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SLC18A3 is a member of the vesicular amine transporter family. Zusätzlich bieten wir Ihnen Solute Carrier Family 18 (Vesicular Acetylcholine), Member 3 Kits (12) und und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal SLC18A3 Primary Antibody für IEM, ICC - ABIN1526179
Wang, Guan, Ochiai, Nakai: An electron microscopic observation of the vesicular acetylcholine transporter-immunoreactive fibers in the rat dorsal raphe nucleus. in Brain research bulletin 1998
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Mammalian Monoclonal SLC18A3 Primary Antibody für - ABIN1305040
Perez-Gonzalez, Albrecht, Blasi, Llobet: Schwann cells modulate short-term plasticity of cholinergic autaptic synapses. in The Journal of physiology 2008
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Rat (Rattus) Polyclonal SLC18A3 Primary Antibody für IHC, WB - ABIN1742304
Gallart-Palau, Tarabal, Casanovas, Sábado, Correa, Hereu, Piedrafita, Calderó, Esquerda: Neuregulin-1 is concentrated in the postsynaptic subsurface cistern of C-bouton inputs to α-motoneurons and altered during motoneuron diseases. in FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2014
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Human Polyclonal SLC18A3 Primary Antibody für IHC (fro), IHC (p) - ABIN259170
Ezkurdia, Coll, Raurell, Rodriguez, Cuenca, González, Guardia, Esteban, Genescà, Martell: Blockage of the afferent sensitive pathway prevents sympathetic atrophy and hemodynamic alterations in rat portal hypertension. in Liver international : official journal of the International Association for the Study of the Liver 2012
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Human Polyclonal SLC18A3 Primary Antibody für IHC - ABIN926164
Schmidt, Xie, Lyte, Vulchanova, Brown: Autonomic neurotransmitters modulate immunoglobulin A secretion in porcine colonic mucosa. in Journal of neuroimmunology 2007
The results of this study suggest that the Gly360Arg mutant VAChT protein undergoes posttranslational degradation.
PCMC expression of ADAM29 (zeige ADAM29 Antikörper), FLRT2 (zeige FLRT2 Antikörper), 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 (zeige LHX8 Antikörper).
alpha-Synuclein expression in axons to the distal gut (zeige GUSB Antikörper) 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 (zeige ChT Antikörper) gene but not the VACHT gene
Mutations in the vesicular acetylcholine transporter demonstrate decreased affinity for acetylcholine and vesamicol.
The colocalisation of CHT1 (zeige ChT Antikörper) immunoreactivity with VAChT immunoreactivity in cholinergic enteric nerves in the human bowel thus suggests that CHT1 (zeige ChT Antikörper) 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.
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
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 (zeige FGFR3 Antikörper) content affects vesicles shape.
we conclude that VAChT overexpression is sufficient to enhance ACh (zeige FGFR3 Antikörper) 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.
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