Monisankar Ghosh

Introduction Bromodomain-containing protein 4 (BRD4) is a key regulator of development, tumorigenesis, inflammation, and fibrosis in mammalian organisms (1–5). In the context of airway inflammation, aeroallergens and airway pathogens trigger NF-κB/BRD4-mediated innate inflammation via activation of upstream pattern recognition receptors (6).

1 Introduction TANK-binding kinase (TBK1) plays a crucial role in the host defense against pathogens by functioning as a signaling intermediate downstream of cytosolic or endosomal nucleic acid-sensing pattern recognition receptors (PRRs). Upon PRR activation, TBK1 promotes the C-terminal phosphorylation and activation of the transcription factors interferon-regulatory factor 3 (IRF3) and IRF7 (1, 2).

Tumor suppression by TP53 involves cell-autonomous and non-cell-autonomous mechanisms. TP53 can suppress tumor growth by modulating immune system functions; however, the mechanistic basis for this activity is not well understood. We report that p53 promotes the degradation of the DNA exonuclease TREX1, resulting in cytosolic dsDNA accumulation. We demonstrate that p53 requires the ubiquitin ligase TRIM24 to induce TREX1 degradation.