Gotowe bibliografie tematyczne / Human TREK1

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Gotowa bibliografia na temat „Human TREK1”

Autor: Grafiati

Data publikacji: 6 września 2023

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Artykuły w czasopismach na temat "Human TREK1"

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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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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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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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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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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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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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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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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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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Nayak, Tapan K., S. Harinath, S. Nama, K. Somasundaram i S. K. Sikdar. "Inhibition of Human Two-Pore Domain K+ Channel TREK1 by Local Anesthetic Lidocaine: Negative Cooperativity and Half-of-Sites Saturation Kinetics". Molecular Pharmacology 76, nr 4 (21.07.2009): 903–17. http://dx.doi.org/10.1124/mol.109.056838.

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Rozprawy doktorskie na temat "Human TREK1"

Yuan, Fenghua, Tanmay Dutta, Ling Wang, Lei Song, Liya Gu, Liangyue Qian, Anaid Benitez i in. "Human DNA Exonuclease TREX1 Is Also an Exoribonuclease That Acts on Single-stranded RNA". Digital Commons @ East Tennessee State University, 2015. https://dc.etsu.edu/etsu-works/6537.

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3′ repair exonuclease 1 (TREX1) is a known DNA exonuclease involved in autoimmune disorders and the antiviral response. In this work, we show that TREX1 is also a RNA exonuclease. Purified TREX1 displays robust exoribonuclease activity that degrades single-stranded, but not double-stranded, RNA. TREX1-D200N, an Aicardi-Goutieres syndrome disease-causing mutant, is defective in degrading RNA. TREX1 activity is strongly inhibited by a stretch of pyrimidine residues as is a bacterial homolog, RNase T. Kinetic measurements indicate that the apparent Km of TREX1 for RNA is higher than that for DNA. Like RNase T, human TREX1 is active in degrading native tRNA substrates. Previously reported TREX1 crystal structures have revealed that the substrate binding sites are open enough to accommodate the extra hydroxyl group in RNA, further supporting our conclusion that TREX1 acts on RNA. These findings indicate that its RNase activity needs to be taken into account when evaluating the physiological role of TREX1.

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Gowher, Ali. "Characterization of protein factors targeting RNA into human mitochondria". Phd thesis, Université de Strasbourg, 2013. http://tel.archives-ouvertes.fr/tel-01071841.

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The import of yeast tRNALys (tRK1) into human mitochondria in the presence of cytosolic extract suggests that human cell possesses machinery for tRK1 import. Here, we show that precursor of mitochondrial lysyl-tRNA synthetase (preKARS2) interact with tRK1 and its derivatives containing tRK1 import determinants, and facilitates their import into isolated mitochondria and in vivo, when preKARS2 was overexpressed or downregulated. tRK1 import efficiency increased upon addition of glycolytic enzyme enolase, previously found as an actor of RNA import in yeast. We found that tRK1 and its derivatives translocate into mitochondrial matrix in polynucleotide phosphorylase (PNPase) dependent manner. Furthermore, a point mutation preventing trimerization of PNPase affect import of 5S rRNA and MRP RNA into mitochondria and subsequently mitochondrial translation. Overexpression of the wild-type PNPase induced an increase of 5S rRNA import into mitochondria and rescued translation.

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Harinath, S. "Pharmacological Modulation Of Recombinant Human Two-Pore Domain K+ Channels : Whole-Cell patch-Clamp Analysis". Thesis, 2005. http://etd.iisc.ernet.in/handle/2005/1501.

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Background potassium currents play an important role in the regulation of the resting membrane potential and excitability of mammalian neurons. Recently cloned two- pore domain potassium channels (K2p) are believed to underlie these currents. The roles of K2P channels in general anesthesia and neuroprotection have been proposed recently. In view of this, we investigated the ability of trichloroethanol (an active metabolite of the non-volatile general anesthetic cldoral hydrate, widely used as a pediatric sedative) to modulate the activity of human TREK-1 and TRAAK channels. We found that trichloroethanol potently activates both hTREK-1 and hTRAAK channels at pharmacologically relevant concentrations. The parent compound chloral hydrate was also found to augtnent the activity of both the channels reversibly. Studies with carboxy- terminal deletion mutants (hTREK-1A89, hTREK-1 A100 and hTREK-1 A1 19), suggested that C-terminal tail is not essential for the activation of TREK-1 by trichloroethanol. Our findings identify TREK-1 and TRCL4K channels as molecular targets for trichloroethanol and we propose that activation of both these channels might contribute to the CNS depressant effects of chloral hydrate. Another channel TASK-2, which is essentially absent in the human brain was also found to be potently activated by both trichloroethanol and chloral hydrate. In another series of experiments, we studied the effects of methyl xanthines caffeine and theophylline on hTREK-1 channels. Caffeine and theophylline are used for therapeutic purposes and frequently cause life-threatening convulsive seizures due to systemic toxicity. The mechanisms for the epileptogenicity of caffeine and theophylline are not clear. Recent experiments using knockout mice provided direct evidence for a role for TREK-1 in the control of epileptogenesis. We hypothesized that the epileptogenicity of caffeine and theophylline may be related to the inhibition of TREK-1 channels. We investigated this possibility and observed massive inhibition of TREK-1 channels at toxicologically relevant concentrations. Experiments with the mutant TREK-1 channel (S348A mutant) suggested the involvement of cANP/PKA pathway in the inhibition of TREK-1 channels by caffeine and theophylline. We suggest that inhibition of TREK-1 channels may contribute to the convulsive seizures induced by toxic levels of caffeine and theophylline. Local anesthetics exhibit their clinical effects not only by binding to voltage-gated sodium channels, but also by interacting with other ion channels such as potassium channels. Because of the physiological significance of TREK-1 channels and their abundant expression in peripheral sensory neurons, we investigated the effects of lidocaine to see whether its interaction with 'REK-1 channels contribute to the conduction blockade. Lidocaine caused dose-dependent inhibition of TREK-1channels and the inhibition was voltage-independent. Cytoplasmic C-terminal tail is critically required for lidocaine action. Inhibition of TREK-1 channels is achieved at concentrations for iiz vivo action and this effect may have implications for the clinically observed drug action of lidocaine.

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Książki na temat "Human TREK1"

Duncan, Barrett, red. Star Trek: The Human Frontier. Cambridge: Polity Press, 2001.

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Copyright Paperback Collection (Library of Congress), red. Being Human: Star Trek: New Frontier #12. New York: Pocket Books, 2001.

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Hanley, Richard. Is Data Human?: The Metaphysics of Star Trek. New York: Basic Books, 1998.

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Randolph, Blake, red. Star Trek on the brain: Alien minds, human minds. New York: W.H. Freeman, 1998.

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Johnson, Mike. Star Trek: Boldly go. San Diego, California: Idea & Design Works, LLC, 2018.

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Bonanno, Margaret Wander. Star trek: Strangers from the sky. New York: Simon & Schuster, 1989.

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Stockmyer, John. Life trek: The odyssey of adult development. Atlanta, Ga: Humanics New Age, 1988.

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The double vision of Star Trek: Half-humans, evil twins, and science fiction. Chicago: Cornerstone Press, 1998.

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Carey, Diane. Equinox: Star Trek: Voyager. New York: Pocket, 1999.

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Galanter, Dave. Troublesome Minds: Star Trek. New York: Pocket Books, 2009.

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Części książek na temat "Human TREK1"

Decker, Kevin S. "“The Human Adventure Is Just Beginning”: Star Trek's Secular Society". W The Ultimate Star Trek and Philosophy, 326–39. Oxford, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781119146032.ch31.

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Jaworski, William. "“Today Is a Good Day to Die!” Transporters and Human Extinction". W The Ultimate Star Trek and Philosophy, 148–61. Oxford, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781119146032.ch14.

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Weiss, Dennis M. "Humans, Androids, Cyborgs, and Virtual Beings: All aboard the Enterprise". W The Ultimate Star Trek and Philosophy, 180–89. Oxford, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781119146032.ch17.

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Wassmann, Claudia. "Emotions in Star Trek and Battlestar Galactica: What Makes Us Human". W Emotions in Contemporary TV Series, 205–22. London: Palgrave Macmillan UK, 2016. http://dx.doi.org/10.1007/978-1-137-56885-4_13.

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Vongehr, Frederik. "“A Difficult Weapon to Confiscate” – Ethical Implications of Military Human Enhancement as Reflected in the Science Fiction Genre, Taking Star Trek as an Example". W Ethics of Medical Innovation, Experimentation, and Enhancement in Military and Humanitarian Contexts, 235–60. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-36319-2_14.

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"Space: the human frontier". W Star Trek, 146. Routledge, 2016. http://dx.doi.org/10.4324/9781315516493-31.

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Andrade, Stephen C., i Hilary Mason. "Digital Imaging Trek". W Human Computer Interaction, 2590–613. IGI Global, 2009. http://dx.doi.org/10.4018/978-1-87828-991-9.ch171.

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This chapter introduces the concept and activities of the digitally enabled tourist and the impact such as tourist has on the travel and tourism industry. It summarizes the existing and emerging technical environments that encourage the use of hand held digital recording devices and personal Internet communications. Additionally, it looks at ways tourists publish and exhibit digital visual and written artifacts of their travel experience. The chapter introduces general types of digital communication infrastructure to be considered by the industry to create an experience to support this type of tourism. The authors hope that further understanding of the digitally enabled tourist will inform travel professionals to better facilitate commerce and practice in the industry.

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Andrade, Stephen C., i Hilary Mason. "Digital Imaging Trek". W Selected Readings on the Human Side of Information Technology, 475–98. IGI Global, 2009. http://dx.doi.org/10.4018/978-1-60566-088-2.ch027.

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"A Technological Yet Truly Human Future—as Depicted in Star Trek". W Truly Human Enhancement. The MIT Press, 2013. http://dx.doi.org/10.7551/mitpress/9757.003.0013.

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Agar, Nicholas. "A Technological Yet Truly Human Future—as Depicted in Star Trek". W Truly Human Enhancement, 195–200. The MIT Press, 2014. http://dx.doi.org/10.7551/mitpress/9780262026635.003.0010.

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Streszczenia konferencji na temat "Human TREK1"

Marques, Leonardo, Mauro Amazonas, Thais Castro, Willian Assuncao, Luciana Zaina, Bruno Gadelha i Tayana Conte. "UX trek". W IHC '20: XIX Brazilian Symposium on Human Factors in Computing Systems. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3424953.3426547.

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Axtell, Benett, i Cosmin Munteanu. "Tea, Earl Grey, Hot: Designing Speech Interactions from the Imagined Ideal of Star Trek". W CHI '21: CHI Conference on Human Factors in Computing Systems. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3411764.3445640.

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Neilan, James H., Charles D. Cross, Henry Fan, William L. Fehlman, Lucas Hempley, Mark A. Motter, Garry Qualls, Paul M. Rothhaar, Anna Trujillo i Bonnie D. Allen. "Using Multimodal Input for Autonomous Decision Making for Unmanned Systems - “What it needs in order to evolve, is a human quality. Our capacity to leap beyond logic.” - Capt. Kirk, Star Trek: The Motion Picture". W 15th AIAA Aviation Technology, Integration, and Operations Conference. Reston, Virginia: American Institute of Aeronautics and Astronautics, 2015. http://dx.doi.org/10.2514/6.2015-3032.

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