ArticleCell reports2020
Critical Role of Lipid Scramblase TMEM16F in Phosphatidylserine Exposure and Repair of Plasma Membrane after Pore Formation.
Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
61 citing papers in PubMed, 107 citations in OpenAlex.
- TMEM16F deficiency alleviates sepsis-induced acute lung injury through regulating macrophage polarization.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Protocol for laser-induced plasma membrane and cell wall damage in budding yeast.STAR protocols · 2026Article
- The Xkr protein family-From apoptosis executors to diverse physiological functions regulators.FEBS letters · 2026Review
- Niflumic acid suppresses NLRP3 inflammasome activation by limiting chloride efflux and mitochondrial ROS production.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Peculiarities of Phosphatidylserine Externalization by Nano- and Microsecond Electric Pulses.The Journal of membrane biology · 2026Article
- Recent advances in TMEM16F: structural plasticity, functional versatility, and implications for human diseases.Cell communication and signaling : CCS · 2026Review
- Lipid asymmetry disruption by XKR8 orchestrates neutrophil extracellular trap formation and inhibits fungal infection.Nature immunology · 2026Article
- Calcium dependent activation of the TMEM16F scramblase and ion channel.Nature structural & molecular biology · 2026Article
- Article
- The fungal peptide toxin candidalysin induces distinct membrane repair mechanisms compared to bacterial pore-forming toxins.Cell death discovery · 2025Article
- Phospholipid scramblases TMEM16F and Xkr8 mediate distinct features of phosphatidylserine (PS) externalization and immune suppression to promote tumor growth.Cell death discovery · 2025Article
- A cell-based scrambling assay reveals the phospholipid headgroup preference of TMEM16F on the plasma membrane.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Assessing Extracellular Vesicle Turnover In Vivo Using Highly Sensitive Phosphatidylserine-Binding Reagents.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cellular Adaptation to Mechanical Stress Emerges via Cell Shrinkage Triggered by Nonlinear Calcium Elevation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Targeting lipid scrambling potentiates ferroptosis and triggers tumor immune rejection.Science advances · 2025Article
- Calpains orchestrate secretion of annexin-containing microvesicles during membrane repair.The Journal of cell biology · 2025Article
- A cell-based scrambling assay reveals phospholipid headgroup preference of TMEM16F on the plasma membrane.bioRxiv : the preprint server for biology · 2025Article
- The Multifaceted Role of Calcium Signaling in Regulated Necrosis.Biomolecules · 2025Review
- CD200R1-CD200 checkpoint inhibits phagocytosis differently from SIRPα-CD47 to suppress tumor growth.Nature communications · 2025Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 8 institutions in 3 countries.
Funding
Abstract
Plasma membrane damage and cell death during processes such as necroptosis and apoptosis result from cues originating intracellularly. However, death caused by pore-forming agents, like bacterial toxins or complement, is due to direct external injury to the plasma membrane. To prevent death, the plasma membrane has an intrinsic repair ability. Here, we found that repair triggered by pore-forming agents involved TMEM16F, a calcium-activated lipid scramblase also mutated in Scott's syndrome. Upon pore formation and the subsequent influx of intracellular calcium, TMEM16F induced rapid "lipid scrambling" in the plasma membrane. This response was accompanied by membrane blebbing, extracellular vesicle release, preserved membrane integrity, and increased cell viability. TMEM16F-deficient mice exhibited compromised control of infection by Listeria monocytogenes associated with a greater sensitivity of neutrophils to the pore-forming Listeria toxin listeriolysin O (LLO). Thus, the lipid scramblase TMEM16F is critical for plasma membrane repair after injury by pore-forming agents.
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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.