ArticleCell death and differentiation2017
Pathogen-induced ubiquitin-editing enzyme A20 bifunctionally shuts off NF-κB and caspase-8-dependent apoptotic cell death.
Article in Cell death and differentiation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 65 citations in OpenAlex.
- The ubiquitin-editing enzyme A20 (TNFAIP3): mechanisms of activation, biological function, diseases and therapeutic targets.Molecular biomedicine · 2026Review
- Sphingomonas paucimobilis-Driven Epithelial-Endothelial Transition in Adenomyosis Pathogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Exploring the role of the key gene TNFAIP3 between periodontitis and influenza A through bioinformatic analysis and molecular docking.PloS one · 2026Article
- Interplay between pathogen-mediated immune evasion and innate immune negative regulation in gastrointestinal tumors.Frontiers in immunology · 2026Review
- Update on the pathogenesis and clinical management ofWorld journal of gastrointestinal pathophysiology · 2025Review
- Dissecting the dual role of OTU family proteins in tumor progression and immune escape.Frontiers in immunology · 2025Review
- Inflammatory factors collaboratively linkFrontiers in immunology · 2025Review
- Differential expression of the ubiquitin-editing enzyme A20 in gastric biopsies indicates the severity of disease.Histochemistry and cell biology · 2024Article
- Genetic Mutations Associated With TNFAIP3 (A20) Haploinsufficiency and Their Impact on Inflammatory Diseases.International journal of molecular sciences · 2024Review
- Cytoplasmic TP53INP2 acts as an apoptosis partner in TRAIL treatment: the synergistic effect of TRAIL with venetoclax in TP53INP2-positive acute myeloid leukemia.Journal of experimental & clinical cancer research : CR · 2024Article
- The Complexity of Being A20: From Biological Functions to Genetic Associations.Journal of clinical immunology · 2024Review
- NF-κB/RelA controlled A20 limits TRAIL-induced apoptosis in pancreatic cancer.Cell death & disease · 2023Article
- The emerging role and therapeutic implications of bacterial and parasitic deubiquitinating enzymes.Frontiers in immunology · 2023Review
- Gastric Epithelial Barrier Disruption, Inflammation and Oncogenic Signal Transduction by Helicobacter pylori.Current topics in microbiology and immunology · 2023Review
- Review
- USP48 and A20 synergistically promote cell survival in Helicobacter pylori infection.Cellular and molecular life sciences : CMLS · 2022Article
- A20 undermines alternative NF-κB activity and expression of anti-apoptotic genes in Helicobacter pylori infection.Cellular and molecular life sciences : CMLS · 2022Article
- Helicobacter pylori-induced reactive oxygen species direct turnover of CSN-associated STAMBPL1 and augment apoptotic cell death.Cellular and molecular life sciences : CMLS · 2022Article
- Advances in the Study of the Ubiquitin-Editing Enzyme A20.Frontiers in pharmacology · 2022Review
- An Overview of Autophagy inFrontiers in cellular and infection microbiology · 2022Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human pathogen Helicobacter pylori infects more than half of the world's population and is a paradigm for persistent yet asymptomatic infection but increases the risk for chronic gastritis and gastric adenocarcinoma. For successful colonization, H. pylori needs to subvert the host cell death response, which serves to confine pathogen infection by killing infected cells and preventing malignant transformation. Infection of gastric epithelial cells by H. pylori provokes direct and fast activation of the proinflammatory and survival factor NF-κB, which regulates target genes, such as CXCL8, BIRC3 and TNFAIP3. However, it is not known how H. pylori exploits NF-κB activation and suppresses the inflammatory response and host apoptotic cell death, in order to avert the innate immune response and avoid cell loss, and thereby enhance colonization to establish long-term infection. Here we assign for the first time that H. pylori and also Campylobacter jejuni-induced ubiquitin-editing enzyme A20 bifunctionally terminates NF-κB activity and negatively regulates apoptotic cell death. Mechanistically, we show that the deubiquitinylase activity of A20 counteracts cullin3-mediated K63-linked ubiquitinylation of procaspase-8, therefore restricting the activity of caspase-8. Interestingly, another inducible NF-κB target gene, the scaffold protein p62, ameliorates the interaction of A20 with procaspase-8. In conclusion, pathogen-induced de novo synthesis of A20 regulates the shut-off of the survival factor NF-κB but, on the other hand, also impedes caspase-8-dependent apoptotic cell death so as to promote the persistence of pathogens.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.