Evidence map›Paper›PMID 33891947›Full record

ReviewThe Journal of biological chemistry

Repression of transcription by the glucocorticoid receptor: A parsimonious model for the genomics era.

Anthony N Gerber, Robert Newton, Sarah K Sasse

Abstract readReview
In one paragraph

Review in The Journal of biological chemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
–field-weighted citation impact
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

46 citing papers in PubMed.

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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.

Anthony N GerberDepartment of Medicine, National Jewish Health, Denver, Colorado, USA; Department of Immunology and Genomic Medicine, National Jewish Health, Denver, Colorado, USA; Department of Medicine, University of Colorado, Aurora, Colorado, USA. Electronic address: gerbera@njhealth.org.
Robert NewtonDepartment of Physiology & Pharmacology and Snyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Sarah K SasseDepartment of Medicine, National Jewish Health, Denver, Colorado, USA.

Funding

Role of Klf15 in airway smooth muscle and the response to glucocorticoidsR01HL109557 · NHLBI · NATIONAL JEWISH HEALTH · PI GERBER, ANTHONY N · 2012 to 2025
$7.2M
NHLBI NIH HHS R01 HL109557
6 · The paper itself

Abstract

Glucocorticoids are potent anti-inflammatory drugs that are used to treat an extraordinary range of human disease, including COVID-19, underscoring the ongoing importance of understanding their molecular mechanisms. Early studies of GR signaling led to broad acceptance of models in which glucocorticoid receptor (GR) monomers tether repressively to inflammatory transcription factors, thus abrogating inflammatory gene expression. However, newer data challenge this core concept and present an exciting opportunity to reframe our understanding of GR signaling. Here, we present an alternate, two-part model for transcriptional repression by glucocorticoids. First, widespread GR-mediated induction of transcription results in rapid, primary repression of inflammatory gene transcription and associated enhancers through competition-based mechanisms. Second, a subset of GR-induced genes, including targets that are regulated in coordination with inflammatory transcription factors such as NF-κB, exerts secondary repressive effects on inflammatory gene expression. Within this framework, emerging data indicate that the gene set regulated through the cooperative convergence of GR and NF-κB signaling is central to the broad clinical effectiveness of glucocorticoids in terminating inflammation and promoting tissue repair.

Indexed as

COVID-19 Drug TreatmentAnimalsAnti-Inflammatory AgentsCOVID-19DexamethasoneGene Expression RegulationGenomicsGlucocorticoidsHumansInflammationModels, GeneticNF-kappa BReceptors, GlucocorticoidSARS-CoV-2Signal TransductionTranscription, GeneticAnti-Inflammatory AgentsDexamethasoneGlucocorticoidsNF-kappa BReceptors, Glucocorticoidglucocorticoid receptorinflammationnegative feedbackrepressiontranscriptional enhancer

Identifiers

PMID33891947
PMCPMC8141881

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.