Tumor necrosis factor, alpha-induced protein 3 (TNFAIP3 (A20))

Tumor necrosis factor, alpha-induced protein 3 (TNFAIP3, also known as A20), is a zinc finger protein that acts as both a deubiquitinase and E3 ubiquitin ligase, playing a crucial role in the negative regulation and termination of the NF-κB signaling pathway. TNFAIP3 is essential for immune homeostasis, restricting excess or chronic inflammation by removing polyubiquitin chains from key signaling proteins and promoting their degradation, thereby blocking NF-κB activation. Dysregulation or mutation of TNFAIP3 is linked to a variety of autoimmune, inflammatory, and malignant diseases, making it a significant therapeutic target for modulating immune and inflammatory responses. Genetic variants in TNFAIP3 are associated with increased risk of autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis.

Other names

A20Tumor necrosis factor alpha-induced protein 3

Inhibition of NF-κB activation (via modulation/increase of TNFAIP3 function); Downregulation of inflammatory cytokine production by suppression of NF-κB transcriptional activity; Promotion of apoptosis by suppressing pro-survival NF-κB target genes.