DOCSLIB.ORG

Table S2 Differentially Expressed Genes Between Oncogene-Introduced Wild-Type and Atf4-/- Cells

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Table S2 Differentially Expressed Genes Between Oncogene-Introduced Wild-Type and Atf4-/- Cells Table S2 Differentially expressed genes between oncogene-introduced wild-type and Atf4-/- cells GeneSymbol Gene Name Zscore ratio Genbank Accession Cfd complement factor D 12.714 25036.184 NM_013459 Saa3 serum amyloid A 3 11.189 7437.106 NM_011315 Hp haptoglobin 10.836 5613.776 NM_017370 Prl2c5 prolactin family 2, subfamily c, member 5 7.688 92.732 NM_181852 Cidec cell death-inducing DFFA-like effector c 7.611 982.214 NM_178373 Nrap nebulin-related anchoring protein 7.569 945.372 NM_008733 Adipoq adiponectin, C1Q and collagen domain containing 7.563 940.547 NM_009605 C3 complement component 3 7.310 339.287 NM_009778 Trim12a tripartite motif-containing 12A 7.214 685.215 NM_023835 Apoc1 apolipoprotein C-I 7.026 270.661 NM_007469 Saa1 serum amyloid A 1 6.880 77.790 NM_009117 Lcn2 lipocalin 2 6.658 201.906 NM_008491 Ddx3y DEAD (Asp-Glu-Ala-Asp) box polypeptide 3, Y-linked 6.620 400.047 NM_012008 Pxt1 peroxisomal, testis specific 1 6.470 349.122 NM_153390 Dll4 delta-like 4 6.455 344.263 NM_019454 Lrg1 leucine-rich alpha-2-glycoprotein 1 6.398 326.917 NM_029796 Dcn decorin 6.335 41.800 NM_007833 Rarres2 retinoic acid receptor responder (tazarotene induced) 2 5.985 118.167 NM_027852 Ccl2 chemokine (C-C motif) ligand 2 5.980 12.764 NM_011333 Cyp2f2 cytochrome P450, family 2, subfamily f, polypeptide 2 5.944 584.071 NM_007817 Ccl11 chemokine (C-C motif) ligand 11 5.936 579.003 NM_011330 Plin1 perilipin 1 5.846 198.287 NM_175640 Gsta3 glutathione S-transferase, alpha 3 5.842 105.447 NM_001077353 Barx2 BarH-like homeobox 2 5.836 40.178 NM_013800 Gpd1 glycerol-3-phosphate dehydrogenase 1 5.761 98.835 NM_010271 Fabp4 fatty acid binding protein 4, adipocyte 5.667 28.197 NM_024406 Ifi27l2a interferon, alpha-inducible protein 27 like 2A 5.665 91.632 NM_029803 Eif2s3y eukaryotic translation initiation factor 2, subunit 3, structural gene Y-linked 5.562 153.234 NM_012011 Mnda myeloid cell nuclear differentiation antigen 5.513 368.786 NM_001033450 Prl2c1 Prolactin family 2, subfamily c, member 1 5.478 25.230 NM_001045532 Plin4 perilipin 4 5.412 30.703 NM_020568 Trf transferrin 5.145 60.553 NM_133977 Klra2 killer cell lectin-like receptor, subfamily A, member 2 5.046 223.985 NM_001170851 Cfb complement factor B 5.043 95.684 NM_008198 Dpt dermatopontin 5.001 92.155 NM_019759 Brs3 bombesin-like receptor 3 4.985 209.917 NM_009766 Fth1 ferritin heavy chain 1 4.961 3.041 NM_010239 C1s complement component 1, s subcomponent 4.890 49.443 NM_144938 Angptl4 angiopoietin-like 4 4.853 21.563 NM_020581 Pdpn podoplanin 4.852 17.453 NM_010329 Tmem14c transmembrane protein 14C 4.782 45.344 NM_025387 Cp ceruloplasmin 4.759 44.548 NM_007752 Il4ra interleukin 4 receptor, alpha 4.750 73.367 NM_001008700 Cck cholecystokinin 4.734 7.486 NM_031161 Tmem176b transmembrane protein 176B 4.725 7.458 NM_023056 Vstm2a V-set and transmembrane domain containing 2A 4.687 152.663 NM_145967 Ccl7 chemokine (C-C motif) ligand 7 4.614 7.112 NM_013654 Snhg11 small nucleolar RNA host gene 11 4.531 129.291 NM_175692 Tekt5 tektin 5 4.531 129.200 NM_001099275 Gstm6 glutathione S-transferase, mu 6 4.438 55.291 NM_008184 Lgals3bp lectin, galactoside-binding, soluble, 3 binding protein 4.437 13.666 NM_011150 Mefv Mediterranean fever 4.433 55.046 NM_019453 Cxcl1 chemokine (C-X-C motif) ligand 1 4.425 16.435 NM_008176 Thrsp thyroid hormone responsive SPOT14 homolog 4.414 114.129 NM_009381 Islr immunoglobulin superfamily containing leucine-rich repeat 4.396 33.351 NM_012043 Gfra2 glial cell line derived neurotrophic factor family receptor alpha 2 4.351 32.181 NM_008115 Pck1 phosphoenolpyruvate carboxykinase 1, cytosolic 4.348 106.318 NM_011044 Penk preproenkephalin 4.339 15.570 NM_001002927 Ces2e carboxylesterase 2E 4.324 31.510 NM_172759 Acyp2 acylphosphatase 2, muscle type 4.321 49.721 NM_029344 Ifi27l1 interferon, alpha-inducible protein 27 like 1 4.310 12.680 NM_026790 Grin3b glutamate receptor, ionotropic, NMDA3B 4.304 48.978 NM_130455 Samd4 sterile alpha motif domain containing 4 4.251 29.733 NM_001037221 Gdf10 growth differentiation factor 10 4.246 46.446 NM_145741 Caskin2 CASK-interacting protein 2 4.220 14.441 NM_080643 Ugt1a6b UDP glucuronosyltransferase 1 family, polypeptide A6B 4.183 14.104 NM_201410 Ly6g lymphocyte antigen 6 complex, locus G 4.180 28.082 XM_001475753 Tmem45b transmembrane protein 45b 4.178 88.645 NM_144936 Atp1a2 ATPase, Na+/K+ transporting, alpha 2 polypeptide 4.145 85.624 NM_178405 Grem1 gremlin 1 4.099 11.198 NM_011824 Ccl8 chemokine (C-C motif) ligand 8 4.088 26.107 NM_021443 Cdkn2a cyclin-dependent kinase inhibitor 2A 4.074 11.038 NM_009877 H2-Ab1 histocompatibility 2, class II antigen A, beta 1 4.068 25.690 NM_207105 Mfsd6l major facilitator superfamily domain containing 6-like 4.065 78.602 NM_146004 Fmo2 flavin containing monooxygenase 2 4.041 76.607 NM_018881 Ctsk cathepsin K 4.033 12.829 NM_007802 Mrap melanocortin 2 receptor accessory protein 3.990 36.831 NM_029844 Mmp10 matrix metallopeptidase 10 3.989 24.129 NM_019471 Cidea cell death-inducing DNA fragmentation factor, alpha subunit-like effector A 3.976 36.362 NM_007702 Sepp1 selenoprotein P, plasma, 1 3.976 12.368 NM_001042614 Cox8b cytochrome c oxidase, subunit VIIIb 3.968 70.884 NM_007751 Camp cathelicidin antimicrobial peptide 3.962 35.923 NM_009921 Hsd3b6 hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid 3.953 69.740 NM_013821 delta-isomerase 6 Aoc3 amine oxidase, copper containing 3 3.950 35.512 NM_009675 Fgf23 fibroblast growth factor 23 3.944 5.338 NM_022657 Retn resistin 3.942 68.952 NM_001204959 Nlrc5 NLR family, CARD domain containing 5 3.929 34.840 NM_001033207 Wdr92 WD repeat domain 92 3.924 11.971 NM_178909 Cpz carboxypeptidase Z 3.900 22.470 NM_153107 Lce1g late cornified envelope 1G 3.897 9.945 NM_025413 Clstn2 calsyntenin 2 3.878 22.092 NM_022319 Idua iduronidase, alpha-L- 3.858 5.147 NM_008325 Tusc5 tumor suppressor candidate 5 3.830 61.160 NM_177709 Uts2d urotensin 2 domain containing 3.821 60.551 NM_198166 Dbp D site albumin promoter binding protein 3.815 21.000 NM_016974 Gvin1 GTPase, very large interferon inducible 1 3.805 20.833 NM_029000 Car8 carbonic anhydrase 8 3.801 59.322 NM_007592 Prl3c1 prolactin family 3, subfamily c, member 1 3.790 58.571 NM_013766 Cpxm1 carboxypeptidase X 1 (M14 family) 3.786 10.967 NM_019696 Snap25 synaptosomal-associated protein 25 3.784 4.985 NM_011428 Slc36a2 solute carrier family 36 (proton/amino acid symporter), member 2 3.778 57.857 NM_153170 Agtr2 angiotensin II receptor, type 2 3.775 30.307 NM_007429 Bst2 bone marrow stromal cell antigen 2 3.755 10.755 NM_198095 Itgam integrin alpha M 3.753 4.919 NM_001082960 Kcng2 potassium voltage-gated channel, subfamily G, member 2 3.742 29.407 NM_001190373 Nrn1 neuritin 1 3.740 19.790 NM_153529 Ftl1 ferritin light chain 1 3.731 4.873 NM_010240 Apoa2 apolipoprotein A-II 3.729 54.913 NM_013474 Pamr1 peptidase domain containing associated with muscle regeneration 1 3.724 19.534 NM_173749 Zfp874a zinc finger protein 874a 3.720 54.366 NM_177712 Ch25h cholesterol 25-hydroxylase 3.717 19.438 NM_009890 Ppp1r3c protein phosphatase 1, regulatory (inhibitor) subunit 3C 3.712 53.933 NM_016854 Unc5a unc-5 homolog A 3.707 28.494 NM_153131 Prdm9 PR domain containing 9 3.702 19.206 NM_144809 Il6 interleukin 6 3.698 19.133 NM_031168 Hexim2 hexamthylene bis-acetamide inducible 2 3.693 4.795 NM_027658 Il23a interleukin 23, alpha subunit p19 3.677 51.918 NM_031252 Cygb cytoglobin 3.668 18.694 NM_030206 Hist1h2ba histone cluster 1, H2ba 3.658 10.117 NM_175663 Serpina3c serine (or cysteine) peptidase inhibitor, clade A, member 3C 3.643 50.071 NM_008458 Spag17 sperm associated antigen 17 3.633 49.580 NM_028892 Tnfrsf18 tumor necrosis factor receptor superfamily, member 18 3.617 26.269 NM_009400 Orm2 orosomucoid 2 3.593 47.499 NM_011016 Mmp3 matrix metallopeptidase 3 3.584 8.272 NM_010809 Cd40 CD40 antigen 3.578 17.394 NM_011611 Glyat glycine-N-acyltransferase 3.557 45.704 NM_145935 Nnmt nicotinamide N-methyltransferase 3.550 17.014 NM_010924 Nrxn2 neurexin II 3.536 16.829 NM_001205234 Ubd ubiquitin D 3.532 44.518 NM_023137 Xdh xanthine dehydrogenase 3.527 16.703 NM_011723 Tmem176a transmembrane protein 176A 3.522 9.279 NM_025326 Lpl lipoprotein lipase 3.520 9.270 NM_008509 Nudt18 nudix (nucleoside diphosphate linked moiety X)-type motif 18 3.498 23.577 NM_153136 Serpina3g serine (or cysteine) peptidase inhibitor, clade A, member 3G 3.485 9.066 NM_009251 Krt222 keratin 222 3.470 7.733 NM_172946 Tmem179 transmembrane protein 179 3.465 15.897 NM_178915 Gpm6b glycoprotein m6b 3.464 15.883 NM_001177956 Gch1 GTP cyclohydrolase 1 3.457 8.909 NM_008102 Bace2 beta-site APP-cleaving enzyme 2 3.427 39.787 NM_019517 Hmox1 heme oxygenase (decycling) 1 3.421 7.514 NM_010442 Slc8a3 solute carrier family 8 (sodium/calcium exchanger), member 3 3.418 7.500 NM_080440 Plin5 perilipin 5 3.415 39.259 NM_001077348 Dnmt3l DNA (cytosine-5-) 3.406 21.700 NM_019448 -methyltransferase 3-like C1ra complement component 1, r subcomponent A 3.397 15.057 NM_023143 C4b complement component 4B (Childo blood group) 3.392 21.417 NM_009780 Ltbp2 latent transforming growth factor beta binding protein 2 3.391 4.212 NM_013589 S100a8 S100 calcium binding protein A8 (calgranulin A) 3.371 21.012 NM_013650 Sult4a1 sulfotransferase family 4A, member 1 3.370 14.743 NM_013873 Trim30a tripartite motif-containing 30A 3.361 37.054 NM_009099 S100b S100 protein, beta polypeptide, neural 3.354 14.556 NM_009115 Cyp1a1 cytochrome P450, family 1, subfamily a, polypeptide 1 3.351 36.694 NM_009992 Fgf1 fibroblast growth factor 1 3.341 36.288 NM_010197 C1qtnf7 C1q and
Load more

Recommended publications
  • Strategies to Increase ß-Cell Mass Expansion
    This electronic thesis or dissertation has been downloaded from the King’s Research Portal at https://kclpure.kcl.ac.uk/portal/ Strategies to increase -cell mass expansion Drynda, Robert Lech Awarding institution: King's College London The copyright of this thesis rests with the author and no quotation from it or information derived from it may be published without proper acknowledgement. END USER LICENCE AGREEMENT Unless another licence is stated on the immediately following page this work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International licence. https://creativecommons.org/licenses/by-nc-nd/4.0/ You are free to copy, distribute and transmit the work Under the following conditions: Attribution: You must attribute the work in the manner specified by the author (but not in any way that suggests that they endorse you or your use of the work). Non Commercial: You may not use this work for commercial purposes. No Derivative Works - You may not alter, transform, or build upon this work. Any of these conditions can be waived if you receive permission from the author. Your fair dealings and other rights are in no way affected by the above. Take down policy If you believe that this document breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim. Download date: 02. Oct. 2021 Strategies to increase β-cell mass expansion A thesis submitted by Robert Drynda For the degree of Doctor of Philosophy from King’s College London Diabetes Research Group Division of Diabetes & Nutritional Sciences Faculty of Life Sciences & Medicine King’s College London 2017 Table of contents Table of contents .................................................................................................
    [Show full text]
  • Kinesin Family Member 18B Regulates the Proliferation and Invasion Of
    Wu et al. Cell Death and Disease (2021) 12:302 https://doi.org/10.1038/s41419-021-03582-2 Cell Death & Disease ARTICLE Open Access Kinesin family member 18B regulates the proliferation and invasion of human prostate cancer cells Yu-Peng Wu 1,Zhi-BinKe 1, Wen-Cai Zheng 1, Ye-Hui Chen 1,Jun-MingZhu 1,FeiLin 1,Xiao-DongLi 1, Shao-Hao Chen 1,HaiCai 1, Qing-Shui Zheng 1, Yong Wei 1, Xue-Yi Xue 1 and Ning Xu 1 Abstract Expression of kinesin family member 18B (KIF18B), an ATPase with key roles in cell division, is deregulated in many cancers, but its involvement in prostate cancer (PCa) is unclear. Here, we investigated the expression and function of KIF18B in human PCa specimens and cell lines using bioinformatics analyses, immunohistochemical and immunofluorescence microscopy, and RT-qPCR and western blot analyses. KIF18B was overexpressed in PCa specimens compared with paracancerous tissues and was associated with poorer disease-free survival. In vitro, KIF18B knockdown in PCa cell lines promoted cell proliferation, migration, and invasion, and inhibited cell apoptosis, while KIF18B overexpression had the opposite effects. In a mouse xenograft model, KIF18B overexpression accelerated and promoted the growth of PCa tumors. Bioinformatics analysis of control and KIF18B-overexpressing PCa cells showed that genes involved in the PI3K–AKT–mTOR signaling pathway were significantly enriched among the differentially expressed genes. Consistent with this observation, we found that KIF18B overexpression activates the PI3K–AKT–mTOR signaling pathway in PCa cells both in vitro and in vivo. Collectively, our results suggest that KIF18B plays a crucial role – – 1234567890():,; 1234567890():,; 1234567890():,; 1234567890():,; in PCa via activation of the PI3K AKT mTOR signaling pathway, and raise the possibility that KIF18B could have utility as a novel biomarker for PCa.
    [Show full text]
  • 0.5) in Stat3∆/∆ Compared with Stat3flox/Flox
    Supplemental Table 2 Genes down-regulated (<0.5) in Stat3∆/∆ compared with Stat3flox/flox Probe ID Gene Symbol Gene Description Entrez gene ID 1460599_at Ermp1 endoplasmic reticulum metallopeptidase 1 226090 1460463_at H60c histocompatibility 60c 670558 1460431_at Gcnt1 glucosaminyl (N-acetyl) transferase 1, core 2 14537 1459979_x_at Zfp68 zinc finger protein 68 24135 1459747_at --- --- --- 1459608_at --- --- --- 1459168_at --- --- --- 1458718_at --- --- --- 1458618_at --- --- --- 1458466_at Ctsa cathepsin A 19025 1458345_s_at Colec11 collectin sub-family member 11 71693 1458046_at --- --- --- 1457769_at H60a histocompatibility 60a 15101 1457680_a_at Tmem69 transmembrane protein 69 230657 1457644_s_at Cxcl1 chemokine (C-X-C motif) ligand 1 14825 1457639_at Atp6v1h ATPase, H+ transporting, lysosomal V1 subunit H 108664 1457260_at 5730409E04Rik RIKEN cDNA 5730409E04Rik gene 230757 1457070_at --- --- --- 1456893_at --- --- --- 1456823_at Gm70 predicted gene 70 210762 1456671_at Tbrg3 transforming growth factor beta regulated gene 3 21378 1456211_at Nlrp10 NLR family, pyrin domain containing 10 244202 1455881_at Ier5l immediate early response 5-like 72500 1455576_at Rinl Ras and Rab interactor-like 320435 1455304_at Unc13c unc-13 homolog C (C. elegans) 208898 1455241_at BC037703 cDNA sequence BC037703 242125 1454866_s_at Clic6 chloride intracellular channel 6 209195 1453906_at Med13l mediator complex subunit 13-like 76199 1453522_at 6530401N04Rik RIKEN cDNA 6530401N04 gene 328092 1453354_at Gm11602 predicted gene 11602 100380944 1453234_at
    [Show full text]
  • Application to Acetaminophen Anaïs Michaut, Dounia Le Guillou, Caroline Moreau, Simon Bucher, Mitchell R
    A cellular model to study drug-induced liver injury in nonalcoholic fatty liver disease: application to acetaminophen Anaïs Michaut, Dounia Le Guillou, Caroline Moreau, Simon Bucher, Mitchell R. Mcgill, Sophie Martinais, Thomas Gicquel, Isabelle Morel, Marie-Anne Robin, Hartmut Jaeschke, et al. To cite this version: Anaïs Michaut, Dounia Le Guillou, Caroline Moreau, Simon Bucher, Mitchell R. Mcgill, et al.. A cellular model to study drug-induced liver injury in nonalcoholic fatty liver disease: applica- tion to acetaminophen. Toxicology and Applied Pharmacology, Elsevier, 2016, 292, pp.40-55. 10.1016/j.taap.2015.12.020. hal-01255826 HAL Id: hal-01255826 https://hal-univ-rennes1.archives-ouvertes.fr/hal-01255826 Submitted on 29 Jan 2016 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. ACCEPTED MANUSCRIPT A cellular model to study drug-induced liver injury in nonalcoholic fatty liver disease: application to acetaminophen Anaïs Michauta, Dounia Le Guilloua, Caroline Moreaua,b, Simon Buchera, Mitchell R. McGillc, Sophie Martinaisa, Thomas Gicquela,b, Isabelle Morela,b, Marie-Anne Robina, Hartmut Jaeschkec, and Bernard Fromentya,* aINSERM, U991, Université de Rennes 1, Rennes, France, bService de Biochimie et Toxicologie, CHU Pontchaillou, Rennes, France, cDepartment of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS, USA *To whom correspondenceACCEPTED should be addressed MANUSCRIPT at INSERM U991, Université de Rennes 1, 35043 Rennes Cedex, France.
    [Show full text]
  • Original Article Colonic Mucosal Gene Expression in Irritable Bowel Syndrome Rats by the Liquid Chip Technology
    Int J Clin Exp Pathol 2016;9(10):10751-10755 www.ijcep.com /ISSN:1936-2625/IJCEP0036079 Original Article Colonic mucosal gene expression in irritable bowel syndrome rats by the liquid chip technology Guanqun Chao1, Yingying Wang2, Shuo Zhang2 1Department of Family Medicine, Sir Run Run Shaw Hospital, Zhejiang University, Zhejiang, China; 2Department of Gastroenterology, The First Affiliated Hospital, Zhejiang Chinese Medical University, Zhejiang, China Received July 18, 2016; Accepted August 27, 2016; Epub October 1, 2016; Published October 15, 2016 Abstract: Background: Irritable bowel syndrome (IBS) is one of the most frequent GI disorders. The etiology and pathogenesis underlying IBS are currently unclear. Gene influence a number of chronic disease processes and may also be involved in regulating disease activity in gastrointestinal disorders, but few studies of IBS have focused on gene expression. Objective: The objective of this study was to screen the differentially expressed colonic mucosal genes in IBS rats to build the expression profile of genes in the colon of IBS rats. Methods: Twenty SD rats were divided randomly into two groups: the rats of control group were normal rats; the rats of model group were induced by conditioned stimulus and unconditioned stimulus. The rats’ visceral sensitivity was evaluated by abdominal with- draw reaction. Then we screened differential expression of colonic mucosal gene by the liquid chip technology and verified by RT-PCR technology. Results: The IBS model was successfully established. Compared with control group, the dose of injection water was decreased in model group (P<0.01). We screened htr4, htr1a, 2rl3, nos1, Calca, npy, crhr2, il1b, p2rx3, nos2, tph1, crhr1, hmox1, trpv1, Vip, f2rl, tgfb1, htr3a, slc6a4, tff2, aqp8 from the colon, but we found that only the expression of nos1, il1b, htr3a in model group was up-regulated (P<0.05).
    [Show full text]
  • Differential Gene Expression in Oligodendrocyte Progenitor Cells, Oligodendrocytes and Type II Astrocytes
    Tohoku J. Exp. Med., 2011,Differential 223, 161-176 Gene Expression in OPCs, Oligodendrocytes and Type II Astrocytes 161 Differential Gene Expression in Oligodendrocyte Progenitor Cells, Oligodendrocytes and Type II Astrocytes Jian-Guo Hu,1,2,* Yan-Xia Wang,3,* Jian-Sheng Zhou,2 Chang-Jie Chen,4 Feng-Chao Wang,1 Xing-Wu Li1 and He-Zuo Lü1,2 1Department of Clinical Laboratory Science, The First Affiliated Hospital of Bengbu Medical College, Bengbu, P.R. China 2Anhui Key Laboratory of Tissue Transplantation, Bengbu Medical College, Bengbu, P.R. China 3Department of Neurobiology, Shanghai Jiaotong University School of Medicine, Shanghai, P.R. China 4Department of Laboratory Medicine, Bengbu Medical College, Bengbu, P.R. China Oligodendrocyte precursor cells (OPCs) are bipotential progenitor cells that can differentiate into myelin-forming oligodendrocytes or functionally undetermined type II astrocytes. Transplantation of OPCs is an attractive therapy for demyelinating diseases. However, due to their bipotential differentiation potential, the majority of OPCs differentiate into astrocytes at transplanted sites. It is therefore important to understand the molecular mechanisms that regulate the transition from OPCs to oligodendrocytes or astrocytes. In this study, we isolated OPCs from the spinal cords of rat embryos (16 days old) and induced them to differentiate into oligodendrocytes or type II astrocytes in the absence or presence of 10% fetal bovine serum, respectively. RNAs were extracted from each cell population and hybridized to GeneChip with 28,700 rat genes. Using the criterion of fold change > 4 in the expression level, we identified 83 genes that were up-regulated and 89 genes that were down-regulated in oligodendrocytes, and 92 genes that were up-regulated and 86 that were down-regulated in type II astrocytes compared with OPCs.
    [Show full text]
  • Microrna-7-5P Mediates the Signaling of Hepatocyte Growth
    www.nature.com/scientificreports OPEN MicroRNA-7-5p mediates the signaling of hepatocyte growth factor to suppress oncogenes in the Received: 30 August 2017 Accepted: 2 November 2017 MCF-10A mammary epithelial cell Published: xx xx xxxx Dawoon Jeong1, Juyeon Ham1, Sungbin Park1, Seungyeon Lee 1, Hyunkyung Lee1, Han-Sung Kang2 & Sun Jung Kim1 MicroRNA-7 (miR-7) is a non-coding RNA of 23-nucleotides that has been shown to act as a tumor suppressor in various cancers including breast cancer. Although there have been copious studies on the action mechanisms of miR-7, little is known about how the miR is controlled in the mammary cell. In this study, we performed a genome-wide expression analysis in miR-7-transfected MCF-10A breast cell line to explore the upstream regulators of miR-7. Analysis of the dysregulated target gene pool predicted hepatocyte growth factor (HGF) as the most plausible upstream regulator of miR-7. MiR-7 was upregulated in MCF-10A cells by HGF, and subsequently downregulated upon treatment with siRNA against HGF. However, the expression of HGF did not signifcantly change through either an upregulation or downregulation of miR-7 expression, suggesting that HGF acts upstream of miR-7. In addition, the target genes of miR-7, such as EGFR, KLF4, FAK, PAK1 and SET8, which are all known oncogenes, were downregulated in HGF-treated MCF-10A; in contrast, knocking down HGF recovered their expression. These results indicate that miR-7 mediates the activity of HGF to suppress oncogenic proteins, which inhibits the development of normal cells, at least MCF-10A, into cancerous cells.
    [Show full text]
  • 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]
  • Identification of Potential Key Genes and Pathway Linked with Sporadic Creutzfeldt-Jakob Disease Based on Integrated Bioinformatics Analyses
    medRxiv preprint doi: https://doi.org/10.1101/2020.12.21.20248688; this version posted December 24, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. Identification of potential key genes and pathway linked with sporadic Creutzfeldt-Jakob disease based on integrated bioinformatics analyses Basavaraj Vastrad1, Chanabasayya Vastrad*2 , Iranna Kotturshetti 1. Department of Biochemistry, Basaveshwar College of Pharmacy, Gadag, Karnataka 582103, India. 2. Biostatistics and Bioinformatics, Chanabasava Nilaya, Bharthinagar, Dharwad 580001, Karanataka, India. 3. Department of Ayurveda, Rajiv Gandhi Education Society`s Ayurvedic Medical College, Ron, Karnataka 562209, India. * Chanabasayya Vastrad [email protected] Ph: +919480073398 Chanabasava Nilaya, Bharthinagar, Dharwad 580001 , Karanataka, India NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice. medRxiv preprint doi: https://doi.org/10.1101/2020.12.21.20248688; this version posted December 24, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. Abstract Sporadic Creutzfeldt-Jakob disease (sCJD) is neurodegenerative disease also called prion disease linked with poor prognosis. The aim of the current study was to illuminate the underlying molecular mechanisms of sCJD. The mRNA microarray dataset GSE124571 was downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) were screened.
    [Show full text]
  • Impaired Angiogenesis and Tumor Development by Inhibition of the Mitotic Kinesin Eg5
    Oncotarget, December, Vol.4, No 12 Impaired angiogenesis and tumor development by inhibition of the mitotic kinesin Eg5 Prisca Exertier1,2, Sophie Javerzat1,2, Baigang Wang3,8, Mélanie Franco1,2, John Herbert4, Natalia Platonova1,2, Marie Winandy5, Nadège Pujol1,2, Olivier Nivelles6, Sandra Ormenese7, Virginie Godard1,2, Jürgen Becker8, Roy Bicknell4, Raphael Pineau9, Jörg Wilting8*, Andreas Bikfalvi1,2*, Martin Hagedorn1,2* 1 Univ. Bordeaux, LAMC, UMR 1029, F-33405 Talence, France 2 INSERM, LAMC, UMR 1029, F-33405 Talence, France 3 Ruhr-Universität Bochum, Medizinische Fakultät; Abt. f. Anatomie und Embryologie, D-44780 Bochum, Germany 4 Molecular Angiogenesis Group, Institute of Biomedical Research, Univ Birmingham, Medical School, Edgbaston, Birmingham, UK 5 GIGA, Zebrafish Facility, Tour B34, Université de Liège, Belgium 6 GIGA, Unité de Biologie Moléculaire et Génie Génétique, Tour B34, Université de Liège, Belgium 7 GIGA, Imaging and Flow Cytometry Facility, Tour B34, Université de Liege, Belgium 8 Zentrum Anatomie, Abteilung Anatomie und Zellbiologie, Georg-August-Universität Goettingen, Germany 9 Animalerie mutualisée, University of Bordeaux I, Talence, France * Co-PIs Correspondence to: Martin Hagedorn, email: [email protected] Keywords: Angiogenesis, Eg5 kinesin, Mklp2 kinesin, VEGF, ispinesib Received: October 11, 2013 Accepted: October 24, 2013 Published: October 26, 2013 This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACT: Kinesin motor proteins exert essential cellular functions in all eukaryotes. They control mitosis, migration and intracellular transport through interaction with microtubules. Small molecule inhibitors of the mitotic kinesin KiF11/Eg5 are a promising new class of anti-neoplastic agents currently evaluated in clinical cancer trials for solid tumors and hematological malignancies.
    [Show full text]
  • Areca Catechu-(Betel-Nut)-Induced Whole Transcriptome Changes Associated With
    bioRxiv preprint doi: https://doi.org/10.1101/2020.08.03.233932; this version posted August 3, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. 1 Areca catechu-(Betel-nut)-induced whole transcriptome changes associated with 2 diabetes, obesity and metabolic syndrome in a human monocyte cell line 3 4 Short title: Betel-nut induced whole transcriptome changes 5 6 7 Shirleny Cardoso1¶ , B. William Ogunkolade1¶, Rob Lowe2, Emanuel Savage3, Charles A 8 Mein3, Barbara J Boucher1, Graham A Hitman1* 9 10 11 1Centre for Genomics and Child Health, Blizard Institute, Barts and the London School of 12 Medicine and Dentistry, Queen Mary University of London, United Kingdom 13 14 2Omnigen Biodata Ltd, Cambridge, United Kingdom 15 16 3Barts and The London Genome Centre, Blizard Institute, Queen Mary University of London, 17 United Kingdom 18 19 * Corresponding author 20 Email: [email protected] 21 22 ¶These authors contributed equally to the work 23 24 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.08.03.233932; this version posted August 3, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. 25 Abstract 26 Betel-nut consumption is the fourth most common addictive habit globally and there is good 27 evidence to link it with obesity, type 2 diabetes and the metabolic syndrome.
    [Show full text]
  • Molecular Features of Triple Negative Breast Cancer Cells by Genome-Wide Gene Expression Profiling Analysis
    478 INTERNATIONAL JOURNAL OF ONCOLOGY 42: 478-506, 2013 Molecular features of triple negative breast cancer cells by genome-wide gene expression profiling analysis MASATO KOMATSU1,2*, TETSURO YOSHIMARU1*, TAISUKE MATSUO1, KAZUMA KIYOTANI1, YASUO MIYOSHI3, TOSHIHITO TANAHASHI4, KAZUHITO ROKUTAN4, RUI YAMAGUCHI5, AYUMU SAITO6, SEIYA IMOTO6, SATORU MIYANO6, YUSUKE NAKAMURA7, MITSUNORI SASA8, MITSUO SHIMADA2 and TOYOMASA KATAGIRI1 1Division of Genome Medicine, Institute for Genome Research, The University of Tokushima; 2Department of Digestive and Transplantation Surgery, The University of Tokushima Graduate School; 3Department of Surgery, Division of Breast and Endocrine Surgery, Hyogo College of Medicine, Hyogo 663-8501; 4Department of Stress Science, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima 770-8503; Laboratories of 5Sequence Analysis, 6DNA Information Analysis and 7Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo 108-8639; 8Tokushima Breast Care Clinic, Tokushima 770-0052, Japan Received September 22, 2012; Accepted November 6, 2012 DOI: 10.3892/ijo.2012.1744 Abstract. Triple negative breast cancer (TNBC) has a poor carcinogenesis of TNBC and could contribute to the develop- outcome due to the lack of beneficial therapeutic targets. To ment of molecular targets as a treatment for TNBC patients. clarify the molecular mechanisms involved in the carcino- genesis of TNBC and to identify target molecules for novel Introduction anticancer drugs, we analyzed the gene expression profiles of 30 TNBCs as well as 13 normal epithelial ductal cells that were Breast cancer is one of the most common solid malignant purified by laser-microbeam microdissection. We identified tumors among women worldwide. Breast cancer is a heteroge- 301 and 321 transcripts that were significantly upregulated neous disease that is currently classified based on the expression and downregulated in TNBC, respectively.
    [Show full text]