DOCSLIB.ORG

Vascular Endothelial Growth Factor Receptor 2

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Vascular Endothelial Growth Factor Receptor 2 Volume 1 - Number 1 May - September 1997 Volume 20 - Number 7 July 2016 Atlas of Genetics and Cytogenetics in Oncology and Haematology OPEN ACCESS JOURNAL INIST-CNRS Scope The Atlas of Genetics and Cytogenetics in Oncology and Haematology is a peer reviewed on-line journal in open access, devoted to genes, cytogenetics, and clinical entities in cancer, and cancer-prone diseases. It is made for and by: clinicians and researchers in cytogenetics, molecular biology, oncology, haematology, and pathology. One main scope of the Atlas is to conjugate the scientific information provided by cytogenetics/molecular genetics to the clinical setting (diagnostics, prognostics and therapeutic design), another is to provide an encyclopedic knowledge in cancer genetics. The Atlas deals with cancer research and genomics. It is at the crossroads of research, virtual medical university (university and post-university e-learning), and telemedicine. It contributes to "meta-medicine", this mediation, using information technology, between the increasing amount of knowledge and the individual, having to use the information. Towards a personalized medicine of cancer. It presents structured review articles ("cards") on: 1- Genes, 2- Leukemias, 3- Solid tumors, 4- Cancer-prone diseases, and also 5- "Deep insights": more traditional review articles on the above subjects and on surrounding topics. It also present 6- Case reports in hematology and 7- Educational items in the various related topics for students in Medicine and in Sciences. The Atlas of Genetics and Cytogenetics in Oncology and Haematology does not publish research articles. See also: http://documents.irevues.inist.fr/bitstream/handle/2042/56067/Scope.pdf Editorial correspondance Jean-Loup Huret, MD, PhD, Genetics, Department of Medical Information, University Hospital F-86021 Poitiers, France phone +33 5 49 44 45 46 [email protected] or [email protected] . Editor, Editorial Board and Publisher See:http://documents.irevues.inist.fr/bitstream/handle/2042/48485/Editor-editorial-board-and-publisher.pdf The Atlas of Genetics and Cytogenetics in Oncology and Haematology is published 12 times a year by ARMGHM, a non profit organisation, and by the INstitute for Scientific and Technical Information of the French National Center for Scientific Research (INIST-CNRS) since 2008. The Atlas is hosted by INIST-CNRS (http://www.inist.fr) Staff: Vanessa Le Berre Philippe Dessen is the Database Directorof the on-line version (Gustave Roussy Institute – Villejuif – France). Publisher Contact: INIST-CNRS Mailing Address: Catherine Morel, 2,Allée du Parc de Brabois, CS 10130, 54519 Vandoeuvre-lès-Nancy France. Email Address:[email protected] Articles of the ATLAS are free in PDF format, and metadata are available on the web in Dublin Core XML format and freely harvestable.A Digital object identifier (DOI®), recorded at the International Agency CrossRefhttp://www.crossref.org/ is assigned to each article. http://AtlasGeneticsOncology.org © ATLAS - ISSN 1768-3262 The PDF version of the Atlas of Genetics and Cytogenetics in Oncology and Haematology is a reissue of the original articles published in collaboration with the Institute for Scientific and Technical Information (INstitut de l’Information Scientifique et Technique - INIST) of the French National Center for Scientific Research (CNRS) on its electronic publishing platform I-Revues. Online and PDF versions of the Atlas of Genetics and Cytogenetics in Oncology and Haematology are hosted by INIST-CNRS. Atlas of Genetics and Cytogenetics in Oncology and Haematology OPEN ACCESS JOURNAL INIST-CNRS Editor-in-Chief Jean-Loup Huret (Poitiers, France) Lymphomas Section Editor Antonino Carbone (Aviano, Italy) Myeloid Malignancies Section Editor Robert S. Ohgami (Stanford, California) Bone Tumors Section Editor Judith Bovee (Leiden, Netherlands) Head and Neck Tumors Section Editors Cécile Badoual and Hélène Blons (Paris, France) Urinary Tumors Section Editor Paola Dal Cin (Boston, Massachusetts) Pediatric Tumors Section Editor Frederic G. Barr (Bethesda, Maryland) Cancer Prone Diseases Section Editor Gaia Roversi (Milano, Italy) Cell Cycle Section Editor João Agostinho Machado-Neto (São Paulo, Brazil) DNA Repair Section Editor Godefridus Peters (Amsterdam, Netherlands) Hormones and Growth factors Section Editor Gajanan V. Sherbet (Newcastle upon Tyne, UK) Mitosis Section Editor Patrizia Lavia (Rome, Italy) WNT pathway Section Editor Alessandro Beghini (Milano, Italy) Board Members Sreeparna Department of Biological Sciences, Middle East Technical University, Ankara, Turkey; [email protected] Banerjee Alessandro Department of Health Sciences, University of Milan, Italy; [email protected] Beghini Judith Bovée 2300 RC Leiden, The Netherlands; [email protected] Dipartimento di ScienzeMediche, Sezione di Ematologia e Reumatologia Via Aldo Moro 8, 44124 - Ferrara, Italy; Antonio Cuneo [email protected] Paola Dal Cin Department of Pathology, Brigham, Women's Hospital, 75 Francis Street, Boston, MA 02115, USA; [email protected] François IRBA, Departement Effets Biologiques des Rayonnements, Laboratoire de Dosimetrie Biologique des Irradiations, Dewoitine C212, Desangles 91223 Bretigny-sur-Orge, France; [email protected] Molecular and Population Genetics Laboratory, Wellcome Trust Centre for Human Genetics, Roosevelt Dr. Oxford, OX37BN, UK Enric Domingo [email protected] Ayse Elif Erson- Department of Biological Sciences, Middle East Technical University, Ankara, Turkey; [email protected] Bensan Ad Geurts van Department of Human Genetics, Radboud University Medical Center, Radboud Institute for Molecular Life Sciences, 6500 HB Kessel Nijmegen, The Netherlands; [email protected] Department of Pediatrics and Adolescent Medicine, St. Anna Children's Hospital, Medical University Vienna, Children's Cancer Oskar A. Haas Research Institute Vienna, Vienna, Austria. [email protected] Anne Hagemeijer Center for Human Genetics, University Hospital Leuven and KU Leuven, Leuven, Belgium; [email protected] Department of Pathology, The Ohio State University, 129 Hamilton Hall, 1645 Neil Ave, Columbus, OH 43210, USA; Nyla Heerema [email protected] Sakari Knuutila Hartmann Institute and HUSLab, University of Helsinki, Department of Pathology, Helsinki, Finland; [email protected] Lidia Larizza Lab Centro di Ricerche e TecnologieBiomedicheIRCCS-IstitutoAuxologico Italiano Milano, Italy; l.larizza@auxologico Department of Human, Animal Cell Lines, Leibniz-Institute DSMZ-German Collection of Microorganisms, Cell Cultures, Roderick Mc Leod Braunschweig, Germany; [email protected] Cristina Mecucci Hematology University of Perugia, University Hospital S.Mariadella Misericordia, Perugia, Italy; [email protected] Department of Clinical Genetics, University and Regional Laboratories, Lund University, SE-221 85 Lund, Sweden; Fredrik Mertens [email protected] Konstantin Miller Institute of Human Genetics, Hannover Medical School, 30623 Hannover, Germany; [email protected] Department of Clinical Genetics, University and Regional Laboratories, Lund University, SE-221 85 Lund, Sweden; Felix Mitelman [email protected] Hossain Mossafa Laboratoire CERBA, 95066 Cergy-Pontoise cedex 9, France; [email protected] Department of Human, Animal Cell Lines, Leibniz-Institute DSMZ-German Collection of Microorganisms, Cell Cultures, Stefan Nagel Braunschweig, Germany; [email protected] Florence Laboratory of Solid Tumors Genetics, Nice University Hospital, CNRSUMR 7284/INSERMU1081, France; Pedeutour [email protected] Department of Pathology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Mail Stop 250, Memphis, Tennessee Susana Raimondi 38105-3678, USA; [email protected] Clelia Tiziana Department of Biology, University of Bari, Bari, Italy; [email protected] Storlazzi Sabine Strehl CCRI, Children's Cancer Research Institute, St. Anna Kinderkrebsforschunge.V., Vienna, Austria; [email protected] Nancy Uhrhammer Laboratoire Diagnostic Génétique et Moléculaire, Centre Jean Perrin, Clermont-Ferrand, France; [email protected] Dan L. Van Dyke Mayo Clinic Cytogenetics Laboratory, 200 First St SW, Rochester MN 55905, USA; [email protected] Universita di Cagliari, Dipartimento di ScienzeBiomediche(DiSB), CittadellaUniversitaria, 09042 Monserrato (CA) - Italy; Roberta Vanni [email protected] Service d'Histologie-Embryologie-Cytogénétique, Unité de Cytogénétique Onco-Hématologique, Hôpital Universitaire Necker-Enfants Franck Viguié Malades, 75015 Paris, France; [email protected] Atlas Genet Cytogenet Oncol Haematol. 2016; 20(7) Atlas of Genetics and Cytogenetics in Oncology and Haematology OPEN ACCESS JOURNAL INIST-CNRS Volume 20, Number 7, July 2016 Table of contents Gene Section PIP4K2A (phosphatidylinositol-5-phosphate 4-kinase, type II, alpha) 380 Keli Lima, João Agostinho Machado-Neto ZAP70 (zeta-chain (TCR) associated protein kinase 70kDa) 385 Payam Delfani, Zahra El-Schich and Anette Gjörloff Wingren KDR (kinase insert domain receptor)/Vascular Endothelial Growth Factor Receptor 2 (VEGFR2) 392 Noah Sorrelle, Rolf Brekken HMGA2 (high mobility group AT-hook 2) 403 Jian-Jun Wei NDRG1 (N-myc downstream regulated 1) 413 Maria A Nagai, Flavia R Mangone CYB5A (Cytochrome B5 Type A (microsomal)) 421 Valentina E Gomez, Amir Avan, Godefridus J Peters, Elisa Giovannetti Leukaemia Section der(20)t(1;20)(q10-21;q11-13)
Load more

Recommended publications
  • Protein Identities in Evs Isolated from U87-MG GBM Cells As Determined by NG LC-MS/MS
    Protein identities in EVs isolated from U87-MG GBM cells as determined by NG LC-MS/MS. No. Accession Description Σ Coverage Σ# Proteins Σ# Unique Peptides Σ# Peptides Σ# PSMs # AAs MW [kDa] calc. pI 1 A8MS94 Putative golgin subfamily A member 2-like protein 5 OS=Homo sapiens PE=5 SV=2 - [GG2L5_HUMAN] 100 1 1 7 88 110 12,03704523 5,681152344 2 P60660 Myosin light polypeptide 6 OS=Homo sapiens GN=MYL6 PE=1 SV=2 - [MYL6_HUMAN] 100 3 5 17 173 151 16,91913397 4,652832031 3 Q6ZYL4 General transcription factor IIH subunit 5 OS=Homo sapiens GN=GTF2H5 PE=1 SV=1 - [TF2H5_HUMAN] 98,59 1 1 4 13 71 8,048185945 4,652832031 4 P60709 Actin, cytoplasmic 1 OS=Homo sapiens GN=ACTB PE=1 SV=1 - [ACTB_HUMAN] 97,6 5 5 35 917 375 41,70973209 5,478027344 5 P13489 Ribonuclease inhibitor OS=Homo sapiens GN=RNH1 PE=1 SV=2 - [RINI_HUMAN] 96,75 1 12 37 173 461 49,94108966 4,817871094 6 P09382 Galectin-1 OS=Homo sapiens GN=LGALS1 PE=1 SV=2 - [LEG1_HUMAN] 96,3 1 7 14 283 135 14,70620005 5,503417969 7 P60174 Triosephosphate isomerase OS=Homo sapiens GN=TPI1 PE=1 SV=3 - [TPIS_HUMAN] 95,1 3 16 25 375 286 30,77169764 5,922363281 8 P04406 Glyceraldehyde-3-phosphate dehydrogenase OS=Homo sapiens GN=GAPDH PE=1 SV=3 - [G3P_HUMAN] 94,63 2 13 31 509 335 36,03039959 8,455566406 9 Q15185 Prostaglandin E synthase 3 OS=Homo sapiens GN=PTGES3 PE=1 SV=1 - [TEBP_HUMAN] 93,13 1 5 12 74 160 18,68541938 4,538574219 10 P09417 Dihydropteridine reductase OS=Homo sapiens GN=QDPR PE=1 SV=2 - [DHPR_HUMAN] 93,03 1 1 17 69 244 25,77302971 7,371582031 11 P01911 HLA class II histocompatibility antigen,
    [Show full text]
  • Inhibiting TG2 Sensitizes Lung Cancer to Radiotherapy Through Interfering
    bioRxiv preprint doi: https://doi.org/10.1101/597112; this version posted April 6, 2019. 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 Title page 2 3 Inhibiting TG2 sensitizes lung cancer to radiotherapy through interfering 4 TOPOIIα-mediated DNA repair 5 6 Xiao Lei#, Zhe Liu#, Kun Cao#, Yuanyuan Chen#, Jianming Cai, Fu Gao*, Yanyong 7 Yang* 8 9 #Authors contributed equally to this work. 10 11 Department of Radiation Medicine, Faculty of Naval Medicine, Second Military 12 Medical University, 800, Xiangyin Road, 200433, Shanghai, P.R. China; 13 14 *Corresponding author: Yanyong Yang, Fu Gao and Jianming Cai. 15 Address: Department of Radiation Medicine, Faculty of Naval Medicine, Second 16 Military Medical University; 800, Xiangyin Road, 200433, Shanghai, P.R. China. Fax: 17 +86-21-81871148. E-mail: [email protected], [email protected], 18 [email protected]; 19 20 Running title: Targeting TG2 sensitizes lung cancer to radiotherapy 21 22 Keywords: TG2, Radiosensitization, TOPOIIα, NSCLC, DNA repair 23 24 Conflicts of interest 25 The authors have no conflicts of interest to disclose. 26 1 bioRxiv preprint doi: https://doi.org/10.1101/597112; this version posted April 6, 2019. 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. 27 Abstract 28 Radiotherapy is an indispensable strategy for lung cancer, however, treatment failure 29 or reoccurrence is often found in patients due to the developing radioresistance.
    [Show full text]
  • Supplementary Material Computational Prediction of SARS
    Supplementary_Material Computational prediction of SARS-CoV-2 encoded miRNAs and their putative host targets Sheet_1 List of potential stem-loop structures in SARS-CoV-2 genome as predicted by VMir. Rank Name Start Apex Size Score Window Count (Absolute) Direct Orientation 1 MD13 2801 2864 125 243.8 61 2 MD62 11234 11286 101 211.4 49 4 MD136 27666 27721 104 205.6 119 5 MD108 21131 21184 110 204.7 210 9 MD132 26743 26801 119 188.9 252 19 MD56 9797 9858 128 179.1 59 26 MD139 28196 28233 72 170.4 133 28 MD16 2934 2974 76 169.9 71 43 MD103 20002 20042 80 159.3 403 46 MD6 1489 1531 86 156.7 171 51 MD17 2981 3047 131 152.8 38 87 MD4 651 692 75 140.3 46 95 MD7 1810 1872 121 137.4 58 116 MD140 28217 28252 72 133.8 62 122 MD55 9712 9758 96 132.5 49 135 MD70 13171 13219 93 130.2 131 164 MD95 18782 18820 79 124.7 184 173 MD121 24086 24135 99 123.1 45 176 MD96 19046 19086 75 123.1 179 196 MD19 3197 3236 76 120.4 49 200 MD86 17048 17083 73 119.8 428 223 MD75 14534 14600 137 117 51 228 MD50 8824 8870 94 115.8 79 234 MD129 25598 25642 89 115.6 354 Reverse Orientation 6 MR61 19088 19132 88 197.8 271 10 MR72 23563 23636 148 188.8 286 11 MR11 3775 3844 136 185.1 116 12 MR94 29532 29582 94 184.6 271 15 MR43 14973 15028 109 183.9 226 27 MR14 4160 4206 89 170 241 34 MR35 11734 11792 111 164.2 37 52 MR5 1603 1652 89 152.7 118 53 MR57 18089 18132 101 152.7 139 94 MR8 2804 2864 122 137.4 38 107 MR58 18474 18508 72 134.9 237 117 MR16 4506 4540 72 133.8 311 120 MR34 10010 10048 82 132.7 245 133 MR7 2534 2578 90 130.4 75 146 MR79 24766 24808 75 127.9 59 150 MR65 21528 21576 99 127.4 83 180 MR60 19016 19049 70 122.5 72 187 MR51 16450 16482 75 121 363 190 MR80 25687 25734 96 120.6 75 198 MR64 21507 21544 70 120.3 35 206 MR41 14500 14542 84 119.2 94 218 MR84 26840 26894 108 117.6 94 Sheet_2 List of stable stem-loop structures based on MFE.
    [Show full text]
  • Oviductal Response to Gametes and Early Embryos in Mammals
    REPRODUCTIONREVIEW Oviductal response to gametes and early embryos in mammals Veronica Maillo1, Maria Jesus Sánchez-Calabuig1, Ricaurte Lopera-Vasquez1, Meriem Hamdi1, Alfonso Gutierrez-Adan1, Patrick Lonergan2 and Dimitrios Rizos1 1Departamento de Reproducción Animal, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria (INIA), Madrid, Spain and 2School of Agriculture and Food Science, University College Dublin, Belfield, Dublin 4, Ireland Correspondence should be addressed to D Rizos; Email: [email protected] Abstract The oviduct is a complex and organized thin tubular structure connecting the ovary with the uterus. It is the site of final sperm capacitation, oocyte fertilization and, in most species, the first 3–4 days of early embryo development. The oviductal epithelium is made up of ciliary and secretory cells responsible for the secretion of proteins and other factors which contribute to the formation of the oviductal fluid. Despite significant research, most of the pathways and oviductal factors implicated in the crosstalk between gametes/early embryo and the oviduct remain unknown. Therefore, studying the oviductal environment is crucial to improve our understanding of the regulatory mechanisms controlling fertilization and embryo development. In vitro systems are a valuable tool to study in vivo pathways and mechanisms, particularly those in the oviducts which in livestock species are challenging to access. In studies of gamete and embryo interaction with the reproductive tract, oviductal epithelial cells, oviductal fluid and microvesicles co-cultured with gametes/embryos represent the most appropriate in vitro models to mimic the physiological conditions in vivo. Reproduction (2016) 152 R127–R141 Introduction Despite significant research, most of the pathways and oviductal factors implicated in the crosstalk between The oviducts (or fallopian tubes, uterine tubes) the gametes/early embryo(s) and the oviduct remain were described for the first time by the 16th century unknown.
    [Show full text]
  • Characterizing Genomic Duplication in Autism Spectrum Disorder by Edward James Higginbotham a Thesis Submitted in Conformity
    Characterizing Genomic Duplication in Autism Spectrum Disorder by Edward James Higginbotham A thesis submitted in conformity with the requirements for the degree of Master of Science Graduate Department of Molecular Genetics University of Toronto © Copyright by Edward James Higginbotham 2020 i Abstract Characterizing Genomic Duplication in Autism Spectrum Disorder Edward James Higginbotham Master of Science Graduate Department of Molecular Genetics University of Toronto 2020 Duplication, the gain of additional copies of genomic material relative to its ancestral diploid state is yet to achieve full appreciation for its role in human traits and disease. Challenges include accurately genotyping, annotating, and characterizing the properties of duplications, and resolving duplication mechanisms. Whole genome sequencing, in principle, should enable accurate detection of duplications in a single experiment. This thesis makes use of the technology to catalogue disease relevant duplications in the genomes of 2,739 individuals with Autism Spectrum Disorder (ASD) who enrolled in the Autism Speaks MSSNG Project. Fine-mapping the breakpoint junctions of 259 ASD-relevant duplications identified 34 (13.1%) variants with complex genomic structures as well as tandem (193/259, 74.5%) and NAHR- mediated (6/259, 2.3%) duplications. As whole genome sequencing-based studies expand in scale and reach, a continued focus on generating high-quality, standardized duplication data will be prerequisite to addressing their associated biological mechanisms. ii Acknowledgements I thank Dr. Stephen Scherer for his leadership par excellence, his generosity, and for giving me a chance. I am grateful for his investment and the opportunities afforded me, from which I have learned and benefited. I would next thank Drs.
    [Show full text]
  • Gene Section Review
    Atlas of Genetics and Cytogenetics in Oncology and Haematology OPEN ACCESS JOURNAL INIST-CNRS Gene Section Review CYB5A (Cytochrome B5 Type A (microsomal)) Valentina E Gomez, Amir Avan, Godefridus J Peters, Elisa Giovannetti Department of Medical Oncology, VU University Medical Center, Amsterdam, De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands.(VEG, GJP, EG) [email protected]; [email protected]; Molecular Medicine group, Department of Modern Sciences and Technologies, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran (AA) [email protected]; Cancer Pharmacology Lab, AIRC Start-Up Unit, University of Pisa, Pisa , Italy (EG) [email protected] Published in Atlas Database: November 2015 Online updated version : http://AtlasGeneticsOncology.org/Genes/CYB5AID53723ch18q22.html Printable original version : http://documents.irevues.inist.fr/bitstream/handle/2042/66058/11-2015-CYB5AID53723ch18q22.pdf DOI: 10.4267/2042/66058 This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 2.0 France Licence. © 2016 Atlas of Genetics and Cytogenetics in Oncology and Haematology -FAUP1 (FBR-MuSV-Associated Ubiquitously Abstract Expressed (fox derived) Pseudogene 1; 18q22.3 Review on Cytochrome B5 Type A, with data on DNA/RNA DNA/RNA, on the protein encoded and the diseases in which the gene has been implicated. Description The CYB5A gene is situated on chromosome 18, Identity starting from 74250847 and ending at 74292016 bp. The gene encodes a membrane-bound cytochrome Other names: MCB5, CYB5 protein. HGNC (Hugo): CYB5A Transcription Location: 18q22.3 For this gene, seven alternatively spliced transcript Local order variants have been identified (CYB5A-001, -002, - Based on MapViewer, genes flanking are: 003, -004, -005, -006 and -007).
    [Show full text]
  • Supplementary Figures and Tables 1 2 3 Time Course
    1 Supplementary Figures and Tables 2 3 for manuscript: 4 Time course analysis of the brain transcriptome during transitions between brood care and 5 reproduction in the clonal raider ant 6 Romain Libbrecht*1,2, Peter R. Oxley*1,3, Daniel J. C. Kronauer1 7 *co-first authors 8 1 Laboratory of Social Evolution and Behavior, The Rockefeller University, 1230 York Avenue, New York, 9 NY 10065, USA 10 2 Institute of Organismic and Molecular Evolution, Johannes Gutenberg University, Johannes-von-Müller- 11 Weg 6, 55128 Mainz, Germany 12 3 Samuel J. Wood Library, Weill Cornell Medicine, 1300 York Avenue, New York, NY 10065, USA 13 Correspondence: [email protected] 14 [email protected] 15 A B C 1.5 RC12 Number of genes with more 0.0 than 2-fold change in expression RC06 RC12 RB12 BR96 RB06 BC06 RB24 BR06 RC06 12- through 96-hour time points RB48 RB06 BR96 BC06 RB96 BR12 BR48 BC12 564 BC12 BR06 BR24 BR12 BR48 RB96 BR24 RB12 RB24 18 RB48 16 34 6-hour BR 0 1 4 6-hour RB 16 RC12 BR96 BC06 BR06 RC06 RB06 RB96 BC12 BR12 BR48 BR24 RB12 RB24 RB48 17 Supplementary Figure 1 18 Outlier analysis. PCA and distance map of genes showing greater than 2-fold change in 19 expression. A) PCA plot of brood-swap and control samples. Clustering was based on the mean 20 gene expression of each group, for 967 genes with more than 2-fold change in expression 21 between samples. Percentages on each axis indicate the proportion of variance explained by 22 the indicated principal component.
    [Show full text]
  • PRODUCT SPECIFICATION Product Datasheet
    Product Datasheet QPrEST PRODUCT SPECIFICATION Product Name QPrEST CR063 Mass Spectrometry Protein Standard Product Number QPrEST28820 Protein Name Uncharacterized protein C18orf63 Uniprot ID Q68DL7 Gene C18orf63 Product Description Stable isotope-labeled standard for absolute protein quantification of Uncharacterized protein C18orf63. Lys (13C and 15N) and Arg (13C and 15N) metabolically labeled recombinant human protein fragment. Application Absolute protein quantification using mass spectrometry Sequence (excluding KLPHICGFPIKMTSKPCYYTQELTKPNIQEHKVKPPNLTTKKMLRASLTQ fusion tag) ATSRKPACAQSLLPCSVAVDHKVELSVSQPTSGIFSALHLQP Theoretical MW 27984 Da including N-terminal His6ABP fusion tag Fusion Tag A purification and quantification tag (QTag) consisting of a hexahistidine sequence followed by an Albumin Binding Protein (ABP) domain derived from Streptococcal Protein G. Expression Host Escherichia coli LysA ArgA BL21(DE3) Purification IMAC purification Purity >90% as determined by Bioanalyzer Protein 230 Purity Assay Isotopic Incorporation >99% Concentration >5 μM after reconstitution in 100 μl H20 Concentration Concentration determined by LC-MS/MS using a highly pure amino acid analyzed internal Determination reference (QTag), CV ≤10%. Amount >0.5 nmol per vial, two vials supplied. Formulation Lyophilized in 100 mM Tris-HCl 5% Trehalose, pH 8.0 Instructions for Spin vial before opening. Add 100 μL ultrapure H2O to the vial. Vortex thoroughly and spin Reconstitution down. For further dilution, see Application Protocol. Shipping Shipped at ambient temperature Storage Lyophilized product shall be stored at -20°C. See COA for expiry date. Reconstituted product can be stored at -20°C for up to 4 weeks. Avoid repeated freeze-thaw cycles. Notes For research use only Product of Sweden. For research use only. Not intended for pharmaceutical development, diagnostic, therapeutic or any in vivo use.
    [Show full text]
  • GRADY-DISSERTATION-2017.Pdf (6.311Mb)
    EFFECT OF MESENCHYMAL STEM CELLS ON EQUINE OVARIAN FOLLICULAR DEVELOPMENT AND GENE EXPRESSION A Dissertation by SICILIA TATIANA GRADY Submitted to the Office of Graduate and Professional Studies of Texas A&M University in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY Chair of Committee, Katrin Hinrichs Committee Members, Scott V. Dindot Qinglei Li Ashlee E. Watts Head of Department, Larry J. Suva August 2017 Major Subject: Biomedical Sciences Copyright 2017 Sicilia Tatiana Grady ABSTRACT Aging affects the reproductive efficiency of females. In rodent models, injection of mesenchymal stem cells (MSCs) improves function and induces trophic mRNA expression in ovaries compromised by chemotherapy. However, little information is available on the effect of MSCs in the aging ovary, an application which if effective in increasing fertility, would have an impact in both human and equine reproduction. The aim of the research outlined in this dissertation was to investigate this area. We hypothesized that injection of MSCs into the ovaries of old mares would increase follicle numbers and increase expression of genes related to follicle growth. We examined for the first time the use of fluorescent quantum dots (QDs) to label equine MSCs, to see if this would allow them to be tracked after injection. We found that QD-labeled MSCs retain their ability to proliferate and differentiate. The QDs were maintained in MSCs induced to differentiate into chondrocytes (non-proliferating), but the percentage of labeled cells and the fluorescence intensity decreased to essentially non-detectable within 3 to 5 days in rapidly proliferating cells. Co-culture of equine ovarian tissue with MSCs was not effective due to tissue degradation in culture; however, we used this trial to develop effective methods for isolation of RNA from the extremely fibrous equine ovarian tissue.
    [Show full text]
  • Supplementary Information
    Supplementary Information Supplementary Figure 1 2 Supplementary Figure 2 3 Supplementary Figure 3 4 Supplementary Figure 4 5 Supplementary Figure 5 6 Supplementary Figure 6 7 Supplementary Figure 7 8 Supplementary Table 1 9 Supplementary Table 2 23 Supplementary Table 3 25 Supplementary References 26 1 Supplementary Figure 1 Supplementary Figure 1. Testing cell-specific dataset by differential expression analysis and known marker genes for gene transcriptions. (A) Differential gene expression analysis of human spermatogenesis dataset provided by Xia B., et al. (2020) shows unique expression sets among individual cell stages defined by binary logarithmic Fold Change (log2FC) of gene expression at a threshold of 0.25. (B) PCA-based trajectory analysis is consistent with gene sets for cell-stage identifications as reported in human single-cell atlas (Guo et al., 2018). List of gene marker clusters in individual stages is provided in Supplementary Table 1. (C,D,E) Normalized 2 absolute spermatogenesis transcriptome shows total cellular gene transcription, mitochondrial gene transcription, and RNF20 expression known for TCEA inhibition. [all statistical analysis provided in the figure was tested by Pearson’s correlation at a cut-off p-value < 0.001] Supplementary Figure 2 Supplementary Figure 2. TCEA expression profile in human embryogenesis. (A,B) TCEA expression profile of human embryogenesis classified by days [day 3-7] (left) and tissue types [epiblast, not applicable, primitive endoderm, and trophectoderm] (right) provided by (Sladitschek et al., 2020). (C,D) Correlation analyses between embryogene-related gene transcription and TCEA1 (left) and TCEA2 (right). [all statistical analysis provided in the figure was tested by Pearson’s correlation at a cut-off p-value < 0.001] 3 Supplementary Figure 3 Supplementary Figure 3.
    [Show full text]
  • Exome Sequencing Enhanced Package Department of Pathology and Laboratory Medicine Feb 2012 UCLA Molecular Diagnostics Laboratories Page:1
    UCLA Health System Clinical Exome Sequencing Enhanced Package Department of Pathology and Laboratory Medicine Feb 2012 UCLA Molecular Diagnostics Laboratories Page:1 Gene_Symbol Total_coding_bp %_bp_>=10X Associated_Disease(OMIM) MARC1 1093 80% . MARCH1 1005 100% . MARC2 1797 92% . MARCH3 802 100% . MARCH4 1249 99% . MARCH5 861 96% . MARCH6 2907 100% . MARCH7 2161 100% . MARCH8 900 100% . MARCH9 1057 73% . MARCH10 2467 100% . MARCH11 1225 56% . SEPT1 1148 100% . SEPT2 1341 100% . SEPT3 1175 100% . SEPT4 1848 96% . SEPT5 1250 94% . SEPT6 1440 96% . SEPT7 1417 96% . SEPT8 1659 98% . SEPT9 2290 96% Hereditary Neuralgic Amyotrophy SEPT10 1605 98% . SEPT11 1334 98% . SEPT12 1113 100% . SEPT14 1335 100% . SEP15 518 100% . DEC1 229 100% . A1BG 1626 82% . A1CF 1956 100% . A2LD1 466 42% . A2M 4569 100% . A2ML1 4505 100% . UCLA Health System Clinical Exome Sequencing Enhanced Package Department of Pathology and Laboratory Medicine Feb 2012 UCLA Molecular Diagnostics Laboratories Page:2 Gene_Symbol Total_coding_bp %_bp_>=10X Associated_Disease(OMIM) A4GALT 1066 100% . A4GNT 1031 100% . AAAS 1705 100% Achalasia‐Addisonianism‐Alacrima Syndrome AACS 2091 94% . AADAC 1232 100% . AADACL2 1226 100% . AADACL3 1073 100% . AADACL4 1240 100% . AADAT 1342 97% . AAGAB 988 100% . AAK1 3095 100% . AAMP 1422 100% . AANAT 637 93% . AARS 3059 100% Charcot‐Marie‐Tooth Neuropathy Type 2 AARS 3059 100% Charcot‐Marie‐Tooth Neuropathy Type 2N AARS2 3050 100% . AARSD1 1902 98% . AASDH 3391 100% . AASDHPPT 954 100% . AASS 2873 100% Hyperlysinemia AATF 1731 99% . AATK 4181 78% . ABAT 1563 100% GABA‐Transaminase Deficiency ABCA1 6991 100% ABCA1‐Associated Familial High Density Lipoprotein Deficiency ABCA1 6991 100% Familial High Density Lipoprotein Deficiency ABCA1 6991 100% Tangier Disease ABCA10 4780 100% .
    [Show full text]
  • L‑Lactate Dehydrogenase B May Be a Predictive Marker for Sensitivity to Anti‑EGFR Monoclonal Antibodies in Colorectal Cancer Cell Lines
    4710 ONCOLOGY LETTERS 17: 4710-4716, 2019 L‑Lactate dehydrogenase B may be a predictive marker for sensitivity to anti‑EGFR monoclonal antibodies in colorectal cancer cell lines AYUMU NAGAMINE1,2, TAKUYA ARAKI1,2, DAISUKE NAGANO1, MITSUE MIYAZAKI3 and KOUJIROU YAMAMOTO1,2 1Department of Clinical Pharmacology and Therapeutics, Gunma University Graduate School of Medicine; 2Department of Pharmacy, Gunma University Hospital; 3Division of Endocrinology Metabolism and Signal Research, Gunma University Initiative for Advanced Research and Institute for Molecular and Cellular Regulation, Maebashi, Gunma 371‑8511, Japan Received October 15, 2018; Accepted January 31, 2019 DOI: 10.3892/ol.2019.10075 Abstract. Recently, proteins derived from cancer cells have Introduction been widely investigated as biomarkers for predicting the efficacy of chemotherapy. In this study, to identify a sensitive Various factors such as genetic variations and changes in biomarker for the efficacy of anti‑epidermal growth factor mRNA expression patterns are known to influence drug effi- receptor monoclonal antibodies (anti-EGFR mAbs), proteins cacy, and such factors have been studied extensively. However, derived from 6 colorectal cancer (CRC) cell lines with drug responses are affected by changes in the conformation, different sensitivities to cetuximab, an anti‑EGFR mAb, were localization, and expression of numerous proteins, which analyzed. Cytoplasmic and membrane proteins extracted from are regulated by mutations and mRNA expression levels. In each CRC cell line were digested using trypsin and analyzed 2014, Zhang et al reported that only 32% of the genes showed comprehensively using mass spectrometry. As a result, 148 and statistically significant positive mRNA-protein correlation 146 peaks from cytoplasmic proteins and 363 and 267 peaks in 86 CRC samples (1).
    [Show full text]