Evidence map›Paper›PMID 30895337›Full record

ArticleCellular and molecular life sciences : CMLS2019

E2F1 mediates the downregulation of POLD1 in replicative senescence.

Shichao Gao, Qiao Song, Jing Liu, Xiaomin Zhang, Xunming Ji, Peichang Wang

Open access · hybridAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 40 citations in OpenAlex.

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  8. Transferrin Receptor-Mediated Iron Uptake Promotes Colon Tumorigenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
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  11. Article
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  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. CTCF Mediates Replicative Senescence Through POLD1.Frontiers in cell and developmental biology · 2021
    Article
  20. Aberrant Methylation of Aging-Related Genes in Asthma.Frontiers in molecular biosciences · 2021
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Shichao GaoClinical Laboratory of Xuanwu Hospital, Capital Medical University, Beijing, 100053, People's Republic of China.
Qiao SongClinical Laboratory of Xuanwu Hospital, Capital Medical University, Beijing, 100053, People's Republic of China.
Jing LiuClinical Laboratory of Xuanwu Hospital, Capital Medical University, Beijing, 100053, People's Republic of China.
Xiaomin ZhangClinical Laboratory of Xuanwu Hospital, Capital Medical University, Beijing, 100053, People's Republic of China.
Xunming JiBeijing Institute of Brain Disorders, Capital Medical University, Beijing, 100053, People's Republic of China.
Peichang WangClinical Laboratory of Xuanwu Hospital, Capital Medical University, Beijing, 100053, People's Republic of China. pcw1905@126.com.ORCID http://orcid.org/0000-0002-7970-9797
Capital Medical University · CN

Funding

Beijing Municipal Administration of Hospital's Ascent Plan DFL20180803National Natural Science Foundation of China 81271924National Natural Science Foundation of China 81472007National Natural Science Foundation of China 81871714
6 · The paper itself

Abstract

POLD1, the catalytic subunit of DNA Pol δ, plays an important role in DNA synthesis and DNA damage repair, and POLD1 is downregulated in replicative senescence and mediates cell aging. However, the mechanisms of age-related downregulation of POLD1 expression have not been elucidated. In this study, four potential CpG islands in the POLD1 promoter were found, and the methylation levels of the POLD1 promoter were increased in aging 2BS cells, WI-38 cells and peripheral blood lymphocytes, especially at a single site, CpG 36, in CpG island 3. Then, the transcription factor E2F1 was observed to bind to these sites. The binding affinity of E2F1 for the POLD1 promoter was found to show age-related attenuation and was confirmed to be positively regulated by the E2F1 level and negatively regulated by POLD1 promoter methylation. Moreover, cell senescence characteristics were observed in the cells transfected with shRNA-E2F1 and could contribute to the downregulation of POLD1 induced by the E2F1 decline. Collectively, these results indicated that the attenuation of the binding affinity of E2F1 for the POLD1 promoter, mediated by an age-related decline in E2F1 and increased methylation of CpG island 3, downregulates POLD1 expression in aging.

Indexed as

Cellular SenescenceGene Expression RegulationAdultAgedAged, 80 and overCells, CulturedCpG IslandsDNA MethylationDNA Polymerase IIIDNA RepairDNA ReplicationDown-RegulationE2F1 Transcription FactorFemaleHealthy VolunteersHumansDNA Polymerase IIIE2F1 protein, humanE2F1 Transcription FactorPOLD1 protein, humanDNA methylationE2F1POLD1Replicative senescenceTranscription factor

Identifiers

PMID30895337
PMCPMC6588650
OpenAlexW2925157746

What OpenQuestion holds

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Registered trials

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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.