The bromodomain protein BRD4 positively regulates necroptosis via modulating MLKL expression View Full Text


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Article Info

DATE

2019-01-15

AUTHORS

Yu Xiong, Linli Li, Liting Zhang, Yangyang Cui, Chengyong Wu, Hui Li, Kai Chen, Qiuyuan Yang, Rong Xiang, Yiguo Hu, Shile Huang, Yuquan Wei, Shengyong Yang

ABSTRACT

Necroptosis is a programmed form of necrotic cell death, which is tightly regulated by the necroptotic signaling pathway containing receptor-interacting protein (RIP)1, RIP3, and mixed-lineage kinase domain-like (MLKL) protein. In addition to the RIP1-RIP3-MLKL axis, other factors regulating necroptosis are still largely unknown. Here a cell-based small-molecule screening led to the finding that BET inhibitors protected cells from necroptosis in the TNFα/Smac-mimetic/Z-VAD-FMK (TSZ)-induced cell necroptosis model. Mechanistic studies revealed that BET inhibitors acted by downregulating MLKL expression. Further research demonstrated that BRD4, IRF1, P-TEFb, and RNA polymerase II formed a transcription complex to regulate the expression of MLKL, and BET inhibitors interfered with the transcription complex formation. In necroptosis-related disease model, the BET inhibitor JQ-1 showed promising therapeutic effects. Collectively, our studies establish, for the first time, BRD4 as a new epigenetic factor regulating necroptosis, and highlight the potential of BET inhibitors in the treatment of necroptosis-related diseases. More... »

PAGES

1-13

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41418-018-0262-9

    DOI

    http://dx.doi.org/10.1038/s41418-018-0262-9

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1111407340

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30644439


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