ArticleNucleic acids research2013
The coactivator role of histone deacetylase 3 in IL-1-signaling involves deacetylation of p65 NF-κB.
Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 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
78 citing papers in PubMed, 122 citations in OpenAlex.
- HDAC3 Inhibitor RGFP966 Enhances Memory Persistence in a Biphasic Manner and Modulates NF-kB Nuclear Localization.Molecular neurobiology · 2026Article
- Innate immunity: current understandings and future perspectives.Signal transduction and targeted therapy · 2026Review
- HDAC3 as an Immunometabolic Rheostat: Molecular Mechanisms of Deacylation Plasticity, Lactylation Dynamics, and Spatiotemporal Regulation.Biomolecules · 2026Review
- Neointimal hyperplasia and vascular restenosis: from molecular mechanisms to therapeutic interventions.Molecular biomedicine · 2026Review
- The role and mechanism of histone deacetylase in COPD.Molecular and cellular biochemistry · 2026Review
- Constitutive expression of the transcriptional co-activator IκBζ promotes melanoma growth and immunotherapy resistance.Nature communications · 2025Article
- The Role of HDAC3 in Pulmonary Diseases.Lung · 2025Review
- HDAC3 in action: Expanding roles in inflammation and inflammatory diseases.Cell proliferation · 2025Review
- Expression of glucocorticoid receptor and HDACs in airway smooth muscle cells is associated with response to steroids in COPD.Respiratory research · 2024Article
- Deficiency of histone deacetylases 3 in macrophage alleviates monosodium urate crystals-induced gouty inflammation in mice.Arthritis research & therapy · 2024Article
- Critical Role of histone deacetylase 3 in the regulation of kidney inflammation and fibrosis.Kidney international · 2024Article
- Zinc-Dependent Histone Deacetylases in Lung Endothelial Pathobiology.Biomolecules · 2024Review
- Integrative function of histone deacetylase 3 in inflammation.Molecular biology reports · 2024Review
- The involvement of HDAC3 in the pathogenesis of lung injury and pulmonary fibrosis.Frontiers in immunology · 2024Review
- The role of HDAC3 in inflammation: mechanisms and therapeutic implications.Frontiers in immunology · 2024Review
- CUL4B functions as a tumor suppressor in KRAS-driven lung tumors by inhibiting the recruitment of myeloid-derived suppressor cells.Oncogene · 2023Article
- The effect of epigenetic reprogramming using MI192 HDAC inhibitor on enhancing the osteogenesis of human adipose-derived stem cells in vitro.Bioscience reports · 2023Article
- Butyrate limits inflammatory macrophage niche in NASH.Cell death & disease · 2023Article
- RELA tunes innate-like interferon I/III responses in human T cells.The Journal of experimental medicine · 2023Article
- Intestinal epithelial HDAC3 and MHC class II coordinate microbiota-specific immunity.The Journal of clinical investigation · 2023Article
18 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
18 authors at 6 institutions in 4 countries.
Funding
Abstract
Histone deacetylase (HDAC) 3, as a cofactor in co-repressor complexes containing silencing mediator for retinoid or thyroid-hormone receptors (SMRT) and nuclear receptor co-repressor (N-CoR), has been shown to repress gene transcription in a variety of contexts. Here, we reveal a novel role for HDAC3 as a positive regulator of IL-1-induced gene expression. Various experimental approaches involving RNAi-mediated knockdown, conditional gene deletion or small molecule inhibitors indicate a positive role of HDAC3 for transcription of the majority of IL-1-induced human or murine genes. This effect was independent from the gene regulatory effects mediated by the broad-spectrum HDAC inhibitor trichostatin A (TSA) and thus suggests IL-1-specific functions for HDAC3. The stimulatory function of HDAC3 for inflammatory gene expression involves a mechanism that uses binding to NF-κB p65 and its deacetylation at various lysines. NF-κB p65-deficient cells stably reconstituted to express acetylation mimicking forms of p65 (p65 K/Q) had largely lost their potential to stimulate IL-1-triggered gene expression, implying that the co-activating property of HDAC3 involves the removal of inhibitory NF-κB p65 acetylations at K122, 123, 314 and 315. These data describe a novel function for HDAC3 as a co-activator in inflammatory signaling pathways and help to explain the anti-inflammatory effects frequently observed for HDAC inhibitors in (pre)clinical use.
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.