ArticleGenes & development2012
ZRANB3 is a structure-specific ATP-dependent endonuclease involved in replication stress response.
Article in Genes & development, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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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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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
76 citing papers in PubMed, 123 citations in OpenAlex.
- Article
- FBH1 Reverses Stalled Replication Forks via Sequential Unwinding of Nascent Strands.bioRxiv : the preprint server for biology · 2026Article
- The Zinc Finger Ran-Binding Protein 3 (ZRANB3): An Advanced Perspective.International journal of molecular sciences · 2026Review
- Thioether-mediated protein ubiquitination in constructing affinity- and activity-based ubiquitinated protein probes.Nature protocols · 2025Review
- Widespread impact of nucleosome remodelers on transcription at cis-regulatory elements.Cell reports · 2025Article
- Digital Image Processing to Detect Adaptive Evolution.Molecular biology and evolution · 2024Article
- Mechanisms and regulation of replication fork reversal.DNA repair · 2024Review
- ATAD5 functions as a regulatory platform for Ub-PCNA deubiquitination.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Article
- How to sensitize glioblastomas to temozolomide chemotherapy: a gap-centered view.Frontiers in cell and developmental biology · 2024Review
- Genome maintenance meets mechanobiology.Chromosoma · 2024Review
- Cellular Responses to Widespread DNA Replication Stress.International journal of molecular sciences · 2023Review
- An inventory of crosstalk between ubiquitination and other post-translational modifications in orchestrating cellular processes.iScience · 2023Review
- RFWD3 promotes ZRANB3 recruitment to regulate the remodeling of stalled replication forks.The Journal of cell biology · 2023Article
- ERCC6L2 mitigates replication stress and promotes centromere stability.Cell reports · 2023Article
- PARP1 recruits DNA translocases to restrain DNA replication and facilitate DNA repair.PLoS genetics · 2022Article
- Strand annealing and motor driven activities of SMARCAL1 and ZRANB3 are stimulated by RAD51 and the paralog complex.Nucleic acids research · 2022Article
- Linkage reprogramming by tailor-made E3s reveals polyubiquitin chain requirements in DNA-damage bypass.Molecular cell · 2022Article
- Chromatin-remodeling factor CHR721 with non-canonical PIP-box interacts with OsPCNA in Rice.BMC plant biology · 2022Article
- A fork in the road: Where homologous recombination and stalled replication fork protection part ways.Seminars in cell & developmental biology · 2021Review
16 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
To efficiently duplicate their genomic content, cells must overcome DNA lesions that interfere with processive DNA replication. These lesions may be removed and repaired, rather than just tolerated, to allow continuity of DNA replication on an undamaged DNA template. However, it is unclear how this is achieved at a molecular level. Here we identify a new replication-associated factor, ZRANB3 (zinc finger, RAN-binding domain containing 3), and propose its role in the repair of replication-blocking lesions. ZRANB3 has a unique structure-specific endonuclease activity, which is coupled to ATP hydrolysis. It cleaves branched DNA structures with unusual polarity, generating an accessible 3'-OH group in the template of the leading strand. Furthermore, ZRANB3 localizes to DNA replication sites and interacts with the components of the replication machinery. It is recruited to damaged replication forks via multiple mechanisms, which involve interactions with PCNA, K63-polyubiquitin chains, and branched DNA structures. Collectively, our data support a role for ZRANB3 in the replication stress response and suggest new insights into how DNA repair is coordinated with DNA replication to maintain genome stability.
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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.