Solute Carrier Family 17 (Vesicular Glutamate Transporter), Member 7 Proteins (SLC17A7)

Mouse (Murine) Solute Carrier Family 17 (Vesicular Glutamate Transporter), Member 7 (SLC17A7) interaction partners

1. early VGLUT1-specific parallel fiber synaptic input deficits and dysregulated cerebellar circuit as potential mediators of cerebellar dysfunction in frataxin (show FXN Proteins) knock-in/knockout mice.

2. 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.

3. These findings suggest that nitrosylation of VAChT and VGLUT1 may be associated with dysfunctional acetylcholinergic and glutamatergic neurotransmission in Alzheimer's disease.

4. Study revealed susceptibility of glutamatergic nerve terminals to Abeta (show APP Proteins) 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 (show APP Proteins) induced neuroinflammation and synaptic plasticity disruption.

5. triple KO of Slc17a7, Slc17a6, and Slc17a8 diminished IIIS, which was rescued by exogenously introduced wild-type Slc17a7 or Slc17a6 genes

6. In CA1 pyramidal neurons, a slow excitatory postsynaptic current is absent in the VGLUT1 knockout mouse.

7. Data show that activation of nucleotide receptor P2Y4 (P2Y4 (show P2RY4 Proteins)) in the differentiating embryonic stem cells (ESCs (show NR2E3 Proteins)) resulted in an increased proportion of neurons expressing vesicular glutamate transporter (show SLC1A1 Proteins) (vGluT).

8. 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

9. 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

10. 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.

Human Solute Carrier Family 17 (Vesicular Glutamate Transporter), Member 7 (SLC17A7) interaction partners

1. Study revealed susceptibility of glutamatergic nerve terminals to Abeta (show APP Proteins) 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 (show APP Proteins) induced neuroinflammation and synaptic plasticity disruption.

2. 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.

3. 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

4. Loss of SLC17A7 expression is associated with glioblastoma.

5. Depressed patients showed significant decreases in synaptophysin (SYN (show SYP Proteins)) and VGLUT1 expression, whereas in bipolar patients, decreases in VGLUT1 expression have also been found.

6. 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.

7. We examined the ratio of excitatory to inhibitory vesicular neurotransmitter transporter mRNAs (VGluT1 to VGAT) and their ratio in the dorsolateral prefrontal cortex during normal human development and in people with schizophrenia

8. 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.

9. 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.

10. 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