ArticleMolecular cell2018
MRI Is a DNA Damage Response Adaptor during Classical Non-homologous End Joining.
Article in Molecular cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 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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Who cites it
64 citing papers in PubMed, 112 citations in OpenAlex.
- No Time to Fold: Intrinsically Disordered Microproteins in Action.Biochemistry · 2026Review
- 53BP1 orchestrates sequence feature of RAG targets to balance DNA repair outcomes during V(D)J recombination.Science advances · 2026Article
- Nonhomologous end joining-the importance of end tethering and beyond.Genes & development · 2026Review
- Uncovering genetic interactions in the DNA repair network in response to endogenous damage and ionizing radiation.Cell reports · 2026Article
- The nonamer code for RAG-mediated recombination in vivo.Nucleic acids research · 2025Article
- CRISPR-Cas9 screening reveals microproteins regulating adipocyte proliferation and lipid metabolism.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Senataxin and DNA-PKcs redundantly promote non-homologous end joining repair of DNA double strand breaks during V(D)J recombination.Science advances · 2025Article
- Article
- Nuclear VPS35 attenuates NHEJ repair by sequestering Ku protein.Molecular medicine (Cambridge, Mass.) · 2025Article
- Eukaryotic Microproteins.Annual review of biochemistry · 2025Review
- A large-scale sORF screen identifies putative microproteins involved in cancer cell fitness.iScience · 2025Article
- Homeodomain protein PRRX1 anchors the Ku heterodimers at DNA double-strand breaks to promote nonhomologous end-joining.Nucleic acids research · 2025Article
- THE GID COMPLEX REGULATES DNA END PROCESSING DURING DNA DOUBLE-STRAND BREAK REPAIR BY NONHOMOLOGOUS END JOINING.Transactions of the American Clinical and Climatological Association · 2025Article
- Microprotein-encoding RNA regulation in cells treated with pro-inflammatory and pro-fibrotic stimuli.BMC genomics · 2024Article
- Orientation Regulation of Class-switch Recombination in Human B Cells.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Noncanonical microprotein regulation of immunity.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Review
- Microproteins-Discovery, structure, and function.Proteomics · 2023Review
- Biochemistry and Protein Interactions of the CYREN Microprotein.Biochemistry · 2023Article
- New Facets of DNA Double Strand Break Repair: Radiation Dose as Key Determinant of HR versus c-NHEJ Engagement.International journal of molecular sciences · 2023Review
- Chemical labeling and proteomics for characterization of unannotated small and alternative open reading frame-encoded polypeptides.Biochemical Society transactions · 2023Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
21 authors at 5 institutions in 1 country.
Funding
Abstract
The modulator of retrovirus infection (MRI or CYREN) is a 30-kDa protein with a conserved N-terminal Ku-binding motif (KBM) and a C-terminal XLF-like motif (XLM). We show that MRI is intrinsically disordered and interacts with many DNA damage response (DDR) proteins, including the kinases ataxia telangiectasia mutated (ATM) and DNA-PKcs and the classical non-homologous end joining (cNHEJ) factors Ku70, Ku80, XRCC4, XLF, PAXX, and XRCC4. MRI forms large multimeric complexes that depend on its N and C termini and localizes to DNA double-strand breaks (DSBs), where it promotes the retention of DDR factors. Mice deficient in MRI and XLF exhibit embryonic lethality at a stage similar to those deficient in the core cNHEJ factors XRCC4 or DNA ligase IV. Moreover, MRI is required for cNHEJ-mediated DSB repair in XLF-deficient lymphocytes. We propose that MRI is an adaptor that, through multivalent interactions, increases the avidity of DDR factors to DSB-associated chromatin to promote cNHEJ.
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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.