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. Specifically, we show that mice lacking SRPX2 show a specific reduction in excitatory VGlut2 synapses in the cerebral cortex, while VGlut1 and inhibitory synapses were largely unaffected. SRPX2 KO mice also exhibit an abnormal ultrasonic vocalization ontogenetic profile in neonatal pups, and reduced preference for social novelty.

2. SH3 fusion protein pull downs using ITSN1SH3 A reveal diurnally varying binding of VGLUT1 with slightly reduced VGLUT1/dynamin ratios at the beginning of the light (ZT 0) or the dark (ZT 12) period. Phosphorylation increases binding of VGLUT1 but not of dynamin to EnphSH3. In contrast binding of dynamin to ITSN1SH3 A decreases under phosphorylating conditions with no changes in VGLUT1 binding.

3. Study shows by live-cell imaging with pH- and chloride-sensitive fluorescent probes in cultured hippocampal neurons of wild-type and VGLUT1-deficient mice that in synaptic vesicles VGLUT functions as a glutamate/proton exchanger associated with a channel-like chloride conductance.

4. early VGLUT1-specific parallel fiber synaptic input deficits and dysregulated cerebellar circuit as potential mediators of cerebellar dysfunction in frataxin knock-in/knockout mice.

5. 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.

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

7. Study revealed susceptibility of glutamatergic nerve terminals to Abeta 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 induced neuroinflammation and synaptic plasticity disruption.

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

9. The observed changes in gene and protein expression of vesicular transporter 2, regional architecture, and morphology of mouse auditory forebrain may relate to-and to some extent enable-the emergence of mature sound-evoked activity patterns.

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

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

12. 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

13. 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

14. 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.

15. conclude that VGLUTs contain two anion binding sites and one cation binding site, allowing the transporter to adjust to the changing ionic conditions during vesicle filling without being dependent on other transporters or channels.

16. our genetic analysis provides new in vivo evidence that VGluT1(+) glutamatergic signaling, mediated by the astroglial mGluR5 receptor, regulates the functional maturation of cortical astroglia during development.

17. Targeting of VGLUT-1 in the hippocampus leads to cognitive deficits in a knocked-down adult mouse model.

18. VGLUT1 enhances the tonicity of excitatory synaptic vesicles and stabilises SVs at presynaptic terminals.

19. This study demonstrates a key role for VGLUT1 in long-loop glutamatergic feedback control of 5-HT function.

20. These data indicate that VGluT1, but not VGluT2, plays a role in the neural processes underlying inhibitory learning

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

1. Study revealed susceptibility of glutamatergic nerve terminals to Abeta 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 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) 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

11. Our results suggest that VGLUT1 expression in the prefrontal cortex could be used as a valuable neurochemical marker of dementia in AD.

12. Docking and homology modeling explain the inhibition of VGLUT1.

13. We found increased VGLUT1 transcript and reduced VGLUT1 protein expression in the ACC, but not DLPFC, in schizophrenia.

14. This study found decreased VGLUT1 mRNA expression in both major depressive disorder and bipolar disorder in the entorhinal cortex.

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

1. 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.