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. 2021 Jan 19;6:23. doi: 10.1038/s41392-020-00384-4

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — The role BRD4 in regulating the NF-κB pathway in inflammation and immunity. BRD4 regulates the activation of the NF-κB pathway caused by TLR ligands through at least four pathways: (1) BRD4 directly acetylates RELA through its atypical histone acetyltransferase activity; (2) BRD4 directly promotes the phosphorylation of RELA; and (3–4) BRD4 promotes the phosphorylation of RELA through inhibiting the translation of NFKBIA and increasing the phosphorylation of NFKBIA and IKBKB. Abbreviations: CDK9, cyclin-dependent kinase 9; CHUK, component of inhibitor of nuclear factor kappa B kinase complex; CycT1, cyclin T1; IKBKB, inhibitor of nuclear factor kappa B kinase regulatory subunit beta; IKBKG, inhibitor of nuclear factor kappa B kinase regulatory subunit gamma; NFKBIA, NFKB inhibitor alpha; NFKB1, nuclear factor kappa B subunit 1; p-TEFb, positive transcription elongation factor b; RELA, RELA proto-oncogene; RNA pol II, RNA polymerase II; TLR, toll-like receptor (numbers 1–9)