ArticleThe Journal of biological chemistry2013
Translocation and stability of replicative DNA helicases upon encountering DNA-protein cross-links.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 67 citations in OpenAlex.
- Stable and programmable formation of DNA nanostructures via inter-strand crosslinking by assembly-triggered oxanine and amine linkage.Nucleic acids research · 2026Article
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- Translesion polymerases and DNA-protein crosslink repair shapes the cellular response to formaldehyde-induced DNA damage in ssDNA.Nucleic acids research · 2025Article
- Mechanisms controlling replication fork stalling and collapse at topoisomerase 1 cleavage complexes.Molecular cell · 2024Article
- Transcription-coupled repair of DNA-protein cross-links depends on CSA and CSB.Nature cell biology · 2024Article
- Aldehyde-induced DNA-protein crosslinks- DNA damage, repair and mutagenesis.Frontiers in oncology · 2024Review
- Review
- Review
- DNA Damage and Its Role in Cancer Therapeutics.International journal of molecular sciences · 2023Review
- Mechanisms and Regulation of DNA-Protein Crosslink Repair During DNA Replication by SPRTN Protease.Frontiers in molecular biosciences · 2022Review
- Multistep mechanism of G-quadruplex resolution during DNA replication.Science advances · 2021Article
- A ubiquitin switch controls autocatalytic inactivation of the DNA-protein crosslink repair protease SPRTN.Nucleic acids research · 2021Article
- DNA-protein crosslink proteases in genome stability.Communications biology · 2021Review
- Unraveling Reversible DNA Cross-Links with a Biological Machine.Chemical research in toxicology · 2020Article
- DNA Structure-Specific Cleavage of DNA-Protein Crosslinks by the SPRTN Protease.Molecular cell · 2020Article
- Tandem Deubiquitination and Acetylation of SPRTN Promotes DNA-Protein Crosslink Repair and Protects against Aging.Molecular cell · 2020Article
- GCNA Interacts with Spartan and Topoisomerase II to Regulate Genome Stability.Developmental cell · 2020Article
- DNA-Histone Cross-Links: Formation and Repair.Frontiers in cell and developmental biology · 2020Review
- DNA-protein cross-link repair: what do we know now?Cell & bioscience · 2020Review
- A model of DNA damage response activation at stalled replication forks by SPRTN.Nature communications · 2019Article
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 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA-protein cross-links (DPCs) are formed when cells are exposed to various DNA-damaging agents. Because DPCs are extremely large, steric hindrance conferred by DPCs is likely to affect many aspects of DNA transactions. In DNA replication, DPCs are first encountered by the replicative helicase that moves at the head of the replisome. However, little is known about how replicative helicases respond to covalently immobilized protein roadblocks. In the present study we elucidated the effect of DPCs on the DNA unwinding reaction of hexameric replicative helicases in vitro using defined DPC substrates. DPCs on the translocating strand but not on the nontranslocating strand impeded the progression of the helicases including the phage T7 gene 4 protein, simian virus 40 large T antigen, Escherichia coli DnaB protein, and human minichromosome maintenance Mcm467 subcomplex. The impediment varied with the size of the cross-linked proteins, with a threshold size for clearance of 5.0-14.1 kDa. These results indicate that the central channel of the dynamically translocating hexameric ring helicases can accommodate only small proteins and that all of the helicases tested use the steric exclusion mechanism to unwind duplex DNA. These results further suggest that DPCs on the translocating and nontranslocating strands constitute helicase and polymerase blocks, respectively. The helicases stalled by DPC had limited stability and dissociated from DNA with a half-life of 15-36 min. The implications of the results are discussed in relation to the distinct stabilities of replisomes that encounter tight but reversible DNA-protein complexes and irreversible DPC roadblocks.
Indexed as
Identifiers
What OpenQuestion holds
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.