GPR85 (N-14): Sc-54685

Total Page:16

File Type:pdf, Size:1020Kb

GPR85 (N-14): Sc-54685 SAN TA C RUZ BI OTEC HNOL OG Y, INC . GPR85 (N-14): sc-54685 BACKGROUND APPLICATIONS G protein-coupled receptors (GPRs), also known as seven transmembrane GPR85 (N-14) is recommended for detection of GPR85 of mouse, rat and receptors, heptahelical receptors or 7TM receptors, comprise a superfamily human origin by Western Blotting (starting dilution 1:200, dilution range of proteins that play a role in many different stimulus-response pathways. 1:100-1:1000), immunofluorescence (starting dilution 1:50, dilution range G protein-coupled receptors translate extracellular signals into intracellular 1:50-1:500) and solid phase ELISA (starting dilution 1:30, dilution range signals (G protein activation) and they respond to a variety of signaling mol - 1: 30-1:3000). ecules, such as hormones and neurotransmitters. GPR85 (G protein-coupled GPR85 (N-14) is also recommended for detection of GPR85 in additional receptor 85), also designated SREB2 (super conserved receptor expressed in species, including equine, canine, bovine, porcine and avian. brain 2), is a 370 amino acid multi-pass membrane protein that functions as an orphan receptor and belongs to the GPR family. Highly expressed in testis Suitable for use as control antibody for GPR85 siRNA (h): sc-62403, GPR85 and brain, GPR85 is found at lower levels in spleen, placenta and small siRNA (m): sc-62404, GPR85 shRNA Plasmid (h): sc-62403-SH, GPR85 shRNA intestine, and is encoded by a gene that maps to human chromosome 7q31. Plasmid (m): sc-62404-SH, GPR85 shRNA (h) Lentiviral Particles: sc-62403-V and GPR85 shRNA (m) Lentiviral Particles: sc-62404-V. REFERENCES Molecular Weight of GPR85: 42 kDa. 1. Matsumoto, M., et al. 2000. An evolutionarily conserved G protein-coupled Positive Controls: rat hippocampus tissue extract. receptor family, SREB, expressed in the central nervous system. Biochem. Biophys. Res. Commun. 272: 576-582. RECOMMENDED SECONDARY REAGENTS 2. Hellebrand, S., et al. 2000. The brain-specific G protein-coupled receptor To ensure optimal results, the following support (secondary) reagents are GPR85 with identical protein sequence in man and mouse maps to human recommended: 1) Western Blotting: use donkey anti-goat IgG-HRP: sc-2020 chromosome 7q31. Biochim. Biophys. Acta 1493: 269-272. (dilution range: 1:2000-1:100,000) or Cruz Marker™ compatible donkey 3. Hellebrand, S., et al. 2001. Gpr85, a novel member of the G protein-coupled anti- goat IgG-HRP: sc-2033 (dilution range: 1:2000-1:5000), Cruz Marker™ receptor family, prominently expressed in the developing mouse cerebral Molecular Weight Standards: sc-2035, TBS Blotto A Blocking Reagent: cortex. Brain Res. Gene Expr. Patterns 1: 13-16. sc-2333 and Western Blotting Luminol Reagent: sc-2048. 2) Immunofluo- rescence: use donkey anti-goat IgG-FITC: sc-2024 (dilution range: 1:100- 4. Jeon, J., et al. 2002. Cloning and localization of rgpr85 encoding rat G 1:400) or donkey anti-goat IgG-TR: sc-2783 (dilution range: 1:100-1:400) protein-coupled receptor. Biochem. Biophys. Res. Commun. 298: 613-618. with UltraCruz™ Mounting Medium: sc-24941. 5. Lee, D.K., et al. 2002. Novel G protein-coupled receptor genes expressed in the brain: continued discovery of important therapeutic targets. Expert STORAGE Opin. Ther. Targets 6: 185-202. Store at 4° C, **DO NOT FREEZE**. Stable for one year from the date of 6. Lee, D.K., et al. 2003. Continued discovery of ligands for G protein-coupled shipment. Non-hazardous. No MSDS required. receptors. Life Sci. 74: 293-297. RESEARCH USE 7. Matsumoto, M., et al. 2005. A conserved mRNA expression profile of SREB2 (GPR85) in adult human, monkey, and rat forebrain. Brain Res. Mol. For research use only, not for use in diagnostic procedures. Brain Res. 138: 58-69. PROTOCOLS CHROMOSOMAL LOCATION See our web site at www.scbt.com or our catalog for detailed protocols and Genetic locus: GPR85 (human) mapping to 7q31.1; Gpr85 (mouse) mapping to support products. 6 A1. SOURCE GPR85 (N-14) is an affinity purified goat polyclonal antibody raised against a peptide mapping within an N-terminal extracellular domain of GPR85 of human origin. PRODUCT Each vial contains 200 µg IgG in 1.0 ml of PBS with < 0.1% sodium azide and 0.1% gelatin. Blocking peptide available for competition studies, sc-54685 P, (100 µg pep tide in 0.5 ml PBS containing < 0.1% sodium azide and 0.2% BSA). Santa Cruz Biotechnology, Inc. 1.800.457.3801 831.457.3800 fax 831.457.3801 Europe +00800 4573 8000 49 6221 4503 0 www.scbt.com.
Recommended publications
  • 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]
  • The Effect of Hypoxia on the Expression of CXC Chemokines and CXC Chemokine Receptors—A Review of Literature
    International Journal of Molecular Sciences Review The Effect of Hypoxia on the Expression of CXC Chemokines and CXC Chemokine Receptors—A Review of Literature Jan Korbecki 1 , Klaudyna Kojder 2, Patrycja Kapczuk 1, Patrycja Kupnicka 1 , Barbara Gawro ´nska-Szklarz 3 , Izabela Gutowska 4 , Dariusz Chlubek 1 and Irena Baranowska-Bosiacka 1,* 1 Department of Biochemistry and Medical Chemistry, Pomeranian Medical University in Szczecin, Powsta´nców Wielkopolskich 72 Av., 70-111 Szczecin, Poland; [email protected] (J.K.); [email protected] (P.K.); [email protected] (P.K.); [email protected] (D.C.) 2 Department of Anaesthesiology and Intensive Care, Pomeranian Medical University in Szczecin, Unii Lubelskiej 1, 71-281 Szczecin, Poland; [email protected] 3 Department of Pharmacokinetics and Therapeutic Drug Monitoring, Pomeranian Medical University in Szczecin, Powsta´nców Wielkopolskich 72 Av., 70-111 Szczecin, Poland; [email protected] 4 Department of Medical Chemistry, Pomeranian Medical University in Szczecin, Powsta´nców Wlkp. 72 Av., 70-111 Szczecin, Poland; [email protected] * Correspondence: [email protected]; Tel.: +48-914661515 Abstract: Hypoxia is an integral component of the tumor microenvironment. Either as chronic or cycling hypoxia, it exerts a similar effect on cancer processes by activating hypoxia-inducible factor-1 (HIF-1) and nuclear factor (NF-κB), with cycling hypoxia showing a stronger proinflammatory influ- ence. One of the systems affected by hypoxia is the CXC chemokine system. This paper reviews all available information on hypoxia-induced changes in the expression of all CXC chemokines (CXCL1, CXCL2, CXCL3, CXCL4, CXCL5, CXCL6, CXCL7, CXCL8 (IL-8), CXCL9, CXCL10, CXCL11, CXCL12 Citation: Korbecki, J.; Kojder, K.; Kapczuk, P.; Kupnicka, P.; (SDF-1), CXCL13, CXCL14, CXCL15, CXCL16, CXCL17) as well as CXC chemokine receptors— Gawro´nska-Szklarz,B.; Gutowska, I.; CXCR1, CXCR2, CXCR3, CXCR4, CXCR5, CXCR6, CXCR7 and CXCR8.
    [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]
  • G-Protein-Coupled Receptors in CNS: a Potential Therapeutic Target for Intervention in Neurodegenerative Disorders and Associated Cognitive Deficits
    cells Review G-Protein-Coupled Receptors in CNS: A Potential Therapeutic Target for Intervention in Neurodegenerative Disorders and Associated Cognitive Deficits Shofiul Azam 1 , Md. Ezazul Haque 1, Md. Jakaria 1,2 , Song-Hee Jo 1, In-Su Kim 3,* and Dong-Kug Choi 1,3,* 1 Department of Applied Life Science & Integrated Bioscience, Graduate School, Konkuk University, Chungju 27478, Korea; shofi[email protected] (S.A.); [email protected] (M.E.H.); md.jakaria@florey.edu.au (M.J.); [email protected] (S.-H.J.) 2 The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, VIC 3010, Australia 3 Department of Integrated Bioscience & Biotechnology, College of Biomedical and Health Science, and Research Institute of Inflammatory Disease (RID), Konkuk University, Chungju 27478, Korea * Correspondence: [email protected] (I.-S.K.); [email protected] (D.-K.C.); Tel.: +82-010-3876-4773 (I.-S.K.); +82-43-840-3610 (D.-K.C.); Fax: +82-43-840-3872 (D.-K.C.) Received: 16 January 2020; Accepted: 18 February 2020; Published: 23 February 2020 Abstract: Neurodegenerative diseases are a large group of neurological disorders with diverse etiological and pathological phenomena. However, current therapeutics rely mostly on symptomatic relief while failing to target the underlying disease pathobiology. G-protein-coupled receptors (GPCRs) are one of the most frequently targeted receptors for developing novel therapeutics for central nervous system (CNS) disorders. Many currently available antipsychotic therapeutics also act as either antagonists or agonists of different GPCRs. Therefore, GPCR-based drug development is spreading widely to regulate neurodegeneration and associated cognitive deficits through the modulation of canonical and noncanonical signals.
    [Show full text]
  • Activation of the Orphan G Protein–Coupled Receptor GPR27 by Surrogate Ligands Promotes B-Arrestin 2 Recruitment S
    Supplemental material to this article can be found at: http://molpharm.aspetjournals.org/content/suppl/2017/03/17/mol.116.107714.DC1 1521-0111/91/6/595–608$25.00 https://doi.org/10.1124/mol.116.107714 MOLECULAR PHARMACOLOGY Mol Pharmacol 91:595–608, June 2017 Copyright ª 2017 by The American Society for Pharmacology and Experimental Therapeutics Activation of the Orphan G Protein–Coupled Receptor GPR27 by Surrogate Ligands Promotes b-Arrestin 2 Recruitment s Nadine Dupuis, Céline Laschet, Delphine Franssen, Martyna Szpakowska, Julie Gilissen, Pierre Geubelle, Arvind Soni, Anne-Simone Parent, Bernard Pirotte, Andy Chevigné, Jean- Claude Twizere, and Julien Hanson Laboratory of Molecular Pharmacology, GIGA-Molecular Biology of Diseases (N.D., C.L., J.G., P.G., A.S., J.H.), Laboratory of Medicinal Chemistry, Center for Interdisciplinary Research on Medicines (N.D., B.P., J.H.), Neuroendocrinology Unit, GIGA- Neurosciences (D.F., A.-S.P.), Laboratory of Protein Signaling and Interactions, GIGA-Molecular Biology of Diseases (J.-C.T.), Downloaded from University of Liège, Liège, Belgium; and Department of Infection and Immunity, Luxembourg Institute of Health, Esch-sur- Alzette, Luxembourg (M.S., A.C.) Received December 6, 2016; accepted March 16, 2017 ABSTRACT molpharm.aspetjournals.org Gprotein–coupled receptors are the most important drug targets the presence of membrane-anchored G protein-coupled receptor for human diseases. An important number of them remain devoid kinase-2. Therefore, we optimized a firefly luciferase complemen- of confirmed ligands. GPR27 is one of these orphan receptors, tation assay to screen against this chimeric receptor. We identified characterized by a high level of conservation among vertebrates two compounds [N-[4-(anilinocarbonyl)phenyl]-2,4-dichloroben- and a predominant expression in the central nervous system.
    [Show full text]
  • 1 1 2 3 Cell Type-Specific Transcriptomics of Hypothalamic
    1 2 3 4 Cell type-specific transcriptomics of hypothalamic energy-sensing neuron responses to 5 weight-loss 6 7 Fredrick E. Henry1,†, Ken Sugino1,†, Adam Tozer2, Tiago Branco2, Scott M. Sternson1,* 8 9 1Janelia Research Campus, Howard Hughes Medical Institute, 19700 Helix Drive, Ashburn, VA 10 20147, USA. 11 2Division of Neurobiology, Medical Research Council Laboratory of Molecular Biology, 12 Cambridge CB2 0QH, UK 13 14 †Co-first author 15 *Correspondence to: [email protected] 16 Phone: 571-209-4103 17 18 Authors have no competing interests 19 1 20 Abstract 21 Molecular and cellular processes in neurons are critical for sensing and responding to energy 22 deficit states, such as during weight-loss. AGRP neurons are a key hypothalamic population 23 that is activated during energy deficit and increases appetite and weight-gain. Cell type-specific 24 transcriptomics can be used to identify pathways that counteract weight-loss, and here we 25 report high-quality gene expression profiles of AGRP neurons from well-fed and food-deprived 26 young adult mice. For comparison, we also analyzed POMC neurons, an intermingled 27 population that suppresses appetite and body weight. We find that AGRP neurons are 28 considerably more sensitive to energy deficit than POMC neurons. Furthermore, we identify cell 29 type-specific pathways involving endoplasmic reticulum-stress, circadian signaling, ion 30 channels, neuropeptides, and receptors. Combined with methods to validate and manipulate 31 these pathways, this resource greatly expands molecular insight into neuronal regulation of 32 body weight, and may be useful for devising therapeutic strategies for obesity and eating 33 disorders.
    [Show full text]
  • In Vitro Profiling of Orphan G Protein Coupled Receptor (GPCR)
    bioRxiv preprint doi: https://doi.org/10.1101/2021.03.10.434788; this version posted March 11, 2021. 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. 1 2 In vitro profiling of orphan G protein coupled receptor (GPCR) 3 constitutive activity 4 5 Lyndsay R. Watkins and Cesare Orlandi * 6 Department of Pharmacology and Physiology, University of Rochester Medical Center, 7 Rochester, NY 14642, USA 8 * Correspondence: [email protected] 9 10 11 12 13 14 15 16 17 18 19 20 Running title: 21 Orphan GPCR constitutive activity 22 23 Keywords: 24 G protein‐coupled receptor (GPCR); constitutive activity; cell signaling; molecular pharmacology. 1 bioRxiv preprint doi: https://doi.org/10.1101/2021.03.10.434788; this version posted March 11, 2021. 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. 25 Abstract 26 Background and Purpose 27 Members of the G protein coupled receptor (GPCR) family are targeted by a significant fraction 28 of the available FDA-approved drugs. However, the physiological role and pharmacological 29 properties of many GPCRs remain unknown, representing untapped potential in drug design. Of 30 particular interest are ~100 less-studied GPCRs known as orphans because their endogenous 31 ligands are unknown. Intriguingly, disease-causing mutations identified in patients, together with 32 animal studies, have demonstrated that many orphan receptors play crucial physiological roles, 33 and thus, represent attractive drug targets.
    [Show full text]
  • G Protein-Coupled Receptors
    Alexander, S. P. H., Christopoulos, A., Davenport, A. P., Kelly, E., Marrion, N. V., Peters, J. A., Faccenda, E., Harding, S. D., Pawson, A. J., Sharman, J. L., Southan, C., Davies, J. A. (2017). THE CONCISE GUIDE TO PHARMACOLOGY 2017/18: G protein-coupled receptors. British Journal of Pharmacology, 174, S17-S129. https://doi.org/10.1111/bph.13878 Publisher's PDF, also known as Version of record License (if available): CC BY Link to published version (if available): 10.1111/bph.13878 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.13878 . 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: G protein-coupled receptors. British Journal of Pharmacology (2017) 174, S17–S129 THE CONCISE GUIDE TO PHARMACOLOGY 2017/18: G protein-coupled receptors Stephen PH Alexander1, Arthur Christopoulos2, Anthony P Davenport3, Eamonn Kelly4, Neil V Marrion4, John A Peters5, Elena Faccenda6, Simon D Harding6,AdamJPawson6, Joanna L Sharman6, Christopher Southan6, Jamie A Davies6 and CGTP Collaborators 1 School of Life Sciences,
    [Show full text]
  • SREB2/GPR85, a Schizophrenia Risk Factor, Negatively Regulates Hippocampal Adult Neurogenesis and Neurogenesis- Dependent Learning and Memory
    European Journal of Neuroscience European Journal of Neuroscience, pp. 1–12, 2012 doi:10.1111/j.1460-9568.2012.08180.x SREB2/GPR85, a schizophrenia risk factor, negatively regulates hippocampal adult neurogenesis and neurogenesis- dependent learning and memory Qian Chen,1 Jeffrey H. Kogan,1 Adam K. Gross,1 Yuan Zhou,2 Noah M. Walton,1 Rick Shin,1 Carrie L. Heusner,1 Shinichi Miyake,1 Katsunori Tajinda,1 Kouichi Tamura1 and Mitsuyuki Matsumoto1 1CNS, Astellas Research Institute of America LLC, Skokie, IL 60077, USA 2Master of Biotechnology Program, Northwestern University, Evanston, IL, USA Keywords: bromodeoxyuridine, cognition, dentate gyrus, mutant mouse, psychiatric disease Abstract SREB2 ⁄ GPR85, a member of the super-conserved receptor expressed in brain (SREB) family, is the most conserved G-protein- coupled receptor in vertebrate evolution. Previous human and mouse genetic studies have indicated a possible link between SREB2 and schizophrenia. SREB2 is robustly expressed in the hippocampal formation, especially in the dentate gyrus, a structure with an established involvement in psychiatric disorders and cognition. However, the function of SREB2 in the hippocampus remains elusive. Here we show that SREB2 regulates hippocampal adult neurogenesis, which impacts on cognitive function. Bromodeoxyuridine incorporation and immunohistochemistry were conducted in SREB2 transgenic (Tg, over-expression) and knockout (KO, null-mutant) mice to quantitatively assay adult neurogenesis and newborn neuron dendritic morphology. Cognitive responses associated with adult neurogenesis alteration were evaluated in SREB2 mutant mice. In SREB2 Tg mice, both new cell proliferation and new neuron survival were decreased in the dentate gyrus, whereas an enhancement of new neuron survival occurred in SREB2 KO mouse dentate gyrus.
    [Show full text]
  • The Association of GPR85 with PSD-95
    Fujita-Jimbo et al. Molecular Autism (2015) 6:17 DOI 10.1186/s13229-015-0012-5 RESEARCH Open Access The association of GPR85 with PSD-95-neuroligin complex and autism spectrum disorder: a molecular analysis Eriko Fujita-Jimbo1,2†, Yuko Tanabe2†, Zhiling Yu1,3†, Karin Kojima1, Masato Mori1, Hong Li1,4, Sadahiko Iwamoto5, Takanori Yamagata1, Mariko Y Momoi1,2* and Takashi Momoi2* Abstract Background: Autism spectrum disorder (ASD) has a complex genetic etiology. Some symptoms and mutated genes, including neuroligin (NLGN), neurexin (NRXN), and SH3 and multiple ankyrin repeat domains protein (SHANK), are shared by schizophrenia and ASD. Little is known about the molecular pathogenesis of ASD. One of the possible molecular pathogenesis is an imbalance of excitatory and inhibitory receptors linked with the NLGN-PSD-95-SHANK complex via postsynaptic density protein/Drosophila disc large tumor suppressor/zonula occludens-1 protein (PDZ) binding. In the present study, we focused on GPR85 as a candidate gene for ASD because the C-terminal amino acid sequence of GPR85 [Thr-Cys-Val-Ile (YCVI)] is classified as a type II PDZ-binding motif, and GPR85 is a risk factor for schizophrenia. GPR85 is an orphan receptor that regulates neural and synaptic plasticity and modulates diverse behaviors, including learning and memory. While searching for molecules that associate with GPR85, we found that GPR85 was associated with postsynaptic density protein (PSD)-95 linked with NLGN in the brain. Methods: We examined the proteins that associate with the C-terminal sequence of GPR85 by pull-down assay and immunoblot analysis and searched for a mutation of the GPR85 gene in patients with ASD.
    [Show full text]
  • GPR85) on Functional MRI Phenotypes in Healthy Volunteers
    Neuropsychopharmacology (2013) 38, 341–349 & 2013 American College of Neuropsychopharmacology. All rights reserved 0893-133X/13 www.neuropsychopharmacology.org Effect of Schizophrenia Risk-Associated Alleles in SREB2 (GPR85) on Functional MRI Phenotypes in Healthy Volunteers 1,3 1,4 1,5 1 1,5 Eugenia Radulescu , Fabio Sambataro , Venkata S Mattay , Joseph H Callicott , Richard E Straub , 2 1,5 ,1 Mitsuyuki Matsumoto , Daniel R Weinberger and Stefano Marenco* 1 2 Clinical Brain Disorders Branch, GCAP, IRP, NIMH, Bethesda, MD, USA; CNS, Astellas Research Institute of America LLC, Skokie, IL, USA Genetic variants in GPR85 (SREB2: rs56080411 and rs56039557) have been associated with risk for schizophrenia. Here, we test the hypothesis that these variants impact on brain function in normal subjects, measured with functional magnetic resonance imaging (fMRI) paradigms that target regions with greatest SREB2 expression (hippocampal formation and amygdaloid complex). During a facial emotion recognition paradigm, a significant interaction of rs56080411 genotype by sex was found in the left amygdaloid complex (male risk allele carriers showed less activation than male homozygotes for the non-risk allele, while females showed the opposite pattern). During aversive encoding of an emotional memory paradigm, we found that risk allele carriers for rs56080411 had greater activation in the right inferior frontal gyrus. Trends in the same direction were present for rs56039557 in the right occipital cortex and right fusiform gyrus. During a working memory paradigm, a significant sex-by-genotype interaction was found with male risk allele carriers of rs56080411 having inefficient activation within the left dorsolateral prefrontal cortex (DLPFC), compared with same sex non-risk carriers, while females revealed an opposite pattern, despite similar levels of performance.
    [Show full text]