Evidence map›Paper›PMID 29879550›Full record

ArticleRedox biology2018

Loss of the ubiquitin conjugating enzyme UBE2E3 induces cellular senescence.

Kendra S Plafker, Katarzyna Zyla, William Berry, Scott M Plafker

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

18 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Ubiquitin-conjugating Enzymes in Cancer.International journal of biological sciences · 2026
    Review
  4. Cellular senescence in kidney diseases.Chinese medical journal · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Inhibition ofCells · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Comprehensive Analysis of Differently Expressed and Methylated Genes in Preeclampsia.Computational and mathematical methods in medicine · 2020
    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 at 2 institutions in 1 country.

Kendra S PlafkerAging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.
Katarzyna ZylaAging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.
William BerryDepartment of Surgery, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Scott M PlafkerAging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA; Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. Electronic address: plafkers@omrf.org.
Oklahoma Medical Research Foundation · USUniversity of Oklahoma Health Sciences Center · US

Funding

Tissue Pathology Shared ResourceP30CA225520 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Wade Williams · 2018 to 2026
$27.1M
Mitochondrial Dynamics in RPE Homeostasis and DiseaseR01EY024944 · NEI · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI PLAFKER, SCOTT M · 2018 to 2021
$2.2M
NCI NIH HHS P30 CA225520NEI NIH HHS R01 EY024944
6 · The paper itself

Abstract

Cellular senescence plays essential roles in tissue homeostasis as well as a host of diseases ranging from cancers to age-related neurodegeneration. Various molecular pathways can induce senescence and these different pathways dictate the phenotypic and metabolic changes that accompany the transition to, and maintenance of, the senescence state. Here, we describe a novel senescence phenotype induced by depletion of UBE2E3, a highly-conserved, metazoan ubiquitin conjugating enzyme. Cells depleted of UBE2E3 become senescent in the absence of overt DNA damage and have a distinct senescence-associated secretory phenotype, increased mitochondrial and lysosomal mass, an increased sensitivity to mitochondrial and lysosomal poisons, and an increased basal autophagic flux. This senescence phenotype can be partially suppressed by co-depletion of either p53 or its cognate target gene, p21

Indexed as

AutophagyCellular SenescenceCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21DNA DamageHomeostasisHumansMitochondriaTumor Suppressor Protein p53UbiquitinUbiquitin-Conjugating EnzymesCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21Tumor Suppressor Protein p53UBE2E3 protein, humanUbiquitinUbiquitin-Conjugating EnzymesAutophagyMitochondriaSenescenceUBE2E3Ubiquitin

Identifiers

PMID29879550
PMCPMC6007080
OpenAlexW2803393454

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.