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these findings suggest that disrupting 5-HT6 receptor-neurofibromin (show NF1 Proteins) interaction prevents agonist-independent 5-HT6 receptor-operated cAMP signaling in prefrontal cortex, an effect that might underlie neuronal abnormalities in NF1 (show NF1 Proteins) patients.
Results implicate a role of 5-HT6 receptor signaling in primary cilia morphology, suggest that 5-HT6 receptor research should consider relative levels of receptor expression when evaluating their impact on primary cilia function.
5-HT6/7 receptor antagonist ADN (show CFD Proteins)-1184 displays anxiolytic-like activity in animal models of anxiety which employed punished stimuli.
SNX14 (show SNX14 Proteins) is a dual endogenous negative regulator in 5-HT6R-mediated signaling pathway.
Constitutive expression of 5-HT6R controls pyramidal neuron migration through an agonist-independent mechanism that requires Cdk5 (show CDK5 Proteins) activity.
Knockdown of MAO-A (show MAOA Proteins) expression in embryos induces high serotonin levels and abnormal brain development, which can be rescued by inactivation of serotonin receptor-6.
Coexpression of 5HT6 with adenylyl cyclase type III (show ADCY3 Proteins) normalizes cilia structure and restores dendrite outgrowth.
Serotonergic stimulation of 5-HT6 serotonin receptors augments extrapyramidal motor symptoms; antagonism of 5-HT6 receptors alleviates the symptoms.
5-HT6 receptors were expressed in embryonic mouse cortical interneurons and that 5-HT6 receptor activation decreased interneuron migration, whereas 5-HT6 receptor blockade prevented the migratory effects induced by 5-HT (show DDC Proteins).
that HTR6 plays an important role in modulating seizure activity and that the blockade of the 5-HT6 receptor/mTOR (show FRAP1 Proteins) pathway could be a potential therapeutic target for epilepsy treatment
Studies indicate that serotonin 5-HT6 receptor (5-HT6R) has been proposed as a promising drug target for cognition enhancement in Alzheimer's disease (AD).
[review] Controlling the activity of 5-HTR6 receptors seems to provide benefits by alleviating cognitive impairments.
Data indicate that hydrogen-bond formation of a methoxy or hydroxy group is not important for binding at the 5-HT6 receptor.
The human cloned 5-HT6 receptor is stably transfected in HeLa cells.
When expressed in pyramidal neuron progenitors, serotonin receptor (show HTR1B Proteins) 5-HT6 transgene decreases the migration speed of cortical pyramidal neurons, thereby affecting a fundamental step in the assembly of neural circuits.
These observations suggest that recruitment of mTOR (show FRAP1 Proteins) by prefrontal 5-HT(6) receptors contributes to the perturbed cognition in schizophrenia, offering new vistas for its therapeutic control.
There was a statistically significant difference in semantic memory scores among the three genotype groups of T267C in 5-HT6.
present findings showed the presence of a higher density of 5-HT(6) receptors, as labeled by [(125)I]SB-258585, in striatum than in hippocampus and prefrontal cortex, and specifically within the neuronal body
results indicate that tagging SNPs in HTR6 may not play a role in the pathophysiology of schizophrenia.
This is one of the several different receptors for 5- hydroxytryptamine (serotonin), a biogenic hormone that function as a neurotransmitter, a hormone, and a mitogen. The activity of this receptor is mediated by G proteins that stimulate adenylate cyclase. It has a high affinity for tricyclic psychotropic drugs (By similarity).
, 5-hydroxytryptamine receptor 6
, serotonin receptor 6
, 5-alpha-hydroxytryptamine receptor 6