ArticleScience advances2022
Membrane repair triggered by cholesterol-dependent cytolysins is activated by mixed lineage kinases and MEK.
Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- From pathogenic to reparative: Context-Dependent function of extracellular vesicles in osteoarthritis.Bioactive materials · 2027Review
- Vav2 is a master regulator of repair against bacterial pore-forming toxins.Life science alliance · 2026Article
- Epigenetic Mechanisms in Sepsis-Induced Cardiomyopathy: From Pathophysiology to Therapeutic Targets.International journal of molecular sciences · 2026Review
- Functional Dissection ofToxins · 2026Article
- The fungal peptide toxin candidalysin induces distinct membrane repair mechanisms compared to bacterial pore-forming toxins.Cell death discovery · 2025Article
- Type A cholesterol-dependent cytolysins translocate to the trans-Golgi network for NLRP3 inflammasome activation.Nature immunology · 2025Article
- The septin cytoskeleton is required for plasma membrane repair.EMBO reports · 2024Article
- Deficiency of macrophage-derived Dnase1L3 causes lupus-like phenotypes in mice.Journal of leukocyte biology · 2023Article
- Early Endosomes Undergo Calcium-Triggered Exocytosis and Enable Repair of Diffuse and Focal Plasma Membrane Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Translational implications of targeting annexin A2: From membrane repair to muscular dystrophy, cardiovascular disease and cancer.Clinical and translational discovery · 2023Article
- Patch repair protects cells from the small pore-forming toxin aerolysin.Journal of cell science · 2023Article
- Deciphering the Molecular Mechanism and Function of Pore-Forming Toxins using Leishmania major.Journal of visualized experiments : JoVE · 2022Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Repair of plasma membranes damaged by bacterial pore-forming toxins, such as streptolysin O or perfringolysin O, during septic cardiomyopathy or necrotizing soft tissue infections is mediated by several protein families. However, the activation of these proteins downstream of ion influx is poorly understood. Here, we demonstrate that following membrane perforation by bacterial cholesterol-dependent cytolysins, calcium influx activates mixed lineage kinase 3 independently of protein kinase C or ceramide generation. Mixed lineage kinase 3 uncouples mitogen-activated kinase kinase (MEK) and extracellular-regulated kinase (ERK) signaling. MEK signals via an ERK-independent pathway to promote rapid annexin A2 membrane recruitment and enhance microvesicle shedding. This pathway accounted for 70% of all calcium ion-dependent repair responses to streptolysin O and perfringolysin O, but only 50% of repair to intermedilysin. We conclude that mixed lineage kinase signaling via MEK coordinates microvesicle shedding, which is critical for cellular survival against cholesterol-dependent cytolysins.
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Registered trials
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