Evidence map›Paper›PMID 26417084›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2015

TMEM16F is required for phosphatidylserine exposure and microparticle release in activated mouse platelets.

Toshihiro Fujii, Asuka Sakata, Satoshi Nishimura, Koji Eto, Shigekazu Nagata

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers.

0numbers the graph read from it
0cells of the map it votes in
149citing papers in PubMed
8.3field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

149 citing papers in PubMed, 250 citations in OpenAlex.

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  10. Platelet effector functions in inflammation.Research and practice in thrombosis and haemostasis · 2026
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89 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 4 institutions in 1 country.

Toshihiro FujiiLaboratory of Biochemistry & Immunology, Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan; Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Saitama 332-0012, Japan;
Asuka SakataCenter for Molecular Medicine, Jichi Medical University, Tochigi 329-0498, Japan;
Satoshi NishimuraCenter for Molecular Medicine, Jichi Medical University, Tochigi 329-0498, Japan; Department of Cardiovascular Medicine, The University of Tokyo, Tokyo 113-0033, Japan;
Koji EtoDepartment of Clinical Application, Center for iPS Cell Research and Application, Kyoto University, Kyoto 606-8507, Japan.
Shigekazu NagataLaboratory of Biochemistry & Immunology, Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan; Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Saitama 332-0012, Japan; snagata@ifrec.osaka-u.ac.jp.
Osaka University · JPJichi Medical University · JPKyoto University · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phosphatidylserine (PtdSer) exposure on the surface of activated platelets requires the action of a phospholipid scramblase(s), and serves as a scaffold for the assembly of the tenase and prothrombinase complexes involved in blood coagulation. Here, we found that the activation of mouse platelets with thrombin/collagen or Ca(2+) ionophore at 20 °C induces PtdSer exposure without compromising plasma membrane integrity. Among five transmembrane protein 16 (TMEM16) members that support Ca(2+)-dependent phospholipid scrambling, TMEM16F was the only one that showed high expression in mouse platelets. Platelets from platelet-specific TMEM16F-deficient mice exhibited defects in activation-induced PtdSer exposure and microparticle shedding, although α-granule and dense granule release remained intact. The rate of tissue factor-induced thrombin generation by TMEM16F-deficient platelets was severely reduced, whereas thrombin-induced clot retraction was unaffected. The imaging of laser-induced thrombus formation in whole animals showed that PtdSer exposure on aggregated platelets was TMEM16F-dependent in vivo. The phenotypes of the platelet-specific TMEM16F-null mice resemble those of patients with Scott syndrome, a mild bleeding disorder, indicating that these mice may provide a useful model for human Scott syndrome.

Indexed as

Platelet ActivationAnimalsAnoctaminsBlood CoagulationBlood Coagulation DisordersBlood PlateletsCalciumCell-Derived MicroparticlesDisease Models, AnimalHumansMiceMice, Mutant StrainsPhosphatidylserinesPhospholipid Transfer ProteinsThrombinANO6 protein, humanANO6 protein, mouseAnoctaminsCalciumPhosphatidylserinesPhospholipid Transfer ProteinsThrombincalciummicrovesiclesphosphatidylserineplateletsscramblase

Identifiers

PMID26417084
PMCPMC4611630
OpenAlexW2197048458

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.