Trace Amine Receptor (Version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database
Total Page：16
File Type：pdf, Size：1020Kb
Load more
Recommended publications
-
Downloaded for Further Analysis
bioRxiv preprint doi: https://doi.org/10.1101/2020.09.10.288951; this version posted September 11, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Coordination of two enhancers drives expression of olfactory trace amine- associated receptors Aimei Fei1,8, Wanqing Wu1,8, Longzhi Tan3,8, Cheng Tang4,8, Zhengrong Xu1, Xiaona Huo4, Hongqiang Bao1, Mark Johnson5, Griffin Hartmann5, Mustafa Talay5, Cheng Yang1, Clemens Riegler6, Kristian Joseph6, Florian Engert6, X. Sunney Xie3, Gilad Barnea5, Stephen D. Liberles7, Hui Yang4, and Qian Li1,2,* 1Center for Brain Science, Shanghai Children's Medical Center, Department of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China; 2Shanghai Research Center for Brain Science and Brain-Inspired Intelligence, Shanghai 201210, China; 3Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138, USA; 4Institute of Neuroscience, State Key Laboratory of Neuroscience, Key Laboratory of Primate Neurobiology, CAS Center for Excellence in Brain Science and Intelligence Technology, Shanghai Research Center for Brain Science and Brian-Inspired Intelligence, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China; 5Department of Neuroscience, Division of Biology and Medicine, Brown University, Providence, RI 02912, USA; 6Department of Molecular and Cellular Biology and Center for Brain Science, Harvard University, Cambridge, MA 02138, USA; 7Howard Hughes Medical Institute, Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA; 8These authors contributed equally to this work. *Correspondence to [email protected], phone: +86-21-63846590 ext. 776985 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.09.10.288951; this version posted September 11, 2020. -
Is TAAR1 a Potential Therapeutic Target for Immune Dysregulation In
Graduate Physical and Life Sciences PhD Pharmacology Abstract ID# 1081 Is TAAR1 a Potential Therapeutic Target for Immune Dysregulation in Drug Abuse? Fleischer, Lisa M; Tamashunas, Nina and Miller, Gregory M Addiction Sciences Laboratory, Northeastern University, Boston MA 02115 Abstract Discovered in 2001, Trace Amine Associated Receptor 1 (TAAR1) is a direct target of Data and Results amphetamine, methamphetamine and MDMA. It is expressed in the brain reward circuity and modulates dopamine transporter function and dopamine neuron firing rates. Newly-developed compounds that specifically target TAAR1 have recently been investigated in animal models In addition to brain, TAAR1 is expressed in immune cells METH promotes PKA and PKC Phosphorylation through TAAR1 as candidate therapeutics for methamphetamine, cocaine and alcohol abuse. These studies • We treated HEK/TAAR1 cells and HEK293 involving classic behavioral measures of drug response, as well as drug self-administration, Rhesus and Human cells with vehicle or METH, with and without strongly implicate TAAR1 as a potential therapeutic target for the treatment of addiction. In activators and inhibitors of PKA and PKC. addition to its central actions, we demonstrated that TAAR1 is upregulated in peripheral blood Cells Lines mononuclear cells (PBMC) and B cells following immune activation, and that subsequent • We performed Western blotting experiments to activation of TAAR1 by methamphetamine stimulates cAMP, similar to the function of measure levels of phospho-PKA and phospho- adenosine A2 receptors which are also present in immune cells and play a critical role in the PKC. immune response. Here, we are investigating the relationship between TAAR1 and the • We found that specific activators of PKA and adenosine A2 receptor at the level of cellular signaling and receptor dimerization. -
Functional Selectivity and Partial Efficacy at the Monoamine Transporters: a Unified Model of Allosteric Modulation and Amphetamine-Induced Substrate Release
1521-0111/95/3/303–312$35.00 https://doi.org/10.1124/mol.118.114793 MOLECULAR PHARMACOLOGY Mol Pharmacol 95:303–312, March 2019 Copyright ª 2019 by The Author(s) This is an open access article distributed under the CC BY-NC Attribution 4.0 International license. MINIREVIEW Functional Selectivity and Partial Efficacy at the Monoamine Transporters: A Unified Model of Allosteric Modulation and Amphetamine-Induced Substrate Release Peter S. Hasenhuetl,1,2 Shreyas Bhat,2 Michael Freissmuth, and Walter Sandtner Downloaded from Institute of Pharmacology, Gaston H. Glock Research Laboratories for Exploratory Drug Development, Center of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria Received October 2, 2018; accepted December 13, 2018 ABSTRACT molpharm.aspetjournals.org All clinically approved drugs targeting the plasmalemmal trans- allosteric inhibition and stimulation of MATs, which can be porters for dopamine, norepinephrine, and serotonin act either functionally selective for either substrate uptake or amphetamine- as competitive uptake inhibitors or as amphetamine-like releas- induced release. These concepts are integrated into a parsimonious ers. Monoamine transporter (MAT) ligands that allosterically kinetic framework, which relies exclusively on physiologic transport affect MAT-mediated substrate uptake, release, or both were modes (without any deviation from an alternating access mecha- recently discovered. Their modes of action have not yet been nism). The model posits cooperative substrate and Na1 binding and explained in a unified framework. Here, we go beyond compet- functional selectivity by conformational selection (i.e., preference of itive inhibitors and classic amphetamines and introduce con- the allosteric modulators for the substrate-loaded or substrate-free cepts for partial efficacy at and allosteric modulation of MATs. -
Certificate of Analysis
Print Date: Jan 3rd 2020 Certificate of Analysis www.tocris.com Product Name: EPPTB Catalog No.: 4518 Batch No.: 1 CAS Number: 1110781-88-8 IUPAC Name: N-(3-Ethoxyphenyl)-4-(1-pyrrolidinyl)-3-(trifluoromethyl)benzamide 1. PHYSICAL AND CHEMICAL PROPERTIES Batch Molecular Formula: C20H21F3N2O2 Batch Molecular Weight: 378.39 Physical Appearance: White solid Solubility: DMSO to 100 mM ethanol to 100 mM Storage: Store at +4°C Batch Molecular Structure: 2. ANALYTICAL DATA TLC: Rf = 0.2 (Ethyl acetate:Petroleum ether [4:1]) HPLC: Shows 99.9% purity 1H NMR: Consistent with structure Mass Spectrum: Consistent with structure Microanalysis: Carbon Hydrogen Nitrogen Theoretical 63.48 5.59 7.4 Found 63.37 5.53 7.44 Caution - Not Fully Tested • Research Use Only • Not For Human or Veterinary Use bio-techne.com North America China Europe Middle East Africa Rest of World [email protected] Tel: (800) 343 7475 [email protected] Tel: +44 (0)1235 529449 www.tocris.com/distributors [email protected] Tel: +86 (21) 52380373 Tel:+1 612 379 2956 Print Date: Jan 3rd 2020 Product Information www.tocris.com Product Name: EPPTB Catalog No.: 4518 Batch No.: 1 CAS Number: 1110781-88-8 IUPAC Name: N-(3-Ethoxyphenyl)-4-(1-pyrrolidinyl)-3-(trifluoromethyl)benzamide Description: Storage: Store at +4°C Trace amine 1 (TA ) receptor antagonist/inverse agonist; 1 Solubility & Usage Info: exhibits a higher potency at the mouse TA1 receptor than the rat DMSO to 100 mM and human TA150 receptors (IC values are 27.5, 4539 and 7487 ethanol to 100 mM nM, respectively). -
Modulation by Trace Amine-Associated Receptor 1 of Experimental Parkinsonism, L-DOPA Responsivity, and Glutamatergic Neurotransmission
The Journal of Neuroscience, October 14, 2015 • 35(41):14057–14069 • 14057 Neurobiology of Disease Modulation by Trace Amine-Associated Receptor 1 of Experimental Parkinsonism, L-DOPA Responsivity, and Glutamatergic Neurotransmission Alexandra Alvarsson,1* Xiaoqun Zhang,1* Tiberiu L Stan,1 Nicoletta Schintu,1 Banafsheh Kadkhodaei,2 Mark J. Millan,3 Thomas Perlmann,2,4 and Per Svenningsson1 1Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, SE-17176 Stockholm, Sweden, 2Ludwig Institute for Cancer Research, SE-17177 Stockholm, Sweden, 3Pole of Innovation in Neuropsychiatry, Institut de Recherches Servier, Centre de Recherches de Croissy, Paris 87290, France, and 4Department of Cell and Molecular Biology, Karolinska Institutet, SE-17177 Stockholm, Sweden Parkinson’s disease (PD) is a movement disorder characterized by a progressive loss of nigrostriatal dopaminergic neurons. Restoration of dopamine transmission by L-DOPA relieves symptoms of PD but causes dyskinesia. Trace Amine-Associated Receptor 1 (TAAR1) modulates dopaminergic transmission, but its role in experimental Parkinsonism and L-DOPA responses has been neglected. Here, we report that TAAR1 knock-out (KO) mice show a reduced loss of dopaminergic markers in response to intrastriatal 6-OHDA administra- tion compared with wild-type (WT) littermates. In contrast, the TAAR1 agonist RO5166017 aggravated degeneration induced by intra- striatal6-OHDAinWTmice.Subchronic L-DOPAtreatmentofTAAR1KOmiceunilaterallylesionedwith6-OHDAinthemedialforebrain bundle resulted in more pronounced rotational behavior and dyskinesia than in their WT counterparts. The enhanced behavioral sensitization to L-DOPA in TAAR1 KO mice was paralleled by increased phosphorylation of striatal GluA1 subunits of AMPA receptors. Conversely, RO5166017 counteracted both L-DOPA-induced rotation and dyskinesia as well as AMPA receptor phosphorylation. -
TRAR4 (TAAR6) (NM 175067) Human Tagged ORF Clone Lentiviral Particle Product Data
OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for RC220756L3V TRAR4 (TAAR6) (NM_175067) Human Tagged ORF Clone Lentiviral Particle Product data: Product Type: Lentiviral Particles Product Name: TRAR4 (TAAR6) (NM_175067) Human Tagged ORF Clone Lentiviral Particle Symbol: TAAR6 Synonyms: TA4; taR-4; taR-6; TAR4; TAR6; TRAR4 Vector: pLenti-C-Myc-DDK-P2A-Puro (PS100092) ACCN: NM_175067 ORF Size: 1035 bp ORF Nucleotide The ORF insert of this clone is exactly the same as(RC220756). Sequence: OTI Disclaimer: The molecular sequence of this clone aligns with the gene accession number as a point of reference only. However, individual transcript sequences of the same gene can differ through naturally occurring variations (e.g. polymorphisms), each with its own valid existence. This clone is substantially in agreement with the reference, but a complete review of all prevailing variants is recommended prior to use. More info OTI Annotation: This clone was engineered to express the complete ORF with an expression tag. Expression varies depending on the nature of the gene. RefSeq: NM_175067.1, NP_778237.1 RefSeq Size: 1038 bp RefSeq ORF: 1038 bp Locus ID: 319100 UniProt ID: Q96RI8 Protein Families: Druggable Genome, GPCR, Transmembrane Protein Pathways: Neuroactive ligand-receptor interaction MW: 38.3 kDa Gene Summary: This gene encodes a seven-transmembrane G-protein-coupled receptor that likely functions as a receptor for endogenous trace amines. Mutations in this gene may be associated with schizophrenia.[provided by RefSeq, Feb 2010] This product is to be used for laboratory only. -
Ageing, Sex and Cardioprotection Marisol Ruiz-Meana1,2, Kerstin Boengler3, David Garcia-Dorado1,2, Derek J
Kaambre Tuuli (Orcid ID: 0000-0001-5755-4694) Kararigas Georgios (Orcid ID: 0000-0002-8187-0176) Ageing, sex and cardioprotection Marisol Ruiz-Meana1,2, Kerstin Boengler3, David Garcia-Dorado1,2, Derek J. Hausenloy4,5,6,7,8,9, Tuuli Kaambre10, Georgios Kararigas11,12, Cinzia Perrino13, Rainer Schulz3, Kirsti Ytrehus14. 1 Hospital Universitari Vall d’Hebron, Department of Cardiology. Vall d’Hebron Institut de Recerca (VHIR).Universitat Autonoma de Barcelona, Spain. 2 Centro de Investigación Biomédica en Red-CV, CIBER-CV, Spain. 3Institute of Physiology, Justus-Liebig University Giessen. Giessen 35392, Aulweg 129, Germany. 4Cardiovascular & Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore. 5National Heart Research Institute Singapore, National Heart Centre, Singapore. 6Yong Loo Lin School of Medicine, National University Singapore, Singapore. 7The Hatter Cardiovascular Institute, University College London, London, UK. 8The National Institute of Health Research University College London Hospitals Biomedical Research Centre, Research & Development, London, UK. 9Tecnologico de Monterrey, Centro de Biotecnologia-FEMSA, Nuevo Leon, Mexico. 10Laboratory of Chemical Biology, National Institute of Chemical Physics and Biophysics, Akadeemia tee 23, 12618 Tallinn, Estonia. 11Charité – Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany. 12DZHK (German Centre for Cardiovascular Research), partner site Berlin, -
Jenna K. Caines, Sherri L. Christian, Mark D. Berry Department of Biochemistry, Memorial University of Newfoundland, St. John'
Trace Amine-Associated Receptors in Monocytes: A Constant Low-Level Expression Jenna K. Caines, Sherri L. Christian, Mark D. Berry Department of Biochemistry, Memorial University of Newfoundland, St. John’s NL Trace amine-associated receptors (TAARs) Is TAAR1 differentially expressed in response to Pro- and Are any TAARs differentially expressed between § G protein-coupled receptors anti-inflammatory stimuli? monocyte and macrophage lineages? § Established throughout the body in vertebrates Table 1: Datasets with n ≥ 3 examining human and mice macrophages Table 2: Datasets with n ≥ 3 containing several monocyte and § Humans have 6 functional isoforms: TAAR1, TAAR2, TAAR5, TAAR6, TAAR8, and TAAR9 treated with pro- and anti-inflammatory stimuli macrophage lineages from mice TAARs and the immune system Dataset Treatment Time TAAR1 p-value Dataset Cell type Number of lineages Treatment § Found in leukocyte populations1 GSE53986 Untreated (control) 0h examined INFγ 24h 0.8 GSE15907 Lung Macrophage 2 NA 1 § TAAR1 suspected of regulating immune response GSE60290 Untreated (control) 0h Peritoneal Macrophage 6 NA § Potential target for pharmacological treatment of immune disorders2 INFγ 18h 0.3 Spleen Macrophage NA GSE43075 Untreated (control) 0h Blood Monocyte 2 NA Hypothesis LPS 4h 0.45 Mesenteric LN monocyte 1 NA GSE121646 Untreated (control) 0h Oral Salmonella § TAAR1 will show differential expression upon activation and LPS 8h 0.7 Small intestine macrophage 2 Typhimurium(72 h) GSE19315 Untreated (control) 0h between leukocyte populations -
Full-Text PDF (Final Published Version)
Alexander, S. P. H., Cidlowski, J. A., Kelly, E., Marrion, N. V., Peters, J. A., Faccenda, E., Harding, S. D., Pawson, A. J., Sharman, J. L., Southan, C., Davies, J. A., & CGTP Collaborators (2017). THE CONCISE GUIDE TO PHARMACOLOGY 2017/18: Nuclear hormone receptors. British Journal of Pharmacology, 174, S208-S224. https://doi.org/10.1111/bph.13880 Publisher's PDF, also known as Version of record License (if available): CC BY Link to published version (if available): 10.1111/bph.13880 Link to publication record in Explore Bristol Research PDF-document This is the final published version of the article (version of record). It first appeared online via Wiley at https://doi.org/10.1111/bph.13880 . Please refer to any applicable terms of use of the publisher. University of Bristol - Explore Bristol Research General rights This document is made available in accordance with publisher policies. Please cite only the published version using the reference above. Full terms of use are available: http://www.bristol.ac.uk/red/research-policy/pure/user-guides/ebr-terms/ S.P.H. Alexander et al. The Concise Guide to PHARMACOLOGY 2017/18: Nuclear hormone receptors. British Journal of Pharmacology (2017) 174, S208–S224 THE CONCISE GUIDE TO PHARMACOLOGY 2017/18: Nuclear hormone receptors Stephen PH Alexander1, John A Cidlowski2, Eamonn Kelly3, Neil V Marrion3, John A Peters4, Elena Faccenda5, Simon D Harding5,AdamJPawson5, Joanna L Sharman5, Christopher Southan5, Jamie A Davies5 and CGTP Collaborators 1School of Life Sciences, University of Nottingham Medical -
File Download
Anatomical and functional evidence for trace amines as unique modulators of locomotor function in the mammalian spinal cord Elizabeth A. Gozal, Emory University Brannan E. O'Neill, Emory University Michael A. Sawchuk, Emory University Hong Zhu, Emory University Mallika Halder, Emory University Chou Ching-Chieh , Emory University Shawn Hochman, Emory University Journal Title: Frontiers in Neural Circuits Volume: Volume 8 Publisher: Frontiers | 2014-11-07, Pages 134-134 Type of Work: Article | Final Publisher PDF Publisher DOI: 10.3389/fncir.2014.00134 Permanent URL: https://pid.emory.edu/ark:/25593/mr95r Final published version: http://dx.doi.org/10.3389/fncir.2014.00134 Copyright information: © 2014 Gozal, O'Neill, Sawchuk, Zhu, Halder, Chou and Hochman. This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits distribution of derivative works, making multiple copies, distribution, public display, and publicly performance, provided the original work is properly cited. This license requires credit be given to copyright holder and/or author, copyright and license notices be kept intact. Accessed September 27, 2021 11:18 AM EDT ORIGINAL RESEARCH ARTICLE published: 07 November 2014 NEURAL CIRCUITS doi: 10.3389/fncir.2014.00134 Anatomical and functional evidence for trace amines as unique modulators of locomotor function in the mammalian spinal cord Elizabeth A. Gozal , Brannan E. O’Neill , Michael A. Sawchuk , Hong Zhu , Mallika Halder , Ching-Chieh Chou and Shawn Hochman* Physiology Department, Emory University, Atlanta, GA, USA Edited by: The trace amines (TAs), tryptamine, tyramine, and β-phenylethylamine, are synthesized Brian R. -
Insights Into Nuclear G-Protein-Coupled Receptors As Therapeutic Targets in Non-Communicable Diseases
pharmaceuticals Review Insights into Nuclear G-Protein-Coupled Receptors as Therapeutic Targets in Non-Communicable Diseases Salomé Gonçalves-Monteiro 1,2, Rita Ribeiro-Oliveira 1,2, Maria Sofia Vieira-Rocha 1,2, Martin Vojtek 1,2 , Joana B. Sousa 1,2,* and Carmen Diniz 1,2,* 1 Laboratory of Pharmacology, Department of Drug Sciences, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal; [email protected] (S.G.-M.); [email protected] (R.R.-O.); [email protected] (M.S.V.-R.); [email protected] (M.V.) 2 LAQV/REQUIMTE, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal * Correspondence: [email protected] (J.B.S.); [email protected] (C.D.) Abstract: G-protein-coupled receptors (GPCRs) comprise a large protein superfamily divided into six classes, rhodopsin-like (A), secretin receptor family (B), metabotropic glutamate (C), fungal mating pheromone receptors (D), cyclic AMP receptors (E) and frizzled (F). Until recently, GPCRs signaling was thought to emanate exclusively from the plasma membrane as a response to extracellular stimuli but several studies have challenged this view demonstrating that GPCRs can be present in intracellular localizations, including in the nuclei. A renewed interest in GPCR receptors’ superfamily emerged and intensive research occurred over recent decades, particularly regarding class A GPCRs, but some class B and C have also been explored. Nuclear GPCRs proved to be functional and capable of triggering identical and/or distinct signaling pathways associated with their counterparts on the cell surface bringing new insights into the relevance of nuclear GPCRs and highlighting the Citation: Gonçalves-Monteiro, S.; nucleus as an autonomous signaling organelle (triggered by GPCRs). -
Modulatory Roles of ATP and Adenosine in Cholinergic Neuromuscular Transmission
International Journal of Molecular Sciences Review Modulatory Roles of ATP and Adenosine in Cholinergic Neuromuscular Transmission Ayrat U. Ziganshin 1,* , Adel E. Khairullin 2, Charles H. V. Hoyle 1 and Sergey N. Grishin 3 1 Department of Pharmacology, Kazan State Medical University, 49 Butlerov Street, 420012 Kazan, Russia; [email protected] 2 Department of Biochemistry, Laboratory and Clinical Diagnostics, Kazan State Medical University, 49 Butlerov Street, 420012 Kazan, Russia; [email protected] 3 Department of Medical and Biological Physics with Computer Science and Medical Equipment, Kazan State Medical University, 49 Butlerov Street, 420012 Kazan, Russia; [email protected] * Correspondence: [email protected]; Tel.: +7-843-236-0512 Received: 30 June 2020; Accepted: 1 September 2020; Published: 3 September 2020 Abstract: A review of the data on the modulatory action of adenosine 5’-triphosphate (ATP), the main co-transmitter with acetylcholine, and adenosine, the final ATP metabolite in the synaptic cleft, on neuromuscular transmission is presented. The effects of these endogenous modulators on pre- and post-synaptic processes are discussed. The contribution of purines to the processes of quantal and non- quantal secretion of acetylcholine into the synaptic cleft, as well as the influence of the postsynaptic effects of ATP and adenosine on the functioning of cholinergic receptors, are evaluated. As usual, the P2-receptor-mediated influence is minimal under physiological conditions, but it becomes very important in some pathophysiological situations such as hypothermia, stress, or ischemia. There are some data demonstrating the same in neuromuscular transmission. It is suggested that the role of endogenous purines is primarily to provide a safety factor for the efficiency of cholinergic neuromuscular transmission.