Relevant bibliographies by topics / GluK1 receptors

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  2. Dissertations / Theses
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Academic literature on the topic 'GluK1 receptors'

Author: Grafiati
Published: 14 March 2023

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Journal articles on the topic "GluK1 receptors"

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Chałupnik, Paulina, Alina Vialko, Darryl S. Pickering, Markus Hinkkanen, Stephanie Donbosco, Thor C. Møller, Anders A. Jensen, et al. "Discovery of the First Highly Selective Antagonist of the GluK3 Kainate Receptor Subtype." International Journal of Molecular Sciences 23, no. 15 (August 8, 2022): 8797. http://dx.doi.org/10.3390/ijms23158797.

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Kainate receptors belong to the family of glutamate receptors ion channels, which are responsible for the majority of rapid excitatory synaptic transmission in the central nervous system. The therapeutic potential of kainate receptors is still poorly understood, which is also due to the lack of potent and subunit-selective pharmacological tools. In search of selective ligands for the GluK3 kainate receptor subtype, a series of quinoxaline-2,3-dione analogues was synthesized and pharmacologically characterized at selected recombinant ionotropic glutamate receptors. Among them, compound 28 was found to be a competitive GluK3 antagonist with submicromolar affinity and unprecedented high binding selectivity, showing a 400-fold preference for GluK3 over other homomeric receptors GluK1, GluK2, GluK5 and GluA2. Furthermore, in functional assays performed for selected metabotropic glutamate receptor subtypes, 28 did not show agonist or antagonist activity. The molecular determinants underlying the observed affinity profile of 28 were analyzed using molecular docking and molecular dynamics simulations performed for individual GluK1 and GluK3 ligand-binding domains.
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Jaremko, William, Zhen Huang, Nicholas Karl, Vincen D. Pierce, Janet Lynch, and Li Niu. "A kainate receptor–selective RNA aptamer." Journal of Biological Chemistry 295, no. 19 (March 11, 2020): 6280–88. http://dx.doi.org/10.1074/jbc.ra119.011649.

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Kainate and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors are two major, closely related receptor subtypes in the glutamate ion channel family. Excessive activities of these receptors have been implicated in a number of central nervous system diseases. Designing potent and selective antagonists of these receptors, especially of kainate receptors, is useful for developing potential treatment strategies for these neurological diseases. Here, we report on two RNA aptamers designed to individually inhibit kainate and AMPA receptors. To improve the biostability of these aptamers, we also chemically modified these aptamers by substituting their 2′-OH group with 2′-fluorine. These 2′-fluoro aptamers, FB9s-b and FB9s-r, were markedly resistant to RNase-catalyzed degradation, with a half-life of ∼5 days in rat cerebrospinal fluid or serum-containing medium. Furthermore, FB9s-r blocked AMPA receptor activity. Aptamer FB9s-b selectively inhibited GluK1 and GluK2 kainate receptor subunits, and also GluK1/GluK5 and GluK2/GluK5 heteromeric kainate receptors with equal potency. This inhibitory profile makes FB9s-b a powerful template for developing tool molecules and drug candidates for treatment of neurological diseases involving excessive activities of the GluK1 and GluK2 subunits.
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Sheng, Nengyin, Yun Stone Shi, and Roger A. Nicoll. "Amino-terminal domains of kainate receptors determine the differential dependence on Neto auxiliary subunits for trafficking." Proceedings of the National Academy of Sciences 114, no. 5 (January 18, 2017): 1159–64. http://dx.doi.org/10.1073/pnas.1619253114.

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The kainate receptor (KAR), a subtype of glutamate receptor, mediates excitatory synaptic responses at a subset of glutamatergic synapses. However, the molecular mechanisms underlying the trafficking of its different subunits are poorly understood. Here we use the CA1 hippocampal pyramidal cell, which lacks KAR-mediated synaptic currents, as a null background to determine the minimal requirements for the extrasynaptic and synaptic expression of the GluK2 subunit. We find that the GluK2 receptor itself, in contrast to GluK1, traffics to the neuronal surface and synapse efficiently and the auxiliary subunits Neto1 and Neto2 caused no further enhancement of these two trafficking processes. However, the regulation of GluK2 biophysical properties by Neto proteins is the same as that of GluK1. We further determine that it is the amino-terminal domains (ATDs) of GluK1 and GluK2 that control the strikingly different trafficking properties between these two receptors. Moreover, the ATDs are critical for synaptic expression of heteromeric receptors at mossy fiber–CA3 synapses and also mediate the differential dependence on Neto proteins for surface and synaptic trafficking of GluK1 and GluK2. These results highlight the fundamental differences between the two major KAR subunits and their interplay with Neto auxiliary proteins.
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Pollok, Stefan, and Andreas Reiner. "Subunit-selective iGluR antagonists can potentiate heteromeric receptor responses by blocking desensitization." Proceedings of the National Academy of Sciences 117, no. 41 (September 30, 2020): 25851–58. http://dx.doi.org/10.1073/pnas.2007471117.

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Ionotropic glutamate receptors (iGluRs) are key molecules for synaptic signaling in the central nervous system, which makes them promising drug targets. Intensive efforts are being devoted to the development of subunit-selective ligands, which should enable more precise pharmacologic interventions while limiting the effects on overall neuronal circuit function. However, many AMPA and kainate receptor complexes in vivo are heteromers composed of different subunits. Despite their importance, little is known about how subunit-selective ligands affect the gating of heteromeric iGluRs, namely their activation and desensitization properties. Using fast ligand application experiments, we studied the effects of competitive antagonists that block glutamate from binding at part of the four subunits. We found that UBP-310, a kainate receptor antagonist with high selectivity for GluK1 subunits, reduces the desensitization of GluK1/GluK2 heteromers and fully abolishes the desensitization of GluK1/GluK5 heteromers. This effect is mirrored by subunit-selective agonists and heteromeric receptors that contain binding-impaired subunits, as we show for both kainate and GluA2 AMPA receptors. These findings are consistent with a model in which incomplete agonist occupancy at the four receptor subunits can provide activation without inducing desensitization. However, we did not detect significant steady-state currents during UBP-310 dissociation from GluK1 homotetramers, indicating that antagonist dissociation proceeds in a nonuniform and cooperativity-driven manner, which disfavors nondesensitizing occupancy states. Besides providing mechanistic insights, these results have direct implications for the use of subunit-selective antagonists in neuroscience research and envisioned therapeutic interventions.
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Jaremko, William J., Zhen Huang, Wei Wen, Andrew Wu, Nicholas Karl, and Li Niu. "Identification and characterization of RNA aptamers: A long aptamer blocks the AMPA receptor and a short aptamer blocks both AMPA and kainate receptors." Journal of Biological Chemistry 292, no. 18 (March 21, 2017): 7338–47. http://dx.doi.org/10.1074/jbc.m116.774752.

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AMPA and kainate receptors, along with NMDA receptors, represent different subtypes of glutamate ion channels. AMPA and kainate receptors share a high degree of sequence and structural similarities, and excessive activity of these receptors has been implicated in neurological diseases such as epilepsy. Therefore, blocking detrimental activity of both receptor types could be therapeutically beneficial. Here, we report the use of an in vitro evolution approach involving systematic evolution of ligands by exponential enrichment with a single AMPA receptor target (i.e. GluA1/2R) to isolate RNA aptamers that can potentially inhibit both AMPA and kainate receptors. A full-length or 101-nucleotide (nt) aptamer selectively inhibited GluA1/2R with a KI of ∼5 μm, along with GluA1 and GluA2 AMPA receptor subunits. Of note, its shorter version (55 nt) inhibited both AMPA and kainate receptors. In particular, this shorter aptamer blocked equally potently the activity of both the GluK1 and GluK2 kainate receptors. Using homologous binding and whole-cell recording assays, we found that an RNA aptamer most likely binds to the receptor's regulatory site and inhibits it noncompetitively. Our results suggest the potential of using a single receptor target to develop RNA aptamers with dual activity for effectively blocking both AMPA and kainate receptors.
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Koga, Kohei, Su-Eon Sim, Tao Chen, Long-Jun Wu, Bong-Kiun Kaang, and Min Zhuo. "Kainate receptor-mediated synaptic transmissions in the adult rodent insular cortex." Journal of Neurophysiology 108, no. 7 (October 1, 2012): 1988–98. http://dx.doi.org/10.1152/jn.00453.2012.

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Kainate (KA) receptors are expressed widely in the central nervous system and regulate both excitatory and inhibitory synaptic transmission. KA receptors play important roles in fear memory, anxiety, and pain. However, little is known about their function in synaptic transmission in the insular cortex (IC), a critical region for taste, memory, and pain. Using whole cell patch-clamp recordings, we have shown that KA receptors contribute to fast synaptic transmission in neurons in all layers of the IC. In the presence of the GABAA receptor antagonist picrotoxin, the NMDA receptor antagonist AP-5, and the selective AMPA receptor antagonist GYKI 53655, KA receptor-mediated excitatory postsynaptic currents (KA EPSCs) were revealed. We found that KA EPSCs are ∼5–10% of AMPA/KA EPSCs in all layers of the adult mouse IC. Similar results were found in adult rat IC. KA EPSCs had a significantly slower rise time course and decay time constant compared with AMPA receptor-mediated EPSCs. High-frequency repetitive stimulations at 200 Hz significantly facilitated the summation of KA EPSCs. In addition, genetic deletion of GluK1 or GluK2 subunit partially reduced postsynaptic KA EPSCs, and exposure of GluK2 knockout mice to the selective GluK1 antagonist UBP 302 could significantly reduce the KA EPSCs. These data suggest that both GluK1 and GluK2 play functional roles in the IC. Our study may provide the synaptic basis for the physiology and pathology of KA receptors in the IC-related functions.
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Anna Kaczor, Agnieszka, Christiane Kronbach, Klaus Unverferth, Kalevi Pihlaja, Kirsti Wiinamaki, Jari Sinkkonen, Urszula Kijkowska-Murak, Tomasz Wrobel, Tomasz Stachal, and Dariusz Matosiuk. "Novel Non-Competitive Antagonists of Kainate GluK1/GluK2 Receptors." Letters in Drug Design & Discovery 9, no. 10 (December 1, 2012): 891–98. http://dx.doi.org/10.2174/157018012804586978.

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Anna Kaczor, Agnieszka, Christiane Kronbach, Klaus Unverferth, Kalevi Pihlaja, Kirsti Wiinamaki, Jari Sinkkonen, Urszula Kijkowska-Murak, Tomasz Wrobel, Tomasz Stachal, and Dariusz Matosiuk. "Novel Non-Competitive Antagonists of Kainate GluK1/GluK2 Receptors." Letters in Drug Design & Discovery 9, no. 10 (October 24, 2012): 891–98. http://dx.doi.org/10.2174/1570180811209050891.

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Masocha, Willias. "Astrocyte activation in the anterior cingulate cortex and altered glutamatergic gene expression during paclitaxel-induced neuropathic pain in mice." PeerJ 3 (October 22, 2015): e1350. http://dx.doi.org/10.7717/peerj.1350.

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Spinal astrocyte activation contributes to the pathogenesis of paclitaxel-induced neuropathic pain (PINP) in animal models. We examined glial fibrillary acidic protein (GFAP; an astrocyte marker) immunoreactivity and gene expression of GFAP, glutamate transporters and receptor subunits by real time PCR in the anterior cingulate cortex (ACC) at 7 days post first administration of paclitaxel, a time point when mice had developed thermal hyperalgesia. The ACC, an area in the brain involved in pain perception and modulation, was chosen because changes in this area might contribute to the pathophysiology of PINP. GFAP transcripts levels were elevated by more than fivefold and GFAP immunoreactivity increased in the ACC of paclitaxel-treated mice. The 6 glutamate transporters (GLAST, GLT-1 EAAC1, EAAT4, VGLUT-1 and VGLUT-2) quantified were not significantly altered by paclitaxel treatment. Of the 12 ionotropic glutamate receptor subunits transcripts analysed 6 (GLuA1, GLuA3, GLuK2, GLuK3, GLuK5 and GLuN1) were significantly up-regulated, whereas GLuA2, GLuK1, GLuK4, GLuN2A and GLuN2B were not significantly altered and GLuA4 was lowly expressed. Amongst the 8 metabotropic receptor subunits analysed only mGLuR8 was significantly elevated. In conclusion, during PINP there is astrocyte activation, with no change in glutamate transporter expression and differential up-regulation of glutamate receptor subunits in the ACC. Thus, targeting astrocyte activation and the glutamatergic system might be another therapeutic avenue for management of PINP.
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Bartyzel, Agata, Agnieszka A. Kaczor, Ghodrat Mahmoudi, Ardavan Masoudiasl, Tomasz M. Wróbel, Monika Pitucha, and Dariusz Matosiuk. "Experimental and Computational Structural Studies of 2,3,5-Trisubstituted and 1,2,3,5-Tetrasubstituted Indoles as Non-Competitive Antagonists of GluK1/GluK2 Receptors." Molecules 27, no. 8 (April 12, 2022): 2479. http://dx.doi.org/10.3390/molecules27082479.

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The blockade of kainate receptors, in particular with non-competitive antagonists, has—due to their anticonvulsant and neuroprotective properties—therapeutic potential in many central nervous system (CNS) diseases. Deciphering the structural properties of kainate receptor ligands is crucial to designing medicinal compounds that better fit the receptor binding pockets. In light of that fact, here, we report experimental and computational structural studies of four indole derivatives that are non-competitive antagonists of GluK1/GluK2 receptors. We used X-ray studies and Hirshfeld surface analysis to determine the structure of the compounds in the solid state and quantum chemical calculations to compute HOMO and LUMO orbitals and the electrostatic potential. Moreover, non-covalent interaction maps were also calculated. It is worth emphasizing that compounds 3 and 4 are achiral molecules crystallising in non-centrosymmetric space groups, which is a relatively rare phenomenon.
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Dissertations / Theses on the topic "GluK1 receptors"

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Carreno, Velazquez Thalia Lizbeth. "Structure-based drug discovery approaches to identify modulators of the Nrf2 pathway and glutamate receptors AMPA GluA2 and Kainate GluK1 and GluK2." Thesis, University of Sussex, 2018. http://sro.sussex.ac.uk/id/eprint/75046/.

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Nrf2 project: The protein nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor that provides protection against oxidative stress and the dysfunction of this pathway has been suggested to be implicated in many neurodegenerative diseases. The aim of this thesis was to identify novel Nrf2 activators that disrupt the protein-protein interaction between Nrf2 and Keap1 and thereby induce increased expression of antioxidant enzymes and protective genes. The crystal structure of the Keap1-Nrf2 interface was used to perform a virtual screen and compounds from the screen were assayed using a cellular nuclear complementation assay that measures the nuclear translocation of Nrf2 from the cytosol. Although two novel compounds were found to increase the Nrf2 nuclear translocation, they had low activity and further characterisation did not provide sufficient evidence of a Nrf2-Keap1 robust interaction. iGluRs project: AMPA and kainate receptors are ionotropic glutamate receptors (iGluRs) that are important for excitatory transmission and synaptic plasticity and are linked to several neurological disorders such as epilepsy, schizophrenia and autism. This project aimed to find novel allosteric modulators binding in the ligand-binding domain (LBD) of the GluA2 and GluK1 and GluK2 subtypes of AMPA and kainate receptors, respectively, using protein purification and X-ray crystallography methodologies. Fragment screening for GluA2 identified eight novel fragments, five of which were located at the dimer interface and three located in a novel site near the glycine-threonine dipeptide linker. As regards kainate receptors, structural information on the Gluk1 and GluK2 LBD was obtained, both proteins were soaked with in-house fragments with one compound displaying 20% occupancy in the GluK2 dimer interface. These data form the basis of future studies in the search for novel drugs for the treatment of epilepsy and schizophrenia.
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Fachim, Helene Aparecida. "Estudo da expressão das subunidades GluR1 e GluR2 no hipocampo de ratos após lesão por NMDA e avaliação do efeito neuroprotetor da Parawixina 10." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/59/59134/tde-25032013-144441/.

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Tem sido demonstrado o envolvimento do glutamato, através de diferentes receptores, nos mecanismos excitotóxicos que levam à morte neuronal na maioria das doenças neurodegenerativas do Sistema Nervoso Central (SNC). Adicionalmente, a Parawixina 10 (Pwx 10) tem sido demonstrada possuir efeito neuroprotetor em modelos de lesão atuando sobre o transporte de glutamato. Os objetivos gerais deste trabalho foram: i) estudar, em um curso temporal (24h, 1, 2 e 4 semanas), as alterações na expressão dos receptores AMPA no hipocampo de ratos induzidas pela injeção local de NMDA e ii) estudar o efeito neuroprotetor da Pwx 10 neste modelo. Foram utilizados ratos Wistar machos, submetidos à cirurgia estereotáxica para a microinjeção de salina ou NMDA no hipocampo dorsal. Alguns grupos de animais foram tratados com Pwx 10 a partir de 1h ou 24h após NMDA. O teste comportamental no labirinto aquático de Morris (LAM) e a coloração de Nissl foram realizados para verificar a extensão e eficácia da lesão por NMDA e o efeito neuroprotetor da Pwx 10. A expressão dos receptores foi estudada através do método de imunoistoquímica. Foram também realizados experimentos de imunofluorescência para GFAP e NeuN para avaliação da gliose e presença de neurônios na área lesada. Foi observado comprometimento das funções de aprendizado e memória no LAM, além de intensa perda de células neuronais e proliferação glial na região do CA1 que recebeu o NMDA, comprovando a eficiência da lesão pelo agonista. Observamos um curso temporal de diferentes alterações na expressão das subunidades GluR1 e GluR2 dos receptors AMPA no hipocampo, que podem ser relacionadas ao complexo mecanismo que ocorre em resposta à microinjeção de NMDA resultando em uma lesão local e na ativação da plasticidade neuronal. O tratamento com Pwx 10 apresentou efeito neuroprotetor, sendo este mais pronunciado quando a toxina foi administrada a partir de 1h após o agonista.
It has been shown the involvement of glutamate, through different receptors, on the excitotoxic mechanisms which result on the neuronal death reported in most neurodegenerative disorders of the CNS. In addition, Parawixina 10 (Pwx 10) has been demonstrated to act as neuroprotective in models of injury regulating the glutamatergic neurotransmission through glutamate transporters. The aims of this work were: i) to study, in a time course (24h, 1, 2 and 4 weeks), the changes on the expression of AMPA receptors in rat hippocampus induced by NMDA intrahippocampal injection, and ii) to study the neuroprotective effect of Pwx 10 in this moldel. Male Wistar rats has been used, submitted to stereotaxic surgery for saline or NMDA microinjection into dorsal hippocampus. Some groups of animals were treated with Pwx 10 from 1h or 24h after NMDA. The behavioral test on Morris water maze (MWM) and the Nissl staining were performed for evaluating the extension and efficacy of the NMDA injury and the neuroprotective effect of the Pwx 10 . The expression of the receptors was analyzed by immunohistochemistry. The expression of GFAP and NeuN on the lesioned area has also been investigated by immunofluorescency. It was observed the impaiment of learning and memory functions in the MWM, and intense loss of neuronal cells and glial proliferation in CA1 that received the NMDA, confirming the efficiency of the injury by the agonist. We observed a time course of distinct changes on the expression of GluR1 and GluR2 subunits of AMPA receptors in hippocampus, which may be related to the complex mechanism triggered in response to NMDA injection resulting in a local injury and on the activation of neuronal plasticity. The treatment with Pwx 10 showed neuroprotective effect, being most pronounced when the toxin was administrated from 1h after NMDA.
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Gitelman, Julian. "Synaptic incorporation of GluA1-containing AMPA receptors during memory processes." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=110505.

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It is generally understood that modifications in synaptic strength are the basis for learning and memory and that the strength of a synapse is largely governed by the abundance and distribution of synaptic receptors, especially alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptors (AMPA receptors), which mediate most of the fast synaptic transmission in the brain. GluA1-containing AMPARs are incorporated into the synapse following activity and posttranslational modifications to the carboxyl-terminus affect which proteins interact with the receptor and determine whether the receptor is inserted or removed from the synapse. In vitro research has discovered that the phosphorylation of three serine residues contained on the carboxyl-terminus (Ser 818, Ser-831 and Ser-845) regulates GluA1 synaptic incorporation; however, in vivo research investigating the relative importance of these phosphorylation sites on long-term memory formation is currently limited to knock in studies.To block the interactions between these phosphorylation sites and their binding partners in an inducible, temporally sensitive manner, we infused interference peptides containing these residues during consolidation and reconsolidation. We hypothesized that if the synaptic incorporation of GluA1 containing AMPA receptors is required for memory formation, and if this incorporation required the residues contained on the interference peptide, we would see an impairment in long-term memory expression when the peptide was infused at the time of training, or at the time of retrieval.Infusing the interference peptide GluA1-CT, containing Ser-831 and Ser 845, 1 hour before auditory fear conditioning produced no impairment in memory expression 24 hours later. However, infusing the interference peptide GluA1-MPR, containing Ser-818, 1 hour before training did produce an impairment in memory expression 24 hours later. We did not observe an impairment in long-term memory expression when both peptides were infused 1 hour before memory reactivation.
Il est généralement accepté que les modifications de la force synaptique sont à la base de l'apprentissage et la mémoire et que la force d'une synapse est largement régie par l'abondance et la distribution de récepteurs synaptiques, en particulier de récepteurs alpha-amino-3-hydroxy-5-méthyl-4- isoxazole propionate (récepteurs AMPA), qui interviennent dans la plupart des transmissions synaptiques rapides dans le cerveau. Les récepteurs AMPA contenant la sous-unité GluA1 sont incorporés dans la synapse suite à son activation et des modifications post-traductionnelles de l'extrémité carboxy-terminale influencent quelles protéines interagissent avec le récepteur et détermine si le récepteur est inséré ou retiré de la synapse. Des recherches in vitro ont découvert que la phosphorylation de trois résidus sérine contenus sur l'extrémité carboxy-terminale (Ser-818, Ser-831 et Ser-845) régie l'incorporation synaptique de GluA1; cependant, les recherches in vivo étudiant l'importance de ces sites de phosphorylation sur la formation de la mémoire à long terme est actuellement limitée à des études utilisant des « knock in ». Pour bloquer les interactions entre ces sites de phosphorylation et de leurs partenaires de liaison de manière inductible et temporellement sensibles, nous avons infusé des peptides d'interférence contenant ces résidus lors de la consolidation et la reconsolidation. Nous émettons l'hypothèse que si l'incorporation synaptique des récepteurs AMPA contenant GluA1 est nécessaire à la formation de la mémoire, et si cette incorporation exige les résidus contenus dans le peptide d'interférence, nous verrions une déficience dans l'expression de mémoire à long terme lorsque le peptide a été infusé au moment du conditionnement ou du rappel du souvenir.L'infusion du peptide d'interférence GluA1-CT, contenant les sérines Ser 831 et Ser-845, 1 heure avant le conditionnement de peur auditive n'a produit aucune altération dans l'expression de mémoire 24 heures plus tard. Cependant, l'infusion du peptide d'interférence GluA1-MPR, contenant la sérine Ser-818, 1 heure avant le conditionnement a produit une déficience dans l'expression de mémoire 24 heures plus tard. Nous n'avons pas observé d'altération dans l'expression de mémoire à long terme lorsque les deux peptides ont été infusés 1 heure avant la réactivation.
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Teixidó, Viyuela Laura. "Factors sèrics en l’Esclerosi Lateral Amiotròfica. Modulació del receptor de glutamat de tipus NMDA GluN1/GluN2A." Doctoral thesis, Universitat de Barcelona, 2011. http://hdl.handle.net/10803/79039.

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L’Esclerosi Lateral Amiotròfica (ELA o ALS) és una malaltia neuromuscular caracteritzada per la degeneració selectiva de les motoneurones (MN) superiors e inferiors del còrtex motor, el tronc de l’encèfal i la medul•la espinal, que resulta en una debilitat, espasticitat i atròfia progressives de la musculatura. Menys del 10% dels casos corresponen a la forma familiar de la malaltia, i un 20% d’aquests estan relacionats a mutacions en el gen de l’enzim superòxid dismutasa 1 (mSOD1). La resta de casos corresponen a la forma esporàdica. Les causes implicades en la degeneració selectiva de les MN en la ELA són encara desconegudes. La seva patogènesi s’ha atribuït a diversos mecanismes com serien l’estrès oxidatiu, l’agregació proteica anormal, la disfunció mitocondrial, el transport axonal aberrant, la neuroinflamació, l’autoimmunitat o l’excitotoxicitat per glutamat. En el present estudi hem treballat amb dues d’aquestes hipòtesis en avaluar l’efecte dels sèrums de pacients amb ELA i altres malalties de la MN sobre l’activitat del receptor ionotròpic de glutamat de tipus N-metil-D-Aspartat (NMDAR), expressat en el model d’oòcit de Xenopus laevis. Mitjançant assaigs de ELISA hem analitzat la presència d’autoanticossos associats a ELA en el sèrum de pacients. L’acció dels sèrums control i patològics en els oòcits de Xenopus produïa la generació de corrents oscil•latoris de clorur (Cl-). Aquests corrents havien estat prèviament descrits en aquestes cèl•lules i són deguts a l’activació dels canals de Cl- dependents de calci (Ca2+), endògens en els oòcits de Xenopus, a causa de la mobilització de Ca2+ intracel•lular. L’alliberació de Ca2+ dels compartiments intracel•lulars es activada per l’acció d’un factor sèric, anomenat àcid lisofosfatídic o lisofosfatidat (LPA), sobre el seu receptor, present en la membrana dels oòcits, i a través d’una via de senyalització de segons missatgers. Així doncs, en aquest model, la generació de corrents oscil•latoris de Cl- és una mesura indirecta de la mobilització intracel•lular de Ca2+. En presència del NMDAR, les respostes generades pel sèrum ELA eren significativament superiors a les activades pel sèrum d’individus sans i d’altres malalties de la MN. La resposta generada pel sèrum ELA presentava una dependència respecte de la presència de les dues subunitats del NMDAR i era sensible al bloqueig del receptor amb MK-801, un antagonista no competitiu. Vàrem reproduir els experiments amb sèrums del model de rata transgènica mSOD1 G93A, considerat un model de la forma familiar de la malaltia. Les mostres de sèrum mSOD1 G93A generaven, en presència del NMDAR, respostes significativament superiors a les activades pel sèrum de rata WT. En analitzar l’acció de la fracció de IgG purificada dels sèrums control i patològics en el model d’oòcit de Xenopus, es generaven corrents transitoris d’entrada de tipus no oscil•latori, els quals diferien dels generats en el cas del sèrum complet. La resposta activada per IgG de pacients amb ELA en presència del NMDAR era també significativament superior a la generada per les IgG d’individus sans. En la segona part d’aquest estudi s’ha comprovat la presència d’anticossos contra la proteïna Semaforina 3A (Sema3A) en alguns sèrums de ELA i Lower Motor Neuron Disease (LMND), una altra forma comuna de malaltia de la MN. La Sema3A és una molècula quimiotàctica de guia axonal recentment relacionada amb la patologia de la ELA en detectar-se una sobreexpressió d’aquesta proteïna en cèl•lules de Schwann terminals del model de ratolí mSOD1 G93A. Tot i descartar-se que els anticossos contra Sema3A siguin un marcador específic de la ELA, al no detectar-se en tots el sèrums de pacients, i alhora, al estar presents també en algunes mostres LMND, aquests autoanticossos podrien tenir un efecte defensiu contra les senyals nocives exercides per Sema3A sobre els axons de les MN.
Amyotrophic lateral sclerosis (ALS) is a devastating neuromuscular disease, characterized by the selective degeneration of the superior motor neurons in the motor cortex and of the inferior motor neurons in the brain-stem and spinal cord. The familial form of the illness is associated with the mutation of the superoxide dismutase enzyme (SOD-1). This and other mutations accounts for fewer than 10% of cases; the rest, more than 90%, correspond to the sporadic form. In this study we tested the effect of sera from sporadic ALS patients and from mutated human SOD-1 (mSOD1 G93A) transgenic rats on N-methyl-D-aspartate receptors (NMDAR). We hypothesize that an endogenous excitotoxic factor is implicated in neuronal death in ALS, mediated by the activation of NMDAR noncanonical signalling pathways. Sera from ALS patients or healthy subjects were pretreated to inactivate complement pathways and dialysed to remove glutamate. Sera from mSOD1 G93A rats were obtained at different stages of the neurodegenerative progression. Sera from transgenic rats were also pretreated to eliminate complement system and glutamate. Immunoglobulins G (IgGs) from ALS patients and healthy subjects were obtained by affinity chromatography and dialyzed against phosphate-buffered saline. Human NMDAR were expressed in Xenopus laevis oocytes, and glutamate-induced currents were recorded using the two electrode voltage clamp technique. We observed that sera from sporadic ALS patients induced transient oscillatory currents in Xenopus oocytes expressing NMDAR with a total electric charge significantly higher than the electric charge carried by currents induced by sera from healthy subjects. The currents were inhibited by MK-801, a noncompetitive blocker of NMDAR. Results of sera from mSOD1 G93A transgenic rats were similar to those of sera from ALS patients; samples from patients with another type of neuromuscular disease did not exert this effect. IgG from ALS patients have a significant effect on NMDAR-injected oocytes and that response was doubled respect to the observed in the case of IgG from healthy subjects. Our data agree with the view that ALS patients sera contain some soluble factors that activates NMDAR, not opening directly the ionic conductance, but activating a non-canonical pathway.
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Guo, Yanan [Verfasser], and M. [Akademischer Betreuer] Elstner. "Theoretical Investigation of Kainate Receptor GluK2 and Channelrhodopsin-2: Structure and Mechanism / Yanan Guo ; Betreuer: M. Elstner." Karlsruhe : KIT-Bibliothek, 2017. http://d-nb.info/1126036862/34.

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Warre, Ruth. "The role of the kainate receptor subunit GluK5 in the epileptiform activity induced by pilocarpine in vitro." Thesis, University of Bristol, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.432945.

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Dachtler, James. "The role of the AMPA receptor subunit GluR1 and nitric oxide in experience-dependent plasticity and memory formation." Thesis, Cardiff University, 2010. http://orca.cf.ac.uk/54169/.

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Neocortical and hippocampal synaptic long-term potentiation (LTP) initially requires the AMPA receptor subunit GluR1, while late-phase LTP depends upon nitric oxide synthase (NOS). To investigate whether this was relevant to in vivo ED potentiation, GluR1 and/or NOS knockout mice were deprived of all whiskers but the D1 to induce barrel cortex synaptic potentiation, which was quantified by single unit recordings. In deprived cortex, D1 whisker responses potentiated approximately 40% less in GluR1 and NOS3 knockout mice than wild-type mice. Potentiation in the NOS1 knockout was influenced by gender; female NOS1 knockout potentiation was similar to wild-types, yet was absent in male NOS1 knockout mice. The ED potentiation in GluR1 knockout mice was dependent upon NOS, supporting LTP studies. However, NOS1 was more important for potentiation. Thus, while potentiation occurred in the GluR1/NOS3 double knockout mice, it was completely absent in the GluR1/NOS1 double knockout. To determine the interaction between GluR1 and NO activity in memory, behavioural studies examined their impact on spatial and contextual memory. The results partly confirmed earlier findings that retention of contextual fear conditioning was sensitive to GluR1 deletion. However, this was only the case in male GluR1 knockout mice. Female GluR1 KO mice were unimpaired. In a spatial radial arm watermaze task, GluR1 knockout mice acquired the location of a submerged platform more slowly than wild-types. Nevertheless, spatial reference memory was comparable to wild-type mice at the end of training and was not influenced by gender. In contrast to predictions, GluR1-indepdnent reference memory was not dependent upon NOS. Therefore while emotional learning requires GluR1 in male mice, spatial reference memory can form in its absence in both genders and is insensitive to NOS antagonism.
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Koesters, Andrew G. "Rab3A as a modulator of homeostatic synaptic plasticity." Wright State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=wright1409319870.

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Nagarajan, Naveen. "Molecular mechanisms of AMPA and kainate receptor gating and its implication in synaptic transmission." Doctoral thesis, [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=965898768.

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Castro, Zavala Adriana 1988. "Effects of maternal separation with early weaning on cocaine addictive behaviour and consequences on neuroplasticity." Doctoral thesis, Universitat Pompeu Fabra, 2020. http://hdl.handle.net/10803/670107.

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Early-life stress is associated with maladaptive long-lasting brain effects. Such alterations increase the likelihood of developing several psychiatric disorders. However, the molecular consequences of early-life stress are poorly understood. Here, we evaluated the impact of maternal separation with early weaning (MSEW) at different phases of cocaine self-administration (SA) and the subsequent molecular alterations in brain reward regions of male and female mice. Our findings show that MSEW affects males while females appear to be resilient to this kind of stress. Maternally separated mice evidence higher percentage of acquisition, more cocaine intake and decrease capacity to extinguish the SA behaviour. Moreover, molecular analyses of the brain areas studied reveal sex-induced alterations in the AMPA receptor composition and MSEW-induced changes in the expression of GluA1, GluA2, pCREB and CREB. Cocaine also alters the expression of these molecules. Together, results suggest that MSEW induces molecular alterations in areas related to reward processing, potentiating the vulnerability to cocaine-seeking behaviour and depression.
El estrés en la etapa temprana de la vida se asocial con efectos cerebrales maladaptativos y duraderos. Dichas alteraciones pueden aumentar la probabilidad de desarrollar diversos trastornos psiquiátricos. Sin embargo, las consecuencias moleculares del estrés en la vida temprana son poco conocidas. En este trabajo evaluamos el impacto de la separación maternal con destete temprano (MSEW, por sus siglas en inglés) en diferentes fases de la autoadministración de cocaína, así como las posteriores alteraciones moleculares en regiones cerebrales asociadas al sistema de recompensa, en ratones machos y hembras. Nuestros resultados muestran que la MSEW afecta a los machos, mientras que las hembras parecen ser resistentes a este tipo de estrés. Los ratones separados maternalmente muestran un mayor porcentaje de adquisición, más consumo de cocaína y una menor capacidad para extinguir el comportamiento de autoadministración. Además, los análisis moleculares de las áreas cerebrales estudiadas revelan alteraciones inducidas por el sexo en la composición del receptor AMPA y cambios inducidos por la MSEW en la expresión de GluA1, GluA2, pCREB y CREB. La cocaína también altera la expresión de estas moléculas. Los resultados en conjunto sugieren que la MSEW induce alteraciones moleculares en áreas relacionadas con el procesamiento de la recompensa, potenciando la vulnerabilidad al comportamiento de búsqueda de cocaína y la depresión.
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Books on the topic "GluK1 receptors"

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Wells, Elizabeth M. Anti-N-Methyl-D-Aspartate Receptor Encephalitis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0091.

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Anti- N-methyl-D-aspartate receptor (NMDAR) encephalitis is a severe but treatable recently identified form of immune-mediated encephalitis associated with antibodies in serum and cerebrospinal fluid (CSF) against the GluN1 subunit of the NMDAR. Research has rapidly expanded the understanding of disease mechanisms and how the condition manifests in different populations (e.g., pediatrics vs. adult, cancer vs. noncancer, male vs. female). Immunocytochemical, physiological, and molecular studies of the effects of human CSF on the rodent and murine brain in vitro and in vivo indicate a noncytotoxic antibody-mediated mechanism of disease pathogenesis. Finding positive antibodies prompts a search for occult neoplasm, most likely ovarian teratoma in young women; other age groups and male patients are less likely to have tumor but need to be screened. Fifty percent of patients respond to first line steroids, IVIG, plasma exchange or a combination, and many others improve with addition of rituximab or cyclophosphamide. Cured patients may have cognitive or motor sequelae, and refractory disease and death may occur despite treatment. Knowledge about etiology and biomarkers of refractory disease are lacking. Additional work is needed to further elucidate the origin of the immune-mediated response, to determine optimal clinical management and develop effective therapies for refractory patients.
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Baker, Chris. The role of serine phosphorylation on the slow inactivation of the GluR1 Lurcher AMPA receptor. 2006.

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Book chapters on the topic "GluK1 receptors"

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Kohda, Kazuhisa, Wataru Kakegawa, and Michisuke Yuzaki. "Delta Glutamate Receptor (GluD1, GluD2)." In Encyclopedia of Signaling Molecules, 1345–52. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_642.

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Kohda, Kazuhisa, Wataru Kakegawa, and Michisuke Yuzaki. "Delta Glutamate Receptor (GluD1, GluD2)." In Encyclopedia of Signaling Molecules, 1–8. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_642-1.

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Lukas, Thomas J., Daniela V. Rosa, Luiz Alexandre V. Magno, Bruno R. Souza, Marco A. Romano-Silva, Hisao Masai, Kazuhisa Kohda, et al. "Delta Glutamate Receptor (GluD1, GluD2)." In Encyclopedia of Signaling Molecules, 514–18. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_642.

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Bruneau, Nadine, and Pierre Szepetowski. "Magnetofection™ of NMDA Receptor Subunits GluN1 and GluN2A Expression Vectors in Non-Neuronal Host Cells." In Methods in Molecular Biology, 129–35. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7321-7_5.

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Doherty, A., A. Irving, G. L. Collingridge, and J. M. Henley. "Localisation and Surface Expression of the AMPA Receptor Subunit GluR1 Using Green Fluorescent Protein and Anti-Peptide Antibodies." In Excitatory Amino Acids, 161–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-03596-2_9.

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Khatib, Thabat, Berndt Müller, and Peter McCaffery. "A Bioluminescence Reporter Assay for Retinoic Acid Control of Translation of the GluR1 Subunit of the AMPA Glutamate Receptor." In Bioluminescence, 197–207. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2453-1_15.

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Nisticò, Robert, Sheila Dargan, Stephen M. Fitzjohn, David Lodge, David E. Jane, Graham L. Collingridge, and Zuner A. Bortolotto. "Chapter 2 Gluk1 Receptor Antagonists and Hippocampal Mossy Fiber Function." In International Review of Neurobiology, 13–27. Elsevier, 2009. http://dx.doi.org/10.1016/s0074-7742(09)85002-2.

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Sanderson, D. J., M. A. Good, P. H. Seeburg, R. Sprengel, J. N. P. Rawlins, and D. M. Bannerman. "Chapter 9 The role of the GluR-A (GluR1) AMPA receptor subunit in learning and memory." In Progress in Brain Research, 159–78. Elsevier, 2008. http://dx.doi.org/10.1016/s0079-6123(07)00009-x.

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Knoers, Nine V. A. M., and Elena N. Levtchenko. "Disorders of tubular electrolyte handling." In Oxford Textbook of Medicine, edited by John D. Firth, 5112–23. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0506.

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Glycosuria—glucose reabsorption in the proximal tubule is carried out by two different pairs of apical Na+-dependent (SGLT1 and -2) and basolateral Na+-independent (GLUT1 and -2) glucose transporters. Abnormalities in renal glucose transport can be seen in association with other defects of proximal tubular transport. Familial renal glycosuria is a rare autosomal recessive condition caused by mutations in the SGLT2-encoding gene, SLC5A2. Phosphate-handling disorders—the plasma concentration of inorganic phosphate depends on the balance between intestinal absorption, renal excretion, and the internal contribution from bone. Changes of serum phosphate levels can be caused by numerous inherited and acquired conditions. Disorders associated with increased urinary phosphate excretion and low serum phosphate levels produce symptoms that mainly affect the bones: rickets in children and osteomalacia in adults. Magnesium-handling disorders—normal plasma magnesium concentration is achieved by variation of urinary magnesium excretion in response to altered uptake by the intestine. The main site of magnesium absorption is the small bowel, via paracellular simple diffusion at high intraluminal concentrations, and via active transcellular uptake through the magnesium channel TRPM6 at low concentrations. Regulation and fine-tuning of serum magnesium concentration occurs primarily in the kidney. Genetic disorders of magnesium handling include Gitelman’s syndrome. Aminoaciduria and renal Fanconi’s syndrome—most amino acids (except for tryptophan, which is protein bound) are freely filtered by the glomerulus, after which 95 to 99.9% are reabsorbed in the proximal tubules by apical Na+-dependent cotransporters and Na+-independent cotransporters. Aminoaciduria is defined as urinary excretion of more than 5% of the filtered load of an amino acid. Renal Fanconi’s syndrome is characterized by a generalized defect of both Na+-coupled and receptor-mediated proximal tubular transport.
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Conference papers on the topic "GluK1 receptors"

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Hargrove-Wiley, Ebony, Daniel Valent, Demond Williams, Wendy Bindeman, and Barbara Fingleton. "Abstract 2446: IL4 receptor-induced proliferation is mediated via Glut1 activity in metastatic breast cancer." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2446.

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Benammar, Sarra, Fatima Mraiche, Jensa Mariam Joseph, and Katerina Gorachinova. "Glucose and Transferrin Liganded PLGA Nanoparticles Internalization in Non-Small Lung Cancer Cells." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0227.

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Introduction: Recently, after a decade of confusing results, several studies pointed out that overexpression of GLUT1 (glucose transporter 1) is a biomarker of worse prognosis in NSCLC. Nonetheless, the presence of transferrin (Tf receptor), which is overexpressed in most cancer tissues and most lung cancers as well, in NSCLC is also an indicator of very poor prognosis. Therefore, these ligands can be used for active targeting of lung cancer cells and improved efficacy of internalization of cancer therapy using nanomedicines. Objectives: Having the background, the main goal of the project was the assessment of the influence of the glucose and transferrin ligands on the efficacy of internalization of the designed (i) glucose decorated PLGA (poly lactic-coglycolic acid) nanoparticles (Glu-PLGA NPs) and (ii) transferrin decorated PLGA nanoparticles (Tf-PLGA NPs) in comparison to (iii) non-liganded PLGA NPs using a A549 lung cancer cells. Methods: Glu-PLGA NPs, Tf-PLGA NPs and PLGA NP - fluorescently labelled), were designed using a sonication assisted nanoprecipitation method. Further, physicochemical properties characterization (particle size analysis, zeta potential, FTIR analysis, DSC analysis), cytotoxicity evaluation using MTT test, and cell internalization studies of DTAF labelled NPs using fluorimetry in A549 NSCLC cell line were performed. Results: The results pointed to a significantly improved internalization rate of the liganded compared to PLGA NPs. Glu-PLGA NPs showed higher internalization rate compared to Tf-PLGA and PLGA NPs, in the serum-supplemented and serumfree medium even at normal levels of glucose in the cell growth medium. Conclusion: The developed nanocarriers offer unique advantages of enhanced targetability, improved cell internalization and decreased toxicity, which makes them promising solution for current therapeutic limitations.
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