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DNA of the impulsive but not the calm subjects was methylated at one DAT SNP.
nitrative damage accumulates in midbrain neurons with age; The capacity of a dopamine neuron to accumulate more cytosolic DA, as inferred from DA transporter expression, is related to accumulation of nitrative damage
Two C-terminal motifs dictate synaptic localization of DAT-1.
Endogenous dopamine actions in C. elegans are tightly regulated by synaptic DAT-1.
loss of UNC-64/DAT-1 interactions leads to enhanced synaptic dopamine release
These results suggest that DAT expression affects TH expression and phosphorylation largely in DA terminal field compartments.
These behavioral and molecular phenotypes indicate that a genetic-driven DAT 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.
This study show that Dopamine transporter is enriched in filopodia and induces filopodia formation.
The sigma-1R deficiency through suppressing NR2B (zeige GRIN2B Proteine) function and DAT expression can reduce MPTP (zeige PTPN2 Proteine)-induced death of dopaminergic neurons and parkinsonism.
DAT gene knockout in mice results dendritic spine loss in pyramidal neurons in the CA1 (zeige CA1 Proteine) field of the hippocampus.
Results show that moderate increases in DAT 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 functioning in mice impaired decision-making.
These results demonstrate that the presence of the N-terminal tag leads to impaired DAT protein expression in vivo due in part to improper trafficking of the tagged transporter.
DAT-mediated dopamine uptake plays a role in the absorption and distribution of dopamine following intranasal administration
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 (zeige DRD4 Proteine) and DAT1, prenatal exposure to alcohol and smoking and interactions on ADHD severity, response inhibition and neural activity. DRD4 (zeige DRD4 Proteine) 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. In addition, several genetic associations with an analogous child task occurred with markers on CHRNA4 (zeige CHRNA4 Proteine), COMT (zeige COMT Proteine), and DRD4 (zeige DRD4 Proteine).
Unsubstituted amphetamine-like cathinones bind more favorably to DAT, due to a Val152 offering more space, as compared to the bulkier Ile172 in SERT (zeige SLC6A4 Proteine). This was supported by uptake inhibition measurements, which showed an increase in activity in SERT (zeige SLC6A4 Proteine)-I172V.
Striatal DAT and diencephalic SERT (zeige SLC6A4 Proteine) binding negatively correlated with food detection speed, but not with food distraction time, ratings of hunger, craving or impulsivity. Striatal DAT and diencephalic SERT (zeige SLC6A4 Proteine) binding did not correlate with free choice food intake.
Participants carrying a copy of the nine-repeat DAT 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 allele-linked to lower phasic dopamine activity-selectively demonstrated an increase in sensitivity to monetary loss within anterior insula following sleep loss.
SLC6A3 gene variants have been reported to be implicated in alcohol addiction, nicotine dependence and other addictive behaviors.
The 3' VNTR polymorphism affects human DAT expression level in iPSC-derived human dopaminergic neurons.
Study measured smooth pursuit in 110 healthy subjects genotyped for two well-documented polymorphisms, the COMT Val(158)Met polymorphism and the SLC6A3 3'-UTR-VNTR polymorphism; modulation of striatal dopamine activity by the SLC6A3 3'-UTR-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 variant II
, sodium-dependent dopamine transporter
, solute carrier family 6 (neurotransmitter transporter, dopamine), member 3
, sodium-dependent dopamine transporter-like
, DA transporter
, dopamine transporter 1
, solute carrier family 6 member 3
, solute carrier family 6, member 3