Evidence map›Paper›PMID 22955275›Full record

ArticleThe Journal of biological chemistry2012

ATF4-dependent regulation of the JMJD3 gene during amino acid deprivation can be rescued in Atf4-deficient cells by inhibition of deacetylation.

Jixiu Shan, Lingchen Fu, Mukundh N Balasubramanian, Tracy Anthony, Michael S Kilberg

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

39 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
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  12. JMJD family proteins in cancer and inflammation.Signal transduction and targeted therapy · 2022
    Review
  13. Article
  14. Review
  15. Article
  16. Activating transcription factor 4 regulates angiogenesis under lipid overload via methionine adenosyltransferase 2A-mediated endothelial epigenetic alteration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  17. Article
  18. 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 3 institutions in 1 country.

Jixiu ShanDepartment of Biochemistry and Molecular Biology, Genetics Institute, Shands Cancer Center, University of Florida College of Medicine, Gainesville, Florida 32610, USA.
Lingchen Fu
Mukundh N Balasubramanian
Tracy Anthony
Michael S Kilberg
Florida College · USUniversity of Florida Health · USRutgers, The State University of New Jersey · US

Funding

Molecular Mechanisms of Adverse Metabolic Events by Asparaginase.R01HD070487 · NICHD · RUTGERS, THE STATE UNIV OF N.J. · PI ANTHONY, TRACY G. · 2011 to 2015
$1.9M
Amino Acid Regulation of Alternative SplicingR01DK092062 · NIDDK · UNIVERSITY OF FLORIDA · PI KILBERG, MICHAEL S. · 2011 to 2014
$1.3M
Amino Acid Regulation of the Fos/Jun Transcription FactorsR01DK094729 · NIDDK · UNIVERSITY OF FLORIDA · PI KILBERG, MICHAEL S. · 2011 to 2014
$1.2M
NICHD NIH HHS HD070487NICHD NIH HHS R01 HD070487NIDDK NIH HHS DK092062NIDDK NIH HHS DK094729NIDDK NIH HHS R01 DK092062NIDDK NIH HHS R01 DK094729
6 · The paper itself

Abstract

Following amino acid deprivation, the amino acid response (AAR) induces transcription from specific genes through a collection of signaling mechanisms, including the GCN2-eIF2-ATF4 pathway. The present report documents that the histone demethylase JMJD3 is an activating transcription factor 4 (ATF4)-dependent target gene. The JMJD3 gene contains two AAR-induced promoter activities and chromatin immunoprecipitation (ChIP) analysis showed that the AAR leads to enhanced ATF4 recruitment to the C/EBP-ATF response element (CARE) upstream of Promoter-1. AAR-induced histone modifications across the JMJD3 gene locus occur upon ATF4 binding. Jmjd3 transcription is not induced in Atf4-knock-out cells, but the AAR-dependent activation was rescued by inhibition of histone deacetylation with trichostatin A (TSA). The TSA rescue of AAR activation in the absence of Atf4 also occurred for the Atf3 and C/EBP homology protein (Chop) genes, but not for the asparagine synthetase gene. ChIP analysis of the Jmjd3, Atf3, and Chop genes in Atf4 knock-out cells documented that activation of the AAR in the presence of TSA led to specific changes in acetylation of histone H4. The results suggest that a primary function of ATF4 is to recruit histone acetyltransferase activity to a sub-set of AAR target genes. Thus, absolute binding of ATF4 to these particular genes is not required and no ATF4 interaction with the general transcription machinery is necessary. The data are consistent with the hypothesis that ATF4 functions as a pioneer factor to alter chromatin structure and thus, enhance transcription in a gene-specific manner.

Indexed as

Response ElementsAcetylationActivating Transcription Factor 4AnimalsChromatinHEK293 CellsHep G2 CellsHistone Deacetylase InhibitorsHistone DeacetylasesHistonesHumansHydroxamic AcidsJumonji Domain-Containing Histone DemethylasesMiceMice, KnockoutTranscription Factor CHOPActivating Transcription Factor 4ATF4 protein, humanAtf4 protein, mouseChromatinDDIT3 protein, humanDdit3 protein, mouseHistone Deacetylase InhibitorsHistone DeacetylasesHistonesHydroxamic AcidsJumonji Domain-Containing Histone DemethylasesKDM6B protein, humanKdm6b protein, mouseTranscription Factor CHOPtrichostatin A

Identifiers

PMID22955275
PMCPMC3476305
OpenAlexW1985786752

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.