ArticleMolecular and cellular biology2008
c-Jun controls histone modifications, NF-kappaB recruitment, and RNA polymerase II function to activate the ccl2 gene.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 87 citations in OpenAlex.
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- The proximity-based protein interactome and regulatory logics of the transcription factor p65 NF-κB/RELA.EMBO reports · 2025Article
- Systemic IFN-I combined with topical TLR7/8 agonists promotes distant tumor suppression by c-Jun-dependent IL-12 expression in dendritic cells.Nature cancer · 2025Article
- N-Acetylgalactosamine-4-sulfatase (Arylsulfatase B) Regulates PD-L1 Expression in Melanoma by an HDAC3-Mediated Epigenetic Mechanism.International journal of molecular sciences · 2024Article
- Low HER2 expression in normal breast epithelium enables dedifferentiation and malignant transformation via chromatin opening.Disease models & mechanisms · 2023Article
- Molecular Mechanisms Underlying the Anti-Inflammatory Properties of (R)-(-)-Carvone: Potential Roles of JNK1, Nrf2 and NF-κB.Pharmaceutics · 2023Article
- Cancer genome and tumor microenvironment: Reciprocal crosstalk shapes lung cancer plasticity.eLife · 2022Review
- Inhibition of Class I Histone Deacetylase Activity Blocks the Induction of TNFAIP3 Both Directly and Indirectly via the Suppression of Endogenous TNF-α.International journal of molecular sciences · 2022Article
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- Comparative transcriptome analysis reveals key epigenetic targets in SARS-CoV-2 infection.NPJ systems biology and applications · 2021Article
- Psoriatic skin inflammation is promoted by c-Jun/AP-1-dependent CCL2 and IL-23 expression in dendritic cells.EMBO molecular medicine · 2021Article
- The endocannabinoid anandamide has an anti-inflammatory effect on CCL2 expression in vascular smooth muscle cells.Basic research in cardiology · 2020Article
- NF-κB p65 dimerization and DNA-binding is important for inflammatory gene expression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Epigenomic analysis reveals DNA motifs regulating histone modifications in human and mouse.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- The Crosstalk of Endoplasmic Reticulum (ER) Stress Pathways with NF-κB: Complex Mechanisms Relevant for Cancer, Inflammation and Infection.Biomedicines · 2018Review
- Chemotherapy Induces Breast Cancer Stemness in Association with Dysregulated Monocytosis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-1 (IL-1)-induced mRNA expression of ccl2 (also called MCP-1), a prototypic highly regulated inflammatory gene, is severely suppressed in cells lacking c-Jun or Jun N-terminal protein kinase 1 (JNK1)/JNK2 genes and is only partially restored in cells expressing a c-Jun(SS63/73AA) mutant protein. We used chromatin immunoprecipitation to identify three c-Jun-binding sites located in the far 5' region close to the transcriptional start site and in the far 3' region of murine and human ccl2 genes. Mutational analysis revealed that the latter two sites contribute to ccl2 transcription in response to the presence of IL-1 or of ectopically expressed c-Jun-ATF-2 dimers. Further experiments comparing wild-type and c-Jun-deficient cells revealed that c-Jun regulates Ser10 phosphorylation of histone H3, acetylation of histones H3 and H4, and recruitment of histone deacetylase 3 (HDAC3), NF-kappaB subunits, and RNA polymerase II across the ccl2 locus. c-Jun also coimmunoprecipitated with p65 NF-kappaB and HDAC3. Based on DNA microarray analysis, c-Jun was required for full expression of 133 out of 162 IL-1-induced genes. For inflammatory genes, these data support the idea of an activator function of c-Jun that is executed by multiple mechanisms, including phosphorylation-dependent interaction with p65 NF-kappaB and HDAC3 at the level of chromatin.
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