DOCSLIB.ORG

IHC Plus Antibodies.Xlsx

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
IHC Plus Antibodies.Xlsx August 2012 MayMay 2011 2011 Catalog CatalogCatalog IHC-plusTM Antibodies TM …..because seeing is believing. IHCIHC--plusplusTM Antibodies Antibodies …..because seeing is believing. …..because seeing is believing. IHC-plus™ Antibodies ...because seeing is believing! LSBio is the world's largest supplier of Immunohistochemistry (IHC) antibodies with more than 27,000 having been tested and approved for use in IHC. More than 7,500 of these antibodies have been further validated specifically for use under LSBio's standardized IHC conditions against formalin-fixed paraffin-embedded human tissues. These are LSBio's premier IHC-plus™ brand antibodies. Visit ww.lsbio.com to learn more about our IHC validation procedure or for the most up to data list of IHC-plusTM antibodies. Host/Reactivity Application CD44 Antigen (CD44) Synaptophysin (SYP) Caspase 3 (CASP3) LS-B1862, IHC, Human skin LS-B3393, IHC, Human adrenal LS-B3404, IHC, Human spleen Clonality Solute Carrier Family 5 (sodium/glucose Histone Deacetylase 1 (HDAC1) ATP-Binding Cassette, Sub-Family B (Mdr/Tap), Cotransporter), Member 10 (SLC5A10) LS-B3438, IHC, Human colon Member 1 (Abcb1) LS-A2800, IHC, Human skeletal muscle LS-B1448, IHC, Human kidney Cyclin D1 (CCND1) Integrin, Alpha X (Antigen CD11C (P150), Alpha Transient Receptor Potential Cation Channel, LS-B3452, IHC, Human testis Polypeptide) (ITGAX) Subfamily A, Member 1 (TRPA1) LS-A9382, IHC, Human tonsil LS-A9098, IHC, Human dorsal root ganglia LSBio IHC‐plus Antibodies Target Antibody Application 12 Lipoxygenase (LS‐B1587): Rabbit anti‐Mouse Polyclonal IHC, WB 14‐3‐3(LS‐B7705): Rabbit anti‐Rat Polyclonal IHC, WB 14‐3‐3(LS‐B6644): Rabbit anti‐Sheep Polyclonal IHC, WB, IP 14‐3‐3(LS‐B7072): Mouse anti‐Human Monoclonal IHC, WB 14‐3‐3 Beta (LS‐B3330): Rabbit anti‐Human Polyclonal IHC 14‐3‐3 Beta (LS‐B1282): Rabbit anti‐Human Polyclonal IHC, WB 14‐3‐3 Beta (LS‐B7147): Rabbit anti‐Human Polyclonal IHC, WB 14‐3‐3 Beta (LS‐B4792): Rabbit anti‐Human Polyclonal IHC, WB, ICC, IF 14‐3‐3 Beta (LS‐B4793): Rabbit anti‐Human Polyclonal IHC, WB, ICC, IF 14‐3‐3 Beta (LS‐B2958): Mouse anti‐Human Monoclonal ELISA, IHC, WB 5 Lipoxygenase (LS‐B2164): Rabbit anti‐Human Polyclonal IHC, WB 5 Lipoxygenase (LS‐B2144): Rabbit anti‐Human Polyclonal IHC, WB 5 Lipoxygenase (LS‐B1499): Rabbit anti‐Human Polyclonal IHC, WB, ICC 5HT1A Receptor (LS‐B6043): Mouse anti‐Rat Monoclonal IHC, WB 5HT1A Receptor (LS‐B970): Rabbit anti‐Human Polyclonal ELISA, IHC, WB 5HT1D Receptor (LS‐B2041): Rabbit anti‐Rat Polyclonal IHC, WB 5HT1E Receptor (LS‐A6374): Rabbit anti‐Human Polyclonal ELISA, IHC 5HT1F Receptor (LS‐A864): Rabbit anti‐Human Polyclonal IHC 5HT2A Receptor (LS‐A1106): Rabbit anti‐Human Polyclonal IHC 5HT2C Receptor (LS‐B4082): Rabbit anti‐Human Polyclonal IHC, WB 5HT3A receptor (LS‐B2042): Rabbit anti‐Rat Polyclonal IHC, WB 5HT3A receptor (LS‐B3945): Goat anti‐Human Polyclonal ELISA, IHC, WB 5HT3A receptor (LS‐B152): Rabbit anti‐Human Polyclonal ELISA, IHC, WB 5HT3B receptor (LS‐B7535): Rabbit anti‐Human Polyclonal IHC, WB 5HT3B receptor (LS‐B971): Rabbit anti‐Human Polyclonal ELISA, IHC, WB 5HT4 Receptor (LS‐B6136): Goat anti‐Human Polyclonal ELISA, IHC 5HT5A receptor (LS‐A6693): Rabbit anti‐Human Polyclonal ELISA, IHC 5HT5A receptor (LS‐A2119): Rabbit anti‐Human Polyclonal ELISA, IHC 5HT5A receptor (LS‐A2118): Rabbit anti‐Human Polyclonal ELISA, IHC 5HT7 Receptor (LS‐A6673): Rabbit anti‐Human Polyclonal IHC 5HT7 Receptor (LS‐A659): Rabbit anti‐Human Polyclonal ELISA, IHC 5HT7 Receptor (LS‐A7991): Rabbit anti‐Human Polyclonal ELISA, IHC A1BG (LS‐B1507): Rabbit anti‐Human Polyclonal IHC, WB A1BG (LS‐B4153): Mouse anti‐Human Monoclonal ELISA, IHC, WB A2M / Alpha‐2‐Macroglobulin (LS‐B3119): Rabbit anti‐Human Polyclonal ELISA, IHC, WB A2M / Alpha‐2‐Macroglobulin (LS‐B4881): Goat anti‐Human Polyclonal ELISA, IHC, WB, IP A2M / Alpha‐2‐Macroglobulin (LS‐B403): Goat anti‐Human Polyclonal ELISA, IHC, WB, IP A2M / Alpha‐2‐Macroglobulin (LS‐B7697): Rabbit anti‐Human Monoclonal IHC, WB AAAS / Adracalin (LS‐B6169): Mouse anti‐Human Monoclonal ELISA, IHC, WB AADAT (LS‐A9490): Rabbit anti‐Human Polyclonal IHC AADAT (LS‐A9495): Rabbit anti‐Human Polyclonal IHC AAK1 (LS‐B3833): Rabbit anti‐Human Polyclonal IHC, WB AAK1 (LS‐B3843): Rabbit anti‐Human Polyclonal IHC, WB, ICC AATF (LS‐B438): Rabbit anti‐Human Polyclonal IHC, WB ABCA1 (LS‐B7326): Rabbit anti‐Human Polyclonal IHC, WB ABCA1 (LS‐B3038): Rabbit anti‐Human Polyclonal IHC, WB, ICC, Flo, IF, IP ABCA1 (LS‐B2384): Mouse anti‐Human Monoclonal ELISA, IHC, WB ABCA5 (LS‐B6852): Rabbit anti‐Human Polyclonal IHC, WB ABCA5 (LS‐B3554): Rabbit anti‐Human Polyclonal ELISA, IHC, WB ABCA7 (LS‐B5766): Rat anti‐Mouse Monoclonal IHC, WB, Flo ABCA7 (LS‐B222): Rat anti‐Mouse Monoclonal IHC, WB, Flo ABCB1 / MDR1 (LS‐A9403): Rabbit anti‐Human Polyclonal IHC ABCB1 / MDR1 (LS‐B4675): Rabbit anti‐Human Polyclonal ELISA, IHC, WB ABCB1 / MDR1 (LS‐B1448): Rabbit anti‐Human Polyclonal ELISA, IHC, WB ABCB1 / MDR1 (LS‐B5171): Mouse anti‐Hamster Monoclonal IHC, WB, Flo, IF ABCB1 / MDR1 (LS‐B5570): Mouse anti‐Human Monoclonal IHC, WB, Flo ABCB11 / BSEP (LS‐B2170): Mouse anti‐Human Monoclonal IHC, WB, ICC ABCB4 (LS‐B4112): Goat anti‐Human Polyclonal IHC ABCB4 (LS‐B5729): Rabbit anti‐Human Polyclonal IHC, WB ABCB5 (LS‐B6371): Rabbit anti‐Human Polyclonal IHC, WB August 2012 www.LSBio.com Page 1 LSBio IHC‐plus Antibodies Target Antibody Application ABCB5 (LS‐B3454): Rabbit anti‐Human Polyclonal ELISA, IHC, WB, Flo ABCB7 (LS‐B791): Rabbit anti‐Human Polyclonal ELISA, IHC ABCB7 (LS‐B7063): Rabbit anti‐Human Polyclonal ELISA, IHC ABCB9 (LS‐B2746): Goat anti‐Human Polyclonal ELISA, IHC ABCC3 / MRP3 (LS‐B7540): Rabbit anti‐Human Polyclonal ELISA, IHC, WB ABCC4 / MRP4 (LS‐B2678): Rabbit anti‐Human Polyclonal IHC, WB ABCC4 / MRP4 (LS‐B4): Goat anti‐Human Polyclonal ELISA, IHC ABCC4 / MRP4 (LS‐B5750): Mouse anti‐Human Monoclonal ELISA, IHC, WB ABCC5 / MRP5 (LS‐B2334): Goat anti‐Human Polyclonal ELISA, IHC, WB ABCC8 / MRP8 (LS‐B5774): Rabbit anti‐Human Polyclonal IHC, WB ABCD1 (LS‐B7120): Rabbit anti‐Human Polyclonal IHC, WB ABCD3 / PMP70 (LS‐B6476): Goat anti‐Human Polyclonal ELISA, IHC, WB ABCD4 (LS‐B4375): Goat anti‐Human Polyclonal ELISA, IHC, WB ABCG1 (LS‐B507): Rabbit anti‐Human Polyclonal IHC, WB ABCG2 (LS‐B6595): Mouse anti‐Human Monoclonal IHC, WB, ICC ABHD4 (LS‐B7686): Rabbit anti‐Human Polyclonal ELISA, IHC ABHD4 (LS‐B2767): Goat anti‐Human Polyclonal ELISA, IHC ABHD5 / CGI‐58 (LS‐B4458): Goat anti‐Human Polyclonal ELISA, IHC, WB ABHD5 / CGI‐58 (LS‐B3990): Rabbit anti‐Human Polyclonal ELISA, IHC, WB ABHD5 / CGI‐58 (LS‐B5751): Mouse anti‐Human Monoclonal ELISA, IHC, WB ABL1 (LS‐B2776): Mouse anti‐Human Monoclonal IHC, WB, IF, IP ABL1 (LS‐B5970): Rabbit anti‐Human Polyclonal ELISA, IHC ABL2 (LS‐B7217): Rabbit anti‐Human Monoclonal IHC, WB, Flo ABTB1 / BPOZ (LS‐B3228): Goat anti‐Human Polyclonal ELISA, IHC, WB ACAA1 (LS‐B4015): Rabbit anti‐Human Polyclonal ELISA, IHC, WB ACAA2 (LS‐B6206): Mouse anti‐Human Monoclonal ELISA, IHC, WB, IF ACADM (LS‐B1500): Rabbit anti‐Human Polyclonal IHC, WB ACADM (LS‐B2993): Goat anti‐Human Polyclonal ELISA, IHC, WB ACADS (LS‐B4087): Rabbit anti‐Human Polyclonal IHC, WB ACAN / Aggrecan (LS‐A1561): Rabbit anti‐Human Polyclonal IHC ACAN / Aggrecan (LS‐A1556): Rabbit anti‐Human Polyclonal IHC ACAP1 / CENTB1 (LS‐B2280): Goat anti‐Human Polyclonal ELISA, IHC, WB ACAP2 / CENTB2 (LS‐B2282): Goat anti‐Human Polyclonal ELISA, IHC, WB ACAT1 (LS‐B6372): Rabbit anti‐Human Polyclonal IHC, WB ACAT1 (LS‐B4679): Rabbit anti‐Human Polyclonal ELISA, IHC, WB ACAT1 (LS‐B6919): Rabbit anti‐Human Polyclonal ELISA, IHC, WB ACAT1 (LS‐B6369): Rabbit anti‐Human Polyclonal ELISA, IHC, WB ACAT1 (LS‐B6286): Rabbit anti‐Human Polyclonal ELISA, IHC, WB ACAT1 (LS‐B6358): Mouse anti‐Human Monoclonal ELISA, IHC, WB ACCN1 (LS‐B4761): Rabbit anti‐Mouse Polyclonal IHC ACCN1 (LS‐B156): Rabbit anti‐Human Polyclonal ELISA, IHC, WB ACCN4 (LS‐B920): Rabbit anti‐Human Polyclonal ELISA, IHC, WB ACE (LS‐B2558): Mouse anti‐Human Monoclonal IHC, WB ACE‐2(LS‐B439): Rabbit anti‐Human Polyclonal IHC, WB ACE‐2(LS‐B5837): Rabbit anti‐Human Polyclonal IHC, WB ACE‐2(LS‐B3196): Rabbit anti‐Human Polyclonal ELISA, IHC, WB ACE‐2(LS‐B3197): Rabbit anti‐Human Polyclonal ELISA, IHC, WB ACE‐2(LS‐B6672): Rabbit anti‐Human Polyclonal ELISA, IHC, WB ACE‐2(LS‐B6324): Rabbit anti‐Human Monoclonal IHC, WB, ICC, IP ACHE / Acetylcholinesterase (LS‐B1819): Rabbit anti‐Human Polyclonal IHC, WB ACHE / Acetylcholinesterase (LS‐B6676): Rabbit anti‐Human Polyclonal IHC, WB ACHE / Acetylcholinesterase (LS‐B5977): Sheep anti‐Human Polyclonal ELISA, IHC ACIN1 / Acinus (LS‐B224): Rabbit anti‐ Polyclonal IHC, WB ACIN1 / Acinus (LS‐B3189): Rabbit anti‐Human Polyclonal ELISA, IHC, WB, ICC ACIN1 / Acinus (LS‐B3190): Rabbit anti‐Human Polyclonal ELISA, IHC, WB, ICC ACO2 (LS‐B3427): Rabbit anti‐Human Polyclonal ELISA, IHC, WB ACOT11 (LS‐B2961): Mouse anti‐Human Monoclonal ELISA, IHC, WB ACOT13 / THEM2 (LS‐B5012): Rabbit anti‐Human Polyclonal ELISA, IHC, WB ACOT9 (LS‐B4522): Mouse anti‐Human Monoclonal (4E4) ELISA, IHC, WB, IF ACP2 / Acid Phosphatase 2(LS‐B5788): Rabbit anti‐Human Polyclonal ELISA, IHC, WB August 2012 www.LSBio.com Page 2 LSBio IHC‐plus Antibodies Target Antibody Application ACP2 / Acid Phosphatase 2(LS‐B5373): Mouse anti‐Human Monoclonal ELISA, IHC, WB, IF ACSL1 (LS‐B5593): Rabbit anti‐Human Polyclonal IHC, WB ACSL3 (LS‐B1820): Rabbit anti‐Human Polyclonal ELISA, IHC, WB ACSL4 / FACL4 (LS‐B4440): Goat anti‐Human Polyclonal ELISA, IHC, WB ACSL4 / FACL4 (LS‐B5818): Rabbit anti‐Human
Load more

Recommended publications
  • Endothelin System and Therapeutic Application of Endothelin Receptor
    xperim ACCESS Freely available online & E en OPEN l ta a l ic P in h l a C r m f o a c l a o n l o r g u y o J Journal of ISSN: 2161-1459 Clinical & Experimental Pharmacology Research Article Endothelin System and Therapeutic Application of Endothelin Receptor Antagonists Abebe Basazn Mekuria, Zemene Demelash Kifle*, Mohammedbrhan Abdelwuhab Department of Pharmacology, School of Pharmacy, College of Medicine and Health Sciences, University of Gondar, Gondar, Ethiopia ABSTRACT Endothelin is a 21 amino acid molecule endogenous potent vasoconstrictor peptide. Endothelin is synthesized in vascular endothelial and smooth muscle cells, as well as in neural, renal, pulmonic, and inflammatory cells. It acts through a seven transmembrane endothelin receptor A (ETA) and endothelin receptor B (ETB) receptors belongs to G protein-coupled rhodopsin-type receptor superfamily. This peptide involved in pathogenesis of cardiovascular disorder like (heart failure, arterial hypertension, myocardial infraction and atherosclerosis), renal failure, pulmonary arterial hypertension and it also involved in pathogenesis of cancer. Potentially endothelin receptor antagonist helps the treatment of the above disorder. Currently, there are a lot of trails both per-clinical and clinical on endothelin antagonist for various cardiovascular, pulmonary and cancer disorder. Some are approved by FAD for the treatment. These agents are including both selective and non-selective endothelin receptor antagonist (ETA/B). Currently, Bosentan, Ambrisentan, and Macitentan approved
    [Show full text]
  • Dissecting Signaling and Functions of Adhesion G Proteincoupled Receptors
    Ann. N.Y. Acad. Sci. ISSN 0077-8923 ANNALS OF THE NEW YORK ACADEMY OF SCIENCES Issue: Annals Meeting Reports Dissecting signaling and functions of adhesion G protein–coupled receptors Demet Arac¸,1 Gabriela Aust,2 Davide Calebiro,3 Felix B. Engel,4 Caroline Formstone,5 Andre´ Goffinet,6 Jorg¨ Hamann,7 Robert J. Kittel,8 Ines Liebscher,9 Hsi-Hsien Lin,10 Kelly R. Monk,11 Alexander Petrenko,12 Xianhua Piao,13 Simone Promel,¨ 9 HelgiB.Schioth,¨ 14 Thue W. Schwartz,15 Martin Stacey,16 Yuri A. Ushkaryov,17 Manja Wobus,18 Uwe Wolfrum,19 Lei Xu,20 and Tobias Langenhan8 1Stanford University, Stanford, California. 2Department of Surgery, Research Laboratories, University of Leipzig, Leipzig, Germany. 3Institute of Pharmacology and Rudolf Virchow Center, DFG-Research Center for Experimental Biomedicine, University of Wurzburg,¨ Wurzburg,¨ Germany. 4Department of Cardiac Development and Remodelling, Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany, and Laboratory of Experimental Renal and Cardiovascular Research, Department of Nephropathology, Institute of Pathology, University of Erlangen-Nurnberg,¨ Erlangen, Germany. 5MRC Centre for Developmental Neurobiology, King’s College London, New Hunts House, London, United Kingdom. 6Universite´ Catholique de Louvain, Institute of Neuroscience, Developmental Neurobiology, Brussels, Belgium. 7Department of Experimental Immunology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. 8Institute of Physiology, Department of Neurophysiology, University of Wurzburg,¨ Wurzburg,¨ Germany. 9Institute of Biochemistry, Molecular Biochemistry, Medical Faculty, University of Leipzig, Leipzig, Germany. 10Department of Microbiology and Immunology, College of Medicine, Chang Gung University, Tao-Yuan, Taiwan. 11Department of Developmental Biology, Washington University School of Medicine, St. Louis, Missouri. 12Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Moscow, Russia.
    [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]
  • Supplementary Data
    Supplemental Data A novel mouse model of X-linked nephrogenic diabetes insipidus: Phenotypic analysis and therapeutic implications Jian Hua Li, Chung-Lin Chou, Bo Li, Oksana Gavrilova, Christoph Eisner, Jürgen Schnermann, Stasia A. Anderson, Chu-Xia Deng, Mark A. Knepper, and Jürgen Wess Supplemental Methods Metabolic cage studies. Animals were maintained in mouse metabolic cages (Hatteras Instruments, Cary, NC) under controlled temperature and light conditions (12 hr light and dark cycles). Mice received a fixed daily ration of 6.5 g of gelled diet per 20 g of body weight per day. The gelled diet was composed of 4 g of Basal Diet 5755 (Test Diet, Richmond, IN), 2.5 ml of deionized water, and 65 mg agar. Preweighted drinking water was provided ad libitum during the course of the study. Mice were acclimated in the metabolic cages for 1-2 days. Urine was collected under mineral oil in preweighted collection vials for successive 24 hr periods. Analysis of GPCR expression in mouse IMCD cells via TaqMan real-time qRT-PCR. Total RNA prepared from mouse IMCD tubule suspensions was reverse transcribed as described under Experimental Procedures. Tissues from ten 10-week old C57BL/6 WT mice were collected and pooled for each individual experiment. cDNA derived from 640 ng of RNA was mixed with an equal volume of TaqMan gene expression 2 x master mix (Applied Biosystems, Foster City, CA). 100 μl-aliquots of this mixture (corresponding to 80 ng of RNA) were added to each of the 8 fill ports of a 384-well plate of a mouse GPCR array panel (Applied Biosystems).
    [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]
  • Gpcrs Show Widespread Differential Mrna Expression and Frequent Mutation and Copy Number Variation in Solid Tumors
    bioRxiv preprint doi: https://doi.org/10.1101/546481; this version posted February 11, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-ND 4.0 International license. GPCRs show widespread differential mRNA expression and frequent mutation and copy number variation in solid tumors Krishna Sriram1, Kevin Moyung1, Ross Corriden1, Hannah Carter2, Paul A. Insel1, 2 * Departments of Pharmacology1 and Medicine2 University of California, San Diego *: Corresponding Author Contact Information: Email: [email protected] Phone: 858 534 2298 Mailing Address: 9500 Gilman Drive, BSB 3076, Mail Code 0636 La Jolla, CA, 92093 Abstract: G protein-coupled receptors (GPCRs) are the most widely targeted gene family for FDA-approved drugs. To assess possible roles for GPCRs in cancer, we analyzed Cancer Genome Atlas data for mRNA expression, mutations, and copy number variation (CNV) in 20 categories/45 sub-types of solid tumors and quantified differential expression of GPCRs by comparing tumors against normal tissue from the GTEx database. GPCRs are over-represented among coding genes with elevated expression in solid tumors; most tumor types differentially express >50 GPCRs, including many targets for approved drugs, hitherto largely unrecognized as targets of interest in cancer. GPCR mRNA signatures characterize specific tumor types, indicate survival and correlate with expression of cancer-related pathways. Tumor GPCR mRNA signatures have prognostic relevance for survival and correlate with expression of numerous cancer-related genes and pathways. GPCR expression in tumors is largely independent of staging/grading/metastasis/driver mutations and GPCRs expressed in cancer cell lines parallels that measured in tumors.
    [Show full text]
  • GPCR/G Protein
    Inhibitors, Agonists, Screening Libraries www.MedChemExpress.com GPCR/G Protein G Protein Coupled Receptors (GPCRs) perceive many extracellular signals and transduce them to heterotrimeric G proteins, which further transduce these signals intracellular to appropriate downstream effectors and thereby play an important role in various signaling pathways. G proteins are specialized proteins with the ability to bind the nucleotides guanosine triphosphate (GTP) and guanosine diphosphate (GDP). In unstimulated cells, the state of G alpha is defined by its interaction with GDP, G beta-gamma, and a GPCR. Upon receptor stimulation by a ligand, G alpha dissociates from the receptor and G beta-gamma, and GTP is exchanged for the bound GDP, which leads to G alpha activation. G alpha then goes on to activate other molecules in the cell. These effects include activating the MAPK and PI3K pathways, as well as inhibition of the Na+/H+ exchanger in the plasma membrane, and the lowering of intracellular Ca2+ levels. Most human GPCRs can be grouped into five main families named; Glutamate, Rhodopsin, Adhesion, Frizzled/Taste2, and Secretin, forming the GRAFS classification system. A series of studies showed that aberrant GPCR Signaling including those for GPCR-PCa, PSGR2, CaSR, GPR30, and GPR39 are associated with tumorigenesis or metastasis, thus interfering with these receptors and their downstream targets might provide an opportunity for the development of new strategies for cancer diagnosis, prevention and treatment. At present, modulators of GPCRs form a key area for the pharmaceutical industry, representing approximately 27% of all FDA-approved drugs. References: [1] Moreira IS. Biochim Biophys Acta. 2014 Jan;1840(1):16-33.
    [Show full text]
  • Peripheral Regulation of Pain and Itch
    Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine 1596 Peripheral Regulation of Pain and Itch ELÍN INGIBJÖRG MAGNÚSDÓTTIR ACTA UNIVERSITATIS UPSALIENSIS ISSN 1651-6206 ISBN 978-91-513-0746-6 UPPSALA urn:nbn:se:uu:diva-392709 2019 Dissertation presented at Uppsala University to be publicly examined in A1:107a, BMC, Husargatan 3, Uppsala, Friday, 25 October 2019 at 13:00 for the degree of Doctor of Philosophy (Faculty of Medicine). The examination will be conducted in English. Faculty examiner: Professor emeritus George H. Caughey (University of California, San Francisco). Abstract Magnúsdóttir, E. I. 2019. Peripheral Regulation of Pain and Itch. Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine 1596. 71 pp. Uppsala: Acta Universitatis Upsaliensis. ISBN 978-91-513-0746-6. Pain and itch are diverse sensory modalities, transmitted by the somatosensory nervous system. Stimuli such as heat, cold, mechanical pain and itch can be transmitted by different neuronal populations, which show considerable overlap with regards to sensory activation. Moreover, the immune and nervous systems can be involved in extensive crosstalk in the periphery when reacting to these stimuli. With recent advances in genetic engineering, we now have the possibility to study the contribution of distinct neuron types, neurotransmitters and other mediators in vivo by using gene knock-out mice. The neuropeptide calcitonin gene-related peptide (CGRP) and the ion channel transient receptor potential cation channel subfamily V member 1 (TRPV1) have both been implicated in pain and itch transmission. In Paper I, the Cre- LoxP system was used to specifically remove CGRPα from the primary afferent population that expresses TRPV1.
    [Show full text]
  • Single Cell Derived Clonal Analysis of Human Glioblastoma Links
    SUPPLEMENTARY INFORMATION: Single cell derived clonal analysis of human glioblastoma links functional and genomic heterogeneity ! Mona Meyer*, Jüri Reimand*, Xiaoyang Lan, Renee Head, Xueming Zhu, Michelle Kushida, Jane Bayani, Jessica C. Pressey, Anath Lionel, Ian D. Clarke, Michael Cusimano, Jeremy Squire, Stephen Scherer, Mark Bernstein, Melanie A. Woodin, Gary D. Bader**, and Peter B. Dirks**! ! * These authors contributed equally to this work.! ** Correspondence: [email protected] or [email protected]! ! Supplementary information - Meyer, Reimand et al. Supplementary methods" 4" Patient samples and fluorescence activated cell sorting (FACS)! 4! Differentiation! 4! Immunocytochemistry and EdU Imaging! 4! Proliferation! 5! Western blotting ! 5! Temozolomide treatment! 5! NCI drug library screen! 6! Orthotopic injections! 6! Immunohistochemistry on tumor sections! 6! Promoter methylation of MGMT! 6! Fluorescence in situ Hybridization (FISH)! 7! SNP6 microarray analysis and genome segmentation! 7! Calling copy number alterations! 8! Mapping altered genome segments to genes! 8! Recurrently altered genes with clonal variability! 9! Global analyses of copy number alterations! 9! Phylogenetic analysis of copy number alterations! 10! Microarray analysis! 10! Gene expression differences of TMZ resistant and sensitive clones of GBM-482! 10! Reverse transcription-PCR analyses! 11! Tumor subtype analysis of TMZ-sensitive and resistant clones! 11! Pathway analysis of gene expression in the TMZ-sensitive clone of GBM-482! 11! Supplementary figures and tables" 13" "2 Supplementary information - Meyer, Reimand et al. Table S1: Individual clones from all patient tumors are tumorigenic. ! 14! Fig. S1: clonal tumorigenicity.! 15! Fig. S2: clonal heterogeneity of EGFR and PTEN expression.! 20! Fig. S3: clonal heterogeneity of proliferation.! 21! Fig.
    [Show full text]
  • Supplementary Table 1
    Supplementary Table 1. 492 genes are unique to 0 h post-heat timepoint. The name, p-value, fold change, location and family of each gene are indicated. Genes were filtered for an absolute value log2 ration 1.5 and a significance value of p ≤ 0.05. Symbol p-value Log Gene Name Location Family Ratio ABCA13 1.87E-02 3.292 ATP-binding cassette, sub-family unknown transporter A (ABC1), member 13 ABCB1 1.93E-02 −1.819 ATP-binding cassette, sub-family Plasma transporter B (MDR/TAP), member 1 Membrane ABCC3 2.83E-02 2.016 ATP-binding cassette, sub-family Plasma transporter C (CFTR/MRP), member 3 Membrane ABHD6 7.79E-03 −2.717 abhydrolase domain containing 6 Cytoplasm enzyme ACAT1 4.10E-02 3.009 acetyl-CoA acetyltransferase 1 Cytoplasm enzyme ACBD4 2.66E-03 1.722 acyl-CoA binding domain unknown other containing 4 ACSL5 1.86E-02 −2.876 acyl-CoA synthetase long-chain Cytoplasm enzyme family member 5 ADAM23 3.33E-02 −3.008 ADAM metallopeptidase domain Plasma peptidase 23 Membrane ADAM29 5.58E-03 3.463 ADAM metallopeptidase domain Plasma peptidase 29 Membrane ADAMTS17 2.67E-04 3.051 ADAM metallopeptidase with Extracellular other thrombospondin type 1 motif, 17 Space ADCYAP1R1 1.20E-02 1.848 adenylate cyclase activating Plasma G-protein polypeptide 1 (pituitary) receptor Membrane coupled type I receptor ADH6 (includes 4.02E-02 −1.845 alcohol dehydrogenase 6 (class Cytoplasm enzyme EG:130) V) AHSA2 1.54E-04 −1.6 AHA1, activator of heat shock unknown other 90kDa protein ATPase homolog 2 (yeast) AK5 3.32E-02 1.658 adenylate kinase 5 Cytoplasm kinase AK7
    [Show full text]
  • GPCR Expression Profiles Were Determined Using
    Supplemental Figures and Tables for Tischner et al., 2017 Supplemental Figure 1: GPCR expression profiles were determined using the NanoString nCounter System in 250 ng of pooled cell RNA obtained from freshly isolated CD4 T cells from naïve lymph nodes (CD4ln), spinal cord infiltrating CD4 T cells at peak EAE disease (CD4sc), and primary lung endothelial cells (luEC). Supplemental Figure 2: Array design and quality controls. A, Sorted leukocytes or endothelial cells were subjected to single‐cell expression analysis and re‐evaluated based on the expression of various identity‐defining genes. B, Expression of identity‐defining and quality control genes after deletion of contaminating or reference gene‐negative cells. Expression data are calculated as 2(Limit of detection(LoD) Ct – sample Ct) ; LoD Ct was set to 24. Supplemental Figure 3: Overview over GPCR expression frequencies in different freshly isolated immune cell populations and spinal cord endothelial cells as determined by single cell RT‐PCR. Abbreviations: CD4ln‐Tcon/CD4ln‐Treg, conventional (con) and regulatory (reg) CD4 T cells from lymph nodes (CD4ln) of naïve mice; CD4dr/CD4sc, CD4 T cells from draining lymph nodes (dr) or spinal cord (sc) at peak EAE disease; CD4spn2D/ CD4spn2DTh1/ CD4spn2DTh17, splenic CD4 T cells from 2D2 T cell receptor transgenic mice before (2D) and after in vitro differentiation towards Th1 (2DTh1) or Th17 (2DTh17); MonoSpn, splenic monocytes; CD11b_sc, spinal cord infiltrating CD11b‐ positive cells; sc_microglia, Ccr2neg,Cx3cr1pos microglia from spinal cord at peak disease; sc_macrophages, CCr2pos;Cx3cr1lo/neg macrophages from spinal cord at peak disease; BMDM_M1/BMDM_M2, bone marrow‐derived macrophages differentiated towards M1 or M2; ECscN and ECscEAE, spinal cord endothelial cells from naïve mice (N) and at peak EAE disease (EAE); SMC, smooth muscle cells from various vessel types (included as positive control to ascertain primer functionality).
    [Show full text]
  • G Protein-Coupled Receptors at the Crossroad Between Physiologic
    G protein-coupled receptors at the crossroad between physiologic and pathologic angiogenesis : old paradigms and emerging concepts De Francesco, EM, Sotgia, F, Clarke, RB, Lisanti, MP and Maggiolini, M http://dx.doi.org/10.3390/ijms18122713 Title G protein-coupled receptors at the crossroad between physiologic and pathologic angiogenesis : old paradigms and emerging concepts Authors De Francesco, EM, Sotgia, F, Clarke, RB, Lisanti, MP and Maggiolini, M Type Article URL This version is available at: http://usir.salford.ac.uk/id/eprint/44805/ Published Date 2017 USIR is a digital collection of the research output of the University of Salford. Where copyright permits, full text material held in the repository is made freely available online and can be read, downloaded and copied for non-commercial private study or research purposes. Please check the manuscript for any further copyright restrictions. For more information, including our policy and submission procedure, please contact the Repository Team at: [email protected]. International Journal of Molecular Sciences Review G Protein-Coupled Receptors at the Crossroad between Physiologic and Pathologic Angiogenesis: Old Paradigms and Emerging Concepts Ernestina M. De Francesco 1,2, Federica Sotgia 3, Robert B. Clarke 2, Michael P. Lisanti 3 and Marcello Maggiolini 1,* ID 1 Department of Pharmacy, Health and Nutrition Sciences, University of Calabria via Savinio, 87036 Rende, Italy; [email protected] 2 Breast Cancer Now Research Unit, Division of Cancer Sciences, Manchester
    [Show full text]