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These results suggest that DAT (show SLC6A3 Antibodies) expression affects TH expression and phosphorylation largely in DA terminal field compartments.
These behavioral and molecular phenotypes indicate that a genetic-driven DAT (show SLC6A3 Antibodies) hypofunction alters neurodevelopmental trajectories consistent with ADHD, but not with schizophrenia and bipolar disorders.
An exquisite microanatomical regulation of dopamine by the dopamine transporter was identified in striosomes relative to the matrix in the corpus striatum.
Data suggest that environment pollutants methylmercury and 1-methyl-4-phenylpyridinium decrease release of dopamine from dopaminergic neurons; this mechanism involves down-regulation of expression of Slc6a3 (show SLC6A3 Antibodies).
This study show that Dopamine transporter is enriched in filopodia and induces filopodia formation.
The sigma-1R deficiency through suppressing NR2B (show GRIN2B Antibodies) function and DAT (show SLC6A3 Antibodies) expression can reduce MPTP (show PTPN2 Antibodies)-induced death of dopaminergic neurons and parkinsonism.
DAT (show SLC6A3 Antibodies) gene knockout in mice results dendritic spine loss in pyramidal neurons in the CA1 (show CA1 Antibodies) field of the hippocampus.
Results show that moderate increases in DAT (show SLC6A3 Antibodies) function cause spontaneous dopaminergic cell loss, oxidative stress and fine motor impairment that is reversed by l-DOPA treatment
Chronic and acute reductions of DAT (show SLC6A3 Antibodies) functioning in mice impaired decision-making.
These results demonstrate that the presence of the N-terminal tag leads to impaired DAT (show SLC6A3 Antibodies) protein expression in vivo due in part to improper trafficking of the tagged transporter.
The current study, the effect of the dopamine transporter gene DAT1/SLC6A3 on striatal brain volume was investigated in children and adults with ADHD and healthy participants in three different cross-sectional cohorts.
Study analyzed effects of DRD4 (show DRD4 Antibodies) and DAT1, prenatal exposure to alcohol and smoking and interactions on ADHD severity, response inhibition and neural activity. DRD4 (show DRD4 Antibodies) 7-repeat allele associated with less superior frontal and parietal activity & greater activity in frontal pole and occipital cortex. Alcohol-exposed had more activity in lateral orbitofrontal cortex, & DAT1 risk variant associated with lower cerebellar activity.
We investigated genetic associations with reflexive attention measures in infancy and childhood in the same group of children. Performance on the infant task was associated with SLC6A3 (show SLC6A3 Antibodies). In addition, several genetic associations with an analogous child task occurred with markers on CHRNA4 (show CHRNA4 Antibodies), COMT (show COMT Antibodies), and DRD4 (show DRD4 Antibodies).
Unsubstituted amphetamine-like cathinones bind more favorably to DAT (show SLC6A3 Antibodies), due to a Val152 offering more space, as compared to the bulkier Ile172 in SERT (show SLC6A4 Antibodies). This was supported by uptake inhibition measurements, which showed an increase in activity in SERT (show SLC6A4 Antibodies)-I172V.
Striatal DAT (show SLC6A3 Antibodies) and diencephalic SERT (show SLC6A4 Antibodies) binding negatively correlated with food detection speed, but not with food distraction time, ratings of hunger, craving or impulsivity. Striatal DAT (show SLC6A3 Antibodies) and diencephalic SERT (show SLC6A4 Antibodies) binding did not correlate with free choice food intake.
Participants carrying a copy of the nine-repeat DAT (show SLC6A3 Antibodies) allele-linked to higher phasic dopamine activity-expressed amplified striatal response during anticipation of monetary gain following sleep deprivation. Moreover, participants homozygous for the ten-repeat DAT (show SLC6A3 Antibodies) allele-linked to lower phasic dopamine activity-selectively demonstrated an increase in sensitivity to monetary loss within anterior insula following sleep loss.
SLC6A3 (show SLC6A3 Antibodies) gene variants have been reported to be implicated in alcohol addiction, nicotine dependence and other addictive behaviors.
The 3' VNTR polymorphism affects human DAT (show SLC6A3 Antibodies) expression level in iPSC-derived human dopaminergic neurons.
Study measured smooth pursuit in 110 healthy subjects genotyped for two well-documented polymorphisms, the COMT (show COMT Antibodies) Val(158)Met polymorphism and the SLC6A3 (show SLC6A3 Antibodies) 3'-UTR (show UTS2R Antibodies)-VNTR polymorphism; modulation of striatal dopamine activity by the SLC6A3 (show SLC6A3 Antibodies) 3'-UTR (show UTS2R Antibodies)-VNTR polymorphism had no significant functional effect.
Allosteric modulation of human dopamine transporter activity under conditions promoting its dimerization
This gene encodes a dopamine transporter which is a member of the sodium- and chloride-dependent neurotransmitter transporter family. The 3' UTR of this gene contains a 40 bp tandem repeat, referred to as a variable number tandem repeat or VNTR, which can be present in 3 to 11 copies. Variation in the number of repeats is associated with idiopathic epilepsy, attention-deficit hyperactivity disorder, dependence on alcohol and cocaine, susceptibility to Parkinson disease and protection against nicotine dependence.
, dopamine transporter 1
, sodium-dependent dopamine transporter
, solute carrier family 6 member 3
, solute carrier family 6 (neurotransmitter transporter, dopamine), member 3
, LIM domain only protein 3
, LIM domain only 3
, neuronal-specific transcription factor DAT1
, dopamine-inducible LIM-domain transcription factor DAT1
, solute carrier family 6, member 3
, LIM domain only protein 1