Evidence map›Paper›PMID 31276581›Full record

ArticleNucleic acids research2019

Cockayne syndrome group B deficiency reduces H3K9me3 chromatin remodeler SETDB1 and exacerbates cellular aging.

Jong-Hyuk Lee, Tyler G Demarest, Mansi Babbar, Edward W Kim, Mustafa N Okur, Supriyo De, Deborah L Croteau, Vilhelm A Bohr

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

28 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Interrogating the regulatory epigenome of cellular senescence.Cellular and molecular life sciences : CMLS · 2025
    Review
  3. Review
  4. Review
  5. Article
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  7. Article
  8. Article
  9. Review
  10. Article
  11. Genomic Instability and Epigenetic Changes during Aging.International journal of molecular sciences · 2023
    Review
  12. Article
  13. Review
  14. Mitochondrial PARP1 regulates NADExperimental & molecular medicine · 2022
    Article
  15. WTAP-mediated mNature communications · 2022
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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

8 authors at 2 institutions in 2 countries.

Jong-Hyuk LeeLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA.
Tyler G DemarestLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA.
Mansi BabbarLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA.
Edward W KimLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA.
Mustafa N OkurLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA.
Supriyo DeLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA.
Deborah L CroteauLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA.
Vilhelm A BohrLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA.
National Institute on Aging · USNational Institutes of Health · US

Funding

The role of the Cockayne syndrome proteinZIAAG000722 · NIA · NATIONAL INSTITUTE ON AGING · PI FERRUCCI, LUIGI · 2009 to 2023
$9.1M
NIA Interlab: Dissecting novel genoprotective roles of CSB in the epigenome networkZIAAG000788 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 2018 to 2019
$503k
6 · The paper itself

Abstract

Cockayne syndrome is an accelerated aging disorder, caused by mutations in the CSA or CSB genes. In CSB-deficient cells, poly (ADP ribose) polymerase (PARP) is persistently activated by unrepaired DNA damage and consumes and depletes cellular nicotinamide adenine dinucleotide, which leads to mitochondrial dysfunction. Here, the distribution of poly (ADP ribose) (PAR) was determined in CSB-deficient cells using ADPr-ChAP (ADP ribose-chromatin affinity purification), and the results show striking enrichment of PAR at transcription start sites, depletion of heterochromatin and downregulation of H3K9me3-specific methyltransferases SUV39H1 and SETDB1. Induced-expression of SETDB1 in CSB-deficient cells downregulated PAR and normalized mitochondrial function. The results suggest that defects in CSB are strongly associated with loss of heterochromatin, downregulation of SETDB1, increased PAR in highly-transcribed regions, and mitochondrial dysfunction.

Indexed as

Cell Line, TransformedCellular SenescenceChromatinCockayne SyndromeDNADNA DamageDNA HelicasesDNA Repair EnzymesFibroblastsGene Expression RegulationHistone-Lysine N-MethyltransferaseHistonesHumansMethyltransferasesMitochondriaMutationChromatinDNADNA HelicasesDNA Repair EnzymesERCC6 protein, humanERCC8 protein, humanHistone-Lysine N-MethyltransferaseHistonesMethyltransferasesNADPoly Adenosine Diphosphate RibosePoly-ADP-Ribose Binding ProteinsPoly(ADP-ribose) PolymerasesProtein MethyltransferasesRepressor ProteinsSETDB1 protein, humanSUV39H1 protein, humanTranscription Factors

Identifiers

PMID31276581
PMCPMC6895253
OpenAlexW2954437651

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.