ArticleScientific reports2016
Roles of human POLD1 and POLD3 in genome stability.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Pooled it
- Combined immunodeficiency caused by a loss-of-function mutation in DNA polymerase delta 1.The Journal of allergy and clinical immunology · 2020Trial
- Lnc-RAINY regulates genes involved in radiation susceptibility through DNA:DNA:RNA triplex-forming interactions and has tumor therapeutic potential in lung cancers.Non-coding RNA research · 2025Article
- ATR Inhibition Synergizes With Alkylating PI Polyamide Targeting MYCN by Suppressing DNA Repair in MYCN-Amplified Neuroblastoma.Cancer science · 2025Article
- Patulin and Xestoquinol are inhibitors of DNA topoisomerase 1.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Beyond proofreading: POLD1 mutations as dynamic orchestrators of genomic instability and immune evasion in cancer.Frontiers in immunology · 2025Review
- POLD3 haploinsufficiency is linked to non-syndromic sensorineural adult-onset progressive hearing and balance impairments.European journal of human genetics : EJHG · 2025Article
- When do the pathological signs become evident? Study of human mesenchymal stem cells in MDPL syndrome.Aging · 2024Article
- POLD3 as Controller of Replicative DNA Repair.International journal of molecular sciences · 2024Review
- Alternative lengthening of telomeres: mechanism and the pathogenesis of cancer.Journal of clinical pathology · 2024Article
- Regulatory Effect ofPharmaceuticals (Basel, Switzerland) · 2023Article
- Homology directed telomere clustering, ultrabright telomere formation and nuclear envelope rupture in cells lacking TRF2Nature communications · 2023Article
- Timing of Chromosome DNA Integration throughout the Yeast Cell Cycle.Biomolecules · 2023Article
- Loss of p53 activates thyroid hormone via type 2 deiodinase and enhances DNA damage.Nature communications · 2023Article
- Unraveling the impact of a germline heterozygousFrontiers in molecular biosciences · 2023Article
- RAD18 opposes transcription-associated genome instability through FANCD2 recruitment.PLoS genetics · 2022Article
- Review
- Article
- Article
- The stabilized Pol31-Pol3 interface counteracts Pol32 ablation with differential effects on repair.Life science alliance · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA replication is essential for cellular proliferation. If improperly controlled it can constitute a major source of genome instability, frequently associated with cancer and aging. POLD1 is the catalytic subunit and POLD3 is an accessory subunit of the replicative Pol δ polymerase, which also functions in DNA repair, as well as the translesion synthesis polymerase Pol ζ, whose catalytic subunit is REV3L. In cells depleted of POLD1 or POLD3 we found a differential but general increase in genome instability as manifested by DNA breaks, S-phase progression impairment and chromosome abnormalities. Importantly, we showed that both proteins are needed to maintain the proper amount of active replication origins and that POLD3-depletion causes anaphase bridges accumulation. In addition, POLD3-associated DNA damage showed to be dependent on RNA-DNA hybrids pointing toward an additional and specific role of this subunit in genome stability. Interestingly, a similar increase in RNA-DNA hybrids-dependent genome instability was observed in REV3L-depleted cells. Our findings demonstrate a key role of POLD1 and POLD3 in genome stability and S-phase progression revealing RNA-DNA hybrids-dependent effects for POLD3 that might be partly due to its Pol ζ interaction.
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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.