The Activation of IL-1-Induced Enhancers Depends on TAK1 Kinase Activity and NF-κB p65.
Cast your vote
You can rate an item by clicking the amount of stars they wish to award to this item.
When enough users have cast their vote on this item, the average rating will also be shown.
Your vote was cast
Thank you for your feedback
Thank you for your feedback
Saul, Vera V
Schmitz, M Lienhard
MetadataShow full item record
AbstractThe inflammatory gene response requires activation of the protein kinase TAK1, but it is currently unknown how TAK1-derived signals coordinate transcriptional programs in the genome. We determined the genome-wide binding of the TAK1-controlled NF-κB subunit p65 in relation to active enhancers and promoters of transcribed genes by chromatin immunoprecipitation sequencing (ChIP-seq) experiments. Out of 35,000 active enhancer regions, 410 H3K4me1-positive enhancers show interleukin 1 (IL-1)-induced H3K27ac and p65 binding. Inhibition of TAK1 or IKK2 or depletion of p65 blocked inducible enhancer activation and gene expression. As exemplified by the CXC chemokine cluster located on chromosome 4, the TAK1-p65 pathway also regulates the recruitment kinetics of the histone acetyltransferase CBP, of NF-κB p50, and of AP-1 transcription factors to both promoters and enhancers. This study provides a high-resolution view of epigenetic changes occurring during the IL-1 response and allows the genome-wide identification of a distinct class of inducible p65 NF-κB-dependent enhancers in epithelial cells.
CitationThe Activation of IL-1-Induced Enhancers Depends on TAK1 Kinase Activity and NF-κB p65. 2015: Cell Rep
AffiliationHelmholtz Centre for infection research, Inhoffenstr. 7, 38124 Braunschweig, Germany.
The following license files are associated with this item:
- The NF-κB-dependent and -independent transcriptome and chromatin landscapes of human coronavirus 229E-infected cells.
- Authors: Poppe M, Wittig S, Jurida L, Bartkuhn M, Wilhelm J, Müller H, Beuerlein K, Karl N, Bhuju S, Ziebuhr J, Schmitz ML, Kracht M
- Issue date: 2017 Mar
- Distinct IL-1α-responsive enhancers promote acute and coordinated changes in chromatin topology in a hierarchical manner.
- Authors: Weiterer SS, Meier-Soelch J, Georgomanolis T, Mizi A, Beyerlein A, Weiser H, Brant L, Mayr-Buro C, Jurida L, Beuerlein K, Müller H, Weber A, Tenekeci U, Dittrich-Breiholz O, Bartkuhn M, Nist A, Stiewe T, van IJcken WF, Riedlinger T, Schmitz ML, Papantonis A, Kracht M
- Issue date: 2020 Jan 2
- Lingual antimicrobial peptide and IL-8 expression are oppositely regulated by the antagonistic effects of NF-κB p65 and C/EBPβ in mammary epithelial cells.
- Authors: Liu S, Shi X, Bauer I, Günther J, Seyfert HM
- Issue date: 2011 Mar
- Synthetic double-stranded RNA induces interleukin-32 in bronchial epithelial cells.
- Authors: Ota K, Kawaguchi M, Fujita J, Kokubu F, Huang SK, Morishima Y, Matsukura S, Kurokawa M, Ishii Y, Satoh H, Sakamoto T, Hizawa N
- Issue date: 2015
- TAK1 and IKK2, novel mediators of SCF-induced signaling and potential targets for c-Kit-driven diseases.
- Authors: Drube S, Weber F, Göpfert C, Loschinski R, Rothe M, Boelke F, Diamanti MA, Löhn T, Ruth J, Schütz D, Häfner N, Greten FR, Stumm R, Hartmann K, Krämer OH, Dudeck A, Kamradt T
- Issue date: 2015 Oct 6