TMEM16F Forms a Ca2+-Activated Cation Channel Required for Lipid Scrambling in Platelets during Blood Coagulation-Reference-Cited by-同舟云学术

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TMEM16F Forms a Ca2+-Activated Cation Channel Required for Lipid Scrambling in Platelets during Blood Coagulation

Published:2012-09 Issue:1 Volume:151 Page:111-122
ISSN:0092-8674
Container-title:Cell
language:en
Short-container-title:Cell

Author:

Yang Huanghe,Kim Andrew,David Tovo,Palmer Daniel,Jin Taihao,Tien Jason,Huang Fen,Cheng Tong,Coughlin Shaun R.,Jan Yuh Nung,Jan Lily Yeh

Publisher

Elsevier BV

Subject

General Biochemistry, Genetics and Molecular Biology

Reference44 articles.

1. TMEM16 proteins produce volume-regulated chloride currents that are reduced in mice lacking TMEM16A;Almaça;J. Biol. Chem.,2009

2. ANO1 amplification and expression in HNSCC with a high propensity for future distant metastasis and its functions in HNSCC cell lines;Ayoub;Br. J. Cancer,2010

3. Phospholipid scramblase: an update;Bevers;FEBS Lett.,2010

4. Changes in membrane phospholipid distribution during platelet activation;Bevers;Biochim. Biophys. Acta,1983

5. TMEM16A, a membrane protein associated with calcium-dependent chloride channel activity;Caputo;Science,2008

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1. 4D intravital imaging studies identify platelets as the predominant cellular procoagulant surface in a mouse hemostasis model;Blood;2024-09-05

2. SLAPSHOT reveals rapid dynamics of extracellularly exposed proteome in response to calcium-activated plasma membrane phospholipid scrambling;Communications Biology;2024-08-29

3. TMEM16F Expressed in Kupffer Cells Regulates Liver Inflammation and Metabolism to Protect Against Listeria Monocytogenes;Advanced Science;2024-08-13

4. Unexpected bleeding with platelet phosphatidylserine exposure defect: new kindred motivates rethinking Scott syndrome;Journal of Thrombosis and Haemostasis;2024-08

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