Evidence map›Paper›PMID 23269699›Full record

ArticlePhysiological genomics2013

Elevated cJUN expression and an ATF/CRE site within the ATF3 promoter contribute to activation of ATF3 transcription by the amino acid response.

Lingchen Fu, Michael S Kilberg

Abstract read
In one paragraph

Article in Physiological genomics, 2013. 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
1.1field-weighted citation impact, top 25% 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, 24 citations in OpenAlex.

  1. Shared gene targets of the ATF4 and p53 transcriptional networks.bioRxiv : the preprint server for biology · 2023
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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

2 authors at 1 institution in 1 country.

Lingchen FuDepartment of Biochemistry and Molecular Biology, Genetics Institute, Shands Cancer Center, and Center for Nutritional Sciences, University of Florida College of Medicine, Gainesville, Florida, USA.
Michael S Kilberg
Florida College · US

Funding

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
NIDDK NIH HHS DK-92062NIDDK NIH HHS DK-94729NIDDK NIH HHS R01 DK092062NIDDK NIH HHS R01 DK094729
6 · The paper itself

Abstract

Mammalian cells respond to amino acid deprivation through multiple signaling pathways referred to as the amino acid response (AAR). Transcription factors mediate the AAR after their activation by several mechanisms; examples include translational control (activating transcription factor 4, ATF4), phosphorylation (p-cJUN), and transcriptional control (ATF3). ATF4 induces ATF3 transcription through a promoter-localized C/EBP-ATF response element (CARE). The present report characterizes an ATF/CRE site upstream of the CARE that also contributes to AAR-induced ATF3 transcription. ATF4 binds to the ATF/CRE and CARE sequences and both are required for a maximal response to ATF4 induction. ATF3, which antagonizes ATF4 and represses its own gene, also exhibited binding activity to the ATF/CRE and CARE sequences. The AAR resulted in elevated total cJUN and p-cJUN protein levels and both forms exhibited binding activity to the ATF/CRE and CARE ATF3 sequences. Knockdown of AAR-enhanced cJUN expression blocked induction of the ATF3 gene and mutation of either the ATF/CRE or the CARE site prevented the cJUN-dependent increase in ATF3-driven luciferase activity. The results indicate that both increased cJUN and the cis-acting ATF/CRE sequence within the ATF3 promoter contribute to the transcriptional activation of the gene during the AAR.

Indexed as

Activating Transcription Factor 3Activating Transcription Factor 4Amino AcidsBase SequenceBinding SitesCCAAT-Enhancer-Binding Protein-betaGene Expression Regulation, NeoplasticHep G2 CellsHistidinolHumansImmunoblottingMolecular Sequence DataPromoter Regions, GeneticProtein BindingProto-Oncogene Proteins c-junResponse ElementsActivating Transcription Factor 3Activating Transcription Factor 4Amino AcidsATF3 protein, humanCCAAT-Enhancer-Binding Protein-betaHistidinolProto-Oncogene Proteins c-jun

Identifiers

PMID23269699
PMCPMC3568878
OpenAlexW2063338364

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.