Gotowa bibliografia na temat „Glutamate transporter GLAST”
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Artykuły w czasopismach na temat "Glutamate transporter GLAST"
Chen, Zhiqiang, Sharon G. Kujawa i William F. Sewell. "Functional Roles of High-Affinity Glutamate Transporters in Cochlear Afferent Synaptic Transmission in the Mouse". Journal of Neurophysiology 103, nr 5 (maj 2010): 2581–86. http://dx.doi.org/10.1152/jn.00018.2010.
Pełny tekst źródłaSARTHY, VIJAY P., V. JOSEPH DUDLEY i KOHICHI TANAKA. "Retinal glucose metabolism in mice lacking the L-glutamate/aspartate transporter". Visual Neuroscience 21, nr 4 (lipiec 2004): 637–43. http://dx.doi.org/10.1017/s0952523804214122.
Pełny tekst źródłaFujita, Hiroko, Kohji Sato, Tong-Chun Wen, Yi Peng i Masahiro Sakanaka. "Differential Expressions of Glycine Transporter 1 and Three Glutamate Transporter mRNA in the Hippocampus of Gerbils with Transient Forebrain Ischemia". Journal of Cerebral Blood Flow & Metabolism 19, nr 6 (czerwiec 1999): 604–15. http://dx.doi.org/10.1097/00004647-199906000-00003.
Pełny tekst źródłaHernández-Melchor, Dinorah, Leticia Ramírez-Martínez, Luis Cid, Cecilia Palafox-Gómez, Esther López-Bayghen i Arturo Ortega. "EAAT1-dependent slc1a3 Transcriptional Control depends on the Substrate Translocation Process". ASN Neuro 14 (styczeń 2022): 175909142211165. http://dx.doi.org/10.1177/17590914221116574.
Pełny tekst źródłaTAMAHARA, Satoshi, Mutsumi INABA, Kota SATO, Naoaki MATSUKI, Yoshiaki HIKASA i Ken-ichiro ONO. "Non-essential roles of cysteine residues in functional expression and redox regulatory pathways for canine glutamate/aspartate transporter based on mutagenic analysis". Biochemical Journal 367, nr 1 (1.10.2002): 107–11. http://dx.doi.org/10.1042/bj20011843.
Pełny tekst źródłaDeng, Yu, Zhao-Fa Xu, Wei Liu, Bin Xu, Hai-Bo Yang i Yan-Gang Wei. "Riluzole-Triggered GSH Synthesis via Activation of Glutamate Transporters to Antagonize Methylmercury-Induced Oxidative Stress in Rat Cerebral Cortex". Oxidative Medicine and Cellular Longevity 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/534705.
Pełny tekst źródłaHuggett, J. F., A. Mustafa, L. O'Neal i D. J. Mason. "The glutamate transporter GLAST-I (EAAT-I) is expressed in the plasma membrane of osteocytes and is responsive to extracellular glutamate concentration". Biochemical Society Transactions 30, nr 6 (1.11.2002): 890–93. http://dx.doi.org/10.1042/bst0300890.
Pełny tekst źródłaPiao, Chun-Shu, Ashley L. Holloway, Sue Hong-Routson i Mark S. Wainwright. "Depression following traumatic brain injury in mice is associated with down-regulation of hippocampal astrocyte glutamate transporters by thrombin". Journal of Cerebral Blood Flow & Metabolism 39, nr 1 (14.11.2017): 58–73. http://dx.doi.org/10.1177/0271678x17742792.
Pełny tekst źródłaMoshrefi-Ravasdjani, Behrouz, Daniel Ziemens, Nils Pape, Marcel Färfers i Christine Rose. "Action Potential Firing Induces Sodium Transients in Macroglial Cells of the Mouse Corpus Callosum". Neuroglia 1, nr 1 (3.07.2018): 106–25. http://dx.doi.org/10.3390/neuroglia1010009.
Pełny tekst źródłaMiyazaki, Taisuke, Miwako Yamasaki, Kouichi Hashimoto, Kazuhisa Kohda, Michisuke Yuzaki, Keiko Shimamoto, Kohichi Tanaka, Masanobu Kano i Masahiko Watanabe. "Glutamate transporter GLAST controls synaptic wrapping by Bergmann glia and ensures proper wiring of Purkinje cells". Proceedings of the National Academy of Sciences 114, nr 28 (27.06.2017): 7438–43. http://dx.doi.org/10.1073/pnas.1617330114.
Pełny tekst źródłaRozprawy doktorskie na temat "Glutamate transporter GLAST"
Kinoshita, Nagatoki. "Mammalian septin Sept2 modulates the activity of GLAST, a glutamate transporter in astrocytes". Kyoto University, 2004. http://hdl.handle.net/2433/147473.
Pełny tekst źródłaNguyen, Khoa Thuy Diem. "Energy metabolism in the brain and rapid distribution of glutamate transporter GLAST in astrocytes". Thesis, The University of Sydney, 2008. http://hdl.handle.net/2123/3996.
Pełny tekst źródłaNguyen, Khoa Thuy Diem. "Energy metabolism in the brain and rapid distribution of glutamate transporter GLAST in astrocytes". University of Sydney, 2008. http://hdl.handle.net/2123/3996.
Pełny tekst źródłaGlutamate transporters play a role in removing extracellular excitatory neurotransmitter, L-glutamate into the cells. The rate of the uptake depends on the density of the transporters at the membrane. Some studies claimed that glutamate transporters could transit between the cytoplasm and the membrane on a time-scale of minutes. The present study examined the distribution of glutamate transporter GLAST predominantly expressed in rat cortical cultured astrocytes between the membrane and the cytoplasm by using deconvolution microscopy and then analyzing the images. The regulation of the distribution of GLAST was studied in the presence of glutamate transporter substrate (D-aspartate), purinergic receptor activators (α,β-methylene ATP, adenosine), neuroleptic drugs (clozapine, haloperidol), ammonia (hyperammonia) and Na+/K+-ATPase inhibitors (ouabain, digoxin and FCCP). It was demonstrated that the translocation of GLAST towards the plasma membrane was induced by D-aspartate, α,β-methylene ATP, adenosine, clozapine and ammonia (at 100 μM and very high concentrations of 10 mM). However, the inhibition of Na+/K+-ATPase activity had an opposite effect, resulting in redistribution of GLAST away from the membrane. It has previously been claimed that the membrane-cytoplasm trafficking of GLAST was regulated by phosphorylation catalysed by protein kinase C delta (PKC-delta). Involvement of this mechanism has, however, been put to doubt when rottlerin, a PKC-delta inhibitor, used to test the hypothesis showed to inhibit Na+/K+-ATPase-mediated uptake of Rb+, suggesting that rottlerin influenced the activity of Na+/K+-ATPase. As Na+/K+-ATPase converts ATP to energy and pumps Na+, K+ ions, thus helping to maintain normal electrochemical and ionic gradients across the cell membrane. Its inhibition also reduced D-aspartate transport and could impact on the cytoplasm-to-membrane traffic of GLAST molecules. Furthermore, rottlerin decreased the activity of Na+/K+-ATPase by acting as a mitochondrial inhibitor. The present study has focused on the inhibition of Na+/K+-ATPase activity by rottlerin, ouabain and digoxin in homogenates prepared from rat kidney and cultured astrocytes. The activity of Na+/K+-ATPase was measured by the absorption of inorganic phosphate product generated from the hydrolysis of ATP and the fluorescent transition of the dye RH421 induced by the movement of Na+/K+-ATPase. This approach has a potential to test whether the rottlerin effect on Na+/K+-ATPase is a direct inhibition of the enzyme activity. Rottlerin has been found to block the activity of Na+/K+-ATPase in a dose-dependent manner in both rat kidney and astrocyte homogenates. Therefore, rottlerin inhibited the activity of Na+/K+-ATPase directly in a cell-free preparation, thus strongly indicating that the effect was direct on the enzyme. In parallel experiments, ouabain and digoxin produced similar inhibitions of Na+/K+-ATPase activity in rat kidney while digoxin blocked the activity of Na+/K+-ATPase to a greater extent than ouabain in rat cortical cultured astrocytes. In a separate set of experiments, Na+/K+-ATPase in the astrocytic membrane was found to be unsaturated in E1(Na+)3 conformation in the presence of Na+ ions and this could explain the differences between the effects of digoxin and ouabain on the activity of Na+/K+-ATPase in rat astrocytes. In addition, it was found that at low concentrations of rottlerin, the activity of Na+/K+-ATPase was increased rather than inhibited. This effect was further investigated by studying rottlerin interactions with membrane lipids. The activity of Na+/K+-ATPase has been reported to be regulated by membrane lipids. The enzyme activity can be enhanced by increasing fluidity of the lipid membrane. I have, therefore, proposed that rottlerin binds to the membrane lipids and the effects of rottlerin on Na+/K+-ATPase are mediated by changes in the properties (fluidity) of the membrane. The hypothesis was tested by comparing rottlerin and a detergent, DOC (sodium deoxycholate), for their binding to the lipids by using a DMPC (1,2-Dimyristoyl-sn-Glycero-3-Phosphocholine) monolayer technique. DOC has been shown to both increase and inhibit activity of Na+/K+-ATPase in a manner similar to that displayed by rottlerin. The effects of rottlerin and DOC on the DMPC monolayers were studied by measuring the surface pressure of DMPC monolayers and surface area per DMPC molecule. I established that both rottlerin and DOC decreased the surface pressure of DMPC monolayers and increased the surface area per DMPC molecule. This indicates that both rottlerin and DOC penetrated into the DMPC monolayers. If rottlerin can interact with the lipids, changes in fluidity of the lipid membrane cannot be ruled out and should be considered as a possible factor contributing to the effects of rottlerin on the activity of Na+/K+-ATPase. Overall, the study demonstrates that rottlerin is not only a PKC-delta inhibitor but can have additional effects, both on the enzyme activities (Na+/K+-ATPase) and/or on lipid-containing biological structures such as membranes. The findings have implication not only for studies where rottlerin was used as a supposedly specific PKC-delta inhibitor but also for mechanisms of its toxicity.
Hulme, Julie Anne. "Ultrastructural and immunocytochemical studies of the glutamate/aspartate transporter, GLAST, and its relationship to glutamate handling in the mammalian cochlea". Thesis, Keele University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.401057.
Pełny tekst źródłaMeyer, Logan. "Novel Role of the Nociceptin System as a Regulator of Glutamate Transporter Expression in Developing Astrocytes". VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4931.
Pełny tekst źródłaAlshehri, Fahad. "Role of Modulating Glutamate Transporters on Hydrocodone and Alcohol Co-Abuse inAlcohol-Preferring Rats". University of Toledo Health Science Campus / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=mco153245611012862.
Pełny tekst źródłaColin, Angélique. "Développement d'un vecteur lentiviral ciblant les astrocytes et mise en application dans l'étude des transporteurs au glutamate GLAST et GLT-1". Phd thesis, Université Pierre et Marie Curie - Paris VI, 2008. http://tel.archives-ouvertes.fr/tel-00348988.
Pełny tekst źródłaColin, Angélique. "Développement d’un vecteur lentiviral ciblant les astrocytes in vivo et mise en application dans l’étude des transporteurs au glutamate GLAST et GLT-1". Paris 6, 2008. http://www.theses.fr/2008PA066423.
Pełny tekst źródłaSATO, Kota. "Molecular Pathobiological Studies on Glutamate/Aspartate Transporter (GLAST) in Canine Red Cells : Molecular Basis for Hereditary Deficiency of GLAST in Dogs". Doctoral thesis, 2000. http://hdl.handle.net/2115/28086.
Pełny tekst źródłaCzęści książek na temat "Glutamate transporter GLAST"
Tserga, Evangelia, Peter Damberg, Barbara Canlon i Christopher R. Cederroth. "Auditory synaptopathy in mice lacking the glutamate transporter GLAST and its impact on brain activity". W Progress in Brain Research. Elsevier, 2020. http://dx.doi.org/10.1016/bs.pbr.2020.04.004.
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