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SLC18A3 is a member of the vesicular amine transporter family. Additionally we are shipping Solute Carrier Family 18 (Vesicular Acetylcholine), Member 3 Antibodies (97) and and many more products for this protein.
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The results of this study suggest that the Gly360Arg mutant VAChT protein undergoes posttranslational degradation.
PCMC expression of ADAM29 (show ADAM29 ELISA Kits), FLRT2 (show FLRT2 ELISA Kits), 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
Expression of VAChT is increased in neuronal cell lines following upregulation of Lhx8 (show LHX8 ELISA Kits).
alpha-Synuclein (show SNCA ELISA Kits) expression in axons to the distal gut (show GUSB ELISA Kits) correlates closely with expression of the cholinergic marker, VAChT.
Data indicate that siRNA-mediated attenuation of vesicular acetylcholine transporter (VAChT, SLC18A3) reversed the apoptotic activity of vesamicol.
Multiple abnormalities with intellectual and developmental disability result from recurrent deletions and reciprocal duplications of 10q11.21q11.23 including CHAT and SLC18A3.
overexpressed ChAT enhanced transcription of the CHT1 (show ChT ELISA Kits) gene but not the VACHT gene
Mutations in the vesicular acetylcholine transporter demonstrate decreased affinity for acetylcholine and vesamicol.
The colocalisation of CHT1 (show ChT ELISA Kits) immunoreactivity with VAChT immunoreactivity in cholinergic enteric nerves in the human bowel thus suggests that CHT1 (show ChT ELISA Kits) represents another marker of cholinergic nerves.
Three non-coding SNPs were detected in SLC18A3. None demonstrated any reproducible association with late-onset AD in our samples.
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.
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
These results suggest that the VAChT-Cre lines are Cre-drivers that have selectivity in S and FR motor neurons.
Loss of VAChT expression is associated with pulmonary inflammation.
decreased VAChT levels affect synaptic vesicle biogenesis and distribution whereas a lower ACh (show FGFR3 ELISA Kits) content affects vesicles shape.
we conclude that VAChT overexpression is sufficient to enhance ACh (show FGFR3 ELISA Kits) release in the hippocampal formation
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.
Mice with 65% knockdown of VAChT had normal prepulse inhibition and short-term habituation of startle reaction, whereas long-term habituation was disrupted.
VAChT mutant mice present preserved neuromuscular function, but altered brain cholinergic function and are hyperactive.
These results reveal the dependence of short-term plasticity on the level of VAChT expression and efficient synaptic vesicle filling.
This gene is a member of the vesicular amine transporter family. The encoded transmembrane protein transports acetylcholine into secretory vesicles for release into the extracellular space. Acetylcholine transport utilizes a proton gradient established by a vacuolar ATPase. This gene is located within the first intron of the choline acetyltransferase gene.
, vesicular acetylcholine transporter
, solute carrier family 18 (vesicular acetylcholine), member 3
, vesicular acetylcholine transporter-like
, solute carrier family 18 (vesicular monoamine) member 3
, solute carrier family 18, member 3
, solute carrier family 18 member 3