Last update 01 Nov 2024

α3-AR

Last update 01 Nov 2024

Basic Info

Synonyms-

Introduction-

Drugs associated with α3-AR

YH-200

Target

ADRA1 x ADRA2 x AMPA receptor x D1 receptor x D2 receptor x α1B-AR x α3-AR x β-adrenoceptors

Mechanism

ADRA1 modulators [+7]

Active Org.

Peking University Health Science Center

Originator Org.

Peking University Health Science Center

Active Indication

Depressive Disorder

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with α3-AR

100 Translational Medicine associated with α3-AR

0 Patents (Medical) associated with α3-AR

212

Literatures (Medical) associated with α3-AR

01 May 2018·Thrombosis ResearchQ3 · MEDICINE

SSRI-reduced platelet reactivity in non-responding patients with life-long Recurrent Depressive Disorder: Detection and involved mechanisms

Q3 · MEDICINE

Article

Author: Manusheva, Nensi ; Filipce, Ana ; Vujović, Viktorija ; Neceva, Violeta ; Rendevski, Vladimir ; Sofijanova, Aspazija ; Gjorgoski, Icko ; Aleksovski, Boris ; Novotni, Antoni ; Aleksovski, Vasko ; Spasovska, Anastazija

INTRODUCTIONAdverse effects with bleeding disorders are often associated with the administration of SSRI in depression, although the exact mechanisms remain contradicting. This study is aimed at detecting and exploring the mechanisms of SSRI-induced changes in platelet reactivity in non-responding patients with Recurrent Depressive Disorder (RDD) and life-long exposure to antidepressants.MATERIALS AND METHODSThirty-one patients and thirty-one healthy controls were included in the study. A comprehensive approach which includes evaluation of peripheral markers and microscopic analyses of platelet morphology changes has been used.RESULTSRDD SSRI patients have shown blunted aggregatory responses towards collagen and epinephrine. Evident differences in the microscopic evaluation of platelet morphology were observed between the groups, with inherent absence of micro-aggregates and platelet shape changes within the patients; after quantification, the sensitivity and specificity of this method were assessed as high. The abnormalities were found in association with lower platelet serotonin content and high fluctuations of free plasma serotonin levels. Changes in the levels of CRP, fibrinogen and nitric oxide were not observed. Macroplatelets were also detected within RDD SSRI patients via increased MPV, PDW and P-LCR, which were associated with discoid shape and without procoagulant activity.CONCLUSIONSThe microscopic evaluation might be useful as a simple method for detection of SSRI-reduced platelet function for research purposes or systematic correlations with other biochemical parameters. The mechanisms involved in SSRI-reduced platelet function in non-responding RDD patients are complex, including combined effects of lower platelet serotonin content, high fluctuations in plasma serotonin concentration and abnormal α-AR function.

01 Nov 2012·HepatologyQ1 · MEDICINE

Pericentral activity of alpha-fetoprotein enhancer 3 and glutamine synthetase upstream enhancer in the adult liver are regulated by β-catenin in mice

Q1 · MEDICINE

Article

Author: Butler, James E. ; Clinkenbeard, Erica L. ; Spear, Brett T.

We previously showed that mouse alpha-fetoprotein (AFP) enhancer 3 activity is highly restricted to pericentral hepatocytes in the adult liver. Here, using transgenic mice, we show that the upstream enhancer of the rat glutamine synthetase gene is also active, specifically in pericentral regions. Activity of both enhancers is lost in the absence of β-catenin, a key regulator of zonal gene expression in the adult liver. Both enhancers contain a single, highly conserved T-cell factor/lymphoid enhancer factor binding site that is required for responsiveness to β-catenin. We also show that endogenous AFP messenger RNA levels in the perinatal liver are lower when β-catenin is reduced.Conclusion:These data identify the first distinct zonally active regulatory regions required for β-catenin responsiveness in the adult liver, and suggest that postnatal AFP repression and the establishment of zonal regulation are controlled, at least in part, by the same factors.

01 Jun 2010·European Journal of PharmacologyQ3 · MEDICINE

The point mutation γ2F77I changes the potency and efficacy of benzodiazepine site ligands in different GABAA receptor subtypes

Q3 · MEDICINE

Article

Author: Furtmueller, Roman ; Vogel, Elisabeth ; Huck, Sigismund ; Sieghart, Werner ; Ramerstorfer, Joachim

Benzodiazepine site agonists or inverse agonists enhance or reduce gamma-aminobutyric acid(A) (GABA(A)) receptor-mediated inhibition of neurons, respectively. Recently, it was demonstrated that the point mutation gamma 2F77I causes a drastic change in the affinity of a variety of benzodiazepine agonists or inverse agonists in receptor binding studies. Here we investigated the potency and efficacy of 10 benzodiazepine site ligands from 6 structural classes in wild-type and gamma 2F77I point mutated recombinant GABA(A) receptors composed of alpha 1 beta 3 gamma 2, alpha 2 beta 3 gamma 2, alpha 3 beta 3 gamma 2, alpha 4 beta 3 gamma 2, alpha 5 beta 3 gamma 2, and alpha 6 beta 3 gamma 2 subunits. Results indicate that the effects of the benzodiazepine site ligands zolpidem, zopiclone, Cl218872, L-655,708 and DMCM were nearly completely eliminated in all mutated receptors up to a 1 microM concentration. The effects of bretazenil, Ro15-1788 or abecarnil were eliminated in some, but not all mutated receptors, suggesting that the gamma 2F77I mutation differentially influences the actions of these ligands in different receptor subtypes. In addition, this point mutation also influences the efficacy of diazepam for enhancing GABA-induced chloride flux, suggesting that the amino acid residue gamma 2F77 might also be involved in the transduction of the effect of benzodiazepines from binding to gating. The application of these drugs in a novel mouse model is discussed.

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