ArticleThe Biochemical journal2006
Recruitment of histone deacetylase 4 by transcription factors represses interleukin-5 transcription.
Article in The Biochemical journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 43 citations in OpenAlex.
- GATA-3-dependent Gene Transcription is Impaired upon HDAC Inhibition.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- Genetic Association and Differential RNA Expression of Histone (De)Acetylation-Related Genes in Pemphigus Foliaceus-A Possible Epigenetic Effect in the Autoimmune Response.Life (Basel, Switzerland) · 2023Article
- Review
- Critical Functions of Histone Deacetylases (HDACs) in Modulating Inflammation Associated with Cardiovascular Diseases.Pathophysiology : the official journal of the International Society for Pathophysiology · 2022Review
- GROWTH AND DEVELOPMENT SYMPOSIUM: STEM AND PROGENITOR CELLS IN ANIMAL GROWTH: The regulation of beef quality by resident progenitor cells1.Journal of animal science · 2019Article
- HDAC4 is expressed on multiple T cell lineages but dispensable for their development and function.Oncotarget · 2017Article
- The microRNA miR-22 inhibits the histone deacetylase HDAC4 to promote T(H)17 cell-dependent emphysema.Nature immunology · 2015Article
- Genomics of lymphoid malignancies reveal major activation pathways in lymphocytes.Journal of autoimmunity · 2013Review
- Epigenetic regulation of inflammation: progressing from broad acting histone deacetylase (HDAC) inhibitors to targeting specific HDACs.Inflammopharmacology · 2013Review
- Review
- ATRA inhibits the proliferation of DU145 prostate cancer cells through reducing the methylation level of HOXB13 gene.PloS one · 2012Article
- Modeling the relative relationship of transcription factor binding and histone modifications to gene expression levels in mouse embryonic stem cells.Nucleic acids research · 2012Article
- Mechanisms of intermittent hypoxia induced hypertension.Journal of cellular and molecular medicine · 2010Review
- Th1/Th2 patterns and balance in cytokine production in the parents and infants of a large birth cohort.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- YY1 protects cardiac myocytes from pathologic hypertrophy by interacting with HDAC5.Molecular biology of the cell · 2008Article
- NFATc3 is required for intermittent hypoxia-induced hypertension.American journal of physiology. Heart and circulatory physiology · 2008Article
- Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The critical role of IL-5 (interleukin-5) in eosinophilic inflammation implicates it as a therapeutic target for allergic diseases. The aim of the present study was to elucidate the molecular basis for the involvement of reversible histone acetylation in IL-5 transcriptional regulation. We provide evidence that HDAC4 (histone deacetylase 4) and p300, a known HAT (histone acetyltransferase), reversibly controlled the activity of the IL-5 promoter in vivo and in vitro, with a concurrent alteration of histone H3 acetylation status at the promoter regions. The nucleo-cytoplasmic shuttling of HDAC4 was shown to play an important role in the suppressive function of HDAC4 in IL-5 gene expression. Point mutation and reporter ChIP (chromatin immunoprecipitation) studies determined that the four transcription factors binding on the IL-5 promoter, i.e. C/EBPbeta (CAAT/enhancer-binding protein beta), GATA3 (GATA binding protein 3), NFAT (nuclear factor of activated T cells) and YY1 (Yin and Yang 1), were essential for the recruitment of HDAC4. Consistent with these observations, HDAC4 was found to form protein complexes with GATA3 and YY1, and to co-exist in the nuclei with GATA3. We propose that the unique regulatory mechanism of IL-5 gene transcription involves the reversible histone modification catalysed by HDAC4 and p300, which are recruited by the transcription factors. The dynamic balance in IL-5 transcriptional regulation is achieved through interactions among HATs/HDACs, histones and transcription factors. These data contribute to understanding the molecular mechanisms of IL-5 regulation, which is crucial to the development of new therapeutic strategies for IL-5-related allergic diseases.
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