Solute Carrier Family 18 (Vesicular Acetylcholine), Member 3 (SLC18A3) ELISA Kits

Fruit Fly (Drosophila melanogaster) Solute Carrier Family 18 (Vesicular Acetylcholine), Member 3 (SLC18A3) interaction partners

1. Reduction of the polyQ region, by one glutamine residue (13Q to 12Q), results in a significant increase in both amplitude and frequency of spontaneous cholinergic miniature EPSCs (mEPSCs) recorded in the aCC and RP2 motoneurons; and results in evoked synaptic currents that show increased duration: consistent with increased ACh release.

Human Solute Carrier Family 18 (Vesicular Acetylcholine), Member 3 (SLC18A3) interaction partners

1. The results of this study suggest that the Gly360Arg mutant VAChT protein undergoes posttranslational degradation.

2. PCMC expression of ADAM29, FLRT2, and SLC18A3 could be assessed as part of a routine screen to help identify individuals at risk of severe Obstructive sleep apnea in Asian populations

3. Expression of VAChT is increased in neuronal cell lines following upregulation of Lhx8.

4. alpha-Synuclein expression in axons to the distal gut correlates closely with expression of the cholinergic marker, VAChT.

5. Data indicate that siRNA-mediated attenuation of vesicular acetylcholine transporter (VAChT, SLC18A3) reversed the apoptotic activity of vesamicol.

6. Multiple abnormalities with intellectual and developmental disability result from recurrent deletions and reciprocal duplications of 10q11.21q11.23 including CHAT and SLC18A3.

7. overexpressed ChAT enhanced transcription of the CHT1 gene but not the VACHT gene

8. Mutations in the vesicular acetylcholine transporter demonstrate decreased affinity for acetylcholine and vesamicol.

9. The colocalisation of CHT1 immunoreactivity with VAChT immunoreactivity in cholinergic enteric nerves in the human bowel thus suggests that CHT1 represents another marker of cholinergic nerves.

10. Three non-coding SNPs were detected in SLC18A3. None demonstrated any reproducible association with late-onset AD in our samples.

11. An 11.2 kb transgene (named hV11.2) that spanned about 5 kb upstream of the start of VACHT translation down to the first choline acetyltransferase coding exon gave variable expression in the medial habenular nucleus of transgenic mice

12. presence of VAChT in cutaneous nerves and in both epidermal melanocytes and keratinocytes as well as in their nuclei

13. Time-dependent dissociation of bound [3H]vesamicol is biphasic, but equilibrium saturation curves are not. The contrasting phasicity suggests that the pathway to and from the [3H]vesamicol binding site exists in open and at least partially closed states.

Mouse (Murine) Solute Carrier Family 18 (Vesicular Acetylcholine), Member 3 (SLC18A3) interaction partners

1. Aged VAChT-deficient mice showed a decrease in the number of hippocampal neurons and Alzheimer's-Like Pathology.

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

3. Studied object recognition and spatial location in mice deficient for Vesicular Acetylcholine Transporter (VAChT) within interneurons of the striatum, found: impairment in home cage object recognition with a 15 min retention delay, but not with a 3 h retention delay; no on memory for the location of objects; sex differences in retention

4. VAChT overexpression increases acetylcholine at the synaptic cleft and accelerates aging of neuromuscular junctions. Data demonstrate that increasing levels of acetylcholine at the synaptic cleft promote degeneration of adult neuromuscular junction, contributing to age- and disease-related motor deficits.

5. Old VAChT deficient mice (13-16 months-old) showed more pronounced motor learning/balance deficits on the rotarod, and more pronounced balance deficits on the catwalk

6. These results suggest that the VAChT-Cre lines are Cre-drivers that have selectivity in S and FR motor neurons.

7. Loss of VAChT expression is associated with pulmonary inflammation.

8. decreased VAChT levels affect synaptic vesicle biogenesis and distribution whereas a lower ACh content affects vesicles shape.

9. we conclude that VAChT overexpression is sufficient to enhance ACh release in the hippocampal formation

10. Data indicate that elimination of VAChT had only marginal consequences in striatum-related tasks and did not affect spontaneous locomotion, cocaine-induced hyperactivity, or its reward properties.

11. Mice with 65% knockdown of VAChT had normal prepulse inhibition and short-term habituation of startle reaction, whereas long-term habituation was disrupted.

12. VAChT mutant mice present preserved neuromuscular function, but altered brain cholinergic function and are hyperactive.

13. These results reveal the dependence of short-term plasticity on the level of VAChT expression and efficient synaptic vesicle filling.

14. Results indicated that VAChT mutant mice have profound cardiac remodeling and reactivation of the fetal gene program.

15. Residues 481-490 contain trafficking information necessary for VAChT localization, and within this region L485 and L486 are strictly necessary. Clathrin-mediated endocytosis is required for targeting to microvesicles.

16. Real-time RT-PCR revealed significant decreases in VAChT mRNA in the lung of sensitized and allergen challenged animals.

17. Vesicular acetylcholine transporter-immunoreactive axon terminals enriched in the pontine nuclei of the mouse.

18. Nerve fibers surrounding or within taste buds were immunoreactive for the VAChT antibody.

19. results suggest that in rodent prefrontal cortex, the alpha7nAChR plays a major role in modulation of the postsynaptic excitation in spiny dendrites in contact with vesicular acetylcholine transporter containing axons

20. VAChT is essential to the normal development of motor neurons and the release of acetylcholine