A20 undermines alternative NF-kappa B activity and expression of anti-apoptotic genes in Helicobacter pylori infection

Lim MCC, Maubach G, Birkl-Toeglhofer AM, Haybaeck J, Vieth M, Naumann M (2022)


Publication Type: Journal article

Publication year: 2022

Journal

Book Volume: 79

Journal Issue: 2

DOI: 10.1007/s00018-022-04139-y

Abstract

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-kappa B) pathways, underlying inflammation and cell survival. Here, we report that the classical NF-kappa B target gene product A20 contributes to the negative regulation of alternative NF-kappa B 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-kappa B 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-kappa B pathway in H. pylori infection.

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APA:

Lim, M.C.C., Maubach, G., Birkl-Toeglhofer, A.M., Haybaeck, J., Vieth, M., & Naumann, M. (2022). A20 undermines alternative NF-kappa B activity and expression of anti-apoptotic genes in Helicobacter pylori infection. Cellular and Molecular Life Sciences, 79(2). https://doi.org/10.1007/s00018-022-04139-y

MLA:

Lim, Michelle C. C., et al. "A20 undermines alternative NF-kappa B activity and expression of anti-apoptotic genes in Helicobacter pylori infection." Cellular and Molecular Life Sciences 79.2 (2022).

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