The Activation of IL-1-Induced Enhancers Depends on TAK1 Kinase Activity and NF-κB p65
Open accessAbstract
The 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.
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NF-κB is able to recruit p300/CBP to chromatin and to increase H3K27ac.
“Moreover, NF-κB is able both to recruit p300/CBP to chromatin53 and to increase H3K27ac54, 55.”
From Synergistic gene expression during the acute phase response is characterized by transcription factor assisted loading (2017) · cites this paper as [54]
These observations are consistent with a reported role for NF-κB in modifying the enhancer landscape following stimuli.
“These observations are consistent with a reported role for NF-κB (a classic signal-activated TF) in modifying the enhancer landscape following stimuli54, 55.”
From Synergistic gene expression during the acute phase response is characterized by transcription factor assisted loading (2017) · cites this paper as [54]
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Priester, J., Meier‐Soelch, J., Weiser, H., Heylmann, D., Weber, A., Linne, U., & Kracht, M. (2023) · STAR Protocols · doi:10.1016/j.xpro.2023.102195 · Cited by 1 · see citing works
Self-citationEXPLORING THE GENOME-WIDE IMPACT OF TRANSCRIPTION FACTOR AP-1 IN BREAST CANCER
Qiao, Y. (2015) · Figshare
Testing the Effect of Histone Acetyltransferases on Local Chromatin Compaction
Pfisterer, M., & Schmitz, M. L. (2022) · Methods in molecular biology · doi:10.1007/978-1-0716-2788-4_24
Self-citationXu, F., Sieverding, J., Zhou, P., Sah, S., Weinberger, V., Moissl‐Eichinger, C., Wohlers, I., & Heine, H. (2026) · Nature Communications · doi:10.1101/2025.09.30.679018 · Cited by 1 · see citing works
Gulzar, S.-E.-J., Umar, I., Saravanan, B., Dd, S., Najar, A. H., Farooq, U., Molla, S., Ravikumar, A., Notani, D., & Sundaramurthy, V. (2026) · mBio · doi:10.1128/mbio.01214-26
Interferon crosstalk at the lung barrier in viral and fungal infection
Brochero, M. I. V., & Rivera, A. (2026) · Infection and Immunity · doi:10.1128/iai.00295-26
Sun, G., Sun, L., Jiang, J., Ma, X., Zhong, Y., Li, H., Liu, X., Xue, K., Hu, X., Feng, J., et al. (2026) · International Immunopharmacology · doi:10.1016/j.intimp.2026.117430
- Authors
- Jurida, L., Soelch, J., Bartkuhn, M., Handschick, K., Müller, H., Newel, D., Weber, A., Dittrich-Breiholz, O., Schneider, H., Bhuju, S., Saul, V. V., Schmitz, M. L., & Kracht, M.
- Affiliations
- Justus-Liebig-Universität Gießen (DE)
- Medizinische Hochschule Hannover (DE)
- Helmholtz Centre for Infection Research (DE)
- Corresponding author
- Kracht, Michael
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2015-02
- Volume
- 10
- Issue
- 5
- Pages
- 726-739
- ISSN
- 2211-1247 (ISSN-L)
- OpenAlex
- W2014487118
- Cited by
- 51
- References
- 47
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 3 · 2023: 1 · 2022: 8 · 2021: 4 · 2020: 6 · 2019: 5 · 2018: 5 · 2017: 4 · 2016: 2 · 2015: 2
- FWCI
- 1.43
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- HZI (Helmholtz Centre for Infection Research) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Deutsche Forschungsgemeinschaft
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Keywords
- NF-κB p65, IL-1 signaling, enhancer activation, H3K27ac, H3K4me1, AP-1 transcription factor, NF-κB p50, epithelial cells, IKKβ
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