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Artykuły w czasopismach na temat „TREK1”

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Data publikacji: 6 września 2023

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1

Levitz, Joshua, Perrine Royal, Yannick Comoglio, Brigitte Wdziekonski, Sébastien Schaub, Daniel M. Clemens, Ehud Y. Isacoff i Guillaume Sandoz. "Heterodimerization within the TREK channel subfamily produces a diverse family of highly regulated potassium channels". Proceedings of the National Academy of Sciences 113, nr 15 (28.03.2016): 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 single-molecule pull-down (SiMPull) from HEK cell lysate and subunit counting in the plasma membrane of living cells, we show that TREK1, TREK2, and TRAAK readily coassemble. TREK1 and TREK2 can each heterodimerize with TRAAK, but do so less efficiently than with each other. We functionally characterized the heterodimers and found that all combinations form outwardly rectifying potassium-selective channels but with variable voltage sensitivity and pH regulation. TREK1-TREK2 heterodimers show low levels of activity at physiological external pH but, unlike their corresponding homodimers, are activated by both acidic and alkaline conditions. Modeling based on recent crystal structures, along with mutational analysis, suggests that each subunit within a TREK1-TREK2 channel is regulated independently via titratable His. Finally, TREK1/TRAAK heterodimers differ in function from TRAAK homodimers in two critical ways: they are activated by both intracellular acidification and alkalinization and are regulated by the enzyme phospholipase D2. Thus, heterodimerization provides a means for diversifying functionality through an expansion of the channel types within the K2P channels.

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2

Kim, Seong-Seop, Jimin Park, Eunju Kim, Eun Mi Hwang i Jae-Yong Park. "β-COP Suppresses the Surface Expression of the TREK2". Cells 12, nr 11 (29.05.2023): 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 subfamily, including TREK2 and the TRAAK (TWIK-related acid-arachidonic activated K+ channel). In contrast to TREK1, β-COP binds to the C-terminus of TREK2 and reduces its cell surface expression but does not bind to TRAAK. Furthermore, β-COP cannot bind to TREK2 mutants with deletions or point mutations in the C-terminus and does not affect the surface expression of these TREK2 mutants. These results emphasize the unique role of β-COP in regulating the surface expression of the TREK family.

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3

Bai, Xilian, George J. Bugg, Susan L. Greenwood, Jocelyn D. Glazier, Colin P. Sibley, Philip N. Baker, Michael J. Taggart i Gregor K. Fyfe. "Expression of TASK and TREK, two-pore domain K+ channels, in human myometrium". Reproduction 129, nr 4 (kwiecień 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 RT-PCR the mRNA expression of TASK and TREK isoforms was examined in myometrial tissue from pregnant women. mRNAs encoding TASK1, 4 and 5 and TREK1 were detected whereas weak or no signals were observed for TASK2, TASK3 and TREK2. Western blotting for TASK1 gave two bands of approximately 44 and 65 kDa, whereas TREK1 gave bands of approximately 59 and 90 kDa in myometrium from pregnant women. TASK1 and TREK1 immunofluorescence was prominent in intracellular and plasmalemmal locations within myometrial cells. Therefore, we conclude that the human myometrium is a site of expression for the two-pore domain K+channel proteins TASK1 and TREK1.

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4

Afzali, Ali M., Tobias Ruck, Alexander M. Herrmann, Janette Iking, Claudia Sommer, Christoph Kleinschnitz, Corinna Preuβe i in. "The potassium channels TASK2 and TREK1 regulate functional differentiation of murine skeletal muscle cells". American Journal of Physiology-Cell Physiology 311, nr 4 (1.10.2016): 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 quantitative PCR, Western blotting, and immunohistochemical stainings as well as functional analysis including patch-clamp measurements and Ca2+ imaging. Mouse SkMC express TWIK-related acid-sensitive K+ channel (TASK) 2, TWIK-related K+ channel (TREK) 1, TREK2, and TWIK-related arachidonic acid stimulated K+ channel (TRAAK). Except TASK2 all mentioned channels were upregulated in vitro during differentiation from myoblasts to myotubes. TASK2 and TREK1 were also functionally expressed and upregulated in PMMs isolated from mouse muscle tissue. Inhibition of TASK2 and TREK1 during differentiation revealed a morphological impairment of myoblast fusion accompanied by a downregulation of maturation markers. TASK2 and TREK1 blockade led to a decreased K+ outward current and a decrease of ACh-dependent Ca2+ influx in C2C12 cells as potential underlying mechanisms. K2P-channel expression was also detected in human muscle tissue by immunohistochemistry pointing towards possible relevance for human muscle cell maturation and function. In conclusion, our findings for the first time demonstrate the functional expression of TASK2 and TREK1 in muscle cells with implications for differentiation processes warranting further investigations in physiologic and pathophysiologic scenarios.

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5

Blin, Sandy, Ismail Ben Soussia, Eun-Jin Kim, Frédéric Brau, Dawon Kang, Florian Lesage i Delphine Bichet. "Mixing and matching TREK/TRAAK subunits generate heterodimeric K2P channels with unique properties". Proceedings of the National Academy of Sciences 113, nr 15 (28.03.2016): 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 channels have emerged as promising targets for the development of new classes of anesthetics, analgesics, antidepressants, neuroprotective agents, and drugs against addiction. Here, we show that the TREK1, TREK2, and TRAAK subunits assemble and form active heterodimeric channels with electrophysiological, regulatory, and pharmacological properties different from those of homodimeric channels. Heteromerization occurs between all TREK variants produced by alternative splicing and alternative translation initiation. These results unveil a previously unexpected diversity of K2P channels that will be challenging to analyze in vivo, but which opens new perspectives for the development of clinically relevant drugs.

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6

Hermanstyne, T. O., K. Markowitz, L. Fan i M. S. Gold. "Mechanotransducers in Rat Pulpal Afferents". Journal of Dental Research 87, nr 9 (wrzesień 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 inflammation. ASIC3, TRPA1, TREK1, and TREK2 were present in ~67%, 64%, 14%, and 10% of pulpal neurons, respectively. There was no detectable influence of inflammation on the proportion of neurons expressing these mechanotransducers. Given that the majority of pulpal afferents express ASIC3 and TRPA1, our results raise the possibility that these channels may be novel targets for the treatment of dentin sensitivity.

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7

Peng, Yuanzhi, Qingqing Zhang, Hao Cheng, Saie Shen i Xiaojian Weng. "Activation of TREK1 Channel in the Anterior Cingulate Cortex Improves Neuropathic Pain in a Rat Model". Computational Intelligence and Neuroscience 2022 (30.09.2022): 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 CCI rats and the expression of TREK1 protein were reversed. The expression of TREK1 was downregulated in the ACC area of CCI rats and the current of TREK1 was decreased, which played an important role in the regulation of neuropathic pain.

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8

Kim, Seong-Seop, Yeonju Bae, Osung Kwon, Seung-Hae Kwon, Jong Bok Seo, Eun Mi Hwang i Jae-Yong Park. "β-COP Regulates TWIK1/TREK1 Heterodimeric Channel-Mediated Passive Conductance in Astrocytes". Cells 11, nr 20 (21.10.2022): 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 expression and activity of the TWIK1/TREK1 heterodimeric channels in astrocytes. β-COP binds directly to TREK1 but not TWIK1 in a heterologous expression system. However, β-COP also interacts with the TWIK1/TREK1 heterodimeric channel in a TREK1 dependent manner and enhances the surface expression of the heterodimeric channel in astrocytes. Consequently, it regulates TWIK1/TREK1 heterodimeric channel-mediated passive conductance in astrocytes in the mouse brain. Taken together, these results suggest that β-COP is a potential regulator of astrocytic passive conductance in the brain.

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9

Royal, Perrine, Pablo Ávalos Prado, Brigitte Wdziekonski i Guillaume Sandoz. "Canaux potassiques à deux domaines P (K2P) et migraine". Biologie Aujourd'hui 213, nr 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 sont pas liés à la migraine. Notre étude montre que les mutations délétères du gène TRESK impliquées dans la migraine entraînent la formation de deux protéines au lieu d’une (comme attendu du gène non muté), via un nouveau mécanisme appelé fsATI (initiation alternative de la traduction induite par déplacement du cadre de lecture). L’une est inactive et l’autre, en ciblant d’autres canaux K2P, TREK1 et TREK2, stimule fortement l’activité électrique des neurones provoquant ainsi des crises migraineuses. Cette découverte a permis l’identification de deux nouvelles cibles dans le traitement de la migraine, TREK1 et TREK2, et suggère que les mutations induisant une traduction alternative due à un déplacement du cadre de lecture (fsATI) doivent être considérées comme une classe distincte de mutations lors de l’étude des mutations impliquées dans les pathologies humaines.

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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, nr 1 (31.08.2015): 20–32. http://dx.doi.org/10.1111/nyas.12874.

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11

Unnithan, Afeesh Rajan, Michael Rotherham, Hareklea Markides i 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, nr 4 (8.02.2023): 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 (Arginylglycylaspartic acid) motifs or TREK1 (KCNK2, potassium channel subfamily K member 2) ion channels can stimulate the ERK pathway and intracellular calcium levels compared to non-MICA controls. This screening assay offers a powerful tool, which aligns with existing high-throughput drug screening platforms for use in the assessment of drugs that interact with ion channels and influence ion channel-modulated diseases.

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12

Honoré, Eric. "The neuronal background K2P channels: focus on TREK1". Nature Reviews Neuroscience 8, nr 4 (kwiecień 2007): 251–61. http://dx.doi.org/10.1038/nrn2117.

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13

Sandoz, G., D. Douguet, F. Chatelain, M. Lazdunski i 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, nr 34 (10.08.2009): 14628–33. http://dx.doi.org/10.1073/pnas.0906267106.

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14

Park, Kyoung Sun, i 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, nr 3 (31.03.2015): 1964–71. http://dx.doi.org/10.5762/kais.2015.16.3.1964.

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15

Gil, V., D. Gallego, H. Moha Ou Maati, R. Peyronnet, M. Martínez-Cutillas, C. Heurteaux, M. Borsotto i M. Jiménez. "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, nr 3 (1.08.2012): 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) in basal conditions 2) activated by stretch, and 3) with arachidonic acid (AA; 10 μM). l-Methionine (1 mM) or l-cysteine (1 mM) did not modify currents activated by AA. Microelectrode and muscle bath studies were performed on rat colon samples. l-Methionine (2 mM), apamin (1 μM), ODQ (10 μM), and Nω-nitro-l-arginine (l-NNA; 1 mM) depolarized smooth muscle cells and increased motility. These effects were not observed with spadin (1 μM). Purinergic and nitrergic inhibitory junction potentials (IJP) were studied by incubating the tissue with l-NNA (1 mM) or MRS2500 (1 μM). Both purinergic and nitrergic IJP were unaffected by spadin. Apamin reduced both IJP with a different potency and maximal effect for each. ODQ concentration dependently abolished nitrergic IJP without affecting purinergic IJP. Similar effects were observed in hyperpolarizations induced by sodium nitroprusside (1 μM) and nitrergic relaxations induced by electrical stimulation. We propose a pharmacological approach to characterize the pathways and function of purinergic and nitrergic neurotransmission. Nitrergic neurotransmission, which is mediated by cyclic guanosine monophosphate, is insensitive to spadin, an effective TREK1 channel inhibitor. Both purinergic and nitrergic neurotransmission are inhibited by apamin but with different relative sensitivity.

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16

Schmidpeter, Philipp, Aboubacar Wague, John T. Petroff, Wayland W. Cheng, Crina M. Nimigean i Paul M. Riegelhaupt. "Membrane phospholipids control activity of the mechanosensitive K2P channel TREK1". Biophysical Journal 121, nr 3 (luty 2022): 433a. http://dx.doi.org/10.1016/j.bpj.2021.11.606.

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Ghatak, Swagata, i Sujit Kumar Sikdar. "Lactate modulates the intracellular pH sensitivity of human TREK1 channels". Pflügers Archiv - European Journal of Physiology 468, nr 5 (3.02.2016): 825–36. http://dx.doi.org/10.1007/s00424-016-1795-8.

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Ford, Kevin J., David A. Arroyo, Jeremy N. Kay, Eric E. Lloyd, Robert M. Bryan, Joshua R. Sanes i Marla B. Feller. "A role for TREK1 in generating the slow afterhyperpolarization in developing starburst amacrine cells". Journal of Neurophysiology 109, nr 9 (1.05.2013): 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 conductance under different pharmacological conditions. We find that this conductance was calcium dependent, reversed at EK, blocked by barium, insensitive to apamin and TEA, and activated by arachidonic acid. In addition, pharmacological inhibition of calcium-activated phosphodiesterase reduced the sAHP. Second, we performed gene profiling on isolated SACs and found that they showed strong preferential expression of the two-pore channel gene kcnk2 that encodes TREK1. Third, we demonstrated that TREK1 knockout animals exhibited an altered frequency of retinal waves, a frequency that is set by the sAHPs in SACs. With these results, we propose a model in which depolarization-induced decreases in cAMP lead to disinhibition of the two-pore potassium channels and in which the kinetics of this biochemical pathway dictate the slow activation and deactivation of the sAHP conductance. Our model offers a novel pathway for the activation of a conductance that is physiologically important.

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Sandoz, G., S. C. Bell i E. Y. Isacoff. "Optical probing of a dynamic membrane interaction that regulates the TREK1 channel". Proceedings of the National Academy of Sciences 108, nr 6 (24.01.2011): 2605–10. http://dx.doi.org/10.1073/pnas.1015788108.

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

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Al-Moubarak, Ehab, i Alistair Mathie. "Enhancement of Current through Trek1 Two Pore Domain Channels by Flufenamic Acid". Biophysical Journal 106, nr 2 (styczeń 2014): 748a. http://dx.doi.org/10.1016/j.bpj.2013.11.4121.

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Srisomboon, Yotesawee, Nathan A. Zaidman, Peter J. Maniak, Chatsri Deachapunya i 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, nr 5 (1.05.2018): 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 KCa3.1 channel blocker TRAM-34 produced an increase in current resulting from inhibition of basal K+ efflux. Treatment with two-pore potassium (K2P) channel blockers quinidine, bupivacaine and a selective TASK1/TASK3 inhibitor (PK-THPP) all produced concentration-dependent inhibition of apical K+ efflux. qRT-PCR experiments detected mRNA expression for nine K2P channel subtypes. Western blot analysis of biotinylated apical membranes and confocal immunocytochemistry revealed that at least five K2P subtypes (TWIK1, TREK1, TREK2, TASK1, and TASK3) are expressed in the apical membrane. Apical UTP also increased the current, but pretreatment with the PKC inhibitor GF109203X blocked the response. Similarly, direct activation of PKC with phorbol 12-myristate 13-acetate produced a similar increase in current as observed with UTP. These results support the conclusion that the basal level of K+ secretion involves constitutive activity of apical KCa3.1 channels and multiple K2P channel subtypes. Apical UTP evoked a transient increase in KCa3.1 channel activity, but over time caused persistent inhibition of K2P channel function leading to an overall decrease in K+ secretion.

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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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Busserolles, Jérôme, Ismail Ben Soussia, Laetitia Pouchol, Nicolas Marie, Mathieu Meleine, Maïly Devilliers, Céline Judon i in. "TREK1 channel activation as a new analgesic strategy devoid of opioid adverse effects". British Journal of Pharmacology 177, nr 20 (21.09.2020): 4782–95. http://dx.doi.org/10.1111/bph.15243.

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Huang, Huang, Jiang-Qi Liu, Yong Yu, Li-Hua Mo, Rong-Ti Ge, Huan-Ping Zhang, Zhi-Gang Liu, Peng-Yuan Zheng i Ping-Chang Yang. "Regulation of TWIK-related potassium channel-1 (Trek1) restitutes intestinal epithelial barrier function". Cellular & Molecular Immunology 13, nr 1 (16.02.2015): 110–18. http://dx.doi.org/10.1038/cmi.2014.137.

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Yin, Xin, Binxiao Su, Haopeng Zhang, Wenying Song, Hao Wu, Xiaomei Chen, Xijing Zhang, Hailong Dong i Lize Xiong. "TREK1 activation mediates spinal cord ischemic tolerance induced by isoflurane preconditioning in rats". Neuroscience Letters 515, nr 2 (maj 2012): 115–20. http://dx.doi.org/10.1016/j.neulet.2012.03.006.

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Veale, Emma L., Kathryn A. Rees, Alistair Mathie i Stefan Trapp. "Dominant Negative Effects of a Non-conducting TREK1 Splice Variant Expressed in Brain". Journal of Biological Chemistry 285, nr 38 (6.07.2010): 29295–304. http://dx.doi.org/10.1074/jbc.m110.108423.

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Kim, Eunju, Eun Mi Hwang, Oleg Yarishkin, Jae Cheal Yoo, Donggyu Kim, Nammi Park, Minhee Cho i in. "Enhancement of TREK1 channel surface expression by protein–protein interaction with β-COP". Biochemical and Biophysical Research Communications 395, nr 2 (kwiecień 2010): 244–50. http://dx.doi.org/10.1016/j.bbrc.2010.03.171.

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Wang, Yuzhi, Lingyan Lv, Hongrui Zang, Zhenfeng Gao, Feng Zhang, Xingjie Wang i Xuanyan Zhou. "Regulation of Trek1 expression in nasal mucosa with allergic rhinitis by specific immunotherapy". Cell Biochemistry and Function 33, nr 1 (22.12.2014): 23–28. http://dx.doi.org/10.1002/cbf.3075.

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Miller, Paula, Chris Peers i 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, nr 2 (luty 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 potent TREK activator and ischemia-related event, intracellular acidification, is similarly without effect during compromised O2 availability. This occlusion is observed in either recording condition, and even the concerted actions of both arachidonic acid and intracellular acidosis are unable to activate hTREK1 during hypoxia. Conversely, intracellular alkalinization is a potent channel inhibitor, and hypoxia does not reverse this inhibition. However, increases in intracellular pH are unable to occlude either arachidonic acid activation or hypoxic inhibition. These data highlight two important points. First, during hypoxia, modulation of hTREK1 cannot be accomplished by parameters known to be perturbed in brain ischemia (increased extracellular fatty acids and intracellular acidification). Second, the mechanism of regulation by intracellular alkalinization is distinct from the overlapping structural requirements known to exist for regulation by arachidonic acid, membrane distortion, and acidosis. Thus it seems likely that hTREK1 regulation in the brain will be physiologically more relevant during alkalosis than during ischemia or acidosis.

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Kondo, Rubii, Akari Deguchi, Naoki Kawata, Yoshiaki Suzuki i Hisao Yamamura. "Involvement of TREK1 channels in the proliferation of human hepatic stellate LX-2 cells". Journal of Pharmacological Sciences 148, nr 3 (marzec 2022): 286–94. http://dx.doi.org/10.1016/j.jphs.2022.01.003.

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Bittner, Stefan, Tobias Ruck, Michael K. Schuhmann, Alexander M. Herrmann, Hamid Moha ou Maati, Nicole Bobak, Kerstin Göbel i in. "Endothelial TWIK-related potassium channel-1 (TREK1) regulates immune-cell trafficking into the CNS". Nature Medicine 19, nr 9 (11.08.2013): 1161–65. http://dx.doi.org/10.1038/nm.3303.

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Tong, L., M. Cai, Y. Huang, H. Zhang, B. Su, Z. Li i H. Dong. "Activation of K 2 P channel–TREK1 mediates the neuroprotection induced by sevoflurane preconditioning". British Journal of Anaesthesia 113, nr 1 (lipiec 2014): 157–67. http://dx.doi.org/10.1093/bja/aet338.

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Brohawn, Stephen G., Zhenwei Su i Roderick MacKinnon. "Mechanosensitivity is mediated directly by the lipid membrane in TRAAK and TREK1 K+channels". Proceedings of the National Academy of Sciences 111, nr 9 (18.02.2014): 3614–19. http://dx.doi.org/10.1073/pnas.1320768111.

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Ye, Dongqing, Yang Li, Xiangrong Zhang, Fei Guo, Leiyu Geng, Qi Zhang i Zhijun Zhang. "TREK1 channel blockade induces an antidepressant-like response synergizing with 5-HT1A receptor signaling". European Neuropsychopharmacology 25, nr 12 (grudzień 2015): 2426–36. http://dx.doi.org/10.1016/j.euroneuro.2015.09.007.

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Viswanath, Ambily Nath Indu, Seo Yun Jung, Eun Mi Hwang, Ki Duk Park, Sang Min Lim, Sun-Joon Min, Yong Seo Cho i Ae Nim Pae. "Identification of the firstin silico-designed TREK1 antagonists that block channel currents dose dependently". Chemical Biology & Drug Design 88, nr 6 (27.07.2016): 807–19. http://dx.doi.org/10.1111/cbdd.12810.

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Fan, Jing, Junxi Du, Zhongwei Zhang, Wenjing Shi, Binyan Hu, Jiaqin Hu, Yan Xue i in. "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, nr 5 (25.02.2022): 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 reduced while anti-apoptotic protein Bcl-2 levels were increased. The levels of cleaved caspase-9 and cleaved caspase-3 were also reduced in the plasma. The endoplasmic reticulum stress (ERS) was decreased, which in turns the survival rate of nerve cells was increased, so that the ischemic injury of neurons was protected accordingly. MTC activated the MEK-ERK signaling pathway and promoted axonal regeneration in primary neurons of the neonatal rat. The pretreatment of MEK-ERK pathway inhibitor PD98059 and PI3K/AKT pathway inhibitor LY294002 partially attenuated the protective effect of MTC. Using a MCAO rat model indicated that MTC could reduce cerebral ischemia-reperfusion injury and decrease the expression of proinflammatory factors. The neuroprotective effect of MTC may be due to inhibition of the over-activation of the TREK-1 channel and reduction of the current density of the TREK1 channel. These results suggested that MTC has a protective effect on neuronal injury induced by ischemia reperfusion, so it may have the potential to become a new type of neuro-ischemic drug candidate.

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Veale, Emma L., Ehab Al-Moubarak, Naina Bajaria, Kiyoyuki Omoto, Lishuang Cao, Stephen J. Tucker, Edward B. Stevens i Alistair Mathie. "Influence of the N Terminus on the Biophysical Properties and Pharmacology of TREK1 Potassium Channels". Molecular Pharmacology 85, nr 5 (7.02.2014): 671–81. http://dx.doi.org/10.1124/mol.113.091199.

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

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Zhi, Yuanxing, Jin Liu, Peihua Kuang, Xin Zhang, Ziwei Xu, Yanshan Chen, Xiuling Lin, Xiaoyan Wu, Pingzheng Zhou i Jianjun Chen. "Novel DCPIB analogs as dual inhibitors of VRAC/TREK1 channels reduced cGAS-STING mediated interferon responses". Biochemical Pharmacology 199 (maj 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 i Stanislav S. Kolesnikov. "Arachidonic acid hyperpolarizes mesenchymal stromal cells from the human adipose tissue by stimulating TREK1 K+ channels". Channels 13, nr 1 (1.01.2019): 36–47. http://dx.doi.org/10.1080/19336950.2019.1565251.

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Qi, Xinyang, Hua Xu, Liping Wang i Zhijun Zhang. "Comparison of Therapeutic Effects of TREK1 Blockers and Fluoxetine on Chronic Unpredicted Mild Stress Sensitive Rats". ACS Chemical Neuroscience 9, nr 11 (28.06.2018): 2824–31. http://dx.doi.org/10.1021/acschemneuro.8b00225.

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Banerjee, Aditi, Swagata Ghatak i Sujit Kumar Sikdar. "l -Lactate mediates neuroprotection against ischaemia by increasing TREK1 channel expression in rat hippocampal astrocytes in vitro". Journal of Neurochemistry 138, nr 2 (26.05.2016): 265–81. http://dx.doi.org/10.1111/jnc.13638.

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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 (16.08.2023): 1. http://dx.doi.org/10.1155/2023/9768435.

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Wang, Kun, i Xiangang Kong. "Isoflurane Preconditioning Induces Neuroprotection by Up-Regulation of TREK1 in a Rat Model of Spinal Cord Ischemic Injury". Biomolecules & Therapeutics 24, nr 5 (1.09.2016): 495–500. http://dx.doi.org/10.4062/biomolther.2015.206.

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Henstock, James R., Michael Rotherham i 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 (styczeń 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 contributions of stem cells and surrounding host tissue has not been resolved, that is, are the mesenchymal stem cells solely responsible for the observed mineralisation or do mechanically stimulated mesenchymal stem cells also promote a host-tissue mineralisation response? To address this, we established a novel two-dimensional co-culture assay, which indicated that magnetic ion channel activation stimulation of human mesenchymal stem cells does not significantly promote migration but does enhance collagen deposition and mineralisation in the surrounding cells. We conclude that one of the important functions of injected human mesenchymal stem cells is to release biological factors (e.g., cytokines and microvesicles) which guide the surrounding tissue response, and that remote control of this signalling process using magnetic ion channel activation technology may be a useful way to both drive and regulate tissue regeneration and healing.

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Garry, Ambroise, Bérengère Fromy, Nicolas Blondeau, Daniel Henrion, Frédéric Brau, Pierre Gounon, Nicolas Guy, Catherine Heurteaux, Michel Lazdunski i Jean Louis Saumet. "Altered acetylcholine, bradykinin and cutaneous pressure‐induced vasodilation in mice lacking the TREK1 potassium channel: the endothelial link". EMBO reports 8, nr 4 (9.03.2007): 354–59. http://dx.doi.org/10.1038/sj.embor.7400916.

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Sandoz, Guillaume, Joshua Levitz, Richard H. Kramer i Ehud Y. Isacoff. "Optical Control of Endogenous Proteins with a Photoswitchable Conditional Subunit Reveals a Role for TREK1 in GABAB Signaling". Neuron 74, nr 6 (czerwiec 2012): 1005–14. http://dx.doi.org/10.1016/j.neuron.2012.04.026.

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Riegelhaupt, Paul M., Kellie A. Woll, Thomas T. Joseph, Kiran A. Vaidya, Crina M. Nimigean i Roderic G. Eckenhoff. "Identification of a Modulatory Site of Action for the Volatile Anesthetic Isoflurane in TREK1 Tandem Pore Potassium Channels". Biophysical Journal 114, nr 3 (luty 2018): 487a—488a. http://dx.doi.org/10.1016/j.bpj.2017.11.2675.

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Lane, Cemantha, Xianyao Xu, Xiaoping Wan, Isabelle Deschenes i Thomas J. Hund. "PO-01-241 ROLE OF THE TWO-PORE K CHANNEL TREK1 IN REGULATING HEART FAILURE-INDUCED VENTRICULAR ARRHYTHMIA". Heart Rhythm 20, nr 5 (maj 2023): S166. http://dx.doi.org/10.1016/j.hrthm.2023.03.537.

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