Abstract:
:Tumor necrosis factor alpha (TNF-α) is a prototypical proinflammatory cytokine that can elicit strong inflammation in macrophages by activating NF-κB. The underlying epigenetic mechanism is obscure. We show here that megakaryocytic leukemia 1 (MKL1) is an epigenetic mediator of TNF-α-induced proinflammatory transcription. Overexpression of a dominant negative form of MKL1 abrogates TNF-α-induced transactivation of proinflammatory genes. Proteomic analysis identifies the histone H3K4 trimethyltransferase ASH2 as a potential cofactor for MKL1. In response to TNF-α stimulation, ASH2 is recruited by MKL1 and interacts with MKL1 to catalyze H3K4 di- and trimethylation. ASH2 modulates proinflammatory transcription at least in part by altering the affinity of p65 for target promoters. Together, our data support an interplay between MKL1 and ASH2 to promote TNF-α-induced proinflammatory transcription in macrophages.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Song M,Fang F,Dai X,Yu L,Fang M,Xu Ydoi
10.1002/1873-3468.12601subject
Has Abstractpub_date
2017-03-01 00:00:00pages
934-945issue
6eissn
0014-5793issn
1873-3468journal_volume
591pub_type
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