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A20 undermines alternative NF-κB activity and expression of anti-apoptotic genes in Helicobacter pylori infection
Ist Teil von
Cellular and molecular life sciences : CMLS, 2022-02, Vol.79 (2), p.102-102, Article 102
Ort / Verlag
Cham: Springer International Publishing
Erscheinungsjahr
2022
Link zum Volltext
Quelle
MEDLINE
Beschreibungen/Notizen
A hallmark of infection by the pathogen
Helicobacter pylori
, which colonizes the human gastric epithelium, is the simultaneous activation of the classical and alternative nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathways, underlying inflammation and cell survival. Here, we report that the classical NF-κB target gene product A20 contributes to the negative regulation of alternative NF-κB signaling in gastric epithelial cells infected by
H. pylori
. Mechanistically, the de novo synthesized A20 protein interacts with tumor necrosis factor receptor-associated factor-interacting protein with forkhead-associated domain (TIFA) and thereby interferes with the association of TIFA with the NIK regulatory complex. We also show that alternative NF-κB activity contributes to the up-regulation of anti-apoptotic genes, such as baculoviral IAP repeat containing 2 (
BIRC2)
,
BIRC3
and B-cell lymphoma 2-related protein A1 (
BCL2A1)
in gastric epithelial cells. Furthermore, the observed over-expression of RelB in human gastric biopsies with type B gastritis and RelB-dependent suppression of apoptotic cell death emphasize an important role of the alternative NF-κB pathway in
H. pylori
infection.