ArticleNature2010
Calcium-dependent phospholipid scrambling by TMEM16F.
Article in Nature, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 540 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
540 citing papers in PubMed, 969 citations in OpenAlex.
- Lipid flip-flop in biological membranes: through the lens of TMEM16F.Physiological reviews · 2027Review
- Towards a systematic understanding of the diverse subtypes, biogenesis and functions of large extracellular vesicles.Nature reviews. Molecular cell biology · 2026Review
- Review
- NINJ1: implications for plasma membrane rupture and disease.Biochemical Society transactions · 2026Review
- Distinct structural mechanisms drive gain-of-function activation of TMEM16E in gnathodiaphyseal dysplasia.Research square · 2026Article
- Protocol for laser-induced plasma membrane and cell wall damage in budding yeast.STAR protocols · 2026Article
- Article
- RAP1-RHO small GTPase cross-talk mediates integrindependent and -independent platelet procoagulant response.Haematologica · 2026Article
- The membrane transition strongly enhances biopolymer condensation through prewetting.Nature chemical biology · 2026Article
- The Xkr protein family-From apoptosis executors to diverse physiological functions regulators.FEBS letters · 2026Review
- Quantifying interleaflet coupling of phase behavior and observing anti-registered phases in asymmetric lipid bilayers.Biophysical journal · 2026Article
- Phosphatidylserine exposure and cancer immune evasion.Cell research · 2026Article
- Physical and Mechanobiological Basis of Biological Functions of Platelets.Thrombosis and haemostasis · 2026Review
- Procoagulant platelets: linking coagulation and thromboinflammation in cardiovascular disease.Nature reviews. Cardiology · 2026Review
- A single-vesicle fluorescence microscopy platform to quantify phospholipid scrambling.Nature structural & molecular biology · 2026Article
- Anoctamin 5 as a protective factor in prostate cancer: Insights from WGCNA, machine learning, and experimental analysis, with a focus on the anoctamin family.Translational oncology · 2026Article
- An ER-IMC bridge protein TgVPS13A and an IMC-resident scramblase TgDAT1 drive daughter budding in Toxoplasma gondii.PLoS pathogens · 2026Article
- Four subtypes of disease-causing missense mutations underlie pathogenic protein interactions in neurodegenerative VPS13A disease.The Journal of clinical investigation · 2026Article
- Flipping sides in NETosis.Nature immunology · 2026Article
- Functional Divergence and Emerging Roles of the ANO-TMC-TMEM63 Channel Families in Olfaction and Gustation.International journal of molecular sciences · 2026Review
480 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In all animal cells, phospholipids are asymmetrically distributed between the outer and inner leaflets of the plasma membrane. This asymmetrical phospholipid distribution is disrupted in various biological systems. For example, when blood platelets are activated, they expose phosphatidylserine (PtdSer) to trigger the clotting system. The PtdSer exposure is believed to be mediated by Ca(2+)-dependent phospholipid scramblases that transport phospholipids bidirectionally, but its molecular mechanism is still unknown. Here we show that TMEM16F (transmembrane protein 16F) is an essential component for the Ca(2+)-dependent exposure of PtdSer on the cell surface. When a mouse B-cell line, Ba/F3, was treated with a Ca(2+) ionophore under low-Ca(2+) conditions, it reversibly exposed PtdSer. Using this property, we established a Ba/F3 subline that strongly exposed PtdSer by repetitive fluorescence-activated cell sorting. A complementary DNA library was constructed from the subline, and a cDNA that caused Ba/F3 to expose PtdSer spontaneously was identified by expression cloning. The cDNA encoded a constitutively active mutant of TMEM16F, a protein with eight transmembrane segments. Wild-type TMEM16F was localized on the plasma membrane and conferred Ca(2+)-dependent scrambling of phospholipids. A patient with Scott syndrome, which results from a defect in phospholipid scrambling activity, was found to carry a mutation at a splice-acceptor site of the gene encoding TMEM16F, causing the premature termination of the protein.
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What OpenQuestion holds
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.