ArticleMolecular cell2021
The Protexin complex counters resection on stalled forks to promote homologous recombination and crosslink repair.
Article in Molecular cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Human TLS DNA polymerase: saviors or threats under replication stress?Molecular and cellular biochemistry · 2025Review
- EXO1's pan-cancer roles: diagnostic, prognostic, and immunological analyses through bioinformatics.Discover oncology · 2025Article
- Repair of genomic interstrand crosslinks.DNA repair · 2024Review
- A sophisticated mechanism governs Pol ζ activity in response to replication stress.Nature communications · 2024Article
- Cyclin F-EXO1 axis controls cell cycle-dependent execution of double-strand break repair.Science advances · 2024Article
- Replication-Independent ICL Repair: From Chemotherapy to Cell Homeostasis.Journal of molecular biology · 2024Review
- FLIP(C1orf112)-FIGNL1 complex regulates RAD51 chromatin association to promote viability after replication stress.Nature communications · 2024Article
- Targeted DNA integration in human cells without double-strand breaks using CRISPR-associated transposases.Nature biotechnology · 2024Article
- REV7 Monomer Is Unable to Participate in Double Strand Break Repair and Translesion Synthesis but Suppresses Mitotic Errors.International journal of molecular sciences · 2023Article
- FIRRM cooperates with FIGNL1 to promote RAD51 disassembly during DNA repair.Science advances · 2023Article
- Revolutionizing DNA repair research and cancer therapy with CRISPR-Cas screens.Nature reviews. Molecular cell biology · 2023Review
- Targeted DNA integration in human cells without double-strand breaks using CRISPR RNA-guided transposases.bioRxiv : the preprint server for biology · 2023Article
- A genome-wide screen identifies SCAI as a modulator of the UV-induced replicative stress response.PLoS biology · 2022Article
- MAD2L2 promotes replication fork protection and recovery in a shieldin-independent and REV3L-dependent manner.Nature communications · 2022Article
- Walking a tightrope: The complex balancing act of R-loops in genome stability.Molecular cell · 2022Review
- SCAI promotes error-free repair of DNA interstrand crosslinks via the Fanconi anemia pathway.EMBO reports · 2022Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Protection of stalled replication forks is critical to genomic stability. Using genetic and proteomic analyses, we discovered the Protexin complex containing the ssDNA binding protein SCAI and the DNA polymerase REV3. Protexin is required specifically for protecting forks stalled by nucleotide depletion, fork barriers, fragile sites, and DNA inter-strand crosslinks (ICLs), where it promotes homologous recombination and repair. Protexin loss leads to ssDNA accumulation and profound genomic instability in response to ICLs. Protexin interacts with RNA POL2, and both oppose EXO1's resection of DNA on forks remodeled by the FANCM translocase activity. This pathway acts independently of BRCA/RAD51-mediated fork stabilization, and cells with BRCA2 mutations were dependent on SCAI for survival. These data suggest that Protexin and its associated factors establish a new fork protection pathway that counteracts fork resection in part through a REV3 polymerase-dependent resynthesis mechanism of excised DNA, particularly at ICL stalled forks.
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Registered trials
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