Evidence map›Paper›PMID 33077499›Full record

ReviewMolecular and cellular biology2021

Translational Control during Cellular Senescence.

Matthew J Payea, Carlos Anerillas, Ravi Tharakan, Myriam Gorospe

Abstract readReview
In one paragraph

Review in Molecular and cellular biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
–field-weighted citation impact
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

34 citing papers in PubMed.

  1. Article
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  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Genomic Instability and Epigenetic Changes during Aging.International journal of molecular sciences · 2023
    Review
  14. Review
  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

4 authors.

Matthew J PayeaLaboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health, Baltimore, Maryland, USA matthew.payea@nih.gov.
Carlos AnerillasLaboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health, Baltimore, Maryland, USA.
Ravi TharakanLaboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health, Baltimore, Maryland, USA.
Myriam GorospeLaboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health, Baltimore, Maryland, USA.

Funding

Influence of mRNA Turnover on the Biology of Cellular Senescence and AgingZ01AG000393 · NIA · NATIONAL INSTITUTE ON AGING · PI GOROSPE, MYRIAM NONE · 2008 to 2008
$265k
Intramural NIH HHS Z01 AG000393
6 · The paper itself

Abstract

Senescence is a state of long-term cell cycle arrest that arises in cells that have incurred sublethal damage. While senescent cells no longer replicate, they remain metabolically active and further develop unique and stable phenotypes that are not present in proliferating cells. On one hand, senescent cells increase in size, maintain an active mTORC1 complex, and produce and secrete a substantial amount of inflammatory proteins as part of the senescence-associated secretory phenotype (SASP). On the other hand, these progrowth phenotypes contrast with the p53-mediated growth arrest typical of senescent cells that is associated with nucleolar stress and an inhibition of rRNA processing and ribosome biogenesis. In sum, translation in senescent cells paradoxically comprises both a global repression of translation triggered by DNA damage and a select increase in the translation of specific proteins, including SASP factors.

Indexed as

Protein Biosynthesisbeta-GalactosidaseBiomarkersCells, CulturedCell SizeCellular SenescenceChemokinesCyclin-Dependent Kinase Inhibitor p21DNA DamageHumansMechanistic Target of Rapamycin Complex 1PhenotypeRNA, RibosomalTumor Suppressor Protein p53beta-GalactosidaseBiomarkersChemokinesCyclin-Dependent Kinase Inhibitor p21Mechanistic Target of Rapamycin Complex 1RNA, RibosomalTumor Suppressor Protein p53agingcellular senescencestress responsetranslational controltranslation elongationtranslation initiation

Identifiers

PMID33077499
PMCPMC8093494

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.