ArticleGenes & development1997
Nuclear hormone receptor antagonism with AP-1 by inhibition of the JNK pathway.
Article in Genes & development, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 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
71 citing papers in PubMed, 337 citations in OpenAlex.
- Roxadustat Activates Thyroid Hormone Receptors α and β at Clinically Relevant Concentrations.Cureus · 2025Article
- The Nuclear Receptor NR1B1/RARα Arrests the Differentiation of Anti-Tumor Effector Cytotoxic T Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Detecting and dissecting signaling crosstalk via the multilayer network integration of signaling and regulatory interactions.Nucleic acids research · 2024Article
- Article
- Glucocorticoid Resistance: Interference between the Glucocorticoid Receptor and the MAPK Signalling Pathways.International journal of molecular sciences · 2021Review
- A review of the molecular design and biological activities of RXR agonists.Medicinal research reviews · 2019Review
- Fighting the Fire: Mechanisms of Inflammatory Gene Regulation by the Glucocorticoid Receptor.Frontiers in immunology · 2019Review
- Isorhapontigenin, a bioavailable dietary polyphenol, suppresses airway epithelial cell inflammation through a corticosteroid-independent mechanism.British journal of pharmacology · 2017Article
- Article
- Membrane glucocorticoid receptors are localised in the extracellular matrix and signal through the MAPK pathway in mammalian skeletal muscle fibres.The Journal of physiology · 2015Article
- Regulation of the nongenomic actions of retinoid X receptor-α by targeting the coregulator-binding sites.Acta pharmacologica Sinica · 2015Review
- Gαi3-Dependent Inhibition of JNK Activity on Intracellular Membranes.Frontiers in bioengineering and biotechnology · 2015Article
- Lipid raft- and protein kinase C-mediated synergism between glucocorticoid- and gonadotropin-releasing hormone signaling results in decreased cell proliferation.The Journal of biological chemistry · 2014Article
- Selective modulation of the glucocorticoid receptor can distinguish between transrepression of NF-κB and AP-1.Cellular and molecular life sciences : CMLS · 2014Article
- Article
- In vivo JNK activation in pancreatic β-cells leads to glucose intolerance caused by insulin resistance in pancreas.Diabetes · 2013Article
- Erg and AP-1 as determinants of glucocorticoid response in acute lymphoblastic leukemia.Oncogene · 2013Article
- THRAP3 interacts with HELZ2 and plays a novel role in adipocyte differentiation.Molecular endocrinology (Baltimore, Md.) · 2013Article
- The five Rs of glucocorticoid action during inflammation: ready, reinforce, repress, resolve, and restore.Trends in endocrinology and metabolism: TEM · 2013Review
- Chronic isolation stress compromises JNK/c-Jun signaling in rat brain.Journal of neural transmission (Vienna, Austria : 1996) · 2012Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The activity of c-Jun, the major component of the transcription factor AP-1, is potentiated by amino-terminal phosphorylation on serines 63 and 73 (Ser-63/73). This phosphorylation is mediated by the Jun amino-terminal kinase (JNK) and required to recruit the transcriptional coactivator CREB-binding protein (CBP). AP-1 function is antagonized by activated members of the steroid/thyroid hormone receptor superfamily. Recently, a competition for CBP has been proposed as a mechanism for this antagonism. Here we present evidence that hormone-activated nuclear receptors prevent c-Jun phosphorylation on Ser-63/73 and, consequently, AP-1 activation, by blocking the induction of the JNK signaling cascade. Consistently, nuclear receptors also antagonize other JNK-activated transcription factors such as Elk-1 and ATF-2. Interference with the JNK signaling pathway represents a novel mechanism by which nuclear hormone receptors antagonize AP-1. This mechanism is based on the blockade of the AP-1 activation step, which is a requisite to interact with CBP. In addition to acting directly on gene transcription, regulation of the JNK cascade activity constitutes an alternative mode whereby steroids and retinoids may control cell fate and conduct their pharmacological actions as immunosupressive, anti-inflammatory, and antineoplastic agents.
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.