https://orcid.org/0000-0002-2728-2859View further author information & https://orcid.org/0000-0002-8000-3708View further author informationFigure 1. A working model to elucidate that OPTN-mediated selective autophagic degradation of KDM4D epigenetically regulates inflammation. The TRIM14-USP14-BRCC3 complex reduces the K63-linked ubiquitin chains of KDM4D to inhibit OPTN-mediated autophagic degradation of KDM4D, which is responsible for removing the H3K9me3 modification at Il12 and Il23 promoters to promote the expression of proinflammatory cytokines IL12 and IL23 to enhance inflammation. LPS, lipopolysaccharide.
Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?
To request a reprint or corporate permissions for this article, please click on the relevant link below:
Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?
Obtain permissions instantly via Rightslink by clicking on the button below:
If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.
