Evidence map›Paper›PMID 21708927›Full record

ArticleThe Journal of experimental medicine2011

E4F1 deficiency results in oxidative stress-mediated cell death of leukemic cells.

Elodie Hatchi, Genevieve Rodier, Matthieu Lacroix, Julie Caramel, Olivier Kirsh, Chantal Jacquet, Emilie Schrepfer, Sylviane Lagarrigue, Laetitia Karine Linares, Gwendaline Lledo and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Regulation of the p53 Family Proteins by the Ubiquitin Proteasomal Pathway.International journal of molecular sciences · 2019
    Review
  10. Article
  11. Glucocorticoid Receptor Binding Inhibits an IntronicInternational journal of molecular sciences · 2018
    Article
  12. Article
  13. Article
  14. E4F1-mediated control of pyruvate dehydrogenase activity is essential for skin homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  15. E4F1 controls a transcriptional program essential for pyruvate dehydrogenase activity.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  16. 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

14 authors at 4 institutions in 1 country.

Elodie HatchiInstitut de Génétique Moléculaire de Montpellier, Centre National de la Recherche Scientifique Unité Mixte de Recherche 5535, Institut Fédératif de Recherche 122, Université de Montpellier, Montpellier 34293, France.
Genevieve Rodier
Matthieu Lacroix
Julie Caramel
Olivier Kirsh
Chantal Jacquet
Emilie Schrepfer
Sylviane Lagarrigue
Laetitia Karine Linares
Gwendaline Lledo
Sylvie Tondeur
Pierre Dubus
Claude Sardet
Laurent Le Cam
Institut de Génétique Moléculaire de Montpellier · FRUniversité de Montpellier · FRHôpital Saint Eloi · FRInstitut de Recherche en Cancérologie de Montpellier · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The multifunctional E4F1 protein was originally discovered as a target of the E1A viral oncoprotein. Growing evidence indicates that E4F1 is involved in key signaling pathways commonly deregulated during cell transformation. In this study, we investigate the influence of E4F1 on tumorigenesis. Wild-type mice injected with fetal liver cells from mice lacking CDKN2A, the gene encoding Ink4a/Arf, developed histiocytic sarcomas (HSs), a tumor originating from the monocytic/macrophagic lineage. Cre-mediated deletion of E4F1 resulted in the death of HS cells and tumor regression in vivo and extended the lifespan of recipient animals. In murine and human HS cell lines, E4F1 inactivation resulted in mitochondrial defects and increased production of reactive oxygen species (ROS) that triggered massive cell death. Notably, these defects of E4F1 depletion were observed in HS cells but not healthy primary macrophages. Short hairpin RNA-mediated depletion of E4F1 induced mitochondrial defects and ROS-mediated death in several human myeloid leukemia cell lines. E4F1 protein is overexpressed in a large subset of human acute myeloid leukemia samples. Together, these data reveal a role for E4F1 in the survival of myeloid leukemic cells and support the notion that targeting E4F1 activities might have therapeutic interest.

Indexed as

AnimalsAutophagyBase SequenceCell DeathCell Line, TumorCell Transformation, NeoplasticDNA-Binding ProteinsHistiocytic SarcomaHumansLeukemia, Myeloid, AcuteMacrophagesMiceMice, 129 StrainMice, Inbred C57BLMice, Inbred DBAMice, KnockoutDNA-Binding ProteinsE4F1 protein, humanE4f1 protein, mouseReactive Oxygen SpeciesRepressor ProteinsRNA, Small InterferingTranscription FactorsUbiquitin-Protein Ligases

Identifiers

PMID21708927
PMCPMC3135361
OpenAlexW2110253595

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.