ArticleThe Journal of cell biology2008
Repair of injured plasma membrane by rapid Ca2+-dependent endocytosis.
Article in The Journal of cell biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 248 papers.
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Who cites it
248 citing papers in PubMed.
- Quantitative Analysis of Plasmid DNA Distribution and Transgene Expression Following Cell Squeezing.Annals of biomedical engineering · 2026Article
- The ALS- and FTD-associated proteins annexin A11 and CHMP2B act sequentially in plasma membrane repair.Developmental cell · 2026Article
- Viscous drag-induced self-regeneration of laser-dissected actin stress fibers: A potential mechanism for mechanical memory.Mechanobiology in medicine · 2026Article
- TOLLIP targets GSDME-NT-carrying endocytic vesicles for autophagy to regulate pyroptosis and chemotherapy efficacy.Nature cell biology · 2026Article
- Article
- The toxic effects of α-hemolysin and β-hemolysin produced byFrontiers in immunology · 2026Review
- Organelles and cancer cell pyroptosis: overview and perspectives.Cell death & disease · 2025Review
- Mechanistic insights into the dynamics of plasma membrane repair in cancer.Molecular biology reports · 2025Review
- Lands' Cycle at the Crossroads: Phospholipid Remodelling, Oxidative Stress, Cellular Toxicity, and Therapeutic Targeting.ACS pharmacology & translational science · 2025Review
- Programmed cell revival from imminent cell death enhances tissue repair and regeneration.The EMBO journal · 2025Article
- Cell-Surface LAMP1 is a Senescence Marker in Aging and Idiopathic Pulmonary Fibrosis.Aging cell · 2025Article
- Functional identification of Annexin B1 and Annexin B2 from Cysticercus cellulosae and their mechanism in plasma membrane repair.PLoS neglected tropical diseases · 2025Article
- Holistic Investigation of Graphene Quantum Dot Endocytosis.Small (Weinheim an der Bergstrasse, Germany) · 2025Article
- Activation of TMEM16E scramblase induces ligand independent growth factor receptor signaling and macropinocytosis for membrane repair.Communications biology · 2025Article
- Theoretical Study of Sphingomyelinases fromPathogens (Basel, Switzerland) · 2025Article
- Reversible CaUltrasonics sonochemistry · 2025Article
- Membrane Tension Regulation is Required for Wound Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The septin cytoskeleton is required for plasma membrane repair.EMBO reports · 2024Article
- Bacterial pore-forming toxin pneumolysin drives pathogenicity through host extracellular vesicles released during infection.iScience · 2024Article
- Calcium influx rapidly establishes distinct spatial recruitments of Annexins to cell wounds.Genetics · 2024Article
188 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Ca2+ influx through plasma membrane lesions triggers a rapid repair process that was previously shown to require the exocytosis of lysosomal organelles (Reddy, A., E. Caler, and N. Andrews. 2001. Cell. 106:157-169). However, how exocytosis leads to membrane resealing has remained obscure, particularly for stable lesions caused by pore-forming proteins. In this study, we show that Ca2+-dependent resealing after permeabilization with the bacterial toxin streptolysin O (SLO) requires endocytosis via a novel pathway that removes SLO-containing pores from the plasma membrane. We also find that endocytosis is similarly required to repair lesions formed in mechanically wounded cells. Inhibition of lesion endocytosis (by sterol depletion) inhibits repair, whereas enhancement of endocytosis through disruption of the actin cytoskeleton facilitates resealing. Thus, endocytosis promotes wound resealing by removing lesions from the plasma membrane. These findings provide an important new insight into how cells protect themselves not only from mechanical injury but also from microbial toxins and pore-forming proteins produced by the immune system.
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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.