Name Aliases Binding Partner Physiology / Oncology References

Total Page:16

File Type:pdf, Size:1020Kb

Name Aliases Binding Partner Physiology / Oncology References Name Aliases Binding partner Physiology / Oncology References AJAP1 Adherens junction associated protein 1, ? PHY : Expressed in uterus and pancreas. [1] http://www.uniprot.org/uniprot/Q9UKB5. [2] SHREW1 Plays a role in cell adhesion and migration. McDonald JM, Cancer Biol Ther 2006, 5:300-4 Forms a complex with CDH1 and beta-catenin at adherens junctions [1] ONC : Frequently deleted in oligodendrogliomas, functions to inhibit cell adhesion and migration [2] ALCAM Activated leukocyte cell adhesion CD6 PHY : Adhesion of activated leukocytes and [1] Ofori-Acquah SF, Transl Res 2008, 151:122- molecule, CD166, MEMD (melanoma neurons 8. [2] van Kilsdonk JW, Cancer Res 2008, metastasis clone D) 68:3671-9 ONC : Expressed by different tumor types including melanoma; mediates cancer/ melanoma invasiveness [1,2] AMICA1 Adhesion molecule interacting with CXADR PHY : Expression is restricted to the [1] http://www.uniprot.org/uniprot/Q86YT9. [2] CXADR antigen 1, JAML (junctional hematopoietic tissues with the exception of Moog-Lutz C, Blood 2003, 102:3371-8 adhesion molecule-like) liver. May function in transmigration of leukocytes through epithelial and endothelial tissues. Mediates adhesive interactions with CXADR, a protein of the junctional complex of epithelial cells [1] ONC : Enhances myeloid leukemia cell adhesion to endothelial cells [2] AMIGO1 Amphoterin-induced gene and open AMIGO PHY : May be involved in fasciculation as well [1] http://www.uniprot.org/uniprot/Q86WK6 reading frame 1, Alivin-2 as myelination of developing neural axons. May have a role in regeneration as well as neural plasticity in the adult nervous system. May mediate homophilic as well as heterophilic cell-cell interaction and contribute to signal transduction through its intracellular domain [1] ONC : - AMIGO2 Amphoterin-induced gene and open AMIGO PHY : Highest levels in breast, ovary, cervix, [1] http://www.uniprot.org/uniprot/Q86SJ2. [2] reading frame 2, DEGA (Differentially and uterus. May mediate homophilic as well Rabenau KE, Oncogene 2004, 23:5056-67 expressed in gastric adenocarcinomas) as heterophilic cell-cell interaction with MMMP Biomap #87 Page 1 AMIGO1 or AMIGO3. May contribute to signal transduction through its intracellular domain [1] ONC : High expression in 45% of gastric adenocarcinomas; stable expression of an antisense construct in a gastric adenocarcinoma cell line leads to increased ploidy, chromosomal instability, decreased cell adhesion/ migration and nearly complete abrogation of tumorigenicity in nude mice [2] AMIGO3 Amphoterin-induced gene and open AMIGO PHY : May mediate heterophilic cell-cell [1] http://www.uniprot.org/uniprot/Q86WK7 reading frame 3 interaction. May contribute to signal transduction through its intracellular domain [1] ONC : - BCAM Basal cell adhesion molecule, CD239, Laminins (?) PHY : Associated with basal layer of epithelial [1] Kikkawa Y, Exp Cell Res 2008, 314:2579-90 Lutheran blood group antigen and endothelial cells ONC : Mediates adhesion of hepatocellular carcinoma (HCC) cells to laminin alpha 5 [1] CADM1 Cell adhesion molecule 1, TSLC1 (tumor CADM1 PHY : Calcium-independent homophilic and [1] Murakami Y, Cancer Sci 2005, 96:543-52. [2] suppressor in lung cancer), IGSF4, CADM3 heterophilic cell-cell adhesion Nowacki S, Oncogene 2008, 27:3329-38. [3] SYNCAM1 PVRL3 Kikuchi S, Cancer 2006, 106:1751-8 ONC : Considered a tumor suppressor gene [1], especially for neuroblastoma [2] and lung cancer [3] CADM2 Cell adhesion molecule 2, NECL3, ? PHY : ? [1] http://www.uniprot.org/uniprot/Q8N3J6 SYNCAM2 ONC : - CADM3 Cell adhesion molecule 3, IGSF4B, CADM3 PHY : Calcium-independent homophilic and [1] Fukuhara H, Oncogene 2001, 20:5401-7 TSLL1 (TSLC1-like 1), NECL1, IGSF4 heterophilic cell-cell adhesion activity SYNCAM3 PVRL1 PVRL3 ONC : Possibly involved in cancer biology (CADM1 homologous) [1] CADM4 Cell adhesion molecule 4, IGSF4C, ? PHY : Calcium- and magnesium-independent [1] Fukuhara H, Oncogene 2001, 20:5401-7 TSLL2 (TSLC1-like 2), NECL4, cell-cell adhesion activity SYNCAM4 ONC : Possibly involved in cancer biology MMMP Biomap #87 Page 2 (CADM1 homologous) [1] CD2 CD2 antigen p50, LFA-2, LFA-3 receptor, LFA-3 PHY : CD2 interacts with lymphocyte function- [1] http://www.uniprot.org/uniprot/P06729. [2] rosette receptor, T-cell surface antigen CD48 associated antigen (LFA-3) and CD48 to Perea G, Leuk Res 2005, 29:1109-16 T11/Leu-5 mediate adhesion between T-cells and other cell types. CD2 is implicated in the triggering of T-cells, the cytoplasmic domain is implicated in the signaling function ONC : CD2 (and CD36) expression has an adverse prognostic impact in adult de novo acute myeloid leukemia (AML) patients [2] CD4 CD4 antigen p55, T-cell surface antigen MHC class II PHY : Identifies helper T cells (HTL) and [1] http://www.uniprot.org/uniprot/P01730 T4/Leu-3 suppressor/ regulatory T cells (Treg) that interact with MHC class II bearing targets. Singaling and adhesion coreceptor in class II restricted antigen-induced T cell activation. Primary receptor for HIV virus [1] ONC : - CD6 Tp120 CD166 PHY : Expressed by thymocytes, mature T- [1] http://www.uniprot.org/uniprot/P30203 cells, a subset of B-cells known as B-1 cells, and by some cells in the brain. After T-cell activation, becomes phosphorylated on Ser, Thr and Tyr residues [1] ONC : - CD8a CD8 alpha (p32), T-lymphocyte MHC class I PHY : Identifies cytotoxic T cells (CTL) and [1] Smith TR, Trends Immunol 2008, 29:337-42. differentiation antigen T8/Leu-2 suppressor/ regulatory T cells (Treg) that [2] http://www.uniprot.org/uniprot/P01732 interact with MHC class I bearing targets. Signaling and adhesion coreceptor in class II restricted antigen-induced T cell activation. In general heterodimer of an alpha and a beta chain [2] ONC : - CD8b CD8 beta (p37), T-cell surface MHC class I PHY : Identifies cytotoxic T cells (CTL) and [1] Smith TR, Trends Immunol 2008, 29:337-42. glycoprotein CD8 beta chain suppressor/ regulatory T cells (Treg) that [2] http://www.uniprot.org/uniprot/P10966 interact with MHC class I bearing targets. Signaling and adhesion coreceptor in class II restricted antigen-induced T cell activation. In general heterodimer of an alpha and a beta MMMP Biomap #87 Page 3 chain [2] ONC : - CD9 Tetraspanin-29, Leukocyte antigen MIC3 ? PHY : Involved in platelet activation and [1] http://www.uniprot.org/uniprot/P21926. [2] aggregation. Regulates paranodal junction Ikeyama S, J Exp Med 1993, 177:1231-7. [3] formation. Required for gamete fusion. Miyake M, Oncogene 2000, 19:5221-6. [4] Involved in cell adhesion and motility. Nakazawa Y, Blood 2008, 112:1730-9. [5] De Bruyne E, Clin Cancer Res 2008, 14:2918-26. Expressed by a variety of hematopoietic and [6] Longo N, Blood 2001, 98:3717-26. [7] Hong epithelial cells [1]. CD9 (and CD81) associate IK, Exp Mol Med 2005, 37:230-9. [8] Hemler with phosphatidyl inositol 4-kinase (PI4K), ME, Nat Rev Mol Cell Biol 2005, 6:801-11 which locally produces phosphoinositides (such as phosphatidylinositol-4,5- bisphosphate; this causes the recruitment and activation of SHC (SRC-homology-2-domain- containing transforming protein): subsequent RAS-mediated activation of ERK or p38MAPK or JNK pathways leads to proliferation or apoptosis, respectively [8] ONC : Suppresses cell motility and in vivo metastasis of mouse melanoma [2,3]. CD9 may act as a metastasis suppressor, at least in part, by neutralizing Aggrus-mediated platelet aggregation [4]. In multiple myeloma, CD9 is epigenetically silenced during disease progression and correlates with survival [5]. However, anti-CD9 antibodies inhibit transendothelial migration of melanoma cells [6]; plus, CD9 induces MMP-2 expression by activating c- Jun through p38 MAPK and JNK signaling pathways in human melanoma cells [7] CD33 CD33 antigen (gp67), SIGLEC3 (Sialic Sialic acid containing PHY : Putative adhesion molecule of [1] http://www.uniprot.org/uniprot/P20138. [2] acid-binding Ig-like lectin 3), sialoadhesin proteins myelomonocytic-derived cells that mediates Stasi R, Expert Opin Biol Ther 2008, 8:527-40 sialic-acid dependent binding to cells. Contains 2 copies of a cytoplasmic immunoreceptor tyrosine-based inhibitor motif (ITIM). The phosphorylated ITIM motif can bind the SH2 domain of several SH2- containing phosphatases. In the immune response, may act as an inhibitory receptor upon ligand-induced tyrosine phosphorylation MMMP Biomap #87 Page 4 by recruiting cytoplasmic phosphatase(s) via their SH2 domain(s) that block signal transduction through dephosphorylation of signaling molecules [1] ONC : Is used as a therapeutic target for acute myeloid leukemia [2] CD34 - L-selectin PHY: Adhesion molecule with a role in early [1] http://www.uniprot.org/uniprot/P28906 hematopoiesis by mediating the attachment of stem cells to the bone marrow extracellular matrix or directly to stromal cells. Selectively expressed on hematopoietic progenitor cells and the small vessel endothelium of a variety of tissues [1] ONC : - CD36 GP3B, PAS-4, Platelet collagen receptor, Collagen PHY : Expressed by platelets, macrophages [1] http://www.uniprot.org/uniprot/P16671. [2] Thrombospondin receptor, Fatty acid Thrombospondin and microvascular endothelial cells. McCarty MF, Med Hypotheses 2008, 70:419-23 translocase Scavenger receptor for oxidized LDL. Platelet adhesion. Directly mediates cytoadherence of Plasmodium falciparum parasitized erythrocytes. Defects in CD36 are the cause of platelet glycoprotein IV deficiency [1] ONC : The ability of metronomic chemotherapy to induce endothelial apoptosis
Recommended publications
  • Investigation of the Immune Receptors CEACAM3 and CEACAM4
    Investigation of the human immune receptors CEACAM3 and CEACAM4 Dissertation Zur Erlangung des akademischen Grades eines Doktors der Naturwissenschaften (Dr. rer. nat.) vorgelegt von Julia Delgado Tascón An der Universität Konstanz des Fachbereichs Biologie Konstanz, Oktober 2015 Konstanzer Online-Publikations-System (KOPS) URL: http://nbn-resolving.de/urn:nbn:de:bsz:352-0-306516 Tag der mündlichen Prüfung: 05.11.2015 Vorsitzender und mündlicher Prüfer: Herr Professor Dr. Bürkle 1. Referent und und mündlicher Prüfer: Herr Professor Dr. Hauck 2. Referent und und mündlicher Prüfer: Herr Professor Dr. Tschan, Universität Bern A mi familia Acknowledgements I would like to express my special gratitude to my advisor Prof. Dr. Christof Hauck. His patient guidance and enthusiastic encouragement during these four years of PhD were a crucial aid to my process. I’m very thankful for his willingness and for granting me with his time in search for valuable and constructive suggestions during the planning and development of this research work. This certainly allowed me to grow as a person and as a scientist. I would also like to thank my committee members: to Prof. Dr. Mario Tschan for giving me his academic support at this last phase of my PhD thesis, and to Prof. M.Dr. Alexander Bürkle for his wise advices accompanied with Spanish greetings along this time. My thanks are extended to every member of the AG Hauck as well. To Anne, Susana, Petra and Claudia: thank you very much for your technical and personal guidance during these years. I’m also thankful to my fellow colleagues for countless ‘Kaffeepausen’ full of jokes, nice discussions, and delicious vegan cakes.
    [Show full text]
  • Identification of the Binding Partners for Hspb2 and Cryab Reveals
    Brigham Young University BYU ScholarsArchive Theses and Dissertations 2013-12-12 Identification of the Binding arP tners for HspB2 and CryAB Reveals Myofibril and Mitochondrial Protein Interactions and Non- Redundant Roles for Small Heat Shock Proteins Kelsey Murphey Langston Brigham Young University - Provo Follow this and additional works at: https://scholarsarchive.byu.edu/etd Part of the Microbiology Commons BYU ScholarsArchive Citation Langston, Kelsey Murphey, "Identification of the Binding Partners for HspB2 and CryAB Reveals Myofibril and Mitochondrial Protein Interactions and Non-Redundant Roles for Small Heat Shock Proteins" (2013). Theses and Dissertations. 3822. https://scholarsarchive.byu.edu/etd/3822 This Thesis is brought to you for free and open access by BYU ScholarsArchive. It has been accepted for inclusion in Theses and Dissertations by an authorized administrator of BYU ScholarsArchive. For more information, please contact [email protected], [email protected]. Identification of the Binding Partners for HspB2 and CryAB Reveals Myofibril and Mitochondrial Protein Interactions and Non-Redundant Roles for Small Heat Shock Proteins Kelsey Langston A thesis submitted to the faculty of Brigham Young University in partial fulfillment of the requirements for the degree of Master of Science Julianne H. Grose, Chair William R. McCleary Brian Poole Department of Microbiology and Molecular Biology Brigham Young University December 2013 Copyright © 2013 Kelsey Langston All Rights Reserved ABSTRACT Identification of the Binding Partners for HspB2 and CryAB Reveals Myofibril and Mitochondrial Protein Interactors and Non-Redundant Roles for Small Heat Shock Proteins Kelsey Langston Department of Microbiology and Molecular Biology, BYU Master of Science Small Heat Shock Proteins (sHSP) are molecular chaperones that play protective roles in cell survival and have been shown to possess chaperone activity.
    [Show full text]
  • Propranolol-Mediated Attenuation of MMP-9 Excretion in Infants with Hemangiomas
    Supplementary Online Content Thaivalappil S, Bauman N, Saieg A, Movius E, Brown KJ, Preciado D. Propranolol-mediated attenuation of MMP-9 excretion in infants with hemangiomas. JAMA Otolaryngol Head Neck Surg. doi:10.1001/jamaoto.2013.4773 eTable. List of All of the Proteins Identified by Proteomics This supplementary material has been provided by the authors to give readers additional information about their work. © 2013 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 10/01/2021 eTable. List of All of the Proteins Identified by Proteomics Protein Name Prop 12 mo/4 Pred 12 mo/4 Δ Prop to Pred mo mo Myeloperoxidase OS=Homo sapiens GN=MPO 26.00 143.00 ‐117.00 Lactotransferrin OS=Homo sapiens GN=LTF 114.00 205.50 ‐91.50 Matrix metalloproteinase‐9 OS=Homo sapiens GN=MMP9 5.00 36.00 ‐31.00 Neutrophil elastase OS=Homo sapiens GN=ELANE 24.00 48.00 ‐24.00 Bleomycin hydrolase OS=Homo sapiens GN=BLMH 3.00 25.00 ‐22.00 CAP7_HUMAN Azurocidin OS=Homo sapiens GN=AZU1 PE=1 SV=3 4.00 26.00 ‐22.00 S10A8_HUMAN Protein S100‐A8 OS=Homo sapiens GN=S100A8 PE=1 14.67 30.50 ‐15.83 SV=1 IL1F9_HUMAN Interleukin‐1 family member 9 OS=Homo sapiens 1.00 15.00 ‐14.00 GN=IL1F9 PE=1 SV=1 MUC5B_HUMAN Mucin‐5B OS=Homo sapiens GN=MUC5B PE=1 SV=3 2.00 14.00 ‐12.00 MUC4_HUMAN Mucin‐4 OS=Homo sapiens GN=MUC4 PE=1 SV=3 1.00 12.00 ‐11.00 HRG_HUMAN Histidine‐rich glycoprotein OS=Homo sapiens GN=HRG 1.00 12.00 ‐11.00 PE=1 SV=1 TKT_HUMAN Transketolase OS=Homo sapiens GN=TKT PE=1 SV=3 17.00 28.00 ‐11.00 CATG_HUMAN Cathepsin G OS=Homo
    [Show full text]
  • The Utility of Genetic Risk Scores in Predicting the Onset of Stroke March 2021 6
    DOT/FAA/AM-21/24 Office of Aerospace Medicine Washington, DC 20591 The Utility of Genetic Risk Scores in Predicting the Onset of Stroke Diana Judith Monroy Rios, M.D1 and Scott J. Nicholson, Ph.D.2 1. KR 30 # 45-03 University Campus, Building 471, 5th Floor, Office 510 Bogotá D.C. Colombia 2. FAA Civil Aerospace Medical Institute, 6500 S. MacArthur Blvd Rm. 354, Oklahoma City, OK 73125 March 2021 NOTICE This document is disseminated under the sponsorship of the U.S. Department of Transportation in the interest of information exchange. The United States Government assumes no liability for the contents thereof. _________________ This publication and all Office of Aerospace Medicine technical reports are available in full-text from the Civil Aerospace Medical Institute’s publications Web site: (www.faa.gov/go/oamtechreports) Technical Report Documentation Page 1. Report No. 2. Government Accession No. 3. Recipient's Catalog No. DOT/FAA/AM-21/24 4. Title and Subtitle 5. Report Date March 2021 The Utility of Genetic Risk Scores in Predicting the Onset of Stroke 6. Performing Organization Code 7. Author(s) 8. Performing Organization Report No. Diana Judith Monroy Rios M.D1, and Scott J. Nicholson, Ph.D.2 9. Performing Organization Name and Address 10. Work Unit No. (TRAIS) 1 KR 30 # 45-03 University Campus, Building 471, 5th Floor, Office 510, Bogotá D.C. Colombia 11. Contract or Grant No. 2 FAA Civil Aerospace Medical Institute, 6500 S. MacArthur Blvd Rm. 354, Oklahoma City, OK 73125 12. Sponsoring Agency name and Address 13. Type of Report and Period Covered Office of Aerospace Medicine Federal Aviation Administration 800 Independence Ave., S.W.
    [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]
  • 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]
  • Full Text (PDF)
    Published OnlineFirst January 23, 2019; DOI: 10.1158/0008-5472.CAN-18-1261 Cancer Genome and Epigenome Research Sleeping Beauty Insertional Mutagenesis Reveals Important Genetic Drivers of Central Nervous System Embryonal Tumors Pauline J. Beckmann1, Jon D. Larson1, Alex T. Larsson1, Jason P. Ostergaard1, Sandra Wagner1, Eric P. Rahrmann1,2, Ghaidan A. Shamsan3, George M. Otto1,4, Rory L. Williams1,5, Jun Wang6, Catherine Lee6, Barbara R. Tschida1, Paramita Das1, Adrian M. Dubuc7, Branden S. Moriarity1, Daniel Picard8,9, Xiaochong Wu10, Fausto J. Rodriguez11, Quincy Rosemarie1,12, Ryan D. Krebs1, Amy M. Molan1,13, Addison M. Demer1, Michelle M. Frees1, Anthony E. Rizzardi14, Stephen C. Schmechel14,15, Charles G. Eberhart16, Robert B. Jenkins17, Robert J. Wechsler-Reya6, David J. Odde3, Annie Huang18, Michael D. Taylor10, Aaron L. Sarver1, and David A. Largaespada1 Abstract Medulloblastoma and central nervous system primitive identified several putative proto-oncogenes including Arh- neuroectodermal tumors (CNS-PNET) are aggressive, poorly gap36, Megf10,andFoxr2. Genetic manipulation of these differentiated brain tumors with limited effective therapies. genes demonstrated a robust impact on tumorigenesis Using Sleeping Beauty (SB) transposon mutagenesis, we in vitro and in vivo. We also determined that FOXR2 interacts identified novel genetic drivers of medulloblastoma and with N-MYC, increases C-MYC protein stability, and acti- CNS-PNET. Cross-species gene expression analyses classified vates FAK/SRC signaling. Altogether, our study identified SB-driven tumors into distinct medulloblastoma and several promising therapeutic targets in medulloblastoma CNS-PNET subgroups, indicating they resemble human and CNS-PNET. Sonic hedgehog and group 3 and 4 medulloblastoma and CNS neuroblastoma with FOXR2 activation.
    [Show full text]
  • Learning from Cadherin Structures and Sequences: Affinity Determinants and Protein Architecture
    Learning from cadherin structures and sequences: affinity determinants and protein architecture Klára Fels ıvályi Submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Graduate School of Arts and Sciences COLUMBIA UNIVERSITY 2014 © 2014 Klara Felsovalyi All rights reserved ABSTRACT Learning from cadherin structures and sequences: affinity determinants and protein architecture Klara Felsovalyi Cadherins are a family of cell-surface proteins mediating adhesion that are important in development and maintenance of tissues. The family is defined by the repeating cadherin domain (EC) in their extracellular region, but they are diverse in terms of protein size, architecture and cellular function. The best-understood subfamily is the type I classical cadherins, which are found in vertebrates and have five EC domains. Among the five different type I classical cadherins, the binding interactions are highly specific in their homo- and heterophilic binding affinities, though their sequences are very similar. As previously shown, E- and N-cadherins, two prototypic members of the subfamily, differ in their homophilic K D by about an order of magnitude, while their heterophilic affinity is intermediate. To examine the source of the binding affinity differences among type I cadherins, we used crystal structures, analytical ultracentrifugation (AUC), surface plasmon resonance (SPR), and electron paramagnetic resonance (EPR) studies. Phylogenetic analysis and binding affinity behavior show that the type I cadherins can be further divided into two subgroups, with E- and N-cadherin representing each. In addition to the affinity differences in their wild-type binding through the strand-swapped interface, a second interface also shows an affinity difference between E- and N-cadherin.
    [Show full text]
  • Comprehensive Array CGH of Normal Karyotype Myelodysplastic
    Leukemia (2011) 25, 387–399 & 2011 Macmillan Publishers Limited All rights reserved 0887-6924/11 www.nature.com/leu LEADING ARTICLE Comprehensive array CGH of normal karyotype myelodysplastic syndromes reveals hidden recurrent and individual genomic copy number alterations with prognostic relevance A Thiel1, M Beier1, D Ingenhag1, K Servan1, M Hein1, V Moeller1, B Betz1, B Hildebrandt1, C Evers1,3, U Germing2 and B Royer-Pokora1 1Institute of Human Genetics and Anthropology, Medical Faculty, Heinrich Heine University, Duesseldorf, Germany and 2Department of Hematology, Oncology and Clinical Immunology, Heinrich Heine University, Duesseldorf, Germany About 40% of patients with myelodysplastic syndromes (MDSs) 40–50% of MDS cases have a normal karyotype. MDS patients present with a normal karyotype, and they are facing different with a normal karyotype and low-risk clinical parameters are courses of disease. To advance the biological understanding often assigned into the IPSS low and intermediate-1 risk groups. and to find molecular prognostic markers, we performed a high- resolution oligonucleotide array study of 107 MDS patients In the absence of genetic or biological markers, prognostic (French American British) with a normal karyotype and clinical stratification of these patients is difficult. To better prognosticate follow-up through the Duesseldorf MDS registry. Recurrent these patients, new parameters to identify patients at higher risk hidden deletions overlapping with known cytogenetic aberra- are urgently needed. With the more recently introduced modern tions or sites of known tumor-associated genes were identi- technologies of whole-genome-wide surveys of genetic aberra- fied in 4q24 (TET2, 2x), 5q31.2 (2x), 7q22.1 (3x) and 21q22.12 tions, it is hoped that more insights into the biology of disease (RUNX1, 2x).
    [Show full text]
  • CD Markers Are Routinely Used for the Immunophenotyping of Cells
    ptglab.com 1 CD MARKER ANTIBODIES www.ptglab.com Introduction The cluster of differentiation (abbreviated as CD) is a protocol used for the identification and investigation of cell surface molecules. So-called CD markers are routinely used for the immunophenotyping of cells. Despite this use, they are not limited to roles in the immune system and perform a variety of roles in cell differentiation, adhesion, migration, blood clotting, gamete fertilization, amino acid transport and apoptosis, among many others. As such, Proteintech’s mini catalog featuring its antibodies targeting CD markers is applicable to a wide range of research disciplines. PRODUCT FOCUS PECAM1 Platelet endothelial cell adhesion of blood vessels – making up a large portion molecule-1 (PECAM1), also known as cluster of its intracellular junctions. PECAM-1 is also CD Number of differentiation 31 (CD31), is a member of present on the surface of hematopoietic the immunoglobulin gene superfamily of cell cells and immune cells including platelets, CD31 adhesion molecules. It is highly expressed monocytes, neutrophils, natural killer cells, on the surface of the endothelium – the thin megakaryocytes and some types of T-cell. Catalog Number layer of endothelial cells lining the interior 11256-1-AP Type Rabbit Polyclonal Applications ELISA, FC, IF, IHC, IP, WB 16 Publications Immunohistochemical of paraffin-embedded Figure 1: Immunofluorescence staining human hepatocirrhosis using PECAM1, CD31 of PECAM1 (11256-1-AP), Alexa 488 goat antibody (11265-1-AP) at a dilution of 1:50 anti-rabbit (green), and smooth muscle KD/KO Validated (40x objective). alpha-actin (red), courtesy of Nicola Smart. PECAM1: Customer Testimonial Nicola Smart, a cardiovascular researcher “As you can see [the immunostaining] is and a group leader at the University of extremely clean and specific [and] displays Oxford, has said of the PECAM1 antibody strong intercellular junction expression, (11265-1-AP) that it “worked beautifully as expected for a cell adhesion molecule.” on every occasion I’ve tried it.” Proteintech thanks Dr.
    [Show full text]
  • 140503 IPF Signatures Supplement Withfigs Thorax
    Supplementary material for Heterogeneous gene expression signatures correspond to distinct lung pathologies and biomarkers of disease severity in idiopathic pulmonary fibrosis Daryle J. DePianto1*, Sanjay Chandriani1⌘*, Alexander R. Abbas1, Guiquan Jia1, Elsa N. N’Diaye1, Patrick Caplazi1, Steven E. Kauder1, Sabyasachi Biswas1, Satyajit K. Karnik1#, Connie Ha1, Zora Modrusan1, Michael A. Matthay2, Jasleen Kukreja3, Harold R. Collard2, Jackson G. Egen1, Paul J. Wolters2§, and Joseph R. Arron1§ 1Genentech Research and Early Development, South San Francisco, CA 2Department of Medicine, University of California, San Francisco, CA 3Department of Surgery, University of California, San Francisco, CA ⌘Current address: Novartis Institutes for Biomedical Research, Emeryville, CA. #Current address: Gilead Sciences, Foster City, CA. *DJD and SC contributed equally to this manuscript §PJW and JRA co-directed this project Address correspondence to Paul J. Wolters, MD University of California, San Francisco Department of Medicine Box 0111 San Francisco, CA 94143-0111 [email protected] or Joseph R. Arron, MD, PhD Genentech, Inc. MS 231C 1 DNA Way South San Francisco, CA 94080 [email protected] 1 METHODS Human lung tissue samples Tissues were obtained at UCSF from clinical samples from IPF patients at the time of biopsy or lung transplantation. All patients were seen at UCSF and the diagnosis of IPF was established through multidisciplinary review of clinical, radiological, and pathological data according to criteria established by the consensus classification of the American Thoracic Society (ATS) and European Respiratory Society (ERS), Japanese Respiratory Society (JRS), and the Latin American Thoracic Association (ALAT) (ref. 5 in main text). Non-diseased normal lung tissues were procured from lungs not used by the Northern California Transplant Donor Network.
    [Show full text]
  • Literature Mining Sustains and Enhances Knowledge Discovery from Omic Studies
    LITERATURE MINING SUSTAINS AND ENHANCES KNOWLEDGE DISCOVERY FROM OMIC STUDIES by Rick Matthew Jordan B.S. Biology, University of Pittsburgh, 1996 M.S. Molecular Biology/Biotechnology, East Carolina University, 2001 M.S. Biomedical Informatics, University of Pittsburgh, 2005 Submitted to the Graduate Faculty of School of Medicine in partial fulfillment of the requirements for the degree of Doctor of Philosophy University of Pittsburgh 2016 UNIVERSITY OF PITTSBURGH SCHOOL OF MEDICINE This dissertation was presented by Rick Matthew Jordan It was defended on December 2, 2015 and approved by Shyam Visweswaran, M.D., Ph.D., Associate Professor Rebecca Jacobson, M.D., M.S., Professor Songjian Lu, Ph.D., Assistant Professor Dissertation Advisor: Vanathi Gopalakrishnan, Ph.D., Associate Professor ii Copyright © by Rick Matthew Jordan 2016 iii LITERATURE MINING SUSTAINS AND ENHANCES KNOWLEDGE DISCOVERY FROM OMIC STUDIES Rick Matthew Jordan, M.S. University of Pittsburgh, 2016 Genomic, proteomic and other experimentally generated data from studies of biological systems aiming to discover disease biomarkers are currently analyzed without sufficient supporting evidence from the literature due to complexities associated with automated processing. Extracting prior knowledge about markers associated with biological sample types and disease states from the literature is tedious, and little research has been performed to understand how to use this knowledge to inform the generation of classification models from ‘omic’ data. Using pathway analysis methods to better understand the underlying biology of complex diseases such as breast and lung cancers is state-of-the-art. However, the problem of how to combine literature- mining evidence with pathway analysis evidence is an open problem in biomedical informatics research.
    [Show full text]