Evidence map›Paper›PMID 22723347›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Differentiated embryo-chondrocyte expressed gene 1 regulates p53-dependent cell survival versus cell death through macrophage inhibitory cytokine-1.

Yingjuan Qian, Yong-Sam Jung, Xinbin Chen

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 69 citations in OpenAlex.

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  10. Mutant p53 antagonizes p63/p73-mediated tumor suppression via Notch1.Proceedings of the National Academy of Sciences of the United States of America · 2019
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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

3 authors at 2 institutions in 1 country.

Yingjuan QianComparative Cancer Center, University of California, Davis, CA 95616, USA.
Yong-Sam Jung
Xinbin Chen
Columbia University · USUniversity of California, Davis · US

Funding

Staff InvestigatorsP30CA093373 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI Laura Marcu · 2002 to 2026
$84.9M
Mechanism of p53-Mediated Tumor SuppressionR01CA076069 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHEN, XINBIN · 2002 to 2017
$4.5M
The transcriptional activity of p63, a p53 family memberR01CA102188 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHEN, XINBIN · 2003 to 2012
$2.9M
The role of DNA polymerase eta in DNA damage response and p53 activationR01CA123227 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHEN, XINBIN · 2010 to 2014
$1.4M
MECHANISM OF P53 DEPENDENT APOPTOSISR29CA076069 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHEN, XINBIN · 1998 to 2002
$276k
NCI NIH HHS CA076069NCI NIH HHS CA102188NCI NIH HHS CA123227NCI NIH HHS P30 CA093373NCI NIH HHS R01 CA076069NCI NIH HHS R01 CA102188NCI NIH HHS R01 CA123227NCI NIH HHS R29 CA076069
6 · The paper itself

Abstract

Activation of p53 upon DNA damage induces an array of target genes, leading to cell cycle arrest and/or apoptosis. However, the mechanism by which the cell fate is controlled by p53 remains to be clarified. Previously, we showed that DEC1, a basic helix-loop-helix transcription factor and a target of p53, is capable of inducing cell cycle arrest and mediating DNA damage-induced premature senescence. Here, we found that ectopic expression of DEC1 inhibits, whereas knockdown of DEC1 enhances, DNA damage-induced cell death. Surprisingly, we showed that the anti-cell-death activity of DEC1 is p53 dependent, but DEC1 does not directly modulate p53 expression. Instead, we showed that DEC1 inhibits the ability of p53 to induce macrophage inhibitory cytokine-1 (MIC-1), but not other prosurvival/proapoptotic targets, including p21 and Puma. Importantly, we showed that upon binding to their respective response elements on the MIC-1 promoter, DEC1 and p53 physically interact on the MIC-1 promoter via the basic helix-loop-helix domain in DEC1 and the tetramerization domain in p53, which likely weakens the DNA-binding activity of p53 to the MIC-1 promoter. Finally, we found that depletion of MIC-1 abrogates the ability of DEC1 to attenuate DNA damage-induced cell death. Together, we hypothesize that DEC1 controls the response of p53-dependent cell survival vs. cell death to a stress signal through MIC-1.

Indexed as

Genes, p53ApoptosisCell DeathCell DifferentiationCell SurvivalCellular SenescenceDNA DamageGrowth Differentiation Factor 15HumansPromoter Regions, GeneticTretinoinTumor Suppressor Protein p53Tumor Suppressor ProteinsDELEC1 protein, humanGDF15 protein, humanGrowth Differentiation Factor 15TP53 protein, humanTretinoinTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID22723347
PMCPMC3396538
OpenAlexW2159283173

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.