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

27 Citations (Scopus)

Abstract

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
Volume3
DOIs
Publication statusPublished - 2013 Nov 28

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Acetylation
Metabolic Diseases
Interleukin-8
Oxidation-Reduction
Reactive Oxygen Species
Oxidative Stress
Transcription Factors
Injections
Liver

All Science Journal Classification (ASJC) codes

  • General

Cite this

Hwang, Yu Jin ; Lee, Eun Woo ; Song, Jaewhan ; Kim, Haeng Ran ; Jun, Young Chun ; Hwang, Kyung A. / MafK positively regulates NF-κB activity by enhancing CBP-mediated p65 acetylation. In: Scientific reports. 2013 ; Vol. 3.
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abstract = "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.",
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MafK positively regulates NF-κB activity by enhancing CBP-mediated p65 acetylation. / Hwang, Yu Jin; Lee, Eun Woo; Song, Jaewhan; Kim, Haeng Ran; Jun, Young Chun; Hwang, Kyung A.

In: Scientific reports, Vol. 3, 3242, 28.11.2013.

Research output: Contribution to journalArticle

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AU - Hwang, Yu Jin

AU - Lee, Eun Woo

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AU - Jun, Young Chun

AU - Hwang, Kyung A.

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