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anti-Mouse (Murine) SLC17A8 Antikörper:
anti-Rat (Rattus) SLC17A8 Antikörper:
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Mammalian Monoclonal SLC17A8 Primary Antibody für ISt, IHC - ABIN1305048
Platel, Dave, Gordon, Lacar, Rubio, Bordey: NMDA receptors activated by subventricular zone astrocytic glutamate are critical for neuroblast survival prior to entering a synaptic network. in Neuron 2010
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Mouse (Murine) Polyclonal SLC17A8 Primary Antibody für IHC, WB - ABIN1742302
Cao, Gou, Du, Fan, Liang, Yan, Lin, Jin, Du: Glutamatergic and central cholinergic dysfunction in the CA1, CA2 and CA3 fields on spatial learning and memory in chronic cerebral ischemia-Induced vascular dementia of rats. in Neuroscience letters 2016
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Vesicular glutamate transporter 3 is expressed preferentially in hair cells of the ear, and is required for synaptic transmission in the hair cells in zebrafish.
VGluT3-expressing amacrine cells provide selective glycinergic input to a retinal ganglion cell type suppressed by contrast and motion
Results reveal that VGLUT3 plays an important role in the development of l-DOPA-induced dyskinesia (LID), and should be considered as a potential and promising therapeutic target for prevention of LID
Synaptic excitation of W3 ganglion cells is diminished, and responses to object motion are suppressed in mice lacking VGluT3.
Measurements of time spent in noisy versus attenuated environments reveal noise-avoidance behavior in mice expressing VGLUT3 whereas Vglut3-/- mice showed no preference.
Transient expression of VGLUT3 by a discrete population of neurons in the dorsal horn is required for mechanical pain.
Results showed that VGLUT3 expression has little or no effect on vesicular synergy at the immature glycinergic synapse of brainstem
The possible contribution of VGLUT3 upregulation in the cochlear degeneration is discussed.
Our data demonstrate that VGLUT3 is required for normal cholinergic signaling onto striatal fast-spiking interneurons, as well as for acetylcholine-dependent disynaptic inhibition of medium spiny neurons.
This study demonistrated that vglut3 are present in synaptic vesicles in acetylcholinergic nerve terminals in the striatum.
VGLUT3 contributes to protection against neonatal hypoxic stress
Novel pathogenic splicing mutation in SLC17A8 gene identified in a family with hearing loss.
A point mutation in VGLUT3 dramatically reduces its expression in synaptic terminals without altering its function.
The results of this study identify VGLUT3 as an unexpected regulator of drug abuse.
The results from our study suggest that the p.M206Nfs*4 mutation in the SLC17A8 gene is likely a pathogenic mutation that causes autosomal dominant non-syndromic hearing loss.
The absence of VGLUT3 in transgenic mice leads to an up-regulation of the midbrain dopamine system and ameliorates motor dysfunction in a model of Parkinson's disease.
human vesicular glutamate transporter 3 was cloned, shows 72% identity to both hVGLUT1 and hVGLUT2, and its expression in brain overlaps with hVGLUT1 and hVGLUT2
Docking and homology modeling explain the inhibition of VGLUT3.
VGLUT3 immunoreactivity covered only a limited portion of the possible Glu (zeige DCTN1 Antikörper)-ergic pathways in the human fetal small intestine.
SLC17A8 encodes vesicular glutamate transporter-3, VGLUT3 and its impairment has a role in nonsyndromic deafness DFNA25 and inner hair cell dysfunction
This gene encodes a vesicular glutamate transporter. The encoded protein transports the neurotransmitter glutamate into synaptic vesicles before it is released into the synaptic cleft. Mutations in this gene are the cause of autosomal-dominant nonsyndromic type 25 deafness. Alternate splicing results in multiple transcript variants.
vesicular glutamate transporter 3
, solute carrier family 17 member 8
, vesicular glutamate transporter-3
, solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 8