ArticleMolecular and cellular biology1993
Identification of a novel interleukin-6 response element containing an Ets-binding site and a CRE-like site in the junB promoter.
Article in Molecular and cellular biology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 124 citations in OpenAlex.
- Depletion of JunB increases adipocyte thermogenic capacity and ameliorates diet-induced insulin resistance.Nature metabolism · 2024Article
- NovelInternational journal of molecular sciences · 2021Article
- Anabolic and Pro-metabolic Functions of CREB-CRTC in Skeletal Muscle: Advantages and Obstacles for Type 2 Diabetes and Cancer Cachexia.Frontiers in endocrinology · 2019Review
- The Phosphorylation of CREB at Serine 133 Is a Key Event for Circadian Clock Timing and Entrainment in the Suprachiasmatic Nucleus.Journal of biological rhythms · 2018Article
- A RAS-CaMKKβ-AMPKα2 pathway promotes senescence by licensing post-translational activation of C/EBPβ through a novel 3'UTR mechanism.Oncogene · 2018Article
- Quantitative Analyses of Core Promoters Enable Precise Engineering of Regulated Gene Expression in Mammalian Cells.ACS synthetic biology · 2016Article
- Chromatin loop organization of the junb locus in mouse dendritic cells.Nucleic acids research · 2013Article
- Article
- Hypoxia-inducible factor-1alpha enhances haptoglobin gene expression by improving binding of STAT3 to the promoter.The Journal of biological chemistry · 2011Article
- DNA methyl transferase 1: regulatory mechanisms and implications in health and disease.International journal of biochemistry and molecular biology · 2011Article
- Genome wide prediction of HNF4alpha functional binding sites by the use of local and global sequence context.Genome biology · 2008Article
- STAT3 regulates Nemo-like kinase by mediating its interaction with IL-6-stimulated TGFbeta-activated kinase 1 for STAT3 Ser-727 phosphorylation.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Interleukin-6 represses the transcription of the CCAAT/enhancer binding protein-alpha gene in hepatoma cells by inhibiting its ability to autoactivate the proximal promoter region.Nucleic acids research · 2003Article
- MSK1 and MSK2 are required for the mitogen- and stress-induced phosphorylation of CREB and ATF1 in fibroblasts.Molecular and cellular biology · 2002Article
- NF-Y regulates LIF-induced transcription of the signaling adaptor SKAP55R in myeloid cells.Leukemia · 2001Article
- Tissue-specific autoregulation of the stat3 gene and its role in interleukin-6-induced survival signals in T cells.Molecular and cellular biology · 2001Article
- The YXXQ motif in gp 130 is crucial for STAT3 phosphorylation at Ser727 through an H7-sensitive kinase pathway.Oncogene · 2001Article
- The mammalian Jun proteins: redundancy and specificity.Oncogene · 2001Review
- Independent influence of strain difference and mi transcription factor on the expression of mouse mast cell chymases.The American journal of pathology · 2001Article
- Ets target genes: past, present and future.Oncogene · 2000Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-6 (IL-6) activation of the immediate-early gene junB has been shown to require both a tyrosine kinase and an unknown 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H7)-sensitive pathway. Here we report the identification and characterization of an IL-6 immediate-early response element in the junB promoter (designated JRE-IL6) in HepG2 cells. The JRE-IL6 element, located at -149 to -124, contains two DNA motifs, an Ets-binding site (EBS) (CAGGAAGC) and a CRE-like site (TGACGCGA). Functional studies using variously mutated JRE-IL6 elements showed that both motifs were necessary and sufficient for IL-6 response of the promoter. The EBS of the JRE-IL6 element (JEBS) appears to bind a protein in the Ets family or a related protein which could also form a major complex with the EBSs of the murine sarcoma virus long terminal repeat or human T-cell leukemia virus type 1 long terminal repeat. The CRE-like site appears to weakly bind multiple CREB-ATF family proteins. Despite the similarity in the structure between the JRE-IL6 element and the polyomavirus enhancer PyPEA3, composed of an EBS and an AP1-binding site and known to be activated by a variety of oncogene signals, JRE-IL6 could not be activated by activated Ha-Ras, Raf-1, or 12-O-tetradecanoylphorbol-13-acetate. We show that IL-6 activates JRE-IL6 through an H7-sensitive pathway that does not involve protein kinase C, cyclic AMP-dependent kinase, Ca(2+)- or calmodulin-dependent kinases, Ras, Raf-1, or NF-IL6 (C/EBP beta). The combination of JEBS and the CRE-like site appears to form the basis for the selective and efficient response of JRE-IL6 to IL-6 signals, but not to signals generated by activated Ha-Ras, Raf-1, or protein kinase C.
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