Regulation of inflammatory gene transcription by ubiquitination and deubiquitination

Abstract

Transcriptional responses are initiated immediately after the recognition of pathogen-associated molecular patterns by pattern recognition receptors, enabling host cells to deal with inflammatory stimuli, including microbial infections. In turn, these inflammatory transcriptional programs must be tightly controlled to prevent potential detrimental consequences, such as immunopathological or even fatal outcomes. To date, many well-defined mechanisms have been reported that contribute to the transcriptional control of inflammatory gene expression at multiple levels. Here, I mainly focus on reviewing recent progress in post-translational modifications, in particular, how the ubiquitination–deubiquitination cycle controls inflammatory gene transcription mediated by nuclear factor kappa-light-chain-enhancer of activated B cells and interferon signaling pathways. Lastly, I will emphasize the importance of understanding gene-specific mechanisms in controlling inflammatory gene transcription.