TIFA has dual functions in Helicobacter pylori-induced classical and alternative NF-kB pathways

ABSTRACT: Helicobacter pylori infection constitutes one of the major risk factors for the development of gastric diseases including gastric cancer. Activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) via the classical and alternative pathways is a hallmark of H. pylori infection leading to inflammation in gastric epithelial cells. Tumor necrosis factor receptor associated factor (TRAF) interacting protein with forkhead-associated domain (TIFA) was previously suggested to trigger classical NF-kB activation but its role in alternative NF-kB activation remains unexplored. Here, we identify TRAF6 and TRAF2 as binding partners of TIFA contributing to the formation of TIFAsomes upon H. pylori infection. Importantly, the TIFA/TRAF6 interaction enables binding of TGFb-activa

SUBMITTER: Prof. Michael Naumann 

PROVIDER: S-SCDT-EMBOR-2021-52878V1 | biostudies-other |

REPOSITORIES: biostudies-other