ArticleMolecular and cellular biology2009
Phosphorylation of human DNA ligase I regulates its interaction with replication factor C and its participation in DNA replication and DNA repair.
Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- LIG1 Loss in TP53-mutant Triple Negative Breast Cancer Rewires DNA Repair and Confers Sensitivity to PARP-ATR Inhibitor Combinations.Molecular cancer therapeutics · 2026Article
- Impacts of DNA ligase I genotypes on Taiwan Parkinson's disease.BioMedicine · 2026Article
- Joining of DNA breaks- interplay between DNA ligases and poly (ADP-ribose) polymerases.DNA repair · 2025Review
- Mammalian DNA ligases; roles in maintaining genome integrity.Journal of molecular biology · 2024Review
- Unchanged PCNA and DNMT1 dynamics during replication in DNA ligase I-deficient cells but abnormal chromatin levels of non-replicative histone H1.Scientific reports · 2023Article
- Forkhead box O1 targeting replication factor C subunit 2 expression promotes glioma temozolomide resistance and survival.Annals of translational medicine · 2021Article
- Dynamic DNA-bound PCNA complexes co-ordinate Okazaki fragment synthesis, processing and ligation.Journal of molecular biology · 2020Article
- Altered DNA ligase activity in human disease.Mutagenesis · 2020Review
- Human DNA Ligase I Interacts with and Is Targeted for Degradation by the DCAF7 Specificity Factor of the Cul4-DDB1 Ubiquitin Ligase Complex.The Journal of biological chemistry · 2016Article
- Chronic Replication Problems Impact Cell Morphology and Adhesion of DNA Ligase I Defective Cells.PloS one · 2015Article
- Sulfolobus replication factor C stimulates the activity of DNA polymerase B1.Journal of bacteriology · 2014Article
- DNA ligases as therapeutic targets.Translational cancer research · 2013Article
- Phosphorylation of serine 51 regulates the interaction of human DNA ligase I with replication factor C and its participation in DNA replication and repair.The Journal of biological chemistry · 2012Article
- Phosphorylation of SRSF1 is modulated by replicational stress.Nucleic acids research · 2012Article
- DNA ligase I, the replicative DNA ligase.Sub-cellular biochemistry · 2012Review
- Human Mre11/human Rad50/Nbs1 and DNA ligase IIIalpha/XRCC1 protein complexes act together in an alternative nonhomologous end joining pathway.The Journal of biological chemistry · 2011Article
- A systems view of epithelial-mesenchymal transition signaling states.Clinical & experimental metastasis · 2011Article
- Targeting abnormal DNA double strand break repair in cancer.Cellular and molecular life sciences : CMLS · 2010Review
- Reconstitution of eukaryotic lagging strand DNA replication.Methods (San Diego, Calif.) · 2010Review
- CTG/CAG repeat instability is modulated by the levels of human DNA ligase I and its interaction with proliferating cell nuclear antigen: a distinction between replication and slipped-DNA repair.The Journal of biological chemistry · 2009Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Human DNA ligase I (hLigI) participates in DNA replication and excision repair via an interaction with proliferating cell nuclear antigen (PCNA), a DNA sliding clamp. In addition, hLigI interacts with and is inhibited by replication factor C (RFC), the clamp loader complex that loads PCNA onto DNA. Here we show that a mutant version of hLigI, which mimics the hyperphosphorylated M-phase form of hLigI, does not interact with and is not inhibited by RFC, demonstrating that inhibition of ligation is dependent upon the interaction between hLigI and RFC. To examine the biological relevance of hLigI phosphorylation, we isolated derivatives of the hLigI-deficient cell line 46BR.1G1 that stably express mutant versions of hLigI in which four serine residues phosphorylated in vivo were replaced with either alanine or aspartic acid. The cell lines expressing the phosphorylation site mutants of hLigI exhibited a dramatic reduction in proliferation and DNA synthesis and were also hypersensitive to DNA damage. The dominant-negative effects of the hLigI phosphomutants on replication and repair are due to the activation of cellular senescence, presumably because of DNA damage arising from replication abnormalities. Thus, appropriate phosphorylation of hLigI is critical for its participation in DNA replication and repair.
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