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Artykuły w czasopismach na temat "Glutamate"
Ishikawa, Makoto. "Abnormalities in Glutamate Metabolism and Excitotoxicity in the Retinal Diseases". Scientifica 2013 (2013): 1–13. http://dx.doi.org/10.1155/2013/528940.
Pełny tekst źródłaMatthews, D. E., M. A. Marano i R. G. Campbell. "Splanchnic bed utilization of glutamine and glutamic acid in humans". American Journal of Physiology-Endocrinology and Metabolism 264, nr 6 (1.06.1993): E848—E854. http://dx.doi.org/10.1152/ajpendo.1993.264.6.e848.
Pełny tekst źródłaWelbourne, Tomas, i Itzhak Nissim. "Regulation of mitochondrial glutamine/glutamate metabolism by glutamate transport: studies with 15N". American Journal of Physiology-Cell Physiology 280, nr 5 (1.05.2001): C1151—C1159. http://dx.doi.org/10.1152/ajpcell.2001.280.5.c1151.
Pełny tekst źródłaDarmaun, D., D. E. Matthews i D. M. Bier. "Glutamine and glutamate kinetics in humans". American Journal of Physiology-Endocrinology and Metabolism 251, nr 1 (1.07.1986): E117—E126. http://dx.doi.org/10.1152/ajpendo.1986.251.1.e117.
Pełny tekst źródłaWelbourne, T. C., K. Horton i M. J. Cronin. "Growth hormone and renal glutamine and glutamate handling." Journal of the American Society of Nephrology 2, nr 7 (styczeń 1992): 1171–77. http://dx.doi.org/10.1681/asn.v271171.
Pełny tekst źródłaVaughn, P. R., C. Lobo, F. C. Battaglia, P. V. Fennessey, R. B. Wilkening i G. Meschia. "Glutamine-glutamate exchange between placenta and fetal liver". American Journal of Physiology-Endocrinology and Metabolism 268, nr 4 (1.04.1995): E705—E711. http://dx.doi.org/10.1152/ajpendo.1995.268.4.e705.
Pełny tekst źródłaNissim, I., B. States, M. Yudkoff i S. Segal. "Characterization of amino acid metabolism by cultured rat kidney cells: study with 15N". American Journal of Physiology-Renal Physiology 253, nr 6 (1.12.1987): F1243—F1252. http://dx.doi.org/10.1152/ajprenal.1987.253.6.f1243.
Pełny tekst źródłaLow, S. Y., P. M. Taylor, H. S. Hundal, C. I. Pogson i M. J. Rennie. "Transport of l-glutamine and l-glutamate across sinusoidal membranes of rat liver. Effects of starvation, diabetes and corticosteroid treatment". Biochemical Journal 284, nr 2 (1.06.1992): 333–40. http://dx.doi.org/10.1042/bj2840333.
Pełny tekst źródłaTa, T. C., F. D. H. Macdowall, M. A. Faris i K. W. Joy. "Metabolism of nitrogen fixed by root nodules of alfalfa (Medicago sativa L.): I. Utilization of [14C, 15N]glutamate and [14C, 15N]glutamine in the synthesis of γ-aminobutyrate". Biochemistry and Cell Biology 66, nr 12 (1.12.1988): 1342–48. http://dx.doi.org/10.1139/o88-155.
Pełny tekst źródłaMoores, R. R., P. R. Vaughn, F. C. Battaglia, P. V. Fennessey, R. B. Wilkening i G. Meschia. "Glutamate metabolism in fetus and placenta of late-gestation sheep". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, nr 1 (1.07.1994): R89—R96. http://dx.doi.org/10.1152/ajpregu.1994.267.1.r89.
Pełny tekst źródłaRozprawy doktorskie na temat "Glutamate"
Boulland, Jean-Luc. "Recycling the amino acid neurotransmitter glutamate in the CNS : l'alchimie du glutamate et de la glutamine". Paris 6, 2004. http://www.theses.fr/2004PA066017.
Pełny tekst źródłaCabré, Segura Gisela. "New photopharmacological tools for the light-induced control of neuronal signalling". Doctoral thesis, Universitat Autònoma de Barcelona, 2019. http://hdl.handle.net/10803/668303.
Pełny tekst źródłaThe main objective of neuroscience is the study and control of neuronal systems. Nowadays, this area is being revolutionised by the use of photoresponsive small molecules, a field known as photopharmacology. By enabling remote activation of drugs with light, photopharmacology seeks to tackle some of the main challenges faced by conventional pharmacology, such as poor drug selectivity and side effects.1 Three main strategies have been derived in this area: photocaged ligands (CL), freely diffusing prodrugs the effect of which is triggered by removing photolabile protecting groups upon illumination; photochromic ligands (PCL), which allow reversible modulation of the response of bioactive molecules through photoisomerisation of appended light-responsive moieties; and photoswitched tethered ligands (PTL), a special case of PCLs that are covalently attached to the therapeutic receptor. Although these approaches have proven to be successful for a variety of therapeutic targets in vitro and in vivo, several challenges still remain in the field of photopharmacology. Therefore, in this work we have aimed at the investigation of new photopharmacological strategies that overcome some of the weaknesses of the tools developed so far. We have particularly focused on the photocontrol of ionotropic glutamate receptors (iGluRs), which play a key role in the modulation of neuronal excitability. The novel photopharmacological tools developed along this thesis consist in: (i) a PTL based on push-pull-substituted azobenzene photoswitches that responds to two-photon excitation with NIR light. (ii) a non-destructive caged ligand that enable irreversible and quantitative conversion from the inactive to the active state, thus performing in a similar fashion as CLs but without by-product generation. (iii) a PCL based on C2-bridged azobenzenes which displays a thermodynamically stable inactive form that selectively turns into the biologically-active state when irradiated. This thesis reports the synthesis, photochemical characterisation and biological activity evaluation of these three novel photopharmacological approaches.
Scott-Taggart, Catherine Patricia. "Inhibition of glutamine production increases glutamate metabolism via the GABA shunt". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ27542.pdf.
Pełny tekst źródłaBarel, Itai. "The regulation of glutamine synthetase and glutamate synthase in Schizosaccharomyces pombe". Thesis, University of Cambridge, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.279649.
Pełny tekst źródłaSilva, Jackeline Thaís da. "Aminoácidos limitantes para o desempenho de bezerros leiteiros: avaliação de teores ótimos e via de fornecimento". Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/11/11139/tde-11112014-163521/.
Pełny tekst źródłaThe aim in this work was to evaluate the concentration of essential amino acids (Lysine and Methionine) considered in the literature as ideal, according to feeding route (milk replacer or starter concentrate), and its association with the supplementation of glutamate and glutamine to calves in two feeding systems: conventional or step-down. In the first study, the chemical composition was analyzed and in amino acids of main milk replacer marketed in Brazil. In the second and third studies, 45 Holstein calves were used, in randomized blocks distributed in treatments: 1) Control: without supplementation; 2) Supplementation with lysine and methionine to reach consumption of 17 and 5.3 g/d, respectively, with correction based on the analysis basis of the milk replacer, 3) Supplementation of lysine and methionine to reach consumption of 17 and 5.3 g/d, respectively, with correction based on the analysis basis of starter concentrate. The difference between the experiments was the feeding system applied to the calves: in the second study, the animals received 6 L/d of milk replacer; while in the third study, the animals were submitted to the step-down system (4L/d until the 2nd week; 8L/d of the 3nd to 6th week; 4L/d of the 7th to 8th week). In the fourth study, the same experimental design was used to evaluate, in a conventional feeding system, treatments: 1) Control: without supplementation; 2) AminoGut 0.6%: milk replacer supplemented with Lysine and Methionine, to reach consumption 17 and 5.3g/d, respectively + 0.6% product containing 10% of glutamate and glutamine; 3) AminoGut 1%: milk replacer supplemented with Lysine and Methionine to reach consumption 17 and 5.3g/d + 0.6% product containing 10% of glutamate and glutamine. The animals were housed in individual hutches, with free access to water and starter concentrate. The consumption of starter concentrate and fecal scores of animals were monitored daily. Body growth was weighed and measured weekly. In weeks 2, 4, 6, 8 and 10, blood samples were collected to determine the metabolites as markers of protein status of animals (albumin, total protein, N-urea), energy status (glucose and BHBA), bone growth (alkaline phosphatase) and muscular growth (creatinine). The composition of amino acids of the milk replacer marketed in Brazil was lower than expected for diet that replaces the whole milk. In study 2 and 3, the supplementation of the milk replacer or starter concentrate with lysine and methionine resulted in no benefit on dairy calves performance or metabolism. In study 4 the supplementation of the milk replacer with lysine and methionine in association with glutamate and glutmine had no effect on performance, gut health nor metabolism of dairy calves.
Apricò, Karina 1977. "[3H](2S,4R)-4-methylglutamate as a novel radioligand for brain glutamate transporters". Monash University, Dept. of Pharmacology, 2003. http://arrow.monash.edu.au/hdl/1959.1/5497.
Pełny tekst źródłaGirard, Benoît. "Impact de l’activation du récepteur mGlu7 dans l’épilepsie". Thesis, Montpellier, 2018. http://www.theses.fr/2018MONTT038.
Pełny tekst źródłaEpilepsy affects millions of patients worldwide. The available treatments are symptomatic, they treat seizures without preventing the progression of the disease and have heavy side effects. The discovery of new therapeutic targets and new compounds is therefore essential to overcome the limitations of current therapeutic strategies. Previous studies have demonstrated substantial involvement of the mGlu7 receptor in modulating not only excitability but also hypersynchronization of neural networks, two crucial factors affecting epileptic seizures. These discoveries were at the origin of a first publication that I completed at the beginning of my thesis (Tassin, Girard et al., 2016).Using a new mGlu7 receptor agonist, LSP2-9166, in my thesis I then studied the impact of this receptor in different epilepsy models in mice. Two complementary models were used: kindling, a chemical model induced by pentylenetetrazol (PTZ) which sensitizes the brain to induce generalized tonic-clonic seizures, and intra-hippocampal injection of kainate, mimicking mesial temporal lobe epilepsy in humans.At first, I observed an attenuation of the progression of the seizures severity in the PTZ kindling model, under the activation of the mGlu7 receptor. This effect was correlated with weaker inflammation, and microglial and astrocytic activation. In the intra-hippocampal injection model of KA, considered as drug-resistant, activation of the mGlu7 receptor during the epileptogenesis period increased the duration of interictal periods and decreased the duration of seizures as well as neuronal reorganization. Once chronic seizures were established, acute activation of the mGlu7 receptor decreased the number of seizures as strongly as diazepam, commonly used in clinical settings. Finally, chronic injections of LSP2-9166 into naive (non epileptic) animals do not generate any detectable cognitive or behavioral deficits or changes in mGlu7 receptor mRNA level. The activation of the mGlu7 receptor thus presents a strategic target in our two models.This work provides a better understanding of the role of the mGlu7 receptor in epileptogenesis. It participates in the search for future more adequate treatments
Sachidhanandam, Shankar. "Rôle des récepteurs kaïnate dans le transfert d'information dans l'hippocampe". Bordeaux 2, 2007. http://www.theses.fr/2007BOR21433.
Pełny tekst źródłaKainate receptors (KAR) are ionotropic glutamate receptors implicated in the regulation of synaptic transmission and neuronal excitability. At the mossy fiber (Mf) synapse, KARs can be expressed both pre and postsynaptically. In this study, we examined physiological role of KARs in information transfer at the Mf-CA3 pyramidal cell synapse in the mouse hippocampus. We show that KARs can operate in dual mode, by a direct ionotropic action via GluR6, and an indirect G-protein coupled mechanism requiring the binding of glutamate to KA2, to inhibit the slow afterhyperpolarization (IsAHP), hence enhancing neuronal excitability. Using mice deficient for the various KAR subunits, we show that postsynaptic KARs shape the waveform of unitary EPSPs, and pre and postsynaptic KARs act together to amplify unitary EPSPs, triggering spike discharge under conditions of sustained mossy fiber activity. KARs improve timing precision within a frequency range of 3 to 50 Hz and modulation of IsAHP by KA2 facilitates spike discharge in prolonged stimulus trains. KARs are permissive to the induction of LTP at the associative/commissural input. Physiological patterns of afferent input reproduce the output obtained with controlled stimulus inputs. Hence KARs act as amplifiers of synaptic transmission, to enhance the transfer of information at the Mf-CA3 pyramidal cell synapse
Martin, Emily P. "Expression of glutamate dehydrogenase and glutamine synthetase RNA in preimplantation mouse embryos". Virtual Press, 1999. http://liblink.bsu.edu/uhtbin/catkey/1117849.
Pełny tekst źródłaDepartment of Biology
Saito, Kelly Cristina. "Envolvimento de Rac1 na excitotoxicidade induzida por NMDA na retina de ratos". Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-10022012-132908/.
Pełny tekst źródłaOveractivation of NMDA receptors has been described to trigger neuronal death that occurs in diseases such as glaucoma. It is possible that the combination of subunits (NR2A-D) activate intracellular signaling pathways that result in death or survival. Our aim was to investigate the involvement of NR2 subunits and Rac1, a member of Rho GTPase family, in retinal neuronal death. Glutamate-induced neuronal death in vitro was reduced after Rac1 inhibition and by NR2B blocking, but not NR2C/D subunits. Similar results were obtained in vivo after NMDA intravitreous injection, although active Rac1 was mainly detected in Müller glia processes, and it was inhibited by NR2B blockade. In addition, TNF-α level after NMDA injection were reduced by NR2B blocking and Rac1. Thus, our results suggest that excitotoxicity via NR2B/NMDA receptors activate Rac1 in Müller glia cells, which in turn controls the TNF-α production that triggers retinal ganglion cell death.
Książki na temat "Glutamate"
Schousboe, Arne, i Ursula Sonnewald, red. The Glutamate/GABA-Glutamine Cycle. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-45096-4.
Pełny tekst źródłaAlton, Meister, red. Glutamate, glutamine, glutathione, and related compounds. Orlando, Fla: Academic Press, 1985.
Znajdź pełny tekst źródłaP, Ottersen O., i Storm-Mathisen Jon, red. Glutamate. Amsterdam: Elsevier, 2000.
Znajdź pełny tekst źródłaBurger, Corinna, i Margaret Jo Velardo, red. Glutamate Receptors. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9077-1.
Pełny tekst źródłaHerman, Barbara H., Jerry Frankenheim, Raye Z. Litten, Philip H. Sheridan, Forrest F. Weight i Stephen R. Zukin. Glutamate and Addiction. New Jersey: Humana Press, 2002. http://dx.doi.org/10.1385/1592593062.
Pełny tekst źródłaGereau, Robert W., i Geoffrey T. Swanson, red. The Glutamate Receptors. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-055-3.
Pełny tekst źródłaH, Herman Barbara, i Frankenheim Jerry, red. Glutamate and addiction. Totowa, N.J: Humana Press, 2003.
Znajdź pełny tekst źródłaBaskys, Andrius. Metabotropic glutamate receptors. Austin: R.G. Landes Co., 1994.
Znajdź pełny tekst źródłaPavlovic, Zoran M., red. Glutamate and Neuropsychiatric Disorders. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-87480-3.
Pełny tekst źródłaConn, P. Jeffrey, i Jitendra Patel, red. The Metabotropic Glutamate Receptors. Totowa, NJ: Humana Press, 1994. http://dx.doi.org/10.1007/978-1-4757-2298-7.
Pełny tekst źródłaCzęści książek na temat "Glutamate"
Sanzone, Marla. "Glutamate". W Encyclopedia of Clinical Neuropsychology, 1160–62. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_1661.
Pełny tekst źródłaSanzone, Marla. "Glutamate". W Encyclopedia of Clinical Neuropsychology, 1–3. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56782-2_1661-2.
Pełny tekst źródłaSanzone, Marla. "Glutamate". W Encyclopedia of Clinical Neuropsychology, 1587–89. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_1661.
Pełny tekst źródłaManji, Husseini K., Jorge Quiroz, R. Andrew Chambers, Anthony Absalom, David Menon, Patrizia Porcu, A. Leslie Morrow i in. "Glutamate". W Encyclopedia of Psychopharmacology, 559. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1695.
Pełny tekst źródłaNistri, Andrea. "Glutamate". W Neurotransmitter Actions in the Vertebrate Nervous System, 101–23. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4961-7_4.
Pełny tekst źródłaYuen, Eunice. "Glutamate". W Encyclopedia of Autism Spectrum Disorders, 1–2. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-6435-8_102077-1.
Pełny tekst źródłaDuce, Ian R. "Glutamate". W Comparative Invertebrate Neurochemistry, 42–89. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4615-9804-6_2.
Pełny tekst źródłaMurala, Sireesha, Aditya Boddu i Pradeep C. Bollu. "Glutamate". W Neurochemistry in Clinical Practice, 91–107. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-07897-2_5.
Pełny tekst źródłaYuen, Eunice. "Glutamate". W Encyclopedia of Autism Spectrum Disorders, 2258. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-91280-6_102077.
Pełny tekst źródłaÖz, Gülin, David A. Okar i Pierre-Gilles Henry. "Glutamate-Glutamine Cycle and Anaplerosis". W Neural Metabolism In Vivo, 921–46. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4614-1788-0_32.
Pełny tekst źródłaStreszczenia konferencji na temat "Glutamate"
Syafiie, S., i I. H. Mustafa. "Single compartment modeling glutamine-glutamate-GABA system in neuron". W 2016 IEEE EMBS Conference on Biomedical Engineering and Sciences (IECBES). IEEE, 2016. http://dx.doi.org/10.1109/iecbes.2016.7843506.
Pełny tekst źródłaRahman, M. M., T. Yamazaki, T. Ikeda, M. Ishida i K. Sawada. "Development of a glutamate biosensor based on glutamate oxidase using smart-biochips". W TRANSDUCERS 2009 - 2009 International Solid-State Sensors, Actuators and Microsystems Conference. IEEE, 2009. http://dx.doi.org/10.1109/sensor.2009.5285556.
Pełny tekst źródłaSakinyte-Urbikiene, Ieva, Vidute Gureviciene i Julija Razumiene. "Amperometric Biosensing of L-Glutamate Using Reduced Graphene Oxide and Glutamate Oxidase". W Eurosensors 2023. Basel Switzerland: MDPI, 2024. http://dx.doi.org/10.3390/proceedings2024097005.
Pełny tekst źródłaMacpherson, IR, E. Dornier, N. Rabas, E. Rainero i JC Norman. "Abstract P6-01-06: Glutamine metabolism drives breast cancer invasion by providing a source of extracellular glutamate to activate the GRM3 metabotropic glutamate receptor". W Abstracts: 2016 San Antonio Breast Cancer Symposium; December 6-10, 2016; San Antonio, Texas. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.sabcs16-p6-01-06.
Pełny tekst źródłaBernal-Martínez, Juan. "L-glutamate Receptor In Paramecium". W MEDICAL PHYSICS: Eighth Mexican Symposium on Medical Physics. AIP, 2004. http://dx.doi.org/10.1063/1.1811853.
Pełny tekst źródłaLee, Gija, Seokkeun Choi, Sungwook Kang, Samjin Choi, Jeonghoon Park, Dong Hyun Park, Youngho Park, Kyungsook Kim, Bermseok Oh i Hunkuk Park. "Changes in Extracellular Glutamate Release on Repetitive Transient Occlusion in Global Ischemia Model". W ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206602.
Pełny tekst źródłaMohan, A., J. Gall, S. Nair i P. Kalivas. "Glutamate Dynamics in the PFC-NAC Synapse". W ASME 2006 International Mechanical Engineering Congress and Exposition. ASMEDC, 2006. http://dx.doi.org/10.1115/imece2006-15401.
Pełny tekst źródłaKotake, Naoki, Takafumi Suzuki, Osamu Fukayama i Kunihiko Mabuchi. "A flexible parylene-based glutamate sensor". W 5th International IEEE/EMBS Conference on Neural Engineering (NER 2011). IEEE, 2011. http://dx.doi.org/10.1109/ner.2011.5910550.
Pełny tekst źródłaGao, Yong. "UASB Treatment of Monosodium Glutamate Wastewater". W 2010 4th International Conference on Bioinformatics and Biomedical Engineering (iCBBE). IEEE, 2010. http://dx.doi.org/10.1109/icbbe.2010.5516404.
Pełny tekst źródłaXiao, Guihua, Yilin Song, Song Zhang, Shengwei Xu, Lili Yang, Huiren Xu i Xinxia Cai. "Microelectrode arrays studies of glutamate excitatory pathway in hippocampus CA3 by offside KCl and glutamate stimulating". W 2017 8th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2017. http://dx.doi.org/10.1109/ner.2017.8008333.
Pełny tekst źródłaRaporty organizacyjne na temat "Glutamate"
Niu, Li. Glutamate Receptor Aptamers and ALS. Fort Belvoir, VA: Defense Technical Information Center, styczeń 2008. http://dx.doi.org/10.21236/ada481452.
Pełny tekst źródłaRisbrough, Victoria. Glutamate Transmission Enhancement for Treatment of PTSD. Fort Belvoir, VA: Defense Technical Information Center, marzec 2009. http://dx.doi.org/10.21236/ada506358.
Pełny tekst źródłaMichaelis, Elias K. Molecular Characteristics of Membrane Glutamate Receptor-Ionophore Interaction. Fort Belvoir, VA: Defense Technical Information Center, październik 1988. http://dx.doi.org/10.21236/ada201954.
Pełny tekst źródłaSurmeier, James. Glutamate Signaling and Mitochnodrial Dysfunction in Models of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, grudzień 2012. http://dx.doi.org/10.21236/ada602445.
Pełny tekst źródłaSurmeier, D. J. Glutamate Signaling and Mitochondrial Dysfunction in Models of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, marzec 2014. http://dx.doi.org/10.21236/ada604089.
Pełny tekst źródłaStern, Michael. Group II Metabotropic Glutamate Receptors as Potential Pharmaceutical Targets for Neurofibroma Formation. Fort Belvoir, VA: Defense Technical Information Center, luty 2010. http://dx.doi.org/10.21236/ada542280.
Pełny tekst źródłaStern, Michael. Group II Metabotropic Glutamate Receptors as Potential Pharmaceutical Targets for Neurofibroma Formation. Fort Belvoir, VA: Defense Technical Information Center, luty 2011. http://dx.doi.org/10.21236/ada542347.
Pełny tekst źródłaFromm, Hillel, i Joe Poovaiah. Calcium- and Calmodulin-Mediated Regulation of Plant Responses to Stress. United States Department of Agriculture, wrzesień 1993. http://dx.doi.org/10.32747/1993.7568096.bard.
Pełny tekst źródłaAkanji, Bukunmi Abongwa. Functional expression of a glutamate-gated chloride channel (GLC-3) from adult Brugia malayi. Ames (Iowa): Iowa State University, styczeń 2018. http://dx.doi.org/10.31274/cc-20240624-771.
Pełny tekst źródłaLiu, Ya F. Molecular Analysis of the Common Signaling Mechanism of Neuronal Death Induced by Glutamate and Mutated Huntington. Fort Belvoir, VA: Defense Technical Information Center, marzec 2001. http://dx.doi.org/10.21236/ada393700.
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