Evidence map›Paper›PMID 18375871›Full record

ArticleThe journals of gerontology. Series A, Biological sciences and medical sciences2008

Cells from long-lived mutant mice exhibit enhanced repair of ultraviolet lesions.

Adam B Salmon, Mats Ljungman, Richard A Miller

Open access · bronzeAbstract read
In one paragraph

Article in The journals of gerontology. Series A, Biological sciences and medical sciences, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

17 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Regulation of Age-Related Protein Toxicity.Frontiers in cell and developmental biology · 2021
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Hepatic response to oxidative injury in long-lived Ames dwarf mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. 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

3 authors at 1 institution in 1 country.

Adam B SalmonCellular and Molecular Biology Graduate Program, University of Michigan Comprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, MI, USA.
Mats Ljungman
Richard A Miller
University of Michigan · US

Funding

Systems BiologyU19AG023122 · NIA · TRANSLATIONAL GENOMICS RESEARCH INST · PI Thomas Girke, NICHOLAS Joseph SCHORK · 2004 to 2026
$102.6M
Research Training in BiogerontologyT32AG000114 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SCOTT PLETCHER · 1985 to 2026
$12.4M
Race/Ethnic Differences in Life Course Exposure to Death: Consequences for HealthR01AG054624 · NIA · UNIVERSITY OF TEXAS AT AUSTIN · PI UMBERSON, DEBRA J. · 2018 to 2021
$1.7M
NIA NIH HHS AG023122NIA NIH HHS AG054624NIA NIH HHS R01 AG054624NIA NIH HHS T32 AG000114NIA NIH HHS T32-AG000114NIA NIH HHS U19 AG023122
6 · The paper itself

Abstract

Fibroblasts isolated from long-lived hypopituitary dwarf mice are resistant to many cell stresses, including ultraviolet (UV) light and methyl methane sulfonate (MMS), which induce cell death by producing DNA damage. Here we report that cells from Snell dwarf mice recover more rapidly than controls from the inhibition of RNA synthesis induced by UV damage. Recovery of messenger RNA (mRNA) synthesis in particular is more rapid in dwarf cells, suggesting enhanced repair of the actively transcribing genes in dwarf-derived cells. At early time points, there was no difference in the repair of cyclobutane pyrimidine dimers (CPD) or 6-4 photoproducts (6-4PP) in the whole genome, nor was there any significant difference in the repair of UV lesions in specific genes. However, at later time points we found that more lesions had been removed from the genome of dwarf-derived cells. We have also found that cells from dwarf mice express higher levels of the nucleotide excision repair proteins XPC and CSA, suggesting a causal link to enhanced DNA repair. Overall, these data suggest a mechanism for the UV resistance of Snell dwarf-derived fibroblasts that could contribute to the delay of aging and neoplasia in these mice.

Indexed as

DNA RepairUltraviolet RaysAnimalsBlotting, WesternCells, CulturedDNADNA-Binding ProteinsDNA DamageDNA Excision Repair Protein ERCC-5Dwarfism, PituitaryEndonucleasesEnzyme-Linked Immunosorbent AssayFemaleFibroblastsMaleMiceDNADNA-Binding ProteinsDNA Excision Repair Protein ERCC-5EndonucleasesNuclear ProteinsPyrimidine DimersRNA, MessengerTranscription Factorsxeroderma pigmentosum group F protein

Identifiers

PMID18375871
PMCPMC2711434
OpenAlexW2160881796

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.