| First Author | Hwang YJ | Year | 2013 |
| Journal | Sci Rep | Volume | 3 |
| Pages | 3242 | PubMed ID | 24247732 |
| Mgi Jnum | J:207849 | Mgi Id | MGI:5559813 |
| Doi | 10.1038/srep03242 | Citation | Hwang YJ, et al. (2013) MafK positively regulates NF-kappaB activity by enhancing CBP-mediated p65 acetylation. Sci Rep 3:3242 |
| abstractText | Reactive oxygen species, produced by oxidative stress, initiate and promote many metabolic diseases through activation/suppression of redox-sensitive transcription factors. NF-kappaB 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-kappaB activity. MafK knockdown reduced NF-kappaB activation, whereas MafK overexpression enhanced NF-kappaB function. MafK mediated p65 acetylation by CBP upon LPS stimulation, thereby facilitating recruitment of p65 to NF-kappaB promoters such as IL-8 and TNFalpha. 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-kappaB activity via CBP-mediated p65 acetylation. |
