ArticleNature structural & molecular biology2019
Protection of abasic sites during DNA replication by a stable thiazolidine protein-DNA cross-link.
Article in Nature structural & molecular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed.
- DEPACE-seq enables high-fidelity, single-nucleotide-resolution mapping of abasic sites and characterization of dynamic and long-lived AP landscapes in mammalian genomes.Nucleic acids research · 2026Article
- DeepPANB: integrating protein language model with PaiNN equivariant graph neural networks for prediction of protein-nucleic acid binding sites.Briefings in bioinformatics · 2026Article
- DNA binding and lesion recognition by the bacterial interstrand DNA crosslink glycosylase AlkX.EMBO reports · 2026Article
- Direct Mapping of CDK2 Substrates in Embryonic Stem Cells Uncovers an AP-Site Repair Mechanism via HMCES Phosphorylation.bioRxiv : the preprint server for biology · 2026Article
- Fork Reversal Safeguards Epigenetic Inheritance During Replication Stress.Research square · 2026Article
- Identification of HMCES as the Core Genetic Determinant Underlying theInternational journal of molecular sciences · 2026Article
- DNA binding and lesion recognition by the bacterial interstrand DNA crosslink glycosylase AlkX.bioRxiv : the preprint server for biology · 2025Article
- A comparative study of flaxseed gum effect on Lactobacillus acidophilus genes expression, and textural, sensory, structural, and microbiological properties of synbiotic Iranian white cheese.Scientific reports · 2025Article
- DNA-Protein Cross-Links Derived from Abasic DNA Lesions: Recent Progress and Future Directions.Chemical research in toxicology · 2025Review
- Chemical Switching: A Concept Inspired by Strategies from Biocatalysis and Organocatalysis.Chembiochem : a European journal of chemical biology · 2025Review
- Contributing factors to the oxidation-induced mutational landscape in human cells.Nature communications · 2024Article
- Electro-elution-based purification of covalent DNA-protein cross-links.Nature protocols · 2024Review
- Repair of genomic interstrand crosslinks.DNA repair · 2024Review
- Structure andmBio · 2024Article
- Review
- RPA guides UNG to uracil in ssDNA to facilitate antibody class switching and repair of mutagenic uracil at the replication fork.Nucleic acids research · 2024Article
- Temporary HMCES-DNA cross-link prevents permanent DNA damage.Cell reports · 2024Article
- Self-reversal facilitates the resolution of HMCES DNA-protein crosslinks in cells.Cell reports · 2023Article
- Unprecedented reactivity of polyamines with aldehydic DNA modifications: structural determinants of reactivity, characterization and enzymatic stability of adducts.Nucleic acids research · 2023Article
- A non-proteolytic release mechanism for HMCES-DNA-protein crosslinks.The EMBO journal · 2023Article
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Authors and funding
5 authors.
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Abstract
Abasic (AP) sites are one of the most common DNA lesions that block replicative polymerases. 5-hydroxymethylcytosine binding, embryonic stem cell-specific protein (HMCES) recognizes and processes these lesions in the context of single-stranded DNA (ssDNA). A HMCES DNA-protein cross-link (DPC) intermediate is thought to shield the AP site from endonucleases and error-prone polymerases. The highly evolutionarily conserved SOS-response associated peptidase (SRAP) domain of HMCES and its Escherichia coli ortholog YedK mediate lesion recognition. Here we uncover the basis of AP site protection by SRAP domains from a crystal structure of the YedK DPC. YedK forms a stable thiazolidine linkage between a ring-opened AP site and the α-amino and sulfhydryl substituents of its amino-terminal cysteine residue. The thiazolidine linkage explains the remarkable stability of the HMCES DPC, its resistance to strand cleavage and the proteolysis requirement for resolution. Furthermore, its structure reveals that HMCES has specificity for AP sites in ssDNA at junctions found when replicative polymerases encounter the AP lesion.
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