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Eaat1 expression is promoted by Fringe-mediated neuron-glial communication during development and suggest that Eaat1 plays an essential role in regulating central nervous system neural circuits that control locomotion in Drosophila
dEAAT1 is present at the adult, but surprisingly not at embryonic and larval NMJ, suggesting a physiological maturation of the junction during metamorphosis
Episodic ataxias 6 is caused by heterozygous mutations in SLC1A3, which encodes a subunit of a glial excitatory amino acid transporter, EAAT1.
a novel missense mutation, c.383T>G (p.Met128Arg) in SLC1A3, in an episodic ataxia patient by whole-exome sequencing.
This is the first study to link SLC1A3 and EPHB2 (zeige EPHB2 Proteine) to clinically relevant vertebral osteoporosis phenotypes.
crystal structures of a thermostabilized human SLC1 (zeige MCHR1 Proteine) transporter, the excitatory amino acid transporter 1 (EAAT1), with and without allosteric and competitive inhibitors bound
This study demonstrated that the cytopathology and episodic paralysis in our Drosophila EA6 model stem from a gain-of-function chloride channelopathy of glial cells..
Starvation of Muller cells increased the glutamate (zeige GRIN1 Proteine) uptake capacity as well as the expression of the most abundant glutamate transporter (zeige SLC1A1 Proteine), EAAT1.
A heterozygous SLC1A3 c.1177G4A mutation has been detected in a patient with late-onset episodic ataxia. Same heterozygous mutation was identified in one clinically affected family member and two asymptomatic members.
that Abeta1-42 oligomers could cause disturbances in insulin (zeige INS Proteine)/Akt (zeige AKT1 Proteine)/EAAT (zeige SLC1A2 Proteine) signaling in astrocytes
We consider an association between SLC1A3 and the behavioural problems which can also be considered a contributing factor to behavioural problems in larger duplications overlapping the 5p13 microduplication syndrome region.
In combination with other nearby residues, Arg-388 coordinates anion channel gating and forms part of the missing structural link between the anion conducting and substrate transport states in EAAT1.
Study shows that high-fat feeding induces metabolic disorders and disrupts lactate metabolism in the hippocampus. Glial glutamate transporters GLAST and GLT-1 may contribute to the high-fat diet induced abnormalities of the hippocampal lactate metabolism.
glutamate transporter (zeige SLC1A1 Proteine) function by GLAST on Bergmann glia plays important roles in development and maintenance of proper synaptic wiring and wrapping in Purkinje cells
Loss of EAAT4 (zeige SLC1A6 Proteine) accounts for the initial hyper-excitability of Purkinje cells lacking b-III spectrin and that loss of GLAST appears to work synergistically to worsen motor deficits. When levels of both EAAT4 (zeige SLC1A6 Proteine) and GLAST are compromised in b-III(-/-) mice, the proximal dendrites of Purkinje cells within the posterior cerebellum are the most vulnerable to degeneration.
The results of this study concluded that EAAT (zeige SLC1A2 Proteine) anion channels play an important and unexpected role in adjusting glial intracellular anion concentration during maturation and in response to cerebellar activity.
SLC1A3 maintains a constant import of acidic amino acids independently of nutritional status in adipocytes.
glutamate/aspartate transporter (GLAST) was elevated in 8- to 10- and/or 20- to 22-month GHR (zeige GHR Proteine)-KO mice when comparing genotypes
This study findings demonstrate that Ascl1 (zeige ASCL1 Proteine)(CreERT2) and Glast(CreERT2) mouse lines enable simple and reliable labeling of adult-born GC lineages within restricted time windows.
arundic acid treatment prevented RGC death by upregulating GLAST in heterozygous (GLAST(+/-)) mice
Results show that expression of GLAST is decreased in cerebellar astrocytes in a mouse model of SCA1; decrease occurs in non-cell autonomous manner late in disease and correlates well with the loss of Purkinje neurons
we have demonstrated for the first time that DOR receptor activation induces astrocytic expression of EAAT1 and EAAT2 (zeige SLC1A2 Proteine)
This gene encodes a member of a member of a high affinity glutamate transporter family. Mutations in this gene are associated with episodic ataxia, Type 6. Alternative splicing results in multiple transcript variants.
, drosophila glutamate transporter-1
, excitatory amino acid transporter 1
, glutamate transporter
, sodium-dependent excitatory amino acid transporter 1
, sodium-dependent glutamate transporter
, excitatory amino acid transporter SLC1A3a
, solute carrier family 1 (glial high affinity glutamate transporter), member 3
, Na+-dependent glutamate/aspartate transporter
, Sodium-dependent glutamate/aspartate transporter 1
, excitatory amino acid transporter 1-like
, glial glutamate transporter
, glutamate/aspartate transporter
, sodium-dependent glutamate/aspartate transporter 1
, solute carrier family 1, member 3
, solute carrier family 1 member 3
, glial high affinity glutamate transporter
, high-affinity neuronal glutamate transporter