DOCSLIB.ORG

Table S3a Table

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Table S3a Table Table S3a C2 KEGG Geneset Genesets enriched and upregulated in responders (FDR <0.25) Genesets enriched and upregulated in non-responders (FDR <0.25) HSA04610_COMPLEMENT_AND_COAGULATION_CASCADES HSA00970_AMINOACYL_TRNA_BIOSYNTHESIS HSA04640_HEMATOPOIETIC_CELL_LINEAGE HSA05050_DENTATORUBROPALLIDOLUYSIAN_ATROPHY HSA04060_CYTOKINE_CYTOKINE_RECEPTOR_INTERACTION HSA04514_CELL_ADHESION_MOLECULES HSA04650_NATURAL_KILLER_CELL_MEDIATED_CYTOTOXICITY HSA04630_JAK_STAT_SIGNALING_PATHWAY HSA03320_PPAR_SIGNALING_PATHWAY HSA04080_NEUROACTIVE_LIGAND_RECEPTOR_INTERACTION HSA00980_METABOLISM_OF_XENOBIOTICS_BY_CYTOCHROME_P450 HSA00071_FATTY_ACID_METABOLISM HSA04660_T_CELL_RECEPTOR_SIGNALING_PATHWAY HSA04612_ANTIGEN_PROCESSING_AND_PRESENTATION HSA04662_B_CELL_RECEPTOR_SIGNALING_PATHWAY HSA04920_ADIPOCYTOKINE_SIGNALING_PATHWAY HSA00120_BILE_ACID_BIOSYNTHESIS HSA04670_LEUKOCYTE_TRANSENDOTHELIAL_MIGRATION HSA00641_3_CHLOROACRYLIC_ACID_DEGRADATION HSA04020_CALCIUM_SIGNALING_PATHWAY HSA04940_TYPE_I_DIABETES_MELLITUS HSA04512_ECM_RECEPTOR_INTERACTION HSA00010_GLYCOLYSIS_AND_GLUCONEOGENESIS HSA02010_ABC_TRANSPORTERS_GENERAL HSA04664_FC_EPSILON_RI_SIGNALING_PATHWAY HSA04710_CIRCADIAN_RHYTHM HSA04510_FOCAL_ADHESION HSA04810_REGULATION_OF_ACTIN_CYTOSKELETON HSA00410_BETA_ALANINE_METABOLISM HSA01040_POLYUNSATURATED_FATTY_ACID_BIOSYNTHESIS HSA00532_CHONDROITIN_SULFATE_BIOSYNTHESIS HSA04620_TOLL_LIKE_RECEPTOR_SIGNALING_PATHWAY HSA04010_MAPK_SIGNALING_PATHWAY HSA00561_GLYCEROLIPID_METABOLISM HSA00053_ASCORBATE_AND_ALDARATE_METABOLISM HSA00590_ARACHIDONIC_ACID_METABOLISM HSA01430_CELL_COMMUNICATION HSA04370_VEGF_SIGNALING_PATHWAY HSA00680_METHANE_METABOLISM HSA00603_GLYCOSPHINGOLIPID_BIOSYNTHESIS_GLOBOSERIES HSA00260_GLYCINE_SERINE_AND_THREONINE_METABOLISM HSA04614_RENIN_ANGIOTENSIN_SYSTEM HSA00643_STYRENE_DEGRADATION HSA00624_1_AND_2_METHYLNAPHTHALENE_DEGRADATION HSA05218_MELANOMA HSA04540_GAP_JUNCTION HSA00591_LINOLEIC_ACID_METABOLISM HSA04910_INSULIN_SIGNALING_PATHWAY HSA00785_LIPOIC_ACID_METABOLISM HSA00430_TAURINE_AND_HYPOTAURINE_METABOLISM Table S3b C5 All GO Genesets Genesets enriched and upregulated in responders (FDR <0.1) Genesets enriched and upregulated in non-responders (FDR <0.1) DEFENSE_RESPONSE CHROMOSOME IMMUNE_RESPONSE CHROMOSOMAL_PART IMMUNE_SYSTEM_PROCESS MRNA_METABOLIC_PROCESS HEMOSTASIS RRNA_METABOLIC_PROCESS RESPONSE_TO_WOUNDING CHROMOSOME__PERICENTRIC_REGION EXTRACELLULAR_SPACE REPLICATION_FORK INFLAMMATORY_RESPONSE MITOSIS EXTRACELLULAR_REGION_PART REGULATION_OF_CELLULAR_PH REGULATION_OF_BODY_FLUID_LEVELS NUCLEAR_REPLICATION_FORK CELL_ACTIVATION CONDENSED_CHROMOSOME BLOOD_COAGULATION COAGULATION RESPONSE_TO_EXTERNAL_STIMULUS RHO_GTPASE_ACTIVATOR_ACTIVITY LEUKOCYTE_ACTIVATION RECEPTOR_ACTIVITY EXTRACELLULAR_REGION LYMPHOCYTE_ACTIVATION REGULATION_OF_MULTICELLULAR_ORGANISMAL_PROCESS HEMOPOIETIC_OR_LYMPHOID_ORGAN_DEVELOPMENT HUMORAL_IMMUNE_RESPONSE HEMOPOIESIS IMMUNE_SYSTEM_DEVELOPMENT INTEGRAL_TO_PLASMA_MEMBRANE INTRINSIC_TO_PLASMA_MEMBRANE PEPTIDYL_TYROSINE_MODIFICATION PLASMA_MEMBRANE MONOOXYGENASE_ACTIVITY RAS_GTPASE_ACTIVATOR_ACTIVITY MUSCLE_DEVELOPMENT INTERLEUKIN_BINDING PLASMA_MEMBRANE_PART TRANSMEMBRANE_RECEPTOR_ACTIVITY HEMATOPOIETIN_INTERFERON_CLASS__D200_DOMAIN__CYTOKINE_RECEPTOR_ACTIVITY ANGIOGENESIS SULFUR_METABOLIC_PROCESS CELL_SURFACE_RECEPTOR_LINKED_SIGNAL_TRANSDUCTION_GO_0007166 ANTIGEN_BINDING POSITIVE_REGULATION_OF_IMMUNE_SYSTEM_PROCESS RHODOPSIN_LIKE_RECEPTOR_ACTIVITY INTEGRIN_BINDING G_PROTEIN_COUPLED_RECEPTOR_PROTEIN_SIGNALING_PATHWAY POSITIVE_REGULATION_OF_MULTICELLULAR_ORGANISMAL_PROCESS T_CELL_ACTIVATION REGULATION_OF_IMMUNE_SYSTEM_PROCESS VASCULATURE_DEVELOPMENT SULFOTRANSFERASE_ACTIVITY PHAGOCYTOSIS CELLULAR_DEFENSE_RESPONSE WOUND_HEALING INTRINSIC_TO_MEMBRANE EXTRACELLULAR_MATRIX LEUKOCYTE_DIFFERENTIATION RESPONSE_TO_BIOTIC_STIMULUS CALCIUM_MEDIATED_SIGNALING G_PROTEIN_COUPLED_RECEPTOR_BINDING GTPASE_ACTIVATOR_ACTIVITY INTEGRAL_TO_MEMBRANE AMINO_ACID_TRANSMEMBRANE_TRANSPORTER_ACTIVITY SYSTEM_DEVELOPMENT ANATOMICAL_STRUCTURE_DEVELOPMENT AMINO_ACID_DERIVATIVE_BIOSYNTHETIC_PROCESS OXIDOREDUCTASE_ACTIVITY__ACTING_ON_THE_ALDEHYDE_OR_OXO_GROUP_OF_DONOR S ADAPTIVE_IMMUNE_RESPONSE_GO_0002460 CYTOKINE_BINDING POSITIVE_REGULATION_OF_IMMUNE_RESPONSE PROTEINACEOUS_EXTRACELLULAR_MATRIX CONTRACTILE_FIBER MULTICELLULAR_ORGANISMAL_DEVELOPMENT ACTIVATION_OF_IMMUNE_RESPONSE OXIDOREDUCTASE_ACTIVITY REGULATION_OF_LYMPHOCYTE_ACTIVATION CONTRACTILE_FIBER_PART GROWTH_FACTOR_BINDING IMMUNE_EFFECTOR_PROCESS POSITIVE_REGULATION_OF_RESPONSE_TO_STIMULUS NEGATIVE_REGULATION_OF_MULTICELLULAR_ORGANISMAL_PROCESS CYTOKINE_PRODUCTION PEPTIDYL_TYROSINE_PHOSPHORYLATION INTERLEUKIN_RECEPTOR_ACTIVITY CARBOXYLIC_ACID_TRANSMEMBRANE_TRANSPORTER_ACTIVITY ADAPTIVE_IMMUNE_RESPONSE ORGANIC_ACID_TRANSMEMBRANE_TRANSPORTER_ACTIVITY ORGAN_DEVELOPMENT REGULATION_OF_HEART_CONTRACTION RHO_GUANYL_NUCLEOTIDE_EXCHANGE_FACTOR_ACTIVITY NON_MEMBRANE_SPANNING_PROTEIN_TYROSINE_KINASE_ACTIVITY REGULATION_OF_PEPTIDYL_TYROSINE_PHOSPHORYLATION ORGAN_MORPHOGENESIS MYOFIBRIL RESPONSE_TO_OTHER_ORGANISM NERVOUS_SYSTEM_DEVELOPMENT VITAMIN_TRANSPORT REGULATION_OF_IMMUNE_RESPONSE LIPID_HOMEOSTASIS LOCOMOTORY_BEHAVIOR POSITIVE_REGULATION_OF_CYTOKINE_BIOSYNTHETIC_PROCESS REGULATION_OF_BIOLOGICAL_QUALITY MEMBRANE CYTOKINE_SECRETION G_PROTEIN_COUPLED_RECEPTOR_ACTIVITY RESPONSE_TO_VIRUS TRANSFERASE_ACTIVITY__TRANSFERRING_SULFUR_CONTAINING_GROUPS REGULATION_OF_GENE_SPECIFIC_TRANSCRIPTION POSITIVE_REGULATION_OF_LYMPHOCYTE_ACTIVATION POSITIVE_REGULATION_OF_TRANSLATION ACTIN_FILAMENT_ORGANIZATION AMINE_RECEPTOR_ACTIVITY STEROID_DEHYDROGENASE_ACTIVITY SECOND_MESSENGER_MEDIATED_SIGNALING CELL_RECOGNITION CHEMOKINE_RECEPTOR_BINDING OXIDOREDUCTASE_ACTIVITY L_AMINO_ACID_TRANSMEMBRANE_TRANSPORTER_ACTIVITY POSITIVE_REGULATION_OF_T_CELL_ACTIVATION CHEMICAL_HOMEOSTASIS SMALL_GTPASE_REGULATOR_ACTIVITY ENDOCYTIC_VESICLE REGULATION_OF_T_CELL_ACTIVATION COFACTOR_TRANSPORT BEHAVIOR SUGAR_BINDING ANATOMICAL_STRUCTURE_FORMATION REGULATION_OF_CYTOKINE_BIOSYNTHETIC_PROCESS REGULATION_OF_CYTOKINE_SECRETION CARBOXYLIC_ACID_METABOLIC_PROCESS NEURON_DIFFERENTIATION HOMEOSTATIC_PROCESS PROTEOGLYCAN_METABOLIC_PROCESS JAK_STAT_CASCADE ORGANIC_ACID_METABOLIC_PROCESS AMINO_ACID_AND_DERIVATIVE_METABOLIC_PROCESS STEROID_DEHYDROGENASE_ACTIVITY DEAMINASE_ACTIVITY MEMBRANE_PART REGULATION_OF_ANATOMICAL_STRUCTURE_MORPHOGENESIS CYTOKINE_METABOLIC_PROCESS LYMPHOCYTE_DIFFERENTIATION EXTRACELLULAR_MATRIX_PART PROTEASE_INHIBITOR_ACTIVITY LIPID_TRANSPORT GENERATION_OF_NEURONS NEGATIVE_REGULATION_OF_ANGIOGENESIS AMINE_TRANSMEMBRANE_TRANSPORTER_ACTIVITY REGULATION_OF_G_PROTEIN_COUPLED_RECEPTOR_PROTEIN_SIGNALING_PATHWAY FATTY_ACID_BETA_OXIDATION INTERLEUKIN_1_SECRETION SIGNAL_TRANSDUCTION LIPID_RAFT CHEMOKINE_ACTIVITY CYTOKINE_BIOSYNTHETIC_PROCESS RECEPTOR_BINDING CELL_CELL_ADHESION AMINE_METABOLIC_PROCESS MYELOID_LEUKOCYTE_DIFFERENTIATION GLUTATHIONE_TRANSFERASE_ACTIVITY REGULATION_OF_ANGIOGENESIS SYSTEM_PROCESS RESPONSE_TO_CHEMICAL_STIMULUS IMMUNOLOGICAL_SYNAPSE B_CELL_ACTIVATION ACTIVATION_OF_MAPK_ACTIVITY ICOSANOID_METABOLIC_PROCESS EXTRACELLULAR_STRUCTURE_ORGANIZATION_AND_BIOGENESIS ANATOMICAL_STRUCTURE_MORPHOGENESIS REGULATION_OF_RESPONSE_TO_STIMULUS RECEPTOR_COMPLEX MAPKKK_CASCADE_GO_0000165 COPPER_ION_BINDING MYELOID_CELL_DIFFERENTIATION AMINO_ACID_DERIVATIVE_METABOLIC_PROCESS Table S3c Oxaliplatin Basal in vitro geneset The geneset was enriched and upregulated in the non-responder (FDR <25%) Genes enriched: ADXCRPDRC.12697.C1_s_a t RAB11FIP1 Homo sapiens RAB11 family interacting protein 1 (class I) -2.13973 ADXCRPD.6693.C1_s_at GK5 Homo sapiens glycerol kinase 5 (putative) (GK5) mRNA. -2.00457 ADXCRPD.4652.C1_at FLJ20366 Homo sapiens hypothetical protein FLJ20366 (FLJ20366) mRNA. -1.74485 ADXCRAD_BX503862_at na NULL -1.63943 RDCR489_A06_at LOC728863 PREDICTED: Homo sapiens hypothetical protein LOC728863 (LOC728863) -1.50455 ADXCRAG_BC065304_at DEPDC1 Homo sapiens DEP domain containing 1 (DEPDC1) mRNA. -1.49412 ADXCRIH.301.C1_at na NULL -1.40391 ADXCRAG_BC001557_s_at SMC4 Homo sapiens structural maintenance of chromosomes 4 (SMC4) -1.40388 ADXCRPD.2083.C1_at NCAPG Homo sapiens ligand dependent nuclear receptor corepressor-like -1.39083 ADXCRIH.711.C1_at RAB5A Homo sapiens RAB5A member RAS oncogene family (RAB5A) mRNA. -1.36445 ADXCRIH.2730.C1_s_at SH3D19 Homo sapiens SH3 domain protein D19 (SH3D19) mRNA. -1.34021 ADXCRPDRC.2988.C1_at POLE2 Polymerase (DNA directed) epsilon 2 (p59 subunit) -1.29988 ADXCRPD.2283.C1_at LOC653256 PREDICTED: Homo sapiens similar to RAB member of RAS oncogene -1.26735 ADXCRIHRC.179.C1_s_at NET1 Homo sapiens neuroepithelial cell transforming gene 1 (NET1) -1.24644 ADXCRIH.3632.C1_s_at EMP2 Epithelial membrane protein 2 -1.2335 ADXCRAD_AL541247_at SLC35B3 NULL -1.23243 ADXCRPD.1683.C1_at C10orf57 Homo sapiens chromosome 10 open reading frame 57 (C10orf57) mRNA. -1.22209 ADXCRAG_BC025767_s_at RHPN1 Homo sapiens rhophilin Rho GTPase binding protein 1 (RHPN1) mRNA. -1.21481 ADXCRIHRC.32.C1_at KIAA0101 Homo sapiens KIAA0101 (KIAA0101) transcript variant 2 mRNA. -1.20186 ADXCRAG_NM_001987_at ETV6 Homo sapiens ets variant gene 6 (TEL oncogene) (ETV6) mRNA. -1.19825 ADXCRAD_CN430263_s_at POLD4 NULL -1.19113 ADXCRPD.1683.C1_x_at C10orf57 Homo sapiens chromosome 10 open reading frame 57 (C10orf57) mRNA. -1.18617 ADXCRPD.1045.C1_s_at FBXO45 F-box protein 45 -1.18354 ADXCRAD_CX163692_s_at GAL Homo sapiens galanin (GAL) mRNA. -1.18292 ADXCRAD_CF454650_s_at FAM120A Homo sapiens family with sequence similarity 120A (FAM120A) mRNA. -1.17326 ADXCRAG_BC057824_s_at na NULL -1.15893 ADXCRPD.13858.C1_s_at FLNB
Load more

Recommended publications
  • The Title of the Article
    Mechanism-Anchored Profiling Derived from Epigenetic Networks Predicts Outcome in Acute Lymphoblastic Leukemia Xinan Yang, PhD1, Yong Huang, MD1, James L Chen, MD1, Jianming Xie, MSc2, Xiao Sun, PhD2, Yves A Lussier, MD1,3,4§ 1Center for Biomedical Informatics and Section of Genetic Medicine, Department of Medicine, The University of Chicago, Chicago, IL 60637 USA 2State Key Laboratory of Bioelectronics, Southeast University, 210096 Nanjing, P.R.China 3The University of Chicago Cancer Research Center, and The Ludwig Center for Metastasis Research, The University of Chicago, Chicago, IL 60637 USA 4The Institute for Genomics and Systems Biology, and the Computational Institute, The University of Chicago, Chicago, IL 60637 USA §Corresponding author Email addresses: XY: [email protected] YH: [email protected] JC: [email protected] JX: [email protected] XS: [email protected] YL: [email protected] - 1 - Abstract Background Current outcome predictors based on “molecular profiling” rely on gene lists selected without consideration for their molecular mechanisms. This study was designed to demonstrate that we could learn about genes related to a specific mechanism and further use this knowledge to predict outcome in patients – a paradigm shift towards accurate “mechanism-anchored profiling”. We propose a novel algorithm, PGnet, which predicts a tripartite mechanism-anchored network associated to epigenetic regulation consisting of phenotypes, genes and mechanisms. Genes termed as GEMs in this network meet all of the following criteria: (i) they are co-expressed with genes known to be involved in the biological mechanism of interest, (ii) they are also differentially expressed between distinct phenotypes relevant to the study, and (iii) as a biomodule, genes correlate with both the mechanism and the phenotype.
    [Show full text]
  • Supplemental Table S1
    Entrez Gene Symbol Gene Name Affymetrix EST Glomchip SAGE Stanford Literature HPA confirmed Gene ID Profiling profiling Profiling Profiling array profiling confirmed 1 2 A2M alpha-2-macroglobulin 0 0 0 1 0 2 10347 ABCA7 ATP-binding cassette, sub-family A (ABC1), member 7 1 0 0 0 0 3 10350 ABCA9 ATP-binding cassette, sub-family A (ABC1), member 9 1 0 0 0 0 4 10057 ABCC5 ATP-binding cassette, sub-family C (CFTR/MRP), member 5 1 0 0 0 0 5 10060 ABCC9 ATP-binding cassette, sub-family C (CFTR/MRP), member 9 1 0 0 0 0 6 79575 ABHD8 abhydrolase domain containing 8 1 0 0 0 0 7 51225 ABI3 ABI gene family, member 3 1 0 1 0 0 8 29 ABR active BCR-related gene 1 0 0 0 0 9 25841 ABTB2 ankyrin repeat and BTB (POZ) domain containing 2 1 0 1 0 0 10 30 ACAA1 acetyl-Coenzyme A acyltransferase 1 (peroxisomal 3-oxoacyl-Coenzyme A thiol 0 1 0 0 0 11 43 ACHE acetylcholinesterase (Yt blood group) 1 0 0 0 0 12 58 ACTA1 actin, alpha 1, skeletal muscle 0 1 0 0 0 13 60 ACTB actin, beta 01000 1 14 71 ACTG1 actin, gamma 1 0 1 0 0 0 15 81 ACTN4 actinin, alpha 4 0 0 1 1 1 10700177 16 10096 ACTR3 ARP3 actin-related protein 3 homolog (yeast) 0 1 0 0 0 17 94 ACVRL1 activin A receptor type II-like 1 1 0 1 0 0 18 8038 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 1 0 0 0 0 19 8751 ADAM15 ADAM metallopeptidase domain 15 (metargidin) 1 0 0 0 0 20 8728 ADAM19 ADAM metallopeptidase domain 19 (meltrin beta) 1 0 0 0 0 21 81792 ADAMTS12 ADAM metallopeptidase with thrombospondin type 1 motif, 12 1 0 0 0 0 22 9507 ADAMTS4 ADAM metallopeptidase with thrombospondin type 1
    [Show full text]
  • Progesterone Receptor Membrane Component 1 Promotes Survival of Human Breast Cancer Cells and the Growth of Xenograft Tumors
    Cancer Biology & Therapy ISSN: 1538-4047 (Print) 1555-8576 (Online) Journal homepage: http://www.tandfonline.com/loi/kcbt20 Progesterone receptor membrane component 1 promotes survival of human breast cancer cells and the growth of xenograft tumors Nicole C. Clark, Anne M. Friel, Cindy A. Pru, Ling Zhang, Toshi Shioda, Bo R. Rueda, John J. Peluso & James K. Pru To cite this article: Nicole C. Clark, Anne M. Friel, Cindy A. Pru, Ling Zhang, Toshi Shioda, Bo R. Rueda, John J. Peluso & James K. Pru (2016) Progesterone receptor membrane component 1 promotes survival of human breast cancer cells and the growth of xenograft tumors, Cancer Biology & Therapy, 17:3, 262-271, DOI: 10.1080/15384047.2016.1139240 To link to this article: http://dx.doi.org/10.1080/15384047.2016.1139240 Accepted author version posted online: 19 Jan 2016. Published online: 19 Jan 2016. Submit your article to this journal Article views: 49 View related articles View Crossmark data Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=kcbt20 Download by: [University of Connecticut] Date: 26 May 2016, At: 11:28 CANCER BIOLOGY & THERAPY 2016, VOL. 17, NO. 3, 262–271 http://dx.doi.org/10.1080/15384047.2016.1139240 RESEARCH PAPER Progesterone receptor membrane component 1 promotes survival of human breast cancer cells and the growth of xenograft tumors Nicole C. Clarka,*, Anne M. Frielb,*, Cindy A. Prua, Ling Zhangb, Toshi Shiodac, Bo R. Ruedab, John J. Pelusod, and James K. Prua aDepartment of Animal Sciences,
    [Show full text]
  • Identification of 10 Important Genes with Poor Prognosis in Non-Small Cell Lung Cancer Through Bioinformatical Analysis
    Journal of ISSN: 2581-7388 Inno Biomedical Research and Reviews Volume 3: 2 J Biomed Res Rev 2020 Identification of 10 Important Genes with Poor Prognosis in Non-Small Cell Lung Cancer through Bioinformatical Analysis Wenbin Wu†1 1Experiment Animal Center, Experiment Center for Science and Technology, Shanghai University of Traditional Chinese Medicine, PR China †2,3 Cheng Fang 2Center for Traditional Chinese Medicine and Immunology Research, Shanghai University of Traditional Chinese Medicine, PR China Chaochao Zhang1 3Department of Immunology and Pathogenic Biology, School of Basic Medical Nanhua Hu*4 Sciences, Shanghai University of Traditional Chinese Medicine, PR China 4Department of Hepatopancreatobiliary and Traditional Chinese Medicine, Minhang *2,3 Lixin Wang Branch, Fudan University Shanghai Cancer Center, PR China † These authors contributed equally to this work Abstract Article Information Objective: The lung cancer has become the most lethal cause of Article Type: Research Article cancer-related death in China and is responsible for more than 1 million Article Number: JBRR-143 deaths all over the world every year, especially non-small cell lung cancer Received Date: 16 October, 2020 (NSCLC). Although great advance in pharmaceutical therapies for lung Accepted Date: 11 November, 2020 Published Date: 18 November, 2020 the effective biomarkers in order to improve and predict the prognosis ofcancer lung patients, cancer patients.the overall The survival integrated is still bioinformaticalpoor. It is necessary analysis, to find as out a *Corresponding author: Lixin Wang, Center for useful tool to dig up the valuable clues, can be applied to search new Traditional Chinese Medicine and Immunology Research; effective therapeutic targets.
    [Show full text]
  • Localization of Condensin Subunit XCAP-E in Interphase Nucleus, Nucleoid and Nuclear
    1 Localization of condensin subunit XCAP-E in interphase nucleus, nucleoid and nuclear matrix of XL2 cells. Elmira Timirbulatova, Igor Kireev, Vladimir Ju. Polyakov, and Rustem Uzbekov* Division of Electron Microscopy, A.N.Belozersky Institute of Physico-Chemical Biology, Moscow State University, 119899, Moscow, Russia. *Author for correspondence: telephone. 007-095-939-55-28; FAX 007-095-939-31-81 e-mail: [email protected] Key words: XCAP-E; nucleolus; condensin; nuclear matrix; Xenopus. Abbreviations: DAPI , 4’, 6 diamidino-2-phenylindole; DNP, deoxyribonucleoprotein; DRB, 5,6-dichloro-1b-d-ribofuranosylbenzimidazole; SMC, structural maintenance of chromosomes; XCAP-E, Xenopus chromosome associated protein E. 2 Abstract The Xenopus XCAP-E protein is a component of condensin complex In the present work we investigate its localization in interphase XL2 cells and nucleoids. We shown, that XCAP-E is localizes in granular and in dense fibrillar component of nucleolus and also in small karyoplasmic structures (termed “SMC bodies”). Extraction by 2M NaCl does not influence XCAP-E distribution in nucleolus and “SMC bodies”. DNAse I treatment of interphase cells permeabilized by Triton X-100 or nucleoids resulted in partial decrease of labeling intensity in the nucleus, whereas RNAse A treatment resulted in practically complete loss of labeling of nucleolus and “SMC bodies” labeling. In mitotic cells, however, 2M NaCl extraction results in an intense staining of the chromosome region although the labeling was visible along the whole length of sister chromatids, with a stronger staining in centromore region. The data are discussed in view of a hypothesis about participation of XCAP-E in processing of ribosomal RNA.
    [Show full text]
  • Defining Functional Interactions During Biogenesis of Epithelial Junctions
    ARTICLE Received 11 Dec 2015 | Accepted 13 Oct 2016 | Published 6 Dec 2016 | Updated 5 Jan 2017 DOI: 10.1038/ncomms13542 OPEN Defining functional interactions during biogenesis of epithelial junctions J.C. Erasmus1,*, S. Bruche1,*,w, L. Pizarro1,2,*, N. Maimari1,3,*, T. Poggioli1,w, C. Tomlinson4,J.Lees5, I. Zalivina1,w, A. Wheeler1,w, A. Alberts6, A. Russo2 & V.M.M. Braga1 In spite of extensive recent progress, a comprehensive understanding of how actin cytoskeleton remodelling supports stable junctions remains to be established. Here we design a platform that integrates actin functions with optimized phenotypic clustering and identify new cytoskeletal proteins, their functional hierarchy and pathways that modulate E-cadherin adhesion. Depletion of EEF1A, an actin bundling protein, increases E-cadherin levels at junctions without a corresponding reinforcement of cell–cell contacts. This unexpected result reflects a more dynamic and mobile junctional actin in EEF1A-depleted cells. A partner for EEF1A in cadherin contact maintenance is the formin DIAPH2, which interacts with EEF1A. In contrast, depletion of either the endocytic regulator TRIP10 or the Rho GTPase activator VAV2 reduces E-cadherin levels at junctions. TRIP10 binds to and requires VAV2 function for its junctional localization. Overall, we present new conceptual insights on junction stabilization, which integrate known and novel pathways with impact for epithelial morphogenesis, homeostasis and diseases. 1 National Heart and Lung Institute, Faculty of Medicine, Imperial College London, London SW7 2AZ, UK. 2 Computing Department, Imperial College London, London SW7 2AZ, UK. 3 Bioengineering Department, Faculty of Engineering, Imperial College London, London SW7 2AZ, UK. 4 Department of Surgery & Cancer, Faculty of Medicine, Imperial College London, London SW7 2AZ, UK.
    [Show full text]
  • Download The
    PROBING THE INTERACTION OF ASPERGILLUS FUMIGATUS CONIDIA AND HUMAN AIRWAY EPITHELIAL CELLS BY TRANSCRIPTIONAL PROFILING IN BOTH SPECIES by POL GOMEZ B.Sc., The University of British Columbia, 2002 A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF SCIENCE in THE FACULTY OF GRADUATE STUDIES (Experimental Medicine) THE UNIVERSITY OF BRITISH COLUMBIA (Vancouver) January 2010 © Pol Gomez, 2010 ABSTRACT The cells of the airway epithelium play critical roles in host defense to inhaled irritants, and in asthma pathogenesis. These cells are constantly exposed to environmental factors, including the conidia of the ubiquitous mould Aspergillus fumigatus, which are small enough to reach the alveoli. A. fumigatus is associated with a spectrum of diseases ranging from asthma and allergic bronchopulmonary aspergillosis to aspergilloma and invasive aspergillosis. Airway epithelial cells have been shown to internalize A. fumigatus conidia in vitro, but the implications of this process for pathogenesis remain unclear. We have developed a cell culture model for this interaction using the human bronchial epithelium cell line 16HBE and a transgenic A. fumigatus strain expressing green fluorescent protein (GFP). Immunofluorescent staining and nystatin protection assays indicated that cells internalized upwards of 50% of bound conidia. Using fluorescence-activated cell sorting (FACS), cells directly interacting with conidia and cells not associated with any conidia were sorted into separate samples, with an overall accuracy of 75%. Genome-wide transcriptional profiling using microarrays revealed significant responses of 16HBE cells and conidia to each other. Significant changes in gene expression were identified between cells and conidia incubated alone versus together, as well as between GFP positive and negative sorted cells.
    [Show full text]
  • Meta-Analyses of Expression Profiling Data in the Postmortem
    META-ANALYSES OF EXPRESSION PROFILING DATA IN THE POSTMORTEM HUMAN BRAIN by Meeta Mistry B.Sc., McMaster University, 2005 A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY in THE FACULTY OF GRADUATE STUDIES (Bioinformatics) THE UNIVERSITY OF BRITISH COLUMBIA (Vancouver) July 2012 © Meeta Mistry, 2012 Abstract Schizophrenia is a severe psychiatric illness for which the precise etiology remains unknown. Studies using postmortem human brain have become increasingly important in schizophrenia research, providing an opportunity to directly investigate the diseased brain tissue. Gene expression profiling technologies have been used by a number of groups to explore the postmortem human brain and seek genes which show changes in expression correlated with schizophrenia. While this has been a valuable means of generating hypotheses, there is a general lack of consensus in the findings across studies. Expression profiling of postmortem human brain tissue is difficult due to the effect of various factors that can confound the data. The first aim of this thesis was to use control postmortem human cortex for identification of expression changes associated with several factors, specifically: age, sex, brain pH and postmortem interval. I conducted a meta-analysis across the control arm of eleven microarray datasets (representing over 400 subjects), and identified a signature of genes associated with each factor. These genes provide critical information towards the identification of problematic genes when investigating postmortem human brain in schizophrenia and other neuropsychiatric illnesses. The second aim of this thesis was to evaluate gene expression patterns in the prefrontal cortex associated with schizophrenia by exploring two methods of analysis: differential expression and coexpression.
    [Show full text]
  • Expression of Progesterone Receptor Membrane Component 1, Serpine Mrna Binding Protein 1 and Nuclear Progesterone Receptor Isoforms a and B in the Bovine Myometrium During The
    Journal of Reproduction and Development, Vol. 58, No 3, 2012 —Original Article— Expression of Progesterone Receptor Membrane Component 1, Serpine mRNA Binding Protein 1 and Nuclear Progesterone Receptor Isoforms A and B in the Bovine Myometrium During the Estrous Cycle and Early Pregnancy Dominika SLOnina1), Magdalena K. KOWALik1) and Jan KOTWica1) 1)Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, 10-747 Olsztyn, Poland Abstract. The aim of this study was to investigate the (1) expression of progesterone membrane component 1 (PGRMC1), serpine mRNA binding protein 1 (SERBP1) and progesterone receptor (PR) mRNA and (2) protein expression levels of PGRMC1, SERBP1 and PR isoforms A and B in the bovine myometrium during the estrous cycle and early pregnancy. Uteri from cows on days 1–5, 6–10, 11–16 and 17–21 of the estrous cycle and weeks 3–5, 6–8 and 9–12 of pregnancy were used (n=5–6 per period). There were no changes (P>0.05) in PGRMC1 mRNA expression during the estrous cycle, while expression of SERBP1 and PR mRNA was the lowest (P<0.05) on days 11–16 relative to other days of the cycle. The highest mRNA expression of PGRMC1, SERBP1 and PR was found during pregnancy. There were no changes (P>0.05) in SERBP1 protein expression in cycling and pregnant cows, while the highest (P<0.05) PGRMC1 protein expression was found during weeks 3–5 of pregnancy. Similar protein expression profiles for PRA and PRB were found, and protein levels were highest on days 1–5 of the estrous cycle.
    [Show full text]
  • 1 Supporting Information for a Microrna Network Regulates
    Supporting Information for A microRNA Network Regulates Expression and Biosynthesis of CFTR and CFTR-ΔF508 Shyam Ramachandrana,b, Philip H. Karpc, Peng Jiangc, Lynda S. Ostedgaardc, Amy E. Walza, John T. Fishere, Shaf Keshavjeeh, Kim A. Lennoxi, Ashley M. Jacobii, Scott D. Rosei, Mark A. Behlkei, Michael J. Welshb,c,d,g, Yi Xingb,c,f, Paul B. McCray Jr.a,b,c Author Affiliations: Department of Pediatricsa, Interdisciplinary Program in Geneticsb, Departments of Internal Medicinec, Molecular Physiology and Biophysicsd, Anatomy and Cell Biologye, Biomedical Engineeringf, Howard Hughes Medical Instituteg, Carver College of Medicine, University of Iowa, Iowa City, IA-52242 Division of Thoracic Surgeryh, Toronto General Hospital, University Health Network, University of Toronto, Toronto, Canada-M5G 2C4 Integrated DNA Technologiesi, Coralville, IA-52241 To whom correspondence should be addressed: Email: [email protected] (M.J.W.); yi- [email protected] (Y.X.); Email: [email protected] (P.B.M.) This PDF file includes: Materials and Methods References Fig. S1. miR-138 regulates SIN3A in a dose-dependent and site-specific manner. Fig. S2. miR-138 regulates endogenous SIN3A protein expression. Fig. S3. miR-138 regulates endogenous CFTR protein expression in Calu-3 cells. Fig. S4. miR-138 regulates endogenous CFTR protein expression in primary human airway epithelia. Fig. S5. miR-138 regulates CFTR expression in HeLa cells. Fig. S6. miR-138 regulates CFTR expression in HEK293T cells. Fig. S7. HeLa cells exhibit CFTR channel activity. Fig. S8. miR-138 improves CFTR processing. Fig. S9. miR-138 improves CFTR-ΔF508 processing. Fig. S10. SIN3A inhibition yields partial rescue of Cl- transport in CF epithelia.
    [Show full text]
  • Rabbit Anti-DAZAP1/FITC Conjugated Antibody-SL14200R-FITC
    SunLong Biotech Co.,LTD Tel: 0086-571- 56623320 Fax:0086-571- 56623318 E-mail:[email protected] www.sunlongbiotech.com Rabbit Anti-DAZAP1/FITC Conjugated antibody SL14200R-FITC Product Name: Anti-DAZAP1/FITC Chinese Name: FITC标记的无精症缺失相关蛋白1抗体 DAZ associated protein 1; DAZ-associated protein 1; Dazap1; DAZP1_HUMAN; Alias: Deleted in azoospermia associated protein 1; Deleted in azoospermia-associated protein 1. Organism Species: Rabbit Clonality: Polyclonal React Species: Human,Mouse,Rat,Chicken,Dog,Pig,Cow,Horse,Sheep, ICC=1:50-200IF=1:50-200 Applications: not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. Molecular weight: 43kDa Form: Lyophilized or Liquid Concentration: 1mg/ml immunogen: KLH conjugated synthetic peptide derived from human DAZAP1 Lsotype: IgG Purification: affinity purified by Protein A Storage Buffer: 0.01Mwww.sunlongbiotech.com TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year Storage: when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. background: In mammals, the Y chromosome directs the development of the testes and plays an important role in spermatogenesis. A high percentage of infertile men have deletions that map to regions of the Y chromosome. The DAZ (deleted in azoospermia) gene Product Detail: cluster maps to the AZFc region of the Y chromosome and is deleted in many azoospermic and severely oligospermic men.
    [Show full text]
  • Polychlorinated Biphenyl Ligands of the Aryl Hydrocarbon Receptor Promote Adipocyte-Mediated Diabetes
    University of Kentucky UKnowledge Theses and Dissertations--Nutritional Sciences Nutritional Sciences 2013 POLYCHLORINATED BIPHENYL LIGANDS OF THE ARYL HYDROCARBON RECEPTOR PROMOTE ADIPOCYTE-MEDIATED DIABETES Nicki A. Baker University of Kentucky, [email protected] Right click to open a feedback form in a new tab to let us know how this document benefits ou.y Recommended Citation Baker, Nicki A., "POLYCHLORINATED BIPHENYL LIGANDS OF THE ARYL HYDROCARBON RECEPTOR PROMOTE ADIPOCYTE-MEDIATED DIABETES" (2013). Theses and Dissertations--Nutritional Sciences. 7. https://uknowledge.uky.edu/nutrisci_etds/7 This Doctoral Dissertation is brought to you for free and open access by the Nutritional Sciences at UKnowledge. It has been accepted for inclusion in Theses and Dissertations--Nutritional Sciences by an authorized administrator of UKnowledge. For more information, please contact [email protected]. STUDENT AGREEMENT: I represent that my thesis or dissertation and abstract are my original work. Proper attribution has been given to all outside sources. I understand that I am solely responsible for obtaining any needed copyright permissions. I have obtained and attached hereto needed written permission statements(s) from the owner(s) of each third-party copyrighted matter to be included in my work, allowing electronic distribution (if such use is not permitted by the fair use doctrine). I hereby grant to The University of Kentucky and its agents the non-exclusive license to archive and make accessible my work in whole or in part in all forms of media, now or hereafter known. I agree that the document mentioned above may be made available immediately for worldwide access unless a preapproved embargo applies.
    [Show full text]