| TMEM16F phospholipid scramblase mediates trophoblast fusion and placental development. | TMEM16F phospholipid scramblase mediates trophoblast fusion and placental development.
Zhang Y, Le T, Grabau R, Mohseni Z, Kim H, Natale DR, Feng L, Pan H, Yang H., Free PMC Article | 04/16/2022 |
| TMEM16F mediates bystander TCR-CD3 membrane dissociation at the immunological synapse and potentiates T cell activation. | TMEM16F mediates bystander TCR-CD3 membrane dissociation at the immunological synapse and potentiates T cell activation.
Connolly A, Panes R, Tual M, Lafortune R, Bellemare-Pelletier A, Gagnon E. | 12/18/2021 |
| A novel mechanism of thrombocytopenia by PS exposure through TMEM16F in sphingomyelin synthase 1 deficiency. | A novel mechanism of thrombocytopenia by PS exposure through TMEM16F in sphingomyelin synthase 1 deficiency.
Fujii Y, Taniguchi M, Nagaya S, Ueda Y, Hashizume C, Watanabe K, Takeya H, Kosaka T, Okazaki T., Free PMC Article | 11/6/2021 |
| Anion and Cation Permeability of the Mouse TMEM16F Calcium-Activated Channel. | Anion and Cation Permeability of the Mouse TMEM16F Calcium-Activated Channel.
Stabilini S, Menini A, Pifferi S., Free PMC Article | 09/18/2021 |
| Ano6 disruption impairs acinar cell regulatory volume decrease and protein secretion in murine submandibular salivary glands. | Ano6 disruption impairs acinar cell regulatory volume decrease and protein secretion in murine submandibular salivary glands.
Munemasa T, Gao X, Melvin JE, Mukaibo T. | 03/20/2021 |
| Spinal Motoneuron TMEM16F Acts at C-boutons to Modulate Motor Resistance and Contributes to ALS Pathogenesis. | Spinal Motoneuron TMEM16F Acts at C-boutons to Modulate Motor Resistance and Contributes to ALS Pathogenesis.
Soulard C, Salsac C, Mouzat K, Hilaire C, Roussel J, Mezghrani A, Lumbroso S, Raoul C, Scamps F. | 03/20/2021 |
| Evidence that polyphenols do not inhibit the phospholipid scramblase TMEM16F. | Evidence that polyphenols do not inhibit the phospholipid scramblase TMEM16F.
Le T, Le SC, Zhang Y, Liang P, Yang H., Free PMC Article | 01/23/2021 |
| Critical Role of Lipid Scramblase TMEM16F in Phosphatidylserine Exposure and Repair of Plasma Membrane after Pore Formation. | Critical Role of Lipid Scramblase TMEM16F in Phosphatidylserine Exposure and Repair of Plasma Membrane after Pore Formation.
Wu N, Cernysiov V, Davidson D, Song H, Tang J, Luo S, Lu Y, Qian J, Gyurova IE, Waggoner SN, Trinh VQ, Cayrol R, Sugiura A, McBride HM, Daudelin JF, Labrecque N, Veillette A., Free PMC Article | 10/24/2020 |
| TMEM16F-promoted M1 polarization and -inhibited M1 polarization were largely associated with the suppression of ADAM17. | TMEM16F inhibition limits pain-associated behavior and improves motor function by promoting microglia M2 polarization in mice.
Zhao J, Gao QY. | 06/20/2020 |
| Here, the authors reveal features of murine TMEM16F (mTMEM16F) that underlie its function as a lipid scramblase and an ion channel. The cryo-EM data of mTMEM16F in absence and presence of Ca(2+) define the ligand-free closed conformation of the protein and the structure of a Ca(2+)-bound intermediate. | Cryo-EM structures and functional characterization of the murine lipid scramblase TMEM16F.
Alvadia C, Lim NK, Clerico Mosina V, Oostergetel GT, Dutzler R, Paulino C., Free PMC Article | 03/21/2020 |
| The dynamic change of ion selectivity suggests a charge-screening mechanism for TMEM16F ion conduction. | Dynamic change of electrostatic field in TMEM16F permeation pathway shifts its ion selectivity.
Ye W, Han TW, He M, Jan YN, Jan LY., Free PMC Article | 02/22/2020 |
| Study identified an inner activation gate, which is established by three hydrophobic residues, F518, Y563 and I612, in the middle of the phospholipid permeation pathway of TMEM16F-CaPLSase. Disrupting the inner gate profoundly alters TMEM16F phospholipid permeation. | An inner activation gate controls TMEM16F phospholipid scrambling.
Le T, Jia Z, Le SC, Zhang Y, Chen J, Yang H., Free PMC Article | 06/15/2019 |
| TMEM16F knockout did not affect Ca2+ signaling and Ca2+-activated whole cell currents in podocytes. TMEM16F shows little effect on basal properties of podocytes and does not appear to be essential for renal function. | Regulation and Function of TMEM16F in Renal Podocytes.
Schenk LK, Ousingsawat J, Skryabin BV, Schreiber R, Pavenstädt H, Kunzelmann K., Free PMC Article | 10/13/2018 |
| TMEM16F interaction with phosphatidylinositol-(4, 5)-bisphosphate works synergistically with membrane depolarization to facilitate Ca(2+)-gating of TMEM16F. | Phosphatidylinositol-(4, 5)-bisphosphate regulates calcium gating of small-conductance cation channel TMEM16F.
Ye W, Han TW, Nassar LM, Zubia M, Jan YN, Jan LY., Free PMC Article | 09/8/2018 |
| TMEM16F is an essential component of the microglial response to injury and suggest the importance of microglial phagocytosis in the pathogenesis of neuropathic pain. | TMEM16F Regulates Spinal Microglial Function in Neuropathic Pain States.
Batti L, Sundukova M, Murana E, Pimpinella S, De Castro Reis F, Pagani F, Wang H, Pellegrino E, Perlas E, Di Angelantonio S, Ragozzino D, Heppenstall PA., Free PMC Article | 10/14/2017 |
| The present data demonstrate the activation of ANO6 during necroptosis, which, however, is not essential for cell death. | Ca(2+) signals, cell membrane disintegration, and activation of TMEM16F during necroptosis.
Ousingsawat J, Cabrita I, Wanitchakool P, Sirianant L, Krautwald S, Linkermann A, Schreiber R, Kunzelmann K., Free PMC Article | 08/26/2017 |
| TMEM16F deficiency results in sustained signaling and augmented T cell activation. | Scramblase TMEM16F terminates T cell receptor signaling to restrict T cell exhaustion.
Hu Y, Kim JH, He K, Wan Q, Kim J, Flach M, Kirchhausen T, Vortkamp A, Winau F., Free PMC Article | 08/12/2017 |
| Platelet TMEM16F activity contributes significantly to hemostasis and thrombosis but not cerebral thromboinflammation. | TMEM16F-Mediated Platelet Membrane Phospholipid Scrambling Is Critical for Hemostasis and Thrombosis but not Thromboinflammation in Mice-Brief Report.
Baig AA, Haining EJ, Geuss E, Beck S, Swieringa F, Wanitchakool P, Schuhmann MK, Stegner D, Kunzelmann K, Kleinschnitz C, Heemskerk JW, Braun A, Nieswandt B. | 06/24/2017 |
| ANO6 produces volume-regulated anion currents and controls cell volume in four unrelated cell types. | Cellular volume regulation by anoctamin 6: Ca²⁺, phospholipase A2 and osmosensing.
Sirianant L, Ousingsawat J, Wanitchakool P, Schreiber R, Kunzelmann K. | 10/8/2016 |
| deficiency in Ano6 resulted in reduced viability with increased bleeding time | Survival protein anoctamin-6 controls multiple platelet responses including phospholipid scrambling, swelling, and protein cleavage.
Mattheij NJ, Braun A, van Kruchten R, Castoldi E, Pircher J, Baaten CC, Wülling M, Kuijpers MJ, Köhler R, Poole AW, Schreiber R, Vortkamp A, Collins PW, Nieswandt B, Kunzelmann K, Cosemans JM, Heemskerk JW. | 06/28/2016 |
| Although broadly expressed, Ano6 has no role in intestinal cholinergic Cl- secretion. | Anoctamins support calcium-dependent chloride secretion by facilitating calcium signaling in adult mouse intestine.
Schreiber R, Faria D, Skryabin BV, Wanitchakool P, Rock JR, Kunzelmann K. | 02/13/2016 |
| Ano6 mediates effects essential for innate immunity downstream of P2X7 receptors in macrophages. | Anoctamin 6 mediates effects essential for innate immunity downstream of P2X7 receptors in macrophages.
Ousingsawat J, Wanitchakool P, Kmit A, Romao AM, Jantarajit W, Schreiber R, Kunzelmann K. | 01/30/2016 |
| TMEM16F is required for phosphatidylserine exposure and microparticle release in activated mouse platelets. | TMEM16F is required for phosphatidylserine exposure and microparticle release in activated mouse platelets.
Fujii T, Sakata A, Nishimura S, Eto K, Nagata S., Free PMC Article | 01/30/2016 |
| Ano6 and Ano2 proteins co-localize in the ciliary membrane microdomains, which indicates a role for Ano6 in olfactory signaling. | Co-expression of anoctamins in cilia of olfactory sensory neurons.
Henkel B, Drose DR, Ackels T, Oberland S, Spehr M, Neuhaus EM. | 10/3/2015 |
| human osteoblasts and osteoblasts from Ano6(-/-) and WT mice, we demonstrate that NCX1 requires Ano6 to efficiently translocate Ca(2+) out of osteoblasts into the calcifying bone matrix | Anoctamin-6 controls bone mineralization by activating the calcium transporter NCX1.
Ousingsawat J, Wanitchakool P, Schreiber R, Wuelling M, Vortkamp A, Kunzelmann K., Free PMC Article | 05/23/2015 |