GPR173 Polyclonal Antibody Catalog # AP70181

Total Page：16

File Type：pdf, Size：1020Kb

10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 GPR173 Polyclonal Antibody Catalog # AP70181 Specification GPR173 Polyclonal Antibody - Product Information Application WB Primary Accession Q9NS66 Reactivity Human, Mouse, Rat Host Rabbit Clonality Polyclonal GPR173 Polyclonal Antibody - Additional Information Gene ID 54328 Other Names GPR173; SREB3; Probable G-protein coupled receptor 173; Super conserved receptor expressed in brain 3 Dilution WB~~Western Blot: 1/500 - 1/2000. Immunofluorescence: 1/200 - 1/1000. ELISA: 1/10000. Not yet tested in other applications. Format Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide. Storage Conditions -20℃ GPR173 Polyclonal Antibody - Protein Information Name GPR173 Synonyms SREB3 Function Is a receptor for the SMIM20 derived peptides Phoenixin-14 and Phoenixin-20 (By similarity). It mediates the Phoenixin-14 and Phoenixin-20 augmentation of gonadotropin-releasing hormone (GNRH) signaling in the hypothalamus and pituitary gland (By similarity). In the ovary, it Page 1/2 10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 mediates the effects of Phoenixin-14 and Phoenixin-20 induced granulosa cell proliferation during follicular growth (PubMed:<a href="http://www.uniprot.org/c itations/30933929" target="_blank">30933929</a>). Cellular Location Cell membrane; Multi-pass membrane protein Tissue Location Expressed in the ovary, specifically in granulosa cells of follicles that have passed the primary stage and in oocytes (at protein level) (PubMed:30933929). Expressed at high levels in brain. Lower levels in small intestine. In brain regions, detected in all regions tested. Highest levels in the cerebellum and cerebral cortex. GPR173 Polyclonal Antibody - Protocols Provided below are standard protocols that you may find useful for product applications. • Western Blot • Blocking Peptides • Dot Blot • Immunohistochemistry • Immunofluorescence • Immunoprecipitation • Flow Cytomety • Cell Culture GPR173 Polyclonal Antibody - Background Orphan receptor. Page 2/2 Powered by TCPDF (www.tcpdf.org).

Copy Link

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]
Integrative Analysis of Mirna–Mrna Network in High Altitude Retinopathy by Bioinformatics Analysis
Bioscience Reports (2021) 41 BSR20200776 https://doi.org/10.1042/BSR20200776 Research Article Integrative analysis of miRNA–mRNA network in high altitude retinopathy by bioinformatics analysis Tong Su1,2,*, Chufeng Gu1,2,*,DejiDraga3,*, Chuandi Zhou1,2, Thashi Lhamo3, Zhi Zheng1,2 and Qinghua Qiu1,2,3 1Department of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China; 2National Clinical Research Center for Eye Downloaded from http://portlandpress.com/bioscirep/article-pdf/41/1/BSR20200776/902020/bsr-2020-0776.pdf by guest on 26 September 2021 Diseases; Shanghai Key Laboratory of Ocular Fundus Diseases; Shanghai Engineering Center for Visual Science and Photomedicine; Shanghai Engineering Center for Precise Diagnosis and Treatment of Eye Diseases, Shanghai, P.R. China; 3Department of Ophthalmology, Shigatse People’s Hospital, Shigatse, Xizang, P.R. China Correspondence: Qinghua Qiu ([email protected]) or Zhi Zheng ([email protected]) High-altitude retinopathy (HAR) is an ocular manifestation of acute oxygen deficiency at high altitudes. Although the pathophysiology of HAR has been revealed by many studies in recent years, the molecular mechanism is not yet clear. Our study aimed to systemati- cally identify the genes and microRNA (miRNA) and explore the potential biomarkers asso- ciated with HAR by integrated bioinformatics analysis. The mRNA and miRNA expression profiles were obtained from the Gene Expression Omnibus database. We performed Gene Ontology functional annotations and Kyoto Encyclopedia of Genes and Genomes path- way analysis. Potential target gene analysis and miRNA–mRNA network analysis were also conducted. Quantitative RT-PCR (qRT-PCR) was used to validate the results of the bioinfor- matics analysis.
[Show full text]
G Protein-Coupled Receptors in Stem Cell Maintenance and Somatic Reprogramming to Pluripotent Or Cancer Stem Cells
BMB Reports - Manuscript Submission Manuscript Draft Manuscript Number: BMB-14-250 Title: G protein-coupled receptors in stem cell maintenance and somatic reprogramming to pluripotent or cancer stem cells Article Type: Mini Review Keywords: G protein-coupled receptors; stem cell maintenance; somatic reprogramming; cancer stem cells; pluripotent stem cell Corresponding Author: Ssang-Goo Cho Authors: Ssang-Goo Cho1,*, Hye Yeon Choi1, Subbroto Kumar Saha1, Kyeongseok Kim1, Sangsu Kim1, Gwang-Mo Yang1, BongWoo Kim1, Jin-hoi Kim1 Institution: 1Department of Animal Biotechnology, Animal Resources Research Center, and Incurable Disease Animal Model and Stem Cell Institute (IDASI), Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul 143-701, Republic of Korea, UNCORRECTED PROOF 1 G protein-coupled receptors in stem cell maintenance and somatic reprogramming to 2 pluripotent or cancer stem cells 3 4 Hye Yeon Choi, Subbroto Kumar Saha, Kyeongseok Kim, Sangsu Kim, Gwang-Mo 5 Yang, BongWoo Kim, Jin-hoi Kim, and Ssang-Goo Cho 6 7 Department of Animal Biotechnology, Animal Resources Research Center, and 8 Incurable Disease Animal Model and Stem Cell Institute (IDASI), Konkuk University, 9 120 Neungdong-ro, Gwangjin-gu, Seoul 143-701, Republic of Korea 10 * 11 Address correspondence to Ssang-Goo Cho, Department of Animal Biotechnology and 12 Animal Resources Research Center. Konkuk University, 120 Neungdong-ro, Gwangjin- 13 gu, Seoul 143-701, Republic of Korea. Tel: 82-2-450-4207, Fax: 82-2-450-1044, E-mail: 14 [email protected] 15 16 17 18 19 1 UNCORRECTED PROOF 20 Abstract 21 The G protein-coupled receptors (GPCRs) compose the third largest gene family in the 22 human genome, representing more than 800 distinct genes and 3–5% of the human genome.
[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]
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]
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]
Supplementary Data, Ms Iring Et Al. Re-Revised
Supplementary Data András Iring et al., “Shear stress-induced endothelial adrenomedullin signaling regulates vascular tone and blood pressure” Supplementary Tables Supplementary Table 1. Target sequences of siRNAs used in the siRNA screen (Fig. 4A). Gene Target sequence (5´-3´) ADORA2A CGGAACAGCTCCCAGGTCT ADORA2A GCTGTTAGATCCTCCATGT ADORA2A GGCTTTCCACGGGTTCAGA ADORA2B GAGACTTCCGCTACACTTT ADORA2B GAGCTCATGGATCACTCAA ADORA2B GATGCAGCCACGAACGTGA ADRB1 CAGATCTGGTCATGGGTCT ADRB1 GTGTCATCGCCCTGGACCA ADRB1 CCATCTCGGCGCTGGTGTC ADRB2 CAAGTTCTACTTGAAGGAA ADRB2 CAACTTCTGGTGTGAGTTT ADRB2 GTCATCACAGCCATTGCCA CALCRL GATCAGTTCTGATACGCAA CALCRL GATACTCTCCGTAGTGCAT CALCRL GATTTATGATTTACCTATA CCRL1 GTATGAAGTGATCTGTATA CCRL1 GCTACTTCATCACGGCAAA CCRL1 GCATCAAACATCTGCATTT CCRL2 GACCCTACAATATTGTACT CCRL2 GCTTCTTTACCGGACTTCA CCRL2 CCTGTTGCTCTACTCCATA CELSR1 CTATGAGGAGAATCGAGTA CELSR1 GACTGAAGGTCCAGACGCA CELSR1 CCAACATCGCCACGCTGAA CELSR3 CCTTTGTAACCAGAGAGAT CELSR3 CAGCTTATGATCCAGATGT CELSR3 GCAATACCGGGAGACGCTT CXCR7 GCATGAGTGTGGATCGCTA CXCR7 GCTACGACACGCACTGCTA CXCR7 CTTTGGAGCAGAATGCCAA 2 ELTD1 CTCTTCTAATTCAACTCTT ELTD1 CAAGTTTATTACTAATGAT ELTD1 GTACCATACAGCTATAGTA FZD1 GTAACCAATGCCAAACTTT FZD1 GATTAGCCACCGAAATAAA FZD1 CAGTGTTCCGCCGAGCTCA FZD2 CGCTTTGCGCGCCTCTGGA FZD2 GACATGCAGCGCTTCCGCT FZD2 CGCACTACACGCCGCGCAT FZD4 GTATGTGCTATAATATTTA FZD4 CCATTGTCATCTTGATTAT FZD4 CCAACATGGCAGTGGAAAT FZD5 GGATTTAAGGCCCAGTTTA FZD5 GACCATAACACACTTGCTT FZD5 CAAGTGATCCTGGGAAAGA FZD6 GCATTGTATCTCTTATGTA FZD6 GTGCTTACTGAGTGTCCAA FZD6 CCAATTACTGTTCCCAGAT FZD8 CCATCTGCCTAGAGGACTA
[Show full text]
Expression Map of 78 Brain-Expressed Mouse Orphan Gpcrs Provides a Translational Resource for Neuropsychiatric Research
ARTICLE DOI: 10.1038/s42003-018-0106-7 OPEN Expression map of 78 brain-expressed mouse orphan GPCRs provides a translational resource for neuropsychiatric research Aliza T. Ehrlich1,2, Grégoire Maroteaux2,5, Anne Robe1, Lydie Venteo3, Md. Taufiq Nasseef2, 1234567890():,; Leon C. van Kempen4,6, Naguib Mechawar2, Gustavo Turecki2, Emmanuel Darcq2 & Brigitte L. Kieffer 1,2 Orphan G-protein-coupled receptors (oGPCRs) possess untapped potential for drug dis- covery. In the brain, oGPCRs are generally expressed at low abundance and their function is understudied. Expression profiling is an essential step to position oGPCRs in brain function and disease, however public databases provide only partial information. Here, we fine-map expression of 78 brain-oGPCRs in the mouse, using customized probes in both standard and supersensitive in situ hybridization. Images are available at http://ogpcr-neuromap.douglas. qc.ca. This searchable database contains over 8000 coronal brain sections across 1350 slides, providing the first public mapping resource dedicated to oGPCRs. Analysis with public mouse (60 oGPCRs) and human (56 oGPCRs) genome-wide datasets identifies 25 oGPCRs with potential to address emotional and/or cognitive dimensions of psychiatric conditions. We probe their expression in postmortem human brains using nanoString, and included data in the resource. Correlating human with mouse datasets reveals excellent suitability of mouse models for oGPCRs in neuropsychiatric research. 1 IGBMC, Institut Génétique Biologie Moléculaire Cellulaire, Illkirch, France. 2 Douglas Mental Health University Institute and McGill University, Department of Psychiatry, Montreal, Canada. 3 Label Histologie, 51100 Reims, France. 4 Lady Davis Institute for Medical Research, Jewish General Hospital and McGill University, Department of Pathology, Montreal, Canada.
[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]
Adenylyl Cyclase 2 Selectively Regulates IL-6 Expression in Human Bronchial Smooth Muscle Cells Amy Sue Bogard University of Tennessee Health Science Center
University of Tennessee Health Science Center UTHSC Digital Commons Theses and Dissertations (ETD) College of Graduate Health Sciences 12-2013 Adenylyl Cyclase 2 Selectively Regulates IL-6 Expression in Human Bronchial Smooth Muscle Cells Amy Sue Bogard University of Tennessee Health Science Center Follow this and additional works at: https://dc.uthsc.edu/dissertations Part of the Medical Cell Biology Commons, and the Medical Molecular Biology Commons Recommended Citation Bogard, Amy Sue , "Adenylyl Cyclase 2 Selectively Regulates IL-6 Expression in Human Bronchial Smooth Muscle Cells" (2013). Theses and Dissertations (ETD). Paper 330. http://dx.doi.org/10.21007/etd.cghs.2013.0029. This Dissertation is brought to you for free and open access by the College of Graduate Health Sciences at UTHSC Digital Commons. It has been accepted for inclusion in Theses and Dissertations (ETD) by an authorized administrator of UTHSC Digital Commons. For more information, please contact [email protected]. Adenylyl Cyclase 2 Selectively Regulates IL-6 Expression in Human Bronchial Smooth Muscle Cells Document Type Dissertation Degree Name Doctor of Philosophy (PhD) Program Biomedical Sciences Track Molecular Therapeutics and Cell Signaling Research Advisor Rennolds Ostrom, Ph.D. Committee Elizabeth Fitzpatrick, Ph.D. Edwards Park, Ph.D. Steven Tavalin, Ph.D. Christopher Waters, Ph.D. DOI 10.21007/etd.cghs.2013.0029 Comments Six month embargo expired June 2014 This dissertation is available at UTHSC Digital Commons: https://dc.uthsc.edu/dissertations/330 Adenylyl Cyclase 2 Selectively Regulates IL-6 Expression in Human Bronchial Smooth Muscle Cells A Dissertation Presented for The Graduate Studies Council The University of Tennessee Health Science Center In Partial Fulfillment Of the Requirements for the Degree Doctor of Philosophy From The University of Tennessee By Amy Sue Bogard December 2013 Copyright © 2013 by Amy Sue Bogard.
[Show full text]
Orphan G Protein Coupled Receptors in Affective Disorders
G C A T T A C G G C A T genes Review Orphan G Protein Coupled Receptors in Aﬀective Disorders Lyndsay R. Watkins and Cesare Orlandi * Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY 14642, USA; [email protected] * Correspondence: [email protected] Received: 3 June 2020; Accepted: 21 June 2020; Published: 24 June 2020 Abstract: G protein coupled receptors (GPCRs) are the main mediators of signal transduction in the central nervous system. Therefore, it is not surprising that many GPCRs have long been investigated for their role in the development of anxiety and mood disorders, as well as in the mechanism of action of antidepressant therapies. Importantly, the endogenous ligands for a large group of GPCRs have not yet been identiﬁed and are therefore known as orphan GPCRs (oGPCRs). Nonetheless, growing evidence from animal studies, together with genome wide association studies (GWAS) and post-mortem transcriptomic analysis in patients, pointed at many oGPCRs as potential pharmacological targets. Among these discoveries, we summarize in this review how emotional behaviors are modulated by the following oGPCRs: ADGRB2 (BAI2), ADGRG1 (GPR56), GPR3, GPR26, GPR37, GPR50, GPR52, GPR61, GPR62, GPR88, GPR135, GPR158, and GPRC5B. Keywords: G protein coupled receptor (GPCR); G proteins; orphan GPCR (oGPCR); mood disorders; major depressive disorder (MDD); bipolar disorder (BPD); anxiety disorders; antidepressant; animal models 1. Introduction Mood alterations due to pharmacological treatments that modulate serotonergic and noradrenergic systems laid the foundations for the monoamine hypothesis that has led research on mood disorders since the late 1950s [1–3]. Dopaminergic alterations have also been associated with major depressive disorder (MDD) symptoms, such as anhedonia [4].
[Show full text]
Modeling and Analysis of Acute Leukemia Using Human Hematopoietic Stem and Progenitor Cells
Modeling and analysis of acute leukemia using human hematopoietic stem and progenitor cells A dissertation submitted to the Graduate School of the University of Cincinnati in partial fulfillment of the requirement for the degree of Doctor of Philosophy in the Molecular &Developmental Biology Graduate Program of the College of Medicine by Shan Lin BS, Tsinghua University, 2009 Dissertation Committee: James C. Mulloy, PhD (Chair) Geraldine Guasch, PhD Ashish R. Kumar, MD, PhD Daniel T. Starczynowski, PhD Yi Zheng, PhD Abstract For decades, elegant mouse models have yielded important insights into the complex biology of acute leukemia development. However, species differences between human and mouse could have significant influences on biological and translational applications. Therefore, human primary hematopoietic cells and xenograft mouse models have become important research tools in the field. In this report, we briefly review the methodologies that use human primary hematopoietic cells to model acute leukemia and examine the effects of leukemic oncogenes. The advantages and limitations of the human model system compared to syngeneic mouse models are discussed. The species-related complexity in human disease modeling is highlighted in the study establishing a faithful model of proB-ALL caused by MLL-AF4, the fusion product of the t(4;11). MLL-AF4 proB-ALL has poor prognosis, the lack of an accurate model hampers the study of disease pathobiology and therapeutic testing. We find human AF4 cDNA inhibits retroviral production and efficient transduction, this limitation can be overcome by fusing MLL with murine Af4, highly conserved with human AF4. Whereas MLL-Af4-transduced murine cells induce only AML, transduced human CD34+ cells produce proB-ALL faithful to t(4;11) disease, fully recapitulating the immunophenotypic and molecular aspects of the disease.
[Show full text]