ArticleNucleic acids research2013
Silencing of human DNA polymerase λ causes replication stress and is synthetically lethal with an impaired S phase checkpoint.
Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 32 citations in OpenAlex.
- Complex molecular profile of DNA repair genes in epithelial ovarian carcinoma patients with different sensitivity to platinum-based therapy.Frontiers in oncology · 2022Article
- SOG1 transcription factor promotes the onset of endoreduplication under salinity stress in Arabidopsis.Scientific reports · 2021Article
- A Role for Human DNA Polymerase λ in Alternative Lengthening of Telomeres.International journal of molecular sciences · 2021Article
- Oxidative and genotoxic damages in plants in response to heavy metal stress and maintenance of genome stability.Plant signaling & behavior · 2018Article
- Regulation of human polλ by ATM-mediated phosphorylation during non-homologous end joining.DNA repair · 2017Article
- Homologous Recombination Defective Arabidopsis Mutants Exhibit Enhanced Sensitivity to Abscisic Acid.PloS one · 2017Article
- Estrogen Drives Cellular Transformation and Mutagenesis in Cells Expressing the Breast Cancer-Associated R438W DNA Polymerase Lambda Protein.Molecular cancer research : MCR · 2016Article
- Review
- Article
- Replication stress and cancer.Nature reviews. Cancer · 2015Review
- Understanding the Physical and Molecular Basis of Stability of Arabidopsis DNA Pol λ under UV-B and High NaCl Stress.PloS one · 2015Article
- Whole genome RNAi screens reveal a critical role of REV3 in coping with replication stress.Molecular oncology · 2014Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human DNA polymerase (pol) λ functions in base excision repair and non-homologous end joining. We have previously shown that DNA pol λ is involved in accurate bypass of the two frequent oxidative lesions, 7,8-dihydro-8-oxoguanine and 1,2-dihydro-2-oxoadenine during the S phase. However, nothing is known so far about the relationship of DNA pol λ with the S phase DNA damage response checkpoint. Here, we show that a knockdown of DNA pol λ, but not of its close homologue DNA pol β, results in replication fork stress and activates the S phase checkpoint, slowing S phase progression in different human cancer cell lines. We furthermore show that DNA pol λ protects cells from oxidative DNA damage and also functions in rescuing stalled replication forks. Its absence becomes lethal for a cell when a functional checkpoint is missing, suggesting a DNA synthesis deficiency. Our results provide the first evidence, to our knowledge, that DNA pol λ is required for cell cycle progression and is functionally connected to the S phase DNA damage response machinery in cancer cells.
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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.