ArticleNature communications2020
FAM111A protects replication forks from protein obstacles via its trypsin-like domain.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 2 of them syntheses that pooled it.
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.
The trial behind it
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
82 citing papers in PubMed, 2 syntheses or guidelines pooled it, 113 citations in OpenAlex.
- Expanding TBCE-related phenotype-novel variant causing rigid spine, eosinophilia, neutropenia, and nocturnal hypoxemia.Journal of applied genetics · 2025Pooled it
- Expanding the Phenotypic Spectrum of Kenny-Caffey Syndrome.The Journal of clinical endocrinology and metabolism · 2023Pooled it
- Distinct ATRX functions cooperate with 9-1-1 and CST complexes to safeguard replication and telomere integrity.Nature structural & molecular biology · 2026Article
- Isotope Dilution NanoLC-MS/MS Quantitation of Methylglyoxal DNA-Protein Cross-Links: Formation and Repair in Human Cells.Analytical chemistry · 2026Article
- ACRC/GCNA is an essential protease that repairs DNA-protein crosslinks during vertebrate development.Nucleic acids research · 2026Article
- Living Cells Employ Ubiquitin-Proteasomal System and Nucleotide Excision Repair Pathways to Remove Reactive Oxygen Species-Induced DNA-Protein Crosslinks (ROS-DPCs).bioRxiv : the preprint server for biology · 2026Article
- Targeting DNA Topoisomerase I for the Treatment of Cancer: Past, Present and Future.Journal of molecular biology · 2026Review
- The FAM111A Gene: Genetic, Epigenetic, and Pharmacological Targets and Mechanistic Insights with Clinical Relevance.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Cellular strategies for repairing trapped protein-DNA complexes.Frontiers in pharmacology · 2026Review
- Isotope Dilution nanoLC-MS/MS Quantitation of Methylglyoxal DNA-Protein Crosslinks: Formation and Repair in Human Cells.bioRxiv : the preprint server for biology · 2025Article
- Computational prediction of diagnostic biomarker candidates and prognostic gene signature from DNA replication-related genes in breast cancer.Discover oncology · 2025Article
- Poxvirus Host-Range Determinants: SAMD9/9L and Beyond.Annual review of virology · 2025Review
- Allosteric activation of the SPRTN protease by ubiquitin maintains genome stability.Nature communications · 2025Article
- DNA-Protein Cross-Links Derived from Abasic DNA Lesions: Recent Progress and Future Directions.Chemical research in toxicology · 2025Review
- New insights into the effects of PFOS exposure on rat lung development: morphological, functional, and single-cell sequencing analysis.Archives of toxicology · 2025Article
- The role of FAM111B in the malignant progression and molecular regulation of human glioma through the PI3K/Akt pathway.Chinese neurosurgical journal · 2025Article
- Olfactory ensheathing cells from adult female rats are hybrid glia that promote neural repair.eLife · 2025Article
- Unveiling FAM111B: A Pan-Cancer Biomarker for DNA Repair and Immune Infiltration.International journal of molecular sciences · 2025Article
- Quantitative hypermorphic FAM111A alleles cause autosomal recessive Kenny-Caffey syndrome type 2 and osteocraniostenosis.JCI insight · 2025Article
- Homozygous synonymous FAM111A variant underlies an autosomal recessive form of Kenny-Caffey syndrome.Journal of human genetics · 2025Article
22 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
7 authors at 3 institutions in 1 country.
Funding
Abstract
Persistent protein obstacles on genomic DNA, such as DNA-protein crosslinks (DPCs) and tight nucleoprotein complexes, can block replication forks. DPCs can be removed by the proteolytic activities of the metalloprotease SPRTN or the proteasome in a replication-coupled manner; however, additional proteolytic mechanisms may exist to cope with the diversity of protein obstacles. Here, we show that FAM111A, a PCNA-interacting protein, plays an important role in mitigating the effect of protein obstacles on replication forks. This function of FAM111A requires an intact trypsin-like protease domain, the PCNA interaction, and the DNA-binding domain that is necessary for protease activity in vivo. FAM111A, but not SPRTN, protects replication forks from stalling at poly(ADP-ribose) polymerase 1 (PARP1)-DNA complexes trapped by PARP inhibitors, thereby promoting cell survival after drug treatment. Altogether, our findings reveal a role of FAM111A in overcoming protein obstacles to replication forks, shedding light on cellular responses to anti-cancer therapies.
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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.