Evidence map›Paper›PMID 27345397›Full record

ArticleOncogene2017

Mitochondrial stress-induced p53 attenuates HIF-1α activity by physical association and enhanced ubiquitination.

A Roy Chowdhury, A Long, S Y Fuchs, A Rustgi, N G Avadhani

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. HIF-transcribed p53 chaperones HIF-1α.Nucleic acids research · 2019
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Mitochondrial dysfunction and mitochondrial dynamics-The cancer connection.Biochimica et biophysica acta. Bioenergetics · 2017
    Review
  17. 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

5 authors at 1 institution in 1 country.

A Roy ChowdhuryDepartment of Biomedical Sciences and Mari Lowe Center for Comparative Oncology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.
A LongDivision of Gastroenterology, Department of Medicine and Genetics, Abramson Cancer Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
S Y FuchsDepartment of Biomedical Sciences and Mari Lowe Center for Comparative Oncology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.
A RustgiDivision of Gastroenterology, Department of Medicine and Genetics, Abramson Cancer Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
N G AvadhaniDepartment of Biomedical Sciences and Mari Lowe Center for Comparative Oncology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.
University of Pennsylvania · US

Funding

TRANSGENIC AND CHIMERIC MOUSE COREP30DK050306 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI Ken Hashigiwa Cadwell · 1997 to 2026
$32.5M
Role of HOS in Cell Transformation and ApoptosisR01CA092900 · NCI · UNIVERSITY OF PENNSYLVANIA · PI FUCHS, SERGE Y · 2001 to 2021
$5.3M
Role of Mitochondrial Respiratory Stress Signaling in Cancer ProgressionR01CA022762 · NCI · UNIVERSITY OF PENNSYLVANIA · PI AVADHANI, NARAYAN G · 1985 to 2013
$3.3M
Ahr and OsteoporosisR01AR067066 · NIAMS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI AVADHANI, NARAYAN G, ZAIDI, MONE · 2014 to 2018
$3.3M
CYP2E1 Mediated Mitochondrial Injury and Cell Damage in Alcohol Liver DiseaseR01AA022986 · NIAAA · UNIVERSITY OF PENNSYLVANIA · PI AVADHANI, NARAYAN G, KALYANARAMAN, BALARAMAN · 2015 to 2019
$2.6M
MITOCHONDRIAL D-LOOP DNA MUTATIONS AND GENE EXPRESSIONR37CA022762 · NCI · UNIVERSITY OF PENNSYLVANIA · PI AVADHANI, NARAYAN G · 1994 to 2002
$299k
NCI NIH HHS R01 CA022762NCI NIH HHS R01 CA092900NCI NIH HHS R37 CA022762NIAAA NIH HHS R01 AA022986NIAMS NIH HHS R01 AR067066NIDDK NIH HHS P30 DK050306
6 · The paper itself

Abstract

Retrograde signaling is a mechanism by which mitochondrial dysfunction is communicated to the nucleus for inducing a metabolic shift essential for cell survival. Previously, we showed that partial mitochondrial DNA (mtDNA) depletion in different cell types induced mitochondrial retrograde signaling pathway (MtRS) involving Ca

Indexed as

A549 CellsAnimalsBase SequenceCalcineurinCalciumCell Line, TumorCOS CellsDNA, MitochondrialHCT116 CellsHumansHypoxia-Inducible Factor 1, alpha SubunitMiceMitochondriaProtein BindingRatsSequence DeletionCalcineurinCalciumDNA, MitochondrialHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID27345397
PMCPMC5192009
OpenAlexW2460822625

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.