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Artykuły w czasopismach na temat „TREK1”

Autor: Grafiati

Data publikacji: 6 września 2023

Data aktualizacji: 31 lipca 2025

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1

Levitz, Joshua, Perrine Royal, Yannick Comoglio, et al. "Heterodimerization within the TREK channel subfamily produces a diverse family of highly regulated potassium channels." Proceedings of the National Academy of Sciences 113, no. 15 (2016): 4194–99. http://dx.doi.org/10.1073/pnas.1522459113.

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Twik-related K+ channel 1 (TREK1), TREK2, and Twik-related arachidonic-acid stimulated K+ channel (TRAAK) form the TREK subfamily of two-pore-domain K+ (K2P) channels. Despite sharing up to 78% sequence homology and overlapping expression profiles in the nervous system, these channels show major differences in their regulation by physiological stimuli. For instance, TREK1 is inhibited by external acidification, whereas TREK2 is activated. Here, we investigated the ability of the members of the TREK subfamily to assemble to form functional heteromeric channels with novel properties. Using singl

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2

Kim, Seong-Seop, Jimin Park, Eunju Kim, Eun Mi Hwang та Jae-Yong Park. "β-COP Suppresses the Surface Expression of the TREK2". Cells 12, № 11 (2023): 1500. http://dx.doi.org/10.3390/cells12111500.

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K2P channels, also known as two-pore domain K+ channels, play a crucial role in maintaining the cell membrane potential and contributing to potassium homeostasis due to their leaky nature. The TREK, or tandem of pore domains in a weak inward rectifying K+ channel (TWIK)-related K+ channel, subfamily within the K2P family consists of mechanical channels regulated by various stimuli and binding proteins. Although TREK1 and TREK2 within the TREK subfamily share many similarities, β-COP, which was previously known to bind to TREK1, exhibits a distinct binding pattern to other members of the TREK s

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3

Bai, Xilian, George J. Bugg, Susan L. Greenwood, et al. "Expression of TASK and TREK, two-pore domain K+ channels, in human myometrium." Reproduction 129, no. 4 (2005): 525–30. http://dx.doi.org/10.1530/rep.1.00442.

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Two-pore domain K+channels are an emerging family of K+channels that may contribute to setting membrane potential in both electrically excitable and non-excitable cells and, as such, influence cellular function. The human uteroplacental unit contains both excitable (e.g. myometrial) and non-excitable cells, whose function depends upon the activity of K+channels. We have therefore investigated the expression of two members of this family, TWIK (two-pore domain weak inward rectifying K+channel)-related acid-sensitive K+channel (TASK) and TWIK-related K+channel (TREK) in human myometrium. Using R

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4

Afzali, Ali M., Tobias Ruck, Alexander M. Herrmann, et al. "The potassium channels TASK2 and TREK1 regulate functional differentiation of murine skeletal muscle cells." American Journal of Physiology-Cell Physiology 311, no. 4 (2016): C583—C595. http://dx.doi.org/10.1152/ajpcell.00363.2015.

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Two-pore domain potassium (K2P) channels influence basic cellular parameters such as resting membrane potential, cellular excitability, or intracellular Ca2+-concentration [Ca2+]i. While the physiological importance of K2P channels in different organ systems (e.g., heart, central nervous system, or immune system) has become increasingly clear over the last decade, their expression profile and functional role in skeletal muscle cells (SkMC) remain largely unknown. The mouse SkMC cell line C2C12, wild-type mouse muscle tissue, and primary mouse muscle cells (PMMs) were analyzed using quantitativ

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5

Blin, Sandy, Ismail Ben Soussia, Eun-Jin Kim, et al. "Mixing and matching TREK/TRAAK subunits generate heterodimeric K2P channels with unique properties." Proceedings of the National Academy of Sciences 113, no. 15 (2016): 4200–4205. http://dx.doi.org/10.1073/pnas.1522748113.

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The tandem of pore domain in a weak inwardly rectifying K+ channel (Twik)-related acid-arachidonic activated K+ channel (TRAAK) and Twik-related K+ channels (TREK) 1 and TREK2 are active as homodimers gated by stretch, fatty acids, pH, and G protein-coupled receptors. These two-pore domain potassium (K2P) channels are broadly expressed in the nervous system where they control excitability. TREK/TRAAK KO mice display altered phenotypes related to nociception, neuroprotection afforded by polyunsaturated fatty acids, learning and memory, mood control, and sensitivity to general anesthetics. These

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6

Hermanstyne, T. O., K. Markowitz, L. Fan, and M. S. Gold. "Mechanotransducers in Rat Pulpal Afferents." Journal of Dental Research 87, no. 9 (2008): 834–38. http://dx.doi.org/10.1177/154405910808700910.

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The hydrodynamic theory suggests that pain associated with stimulation of a sensitive tooth ultimately involves mechanotransduction as a consequence of fluid movement within exposed dentinal tubules. To determine whether putative mechanotransducers could underlie mechanotransduction in pulpal afferents, we used a single-cell PCR approach to screen retrogradely labeled pulpal afferents. The presence of mRNA encoding BNC-1, ASIC3, TRPV4, TRPA1, the α, β, and γ subunits of ENaC, and the two pore K+ channels (TREK1, TREK2) and TRAAK were screened in pulpal neurons from rats with and without pulpal

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7

Peng, Yuanzhi, Qingqing Zhang, Hao Cheng, Saie Shen, and Xiaojian Weng. "Activation of TREK1 Channel in the Anterior Cingulate Cortex Improves Neuropathic Pain in a Rat Model." Computational Intelligence and Neuroscience 2022 (September 30, 2022): 1–6. http://dx.doi.org/10.1155/2022/1372823.

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Objective. To explore the biological function and mechanism of TREK1 in neuropathic pain. Thirty-two healthy rats and rats with sciatic nerve chronic press-fitting model (chronic constriction injury of the sciatic nerve, CCI) were selected. Western blot, immunofluorescence staining, and patch clamp technique were performed to explore the biological functions of TREK1. The expression of TREK1 was decreased in the CCI model. The TREK1 channel current in the CCI model was decreased. After local administration of TREK1 channel activator in the anterior cingulate cortex area, the pain behavior of C

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8

Kim, Seong-Seop, Yeonju Bae, Osung Kwon та ін. "β-COP Regulates TWIK1/TREK1 Heterodimeric Channel-Mediated Passive Conductance in Astrocytes". Cells 11, № 20 (2022): 3322. http://dx.doi.org/10.3390/cells11203322.

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Mature astrocytes are characterized by a K+ conductance (passive conductance) that changes with a constant slope with voltage, which is involved in K+ homeostasis in the brain. Recently, we reported that the tandem of pore domains in a weak inward rectifying K+ channel (TWIK1 or KCNK1) and TWIK-related K+ channel 1 (TREK1 or KCNK2) form heterodimeric channels that mediate passive conductance in astrocytes. However, little is known about the binding proteins that regulate the function of the TWIK1/TREK1 heterodimeric channels. Here, we found that β-coat protein (COP) regulated the surface expre

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9

Royal, Perrine, Pablo Ávalos Prado, Brigitte Wdziekonski, and Guillaume Sandoz. "Canaux potassiques à deux domaines P (K2P) et migraine." Biologie Aujourd'hui 213, no. 1-2 (2019): 51–57. http://dx.doi.org/10.1051/jbio/2019020.

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La migraine est un désordre neurologique qui affecte 15 % de la population mondiale. Les crises migraineuses sont liées, entre autres, à l’hyperexcitabilité électrique des neurones trigéminaux. Leur activité électrique est contrôlée par les canaux potassiques à deux domaines P (K2P) dont l’importance dans l’induction du contrôle de l’excitabilité a récemment été mise en évidence par la découverte d’une version mutée de l’un d’eux TRESK, le mutant TRESK-MT, qui est lié à la migraine. Cette découverte a été controversée à la suite du séquençage d’autres canaux TRESK mutés non fonctionnels qui ne

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10

Brohawn, Stephen G. "How ion channels sense mechanical force: insights from mechanosensitive K2P channels TRAAK, TREK1, and TREK2." Annals of the New York Academy of Sciences 1352, no. 1 (2015): 20–32. http://dx.doi.org/10.1111/nyas.12874.

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11

Unnithan, Afeesh Rajan, Michael Rotherham, Hareklea Markides, and Alicia J. El Haj. "Magnetic Ion Channel Activation (MICA)-Enabled Screening Assay: A Dynamic Platform for Remote Activation of Mechanosensitive Ion Channels." International Journal of Molecular Sciences 24, no. 4 (2023): 3364. http://dx.doi.org/10.3390/ijms24043364.

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This study reports results of a mechanical platform-based screening assay (MICA) to evaluate the remote activation of mechanosensitive ion channels. Here, we studied ERK pathway activation and the elevation in intracellular Ca2+ levels in response to the MICA application using the Luciferase assay and Fluo-8AM assay, respectively. Functionalised magnetic nanoparticles (MNPs) targeting membrane-bound integrins and mechanosensitive TREK1 ion channels were studied with HEK293 cell lines under MICA application. The study demonstrated that active targeting of mechanosensitive integrins via RGD (Arg

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12

Honoré, Eric. "The neuronal background K2P channels: focus on TREK1." Nature Reviews Neuroscience 8, no. 4 (2007): 251–61. http://dx.doi.org/10.1038/nrn2117.

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13

Khajoueinejad, Leila, and Paul M. Riegelhaupt. "Engineering novel pharmacology for the TREK1 K2P channel." Biophysical Journal 123, no. 3 (2024): 263a—264a. http://dx.doi.org/10.1016/j.bpj.2023.11.1654.

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14

Sandoz, G., D. Douguet, F. Chatelain, M. Lazdunski, and F. Lesage. "Extracellular acidification exerts opposite actions on TREK1 and TREK2 potassium channels via a single conserved histidine residue." Proceedings of the National Academy of Sciences 106, no. 34 (2009): 14628–33. http://dx.doi.org/10.1073/pnas.0906267106.

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15

Gil, V., D. Gallego, H. Moha Ou Maati, et al. "Relative contribution of SKCa and TREK1 channels in purinergic and nitrergic neuromuscular transmission in the rat colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 303, no. 3 (2012): G412—G423. http://dx.doi.org/10.1152/ajpgi.00040.2012.

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Purinergic and nitrergic neurotransmission predominantly mediate inhibitory neuromuscular transmission in the rat colon. We studied the sensitivity of both purinergic and nitrergic pathways to spadin, a TWIK-related potassium channel 1 (TREK1) inhibitor, apamin, a small-conductance calcium-activated potassium channel blocker and 1H-[1,2,4]oxadiazolo[4,3-α]quinoxalin-1-one (ODQ), a specific inhibitor of soluble guanylate cyclase. TREK1 expression was detected by RT-PCR in the rat colon. Patch-clamp experiments were performed on cells expressing hTREK1 channels. Spadin (1 μM) reduced currents 1)

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16

Riel, Elena B., Louis Goldberg, and Paul M. Riegelhaupt. "Engineering an off-switch for background TREK1 potassium channels." Biophysical Journal 123, no. 3 (2024): 29a. http://dx.doi.org/10.1016/j.bpj.2023.11.274.

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17

Park, Kyoung Sun, and Yangmi Kim. "Functional expression of TREK1 channel in human bone marrow and human umbilical cord vein-derived mesenchymal stem cells." Journal of the Korea Academia-Industrial cooperation Society 16, no. 3 (2015): 1964–71. http://dx.doi.org/10.5762/kais.2015.16.3.1964.

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18

Schmidpeter, Philipp, Aboubacar Wague, John T. Petroff, Wayland W. Cheng, Crina M. Nimigean, and Paul M. Riegelhaupt. "Membrane phospholipids control activity of the mechanosensitive K2P channel TREK1." Biophysical Journal 121, no. 3 (2022): 433a. http://dx.doi.org/10.1016/j.bpj.2021.11.606.

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19

Ghatak, Swagata, and Sujit Kumar Sikdar. "Lactate modulates the intracellular pH sensitivity of human TREK1 channels." Pflügers Archiv - European Journal of Physiology 468, no. 5 (2016): 825–36. http://dx.doi.org/10.1007/s00424-016-1795-8.

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20

Ford, Kevin J., David A. Arroyo, Jeremy N. Kay, et al. "A role for TREK1 in generating the slow afterhyperpolarization in developing starburst amacrine cells." Journal of Neurophysiology 109, no. 9 (2013): 2250–59. http://dx.doi.org/10.1152/jn.01085.2012.

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Slow afterhyperpolarizations (sAHPs) play an important role in establishing the firing pattern of neurons that in turn influence network activity. sAHPs are mediated by calcium-activated potassium channels. However, the molecular identity of these channels and the mechanism linking calcium entry to their activation are still unknown. Here we present several lines of evidence suggesting that the sAHPs in developing starburst amacrine cells (SACs) are mediated by two-pore potassium channels. First, we use whole cell and perforated patch voltage clamp recordings to characterize the sAHP conductan

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21

Sandoz, G., S. C. Bell, and E. Y. Isacoff. "Optical probing of a dynamic membrane interaction that regulates the TREK1 channel." Proceedings of the National Academy of Sciences 108, no. 6 (2011): 2605–10. http://dx.doi.org/10.1073/pnas.1015788108.

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22

Choudhury, Nasreen, та Sujit Kumar Sikdar. "17β-estradiol potentiates TREK1 channel activity through G protein-coupled estrogen receptor". Journal of Steroid Biochemistry and Molecular Biology 183 (жовтень 2018): 94–105. http://dx.doi.org/10.1016/j.jsbmb.2018.06.001.

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23

Al-Moubarak, Ehab, and Alistair Mathie. "Enhancement of Current through Trek1 Two Pore Domain Channels by Flufenamic Acid." Biophysical Journal 106, no. 2 (2014): 748a. http://dx.doi.org/10.1016/j.bpj.2013.11.4121.

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24

Srisomboon, Yotesawee, Nathan A. Zaidman, Peter J. Maniak, Chatsri Deachapunya, and Scott M. O’Grady. "P2Y receptor regulation of K2P channels that facilitate K+ secretion by human mammary epithelial cells." American Journal of Physiology-Cell Physiology 314, no. 5 (2018): C627—C639. http://dx.doi.org/10.1152/ajpcell.00342.2016.

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The objective of this study was to determine the molecular identity of ion channels involved in K+ secretion by the mammary epithelium and to examine their regulation by purinoceptor agonists. Apical membrane voltage-clamp experiments were performed on human mammary epithelial cells where the basolateral membrane was exposed to the pore-forming antibiotic amphotericin B dissolved in a solution with intracellular-like ionic composition. Addition of the Na+ channel inhibitor benzamil reduced the basal current, consistent with inhibition of Na+ uptake across the apical membrane, whereas the KCa3.

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25

Ülkümen, Burak. "Role of Nasal AQP5 And TREK1 Expression in Biomolecular Background of Pregnancy Rhinitis." International Journal of Academic Medicine and Pharmacy Volume: 2 Issue: 3, Volume: 2 Issue: 3 (2020): 197–203. http://dx.doi.org/10.29228/jamp.44176.

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26

Busserolles, Jérôme, Ismail Ben Soussia, Laetitia Pouchol, et al. "TREK1 channel activation as a new analgesic strategy devoid of opioid adverse effects." British Journal of Pharmacology 177, no. 20 (2020): 4782–95. http://dx.doi.org/10.1111/bph.15243.

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27

Huang, Huang, Jiang-Qi Liu, Yong Yu, et al. "Regulation of TWIK-related potassium channel-1 (Trek1) restitutes intestinal epithelial barrier function." Cellular & Molecular Immunology 13, no. 1 (2015): 110–18. http://dx.doi.org/10.1038/cmi.2014.137.

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28

Yin, Xin, Binxiao Su, Haopeng Zhang, et al. "TREK1 activation mediates spinal cord ischemic tolerance induced by isoflurane preconditioning in rats." Neuroscience Letters 515, no. 2 (2012): 115–20. http://dx.doi.org/10.1016/j.neulet.2012.03.006.

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29

Veale, Emma L., Kathryn A. Rees, Alistair Mathie, and Stefan Trapp. "Dominant Negative Effects of a Non-conducting TREK1 Splice Variant Expressed in Brain." Journal of Biological Chemistry 285, no. 38 (2010): 29295–304. http://dx.doi.org/10.1074/jbc.m110.108423.

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30

Kim, Eunju, Eun Mi Hwang, Oleg Yarishkin та ін. "Enhancement of TREK1 channel surface expression by protein–protein interaction with β-COP". Biochemical and Biophysical Research Communications 395, № 2 (2010): 244–50. http://dx.doi.org/10.1016/j.bbrc.2010.03.171.

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31

Wang, Yuzhi, Lingyan Lv, Hongrui Zang, et al. "Regulation of Trek1 expression in nasal mucosa with allergic rhinitis by specific immunotherapy." Cell Biochemistry and Function 33, no. 1 (2014): 23–28. http://dx.doi.org/10.1002/cbf.3075.

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32

Miller, Paula, Chris Peers, and Paul J. Kemp. "Polymodal regulation of hTREK1 by pH, arachidonic acid, and hypoxia: physiological impact in acidosis and alkalosis." American Journal of Physiology-Cell Physiology 286, no. 2 (2004): C272—C282. http://dx.doi.org/10.1152/ajpcell.00334.2003.

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Expression of the human tandem P domain K+ channel, hTREK1, is limited almost exclusively to the central nervous system, where ambient Po2 can be as low as 20 Torr. We have previously shown that this level of hypoxia evokes a maximal inhibitory influence on recombinant hTREK1 and occludes the activation by arachidonic acid; this has cast doubt on the idea that TREK1 activation during brain ischemia could facilitate neuroprotection via hyperpolarizing neurons in which it is expressed. Using both whole cell and cell-attached patch-clamp configurations, we now show that the action of another pote

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33

Kondo, Rubii, Akari Deguchi, Naoki Kawata, Yoshiaki Suzuki, and Hisao Yamamura. "Involvement of TREK1 channels in the proliferation of human hepatic stellate LX-2 cells." Journal of Pharmacological Sciences 148, no. 3 (2022): 286–94. http://dx.doi.org/10.1016/j.jphs.2022.01.003.

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34

Bittner, Stefan, Tobias Ruck, Michael K. Schuhmann, et al. "Endothelial TWIK-related potassium channel-1 (TREK1) regulates immune-cell trafficking into the CNS." Nature Medicine 19, no. 9 (2013): 1161–65. http://dx.doi.org/10.1038/nm.3303.

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35

Tong, L., M. Cai, Y. Huang, et al. "Activation of K 2 P channel–TREK1 mediates the neuroprotection induced by sevoflurane preconditioning." British Journal of Anaesthesia 113, no. 1 (2014): 157–67. http://dx.doi.org/10.1093/bja/aet338.

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36

Brohawn, Stephen G., Zhenwei Su, and Roderick MacKinnon. "Mechanosensitivity is mediated directly by the lipid membrane in TRAAK and TREK1 K+channels." Proceedings of the National Academy of Sciences 111, no. 9 (2014): 3614–19. http://dx.doi.org/10.1073/pnas.1320768111.

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37

Ye, Dongqing, Yang Li, Xiangrong Zhang, et al. "TREK1 channel blockade induces an antidepressant-like response synergizing with 5-HT1A receptor signaling." European Neuropsychopharmacology 25, no. 12 (2015): 2426–36. http://dx.doi.org/10.1016/j.euroneuro.2015.09.007.

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38

Viswanath, Ambily Nath Indu, Seo Yun Jung, Eun Mi Hwang, et al. "Identification of the firstin silico-designed TREK1 antagonists that block channel currents dose dependently." Chemical Biology & Drug Design 88, no. 6 (2016): 807–19. http://dx.doi.org/10.1111/cbdd.12810.

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Fan, Jing, Junxi Du, Zhongwei Zhang, et al. "The Protective Effects of Hydrogen Sulfide New Donor Methyl S-(4-Fluorobenzyl)-N-(3,4,5-Trimethoxybenzoyl)-l-Cysteinate on the Ischemic Stroke." Molecules 27, no. 5 (2022): 1554. http://dx.doi.org/10.3390/molecules27051554.

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In this paper, we report the design, synthesis and biological evaluation of a novel S-allyl-l-cysteine (SAC) and gallic acid conjugate S-(4-fluorobenzyl)-N-(3,4,5-trimethoxybenzoyl)-l-cysteinate (MTC). We evaluate the effects on ischemia-reperfusion-induced PC12 cells, primary neurons in neonatal rats, and cerebral ischemic neuronal damage in rats, and the results showed that MTC increased SOD, CAT, GPx activity and decreased LDH release. PI3K and p-AKT protein levels were significantly increased by activating PI3K/AKT pathway. Mitochondrial pro-apoptotic proteins Bax and Bim levels were reduc

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40

Veale, Emma L., Ehab Al-Moubarak, Naina Bajaria, et al. "Influence of the N Terminus on the Biophysical Properties and Pharmacology of TREK1 Potassium Channels." Molecular Pharmacology 85, no. 5 (2014): 671–81. http://dx.doi.org/10.1124/mol.113.091199.

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41

Kim, Seung Chan, Jae Hyouk Choi, and Eunmi Hwang. "TREK1 channel in DGGCs ameliorates depression-like behaviour and increases adult hippocampal neurogenesis in mice." IBRO Reports 6 (September 2019): S116. http://dx.doi.org/10.1016/j.ibror.2019.07.370.

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42

Zhi, Yuanxing, Jin Liu, Peihua Kuang, et al. "Novel DCPIB analogs as dual inhibitors of VRAC/TREK1 channels reduced cGAS-STING mediated interferon responses." Biochemical Pharmacology 199 (May 2022): 114988. http://dx.doi.org/10.1016/j.bcp.2022.114988.

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Tarasov, Michail V., Polina D. Kotova, Marina F. Bystrova, Natalia V. Kabanova, Veronika Yu Sysoeva, and Stanislav S. Kolesnikov. "Arachidonic acid hyperpolarizes mesenchymal stromal cells from the human adipose tissue by stimulating TREK1 K+ channels." Channels 13, no. 1 (2019): 36–47. http://dx.doi.org/10.1080/19336950.2019.1565251.

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44

Qi, Xinyang, Hua Xu, Liping Wang, and Zhijun Zhang. "Comparison of Therapeutic Effects of TREK1 Blockers and Fluoxetine on Chronic Unpredicted Mild Stress Sensitive Rats." ACS Chemical Neuroscience 9, no. 11 (2018): 2824–31. http://dx.doi.org/10.1021/acschemneuro.8b00225.

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45

Banerjee, Aditi, Swagata Ghatak, and Sujit Kumar Sikdar. "l -Lactate mediates neuroprotection against ischaemia by increasing TREK1 channel expression in rat hippocampal astrocytes in vitro." Journal of Neurochemistry 138, no. 2 (2016): 265–81. http://dx.doi.org/10.1111/jnc.13638.

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46

Intelligence and Neuroscience, Computational. "Retracted: Activation of TREK1 Channel in the Anterior Cingulate Cortex Improves Neuropathic Pain in a Rat Model." Computational Intelligence and Neuroscience 2023 (August 16, 2023): 1. http://dx.doi.org/10.1155/2023/9768435.

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47

Wang, Kun, and Xiangang Kong. "Isoflurane Preconditioning Induces Neuroprotection by Up-Regulation of TREK1 in a Rat Model of Spinal Cord Ischemic Injury." Biomolecules & Therapeutics 24, no. 5 (2016): 495–500. http://dx.doi.org/10.4062/biomolther.2015.206.

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Henstock, James R., Michael Rotherham, and Alicia J. El Haj. "Magnetic ion channel activation of TREK1 in human mesenchymal stem cells using nanoparticles promotes osteogenesis in surrounding cells." Journal of Tissue Engineering 9 (January 2018): 204173141880869. http://dx.doi.org/10.1177/2041731418808695.

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Magnetic ion channel activation technology uses superparamagnetic nanoparticles conjugated with targeting antibodies to apply mechanical force directly to stretch-activated ion channels on the cell surface, stimulating mechanotransduction and downstream processes. This technique has been reported to promote differentiation towards musculoskeletal cell types and enhance mineralisation. Previous studies have shown how mesenchymal stem cells injected into a pre-mineralised environment such as a foetal chick epiphysis, results in large-scale osteogenesis at the target site. However, the relative c

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Garry, Ambroise, Bérengère Fromy, Nicolas Blondeau, et al. "Altered acetylcholine, bradykinin and cutaneous pressure‐induced vasodilation in mice lacking the TREK1 potassium channel: the endothelial link." EMBO reports 8, no. 4 (2007): 354–59. http://dx.doi.org/10.1038/sj.embor.7400916.

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Sandoz, Guillaume, Joshua Levitz, Richard H. Kramer, and Ehud Y. Isacoff. "Optical Control of Endogenous Proteins with a Photoswitchable Conditional Subunit Reveals a Role for TREK1 in GABAB Signaling." Neuron 74, no. 6 (2012): 1005–14. http://dx.doi.org/10.1016/j.neuron.2012.04.026.

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