ArticleCellular and molecular life sciences : CMLS2022
Helicobacter pylori-induced reactive oxygen species direct turnover of CSN-associated STAMBPL1 and augment apoptotic cell death.
Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- Roles of JAMM-family deubiquitinase STAMBPL1 in cellular homeostasis and human cancer.Molecular biology reports · 2026Review
- Determination of microplastic-mediated oxidative stress responses and DNA damage in economically important fish species in the largest dam lakes (Keban, Karakaya, and Atatürk) of Türkiye.Fish physiology and biochemistry · 2026Article
- Cathepsin L deletion enhances sensitivity to anticancer drugs through Parkin-mediated ubiquitination of Bcl-xL and USP53-induced Survivin destabilization.Cell death and differentiation · 2026Article
- Helicobacter pylori activates the TRAF1/OASL/ZBP1-PANoptosome pathway to induce PANoptosis in the gastric mucosa.Apoptosis : an international journal on programmed cell death · 2026Article
- Helicobacter pylori infection promotes the progression of gastric cancer by regulating the expression of DMBT1.World journal of clinical oncology · 2025Article
- CSN-CRL Complexes: New Regulators of Adipogenesis.Biomolecules · 2025Review
- STAMBPL1/TRIM21 Balances AXL Stability Impacting Mesenchymal Phenotype and Immune Response in KIRC.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Dioscin inhibits non-small cell lung cancer cells and activates apoptosis by downregulation of Survivin.Journal of Cancer · 2024Article
- The footprint of gut microbiota in gallbladder cancer: a mechanistic review.Frontiers in cellular and infection microbiology · 2024Review
- Programmed cell death inFrontiers in cellular and infection microbiology · 2024Review
- Survivin degradation by bergenin overcomes pemetrexed resistance.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- Reactive Oxygen Species andAntioxidants (Basel, Switzerland) · 2023Review
- Regulatory mechanisms and therapeutic potential of JAB1 in neurological development and disorders.Molecular medicine (Cambridge, Mass.) · 2023Review
- Article
- Gastric Epithelial Barrier Disruption, Inflammation and Oncogenic Signal Transduction by Helicobacter pylori.Current topics in microbiology and immunology · 2023Review
- USP48 and A20 synergistically promote cell survival in Helicobacter pylori infection.Cellular and molecular life sciences : CMLS · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Deubiquitinylases (DUBs) are central regulators of the ubiquitin system involved in protein regulation and cell signalling and are important for a variety of physiological processes. Most DUBs are cysteine proteases, and few other proteases are metalloproteases of the JAB1/MPN +/MOV34 protease family (JAMM). STAM-binding protein like 1 (STAMBPL1), a member of the JAMM family, cleaves ubiquitin bonds and has a function in regulating cell survival, Tax-mediated nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and epithelial-mesenchymal transition. However, the molecular mechanism by which STAMBPL1 influences cell survival is not well defined, especially with regard to its deubiquitinylation function. Here, we show that reactive oxygen species (ROS) induced by chemotherapeutic agents or the human microbial pathogen Helicobacter pylori can induce cullin 1-RING ubiquitin ligase (CRL1) and 26S proteasome-dependent degradation STAMBPL1. Interestingly, STAMBPL1 has a direct interaction with the constitutive photomorphogenic 9 (COP9 or CSN) signalosome subunits CSN5 and CSN6. The interaction with the CSN is required for the stabilisation and function of the STAMBPL1 protein. In addition, STAMBPL1 deubiquitinylates the anti-apoptotic protein Survivin and thus ameliorates cell survival. In summary, our data reveal a previously unknown mechanism by which the deubiquitinylase STAMBPL1 and the E3 ligase CRL1 balance the level of Survivin degradation and thereby determine apoptotic cell death. In response to genotoxic stress, the degradation of STAMBPL1 augments apoptotic cell death. This new mechanism may be useful to develop therapeutic strategies targeting STAMBPL1 in tumours that have high STAMBPL1 and Survivin protein levels.
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