Excitatory amino acid transporter 3 is a member of the high-affinity glutamate transporters which plays an essential role in transporting glutamate across plasma membranes in neurons. In the brain, excitatory amino acid transporters are crucial in terminating the postsynaptic action of the neurotransmitter glutamate, and in maintaining extracellular glutamate concentrations below neurotoxic levels. EAAT3 also transports aspartate, and mutations in this gene are thought to cause dicarboxylic aminoaciduria, also known as glutamate-aspartate transport defect.[6] EAAT3 is also the major route of neuronal cysteine uptake. Cysteine is a component of the major antioxidant glutathione, and mice lacking EAAT3 exhibit reduced levels of glutathione in neurons, increased oxidative stress, and age-dependent loss of neurons, especially neurons of the substantia nigra. ...
Najimi, Mustapha ; Stéphenne, Xavier ; Sempoux, Christine ; Sokal, Etienne ; Khuu, Ngoc Dung. Modulation of EAAT-2 glutamate transporter expression in human liver cholestasis.21st Biennial Meeting of the International-Society-for-Neurochemistry/38th Annual Meeting of the American-Society-for-Neurochemistry (Cancun (Mexico), Aug 19-24, 2007). In: Journal of Neurochemistry, Vol. 102, p. 46-47 (2007 ...
Sodium-dependent, high-affinity amino acid transporter that mediates the uptake of L-glutamate and also L-aspartate and D-aspartate (PubMed:1280334). Can also transport L-cysteine (By similarity). Functions as a symporter that transports one amino acid molecule together with two or three Na(+) ions and one proton, in parallel with the counter-transport of one K(+) ion (PubMed:1280334). Mediates Cl(-) flux that is not coupled to amino acid transport; this avoids the accumulation of negative charges due to aspartate and Na(+) symport. Plays an important role in L-glutamate and L-aspartate reabsorption in renal tubuli (By similarity). Plays a redundant role in the rapid removal of released glutamate from the synaptic cleft, which is essential for terminating the postsynaptic action of glutamate (By similarity). Negatively regulated by ARL6IP5 (By similarity).
Transports L-glutamate; the L-glutamate uptake is sodium- and voltage-dependent and chloride-independent. Its associated chloride conductance may participate in visual processing.
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Glutamate is the predominant excitatory neurotransmitter in the mammalian central nervous system and extracellular glutamate levels are controlled by a family of transporters known as excitatory amino acid transporters (EAATs). The EAATs transport glutamate and aspartate with similar micromolar affinities and this transport is coupled to the movement of Na(+), K(+), and H(+). The crystal structure of a prokaryotic homologue of the EAATs, aspartate transporter from Pyrococcus horokoshii (Glt(Ph)), has yielded important insights into the architecture of this transporter family. Glt(Ph) is a Na(+)-dependent transporter that has significantly higher affinity for aspartate over glutamate and is not coupled to H(+) or K(+). The highly conserved carboxy-terminal domains of the EAATs and Glt(Ph) contain the substrate and ion binding sites, however, there are a couple of striking differences in this region that we have investigated to better understand the transport mechanism. An arginine residue is in ...
Excitatory amino acid transporters (EAATs) in the CNS maintain extracellular glutamate concentrations below excitotoxic levels and contribute to the clearance o...
It is known that glutamate (Glu), the major excitatory amino acid in the central nervous system, can be an essential source for cell energy metabolism. Here we investigated the role of the plasma membrane Na+/Ca2+ exchanger (NCX) and the Excitatory Amino Acid Transporters (EAATs) in Glu uptake and recycling mechanisms leading to ATP synthesis. We used different cell lines, such as SH-SY5Y neuroblastoma, C6 glioma and H9c2 as neuronal, glial and cardiac models, respectively. We first observed that Glu increased ATP production in SH-SY5Y and C6 cells. Intriguingly, pharmacological inhibition of either EAAT or NCX counteracted the Glu-induced ATP synthesis. Furthermore, Glu induced a plasma membrane depolarization and an intracellular Ca2+ increase and both responses were again abolished by EAAT and NCX blockers. In line with the hypothesis of a mutual interplay between the activities of EAAT and NCX, coimmunoprecipitation studies showed a physical interaction between them. We expanded our studies ...
TY - JOUR. T1 - Role of excitatory amino acid transporter 1 in neonatal rat neuronal damage induced by hypoxia-ischemia. AU - Tao, F.. AU - Lu, S. D.. AU - Zhang, L. M.. AU - Huang, Y. L.. AU - Sun, F. Y.. N1 - Funding Information: We wish to thank Prof. A. Z. Zhang for valuable discussions and suggestions. We also thank W. H. Ge and R. H. Xue for excellent technical assistance. This work was partly supported by grants from the Ninth Five-year Key Medical Research Program of China (No. 96-904-06-04) and the National Nature Science Foundation of China (No. 39570236 and g1999054007). Copyright: Copyright 2017 Elsevier B.V., All rights reserved.. PY - 2001/2/5. Y1 - 2001/2/5. N2 - The role of excitatory amino acid transporter 1 in neonatal rat neuronal damage was studied following hypoxia-ischemia. To induce hypoxia-ischemia injury, rats on postnatal day 7 were exposed to 8% oxygen for 2 h following unilateral common carotid artery ligation. According to brain damage scoring based on Cresyl Violet ...
TY - JOUR. T1 - Effects of the excitatory amino acid transporter subtype 2(EAAT-2) inducer ceftriaxone on different pain modalities in rat. AU - Eljaja, Laila. AU - Bjerrum, Ole Jannik. AU - Honoré, Per Gustaf Hartvig. AU - Abrahamsen, Bjarke. PY - 2011. Y1 - 2011. KW - Det tidligere Farmaceutiske Fakultet. U2 - 10.1016/j.sjpain.2011.03.003. DO - 10.1016/j.sjpain.2011.03.003. M3 - Tidsskriftartikel. VL - 2. SP - 132. EP - 136. JO - Scandinavian Journal of Pain. JF - Scandinavian Journal of Pain. SN - 1877-8860. IS - 3. ER - ...
Glaucoma, a progressive optic neuropathy due to retinal ganglion cell (RGC) degeneration, is one of the leading causes of irreversible blindness. Although glaucoma is often associated with elevated intraocular pressure (IOP), IOP elevation is not detected in a significant subset of glaucomas, such as normal tension glaucoma (NTG). Moreover, in some glaucoma patients, significant IOP reduction does not prevent progression of the disease. Thus, understanding IOP-independent mechanisms of RGC loss is important. Here, we show that mice deficient in the glutamate transporters GLAST or EAAC1 demonstrate spontaneous RGC and optic nerve degeneration without elevated IOP. In GLAST-deficient mice, the glutathione level in Müller glia was decreased; administration of glutamate receptor blocker prevented RGC loss. In EAAC1-deficient mice, RGCs were more vulnerable to oxidative stress. These findings suggest that glutamate transporters are necessary both to prevent excitotoxic retinal damage and to ...
TY - JOUR. T1 - Glial restricted precursors protect against chronic glutamate neurotoxicity of motor neurons in vitro. AU - Maragakis, Nicholas J. AU - Rao, Mahendra S.. AU - Llado, Jeronia. AU - Wong, Victor. AU - Xue, Haipeng. AU - Pardo, Andrea. AU - Herring, Joseph. AU - Kerr, Douglas. AU - Coccia, Carol. AU - Rothstein, Jeffrey D. PY - 2005/4/15. Y1 - 2005/4/15. N2 - We have examined the expression of glutamate transporters in primary and immortalized glial precursors (GRIPs). We subsequently transduced these cells with the GLT1 glutamate transporter and examined the ability of these cells to protect motor neurons in an organotypic spinal cord culture. We show that glial restricted precursors and GRIP-derived astrocytes predominantly express glutamate transporters GLAST and GLT1. Oligodendrocyte differentiation of GRIPs results in downregulation of all glutamate transporter subtypes. Having identified these precursor cells as potential vectors for delivering glutamate transporters to ...
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Anti-EAAT1 (GLAST) (ext.)-FITC Antibody (#AGC-021-F) from Alomone Labs is a highly specific rabbit polyclonal Ab directly conjugated to FITC. Ideal for live cell flow cytometry experiments. Lyophilized. Global shipping at room temperature. Your top supplier for glutamate transporter research!
The Glast Gambit: Hotfix 19.5.7 For those that missed Devstream #85, the cyst cure is aimed to come next week on PC. NOTE: if you were using the ...
SLC1A1, also known as excitatory amino-acid transporter 3 (EAAT3), is a protein that in humans is encoded by the SLC1A1 gene. Excitatory amino-acid transporter 3 is a member of the high-affinity glutamate transporters which plays an essential role in transporting glutamate across plasma membranes in neurons. In the brain, excitatory amino acid transporters are crucial in terminating the postsynaptic action of the neurotransmitter glutamate, and in maintaining extracellular glutamate concentrations below neurotoxic levels. EAAT3 also transports aspartate, and mutations in this gene are thought to cause dicarboxylic aminoaciduria, also known as glutamate-aspartate transport defect. EAAT3 is also the major route of neuronal cysteine uptake. Cysteine is a component of the major antioxidant glutathione, and mice lacking EAAT3 exhibit reduced levels of glutathione in neurons, increased oxidative stress, and age-dependent loss of neurons, especially neurons of the substantia nigra. SLC1A1 has been ...
There are 30,000 cases of ALS at any given time in the United States. Presently there is no cure for ALS and few treatment options. 90 percent of cases have unk...
Glutamate is the major excitatory neurotransmitter in the CNS that is cleared from the extracellular space by a family of high-affinity glutamate transporters. The astroglial glutamate transporter EAAT2 is thought to carry out the uptake of the vast quantity of glutamate, and dysregulation of EAAT2 expression is involved in the pathogenesis of neurological disorders with marked excitotoxic components. Here, we present a novel epigenetic mechanism by which the human EAAT2 gene is kept in a silent state. Sequence inspection identified a classical CpG island at the EAAT2 promoter ...
We cloned and expressed a human metabotropic glutamate receptor 1 alpha (HmGluR1 alpha) in a novel cell line. The human mGluR1 alpha cDNA was found to be 86% identical to rat mGluR1 alpha, and the predicted protein sequence was found to be 93% identical to rat mGluR1 alpha. We expressed HmGluR1 alpha in AV12-664, an adenovirus-transformed Syrian hamster cell line. To prevent tonic activation of HmGluR1 alpha by glutamate that may be released by these cells into the extracellular medium, HmGluR1 alpha was co-expressed in AV12-664 cells with a rat glutamate/aspartate transporter (GLAST). This allowed investigation of the effect that clearance of glutamate from the extracellular space would have on HmGluR1 alpha function. A comparison of mRNA levels revealed that HmGluR1 alpha was similarly expressed in cells with or without co-expression of GLAST. However, HmGluR1 alpha-mediated phosphoinositide hydrolysis was efficiently elicited only in cells co-expressing rat GLAST. Blockade of glutamate ...
Hypoxia inhibits the uptake of glutamate (a major neurotransmitter in the brain closely related to cognitive function) into brain cells, and the initial response of cells to cortical hypoxia depends on glutamate. Previous studies have suggested that magnesium may have protective effects against hypoxic injuries. In particular, magnesium l-threonate (MgT) may increase magnesium ion concentrations in the brain better than MgSO4 and improve cognitive function. We evaluated cell viability under hypoxic conditions in the MgT- and MgSO4-treated human SH-SY5Y neurons, in vivo behavior using the T-maze test following hypoxia in MgT-treated zebrafish, activity of brain mitochondrial dehydrogenase by 2,3,5-triphenyltetrazolium chloride (TTC) staining, and protein expression of the excitatory amino acid transporter (EAAT) 4 glutamate transporter by western blotting. Among the groups treated with hypoxia, cell viability significantly increased when pre-treated with 1 or 10 mM MgT (p = 0.009 and 0.026, respectively)
Hypoxia inhibits the uptake of glutamate (a major neurotransmitter in the brain closely related to cognitive function) into brain cells, and the initial response of cells to cortical hypoxia depends on glutamate. Previous studies have suggested that magnesium may have protective effects against hypoxic injuries. In particular, magnesium l-threonate (MgT) may increase magnesium ion concentrations in the brain better than MgSO4 and improve cognitive function. We evaluated cell viability under hypoxic conditions in the MgT- and MgSO4-treated human SH-SY5Y neurons, in vivo behavior using the T-maze test following hypoxia in MgT-treated zebrafish, activity of brain mitochondrial dehydrogenase by 2,3,5-triphenyltetrazolium chloride (TTC) staining, and protein expression of the excitatory amino acid transporter (EAAT) 4 glutamate transporter by western blotting. Among the groups treated with hypoxia, cell viability significantly increased when pre-treated with 1 or 10 mM MgT (p = 0.009 and 0.026, respectively)
Glutamate transporters (GluTs) maintain a low ambient level of glutamate in the central nervous system (CNS) and shape the activation of glutamate receptors at synapses. Nevertheless, the mechanisms that regulate the trafficking and localization of transporters near sites of glutamate release are poorly understood. Here, we examined the subcellular distribution and dynamic remodeling of the predominant GluT GLT-1 (excitatory amino acid transporter 2, EAAT2) in developing hippocampal astrocytes. Immunolabeling revealed that endogenous GLT-1 is concentrated into discrete clusters along branches of developing astrocytes that were apposed preferentially to synapsin-1 positive synapses. Green fluorescent protein (GFP)-GLT-1 fusion proteins expressed in astrocytes also formed distinct clusters that lined the edges of astrocyte processes, as well as the tips of filopodia and spine-like structures. Time-lapse three-dimensional confocal imaging in tissue slices revealed that GFP-GLT-1 clusters were ...
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Numerous research programs in the laboratory funded under the Direction of A. Nieoullon. Contribution for years to the organisation of numerous national and international scientific meetings in Marseilles and in France.. Scientific production :. More than 180 publications since 1971 (for details, see Pub-Med 156 articles). Publications 2006-2010. · Turle-Lorenzo N., Maurin B., Puma C., Chezaubernard C., Morain P., Baunez C., Nieoullon A., Amalric M. The dopamine agonist piribédil with L-Dopa improves attentional dysfunction : relevance for Parkinsons disease. J. Pharmacol. Exp. Ther., 2006, 319 :914-923. · Nieoullon A., Canolle B., Masmejean F., *Guillet B., Pisano P., Lortet S. The neuronal excitatory amino acid transporter EAAC1/EAAT3 : does it represent a major actor at the brain excitatory synapse ? J. Neurochem., 2006, 98, 1007-1018. · Conductier G., Dusticier N., Lucas G., Cote F., Debonnel G., Daszuta A., Dumuis A., Nieoullon A., Hen R., Bockaert J., Compan V. Adaptives changes in ...
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The videorecord of GLAST launching is available now on the website of Virtual Institute of Astroparticle physics 1-Glast official video 2-Glast launch...
The G.A.R.D. Made Simple I wrote this on June 9, 2005 at the request of a doctor who was interested in this elimination diet for his epileptic patients. Again, this site was originally intended to be used by my clients- lay people searching for answers to medical issues that they did not understand. But I do realize that the length of these papers drives medically-inclined crazy. To be honest, it would me if I was looking for immediate answers for a problem case. BUT, I still contend that the fast-food approach to our problems is totally inadequate, and at some point, we MUST see the big picture again. So, I walk a fine line in my attempt to educate my clients while enlightening my colleagues, often resulting in overly lengthy papers. I guess Id rather over-explain than under-explain. I hope this summary-style paper helps.. The G.A.R.D. originally stood for the glutamate-aspartate restricted diet after its limitation of these two non-essential, neurostimulating amino acids that are also the ...
Coping with dehydration: sympathetic activation and ...TBOA increased renal SNA (top) and MAP (bottom) in both groups, reflecting effects of endogenously released glutamate in the PVN. Responses to TBOA were significantly greater in EH rats (P | 0.05). Prior microinjection of AP5 decreased renal SNA and MAP in the DH rats and effectively prevented sympathoexcitatory and pressor responses to ...Cited by: 11Publish Year: 2014Author: Megan E. Bardgett, Qing-Hui Chen, Qing Guo, Alfredo S Calderon, Mary Ann Andrade, Glenn Matthew Tone...
Happy May day everyone. The new month didnt start off as well for us as we would have liked. As some of you know, our little Maxer dawg has seizures. Hes been pretty regular the last year as in every 28 days, but this was a longer stretch of 37 days and boy, did he make up for it last night and today. He had 7 seizures in less than 50 minutes by the time the 3 valium kicked in - all bad ones, and 2 more this morning, and 2 this afternoon. Honestly, I really thought his number was...
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Excitatory amino acid carrier 1 (EAAC1) is an important subtype of excitatory amino acid transporters (EAATs) and is the route for neuronal cysteine uptake. CoCl 2 is not only a hypoxia-mimetic reagent but also an oxidative stress inducer. Here, we found that CoCl 2 induced significant EAAC1 over...
EAAC1/EAAT3 is a transporter of glutamate (Glu) present at the post‐synaptic neuronal element, in opposition to the two other main transporters, GLAST/EAAT1 and GLT1/EAAT2, expressed at the excitatory amino acid (EAA) synapse by surrounding astrocytes. Although, in the adult, EAAC1/EAAT3 exhibits a rather low expression level and is considered to make a minor contribution to Glu removal from the synapse, its early expression during brain development, before the astrocytes are functional, suggests that such a neuronal transporter is involved in the developmental effects of EAA and, possibly, in the biosynthesis and trophic role of GABA, which is excitatory in nature in different brain regions during the earlier stages of brain development. This neuronal Glu transporter is considered to have a dual action as it is apparently involved in the neuronal uptake of cysteine, which acts as a key substrate for the synthesis of glutathione, a major anti‐oxidant, because the neurones do not express the Xc-
The glutamate transporter GLT-1 is crucial for the maintenance of low interstitial glutamate concentrations. by disrupting the association between Hsp90 and GLT-1. Utilizing a style of TLE, we showed that long-term systemic administration of 17AAG significantly suppressed spontaneous repeated seizures and ameliorated astrogliosis. General, these results claim that up-regulation of GLT-1 by inhibiting Hsp90 in reactive astrocytes could be a potential healing focus on for the treating epilepsy and excitotoxicity. Launch Epilepsy is among the most common chronic neurological illnesses, yet around one-third of affected sufferers do not react to anticonvulsive medications PFI-3 supplier that focus on neurons (Kwan et al., 2011). Latest studies claim that astrocytes certainly are a potential focus on for the healing treatment of intractable epilepsy (Hja, 2014; Robel et al., 2015). GLT-1 (EAAT2; slc1a2) is normally predominantly portrayed in astrocytes and in charge of maintaining low extracellular ...
Gap detection or gap pre-pulse inhibition of the acoustic startle (GPIAS) has been successfully used in rat and guinea pig models of tinnitus, yet this system has proven to have low efficacy in CBA mice, with low basal GPIAS and subtle tinnitus like effects. Here, we tested five mouse strains (CBA, BalbC, CD-1, C57BL/6 and sv129) for pre-pulse inhibition and gap detection with varying interstimulus intervals (ISI) and found the that mice from a CBA genetic background had the poorest capacities of suppressing the startle response in presence of a pre-pulse or a gap. CD-1 mice displayed variable responses throughout all ISI. Interestingly, C57BL/6, sv129 and BalbC showed efficient suppression with either pre-pulses or gaps with shorter ISI. The glutamate aspartate transporter (GLAST) is expressed in support cells from the cochlea and buffers the excess of glutamate. We hypothesized that loss of GLAST function could sensitize the ear to tinnitus-inducing agents, such as salicylate. Using shorter ISI to
In the brain, termination of glutamatergic neurotransmission is achieved predominantly by rapid uptake of synaptically released glutamate into astrocytes through the sodium-dependent glutamate transporters GLT-1 and GLAST and its subsequent conversion to glutamine by the enzyme GS (Rothstein et al., 1996; Sonnewald et al., 1997). To date, several factors, including glutamate itself, have been identified that rapidly alter the activity of the glutamate uptake process by post-translational modification of glutamate transporters (for review, see Gegelashvili and Schousboe, 1998). However, the factor or factors regulating the expression of glial glutamate transporter as well as of GS are still unknown. Pronounced increases in glial expression levels of GLT-1, GLAST, and GS have been observed in coculture systems with neurons (Hayashi et al., 1988; Swanson et al., 1997; Schlag et al., 1998). Although originally it had been suggested that these effects involve glutamate signaling, recent work by ...
Our study indicates that glutamate transporter activity regulates AMPAR synaptic accumulation and stability. After glutamate transport inhibition, glutamate presumably diffuses to the edges of synaptic cleft, in which it binds to parasynaptically localized NMDARs. Stimulation of NR2B-NMDARs leads to AMPAR ubiquitination, internalization, and proteasome-mediated degradation. Furthermore, we show that the effect of EAAT suppression on AMPAR reduction is mediated mainly by the neuronal transporter EAAT3. Inhibition of glial transporters has no effect on AMPARs, and the reduction in AMPARs after EAAT inhibition remains in the absence of glia in the culture, suggesting a minimal role of glial glutamate transporters. Moreover, the knockdown of EAAT3 by siRNA caused similar effects on AMPAR expression to that of EAAT inhibition. In addition, we show that the population of EAAT3 at the postsynaptic, rather than the presynaptic, site is responsible for AMPAR regulation. These findings indicate that the ...
In amyotrophic lateral sclerosis, down-regulation of the astrocyte-specific glutamate excitatory amino acid transporter 2 is hypothesized to increase extracellular glutamate, thereby leading to excitotoxic motor neuron death. The antibiotic ceftriaxone was recently reported to induce excitatory amin …
In this article, David Nicholls and David Attwell describe recent advances in our understanding of the mechanisms by which excitatory amino acids are released from cells, and of the way in which a low extracellular glutamate concentration is maintained. Glutamate can be released from cells by two me …
WAY-213613 hydrochloride 是一种有效的,选择性的 GLT-1/EAAT2 (功能性谷氨酸转运蛋白/兴奋性氨基酸转运蛋白) 非底物抑制剂,对于 EAAT2,EAAT1 和 EAAT3 的 IC50 分别为 85 nM,5 μM 和 3.8 μM。WAY-213613 hydrochloride 是高度首选 EAAT2 的转运蛋白配体,抑制大鼠皮质突出体对谷氨酸的摄取 ...
Expression of UFL1 (KIAA0776, Maxer, NLBP, RCAD) in hippocampus tissue. Antibody staining with HPA030558, HPA030559 and HPA030560 in immunohistochemistry.
Expression of UFL1 (KIAA0776, Maxer, NLBP, RCAD) in cancer tissue. The cancer tissue page shows antibody staining of the protein in 20 different cancers.
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EAAT2小鼠单克隆抗体(ab77039)可与人样本反应并经WB, ELISA, IHC实验严格验证,被1篇文献引用。所有产品均提供质保服务,中国75%以上现货。
GLT25D2兔多克隆抗体(ab122192)可与小鼠, 大鼠, 人样本反应并经WB, IHC, ICC/IF实验严格验证。所有产品均提供质保服务,中国75%以上现货。
Cortical dysplasia is associated with intractable epilepsy and developmental delay in young children. Recent work with the rat freeze-induced focal cortical dysplasia (FCD) model has demonstrated that hyperexcitability in the dysplastic cortex is due in part to higher levels of extracellular glutamate. Astrocyte glutamate transporters play a pivotal role in cortical maintaining extracellular glutamate concentrations. Here we examined the function of astrocytic glutamate transporters in a FCD model in rats. Neocortical freeze lesions were made in postnatal day (PN) 1 rat pups and whole cell electrophysiological recordings and biochemical studies were performed at PN 21-28. Synaptically evoked glutamate transporter currents in astrocytes showed a near 10-fold reduction in amplitude compared to sham operated controls. Astrocyte glutamate transporter currents from lesioned animals were also significantly reduced when challenged exogenously applied glutamate. Reduced astrocytic glutamate transport ...
TY - JOUR. T1 - Glutamate transporter function of rat hippocampal astrocytes is impaired following the global ischemia. AU - Yeh, Tu Hsueh. AU - Hwang, Hwa Min. AU - Chen, Jin Jung. AU - Wu, Tony. AU - Li, Allen Hon Lun. AU - Wang, Hung Li. PY - 2005/4. Y1 - 2005/4. N2 - Astroglial glutamate transporters, GLT-1 and GLAST, play an essential role in removing released glutamate from the extracellular space and are essential for maintaining a low concentration of extracellular glutamate in the brain. It was hypothesized that impaired function of glial glutamate transporters induced by transient global ischemia may lead to an elevated level of extracellular glutamate and subsequent excitotoxic neuronal death. To test this hypothesis, in the present study, we performed whole-cell patch-clamp recording of hippocampal CA1 astrocytes in control or postischemic slices, and measured glutamate transporter activity by recording glutamate-evoked transporter currents. Six to 24 h after global ischemia, maximal ...
TY - JOUR. T1 - The role of glutamate transporters in glutamate homeostasis in the brain. AU - Takahashi, Michiko. AU - Billups, Brian. AU - Rossi, David. AU - Sarantis, Monique. AU - Hamann, Martine. AU - Attwell, David. PY - 1997/1. Y1 - 1997/1. N2 - Glutamate transporters in neurones and glia, four of which have been cloned from mammals, play a crucial rule in controlling the extracellular glutamate concentration in the brain. In normal conditions, they remove glutamate from the extracellular space and thereby help to terminate glutamatergic synaptic transmission and to prevent the extracellular glutamate concentration from rising to neurotoxic values. Glutamate transport on these carriers is thought to be driven by the cotransport of Na+, the countertransport of K+, and either the cotransport of H+ or the counter-transport of OH-. Activating the transporters also activates an anion conductance in their structure, the anion flux through which is not coupled to glutamate movement and varies ...
Our data also shed light on functional differences between neural progenitors and differentiated astrocytes. Adult mammalian neural stem cells of the SVZ carry features of astrocytes such as the expression of glial fibrillary acidic protein (GFAP) or the astrocyte-specific glutamate transporter (GLAST) (Ninkovic and Götz, 2007; Wang and Bordey, 2008), and are sometimes also referred to as the astrocytes of the SVZ. We therefore compared receptor profiles and induced signaling pathways between the cultured neural progenitors and cultured astrocytes. The GFAP-positive progenitor cells investigated in this study were multipotential and expressed the stem-cell marker nestin as well as the type-B cell-associated ectonucleotidases NTPDase2 and TNAP (Mishra et al., 2006; Langer et al., 2007), suggesting that they represent type-B cell-like neural precursors. Both RT-PCR and pharmacological experiments suggest that cultured astrocytes express a variety of P2Y and P2X receptors (Jacques-Silva et al., ...
The mammalian genome contains four genes encoding GABA transporters (GAT1, slc6a1; GAT2, slc6a13; GAT3, slc6a11; BGT1, slc6a12) and five glutamate transporter genes (EAAT1, slc1a3; EAAT2, slc1a2; EAAT3, slc1a1; EAAT4, slc1a6; EAAT5, slc1a7). These transporters keep the extracellular levels of GABA and excitatory amino acids low and provide amino acids for metabolic purposes. The various transporters have different properties both with respect to their transport functions and with respect to their ability to act as ion channels. Further, they are differentially regulated. To understand the physiological roles of the individual transporter subtypes, it is necessary to obtain information on their distributions and expression levels. Quantitative data are important as the functional capacity is limited by the number of transporter molecules. The most important and most abundant transporters for removal of transmitter glutamate in the brain are EAAT2 (GLT-1) and EAAT1 (GLAST), while GAT1 and GAT3 are the
Overall Goals: Our laboratory has an interest in examining the in vivo role played by astrocyte glutamate transporters in the etiology and treatment of traumatic spinal cord injury (SCI). SCI represents a debilitating group of conditions that affect approximately 1.3 million individuals in the U.S. alone, resulting in physical and psychological burdens on patients and their families and huge economic costs.. An opportunity exists for preventing secondary cell death following spinal trauma that is responsible for the majority of tissue and functional loss. One of the major causes of secondary injury is excitotoxic cell death due to dysregulation of extracellular levels of the neurotransmitter, glutamate. In the central nervous system (CNS), glutamate is efficiently cleared from the extracellular space by glutamate transporters. Astrocytes are supportive cells with crucial roles in CNS function, outnumbering their neuronal counterparts several-fold. In particular, astrocytes express the major CNS ...
The GLAST1 knockout mouse is a genetically modified mouse strain in which the gene of this member of the superfamily of the glutamate/aspartate transport proteins has been disrupted. - Italia
The following diet is based on the original one by Dr. Jean Dodds and Im pleased that Dr. Dodds has approved it for long term use. Please note that the amounts of food have changed from the original diet and supplementation differs greatly. This diet meets the newest NRC recommended allowances for vitamins and minerals.. We cant expect to see positive results unless the diet is followed as written below. One of the best things about this diet is that you can purchase supplements that are well suited to your dog rather than a blend of things that may upset the gastrointestinal tract. For instance, if zinc citrate is not well tolerated, zinc gluconate can be used. If one manufacturers B-Complex isnt suitable, there are many others available.. This diet has always been positioned to provide dogs with seizure disorders a source of branch chain amino acids and extremely low amounts of glutamate-aspartate. Since these dogs take medication(s) that can be hard on the liver, the diet is ...