MafK positively regulates NF-κB activity by enhancing CBP-mediated p65 acetylation

Yu Jin Hwang, Eun Woo Lee, Jaewhan Song, Haeng Ran Kim, Young Chun Jun, Kyung A. Hwang

Research output: Contribution to journalArticle

30 Citations (Scopus)


Reactive oxygen species produced by oxidative stress initiate and promote many metabolic diseases through activation/suppression of redox-sensitive transcription factors. NF-κB and Nrf2 are important regulators of oxidation resistance and contribute to the pathogenesis of many diseases. We identified MafK, a novel transcriptional regulator that modulates NF-κB activity. MafK knockdown reduced NF-κB activation, whereas MafK overexpression enhanced NF-κB function. MafK mediated p65 acetylation by CBP upon LPS stimulation, thereby facilitating recruitment of p65 to NF-κB promoters such as IL-8 and TNFα. Consistent with these results, MafK-depleted mice showed prolonged survival with a reduced hepatic inflammatory response after LPS and D-GalN injection. Thus, our findings reveal a novel mechanism by which MafK controls NF-κB activity via CBP-mediated p65 acetylation.

Original languageEnglish
Article number3242
JournalScientific reports
Publication statusPublished - 2013

All Science Journal Classification (ASJC) codes

  • General

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