Calcium-dependent phospholipid scrambling by TMEM16F

By Jun Suzuki, M. Umeda, P. Sims, S. Nagata. Nature, 2010

926 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/3ebb6e1c2cb867e07e7d631c2dfcb39c6b00249c

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Citations in the corpus

Phosphatidylserine is a global immunosuppressive signal in efferocytosis, infectious disease, and cancer (2016, background): “Loss-of-function mutation in TMEM16F is associated with Scott’s syndrome, a rare bleeding disorder characterized by defects in calciumdependent phospholipid scrambling, suggesting that it is the predominant scramblase for externalizing PS in platelets.(19,21)”
An Apoptotic 'Eat Me' Signal: Phosphatidylserine Exposure. (2015, background): “Recently, twomembrane proteins responsible for phospholipid scrambling have been identified: transmembrane protein 16F (TMEM16F) and Xk-related protein 8 (Xkr8) [34,35] (Figure 1).”
Handbook of ion channels (2015, background): “TMEM16F is responsible for calcium-dependent phospholipid scrambling, which may be enhanced by an aspartate to glycine mutation of TMEM16F in a B cell line (Suzuki et al., 2010).”
Focus on Extracellular Vesicles: Introducing the Next Small Big Thing (2016, background): “Recent work by Nagata finally identified transmembrane protein 16F (TMEM16F) as the elusive calcium-dependent phospholipid scramblase [75].”
Neuronal Cell Death. (2018, positive): “However, phosphatidylserine can be reversibly exposed on viable cells as a result of calcium activation of the scramblase TMEM16F (658, 660) or temporary lowering of ATP, which is required for translocase activation.”
Extracellular sphingomyelinase activity impairs TNF-α-induced endothelial cell death via ADAM17 activation and TNF receptor 1 shedding (2017, background): “Indeed, the Ca2+-chelator EGTA markedly reduced phospholipid externalization in COS7 cells and in HUVECs (Figure 3A) at any time point without affecting the SMase activity itself (Figure 3B).”
New fundamentals in hemostasis. (2013, background): “On the basis of genetic analysis of patients with Scott syndrome, whose platelets are deficient in phosphatidylserine exposure, the membrane protein TMEM16F has now been recognized as a good candidate protein implicated in phospholipid scrambling (282).”