Evidence map›Paper›PMID 31138644›Full record

ArticleThe Journal of biological chemistry2019

Inhibition of nucleotide synthesis promotes replicative senescence of human mammary epithelial cells.

Alireza Delfarah, Sydney Parrish, Jason A Junge, Jesse Yang, Frances Seo, Si Li, John Mac, Pin Wang, Scott E Fraser, Nicholas A Graham

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Branched-Chain Amino Acid Accumulation Fuels the Senescence-Associated Secretory Phenotype.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  11. Metabolomics to Study Human Aging: A Review.Current molecular medicine · 2024
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

10 authors at 2 institutions in 2 countries.

Alireza DelfarahFrom the Mork Family Department of Chemical Engineering and Materials Science.ORCID 0000-0002-3192-5941
Sydney ParrishFrom the Mork Family Department of Chemical Engineering and Materials Science.
Jason A Jungethe Translational Imaging Center, Molecular and Computational Biology, and.
Jesse YangFrom the Mork Family Department of Chemical Engineering and Materials Science.
Frances SeoFrom the Mork Family Department of Chemical Engineering and Materials Science.
Si LiFrom the Mork Family Department of Chemical Engineering and Materials Science.
John MacFrom the Mork Family Department of Chemical Engineering and Materials Science.
Pin WangFrom the Mork Family Department of Chemical Engineering and Materials Science.
Scott E Fraserthe Translational Imaging Center, Molecular and Computational Biology, and.
Nicholas A GrahamFrom the Mork Family Department of Chemical Engineering and Materials Science, nagraham@usc.edu.ORCID 0000-0002-6811-1941
Imaging Center · USUniversity of Southern California · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular senescence is a mechanism by which cells permanently withdraw from the cell cycle in response to stresses including telomere shortening, DNA damage, or oncogenic signaling. Senescent cells contribute to both age-related degeneration and hyperplastic pathologies, including cancer. In culture, normal human epithelial cells enter senescence after a limited number of cell divisions, known as replicative senescence. Here, to investigate how metabolic pathways regulate replicative senescence, we used LC-MS-based metabolomics to analyze senescent primary human mammary epithelial cells (HMECs). We did not observe significant changes in glucose uptake or lactate secretion in senescent HMECs. However, analysis of intracellular metabolite pool sizes indicated that senescent cells exhibit depletion of metabolites from nucleotide synthesis pathways. Furthermore, stable isotope tracing with

Indexed as

Cellular SenescenceCells, CulturedCRISPR-Cas SystemsEpithelial CellsGene EditingGlucoseHumansMammary Glands, HumanMetabolomicsNucleotidesRibonucleoside Diphosphate ReductaseTelomeraseGlucoseNucleotidesRibonucleoside Diphosphate Reductaseribonucleotide reductase M2Telomeraseagingcell stresscellular senescenceepithelial cellgrowth arrestmetabolomicsnucleoside/nucleotide biosynthesisribonucleotide reductase regulatory subunit M2 (RRM2)systems biology

Identifiers

PMID31138644
PMCPMC6615688
OpenAlexW2950668056

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.