DOCSLIB.ORG

Available Target List for Biologics

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Available Target List for Biologics Distributor eNewsletter | March 2014; vol 9 Applications For Development of Biologics R&D Groups – Cellular Binding, Functional Screening and Potency Determination Manufacturing or Bioanalytical Groups – Bioassays for QC Lot‐release and Stability Testing Clinical Immunology Groups –Cell‐based Assays for Detection of Neutralizing Anti‐Drug Antibodies Download the customer‐facing brochure HERE Available Target List for Biologics GPCR Assays ADCYAP1R ADORA1 ADORA2A ADORA2B ADORA3 ADRA1A ADRA1B ADRA2A ADRA2B ADRA2C 1 ADRB1 ADRB2 ADRB3 AGTR1 AGTRL1 AVPR1A AVPR1B AVPR2 BAI1 BAI2 CALCR + CALCR + BAI3 BDKRB1 BDKRB2 BRS3 C3AR1 C5AR1 C5L2 CALCR RAMP1 RAMP2 CALCR + CALCRL + CALCRL + CALCRL + CASR CCKAR CCKBR CCR1 CCR10 CCR2 RAMP3 RAMP1 RAMP2 RAMP3 CCR3 CCR4 CCR5 CCR6 CCR7 CCR8 CCRL1 cGPR91 CHRM1 CHRM2 CHRM3 CHRM4 CHRM5 CMKLR1 CNR1 CNR2 CRHR1 CRHR2 CRTH2 CXCR1 CXCR2 CXCR3 CXCR4 CXCR5 CXCR6 CXCR7 CYSLTR2 DARC DRD1 DRD2L DRD2S DRD3 DRD4 DRD5 EBI2 EDG1 EDG2 EDG3 EDG4 EDG5 EDG6 EDG7 EDG8 EDNRA EDNRB F2R F2RL1 F2RL3 FFAR1 FFAR2 FFAR3 FPR1 FPR3 FPRL1 FSHR GALR1 GALR2 GCGR GHRHR GHSR GHSR1b GIPR GLP1R GLP2R GNRHR GPBAR1 GPR1 GPR101 GPR103 GPR107 GPR109A GPR109B GPR119 GPR12 GPR120 GPR120S GPR123 GPR132 GPR135 GPR137 GPR139 GPR141 GPR142 GPR143 GPR146 GPR148 GPR149 GPR15 GPR150 GPR151 GPR152 GPR157 GPR161 GPR162 GPR17 GPR171 GPR173 GPR176 GPR18 GPR182 GPR20 GPR23 GPR25 GPR26 GPR27 GPR3 GPR30 GPR31 GPR32 GPR35 GPR37 GPR37L1 GPR39 GPR4 GPR45 GPR50 GPR52 GPR55 GPR6 GPR61 GPR65 GPR75 GPR78 GPR79 GPR81 GPR83 GPR84 GPR85 GPR88 GPR91 GPR92 GPR97 GRM1 GRM2 GRM3 GRM4 GRM5 GRM6 GRM7 GRPR HCRTR1 HCRTR2 HRH1 HRH2 HRH3 HRH4 HTR1A HTR1B HTR1E HTR1F HTR2A HTR2B HTR2C HTR2C(VGV) HTR2C(VNV) HTR2C(VSV) HTR5A HTR6 HTR7A HTR7B mADORA2 HTR7D KISS1R LGR4 LGR5 LGR6 LHCGR LTB4R mADCYAP1R1 mADORA3 B mADRA1B mAGTRL1 mAVPR2 mBRS3 MC1R MC3R MC4R mC5AR1 MC5R mCCKAR mCCR1 mCCR2 mCCR3 mCCR4 mCCR5 mCCR6 mCCR7 mCCR8 mCCR9 MCHR1 MCHR2 mCMKLR1 mCNR1 mCNR2 mCRHR1 mCRTH2 mCX3CR1 mCXCR2 mCXCR3 mCXCR4 mCXCR5 mCXCR6 mCXCR7 mDRD5 mEDG1 mEDG5 mEDG6 mEDNRA mEDNRB mF2RL1 mFPR1 mGALR1 mGALR2 mGCGR mGHSR mGIPR mGLP1R mGPR1 mGPR120 mHCRTR1 mHTR2A mHTR2C mKISS1R MLNR mLTB4R mMC3R mMC4R mMC5R mMCHR1 mNPY1R mNPY2R mOPRD1 mOPRK1 mOPRM1 mOXTR mP2RY12 mP2RY6 mPPYR1 mPTAFR mPTGIR MRGPRD MRGPRE MRGPRF MRGPRX1 MRGPRX2 MRGPRX4 mRXFP3 mRXFP4 mSSTR2 mSSTR5 mTACR1 MTNR1A MTNR1B mUTR2 mVIPR1 NMBR NMU1R NPBWR1 NPBWR2 NPFFR1 NPSR1b NPY1R NPY2R NTSR1 OPN5 OPRD1 OPRK1 OPRL1 OPRM1 OXER1 OXGR1 OXTR P2RY1 P2RY11 P2RY12 P2RY2 P2RY4 P2RY6 P2RY8 PPYR1 Page 3 Distributor eNewsletter | March 2014; vol 9 GPCR Assays (continued) PRLHR PROKR1 PROKR2 PTAFR PTGDR PTGER1 PTGER2 PTGER3 PTGER4 PTGFR PTGIR PTHR1 PTHR2 rCHRM4 rCNR2 rCRTH2 rDRD1 rDRD2L rDRD2S rEDG5 rGPR35 rHTR2C rOPRM1 rPROKR1 rPROKR2 rPTGER4 rVIPR1 RXFP1 RXFP2 RXFP3 RXFP4 SCTR sEDG5 SSTR1 SSTR2 SSTR3 SSTR4 SSTR5 TAAR1 TAAR5 TACR1 TACR2 TACR3 TBXA2R TRHR TSHR(L) UTR2 VIPR1 VIPR2 XCR1 Kinase Assays AXL BLK c‐KIT c‐MET c‐Ret‐GFRα2 CSF3R‐JAK1 DDR1 EphA4 EphA5 EphA7 EphB1 EphB2 EphB3 EphB4 EpoR‐JAK2 ErbB1 ErbB2‐ErbB3 ErbB4 FGFR1 FGFR2 FGR FLT3 FLT4 GHR‐JAK1 GHR‐JAK2 IGF1R INSR INSR JAK3 KDR PDGFRa PDGFRb PRLR‐JAK1 PRLR‐JAK2 SYK TrkA TrkA‐P75 TrkB TrkB‐P75 TrkC TrkC‐P75 TYK2 YES1 Signaling Pathway Assays ACVR1 ACVR1/ACVR2 BAX BCL2‐BIM BCL2L1‐BAX BIM FOXO3 GSK3β IL17RC IκB Keap1 Keap1‐NRF2 NFκB NPR1 P53 SREBP2 TGFBR1 TGFBR1/TGFBR2 TGFBR2 TORC1 TORC2 Wnt3 XBP1 β‐Catenin LeadHunter Services Panel Testing Dates Test Dates Compounds and PO Due Report and Invoicing 4/1/2014 3/28/2014 4/29/2014 gpcrMAX, 5/13/2014 5/9/2014 6/10/2014 orhpanMAX, 6/24/2014 6/20/2014 7/22/2014 Chemokine and gpcrPANELS 8/5/2014 8/1/2014 9/2/2014 (therapeutic) 9/16/2014 9/12/2014 10/14/2014 10/28/2014 10/24/2014 11/25/2014 3/18/2014 3/14/2014 4/15/2014 4/29/2014 4/25/2014 5/27/2014 6/10/2014 6/6/2014 7/8/2014 nhrMAX and tkMAX 7/22/2014 7/18/2014 8/19/2014 9/2/2014 8/29/2014 9/30/2014 10/14/2014 10/10/2014 11/11/2014 11/25/2014 11/21/2014 12/23/2014 Compound Requirements For specific service or panel specific compound requirements, please visit our Compound Submission page. Generally, compounds may be provided as a stock DMSO solution or dry powder. For single concentration (primary) screens, we need 20 µL of 1000x the desired screening concentration for the first target and an additional 2 µL for each target thereafter or an equivalent amount of dry powder such that when reconstituted, will yield the required volume. For orphan GPCR panels, we require 175 µL of 1000X solution. Page 4.
Load more

Recommended publications
  • G Protein-Coupled Receptors As New Therapeutic Targets for Type 2 Diabetes
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Springer - Publisher Connector Diabetologia (2016) 59:229–233 DOI 10.1007/s00125-015-3825-z MINI-REVIEW G protein-coupled receptors as new therapeutic targets for type 2 diabetes Frank Reimann1 & Fiona M. Gribble 1 Received: 31 October 2015 /Accepted: 9 November 2015 /Published online: 12 December 2015 # The Author(s) 2015. This article is published with open access at Springerlink.com Abstract G protein-coupled receptors (GPCRs) in the gut– GLP1R Glucagon-like peptide 1 receptor brain–pancreatic axis are key players in the postprandial con- GPBAR1 G protein-coupled bile acid receptor trol of metabolism and food intake. A number of intestinally GPCR G protein-coupled receptor located receptors have been implicated in the chemo-detection of ingested nutrients, and in the pancreatic islets and nervous system GPCRs play essential roles in the detection of many Therapeutics that promote insulin secretion have been a main- hormones and neurotransmitters. Because of the diversity, stay of type 2 diabetes treatment for many years. However, cell-specific expression and ‘druggability’ of the GPCR su- with the rising impact of obesity on the incidence of type 2 perfamily, these receptors are popular targets for therapeutic diabetes comes an increasing need to target body weight as development. This review will outline current and potential well as blood glucose control. Recent years have witnessed an future approaches to develop GPCR agonists for the treatment increasing interest in the gut endocrine system as a source of of type 2 diabetes.
    [Show full text]
  • Tuft-Cell-Derived Leukotrienes Drive Rapid Anti-Helminth Immunity in the Small Intestine but Are Dispensable for Anti-Protist Immunity
    Article Tuft-Cell-Derived Leukotrienes Drive Rapid Anti- helminth Immunity in the Small Intestine but Are Dispensable for Anti-protist Immunity Graphical Abstract Authors John W. McGinty, Hung-An Ting, Tyler E. Billipp, ..., Hong-Erh Liang, Ichiro Matsumoto, Jakob von Moltke Correspondence [email protected] In Brief Tuft cells regulate type 2 immunity in the small intestine by secreting the cytokine IL-25. McGinty et al. identify cysteinyl leukotriene production as an additional tuft cell effector function. Tuft-cell- derived leukotrienes drive anti-helminth immunity in the intestine but are dispensable for the response induced by tritrichomonad protists. Highlights d Cysteinyl leukotrienes activate intestinal ILC2s d Cysteinyl leukotrienes drive rapid anti-helminth type 2 immune responses d Tuft cells are the source of cysteinyl leukotrienes during helminth infection d Tuft-cell-derived leukotrienes are not required for the anti- protist response McGinty et al., 2020, Immunity 52, 528–541 March 17, 2020 ª 2020 Elsevier Inc. https://doi.org/10.1016/j.immuni.2020.02.005 Immunity Article Tuft-Cell-Derived Leukotrienes Drive Rapid Anti-helminth Immunity in the Small Intestine but Are Dispensable for Anti-protist Immunity John W. McGinty,1 Hung-An Ting,1 Tyler E. Billipp,1 Marija S. Nadjsombati,1 Danish M. Khan,1 Nora A. Barrett,2 Hong-Erh Liang,3,4 Ichiro Matsumoto,5 and Jakob von Moltke1,6,* 1Department of Immunology, University of Washington School of Medicine, Seattle, WA 98109, USA 2Division of Rheumatology, Immunology and Allergy, Jeff
    [Show full text]
  • Gastrointestinal Defense Mechanisms
    REVIEW CURRENT OPINION Gastrointestinal defense mechanisms Hyder Said a,b and Jonathan D. Kaunitzb,c Purpose of review To summarize and illuminate the recent findings regarding gastroduodenal mucosal defense mechanisms and the specific biomolecules involved in regulating this process, such as glucagon-like peptides (GLPs). Recent findings There has been a growing interest in luminal nutrient chemosensing and its physiological effects throughout the digestive system. From the ingestion of food in the oral cavity to the processing and absorption of nutrients in the intestines, nutrient chemosensing receptors signal the production and release of numerous bioactive peptides from enteroendocrine cells, such as the proglucagon-derived peptides. There has been a major emphasis on two proglucagon-derived peptides, namely GLP-1 and GLP-2, due to their apparent beneficial effect on gut structure, function, and on metabolic processes. As an incretin, GLP-1 not only enhances the effect and release of insulin on pancreatic bcells but also has been implicated in having trophic effects on the intestinal epithelium. In addition, GLP-2, the other major proglucagon-derived peptide, has potent intestinotrophic effects, such as increasing the rate of mucosal stem cell proliferation, mucosal blood flow, and fluid absorption, as well as augmenting the rate of duodenal bicarbonate secretion to improve gastric mucosal health and longevity. Summary Understanding the mechanisms underlying nutrient chemosensing and how it relates to GLP release can further elucidate how the gut functions in response to cellular changes and disturbances. Furthermore, a more in-depth comprehension of GLP release and its tissue-specific effects will help improve the utility of GLP-1 and GLP-2 receptor agonists in clinical settings.
    [Show full text]
  • Edinburgh Research Explorer
    Edinburgh Research Explorer International Union of Basic and Clinical Pharmacology. LXXXVIII. G protein-coupled receptor list Citation for published version: Davenport, AP, Alexander, SPH, Sharman, JL, Pawson, AJ, Benson, HE, Monaghan, AE, Liew, WC, Mpamhanga, CP, Bonner, TI, Neubig, RR, Pin, JP, Spedding, M & Harmar, AJ 2013, 'International Union of Basic and Clinical Pharmacology. LXXXVIII. G protein-coupled receptor list: recommendations for new pairings with cognate ligands', Pharmacological reviews, vol. 65, no. 3, pp. 967-86. https://doi.org/10.1124/pr.112.007179 Digital Object Identifier (DOI): 10.1124/pr.112.007179 Link: Link to publication record in Edinburgh Research Explorer Document Version: Publisher's PDF, also known as Version of record Published In: Pharmacological reviews Publisher Rights Statement: U.S. Government work not protected by U.S. copyright General rights Copyright for the publications made accessible via the Edinburgh Research Explorer is retained by the author(s) and / or other copyright owners and it is a condition of accessing these publications that users recognise and abide by the legal requirements associated with these rights. Take down policy The University of Edinburgh has made every reasonable effort to ensure that Edinburgh Research Explorer content complies with UK legislation. If you believe that the public display of this file breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim. Download date: 02. Oct. 2021 1521-0081/65/3/967–986$25.00 http://dx.doi.org/10.1124/pr.112.007179 PHARMACOLOGICAL REVIEWS Pharmacol Rev 65:967–986, July 2013 U.S.
    [Show full text]
  • A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
    Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated.
    [Show full text]
  • Metabolite Sensing Gpcrs: Promising Therapeutic Targets for Cancer Treatment?
    cells Review Metabolite Sensing GPCRs: Promising Therapeutic Targets for Cancer Treatment? Jesús Cosín-Roger 1,*, Dolores Ortiz-Masia 2 , Maria Dolores Barrachina 3 and Sara Calatayud 3 1 Hospital Dr. Peset, Fundación para la Investigación Sanitaria y Biomédica de la Comunitat Valenciana, FISABIO, 46017 Valencia, Spain 2 Departament of Medicine, Faculty of Medicine, University of Valencia, 46010 Valencia, Spain; [email protected] 3 Departament of Pharmacology and CIBER, Faculty of Medicine, University of Valencia, 46010 Valencia, Spain; [email protected] (M.D.B.); [email protected] (S.C.) * Correspondence: [email protected]; Tel.: +34-963851234 Received: 30 September 2020; Accepted: 21 October 2020; Published: 23 October 2020 Abstract: G-protein-coupled receptors constitute the most diverse and largest receptor family in the human genome, with approximately 800 different members identified. Given the well-known metabolic alterations in cancer development, we will focus specifically in the 19 G-protein-coupled receptors (GPCRs), which can be selectively activated by metabolites. These metabolite sensing GPCRs control crucial processes, such as cell proliferation, differentiation, migration, and survival after their activation. In the present review, we will describe the main functions of these metabolite sensing GPCRs and shed light on the benefits of their potential use as possible pharmacological targets for cancer treatment. Keywords: G-protein-coupled receptor; metabolite sensing GPCR; cancer 1. Introduction G-protein-coupled receptors (GPCRs) are characterized by a seven-transmembrane configuration, constitute the largest and most ubiquitous family of plasma membrane receptors, and regulate virtually all known physiological processes in humans [1,2]. This family includes almost one thousand genes that were initially classified on the basis of sequence homology into six classes (A–F), where classes D and E were not found in vertebrates [3].
    [Show full text]
  • Retinal Energy Demands Control Vascular Supply of the Retina in T Development and Disease: the Role of Neuronal Lipid and Glucose Metabolism
    Progress in Retinal and Eye Research 64 (2018) 131–156 Contents lists available at ScienceDirect Progress in Retinal and Eye Research journal homepage: www.elsevier.com/locate/preteyeres Retinal energy demands control vascular supply of the retina in T development and disease: The role of neuronal lipid and glucose metabolism ∗ ∗∗ Jean-Sébastien Joyala,b, , Marin L. Gantnerc, Lois E.H. Smithd, a Department of Pediatrics, Pharmacology and Ophthalmology, CHU Sainte-Justine Research Center, Université de Montréal, Montreal, Qc, Canada b Department of Pharmacology and Therapeutics, McGill University, Montreal, Qc, Canada c The Lowy Medical Research Institute, La Jolla, United States d Department of Ophthalmology, Harvard Medical School, Boston Children's Hospital, 300 Longwood Avenue, Boston MA 02115, United States 1. Introduction The metabolic and energy needs of the retina have been assumed to be met by glucose, as the retina is part of the CNS, and the brain relies Neuronal energy demands are met by a tightly coupled and adaptive almost exclusively on glucose (Mergenthaler et al., 2013). There are vascular network that supplies nutrients and oxygen. The retina is one two primary pathways that cells can use to generate ATP from glucose, of the highest energy-consuming organs, exceeding the metabolic rate glycolysis and oxidative phosphorylation. However, Cohen and Noell of the brain; blood vessels grow and regress in reaction to changes in concluded in 1960 that a substantial portion of the energy produced these high demands (Ames et al., 1992b; Anderson and Saltzman, 1964; through oxidation by the retina (around 65%) was not derived from Yu and Cringle, 2001).
    [Show full text]
  • Bioinformatics Method Identifies Potential Biomarkers of Dilated Cardiomyopathy in a Human Induced Pluripotent Stem Cell‑Derived Cardiomyocyte Model
    EXPERIMENTAL AND THERAPEUTIC MEDICINE 14: 2771-2778, 2017 Bioinformatics method identifies potential biomarkers of dilated cardiomyopathy in a human induced pluripotent stem cell‑derived cardiomyocyte model YU ZHUANG1, YU-JIA GONG2, BEI-FEN ZHONG3, YI ZHOU1 and LI GONG4 1Department of Cardiovascular Surgery, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080; 2Stomatology Faculty, School of Medicine, Nantong University, Nantong, Jiangsu 226000; 3Department of Urology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080; 4Department of Cardiothoracic Surgery, The Affiliated Huai'an Hospital of Xuzhou Medical University, Huai'an, Jiangsu 223002, P.R. China Received February 19, 2016; Accepted February 10, 2017 DOI: 10.3892/etm.2017.4850 Abstract. Dilated cardiomyopathy (DCM) is the most common crucial nodes in module 2, which were linked to each other. type of cardiomyopathy that account for the majority of heart In conclusion, several potential biomarkers for DCM were failure cases. The present study aimed to reveal the under- identified, such as MMP2, FLT1, CDH1, ITGB6, COL6A3, lying molecular mechanisms of DCM and provide potential COL6A1, LAMC2, PENK and APLNR. These genes may serve biomarkers for detection of this condition. The public dataset significant roles in DCM via involvement of various BPs, such of GSE35108 was downloaded, and 4 normal induced pluripo- as blood vessel and vasculature development and cell adhe- tent stem cell (iPSC)-derived cardiomyocytes (N samples) and sion, and the ECM-receptor interaction pathway. 4 DCM iPSC-derived cardiomyocytes (DCM samples) were utilized. Raw data were preprocessed, followed by identifica- Introduction tion of differentially expressed genes (DEGs) between N and DCM samples.
    [Show full text]
  • An Overview on G Protein-Coupled Receptor-Induced Signal Transduction in Acute Myeloid Leukemia
    An overview on G protein-coupled receptor-induced signal transduction in Acute Myeloid Leukemia 1* 1,3 4,5,6 2* Frode Selheim , Elise Aasebø , Catalina Ribas and Anna M. Aragay 1The Proteomics Unit at the University of Bergen, Department of Biomedicine, University of Bergen, Jonas Lies vei 91, 5020 Bergen, Norway; 3 Department of Clinical Science, University of Bergen, Jonas Lies vei 87, 5021 Bergen, Norway; [email protected]. 2Departamento de Biologia Celular. Instituto de Biología Molecular de Barcelona (IBMB-CSIC), Spanish National Research Council (CSIC), Baldiri i Reixac, 15, 08028 Barcelona, Spain; [email protected]. 4Departamento de Biología Molecular and Centro de Biología Molecular “Severo Ochoa” (UAM-CSIC), 28049 Madrid, Spain; 5Instituto de Investigación Sanitaria La Princesa, 28006 Madrid, Spain; 6CIBER de Enfermedades Cardiovasculares, ISCIII (CIBERCV), 28029 Madrid, Spain, [email protected] * Corresponding authors: Frode Selheim Adr: Jonas Lies vei 91, 5020 Bergen, Norway Email: [email protected], Tel:+4755586091 Anna M. Aragay Adr: Baldiri i Reixac, 15, 08028 Barcelona. Spain. E-mail: [email protected]; Tel.: +934098671 1 Abstract Background: Acute myeloid leukemia (AML) is a genetically heterogeneous disease characterized by uncontrolled proliferation of precursor myeloid-lineage cells in the bone marrow. AML is also characterized with patients with poor long-term survival outcomes due to relapse. Many efforts have been made to understand the biological heterogeneity of AML and the challenges to develop new therapies are therefore enormous. G protein-coupled receptors (GPCRs) are a large attractive drug targeted family of transmembrane proteins, and aberrant GPCR expression and GPCR-mediated signaling have been implicated in leukemogenesis of AML.
    [Show full text]
  • G Protein-Coupled Receptors
    S.P.H. Alexander et al. The Concise Guide to PHARMACOLOGY 2015/16: G protein-coupled receptors. British Journal of Pharmacology (2015) 172, 5744–5869 THE CONCISE GUIDE TO PHARMACOLOGY 2015/16: G protein-coupled receptors Stephen PH Alexander1, Anthony P Davenport2, Eamonn Kelly3, Neil Marrion3, John A Peters4, Helen E Benson5, Elena Faccenda5, Adam J Pawson5, Joanna L Sharman5, Christopher Southan5, Jamie A Davies5 and CGTP Collaborators 1School of Biomedical Sciences, University of Nottingham Medical School, Nottingham, NG7 2UH, UK, 2Clinical Pharmacology Unit, University of Cambridge, Cambridge, CB2 0QQ, UK, 3School of Physiology and Pharmacology, University of Bristol, Bristol, BS8 1TD, UK, 4Neuroscience Division, Medical Education Institute, Ninewells Hospital and Medical School, University of Dundee, Dundee, DD1 9SY, UK, 5Centre for Integrative Physiology, University of Edinburgh, Edinburgh, EH8 9XD, UK Abstract The Concise Guide to PHARMACOLOGY 2015/16 provides concise overviews of the key properties of over 1750 human drug targets with their pharmacology, plus links to an open access knowledgebase of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties. The full contents can be found at http://onlinelibrary.wiley.com/doi/ 10.1111/bph.13348/full. G protein-coupled receptors are one of the eight major pharmacological targets into which the Guide is divided, with the others being: ligand-gated ion channels, voltage-gated ion channels, other ion channels, nuclear hormone receptors, catalytic receptors, enzymes and transporters. These are presented with nomenclature guidance and summary information on the best available pharmacological tools, alongside key references and suggestions for further reading.
    [Show full text]
  • 1 Supplemental Material Maresin 1 Activates LGR6 Receptor
    Supplemental Material Maresin 1 Activates LGR6 Receptor Promoting Phagocyte Immunoresolvent Functions Nan Chiang, Stephania Libreros, Paul C. Norris, Xavier de la Rosa, Charles N. Serhan Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA. 1 Supplemental Table 1. Screening of orphan GPCRs with MaR1 Vehicle Vehicle MaR1 MaR1 mean RLU > GPCR ID SD % Activity Mean RLU Mean RLU + 2 SD Mean RLU Vehicle mean RLU+2 SD? ADMR 930920 33283 997486.5381 863760 -7% BAI1 172580 18362 209304.1828 176160 2% BAI2 26390 1354 29097.71737 26240 -1% BAI3 18040 758 19555.07976 18460 2% CCRL2 15090 402 15893.6583 13840 -8% CMKLR2 30080 1744 33568.954 28240 -6% DARC 119110 4817 128743.8016 126260 6% EBI2 101200 6004 113207.8197 105640 4% GHSR1B 3940 203 4345.298244 3700 -6% GPR101 41740 1593 44926.97349 41580 0% GPR103 21413 1484 24381.25067 23920 12% NO GPR107 366800 11007 388814.4922 360020 -2% GPR12 77980 1563 81105.4653 76260 -2% GPR123 1485190 46446 1578081.986 1342640 -10% GPR132 860940 17473 895885.901 826560 -4% GPR135 18720 1656 22032.6827 17540 -6% GPR137 40973 2285 45544.0809 39140 -4% GPR139 438280 16736 471751.0542 413120 -6% GPR141 30180 2080 34339.2307 29020 -4% GPR142 105250 12089 129427.069 101020 -4% GPR143 89390 5260 99910.40557 89380 0% GPR146 16860 551 17961.75617 16240 -4% GPR148 6160 484 7128.848113 7520 22% YES GPR149 50140 934 52008.76073 49720 -1% GPR15 10110 1086 12282.67884
    [Show full text]
  • G Protein‐Coupled Receptors
    S.P.H. Alexander et al. The Concise Guide to PHARMACOLOGY 2019/20: G protein-coupled receptors. British Journal of Pharmacology (2019) 176, S21–S141 THE CONCISE GUIDE TO PHARMACOLOGY 2019/20: G protein-coupled receptors Stephen PH Alexander1 , Arthur Christopoulos2 , Anthony P Davenport3 , Eamonn Kelly4, Alistair Mathie5 , John A Peters6 , Emma L Veale5 ,JaneFArmstrong7 , Elena Faccenda7 ,SimonDHarding7 ,AdamJPawson7 , Joanna L Sharman7 , Christopher Southan7 , Jamie A Davies7 and CGTP Collaborators 1School of Life Sciences, University of Nottingham Medical School, Nottingham, NG7 2UH, UK 2Monash Institute of Pharmaceutical Sciences and Department of Pharmacology, Monash University, Parkville, Victoria 3052, Australia 3Clinical Pharmacology Unit, University of Cambridge, Cambridge, CB2 0QQ, UK 4School of Physiology, Pharmacology and Neuroscience, University of Bristol, Bristol, BS8 1TD, UK 5Medway School of Pharmacy, The Universities of Greenwich and Kent at Medway, Anson Building, Central Avenue, Chatham Maritime, Chatham, Kent, ME4 4TB, UK 6Neuroscience Division, Medical Education Institute, Ninewells Hospital and Medical School, University of Dundee, Dundee, DD1 9SY, UK 7Centre for Discovery Brain Sciences, University of Edinburgh, Edinburgh, EH8 9XD, UK Abstract The Concise Guide to PHARMACOLOGY 2019/20 is the fourth in this series of biennial publications. The Concise Guide provides concise overviews of the key properties of nearly 1800 human drug targets with an emphasis on selective pharmacology (where available), plus links to the open access knowledgebase source of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties. Although the Concise Guide represents approximately 400 pages, the material presented is substantially reduced compared to information and links presented on the website.
    [Show full text]