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The protein encoded by SLC17A7 is a vesicle-bound, sodium-dependent phosphate transporter that is specifically expressed in the neuron-rich regions of the brain. De plus, nous expédions Solute Carrier Family 17 (Vesicular Glutamate Transporter), Member 7 Kits (7) et Solute Carrier Family 17 (Vesicular Glutamate Transporter), Member 7 Protéines (4) et beaucoup plus de produits pour cette protéine.
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Mammalian Monoclonal SLC17A7 Primary Antibody pour ISt, IHC - ABIN1305044
Sotoca, Alvarado, Fuentes-Santamaría, Martinez-Galan, Caminos: Hearing impairment in the P23H-1 retinal degeneration rat model. dans Frontiers in neuroscience 2014
Show all 42 Pubmed References
early VGLUT1-specific parallel fiber synaptic input deficits and dysregulated cerebellar circuit as potential mediators of cerebellar dysfunction in frataxin (Montrer FXN Anticorps) knock-in/knockout mice.
Mice heterozygous for the vesicular glutamate transporter 1 (VGLUT1+/-) were used. Firstly, mRNA expression of the different members of the HDAC superfamily in the prefrontal cortex (PFC) of VGLUT1+/- mice and WT littermates were studied by RT-PCR.
These findings suggest that nitrosylation of VAChT and VGLUT1 may be associated with dysfunctional acetylcholinergic and glutamatergic neurotransmission in Alzheimer's disease.
Study revealed susceptibility of glutamatergic nerve terminals to Abeta (Montrer APP Anticorps) induced toxicity and underlined the importance of VGLUT1 in the progression of Alzheimer's disease, as the decrease of this protein levels could increase the susceptibility to subsequent deleterious inputs by exacerbating Abeta (Montrer APP Anticorps) induced neuroinflammation and synaptic plasticity disruption.
triple KO of Slc17a7, Slc17a6, and Slc17a8 diminished IIIS, which was rescued by exogenously introduced wild-type Slc17a7 or Slc17a6 genes
In CA1 pyramidal neurons, a slow excitatory postsynaptic current is absent in the VGLUT1 knockout mouse.
Data show that activation of nucleotide receptor P2Y4 (P2Y4 (Montrer P2RY4 Anticorps)) in the differentiating embryonic stem cells (ESCs (Montrer NR2E3 Anticorps)) resulted in an increased proportion of neurons expressing vesicular glutamate transporter (Montrer SLC1A1 Anticorps) (vGluT).
Results suggest that activation of JNK in Alzheimer's disease (AD) inhibits insulin signaling which could lead to a decreased expression of VGLUT1, therefore contributing to the glutamatergic deficit in AD
Distribution of VGLUT1 and VGLUT2 in the CN, previously described for guinea pig, was replicated in mouse and showed similar changes in VGLUT1 and 2 distributions after unilateral cochlear insult
Here, we show that VGluT1(+/-) mice acquired the initial visual discrimination at the same rate as controls. However, they failed to suppress responses to the previously rewarded stimulus following reversal of reward contingencies.
This study was the first to demonstrate an association between genetic polymorphism at rs7417284 SNP in the promoter region of the SLC17A7 gene and concussion severity and duration. Based upon these findings, rs74174284 is a potential predictive genetic marker for identifying athletes who are more susceptible for altered recovery times and worse motor speed ImPACT scores after sport-related concussion.
Loss of SLC17A7 expression is associated with glioblastoma.
Depressed patients showed significant decreases in synaptophysin (SYN (Montrer SYP Anticorps)) and VGLUT1 expression, whereas in bipolar patients, decreases in VGLUT1 expression have also been found.
Data indicate that GABAergic axons were labeled with vesicular inhibitory aa transporter (VIAAT) antibodies, whereas glutamatergic axons were detected with antisera against the major vesicular glutamate transporter (VGLUT) isoforms, VGLUT1 and VGLUT2.
We examined the ratio of excitatory to inhibitory vesicular neurotransmitter transporter (Montrer SLC6A2 Anticorps) mRNAs (VGluT1 to VGAT (Montrer SLC32A1 Anticorps)) and their ratio in the dorsolateral prefrontal cortex during normal human development and in people with schizophrenia
this study suggests that the common genetic variants of the VGLUT1 gene appear not play a major role in conferring susceptibility to schizophrenia in Han population of Taiwan.
In schizophrenia, VGLUT1 mRNA was decreased in hippocampal formation and dorsolateral prefrontal cortex. In the hippocampus, the loss of VGLUT1 mRNA supports data indicating that glutamatergic presynaptic deficits are prominent.
Alterations in the pattern of vesicular glutamate transporter 1-immunoreactivity that perfectly matched the neuronal loss and gliosis, as well as the decrease in the number of asymmetrical synapses identified by electron microscopy in this tissue
The protein encoded by this gene is a vesicle-bound, sodium-dependent phosphate transporter that is specifically expressed in the neuron-rich regions of the brain. It is preferentially associated with the membranes of synaptic vesicles and functions in glutamate transport. The protein shares 82% identity with the differentiation-associated Na-dependent inorganic phosphate cotransporter and they appear to form a distinct class within the Na+/Pi cotransporter family.
Brain-specific Na(+)-dependent inorganic phosphate cotransporter
, Solute carrier family 17 member 7
, brain-specific Na(+)-dependent inorganic phosphate cotransporter
, solute carrier family 17 member 7
, vesicular glutamate transporter 1
, brain-specific Na-dependent inorganic phosphate cotransporter
, solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 7
, solute carrier family 17 (vesicular glutamate transporter), member 7