ArticleCellular and molecular life sciences : CMLS2014
Selective modulation of the glucocorticoid receptor can distinguish between transrepression of NF-κB and AP-1.
Article in Cellular and molecular life sciences : CMLS, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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.
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.
Who cites it
46 citing papers in PubMed, 79 citations in OpenAlex.
- Preclinical and clinical studies on Qin-Zhu-Liang-Xue decoction: insights from network pharmacology and implications for atopic dermatitis treatment.Frontiers of medicine · 2025Trial
- Glucocorticoid signalling dysregulation and immune cell adaptation in Anorexia Nervosa.Molecular psychiatry · 2026Article
- Inter-Organ Communication Networks in Systemic Physiology: Glucocorticoid Receptor α as a Central Integrator of Homeostasis.International journal of molecular sciences · 2026Review
- Cardiac Endocrine Function and Hormonal Interplay in Pediatrics: From Development to Clinical Implications.Biomedicines · 2025Review
- The glucocorticoid receptor is affected by its target ZBTB16 in a dissociated manner.The Journal of endocrinology · 2025Article
- Biological Clock Perspective in Rheumatoid Arthritis.Inflammation · 2025Review
- Reactivation of latent HIV-1 by the glucocorticoid receptor modulator AZD9567.Journal of virology · 2025Article
- UV-induced reorganization of 3D genome mediates DNA damage response.Nature communications · 2025Article
- Regulatory mechanisms of steroid hormone receptors on gene transcription through chromatin interaction and enhancer reprogramming.Cellular oncology (Dordrecht, Netherlands) · 2024Review
- Expression of glucocorticoid receptor and HDACs in airway smooth muscle cells is associated with response to steroids in COPD.Respiratory research · 2024Article
- Synephrine and Its Derivative Compound A: Common and Specific Biological Effects.International journal of molecular sciences · 2023Review
- Synergistic effects of hormones on structural and functional maturation of cardiomyocytes and implications for heart regeneration.Cellular and molecular life sciences : CMLS · 2023Review
- Novel Role of Mammalian Cell Senescence-Sustenance of Muscle Larvae ofOxidative medicine and cellular longevity · 2022Article
- Review
- The role of hormones and neurons in cardiomyocyte maturation.Seminars in cell & developmental biology · 2021Review
- Compound A Increases Cell Infiltration in Target Organs of Acute Graft-versus-Host Disease (aGVHD) in a Mouse Model.Molecules (Basel, Switzerland) · 2021Article
- Article
- A Brief Overview of the Paradoxical Role of Glucocorticoids in Breast Cancer.Breast cancer : basic and clinical research · 2020Review
- Nascent transcript analysis of glucocorticoid crosstalk with TNF defines primary and cooperative inflammatory repression.Genome research · 2019Article
- Glucocorticoids and programming of the microenvironment in heart.The Journal of endocrinology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucocorticoids (GCs) block inflammation via interference of the liganded glucocorticoid receptor (GR) with the activity of pro-inflammatory transcription factors NF-κB and AP-1, a mechanism known as transrepression. This mechanism is believed to involve the activity of GR monomers. Here, we explored how the GR monomer-favoring Compound A (CpdA) affects AP-1 activation and activity. Our results demonstrate that non-steroidal CpdA, unlike classic steroidal GCs, blocks NF-κB- but not AP-1-driven gene expression. CpdA rather sustains AP-1-driven gene expression, a result which could mechanistically be explained by the failure of CpdA to block upstream JNK kinase activation and concomitantly also phosphorylation of c-Jun. In concordance and in contrast to DEX, CpdA maintained the expression of the activated AP-1 target gene c-jun, as well as the production of the c-Jun protein. As for the underlying mechanism, GR is a necessary intermediate in the CpdA-mediated gene expression of AP-1-regulated genes, but seems to be superfluous to CpdA-mediated JNK phosphorylation prolongation. The latter phenomenon concurs with the inability of CpdA to stimulate DUSP1 gene expression. ChIP analysis demonstrates that DEX-activated GR, but not CpdA-activated GR, is recruited to AP-1-driven promoters. Furthermore, in mice we observed that CpdA instigates a strong enhancement of TNF-induced AP-1-driven gene expression. Finally, we demonstrate that this phenomenon coincides with an increased sensitivity towards TNF lethality, and implicate again a role for JNK2. In conclusion, our data support the hypothesis that a ligand-induced differential conformation of GR yields a different transcription factor cross-talk profile.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.