ArticleThe Journal of biological chemistry2014
AMPylation of Rho GTPases subverts multiple host signaling processes.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 45 citations in OpenAlex.
- AMPylation: key roles in biological regulation across prokaryotes and eukaryotes.Frontiers in cellular and infection microbiology · 2026Review
- Pseudomonas gelidaquae sp. nov., an Antarctic bacterium with a distinctive Type III Secretion System, isolated from Fildes Bay, King George Island.Antonie van Leeuwenhoek · 2025Article
- Protein feature engineering framework for AMPylation site prediction.Scientific reports · 2024Article
- Mitogen-Activated Protein Kinases (MAPKs) and Enteric Bacterial Pathogens: A Complex Interplay.International journal of molecular sciences · 2023Review
- AMPylation of small GTPases by Fic enzymes.FEBS letters · 2023Review
- Activity-based Tools for Interrogating Host Biology During Infection.Israel journal of chemistry · 2023Article
- Role of Host Small GTPases in Apicomplexan Parasite Infection.Microorganisms · 2022Review
- Persistent Escherichia coli infection in renal tubular cells enhances calcium oxalate crystal-cell adhesion by inducing ezrin translocation to apical membranes via Rho/ROCK pathway.Cellular and molecular life sciences : CMLS · 2022Article
- Bacterial Toxin and Effector Regulation of Intestinal Immune Signaling.Frontiers in cell and developmental biology · 2022Review
- Fic and non-Fic AMPylases: protein AMPylation in metazoans.Open biology · 2021Article
- Manipulation of IRE1-Dependent MAPK Signaling by a Vibrio Agonist-Antagonist Effector Pair.mSystems · 2021Article
- Ubiquitination-Dependent Regulation of Small GTPases in Membrane Trafficking: From Cell Biology to Human Diseases.Frontiers in cell and developmental biology · 2021Review
- MS-BasedACS infectious diseases · 2020Article
- TheScience signaling · 2020Article
- Structural basis of inactivation of Ras and Rap1 small GTPases by Ras/Rap1-specific endopeptidase from the sepsis-causing pathogenThe Journal of biological chemistry · 2018Article
- Article
- rAMPing Up Stress Signaling: Protein AMPylation in Metazoans.Trends in cell biology · 2017Review
- Article
- T3SS effector VopL inhibits the host ROS response, promoting the intracellular survival of Vibrio parahaemolyticus.PLoS pathogens · 2017Article
- The cytotoxic type 3 secretion system 1 ofScience signaling · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Rho GTPases are frequent targets of virulence factors as they are keystone signaling molecules. Herein, we demonstrate that AMPylation of Rho GTPases by VopS is a multifaceted virulence mechanism that counters several host immunity strategies. Activation of NFκB, Erk, and JNK kinase signaling pathways were inhibited in a VopS-dependent manner during infection with Vibrio parahaemolyticus. Phosphorylation and degradation of IKBα were inhibited in the presence of VopS as was nuclear translocation of the NFκB subunit p65. AMPylation also prevented the generation of superoxide by the phagocytic NADPH oxidase complex, potentially by inhibiting the interaction of Rac and p67. Furthermore, the interaction of GTPases with the E3 ubiquitin ligases cIAP1 and XIAP was hindered, leading to decreased degradation of Rac and RhoA during infection. Finally, we screened for novel Rac1 interactions using a nucleic acid programmable protein array and discovered that Rac1 binds to the protein C1QA, a protein known to promote immune signaling in the cytosol. Interestingly, this interaction was disrupted by AMPylation. We conclude that AMPylation of Rho Family GTPases by VopS results in diverse inhibitory consequences during infection beyond the most obvious phenotype, the collapse of the actin cytoskeleton.
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Registered trials
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.