Evidence map›Paper›PMID 23500643›Full record

ArticleStem cell research2013

Mouse embryonic stem cells undergo charontosis, a novel programmed cell death pathway dependent upon cathepsins, p53, and EndoG, in response to etoposide treatment.

Elisia D Tichy, Zachary A Stephan, Andrew Osterburg, Greg Noel, Peter J Stambrook

Open access · greenAbstract read
In one paragraph

Article in Stem cell research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Repetitive Sequence Stability in Embryonic Stem Cells.International journal of molecular sciences · 2024
    Review
  3. Article
  4. Review
  5. Article
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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

5 authors at 2 institutions in 1 country.

Elisia D TichyDepartment of Molecular Genetics, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA. tichyed@mail.uc.edu
Zachary A Stephan
Andrew Osterburg
Greg Noel
Peter J Stambrook
University of Cincinnati Medical Center · USUniversity of Cincinnati · US

Funding

REPRODUCTIVE AND DEVELOPMENTAL TOXICOLOGY RESEARCHP30ES006096 · NIEHS · UNIVERSITY OF CINCINNATI · PI PINNEY, SUSAN MENGEL · 1992 to 2022
$35.4M
Stem Cell/Organoid and Genome Editing CoreP30DK078392 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Alexander Miethke · 2007 to 2026
$24.4M
ENVIRONMETAL CARCINOGENESIS AND MUTAGENESIST32ES007250 · NIEHS · UNIVERSITY OF CINCINNATI · PI MILLER, WILLIAM E · 1988 to 2024
$11.9M
ROLE OF ANGPTL4, AN ANGIOGENIC MEDIATOR, IN ARTHRITISP30AR047363 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI FLICK, MATTHEW J. · 2001 to 2015
$9.2M
Cincinnati Center for Excellence in Molecular HematologyP30DK090971 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI ZHENG, YI · 2010 to 2015
$4.0M
Pathways to Mutagenesis in vivo and in Stem CellsR01ES012695 · NIEHS · UNIVERSITY OF CINCINNATI · PI STAMBROOK, PETER J. · 2006 to 2009
$1.7M
NIAMS NIH HHS P30 AR047363NIDDK NIH HHS P30 DK078392NIDDK NIH HHS P30 DK090971NIEHS NIH HHS P30 ES006096NIEHS NIH HHS R01 ES012695NIEHS NIH HHS R01 ES12695-4S1NIEHS NIH HHS T32 ES007250
6 · The paper itself

Abstract

Embryonic stem cells (ESCs) are hypersensitive to many DNA damaging agents and can rapidly undergo cell death or cell differentiation following exposure. Treatment of mouse ESCs (mESCs) with etoposide (ETO), a topoisomerase II poison, followed by a recovery period resulted in massive cell death with characteristics of a programmed cell death pathway (PCD). While cell death was both caspase- and necroptosis-independent, it was partially dependent on the activity of lysosomal proteases. A role for autophagy in the cell death process was eliminated, suggesting that ETO induces a novel PCD pathway in mESCs. Inhibition of p53 either as a transcription factor by pifithrin α or in its mitochondrial role by pifithrin μ significantly reduced ESC death levels. Finally, EndoG was newly identified as a protease participating in the DNA fragmentation observed during ETO-induced PCD. We coined the term charontosis after Charon, the ferryman of the dead in Greek mythology, to refer to the PCD signaling events induced by ETO in mESCs.

Indexed as

AnimalsAntineoplastic Agents, PhytogenicApoptosisCaspasesCathepsinsCell LineEmbryonic Stem CellsEndodeoxyribonucleasesEtoposideMiceMice, Inbred C57BLTumor Suppressor Protein p53Antineoplastic Agents, PhytogenicCaspasesCathepsinsEndodeoxyribonucleasesendonuclease GEtoposideTumor Suppressor Protein p53

Identifiers

PMID23500643
PMCPMC3924754
OpenAlexW2035449163

What OpenQuestion holds

Textmetadata
LicenceTDM
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.