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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
T23G5.5-transfected HeLa transports dopamine. Weaker activity for other biogenic amines (tyramine, octopamine, serotonin, norepinephrine). Inhibitors include the tricyclics imipramine and desipramine, cocaine, nomifensine, nisoxetine, and D-amphetamine.
snapin/DAT interaction represents a direct link between exocytotic and reuptake mechanisms.
PREP regulates the function of dopamine transporter, possibly by controlling the phosphorylation and transport of dopamine transporter into the striatum or synaptic membrane.
Melatonin MT1 and MT2 receptors interact with dopamine transporter (DAT) in striatum.
Study generated a transgenic rat model that overexpresses the mouse DAT gene via pronuclear microinjection. These rats specifically exhibited behavioral and pharmaco-therapeutic phenotype of repetitive disorders. Together, findings suggest that the DAT rat model will constitute a valuable tool for studying the pathological role of DAT overexpression on neural systems relevant to relevant to neuropsychiatric disorders.
The findings of thuis study indicated that the DAT Val559 variant induces impulsivity behaviors that are dependent upon the reward context, with increased impulsive action observed when mice are required to delay responding for a reward.
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 function and DAT expression can reduce MPTP-induced death of dopaminergic neurons and parkinsonism.
DAT gene knockout in mice results dendritic spine loss in pyramidal neurons in the CA1 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.
studies demonstrate an in vivo functional impact of the DAT Val559 variant, providing support for the ability of DAT dysfunction to impact risk for mental illness.
The data of this study imply that individual differences in DAT expression (either genetically or pharmacologically induced) may affect susceptibility to addiction of different types of psychostimulants.
findings support the idea that altered DAT and VMAT2 expression affect age-related changes in dopaminergic function.
This study demonistrated that environment enhanced slc6a2 expression in brain and enhanced totaroad perfermance and short term working menory.
DAT C-terminal protein-protein interactions are critical for AMPH-evoked DA efflux and suggest that it may be possible to target protein-protein interactions to modulate transporter function and interfere with psychostimulant effects.
DAT-mediated dopamine uptake plays a role in the absorption and distribution of dopamine following intranasal administration
results of study show that there is no difference in l-dopa induced dyskinesias prevalence among carriers of the two DAT gene polymorphisms.
(AZI2)3'UTR confers variant-dependent transcriptional regulation of SLC6A3, a potential risk factor for substance abuse disorders.
attention deficit hyperactivity disorder (ADHD) subtypes showed that the DRD4 VNTRs are associated with combined and hyperactive-impulsive subtype groups (p < 0.05). Therefore, our results suggest that DAT1 VNTRs and DRD4 VNTRs play a role in the genetic etiology of ADHD in Korean children
Significant associations for polymorphisms in CLOCK, NPSR1 and SLC6A3 with traffic crash parameters in professional bus drivers were found.
No DAT1 main effects were found for any of the analyzed personality traits in substance abusers, but the DAT1 main effects approximated to the statistical significance for the agreeability scale.
The authors results suggest that dopamine transporter polymorphisms influence recognition memory.
SLC6A3 (a dopamine transporter gene, formerly known as DAT1) polymorphism was found to be significantly associated with Attention-Deficit Hyperactivity Disorder.
findings support that gain of disruptive functions due to missense mutations in SLC6A3 may be key to understanding how dopaminergic dyshomeostasis arises in heterozygous carriers
Targeting of dopamine transporter to filopodia requires an outward-facing conformation of the dopamine transporter.
After controlling for gender, age, and SES, the three-way interaction of COMT, DAT1, and peer acceptance significantly concurrently predicted adolescent depressive symptoms. Adolescents with ValVal genotype of COMT and CC genotype of DAT1 were more sensitive to acceptance, compared to their counterparts carrying other combined genotypes
The experimentally observed nonuniform surface distribution of DATs emerged as a major modulator of dopamine signaling: reuptake was slower, and the peaks/width of transient DA levels were sharper/wider under nonuniform distribution of DATs, compared with uniform.
genetically determined differences in DAT1 and DRD2 expression modulate functional consequences of sleep deprivation.
SLC6A3 gene moderates the relation between maternal history of maltreatment and infant emotion regulation.
The age-related reduction in striatal DAT density also predicted memory decline, suggesting that a relation between striatal functions and memory decline in aging is multifaceted.
genetic association studies in population of young adults in Columbia: Data suggest that genetic polymorphisms in DRD4 and SLC6A3 are associated with overweight/obesity in the population studied; DRD4 4/4 genotype is associated with lower BMI and SLC6A3 10/10 genotype is associated with higher BMI. (DRD4 = dopamine receptor D4; SLC6A3 = solute carrier family 6 member 3)
Cloninger's (1987) hypothesis about negative relationship between novelty seeking and dopamine was confirmed on allele level, because higher novelty seeking was found in Val allele carriers comparing to Met/Met genotype carriers.
Results indicate that chronic coffee consumption in Parkinson's disease (PD) patients was not associated with significant change in striatal DAT availability, even after taking into account potentially confounding factors that are probably related to dopaminergic neuron decline (age, sex, disease duration, and severity of PD), treatment, and coffee-related habit (cigarette smoking).
This is the first study to investigate the association of rs3910105 in SNCA [SNCA protein, human] with DAT [dopamine transporter] availability. rs3910105 had an effect on DAT availability, and the correlation between DAT availability and SNCA transcripts were significant in CT [computed tomography] genotypes of rs3910105.
Study describes an association between the 6R6R genotype of the intron 8 VNTR of the dopamine transporter (DAT1) gene and crack cocaine addiction.
None of the polymorphisms studied showed a reliable association with response inhibition performance. The methodological and theoretical implications of these findings are discussed.
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