DOCSLIB.ORG

Table 8. 341 Human Cdnas Used for Hierarchical Clustering of DNA

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Table 8. 341 Human Cdnas Used for Hierarchical Clustering of DNA Table 8. 341 human cDNAs used for hierarchical clustering of DNA microarray datasets of human gastric cancers Clone ID Name (Gene Symbol) IMAGE:2014733 activating transcription factor 2 ( ATF2 ) IMAGE:50765 activating transcription factor 2 ( ATF2 ) IMAGE:112371 activating transcription factor 5 ( ATF5 ) IMAGE:814158 activating transcription factor 5 ( ATF5 ) IMAGE:392123 acylphosphatase 2, muscle type ( ACYP2 ) IMAGE:842939 adenosine deaminase, RNA-specific, B1 (RED1 homolog rat) ( ADARB1 ) IMAGE:327635 adenylate kinase 1 ( AK1 ) IMAGE:1503971 ADP-ribosylation factor-like 6 ( ARL6 ) IMAGE:42035 alpha-N-acetylneuraminyl 2,3-betagalactosyl-1,3)-N-acetyl galactosaminide alpha-2,6-sialyltransferase E ( SIAT7E ) IMAGE:1695257 amyloid beta (A4) precursor protein-binding, family B, member 1 interacting protein ( APBB1IP ) IMAGE:1917557 ATP-binding cassette, sub-family A (ABC1), member 1 ( ABCA1 ) IMAGE:827168 ATP-binding cassette, sub-family A (ABC1), member 1 ( ABCA1 ) IMAGE:288736 ATP-binding cassette, sub-family G (WHITE), member 2 ( ABCG2 ) IMAGE:32110 ATP-binding cassette, sub-family G (WHITE), member 2 ( ABCG2 ) IMAGE:415804 ATP-binding cassette, sub-family G (WHITE), member 2 ( ABCG2 ) IMAGE:365098 BCL2/adenovirus E1B 19kDa interacting protein 3-like ( BNIP3L ) IMAGE:814899 BCL2/adenovirus E1B 19kDa interacting protein 3-like ( BNIP3L ) IMAGE:859386 Bernardinelli-Seip congenital lipodystrophy 2 (seipin) ( BSCL2 ) IMAGE:668851 brain-derived neurotrophic factor ( BDNF ) IMAGE:32812 breast carcinoma amplified sequence 2 ( BCAS2 ) IMAGE:1927395 Ca2+-dependent activator protein for secretion ( CADPS ) IMAGE:32304 Ca2+-dependent activator protein for secretion ( CADPS ) IMAGE:325182 cadherin 2, type 1, N-cadherin (neuronal) ( CDH2 ) IMAGE:2112820 calcitonin/calcitonin-related polypeptide, alpha ( CALCA ) IMAGE:50636 calcium/calmodulin-dependent protein kinase (CaM kinase) II beta ( CAMK2B ) IMAGE:2015501 calmodulin 3 (phosphorylase kinase, delta) ( CALM3 ) IMAGE:969854 calmodulin 3 (phosphorylase kinase, delta) ( CALM3 ) IMAGE:256911 cAMP responsive element modulator ( CREM ) IMAGE:745161 cAMP responsive element modulator ( CREM ) IMAGE:789383 cAMP responsive element modulator ( CREM ) IMAGE:40558 carboxypeptidase E ( CPE ) IMAGE:795840 carboxypeptidase E ( CPE ) IMAGE:345538 cathepsin L ( CTSL ) IMAGE:739116 cathepsin Z ( CTSZ ) IMAGE:842994 cathepsin Z ( CTSZ ) IMAGE:1848167 CD53 antigen ( CD53 ) IMAGE:504226 CD53 antigen ( CD53 ) IMAGE:366067 cerebellar degeneration-related protein 2, 62kDa ( CDR2 ) IMAGE:2028984 chemokine (C-X-C motif) ligand 12 (stromal cell-derived factor 1) ( CXCL12 ) IMAGE:2239290 chemokine (C-X-C motif) ligand 12 (stromal cell-derived factor 1) ( CXCL12 ) IMAGE:784337 chemokine (C-X-C motif) ligand 12 (stromal cell-derived factor 1) ( CXCL12 ) IMAGE:1585535 chromogranin A (parathyroid secretory protein 1) ( CHGA ) IMAGE:322148 chromogranin B (secretogranin 1) ( CHGB ) IMAGE:841645 claudin 7 ( CLDN7 ) IMAGE:264692 coagulation factor II (thrombin) receptor ( F2R ) IMAGE:813254 coagulation factor II (thrombin) receptor ( F2R ) IMAGE:122159 collagen, type III, alpha 1 (Ehlers-Danlos syndrome type IV, autosomal dominant) ( COL3A1 ) IMAGE:491692 collagen, type IV, alpha 1 ( COL4A1 ) IMAGE:769959 collagen, type IV, alpha 2 ( COL4A2 ) IMAGE:1434897 collagen, type V, alpha 2 ( COL5A2 ) IMAGE:138991 collagen, type VI, alpha 3 ( COL6A3 ) IMAGE:1662493 collagen, type VIII, alpha 1 ( COL8A1 ) IMAGE:898092 connective tissue growth factor ( CTGF ) IMAGE:132304 contactin 1 ( CNTN1 ) IMAGE:24884 contactin 1 ( CNTN1 ) IMAGE:51226 contactin 1 ( CNTN1 ) IMAGE:51640 contactin 1 ( CNTN1 ) IMAGE:244637 CREBBP/EP300 inhibitory protein 1 ( CRI1 ) IMAGE:111426 CUG triplet repeat, RNA binding protein 2 ( CUGBP2 ) IMAGE:435573 CUG triplet repeat, RNA binding protein 2 ( CUGBP2 ) IMAGE:488956 CUG triplet repeat, RNA binding protein 2 ( CUGBP2 ) IMAGE:742595 cyclin-dependent kinase 5 ( CDK5 ) IMAGE:145503 cyclin-dependent kinase inhibitor 2D (p19, inhibits CDK4) ( CDKN2D ) IMAGE:2119039 cytochrome P450, family 7, subfamily B, polypeptide 1 ( CYP7B1 ) IMAGE:47475 cytoplasmic FMR1 interacting protein 2 ( CYFIP2 ) IMAGE:71902 cytoskeleton associated protein 2 ( CKAP2 ) IMAGE:825228 cytoskeleton associated protein 2 ( CKAP2 ) IMAGE:291537 development and differentiation enhancing factor 1 ( DDEF1 ) IMAGE:428936 development and differentiation enhancing factor 1 ( DDEF1 ) IMAGE:79448 development and differentiation enhancing factor 1 ( DDEF1 ) IMAGE:838872 dickkopf homolog 2 (Xenopus laevis) ( DKK2 ) IMAGE:361688 dipeptidylpeptidase 6 ( DPP6 ) IMAGE:488033 DnaJ (Hsp40) homolog, subfamily B, member 9 ( DNAJB9 ) IMAGE:773278 DnaJ (Hsp40) homolog, subfamily B, member 9 ( DNAJB9 ) IMAGE:384015 dopa decarboxylase (aromatic L-amino acid decarboxylase) ( DDC ) IMAGE:199833 Down syndrome critical region gene 3 ( DSCR3 ) IMAGE:149539 dual specificity phosphatase 16 ( DUSP16 ) IMAGE:277187 dual specificity phosphatase 16 ( DUSP16 ) IMAGE:841094 dual specificity phosphatase 16 ( DUSP16 ) IMAGE:814818 dual specificity phosphatase 6 ( DUSP6 ) IMAGE:854899 dual specificity phosphatase 6 ( DUSP6 ) IMAGE:250069 dual specificity phosphatase 8 ( DUSP8 ) IMAGE:2146264 ELAV (embryonic lethal, abnormal vision, Drosophila)-like 4 (Hu antigen D) ( ELAVL4 ) IMAGE:34517 ELAV (embryonic lethal, abnormal vision, Drosophila)-like 4 (Hu antigen D) ( ELAVL4 ) IMAGE:40618 ELAV (embryonic lethal, abnormal vision, Drosophila)-like 4 (Hu antigen D) ( ELAVL4 ) IMAGE:564382 ELAV (embryonic lethal, abnormal vision, Drosophila)-like 4 (Hu antigen D) ( ELAVL4 ) IMAGE:26294 Enah/Vasp-like ( EVL ) IMAGE:789147 enolase 2, (gamma, neuronal) ( ENO2 ) IMAGE:684842 F-box and WD-40 domain protein 7 (archipelago homolog, Drosophila) ( FBXW7 ) IMAGE:139009 fibronectin 1 ( FN1 ) IMAGE:256820 fibronectin 1 ( FN1 ) IMAGE:362409 glutamate decarboxylase 1 (brain, 67kDa) ( GAD1 ) IMAGE:364141 glutamate receptor, ionotropic, AMPA 2 ( GRIA2 ) IMAGE:49987 glutamate receptor, ionotropic, AMPA 2 ( GRIA2 ) IMAGE:769676 glutathione transferase zeta 1 (maleylacetoacetate isomerase) ( GSTZ1 ) IMAGE:42558 glycine amidinotransferase (L-arginine:glycine amidinotransferase) ( GATM ) IMAGE:1911474 glycine receptor, beta ( GLRB ) IMAGE:810618 glycine receptor, beta ( GLRB ) IMAGE:290039 glycoprotein M6B ( GPM6B ) IMAGE:31251 glycoprotein M6B ( GPM6B ) IMAGE:713660 glycoprotein M6B ( GPM6B ) IMAGE:1656488 glycosylphosphatidylinositol specific phospholipase D1 ( GPLD1 ) IMAGE:293696 glycosylphosphatidylinositol specific phospholipase D1 ( GPLD1 ) IMAGE:1911721 GNAS complex locus ( GNAS ) IMAGE:359933 GNAS complex locus ( GNAS ) IMAGE:417473 GNAS complex locus ( GNAS ) IMAGE:563444 GNAS complex locus ( GNAS ) IMAGE:700724 GNAS complex locus ( GNAS ) IMAGE:85195 growth arrest and DNA-damage-inducible, gamma ( GADD45G ) IMAGE:365826 growth arrest-specific 1 ( GAS1 ) IMAGE:44563 growth associated protein 43 ( GAP43 ) IMAGE:45645 guanine nucleotide binding protein (G protein), beta 5 ( GNB5 ) IMAGE:809835 heterogeneous nuclear ribonucleoprotein C (C1/C2) ( HNRPC ) IMAGE:2018332 Homo sapiens clone TCCCTA00211 mRNA sequence IMAGE:812289 Homo sapiens clone TCCCTA00211 mRNA sequence IMAGE:854760 Homo sapiens clone TCCCTA00211 mRNA sequence IMAGE:840606 hydroxysteroid (17-beta) dehydrogenase 4 ( HSD17B4 ) IMAGE:134829 hypothetical protein FLJ14001 ( FLJ14001 ) IMAGE:195397 hypothetical protein IMPACT ( IMPACT ) IMAGE:66774 hypothetical protein IMPACT ( IMPACT ) IMAGE:46896 hypothetical protein PRO1331 ( PRO1331 ) IMAGE:283191 immunoglobulin superfamily, member 4 ( IGSF4 ) IMAGE:839048 immunoglobulin superfamily, member 4 ( IGSF4 ) IMAGE:703964 inositol polyphosphate phosphatase-like 1 ( INPPL1 ) IMAGE:1700839 integral membrane protein 2C ( ITM2C ) IMAGE:471196 integral membrane protein 2C ( ITM2C ) IMAGE:740476 interferon regulatory factor 1 ( IRF1 ) IMAGE:289496 interferon-induced protein with tetratricopeptide repeats 2 ( IFIT2 ) IMAGE:588492 interferon-induced protein with tetratricopeptide repeats 2 ( IFIT2 ) IMAGE:841140 isoprenylcysteine carboxyl methyltransferase ( ICMT ) IMAGE:784257 kinesin family member 3C ( KIF3C ) IMAGE:460403 laminin, gamma 2 ( LAMC2 ) IMAGE:42123 LanC lantibiotic synthetase component C-like 1 (bacterial) ( LANCL1 ) IMAGE:760298 legumain ( LGMN ) IMAGE:609155 leucine rich repeat neuronal 1 ( LRRN1 ) IMAGE:754250 likely ortholog of mouse tumor differentially expressed 1, like ( TDE1L ) IMAGE:783698 lipin 1 ( LPIN1 ) IMAGE:66437 lipopolysaccharide binding protein ( LBP ) IMAGE:753313 Lysosomal-associated multispanning membrane protein-5 ( LAPTM5 ) IMAGE:248829 lysyl oxidase ( LOX ) IMAGE:262060 lysyl oxidase ( LOX ) IMAGE:341680 lysyl oxidase ( LOX ) IMAGE:345849 lysyl oxidase ( LOX ) IMAGE:591864 major histocompatibility complex, class II, DO beta ( HLA-DOB ) IMAGE:285780 matrix metalloproteinase 13 (collagenase 3) ( MMP13 ) IMAGE:270505 matrix metalloproteinase 14 (membrane-inserted) ( MMP14 ) IMAGE:2304048 mitogen-activated protein kinase 12 ( MAPK12 ) IMAGE:131362 moesin ( MSN ) IMAGE:1750178 multiple PDZ domain protein ( MPDZ ) IMAGE:469981 multiple PDZ domain protein ( MPDZ ) IMAGE:1908758 myelin expression factor 2 ( MYEF2 ) IMAGE:251875 myelin expression factor 2 ( MYEF2 ) IMAGE:898195 myelin expression factor 2 ( MYEF2 ) IMAGE:39127 necdin homolog (mouse) ( NDN ) IMAGE:1883065 neural cell adhesion molecule 1 ( NCAM1 ) IMAGE:1457207 neuronal guanine nucleotide exchange factor ( NGEF ) IMAGE:288681 neuronal guanine nucleotide exchange factor ( NGEF ) IMAGE:971372 neuronal pentraxin
Load more

Recommended publications
  • Chapter 7: Monogenic Forms of Diabetes
    CHAPTER 7 MONOGENIC FORMS OF DIABETES Mark A. Sperling, MD, and Abhimanyu Garg, MD Dr. Mark A. Sperling is Emeritus Professor and Chair, University of Pittsburgh, Department of Pediatrics, Children’s Hospital of Pittsburgh of UPMC, Pittsburgh, PA. Dr. Abhimanyu Garg is Professor of Internal Medicine and Chief of the Division of Nutrition and Metabolic Diseases at University of Texas Southwestern Medical Center, Dallas, TX. SUMMARY Types 1 and 2 diabetes have multiple and complex genetic influences that interact with environmental triggers, such as viral infections or nutritional excesses, to result in their respective phenotypes: young, lean, and insulin-dependence for type 1 diabetes patients or older, overweight, and often manageable by lifestyle interventions and oral medications for type 2 diabetes patients. A small subset of patients, comprising ~2%–3% of all those diagnosed with diabetes, may have characteristics of either type 1 or type 2 diabetes but have single gene defects that interfere with insulin production, secretion, or action, resulting in clinical diabetes. These types of diabetes are known as MODY, originally defined as maturity-onset diabetes of youth, and severe early-onset forms, such as neonatal diabetes mellitus (NDM). Defects in genes involved in adipocyte development, differentiation, and death pathways cause lipodystrophy syndromes, which are also associated with insulin resistance and diabetes. Although these syndromes are considered rare, more awareness of these disorders and increased availability of genetic testing in clinical and research laboratories, as well as growing use of next generation, whole genome, or exome sequencing for clinically challenging phenotypes, are resulting in increased recognition. A correct diagnosis of MODY, NDM, or lipodystrophy syndromes has profound implications for treatment, genetic counseling, and prognosis.
    [Show full text]
  • Human N-Cadherin / CD325 / CDH2 Protein (His & Fc Tag)
    Human N-Cadherin / CD325 / CDH2 Protein (His & Fc Tag) Catalog Number: 11039-H03H General Information SDS-PAGE: Gene Name Synonym: CD325; CDHN; CDw325; NCAD Protein Construction: A DNA sequence encoding the human CDH2 (NP_001783.2) (Met 1-Ala 724) was fused with the C-terminal polyhistidine-tagged Fc region of human IgG1 at the C-terminus. Source: Human Expression Host: HEK293 Cells QC Testing Purity: > 70 % as determined by SDS-PAGE Endotoxin: Protein Description < 1.0 EU per μg of the protein as determined by the LAL method Cadherins are calcium dependent cell adhesion proteins, and they preferentially interact with themselves in a homophilic manner in Stability: connecting cells. Cadherin 2 (CDH2), also known as N-Cadherin (neuronal) (NCAD), is a single-pass tranmembrane protein and a cadherin containing ℃ Samples are stable for up to twelve months from date of receipt at -70 5 cadherin domains. N-Cadherin displays a ubiquitous expression pattern but with different expression levels between endocrine cell types. CDH2 Asp 160 Predicted N terminal: (NCAD) has been shown to play an essential role in normal neuronal Molecular Mass: development, which is implicated in an array of processes including neuronal differentiation and migration, and axon growth and fasciculation. The secreted recombinant human CDH2 is a disulfide-linked homodimeric In addition, N-Cadherin expression was upregulated in human HSC during protein. The reduced monomer comprises 813 amino acids and has a activation in culture, and function or expression blocking of N-Cadherin predicted molecular mass of 89.9 kDa. As a result of glycosylation, it promoted apoptosis. During apoptosis, N-Cadherin was cleaved into 20- migrates as an approximately 114 and 119 kDa band in SDS-PAGE under 100 kDa fragments.
    [Show full text]
  • The N-Cadherin Interactome in Primary Cardiomyocytes As Defined Using Quantitative Proximity Proteomics Yang Li1,*, Chelsea D
    © 2019. Published by The Company of Biologists Ltd | Journal of Cell Science (2019) 132, jcs221606. doi:10.1242/jcs.221606 TOOLS AND RESOURCES The N-cadherin interactome in primary cardiomyocytes as defined using quantitative proximity proteomics Yang Li1,*, Chelsea D. Merkel1,*, Xuemei Zeng2, Jonathon A. Heier1, Pamela S. Cantrell2, Mai Sun2, Donna B. Stolz1, Simon C. Watkins1, Nathan A. Yates1,2,3 and Adam V. Kwiatkowski1,‡ ABSTRACT requires multiple adhesion, cytoskeletal and signaling proteins, The junctional complexes that couple cardiomyocytes must transmit and mutations in these proteins can cause cardiomyopathies (Ehler, the mechanical forces of contraction while maintaining adhesive 2018). However, the molecular composition of ICD junctional homeostasis. The adherens junction (AJ) connects the actomyosin complexes remains poorly defined. – networks of neighboring cardiomyocytes and is required for proper The core of the AJ is the cadherin catenin complex (Halbleib and heart function. Yet little is known about the molecular composition of the Nelson, 2006; Ratheesh and Yap, 2012). Classical cadherins are cardiomyocyte AJ or how it is organized to function under mechanical single-pass transmembrane proteins with an extracellular domain that load. Here, we define the architecture, dynamics and proteome of mediates calcium-dependent homotypic interactions. The adhesive the cardiomyocyte AJ. Mouse neonatal cardiomyocytes assemble properties of classical cadherins are driven by the recruitment of stable AJs along intercellular contacts with organizational and cytosolic catenin proteins to the cadherin tail, with p120-catenin β structural hallmarks similar to mature contacts. We combine (CTNND1) binding to the juxta-membrane domain and -catenin β quantitative mass spectrometry with proximity labeling to identify the (CTNNB1) binding to the distal part of the tail.
    [Show full text]
  • Analysis of the Human Serum Proteome
    Cedarville University DigitalCommons@Cedarville Pharmaceutical Sciences Faculty Publications Department of Pharmaceutical Sciences 6-2004 Analysis of the Human Serum Proteome King C. Chan David A. Lucas Denise Hise Carl F. Schaefer Zhen Xiao See next page for additional authors Follow this and additional works at: https://digitalcommons.cedarville.edu/ pharmaceutical_sciences_publications Part of the Pharmacy and Pharmaceutical Sciences Commons This Article is brought to you for free and open access by DigitalCommons@Cedarville, a service of the Centennial Library. It has been accepted for inclusion in Pharmaceutical Sciences Faculty Publications by an authorized administrator of DigitalCommons@Cedarville. For more information, please contact [email protected]. Authors King C. Chan, David A. Lucas, Denise Hise, Carl F. Schaefer, Zhen Xiao, George M. Janini, Kenneth H. Buetow, Haleem J. Issaq, Timothy D. Veenstra, and Thomas P. Conrads Clinical Proteomics Journal Copyright ©Humana Press Inc. All rights of any nature whatsoever are reserved. ISSN 1542-6416/04/01:101–225/$25.00 Serum/Plasma Proteome Analysis of the Human Serum Proteome King C. Chan,1,† David A. Lucas,1,† Denise Hise,2 Carl F. Schaefer,2 Zhen Xiao,1 George M. Janini,1 Kenneth H. Buetow,2 Haleem J. Issaq,1 Timothy D.Veenstra,1 and Thomas P. Conrads1,* 1Laboratory of Proteomics and Analytical Technologies, National Cancer Institute at Frederick, SAIC-Frederick, Inc, PO Box B, Frederick, MD 21702 2Center for Bioinformatics, National Cancer Institute, Bethesda, MD 20892 †These authors contributed equally to this work. each of which was analyzed by microcapillary Abstract reversed-phase liquid chromatography coupled Changes in serum proteins that signal online with MS/MS analysis.
    [Show full text]
  • Abstracts from the 9Th Biennial Scientific Meeting of The
    International Journal of Pediatric Endocrinology 2017, 2017(Suppl 1):15 DOI 10.1186/s13633-017-0054-x MEETING ABSTRACTS Open Access Abstracts from the 9th Biennial Scientific Meeting of the Asia Pacific Paediatric Endocrine Society (APPES) and the 50th Annual Meeting of the Japanese Society for Pediatric Endocrinology (JSPE) Tokyo, Japan. 17-20 November 2016 Published: 28 Dec 2017 PS1 Heritable forms of primary bone fragility in children typically lead to Fat fate and disease - from science to global policy a clinical diagnosis of either osteogenesis imperfecta (OI) or juvenile Peter Gluckman osteoporosis (JO). OI is usually caused by dominant mutations affect- Office of Chief Science Advsor to the Prime Minister ing one of the two genes that code for two collagen type I, but a re- International Journal of Pediatric Endocrinology 2017, 2017(Suppl 1):PS1 cessive form of OI is present in 5-10% of individuals with a clinical diagnosis of OI. Most of the involved genes code for proteins that Attempts to deal with the obesity epidemic based solely on adult be- play a role in the processing of collagen type I protein (BMP1, havioural change have been rather disappointing. Indeed the evidence CREB3L1, CRTAP, LEPRE1, P4HB, PPIB, FKBP10, PLOD2, SERPINF1, that biological, developmental and contextual factors are operating SERPINH1, SEC24D, SPARC, from the earliest stages in development and indeed across generations TMEM38B), or interfere with osteoblast function (SP7, WNT1). Specific is compelling. The marked individual differences in the sensitivity to the phenotypes are caused by mutations in SERPINF1 (recessive OI type obesogenic environment need to be understood at both the individual VI), P4HB (Cole-Carpenter syndrome) and SEC24D (‘Cole-Carpenter and population level.
    [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]
  • Oegtp - Epilepsy Test Requisition Lab Use Only: Patient Information
    OEGTP - EPILEPSY TEST REQUISITION LAB USE ONLY: PATIENT INFORMATION: Received date: Name: Notes: Address: Date of Birth: YY/MM/DD Sex: M F Health Card No: TEST REQUEST: See page 2 for gene list for each of the panels below Epilepsy Comprehensive panel: 167 genes Childhood Onset Epilepsy panel: 45 genes Focal Epilepsy panel: 14 genes Brain Malformation Epilepsy panel: 44 genes London Health Sciences Centre – (Molecular Genetics) London Health Sciences Centre Progressive Myoclonic Epilepsy panel: 20 genes Actionable Gene Epilepsy panel: 22 genes Early Infantile Epilepsy panel: 51 genes Single gene test: Carrier Testing/ KnownFamily Mutation SAMPLE COLLECTION: Name of index case in the family (include copy of report) Date drawn: YY/MM/DD EDTA blood (lavender top) (5ml at room temp) Affected Unaffected Date of Birth: Relationship to patient: REFERRING PHYSICIAN: Authorized Signature is Required Gene: RefSeq:NM Physician Name (print): Mutation: Signature: Email: REASON FOR REFERRAL: Clinic/Hospital: Diagnostic Testing Address: Clinical Diagnosis: Telephone: Fax: CC report to: Name: Clinical Presentation: Address: Telephone: Fax: Molecular Genetics Laboratory Victoria Hospital, Room B10-123A 800 Commissioners Rd. E. London, Ontario | N6A 5W9 Pathology and Laboratory Medicine Ph: 519-685-8122 | Fax: 519-685-8279 Page 1 of 6 Page OEGTP (2021/05/28) OEGTP - EPILEPSY TEST PANELS Patient Identifier: COMPREHENSIVE EPILEPSY PANEL: 167 Genes ACTB, ACTG1, ADSL, AKT3, ALDH7A1, AMT, AP3B2, ARFGEF2, ARHGEF9, ARV1, ARX, ASAH1, ASNS, ATP1A3, ATP6V0A2, ATP7A,
    [Show full text]
  • Download Download
    Supplementary Figure S1. Results of flow cytometry analysis, performed to estimate CD34 positivity, after immunomagnetic separation in two different experiments. As monoclonal antibody for labeling the sample, the fluorescein isothiocyanate (FITC)- conjugated mouse anti-human CD34 MoAb (Mylteni) was used. Briefly, cell samples were incubated in the presence of the indicated MoAbs, at the proper dilution, in PBS containing 5% FCS and 1% Fc receptor (FcR) blocking reagent (Miltenyi) for 30 min at 4 C. Cells were then washed twice, resuspended with PBS and analyzed by a Coulter Epics XL (Coulter Electronics Inc., Hialeah, FL, USA) flow cytometer. only use Non-commercial 1 Supplementary Table S1. Complete list of the datasets used in this study and their sources. GEO Total samples Geo selected GEO accession of used Platform Reference series in series samples samples GSM142565 GSM142566 GSM142567 GSM142568 GSE6146 HG-U133A 14 8 - GSM142569 GSM142571 GSM142572 GSM142574 GSM51391 GSM51392 GSE2666 HG-U133A 36 4 1 GSM51393 GSM51394 only GSM321583 GSE12803 HG-U133A 20 3 GSM321584 2 GSM321585 use Promyelocytes_1 Promyelocytes_2 Promyelocytes_3 Promyelocytes_4 HG-U133A 8 8 3 GSE64282 Promyelocytes_5 Promyelocytes_6 Promyelocytes_7 Promyelocytes_8 Non-commercial 2 Supplementary Table S2. Chromosomal regions up-regulated in CD34+ samples as identified by the LAP procedure with the two-class statistics coded in the PREDA R package and an FDR threshold of 0.5. Functional enrichment analysis has been performed using DAVID (http://david.abcc.ncifcrf.gov/)
    [Show full text]
  • Supplemental Information IRF4 Transcription Factor-Dependent Cd11b+ Dendritic Cells in Human and Mouse Control Mucosal IL-17 C
    Immunity, Volume 38 Supplemental Information IRF4 Transcription Factor-Dependent CD11b+ Dendritic Cells in Human and Mouse Control Mucosal IL-17 Cytokine Responses Andreas Schlitzer, Naomi McGovern, Pearline Teo, Teresa Zelante, Koji Atarashi, Donovan Low, Adrian W.S. Ho, Peter See, Amanda Shin, Pavandip Singh Wasan, Guillaume Hoeffel, Benoit Malleret, Alexander Heiseke, Samantha Chew, Laura Jardine, Harriet A. Purvis, Catharien M.U. Hilkens, John Tam, Michael Poidinger, E. Richard Stanley, Anne B. K rug, Laurent Renia, Baalasubramanian Sivasankar, Lai Guan Ng, Matthew Collin, Paola Ricciardi-Castagnoli, Kenya Honda, Muzlifah Haniffa, and Florent Ginhoux Supplemental Inventory 1. Supplemental Figures and Tables Figure S1, Related to Figure 1 Figure S2, Related to Figure 2 and 3 Figure S3, Related to Figure 4 Figure S4, Related to Figure 5 Figure S5, Related to Figure 5 Figure S6, Related to Figure 7 Table S1, Related to Figure 3 Table S2, Related to Figure 6 Table S3, Related to Figure 6 2. Supplemental Experimental Procedures 3. Supplemental References Supplementary figure 1 Sorting strategy for mouse lung and small intestinal DC A Sorting strategy, Lung Singlets Dapi-CD45+ 250K 250K 250K 105 200K 200K 200K 104 A I - 150K 150K 150K C P C C 3 10 S A S S 100K 100K S 100K D S S 102 50K 50K 50K 0 0 0 0 0 50K 100K 150K 200K 250K 0 50K 100K 150K 200K 250K 0 103 104 105 0 103 104 105 FSC FSC-W CD45 GR1 Auto Fluor.- MHCII+ GR1- SSClow CD11c+ CD11b+ 250K 105 105 105 200K 4 104 10 104 150K I 3 I 3 4 3 0 10 3 C 2 H 10 10 100K 1 S D C D S C M 2 C 10 50K 0 0 0 0 0 102 103 104 105 0 103 104 105 0 103 104 105 0 103 104 105 Auto fluor.
    [Show full text]
  • Supplementary Table 1: Adhesion Genes Data Set
    Supplementary Table 1: Adhesion genes data set PROBE Entrez Gene ID Celera Gene ID Gene_Symbol Gene_Name 160832 1 hCG201364.3 A1BG alpha-1-B glycoprotein 223658 1 hCG201364.3 A1BG alpha-1-B glycoprotein 212988 102 hCG40040.3 ADAM10 ADAM metallopeptidase domain 10 133411 4185 hCG28232.2 ADAM11 ADAM metallopeptidase domain 11 110695 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 195222 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 165344 8751 hCG20021.3 ADAM15 ADAM metallopeptidase domain 15 (metargidin) 189065 6868 null ADAM17 ADAM metallopeptidase domain 17 (tumor necrosis factor, alpha, converting enzyme) 108119 8728 hCG15398.4 ADAM19 ADAM metallopeptidase domain 19 (meltrin beta) 117763 8748 hCG20675.3 ADAM20 ADAM metallopeptidase domain 20 126448 8747 hCG1785634.2 ADAM21 ADAM metallopeptidase domain 21 208981 8747 hCG1785634.2|hCG2042897 ADAM21 ADAM metallopeptidase domain 21 180903 53616 hCG17212.4 ADAM22 ADAM metallopeptidase domain 22 177272 8745 hCG1811623.1 ADAM23 ADAM metallopeptidase domain 23 102384 10863 hCG1818505.1 ADAM28 ADAM metallopeptidase domain 28 119968 11086 hCG1786734.2 ADAM29 ADAM metallopeptidase domain 29 205542 11085 hCG1997196.1 ADAM30 ADAM metallopeptidase domain 30 148417 80332 hCG39255.4 ADAM33 ADAM metallopeptidase domain 33 140492 8756 hCG1789002.2 ADAM7 ADAM metallopeptidase domain 7 122603 101 hCG1816947.1 ADAM8 ADAM metallopeptidase domain 8 183965 8754 hCG1996391 ADAM9 ADAM metallopeptidase domain 9 (meltrin gamma) 129974 27299 hCG15447.3 ADAMDEC1 ADAM-like,
    [Show full text]
  • A Human Population-Based Organotypic in Vitro Model for Cardiotoxicity Screening1
    ALTEX preprint published July 8, 2018 doi:10.14573/altex.1805301 Research Article A human population-based organotypic in vitro model for cardiotoxicity screening1 Fabian A. Grimm1, Alexander Blanchette1, John S. House2, Kyle Ferguson1, Nan-Hung Hsieh1, Chimeddulam Dalaijamts1, Alec A. Wright1, Blake Anson5, Fred A. Wright3,4, Weihsueh A. Chiu1, Ivan Rusyn1 1Department of Veterinary Integrative Biosciences, Texas A&M University, College Station, TX, USA; 2Bioinformatics Research Center, 3Department of Biological Sciences, and 4Department of Statistics, North Carolina State University, Raleigh, NC, USA; 5Cellular Dynamics International, Madison, WI, USA Abstract Assessing inter-individual variability in responses to xenobiotics remains a substantial challenge, both in drug development with respect to pharmaceuticals and in public health with respect to environmental chemicals. Although approaches exist to characterize pharmacokinetic variability, there are no methods to routinely address pharmacodynamic variability. In this study, we aimed to demonstrate the feasibility of characterizing inter-individual variability in a human in vitro model. Specifically, we hypothesized that genetic variability across a population of iPSC- derived cardiomyocytes translates into reproducible variability in both baseline phenotypes and drug responses. We measured baseline and drug-related effects in iPSC-derived cardiomyocytes from 27 healthy donors on kinetic Ca2+ flux and high-content live cell imaging. Cells were treated in concentration-response with cardiotoxic drugs: isoproterenol (β- adrenergic receptor agonist/positive inotrope), propranolol (β-adrenergic receptor antagonist/negative inotrope), and cisapride (hERG channel inhibitor/QT prolongation). Cells from four of the 27 donors were further evaluated in terms of baseline and treatment-related gene expression. Reproducibility of phenotypic responses was evaluated across batches and time.
    [Show full text]
  • Gene Expression of Osteosarcoma Cells on Various Coated Titanium Materials
    MOLECULAR & CELLULAR TOXICOLOGY, Vol. 3, No. 1, 36-45, March 2007 Gene Expression of Osteosarcoma Cells on Various Coated Titanium Materials Sung-Hwa Sohn1, Jae Bun Lee2, Ki-Nam Kim1, are made with Ti alloys. However, the exact effect of In Kyoung Kim1, Seung Ho Lee1, Hye Won Kim1, Ti on osteoblasts is still unknown2-4. Successful ap- Sang-Hui Seo1, Yu-Ri Kim1, Sang-Wan Shin2, plication of such materials for bone regeneration Jae-Jun Ryu2 & Meyoung-Kon Kim1 often involved mixing with autogenous bone, a sour- ce of osteoblastic cells and precursors2. 1Department of Biochemistry & Molecular Biology Surface topography may affect the formation of a 2Department of Dentistry, College of Medicine, Korea University, fibrous capsule around implants, inflammatory res- Seoul 136-705, Korea ponse at tissue-implant interface, fibroblast attach- Correspondence and requests for materials should be addressed ment, angiogenesis, epithelial down-growth around to M-K. Kim ([email protected]) percutaneous devices, and many cellular processes such as cellular differentiation, transcription, cell Accepted 8 March 2007 metabolism, protein production, and phenotypic ex- pression1,3,5-7. Diverse implant surface may contribute to the regulation of osteoblast differentiation by infl- Abstract uencing the level of gene expression of key osteo- genic factors7,8. Morphometric analyses had shown Several features of the implant surface, such as differences in bone-implant contact percentages with topography, roughness, and composition play a the varying of surface characteristics, as well as a relevant role in implant integration with bone. This sensitivity of cells to surface topography9,10. Gene ex- study was conducted in order to determine the pression in response to the placement of implants effects of different-coatings on Ti surfaces on the with different surface topographies11-16.
    [Show full text]