DOCSLIB.ORG

Keyword Index

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Keyword Index Gene Therapy (1998) 5, 1717–1719 1998 Stockton Press All rights reserved 0969-7128/98 $12.00 http://www.stockton-press.co.uk/gt Keyword Index Volume 5 1998 15-deoxyspergualin 85 (BC) bcl-2 1156 complex stability 137 (BC) 293 cells adenoviral vectors 563 (BC) bicistronic vectors 1566 (BC) computerized tomography 896 5-azacytidine 1299 bidirectional promoter 76 connexin43 1114, 1221, 1372 5-fluorocytosine 507 biodegradable microspheres 740 cord blood 233 6-hydroxydopamine (6-OHDA) 1650 biolistics 692 corneal endothelium 1347 99mTc 798 BMP-7 1098 coronary infusion 1472 bone repair 1098 costimulation 223 AAV 50, 820 bradykinin 630 costimulatory 965 AAV helper genes 938 brain 712 (BC), 820 Cre-mediated recombination 1047 AAV vector production 938 brain tumors 1122 Cre/loxP 684 adeno-associated virus 277 (BC), 1434, breast tumor 240 cyclophosphamide 189 1604, 1642 bronchoscopy 166 cystic fibrosis 91, 131 (BC), 181, 218, 309, adeno-associated virus (AAV) 166 bystander effect 105, 113, 605, 1114, 1221, 345, 583, 1488 adenosine deaminase 320 1372, 1705 cytidine deaminase 1545 adenoviral gene transfer 85 cytochrome P450 1070 adenoviral vectors 309, 869, 1251 C2C12 1014 cytokine gene 1462 adenovirus 8, 19, 131 (BC), 174, 339, 345, CAG 240 cytokine gene transfer 481 352, 473, 507, 605, 621, 630, 740, 747, cancer 728 (R), 1105, 1400, 1462 cytokine receptors 253 778, 938, 975, 995, 1023, 1038, 1130, cancer gene therapy 189, 451, 1171 cytokines 253, 869, 1400 1156, 1213, 1259, 1314, 1363, 1400, 1552, cancer vaccine 247, 1677 cytosine arabinoside 1545 1612 canine 40, 865 cytosine deaminase 1130, 1571 (BC) adenovirus (Ad) 166 capillary permeability 630 cytotoxic T lymphocytes 189, 459 adenovirus infection 1340 capsules 828 adenovirus knob 798 carboxy-terminal deletions 1631 decorin 1187 adenovirus type 41 645 cationic agent 1180 delivery 848 adenovirus type 5 645 cationic lipids 137 (BC), 855 (BC), 995, dendritic cells 264, 700, 718 (BC) adenovirus vectors 465, 497, 965, 1148 1272 diabetes 8 (BC) cationic liposomes 181, 240, 301, 380, 583, DMI-2 1244 adenovirus-mediated gene transfer 361 614, 930, 955, 1531, 1538 DMRIE 1272 adjuvant 1447, 1677 cationic polymers 712 (BC), 1291 (BC) DNA 865, 1235 adoptive immunotherapy 1508 cationic vector 1508 DNA compaction 855 (BC) AIDS 99 CB1954 105, 1061 DNA complexes 1410 + alkyltransferase 835, 842 CD34 blood cells 465 DNA-binding domain 1204 + allogeneic tumour vaccination 1447 CD34 cells 233 dopamine 820 + anemia 1014 CD4 cells 655 drug resistance 1545 angiogenesis 747, 1105 CD40 ligand 431 DTH reactivity 481 animal 1622 CD80 965, 1355 Duchenne muscular dystrophy 59, 369, anti-idiotypic response 828 CEA 865 1340 antibody 459, 995 CEA promoter 1363 dystrophin 19, 59 antibody delivery 828 cell adhesion 913, 1322 dystrophin minigene 1340 antigen 975 cell cycle regulatory gene 761 dystrophin-associated proteins 19 antisense 1455 cell invasion 1105 antisense RNA 1462 cellular 865 E1A 1538 antisense therapy 388 cellulose sulphate matrix 828 EBNA1 1389 APC 431 central nervous system 50, 1137 EBV 1171 aphidicolin 1481 CFU-S 842 EBV LMP1 905 apoptosis 331, 563 (BC), 605, 728 (R) chemokine receptor 984 EBV vector 1031 arteries 1023 chloroquine 409 (BC) ecotropic retrovirus 621 artificial epidermis 1322 cholecystokinin 848 efficiency 621 aspartylglucosaminidase 1314 cholesterol 137 (BC) EGF receptor 521 aspartylglucosaminuria 1314 CIK cells 31 elafin 352 attenuated herpesviruses 160 CNS 740 elastase 1023 attitudes 218 cochlea, hearing disorders 277 (BC) elastase-specific inhibitor 352 collagen-induced arthritis 1584 electroporation 700, 1347 ␤-galactosidase 277 (BC), 301, 1283 (BC) colon carcinoma 507 electroretinogram 1088 ␤-glucuronidase 1642 colorectal cancer 869, 1054 encapsulation 1014, 1070 B16-F10 melanoma 1447 colorectal tumour 223 endoscopy 166 B7.1 965, 1447 complement inhibitors 531 endosomolysis 409 (BC) baculovirus vectors 531 complement system 531 endothelial cell 614 basement membrane 1322 complement-dependent selection 282 (BC) endothelial cell-specific transcription 1656 Keyword index 1718 endothelium 272 (BC), 747 hematopoiesis 692, 755 internal ribosome entry site 65 episomal maintenance 1389 hematopoietic cells 1545, 1575 (BC) intestine 645 Epstein–Barr virus 1389 hematopoietic progenitor cells 718 (BC) intracerebral 121 equine infectious anemia virus 1481 hemophilia B 40, 394 intracerebral gene transfer 1650 erythropoietin 665, 1014 hepatocellular carcinoma 1114 intracoronary gene delivery 301 etoposide 189 hepatocytes 531, 888, 1259 intrakine 984 ex vivo approach 19 hepatoma 880 IRES 635, 1003 (BC), 1441 (BC), 1566 (BC) Exosurf 1333 hepatoma cells 1204 extracellular matrix 1322 HER-2/neu 1538 K562 835 extrusion 1272 herpes simplex thymidine kinase (HTK) eye 1038, 1561 (BC) 1698 lacZ 1347 herpes simplex virus 1517, 1593 lacZ gene 789 FACS 556 (BC) herpes simplex virus thymidine kinase laminin-5 1322 factor IX 40, 394 1372, 1705 late effects 196 Fas ligand 1622 herpes simplex viruses 121 latent membrane protein 1 1171 Fas-mediated apoptosis 1047 herpes vector 718 (BC), 1137 lentiviral vector 1481 Fas/Apo-1 563 (BC) high-density lipoproteins 1434 lentivirus vector 635 Fas/FasL 331 HIV 1665 leukemia/lymphoma 1355 FasL 563 (BC) HIV Env 655 ligament 1165, 1455 FDG 880 HIV-1 65, 233, 946, 984 linamarase/linamarin 1499 flow cytometry 209, 700 HIV-inducible vector 1665 lipofection 380, 542, 708 (BC) fluorescence microscopy 556 (BC) HMG-12 240 lipoplex 542 formulation 1235, 1272 homologous recombination 149 (R) liposome 380, 388, 1165, 1306, 1455, 1488 fusigenic peptides 955 HPV 1462 lipospermine 855 (BC) fusion 770 HSV 491, 594, 1420 liver 431, 552 (BC), 1180, 1259 fusion protein 521 HSV-1 440, 809, 1566 (BC) liver gene therapy 531 HSV-1 thymidine kinase 419 (BC) local therapy 1070 GAL4 521 HSV-thymidine kinase 614, 880 long-term expression 85 ganciclovir 905, 1054, 1363, 1372, 1705 HSVtk 1114, 1122, 1363 long-term gene expression 1031 ganciclovir elaidic ester 419 (BC) human alpha-1-antitrypsin 85 lung 1333 gap junction 1372, 1705 human CD34+ 835 lung cancer 778 gastrointestinal-specific transcription 1656 human monocytes 1508 lung cancer cells 361 gene delivery 645, 955, 1137, 1251, 1272, humoral 865 lung gene therapy 181 1333, 1410, 1434, 1566 (BC) HVJ liposome 1031, 1472 lymphocytes 209, 984 gene expression 253 hybrid cells 1447 lymphoma 403 gene regulation 320, 1604 hybridoma 828 lymphoproliferative diseases 1171 gene targeting 149 (R) lysosomal storage 1314 gene therapeutics 537 ICAM-1 131 (BC) lysosomal storage disease 1642 gene therapy 50, 59, 65, 76, 91, 99, 105, IFN␤ 253 lysosomes 473 131 (BC), 149 (R), 166, 218, 223, 233, 272 IFN-␥ 1508 (BC), 282 (BC), 293, 309, 320, 331, 345, ifosfamide 1070 macrophage depletion 431 352, 419 (BC), 431, 491, 507, 521, 552 IL-12 223 malignant gliomas 160, 293, 1187 (BC), 556 (BC), 583, 605, 614, 621, 630, IL-12 secretion 481 mammary adenocarcinoma 388 665, 692, 708 (BC), 728 (R), 740, 747, IL-2R␣ 635 MBP promoter 50 761, 778, 880, 888, 905, 923, 930, 946, IL2 975 MDR1 671 965, 984, 1003 (BC), 1023, 1054, 1088, imaging 798 mdx 59 1098, 1114, 1122, 1130, 1148 (BC), 1156, immune privilege 563 (BC), 1038 mdx diaphragm 369 1165, 1180, 1187, 1227, 1283 (BC), 1291 immune response 1038, 1561 (BC) mdx mouse 19 (BC), 1299, 1306, 1314, 1347, 1379, 1389, immune system 1187 medulloblastoma 113 1400, 1441 (BC), 1455, 1462, 1488, 1499, immune therapy 1187 melanoma 223, 975, 1130 1531, 1538, 1552, 1561 (BC), 1584, 1612, immunity 309, 789, 809 methotrexate 1379 1642, 1665, 1677, 1685, 1705 immunogene therapy 1195, 1355 methylation 1299 gene transfer 40, 113, 174, 272 (BC), 380, immunosuppression 85, 369, 497, 1612 mGM-CSF 76, 770 403, 465, 514, 542, 575, 655, 671, 700, immunotherapy 869, 1079, 1400 microinjection 409 (BC) 708 (BC), 712 (BC), 809, 855 (BC), 896, importin subunits 1204 micronucleus 842 930, 995, 1079, 1221, 1244, 1259, 1425, in situ PCR 755 migration 1698 1472, 1545, 1593, 1604, 1622 in vivo 1265 MMTV-neu 388 genetic immunization 789 in vivo expression 1545 MnSOD 196 GFAP promoter 440 in vivo gene transduction 459 monkey 820 GFP 684 inborn errors of metabolism 677 monocytes 99 GFP fusion proteins 1420 inducible apoptosis 923 mouse melanoma 247 glial fibrillary acidic protein 1650 induction of apoptosis 1631 mouse models 160, 1314 glioma 121, 809, 1698 INF-␥ 240 mucopolysaccharidosis 1642 glioma therapy 440 INF7 409 (BC) multidrug resistance 403 gliomas 1221 inflammation 1283 (BC) multigene vectors 1517 glucose 8 inflammatory cells 121 multiple sclerosis model 253 GM-CSF 223, 1355 inhibitory cytokine 1265 murine 1265 gp75 975 insulin 888 muscle 40, 272 (BC), 514, 677, 1283 (BC) granulocyte–macrophage colony- integrin 361, 1259, 1488 muscle function 369 stimulating factor 1130 interleukin-1 778 Mycobacterium tuberculosis 247 green fluorescent protein (GFP), 50, 166, interleukin-2 1003 (BC) myelofibrosis 497 700, 1148 (BC) interleukin-3 778 myelosuppression 497 growth hormone 537 interleukin-4 121 myoblast transplantation 1340 interleukin-7 31 myoblasts 1014, 1306 hammerhead ribozyme 1227 interleukin-10, 121 myocardinal infarction 301 heart diseases 630 internal promoter 1299 myocardium 1472 Keyword index 1719 myogenic cells 1306 prodrug 507 spinal cord 1612 myopathy 473 prodrug therapy 1070 sputum 91 promoter 514, 789, 1650 stem cells 149 (R), 692, 913, 1265 protein trafficking 1420 storage disease 473 N13-ras transformation 1227 proteinase inhibitor 352 striatum 594 naked DNA 1531 pseudofection 1410 structure–function relationship 1685 nebulisation 583 Pseudomonas aeruginosa
Load more

Recommended publications
  • Supplementary Table S4. FGA Co-Expressed Gene List in LUAD
    Supplementary Table S4. FGA co-expressed gene list in LUAD tumors Symbol R Locus Description FGG 0.919 4q28 fibrinogen gamma chain FGL1 0.635 8p22 fibrinogen-like 1 SLC7A2 0.536 8p22 solute carrier family 7 (cationic amino acid transporter, y+ system), member 2 DUSP4 0.521 8p12-p11 dual specificity phosphatase 4 HAL 0.51 12q22-q24.1histidine ammonia-lyase PDE4D 0.499 5q12 phosphodiesterase 4D, cAMP-specific FURIN 0.497 15q26.1 furin (paired basic amino acid cleaving enzyme) CPS1 0.49 2q35 carbamoyl-phosphate synthase 1, mitochondrial TESC 0.478 12q24.22 tescalcin INHA 0.465 2q35 inhibin, alpha S100P 0.461 4p16 S100 calcium binding protein P VPS37A 0.447 8p22 vacuolar protein sorting 37 homolog A (S. cerevisiae) SLC16A14 0.447 2q36.3 solute carrier family 16, member 14 PPARGC1A 0.443 4p15.1 peroxisome proliferator-activated receptor gamma, coactivator 1 alpha SIK1 0.435 21q22.3 salt-inducible kinase 1 IRS2 0.434 13q34 insulin receptor substrate 2 RND1 0.433 12q12 Rho family GTPase 1 HGD 0.433 3q13.33 homogentisate 1,2-dioxygenase PTP4A1 0.432 6q12 protein tyrosine phosphatase type IVA, member 1 C8orf4 0.428 8p11.2 chromosome 8 open reading frame 4 DDC 0.427 7p12.2 dopa decarboxylase (aromatic L-amino acid decarboxylase) TACC2 0.427 10q26 transforming, acidic coiled-coil containing protein 2 MUC13 0.422 3q21.2 mucin 13, cell surface associated C5 0.412 9q33-q34 complement component 5 NR4A2 0.412 2q22-q23 nuclear receptor subfamily 4, group A, member 2 EYS 0.411 6q12 eyes shut homolog (Drosophila) GPX2 0.406 14q24.1 glutathione peroxidase
    [Show full text]
  • Common Differentially Expressed Genes and Pathways Correlating Both Coronary Artery Disease and Atrial Fibrillation
    EXCLI Journal 2021;20:126-141– ISSN 1611-2156 Received: December 08, 2020, accepted: January 11, 2021, published: January 18, 2021 Supplementary material to: Original article: COMMON DIFFERENTIALLY EXPRESSED GENES AND PATHWAYS CORRELATING BOTH CORONARY ARTERY DISEASE AND ATRIAL FIBRILLATION Youjing Zheng, Jia-Qiang He* Department of Biomedical Sciences and Pathobiology, College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061, USA * Corresponding author: Jia-Qiang He, Department of Biomedical Sciences and Pathobiology, Virginia Tech, Phase II, Room 252B, Blacksburg, VA 24061, USA. Tel: 1-540-231-2032. E-mail: [email protected] https://orcid.org/0000-0002-4825-7046 Youjing Zheng https://orcid.org/0000-0002-0640-5960 Jia-Qiang He http://dx.doi.org/10.17179/excli2020-3262 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/). Supplemental Table 1: Abbreviations used in the paper Abbreviation Full name ABCA5 ATP binding cassette subfamily A member 5 ABCB6 ATP binding cassette subfamily B member 6 (Langereis blood group) ABCB9 ATP binding cassette subfamily B member 9 ABCC10 ATP binding cassette subfamily C member 10 ABCC13 ATP binding cassette subfamily C member 13 (pseudogene) ABCC5 ATP binding cassette subfamily C member 5 ABCD3 ATP binding cassette subfamily D member 3 ABCE1 ATP binding cassette subfamily E member 1 ABCG1 ATP binding cassette subfamily G member 1 ABCG4 ATP binding cassette subfamily G member 4 ABHD18 Abhydrolase domain
    [Show full text]
  • Human Induced Pluripotent Stem Cell–Derived Podocytes Mature Into Vascularized Glomeruli Upon Experimental Transplantation
    BASIC RESEARCH www.jasn.org Human Induced Pluripotent Stem Cell–Derived Podocytes Mature into Vascularized Glomeruli upon Experimental Transplantation † Sazia Sharmin,* Atsuhiro Taguchi,* Yusuke Kaku,* Yasuhiro Yoshimura,* Tomoko Ohmori,* ‡ † ‡ Tetsushi Sakuma, Masashi Mukoyama, Takashi Yamamoto, Hidetake Kurihara,§ and | Ryuichi Nishinakamura* *Department of Kidney Development, Institute of Molecular Embryology and Genetics, and †Department of Nephrology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan; ‡Department of Mathematical and Life Sciences, Graduate School of Science, Hiroshima University, Hiroshima, Japan; §Division of Anatomy, Juntendo University School of Medicine, Tokyo, Japan; and |Japan Science and Technology Agency, CREST, Kumamoto, Japan ABSTRACT Glomerular podocytes express proteins, such as nephrin, that constitute the slit diaphragm, thereby contributing to the filtration process in the kidney. Glomerular development has been analyzed mainly in mice, whereas analysis of human kidney development has been minimal because of limited access to embryonic kidneys. We previously reported the induction of three-dimensional primordial glomeruli from human induced pluripotent stem (iPS) cells. Here, using transcription activator–like effector nuclease-mediated homologous recombination, we generated human iPS cell lines that express green fluorescent protein (GFP) in the NPHS1 locus, which encodes nephrin, and we show that GFP expression facilitated accurate visualization of nephrin-positive podocyte formation in
    [Show full text]
  • Figure S1. Reverse Transcription‑Quantitative PCR Analysis of ETV5 Mrna Expression Levels in Parental and ETV5 Stable Transfectants
    Figure S1. Reverse transcription‑quantitative PCR analysis of ETV5 mRNA expression levels in parental and ETV5 stable transfectants. (A) Hec1a and Hec1a‑ETV5 EC cell lines; (B) Ishikawa and Ishikawa‑ETV5 EC cell lines. **P<0.005, unpaired Student's t‑test. EC, endometrial cancer; ETV5, ETS variant transcription factor 5. Figure S2. Survival analysis of sample clusters 1‑4. Kaplan Meier graphs for (A) recurrence‑free and (B) overall survival. Survival curves were constructed using the Kaplan‑Meier method, and differences between sample cluster curves were analyzed by log‑rank test. Figure S3. ROC analysis of hub genes. For each gene, ROC curve (left) and mRNA expression levels (right) in control (n=35) and tumor (n=545) samples from The Cancer Genome Atlas Uterine Corpus Endometrioid Cancer cohort are shown. mRNA levels are expressed as Log2(x+1), where ‘x’ is the RSEM normalized expression value. ROC, receiver operating characteristic. Table SI. Clinicopathological characteristics of the GSE17025 dataset. Characteristic n % Atrophic endometrium 12 (postmenopausal) (Control group) Tumor stage I 91 100 Histology Endometrioid adenocarcinoma 79 86.81 Papillary serous 12 13.19 Histological grade Grade 1 30 32.97 Grade 2 36 39.56 Grade 3 25 27.47 Myometrial invasiona Superficial (<50%) 67 74.44 Deep (>50%) 23 25.56 aMyometrial invasion information was available for 90 of 91 tumor samples. Table SII. Clinicopathological characteristics of The Cancer Genome Atlas Uterine Corpus Endometrioid Cancer dataset. Characteristic n % Solid tissue normal 16 Tumor samples Stagea I 226 68.278 II 19 5.740 III 70 21.148 IV 16 4.834 Histology Endometrioid 271 81.381 Mixed 10 3.003 Serous 52 15.616 Histological grade Grade 1 78 23.423 Grade 2 91 27.327 Grade 3 164 49.249 Molecular subtypeb POLE 17 7.328 MSI 65 28.017 CN Low 90 38.793 CN High 60 25.862 CN, copy number; MSI, microsatellite instability; POLE, DNA polymerase ε.
    [Show full text]
  • Characterization of Aspartylglucosaminidase Activation and Aspartylglucosaminuria Mutations
    Arto Pennanen Publications of the National Public Health Institute A 1 / 2004 — INDOOR AIR POLLUTION AND HEALTH RISKS IN FINNISH ICE ARENAS RISKSINFINNISHICE AND HEALTH AIR POLLUTION INDOOR Jani Saarela CHARACTERIZATION OF ASPARTYLGLUCOSAMINIDASE ACTIVATION AND ASPARTYLGLUCOSAMINURIA MUTATIONS ISBN 951-740-485-9 ISSN 0359-3584 ISBN 951-740-486-7 (pdf) Department of Molecular Medicine, ISSN 1458-6290 (pdf) National Public Health Institute, Helsinki, Finland and http://www.ktl.fi /portal/suomi/julkaisut/julkaisusarjat/ Department of Medical Genetics, kansanterveyslaitoksen_julkaisuja_a/ University of Helsinki, Finland Kopijyvä Kuopio 2005 Helsinki 2004 PPennanen_kansi.inddennanen_kansi.indd 1 117.2.20057.2.2005 115:26:195:26:19 CHARACTERIZATION OF ASPARTYLGLUCOSAMINIDASE ACTIVATION AND ASPARTYLGLUCOSAMINURIA MUTATIONS Jani Saarela Department of Molecular Medicine, National Public Health Institute, Helsinki, Finland and Department of Medical Genetics, University of Helsinki, Finland Academic Dissertation To be publicly discussed with the permission of the Medical Faculty of the University of Helsinki, in the lecture room 3 of Biomedicum Helsinki, Haartmaninkatu 8, Helsinki, on January 30th, 2004, at 12 o’clock noon. Helsinki 2004 Supervised by Professor Leena Peltonen-Palotie National Public Health Institute and Department of Medical Genetics University of Helsinki, Helsinki, Finland Reviewed by Professor Ole Kristian Tollersrud and Docent Marc Baumann Department of Medical Biochemistry Protein Chemistry/Proteomics Unit University of Tromsoe and Neuroscience Research Program Tromsoe, Norway University of Helsinki, Helsinki, Finland To be publicly discussed with Professor Marja Makarow Institute of Biotechnology and Department of Applied Biochemistry and Molecular Biology University of Helsinki, Helsinki, Finland Julkaisija-Utgivare-Publisher Kansanterveyslaitos (KTL) Mannerheimintie 166 00300 Helsinki puh. vaihde 09-47441, felefax 09-4744 8408 Folkhälsoinstitutet Mannerheimvägen 166 00300, Helsinki tel.
    [Show full text]
  • Induction of Therapeutic Tissue Tolerance Foxp3 Expression Is
    Downloaded from http://www.jimmunol.org/ by guest on October 2, 2021 is online at: average * The Journal of Immunology , 13 of which you can access for free at: 2012; 189:3947-3956; Prepublished online 17 from submission to initial decision 4 weeks from acceptance to publication September 2012; doi: 10.4049/jimmunol.1200449 http://www.jimmunol.org/content/189/8/3947 Foxp3 Expression Is Required for the Induction of Therapeutic Tissue Tolerance Frederico S. Regateiro, Ye Chen, Adrian R. Kendal, Robert Hilbrands, Elizabeth Adams, Stephen P. Cobbold, Jianbo Ma, Kristian G. Andersen, Alexander G. Betz, Mindy Zhang, Shruti Madhiwalla, Bruce Roberts, Herman Waldmann, Kathleen F. Nolan and Duncan Howie J Immunol cites 35 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription http://www.jimmunol.org/content/suppl/2012/09/17/jimmunol.120044 9.DC1 This article http://www.jimmunol.org/content/189/8/3947.full#ref-list-1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material References Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2012 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of October 2, 2021.
    [Show full text]
  • Open Mithun Shah.Pdf
    The Pennsylvania State University The Graduate School Department of Molecular Medicine ROLE OF SPHINGOLIPID SIGNALING IN PATHOGENESIS OF LARGE GRANULAR LYMPHOCYTE LEUKEMIA A Dissertation in Molecular Medicine by Mithun Vinod Shah © 2009 Mithun Vinod Shah Submitted in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy May 2009 ii The dissertation of Mithun Vinod Shah was reviewed and approved* by the following: Thomas P. Loughran, Jr. Professor of Medicine Dissertation Advisor Co-Chair of Committee Rosalyn B. Irby Assistant Professor of Medicine Co-chair of Committee Gary Clawson Professor of Pathology, and Biochemistry and Molecular Biology Edward J. Gunther Assistant Professor of Medicine Charles H. Lang Director, Molecular Medicine Graduate Program *Signatures are on file in the Graduate School iii ABSTRACT Large granular lymphocyte (LGL) leukemia is a disorder of mature cytotoxic cells. LGL leukemia is characterized by accumulation of cytotoxic cells in blood and infiltration in bone marrow and other tissues. Leukemic LGL could arise from expansion of either CD3+ CD8+ T-cells (T-cell LGL leukemia or T-LGL leukemia) or those arising from CD3- natural killer (NK)-cells (NK-cell LGL leukemia or NK-LGL leukemia). LGL leukemia is a rare disorder consisting of less than 5% of non-B cell leukemia. Clinically, LGL leukemia can manifest along a spectrum of disorders ranging from slowly progressing indolent disorder to an aggressive leukemia that could be fatal within months. About fifty percent of LGL leukemia patients also present with variety of autoimmune conditions, rheumatoid arthritis being the most common one. Normally, following antigen clearance, cytotoxic T-lymphocytes (CTL) become sensitive to Fas-mediated apoptosis resulting in activation-induced cell death (AICD).
    [Show full text]
  • Conventional and Unconventional Therapeutic Strategies for Sialidosis Type I
    Journal of Clinical Medicine Article Conventional and Unconventional Therapeutic Strategies for Sialidosis Type I 1, 1, 1 1,2 Rosario Mosca y, Diantha van de Vlekkert y , Yvan Campos , Leigh E. Fremuth , Jaclyn Cadaoas 3 , Vish Koppaka 3, Emil Kakkis 3, Cynthia Tifft 4, Camilo Toro 5 , Simona Allievi 6,7, Cinzia Gellera 6,7, Laura Canafoglia 7 , Gepke Visser 8 , Ida Annunziata 1 and Alessandra d’Azzo 1,* 1 Department of Genetics, St. Jude Children’s Research Hospital, Memphis, TN 38105, USA; [email protected] (R.M.); [email protected] (D.v.d.V.); [email protected] (Y.C.); [email protected] (L.E.F.); [email protected] (I.A.) 2 Department of Anatomy and Neurobiology, College of Graduate Health Sciences, University of Tennessee Health Science Center, Memphis, TN 38163, USA 3 Ultragenyx Pharmaceutical, Novato, CA 94949, USA; [email protected] (J.C.); [email protected] (V.K.); [email protected] (E.K.) 4 Office of the Clinical Director & Medical Genetics Branch, National Human Genome Research Institute, National Institutes of Health (NHGRI), Bethesda, MD 20892, USA; [email protected] 5 Undiagnosed Disease Network, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA; [email protected] 6 Unit of Genetics of Neurodegenerative and Metabolic Diseases, Fondazione IRCCS Istituto Neurologico Carlo Besta, 20133 Milan, Italy; [email protected] (S.A.); [email protected] (C.G.) 7 Neurophysiopathology, Fondazione IRCCS Istituto Neurologico Carlo Besta, 20133 Milan, Italy; [email protected] 8 Department of Metabolic Diseases, Wilhelmina Children’s Hospital, University Medical Center Utrecht, 3584 CX Utrecht, The Netherlands; [email protected] * Correspondence: [email protected]; Tel.: +1-901-595-2698 These authors contributed equally to this work.
    [Show full text]
  • Supplemental Figures 04 12 2017
    Jung et al. 1 SUPPLEMENTAL FIGURES 2 3 Supplemental Figure 1. Clinical relevance of natural product methyltransferases (NPMTs) in brain disorders. (A) 4 Table summarizing characteristics of 11 NPMTs using data derived from the TCGA GBM and Rembrandt datasets for 5 relative expression levels and survival. In addition, published studies of the 11 NPMTs are summarized. (B) The 1 Jung et al. 6 expression levels of 10 NPMTs in glioblastoma versus non‐tumor brain are displayed in a heatmap, ranked by 7 significance and expression levels. *, p<0.05; **, p<0.01; ***, p<0.001. 8 2 Jung et al. 9 10 Supplemental Figure 2. Anatomical distribution of methyltransferase and metabolic signatures within 11 glioblastomas. The Ivy GAP dataset was downloaded and interrogated by histological structure for NNMT, NAMPT, 12 DNMT mRNA expression and selected gene expression signatures. The results are displayed on a heatmap. The 13 sample size of each histological region as indicated on the figure. 14 3 Jung et al. 15 16 Supplemental Figure 3. Altered expression of nicotinamide and nicotinate metabolism‐related enzymes in 17 glioblastoma. (A) Heatmap (fold change of expression) of whole 25 enzymes in the KEGG nicotinate and 18 nicotinamide metabolism gene set were analyzed in indicated glioblastoma expression datasets with Oncomine. 4 Jung et al. 19 Color bar intensity indicates percentile of fold change in glioblastoma relative to normal brain. (B) Nicotinamide and 20 nicotinate and methionine salvage pathways are displayed with the relative expression levels in glioblastoma 21 specimens in the TCGA GBM dataset indicated. 22 5 Jung et al. 23 24 Supplementary Figure 4.
    [Show full text]
  • Mrna Expression in Human Leiomyoma and Eker Rats As Measured by Microarray Analysis
    Table 3S: mRNA Expression in Human Leiomyoma and Eker Rats as Measured by Microarray Analysis Human_avg Rat_avg_ PENG_ Entrez. Human_ log2_ log2_ RAPAMYCIN Gene.Symbol Gene.ID Gene Description avg_tstat Human_FDR foldChange Rat_avg_tstat Rat_FDR foldChange _DN A1BG 1 alpha-1-B glycoprotein 4.982 9.52E-05 0.68 -0.8346 0.4639 -0.38 A1CF 29974 APOBEC1 complementation factor -0.08024 0.9541 -0.02 0.9141 0.421 0.10 A2BP1 54715 ataxin 2-binding protein 1 2.811 0.01093 0.65 0.07114 0.954 -0.01 A2LD1 87769 AIG2-like domain 1 -0.3033 0.8056 -0.09 -3.365 0.005704 -0.42 A2M 2 alpha-2-macroglobulin -0.8113 0.4691 -0.03 6.02 0 1.75 A4GALT 53947 alpha 1,4-galactosyltransferase 0.4383 0.7128 0.11 6.304 0 2.30 AACS 65985 acetoacetyl-CoA synthetase 0.3595 0.7664 0.03 3.534 0.00388 0.38 AADAC 13 arylacetamide deacetylase (esterase) 0.569 0.6216 0.16 0.005588 0.9968 0.00 AADAT 51166 aminoadipate aminotransferase -0.9577 0.3876 -0.11 0.8123 0.4752 0.24 AAK1 22848 AP2 associated kinase 1 -1.261 0.2505 -0.25 0.8232 0.4689 0.12 AAMP 14 angio-associated, migratory cell protein 0.873 0.4351 0.07 1.656 0.1476 0.06 AANAT 15 arylalkylamine N-acetyltransferase -0.3998 0.7394 -0.08 0.8486 0.456 0.18 AARS 16 alanyl-tRNA synthetase 5.517 0 0.34 8.616 0 0.69 AARS2 57505 alanyl-tRNA synthetase 2, mitochondrial (putative) 1.701 0.1158 0.35 0.5011 0.6622 0.07 AARSD1 80755 alanyl-tRNA synthetase domain containing 1 4.403 9.52E-05 0.52 1.279 0.2609 0.13 AASDH 132949 aminoadipate-semialdehyde dehydrogenase -0.8921 0.4247 -0.12 -2.564 0.02993 -0.32 AASDHPPT 60496 aminoadipate-semialdehyde
    [Show full text]
  • List of Genes Deregulated in HDAC1 KO Vs WT
    Yamaguchi_Suppl. Table 1 List of genes deregulated in HDAC1 KO vs WT Probe Set name fold change 1423327_at RIKEN cDNA 4930517K11 gene 201,6 1426231_at vitrin 33,4 1416368_at glutathione S-transferase, alpha 4 23,2 1435436_at Transcribed locus 20,1 1456379_x_at delta/notch-like EGF-related receptor 15,2 1418175_at vitamin D receptor 14,7 1455642_a_at tetraspanin 17 14,1 1436448_a_at prostaglandin-endoperoxide synthase 1 13,7 1423414_at prostaglandin-endoperoxide synthase 1 12,3 1416710_at transmembrane protein 35 11,8 1454780_at UDP-N-acetyl-alpha-D-galactosamine:polypeptide N-acetylgalactosaminyltransferase-like 4 10,9 1439231_at gb:BG228852 /DB_XREF=gi:12716356 /DB_XREF=ux62e05.x1 /CLONE=IMAGE:3514856 /FEA=EST /CNT=9 /TID=Mm.133155.1 /TIER=Stack10,3 /STK=8 /UG=Mm.133155 /UG_TITLE=ESTs 1416072_at CD34 antigen 10,2 1433529_at RIKEN cDNA E430002G05 gene 9,2 1416203_at aquaporin 1 8,6 1418949_at growth differentiation factor 15 8,3 1435955_at sialic acid binding Ig-like lectin 10 8,2 1416326_at cysteine-rich protein 1 (intestinal) 8,2 1448700_at G0/G1 switch gene 2 8,1 1416271_at PERP, TP53 apoptosis effector 8,0 1418176_at vitamin D receptor 7,8 1439789_at gb:BQ177189 /DB_XREF=gi:20352681 /DB_XREF=UI-M-DJ2-bwa-j-16-0-UI.s1 /CLONE=UI-M-DJ2-bwa-j-16-0-UI /FEA=EST /CNT=16 /TID=7,4 Mm.34073.1 /TIER=ConsEnd /STK=6 /UG=Mm.34073 /UG_TITLE=ESTs 1423627_at NAD(P)H dehydrogenase, quinone 1 7,3 1442174_at tetraspanin 18 7,3 1435945_a_at potassium intermediate/small conductance calcium-activated channel, subfamily N, member 4 6,9 1439362_at Transcribed
    [Show full text]
  • The Endosome Is a Master Regulator of Plasma Membrane Collagen Fibril Assembly
    bioRxiv preprint doi: https://doi.org/10.1101/2021.03.25.436925; this version posted March 25, 2021. 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. The endosome is a master regulator of plasma membrane collagen fibril assembly 1Joan Chang*, 1Adam Pickard, 1Richa Garva, 1Yinhui Lu, 2Donald Gullberg and 1Karl E. Kadler* 1Wellcome Centre for Cell-Matrix Research, Faculty of Biology, Medical and Health, University of Manchester, Michael Smith Building, Oxford Road, Manchester M13 9PT UK, 2Department of Biomedicine and Center for Cancer Biomarkers, Norwegian Center of Excellence, University of Bergen, Norway. * Co-corresponding authors: JC email: [email protected] (orcid.org/0000-0002-7283- 9759); KEK email: [email protected] (orcid.org/0000-0003-4977-4683) Keywords: collagen-I, endocytosis, extracellular matrix, fibril, fibrillogenesis, integrin-a11, trafficking, VPS33b, [abstract] [149 word max] Collagen fibrils are the principal supporting elements in vertebrate tissues. They account for 25% of total protein mass, exhibit a broad range of size and organisation depending on tissue and stage of development, and can be under circadian clock control. Here we show that the remarkable dynamic pleomorphism of collagen fibrils is underpinned by a mechanism that distinguishes between collagen secretion and initiation of fibril assembly, at the plasma membrane. Collagen fibrillogenesis occurring at the plasma membrane requires vacuolar protein sorting (VPS) 33b (which is under circadian clock control), collagen-binding integrin-a11 subunit, and is reduced when endocytosis is inhibited. Fibroblasts lacking VPS33b secrete soluble collagen without assembling fibrils, whereas constitutive over-expression of VPS33b increases fibril number with loss of fibril rhythmicity.
    [Show full text]