Tumor necrosis factor alpha-induced protein 3-interacting protein 3 (TNIP3)

Tumor necrosis factor alpha-induced protein 3-interacting protein 3 (TNIP3) is a cytosolic regulatory protein that interacts with TNFAIP3 (A20) and acts as a negative regulator of NF-kappa-B activation in response to inflammatory stimuli, such as tumor necrosis factor (TNF), Toll-like receptor (TLR) agonists, and interleukin-1. TNIP3 inhibits NF-kappa-B signaling downstream of TRAF6 and upstream of IKK, and its overexpression attenuates inflammatory responses in models of cardiac dysfunction, fibrosis, and nonalcoholic steatohepatitis by modulating PI3K/Akt/NF-kappa-B signaling and shifting macrophage polarization toward an anti-inflammatory (M2) phenotype. TNIP3 is expressed in several tissues and is implicated in inflammatory and fibrotic cardiovascular conditions, as well as in hepatic and infectious disease settings. Its role in disease likely relates to its suppressive effect on pro-inflammatory and pro-fibrotic signaling pathways[1][2][5].

Other names

ABIN3ABIN-3LINDListeria-induced gene proteinFLJ21162TNFAIP3-interacting protein 3A20-binding inhibitor of NF-kappa-B activation 3TNIP3 beta

Negative regulation of inflammatory signaling via inhibition of PI3K/Akt/NF-kappa-B signaling; inhibition of TAK1 activation; promotion of M1 to M2 macrophage polarization