Evidence map›Paper›PMID 23303127›Full record

ArticleCell death & disease2013

Selective glucocorticoid receptor translational isoforms reveal glucocorticoid-induced apoptotic transcriptomes.

I Wu, S C Shin, Y Cao, I K Bender, N Jafari, G Feng, S Lin, J A Cidlowski, R P Schleimer, N Z Lu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
5.8field-weighted citation impact, top 4% 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

34 citing papers in PubMed, 61 citations in OpenAlex.

  1. Glucocorticoid Receptor Translational Isoforms Generate Unique Glucocorticoid Responses in the Mouse Brain.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Review
  3. DAPL1 is activated by Np63 and GRα and regulates lipid metabolism.Journal of molecular medicine (Berlin, Germany) · 2026
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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

10 authors at 4 institutions in 1 country.

I WuDivision of Allergy-Immunology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
S C Shin
Y Cao
I K Bender
N Jafari
G Feng
S Lin
J A Cidlowski
R P Schleimer
N Z Lu
Northwestern University · USIgenbio (United States) · USMarshfield Clinic · USNational Institute of Environmental Health Sciences · US

Funding

Glucocorticosteroid Action In Inflammatory DiseaseR37HL068546 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SCHLEIMER, ROBERT P · 2009 to 2018
$3.5M
Glucocorticoid receptor translational isoforms in asthmaR01HL094558 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LU, NICK · 2009 to 2013
$2.2M
NHLBI NIH HHS 1R01HL094558-01A1NHLBI NIH HHS 2R37HL068546-26NHLBI NIH HHS 3R01HL094558-01A1S1NHLBI NIH HHS R01 HL094558NHLBI NIH HHS R37 HL068546
6 · The paper itself

Abstract

Induction of T-cell apoptosis contributes to the anti-inflammatory and antineoplastic benefits of glucocorticoids. The glucocorticoid receptor (GR) translational isoforms have distinct proapoptotic activities in osteosarcoma cells. Here we determined whether GR isoforms selectively induce apoptosis in Jurkat T lymphoblastic leukemia cells. Jurkat cells stably expressing individual GR isoforms were generated and treated with vehicle or dexamethasone (DEX). DEX induced apoptosis in cells expressing the GR-A, -B, or -C, but not the GR-D, isoform. cDNA microarray analyses of cells sensitive (GR-C3) and insensitive (GR-D3) to DEX revealed glucocorticoid-induced proapoptotic transcriptomes. Genes that were regulated by the proapoptotic GR-C3, but not by the GR-D3, isoform likely contributed to glucocorticoid-induced apoptosis. The identified genes include those that are directly involved in apoptosis and those that facilitate cell killing. Chromatin immunoprecipitation assays demonstrated that distinct chromatin modification abilities may underlie the distinct functions of GR isoforms. Interestingly, all GR isoforms, including the GR-D3 isoform, suppressed mitogen-stimulated cytokines. Furthermore, the GR-C isoforms were selectively upregulated in mitogen-activated primary T cells and DEX treatment induced GR-C target genes in activated T cells. Cell-specific expressions and functions of GR isoforms may help to explain the tissue- and individual-selective actions of glucocorticoids and may provide a basis for developing improved glucocorticoids.

Indexed as

TranscriptomeApoptosisApoptosis Regulatory ProteinsBcl-2-Like Protein 11ChromatinCytokinesDexamethasoneGlucocorticoidsHumansJurkat CellsMembrane ProteinsMicroRNAsProtein IsoformsProto-Oncogene ProteinsProto-Oncogene Proteins c-mycReceptors, GlucocorticoidApoptosis Regulatory ProteinsBCL2L11 protein, humanBcl-2-Like Protein 11ChromatinCytokinesDexamethasoneGlucocorticoidsMembrane ProteinsMicroRNAsProtein IsoformsProto-Oncogene ProteinsProto-Oncogene Proteins c-mycReceptors, Glucocorticoid

Identifiers

PMID23303127
PMCPMC3563981
OpenAlexW2065890957

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.