Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2019 Mar 12;20(5):1241. doi: 10.3390/ijms20051241

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

PMC Copyright notice

Inhibitory effects of GSK3, p52, RelB, and p50 on pro-inflammatory transcription following TNF long term exposure. TNF long term incubation leads to an activation of IDO1 and GSK3. NF-κB2-p100 is degraded to its active form p52 in an IDO-dependent manner. Following translation to the nucleus the non-canonical p52 and RelB homo- and heterodimers, as well as canonical p50, homodimers contribute to the inhibition of pro-inflammatory gene expression. RelB/p52 complexes are also involved in the induction of IDO1 expression. GSK3 mediates phosphorylation of C/EBPβ (T235). Interaction of C/EBPβ with p65 inhibits the transcriptional activity of p65. Please find the relevant literature in the text of the Discussion.