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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
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 (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
DAT-mediated dopamine uptake plays a role in the absorption and distribution of dopamine following intranasal administration
From all the statistically significant CpGs, methylation levels of cg00997378 (SLC6A3 gene) showed the highest differences (p < 0.0001), being associated with prematurity risk factors. SLC6A3 methylation, previously related to attention-deficit/hyperactivity disorder, neuronal function and behavior, might be a potential epigenetic biomarker with value in the early diagnosis and management of neurodevelopmenta
Results show that Gbetagamma activation regulates DAT activity by increasing dopamine (DA) efflux, and suggests that Gbetagamma promotes an efflux-willing state of the transporter and that the activation of a GPCR (zeige NMUR1 Proteine) can lead to a Gbetagamma-dependent DA efflux. Furthermore, the cellular responses that occur following activation of a Galphaq (zeige GNAQ Proteine)-coupled receptor are the result of multiple signaling pathways mediated by Galpha (zeige SUCLG1 Proteine)...
Findings demonstrate that histidine547 on hDAT plays a crucial role in stabilizing basal dopamine transport and Tat (zeige TAT Proteine)-DAT interaction.
In a study of the genetic association between polymorphisms in the DAT1, SERT (zeige SLC6A4 Proteine), COMT (zeige COMT Proteine) and BDNF (zeige BDNF Proteine) genes and attention deficit and hyperactive disorder, transmission disequilibrium test analysis showed that no individual allele of any variant studied has a preferential transmission.
SLC6A3 repeat allele was higher proportion in Indonesian children with ADHD than healthy controls.
This study demonstrate the genetic influence of a family history of alcohol use disorders and DAT and DBH (zeige DBH Proteine) gene polymorphisms on the risk of withdrawal seizures and delirium tremens.
Multilevel models revealed that history of care had a greater influence on maternal baseline cortisol(but not cortisol trajectory)for mothers with more plasticity alleles of SLC6A3 and OXTR (zeige OXTR Proteine), relative to mothers with fewer or no plasticity alleles. Findings indicate that a mother's history of care is related to her cortisol secretion in anticipation of infant stress, but this relation depends on her genetic characteristics
This combined computational-experimental study demonstrates that histidine-547 (H547) of human DAT plays a crucial role in the DAT-HIV-1 Tat (zeige TAT Proteine) binding and dopamine uptake by DAT.
The subjective responses to alcohol consumption in social drinkers were associated with significant epistatic interactions between OPRM1 (zeige OPRM1 Proteine) and DAT1 genotypes.
case-control study by genotyping 7 SNPs of SLC6A2 (zeige SLC6A2 Proteine), SLC6A3 and DRD2 (zeige DRD2 Proteine) in 1034 schizophrenia patients and 1034 controls. No significant difference in the allelic or genotypic frequency was detected between cases and controls
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