · 2021Review
- Regulation of DNA double-strand break repair pathway choice: a new focus on 53BP1.Journal of Zhejiang University. Science. B · 2021Review
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
Abstract
Dynamic protein interaction networks such as DNA double-strand break (DSB) signaling are modulated by post-translational modifications. The DNA repair factor 53BP1 is a rare example of a protein whose post-translational modification-binding function can be switched on and off. 53BP1 is recruited to DSBs by recognizing histone lysine methylation within chromatin, an activity directly inhibited by the 53BP1-binding protein TIRR. X-ray crystal structures of TIRR and a designer protein bound to 53BP1 now reveal a unique regulatory mechanism in which an intricate binding area centered on an essential TIRR arginine residue blocks the methylated-chromatin-binding surface of 53BP1. A 53BP1 separation-of-function mutation that abolishes TIRR-mediated regulation in cells renders 53BP1 hyperactive in response to DSBs, highlighting the key inhibitory function of TIRR. This 53BP1 inhibition is relieved by TIRR-interacting RNA molecules, providing proof-of-principle of RNA-triggered 53BP1 recruitment to DSBs.
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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.