Evidence map›Paper›PMID 19509279›Full record

ArticleThe Journal of biological chemistry2009

Elevated ATF4 expression, in the absence of other signals, is sufficient for transcriptional induction via CCAAT enhancer-binding protein-activating transcription factor response elements.

Jixiu Shan, Daima Ord, Tõnis Ord, Michael S Kilberg

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.7field-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

36 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
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  8. HepaticNutrients · 2021
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  17. Emerging tale of UPR and cancer: an essentiality for malignancy.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
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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

4 authors at 2 institutions in 2 countries.

Jixiu ShanDepartment of Biochemistry and Molecular Biology, Genetics Institute, Shands Cancer Center and Center for Nutritional Sciences, University of Florida College of Medicine, Gainesville, Florida, USA.
Daima Ord
Tõnis Ord
Michael S Kilberg
Estonian Biocentre · EEUniversity of Florida Health · US

Funding

NUTRITIONAL CONTROL OF ASPARAGINE SYNTHETASER01DK052064 · NIDDK · UNIVERSITY OF FLORIDA · PI KILBERG, MICHAEL S. · 1997 to 2010
$3.4M
Nutritional Regulation of Ribosomal Protein ExpressionR01DK059315 · NIDDK · UNIVERSITY OF FLORIDA · PI KILBERG, MICHAEL S. · 2001 to 2005
$1.2M
NIDDK NIH HHS DK-52064NIDDK NIH HHS DK-59315NIDDK NIH HHS R01 DK052064NIDDK NIH HHS R01 DK059315
6 · The paper itself

Abstract

Protein limitation in vivo or amino acid deprivation of cells in culture causes a signal transduction cascade consisting of activation of the kinase GCN2 (general control nonderepressible 2), phosphorylation of eukaryotic initiation factor 2, and increased synthesis of activating transcription factor (ATF) 4 by a translational control mechanism. In a self-limiting transcriptional program, ATF4 transiently activates a wide range of downstream target genes involved in transport, cellular metabolism, and other cell functions. Simultaneous activation of other signal transduction pathways by amino acid deprivation led to the question of whether or not the increased abundance of ATF4 alone was sufficient to trigger the transcriptional control mechanisms. Using 293 cells that ectopically express ATF4 in a tetracycline-inducible manner showed that ATF4 target genes were activated in the absence of amino acid deprivation. Ectopic expression of ATF4 alone resulted in effective recruitment of the general transcription machinery, but some reduction in histone modification was observed. These data document that ATF4 alone is sufficient to trigger the amino acid-responsive transcriptional control program. However, the absolute amount of ectopic ATF4 required to achieve the same degree of transcriptional activation observed after amino acid limitation was greater, suggesting that other factors may serve to enhance ATF4 function.

Indexed as

Activating Transcription Factor 4Amino AcidsBase SequenceCCAAT-Enhancer-Binding ProteinsCell LineDose-Response Relationship, DrugHistonesHumansModels, BiologicalMolecular Sequence DataPhosphorylationProtein BiosynthesisResponse ElementsTranscriptional ActivationTranscription, GeneticActivating Transcription Factor 4Amino AcidsCCAAT-Enhancer-Binding ProteinsHistones

Identifiers

PMID19509279
PMCPMC2755847
OpenAlexW2090952884

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.