ArticleFEBS open bio2017
Proliferating cell nuclear antigen restores the enzymatic activity of a DNA ligase I deficient in DNA binding.
Article in FEBS open bio, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 9 citations in OpenAlex.
- Impacts of DNA ligase I genotypes on Taiwan Parkinson's disease.BioMedicine · 2026Article
- Episomal and chromosomal DNA replication and recombination inFrontiers in molecular biosciences · 2023Review
- Protein Sumoylation Is Crucial for Phagocytosis inInternational journal of molecular sciences · 2021Article
- Intestinal tract and parenteral multi-organ sequential pathological injury caused by necrotizing enterocolitis.BMC pediatrics · 2020Article
- The Conserved ESCRT-III Machinery Participates in the Phagocytosis ofFrontiers in cellular and infection microbiology · 2018Article
- The Sole DNA Ligase inFrontiers in cellular and infection microbiology · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proliferating cell nuclear antigen (PCNA) coordinates multienzymatic reactions by interacting with a variety of protein partners. Family I DNA ligases are multidomain proteins involved in sealing of DNA nicks during Okazaki fragment maturation and DNA repair. The interaction of DNA ligases with the interdomain connector loop (IDCL) of PCNA through its PCNA-interacting peptide (PIP box) is well studied but the role of the interacting surface between both proteins is not well characterized. In this work, we used a minimal DNA ligase I and two N-terminal deletions to establish that DNA binding and nick-sealing stimulation of DNA ligase I by PCNA are not solely dependent on the PIP box-IDCL interaction. We found that a truncated DNA ligase I with a deleted PIP box is stimulated by PCNA. Furthermore, the activity of a DNA ligase defective in DNA binding is rescued upon PCNA addition. As the rate constants for single-turnover ligation for the full-length and truncated DNA ligases are not affected by PCNA, our data suggest that PCNA stimulation is achieved by increasing the affinity for nicked DNA substrate and not by increasing catalytic efficiency. Surprisingly C-terminal mutants of PCNA are not able to stimulate nick-sealing activity of
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Registered trials
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