ID Parametric P

Total Page:16

File Type:pdf, Size:1020Kb

ID Parametric P Geom Geom Ratio of mean mean Parametric p- geom FDR of of Symbol Name value means intensit intensi ID Pla/Bag ies in ties in dapper, antagonist of beta-catenin, homolog 1 (Xenopus 29 1,69E-05 0,0302321 72,8 7,6 9,579 DACT1 laevis) heparan sulfate (glucosamine) 3-O- sulfotransferas 797 0,0011054 0,0757259 237,2 25,7 9,23 HS3ST2 e 2 growth differentiation 874 0,0012657 0,0791194 204,9 23,6 8,682 GDF15 factor 15 potassium voltage-gated channel, Isk- related family, 1756 0,0038928 0,1210936 283,5 37,7 7,52 KCNE1 member 1 membrane- spanning 4- domains, subfamily A, 7305 0,0471766 0,3530226 150,7 20,9 7,211 MS4A1 member 1 POU domain, class 2, associating 5060 0,0248103 0,2680447 58,3 8,6 6,779 POU2AF1 factor 1 442 0,0004744 0,0586829 27,3 4,2 6,5 TSPAN12 tetraspanin 12 44 2,60E-05 0,0312927 57,2 9 6,356 ASTN2 astrotactin 2 266 0,0002545 0,0521767 138,9 21,9 6,342 PRR6 proline rich 6 1218 0,0021841 0,097918 152,7 25,4 6,012 MCOLN3 mucolipin 3 FERM domain 173 0,000154 0,0481428 110 18,7 5,882 FRMD4A containing 4A male sterility domain 4469 0,0199658 0,2442435 1200,3 210,6 5,699 MLSTD1 containing 1 aldehyde dehydrogenas e 1 family, 3738 0,0142747 0,2087933 1816,5 320,1 5,675 ALDH1A2 member A2 deoxyribonucle 779 0,0010754 0,0753005 268 48,3 5,549 DNASE1L3 ase I-like 3 TSC22 domain family, member 944 0,0014302 0,0826707 872,3 158,2 5,514 TSC22D1 1 Male sterility domain 6858 0,0422377 0,3367178 631,6 116,2 5,435 MLSTD1 containing 1 patatin-like phospholipase domain 7 6,60E-06 0,0302321 58,1 10,7 5,43 PNPLA3 containing 3 hypothetical protein 1857 0,0042809 0,126041 52,6 9,8 5,367 FLJ36748 FLJ36748 Fatty acid binding protein 3734 0,014255 0,2087285 1239,5 232,5 5,331 FABP4 4, adipocyte tudor domain 3363 0,0121881 0,1981221 87,4 16,4 5,329 TDRD9 containing 9 deoxyribonucle 332 0,000338 0,0552439 53,4 10,2 5,235 DNASE2B ase II beta aldehyde dehydrogenas e 5 family, member A1 (succinate- semialdehyde dehydrogenas 3016 0,0101106 0,1832002 146,6 28,3 5,18 ALDH5A1 e) phospholipase C, beta 1 (phosphoinositi 1757 0,0038928 0,1210936 61,4 12 5,117 PLCB1 de-specific) FERM domain 110 7,73E-05 0,0382725 370,2 72,6 5,099 FRMD4A containing 4A suppressor of cytokine 2276 0,0061685 0,1481822 173,9 34,2 5,085 SOCS1 signaling 1 hypothetical protein 17 1,34E-05 0,0302321 101,1 19,9 5,08 LOC153577 LOC153577 Similar to Calponin-2 (Calponin H2, smooth muscle) (Neutral 2544 0,0075774 0,1628516 73,9 14,9 4,96 LOC642893 calponin) peptidylprolyl isomerase C 1762 0,0039126 0,121407 107,3 22,3 4,812 PPIC (cyclophilin C) FERM domain 1795 0,0040471 0,1232731 80,7 17 4,747 FRMD4A containing 4A Src-like- adaptor /// Src- 1239 0,0022258 0,0982208 2188 466,7 4,688 SLA like-adaptor peroxisome proliferator- activated receptor 2109 0,0053734 0,1392684 677,5 146,1 4,637 PPARG gamma TIMP metallopeptida se inhibitor 3 (Sorsby fundus dystrophy, pseudoinflamm 630 0,0007657 0,0664245 515 111,3 4,627 TIMP3 atory) TIMP metallopeptida se inhibitor 3 (Sorsby fundus dystrophy, pseudoinflamm 1435 0,0028138 0,1071379 524 113,7 4,609 TIMP3 atory) Leukotriene B4 848 0,0012319 0,0791194 120,8 26,4 4,576 LTB4R receptor Multiple Gene 4620 0,021198 0,2508282 149,7 32,8 4,564 Symbols NA mitochondrial tumor 872 0,0012655 0,0791194 148,2 32,7 4,532 MTUS1 suppressor 1 FERM domain 881 0,0012804 0,079454 270,6 60 4,51 FRMD4A containing 4A chromosome 8 open reading 711 0,0009228 0,0708321 153,3 34 4,509 C8orf72 frame 72 594 0,00072 0,0657513 99 22,6 4,381 PRR6 proline rich 6 Receptor tyrosine kinase- like orphan 27 1,67E-05 0,0302321 39,3 9 4,367 ROR1 receptor 1 solute carrier family 1 (glial high affinity glutamate transporter), 1185 0,0020858 0,0961653 294,1 68 4,325 SLC1A3 member 3 Fms-related tyrosine kinase 1 (vascular endothelial growth factor/vascular permeability 1862 0,0043093 0,1264829 151,6 35,1 4,319 FLT1 factor receptor) protein tyrosine phosphatase- like (proline instead of catalytic arginine), 2654 0,0081664 0,1681297 85,7 20 4,285 PTPLA member A ribosomal protein S6 kinase, 90kDa, 340 0,0003457 0,0552439 242,2 56,7 4,272 RPS6KA2 polypeptide 2 1923 0,0045537 0,1293549 308,6 72,7 4,245 NA NA solute carrier organic anion transporter family, member 3591 0,013433 0,2043749 58,3 13,8 4,225 SLCO4C1 4C1 Fas apoptotic inhibitory molecule 3 /// Fas apoptotic inhibitory 4044 0,0167209 0,2260671 220 52,2 4,215 FAIM3 molecule 3 kelch domain 863 0,001252 0,0791194 71 16,9 4,201 KLHDC5 containing 5 basic helix- loop-helix domain containing, 5648 0,0299771 0,290155 1111,3 265 4,194 BHLHB3 class B, 3 Nedd4 family interacting 883 0,0012847 0,079454 87,8 21 4,181 NDFIP2 protein 2 Eukaryotic translation initiation factor 20 1,40E-05 0,0302321 168,8 40,5 4,168 EIF2C1 2C, 1 Immunoglobuli n heavy constant alpha 1727 0,0037769 0,1195727 343,3 83,3 4,121 IGHA1 1 amidohydrolas e domain 386 0,0004095 0,0577756 33,8 8,3 4,072 AMDHD1 containing 1 patatin-like phospholipase domain 495 0,0005656 0,0624087 108,6 26,8 4,052 PNPLA3 containing 3 ubiquitin carboxyl- terminal esterase L1 (ubiquitin 625 0,0007593 0,0664236 91,9 22,7 4,048 UCHL1 thiolesterase) Src-like- adaptor /// Src- 1593 0,0033554 0,1151642 1824,6 452 4,037 SLA like-adaptor chromosome 11 open reading frame 284 0,0002744 0,0525339 82,7 20,5 4,034 C11orf45 45 TIMP metallopeptida se inhibitor 3 (Sorsby fundus dystrophy, pseudoinflamm 1351 0,0025626 0,1036037 376,9 94,1 4,005 TIMP3 atory) guanylate cyclase activator 1A 3197 0,0112813 0,1929325 67,2 16,8 4 GUCA1A (retina) 5.5 kb mRNA upregulated in retinoic acid treated HL-60 neutrophilic 843 0,0012186 0,0790355 240,9 60,5 3,982 NA cells GM2 ganglioside 1728 0,0037801 0,1196047 878 221,3 3,967 GM2A activator non-SMC condensin I complex, 2296 0,0062576 0,1489073 709,9 180 3,944 NCAPH subunit H transmembran 729 0,0009562 0,071715 185,4 47,2 3,928 TMEM117 e protein 117 solute carrier family 22 (organic cation transporter), 30 1,74E-05 0,0302321 93,8 24,1 3,892 SLC22A16 member 16 pleckstrin homology domain containing, family A 1231 0,0022106 0,0980647 54,2 14 3,871 PLEKHA5 member 5 TPTE 499 0,0005731 0,0626634 61,9 16 3,869 psiTPTE22 pseudogene phosphatidic acid phosphatase 2715 0,0084609 0,1703866 1008,3 264,3 3,815 PPAP2B type 2B 32 1,81E-05 0,0302321 33,1 8,7 3,805 NA NA Malate dehydrogenas e 1, NAD 3884 0,0154747 0,2178371 162,9 43,1 3,78 MDH1 (soluble) transferrin receptor (p90, 2487 0,007256 0,1594541 152,8 40,5 3,773 TFRC CD71) family with sequence similarity 92, member A1 /// FAM92A1 /// similar to 1885 0,0044102 0,1279192 94,4 25,2 3,746 LOC730572 CG6405-PA chromosome 8 open reading 1178 0,0020747 0,0961653 179,4 47,9 3,745 C8orf72 frame 72 transmembran 6727 0,0409647 0,3329486 243,3 65,1 3,737 TMEM130 e protein 130 malic enzyme 1, NADP(+)- dependent, 4064 0,0168471 0,2266524 31,5 8,5 3,706 ME1 cytosolic macrophage scavenger 6751 0,041189 0,3335815 184,8 50,1 3,689 MSR1 receptor 1 LIM domain and actin 2890 0,0093392 0,1765702 556,2 151,5 3,671 LIMA1 binding 1 hypothetical protein 1021 0,0016321 0,0873837 48,6 13,3 3,654 LOC286272 LOC286272 Phosphodieste rase 3B, cGMP- 1197 0,0021249 0,0970402 120,9 33,2 3,642 PDE3B inhibited cytochrome P450, family 4, subfamily V, 2998 0,0100137 0,1825536 42,8 11,8 3,627 CYP4V2 polypeptide 2 HtrA serine 5653 0,0300663 0,2907969 226,8 62,6 3,623 HTRA4 peptidase 4 FERM domain 2767 0,0087787 0,1732398 41,9 11,6 3,612 FRMD4A containing 4A protein kinase, cAMP- dependent, 3780 0,0146005 0,2111806 322,2 89,4 3,604 PRKACB catalytic, beta CDNA FLJ25556 fis, clone 2354 0,0065405 0,1519124 256,2 71,1 3,603 NA JTH02629 phosphodieste rase 3B, cGMP- 148 0,0001225 0,0449393 185,4 51,7 3,586 PDE3B inhibited chromosome 14 open reading frame 1352 0,0025632 0,1036037 73,5 20,5 3,585 C14orf65 65 solute carrier family 6 (neurotransmitt er transporter, betaine/GABA) 157 0,0001304 0,0454116 121,4 34 3,571 SLC6A12 , member 12 peptidylglycine alpha- amidating monooxygenas 237 0,0002189 0,050448 682,7 191,2 3,571 PAM e 5709 0,0305577 0,2926386 94,8 26,6 3,564 FN1 Fibronectin 1 GM2 ganglioside 1837 0,0042158 0,1254704 818,1 230,4 3,551 GM2A activator CDNA FLJ36989 fis, clone BRACE200675 403 0,0004327 0,0577884 3501,3 987,4 3,546 NA 3 phosphatidic acid phosphatase 2492 0,0072711 0,1595295 2284,1 644,8 3,542 PPAP2B type 2B tumor necrosis factor receptor superfamily, member 11a, 1397 0,0026917 0,1053462 131 37 3,541 TNFRSF11A NFKB activator SPOC domain 1429 0,0028067 0,1071379 227,7 64,3 3,541 SPOCD1 containing 1 SPOC domain 6148 0,0349452 0,3107388 451,9 128,1 3,528 SPOCD1 containing 1 Chromosome 9 open reading 1023 0,0016352 0,0873945 173,9 50,4 3,45 C9orf52 frame 52 protein tyrosine phosphatase, non-receptor type 13 (APO- 1/CD95 (Fas)- associated 25 1,58E-05 0,0302321 24 7 3,429 PTPN13 phosphatase) cholesterol 25- 2242 0,0059923 0,1461325 641,2 187,2 3,425 CH25H hydroxylase integrin, alpha 4 (antigen CD49D, alpha 4 subunit of VLA-4 63 4,16E-05 0,0353731 51 14,9 3,423 ITGA4 receptor) malic enzyme 1, NADP(+)- dependent, 6604 0,0393031 0,3253932 173,7 50,8 3,419 ME1 cytosolic Protein tyrosine phosphatase, receptor type, N polypeptide 360 0,00037 0,0561938 107,6 31,5 3,416 PTPRN2 2 Chromosome 9 open reading 1289 0,0024046 0,1019668 106,1 31,1 3,412 C9orf52 frame 52 GM2 ganglioside 1611 0,0034234 0,116061 1005,1 297,4 3,38 GM2A activator HEAT repeat 1664 0,0035687 0,1172588 182,5 54 3,38 HEATR5A containing 5A CDNA FLJ41910 fis, clone PEBLM200783 56 3,42E-05 0,0333908 80 23,7 3,376 NA 4 LIM domain and actin 4102 0,0171483 0,2285213 174,1 51,8 3,361 LIMA1 binding 1 CDNA FLJ37694 fis, clone BRHIP201522 1895 0,0044651 0,128789 43,6 13 3,354 NA 4 peptidylglycine alpha- amidating monooxygenas 178
Recommended publications
  • Binnenwerk Cindy Postma.Indd
    CHAPTER 6 Multiple putative oncogenes at the chromosome 20q amplicon contribute to colorectal adenoma to carcinoma progression Gut 2009, 58: 79-89 Beatriz Carvalho Cindy Postma Sandra Mongera Erik Hopmans Sharon Diskin Mark A. van de Wiel Wim van Criekinge Olivier Thas Anja Matthäi Miguel A. Cuesta Jochim S. Terhaar sive Droste Mike Craanen Evelin Schröck Bauke Ylstra Gerrit A. Meijer 104 | Chapter 6 Abstract Objective: This study aimed to identify the oncogenes at 20q involved in colorectal adenoma to carcinoma progression by measuring the effect of 20q gain on mRNA expression of genes in this amplicon. Methods: Segmentation of DNA copy number changes on 20q was performed by array CGH in 34 non-progressed colorectal adenomas, 41 progressed adenomas (i.e. adenomas that present a focus of cancer) and 33 adenocarcinomas. Moreover, a robust analysis of altered expression of genes in these segments was performed by microarray analysis in 37 adenomas and 31 adenocarcinomas. Protein expression was evaluated by immunohistochemistry on tissue microarrays. Results: The genes C20orf24, AURKA, RNPC1, TH1L, ADRM1, C20orf20 and TCFL5, mapping at 20q were signifi cantly overexpressed in carcinomas compared to adenomas as consequence of copy number gain of 20q. Conclusion: This approach revealed C20orf24, AURKA, RNPC1, TH1L, ADRM1, C20orf20 and TCFL5 genes to be important in chromosomal instability-related adenoma to carcinoma progression. These genes therefore may serve as highly specifi c biomarkers for colorectal cancer with potential clinical applications. Putative oncogenes at chromosome 20q in colorectal carcinogenesis | 105 Introduction The majority of cancers are epithelial in origin and arise through a stepwise progression from normal cells, through dysplasia, into malignant cells that invade surrounding tissues and have metastatic potential.
    [Show full text]
  • Efficacy and Mechanistic Evaluation of Tic10, a Novel Antitumor Agent
    University of Pennsylvania ScholarlyCommons Publicly Accessible Penn Dissertations 2012 Efficacy and Mechanisticv E aluation of Tic10, A Novel Antitumor Agent Joshua Edward Allen University of Pennsylvania, [email protected] Follow this and additional works at: https://repository.upenn.edu/edissertations Part of the Oncology Commons Recommended Citation Allen, Joshua Edward, "Efficacy and Mechanisticv E aluation of Tic10, A Novel Antitumor Agent" (2012). Publicly Accessible Penn Dissertations. 488. https://repository.upenn.edu/edissertations/488 This paper is posted at ScholarlyCommons. https://repository.upenn.edu/edissertations/488 For more information, please contact [email protected]. Efficacy and Mechanisticv E aluation of Tic10, A Novel Antitumor Agent Abstract TNF-related apoptosis-inducing ligand (TRAIL; Apo2L) is an endogenous protein that selectively induces apoptosis in cancer cells and is a critical effector in the immune surveillance of cancer. Recombinant TRAIL and TRAIL-agonist antibodies are in clinical trials for the treatment of solid malignancies due to the cancer-specific cytotoxicity of TRAIL. Recombinant TRAIL has a short serum half-life and both recombinant TRAIL and TRAIL receptor agonist antibodies have a limited capacity to perfuse to tissue compartments such as the brain, limiting their efficacy in certain malignancies. To overcome such limitations, we searched for small molecules capable of inducing the TRAIL gene using a high throughput luciferase reporter gene assay. We selected TRAIL-inducing compound 10 (TIC10) for further study based on its induction of TRAIL at the cell surface and its promising therapeutic index. TIC10 is a potent, stable, and orally active antitumor agent that crosses the blood-brain barrier and transcriptionally induces TRAIL and TRAIL-mediated cell death in a p53-independent manner.
    [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]
  • Effet De La Cryptorchidie Sur Le Transcriptome Testiculaire Humain
    MARIE EVE BERGERON EFFET DE LA CRYPTORCHIDIE SUR LE TRANSCRIPTOME TESTICULAIRE HUMAIN Mémoire présenté à la Faculté des études supérieures et postdoctorales de l’Université Laval dans le cadre du programme de maîtrise en Physiologie-Endocrinologie pour l’obtention du grade de Maître ès sciences (M.Sc.) DÉPARTEMENT D’OBSTÉTRIQUE ET DE GYNÉCOLOGIE FACULTÉ DE MÉDECINE UNIVERSITÉ LAVAL QUÉBEC 2012 © Marie Eve Bergeron, 2012 Résumé Les niveaux d’expression de nombreux gènes peuvent être affectés par l’environnement et mener au développement de la cryptorchidie. Cette malformation congénitale est la plus commune dont une des conséquences majeures est l’infertilité masculine due au testicule non-descendu, auquel un risque plus élevé de cancer testiculaire est associé. L’expression des ARN totaux isolés à partir de biopsies testiculaires ont été analysés par micropuces, puis par une analyse bio-informatique et une validation par RT-qPCR de plusieurs gènes sélectionnés. Ces analyses m’ont permis d’identifier plus de deux milles candidats montrant une expression différente entre des sujets cryptorchides et normaux. Certains de ces gènes sélectionnés peuvent être associés à la descente testiculaire, d’autres au cancer testiculaire ou encore aux divers types cellulaires retrouvés dans cet organe. Les différences dans le transcriptome dues à la cryptorchidie vont nous aider à comprendre la cause génétique de cette maladie. ii Abstract Expression level of numerous genes may be affected by environmental condition and lead to development of cryptorchidism. The most common congenital malformation in male is cryptorchidism. One major consequence of this anomaly is infertility due to undescended testis, to which an increased risk of testicular cancer is associated.
    [Show full text]
  • A Dissertation Entitled the Androgen Receptor
    A Dissertation entitled The Androgen Receptor as a Transcriptional Co-activator: Implications in the Growth and Progression of Prostate Cancer By Mesfin Gonit Submitted to the Graduate Faculty as partial fulfillment of the requirements for the PhD Degree in Biomedical science Dr. Manohar Ratnam, Committee Chair Dr. Lirim Shemshedini, Committee Member Dr. Robert Trumbly, Committee Member Dr. Edwin Sanchez, Committee Member Dr. Beata Lecka -Czernik, Committee Member Dr. Patricia R. Komuniecki, Dean College of Graduate Studies The University of Toledo August 2011 Copyright 2011, Mesfin Gonit This document is copyrighted material. Under copyright law, no parts of this document may be reproduced without the expressed permission of the author. An Abstract of The Androgen Receptor as a Transcriptional Co-activator: Implications in the Growth and Progression of Prostate Cancer By Mesfin Gonit As partial fulfillment of the requirements for the PhD Degree in Biomedical science The University of Toledo August 2011 Prostate cancer depends on the androgen receptor (AR) for growth and survival even in the absence of androgen. In the classical models of gene activation by AR, ligand activated AR signals through binding to the androgen response elements (AREs) in the target gene promoter/enhancer. In the present study the role of AREs in the androgen- independent transcriptional signaling was investigated using LP50 cells, derived from parental LNCaP cells through extended passage in vitro. LP50 cells reflected the signature gene overexpression profile of advanced clinical prostate tumors. The growth of LP50 cells was profoundly dependent on nuclear localized AR but was independent of androgen. Nevertheless, in these cells AR was unable to bind to AREs in the absence of androgen.
    [Show full text]
  • (12) United States Patent (10) Patent No.: US 8.440,393 B2 Birrer Et Al
    USOO8440393B2 (12) United States Patent (10) Patent No.: US 8.440,393 B2 Birrer et al. (45) Date of Patent: May 14, 2013 (54) PRO-ANGIOGENIC GENES IN OVARIAN OTHER PUBLICATIONS TUMORENDOTHELIAL CELL, SOLATES Boyd (The Basic Science of Oncology, 1992, McGraw-Hill, Inc., p. (75) Inventors: Michael J. Birrer, Mt. Airy, MD (US); 379). Tomas A. Bonome, Washington, DC Tockman et al. (Cancer Res., 1992, 52:2711s-2718s).* (US); Anil Sood, Pearland, TX (US); Pritzker (Clinical Chemistry, 2002, 48: 1147-1150).* Chunhua Lu, Missouri City, TX (US) Benedict et al. (J. Exp. Medicine, 2001, 193(1) 89-99).* Jiang et al. (J. Biol. Chem., 2003, 278(7) 4763-4769).* (73) Assignees: The United States of America as Matsushita et al. (FEBS Letters, 1999, vol. 443, pp. 348-352).* Represented by the Secretary of the Singh et al. (Glycobiology, 2001, vol. 11, pp. 587-592).* Department of Health and Human Abbosh et al. (Cancer Res. Jun. 1, 2006 66:5582-55.91 and Supple Services, Washington, DC (US); The mental Figs. S1-S7).* University of MD Anderson Cancer Zhai et al. (Chinese General Practice Aug. 2008, 11(8A): 1366 Center, Houston, TX (US) 1367).* Lu et al. (Cancer Res. Feb. 15, 2007, 64(4): 1757-1768).* (*) Notice: Subject to any disclaimer, the term of this Bagnato et al., “Activation of Mitogenic Signaling by Endothelin 1 in patent is extended or adjusted under 35 Ovarian Carcinoma Cells', Cancer Research, vol. 57, pp. 1306-1311, U.S.C. 154(b) by 194 days. 1997. Bouras et al., “Stanniocalcin 2 is an Estrogen-responsive Gene (21) Appl.
    [Show full text]
  • Supplementary Data
    Supplementary Fig. 1 A B Responder_Xenograft_ Responder_Xenograft_ NON- NON- Lu7336, Vehicle vs Lu7466, Vehicle vs Responder_Xenograft_ Responder_Xenograft_ Sagopilone, Welch- Sagopilone, Welch- Lu7187, Vehicle vs Lu7406, Vehicle vs Test: 638 Test: 600 Sagopilone, Welch- Sagopilone, Welch- Test: 468 Test: 482 Responder_Xenograft_ NON- Lu7860, Vehicle vs Responder_Xenograft_ Sagopilone, Welch - Lu7558, Vehicle vs Test: 605 Sagopilone, Welch- Test: 333 Supplementary Fig. 2 Supplementary Fig. 3 Supplementary Figure S1. Venn diagrams comparing probe sets regulated by Sagopilone treatment (10mg/kg for 24h) between individual models (Welsh Test ellipse p-value<0.001 or 5-fold change). A Sagopilone responder models, B Sagopilone non-responder models. Supplementary Figure S2. Pathway analysis of genes regulated by Sagopilone treatment in responder xenograft models 24h after Sagopilone treatment by GeneGo Metacore; the most significant pathway map representing cell cycle/spindle assembly and chromosome separation is shown, genes upregulated by Sagopilone treatment are marked with red thermometers. Supplementary Figure S3. GeneGo Metacore pathway analysis of genes differentially expressed between Sagopilone Responder and Non-Responder models displaying –log(p-Values) of most significant pathway maps. Supplementary Tables Supplementary Table 1. Response and activity in 22 non-small-cell lung cancer (NSCLC) xenograft models after treatment with Sagopilone and other cytotoxic agents commonly used in the management of NSCLC Tumor Model Response type
    [Show full text]
  • Supplemental Figure S1 Differentially Methylated Regions (Dmrs
    Supplemental Figure S1 '$$#0#,2'**7+#2&7*2#"0#%'-,11 #25##,"'1#1#122#1 '!2-0'*"#.'!2'-,-$122&#20,1'2'-,$0-+2- !"Q !"2-$%," $ 31',% 25-$-*" !&,%# ," ' 0RTRW 1 !32V-$$ !0'2#0'T - #.0#1#,22'-, -$ "'$$#0#,2'**7+#2&7*2#"%#,#11',.0#,2&#1#1,"2&#'0 #&4'-022&#20,1'2'-, #25##,"'$$#0#,2"'1#1#122#1T-*!)00-51',"'!2#&7.#0+#2&7*2#"%#,#1Q%0700-51 &7.-+#2&7*2#"%#,#1Q31',%25-$-*"!&,%#,"'0RTRW1!32V-$$!0'2#0'T-%#,#1 +#22&# -4#!0'2#0'22&#20,1'2'-,$0-+$%2-$Q5#2&#0#$-0#*1-',!*3"#" %#,#15'2&V4*3#0RTRWT$$#!2#"%#,10#&'%&*'%&2#" 712#0'1)1#T Supplemental Figure S2 Validation of results from the HELP assay using Epityper MassarrayT #13*21 $0-+ 2&# 1$ 117 5#0# !-00#*2#" 5'2& /3,2'22'4# +#2&7*2'-, ,*78#" 7 '13*$'2#11007$-04V-,"6U-%#,#.0-+-2#00#%'-,1T11007 51.#0$-0+#"31',%**4'* *#1+.*#1T S Supplemental Fig. S1 A unique hypermethylated genes (methylation sites) 454 (481) 5693 (6747) 120 (122) NLMGUS NEWMM REL 2963 (3207) 1338 (1560) 5 (5) unique hypomethylated genes (methylation sites) B NEWMM 0 (0) MGUS 454 (481) 0 (0) NEWMM REL NL 3* (2) 2472 (3066) NEWMM 2963 REL (3207) 2* (2) MGUS 0 (0) REL 2 (2) NEWMM 0 (0) REL Supplemental Fig. S2 A B ARID4B DNMT3A Methylation by MassArray Methylation by MassArray 0 0.2 0.4 0.6 0.8 1 1.2 0.5 0.6 0.7 0.8 0.9 1 2 0 NL PC MGUS 1.5 -0.5 NEW MM 1 REL MM -1 0.5 -1.5 0 -2 -0.5 -1 -2.5 -1.5 -3 Methylation by HELP Assay Methylation by HELP Methylation by HELP Assay Methylation by HELP -2 -3.5 -2.5 -4 Supplemental tables "3..*#+#,2*6 *#"SS 9*','!*!&0!2#0'12'!1-$.2'#,21+.*#1 DZ_STAGE Age Gender Ethnicity MM isotype PCLI Cytogenetics
    [Show full text]
  • Supplemental Table 3 Site ID Intron Poly(A) Site Type NM/KG Inum
    Supplemental Table 3 Site ID Intron Poly(A) site Type NM/KG Inum Region Gene ID Gene Symbol Gene Annotation Hs.120277.1.10 chr3:170997234:170996860 170996950 b NM_153353 7 CDS 151827 LRRC34 leucine rich repeat containing 34 Hs.134470.1.27 chr17:53059664:53084458 53065543 b NM_138962 10 CDS 124540 MSI2 musashi homolog 2 (Drosophila) Hs.162889.1.18 chr14:80367239:80329208 80366262 b NM_152446 12 CDS 145508 C14orf145 chromosome 14 open reading frame 145 Hs.187898.1.27 chr22:28403623:28415294 28404458 b NM_181832 16 3UTR 4771 NF2 neurofibromin 2 (bilateral acoustic neuroma) Hs.228320.1.6 chr10:115527009:115530350 115527470 b BC036365 5 CDS 79949 C10orf81 chromosome 10 open reading frame 81 Hs.266308.1.2 chr11:117279579:117278191 117278967 b NM_032046 12 CDS 84000 TMPRSS13 transmembrane protease, serine 13 Hs.266308.1.4 chr11:117284536:117281662 117283722 b NM_032046 9 CDS 84000 TMPRSS13 transmembrane protease, serine 13 Hs.2689.1.4 chr10:53492398:53563605 53492622 b NM_006258 7 CDS 5592 PRKG1 protein kinase, cGMP-dependent, type I Hs.280781.1.6 chr18:64715646:64829150 64715837 b NM_024781 4 CDS 79839 C18orf14 chromosome 18 open reading frame 14 Hs.305985.2.25 chr12:8983686:8984438 8983942 b BX640639 17 3UTR NA NA NA Hs.312098.1.36 chr1:151843991:151844258 151844232 b NM_003815 15 CDS 8751 ADAM15 a disintegrin and metalloproteinase domain 15 (metargidin) Hs.314338.1.11 chr21:39490293:39481214 39487623 b NM_018963 41 CDS 54014 BRWD1 bromodomain and WD repeat domain containing 1 Hs.33368.1.3 chr15:92685158:92689361 92688314 b NM_018349 6 CDS 55784 MCTP2 multiple C2-domains with two transmembrane regions 2 Hs.346736.1.21 chr2:99270738:99281614 99272414 b AK126402 10 3UTR 51263 MRPL30 mitochondrial ribosomal protein L30 Hs.445061.1.19 chr16:69322898:69290216 69322712 b NM_018052 14 CDS 55697 VAC14 Vac14 homolog (S.
    [Show full text]
  • Genome-Wide Transcriptome Analysis of Laminar Tissue During the Early Stages of Experimentally Induced Equine Laminitis
    GENOME-WIDE TRANSCRIPTOME ANALYSIS OF LAMINAR TISSUE DURING THE EARLY STAGES OF EXPERIMENTALLY INDUCED EQUINE LAMINITIS A Dissertation by JIXIN WANG Submitted to the Office of Graduate Studies of Texas A&M University in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY December 2010 Major Subject: Biomedical Sciences GENOME-WIDE TRANSCRIPTOME ANALYSIS OF LAMINAR TISSUE DURING THE EARLY STAGES OF EXPERIMENTALLY INDUCED EQUINE LAMINITIS A Dissertation by JIXIN WANG Submitted to the Office of Graduate Studies of Texas A&M University in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY Approved by: Chair of Committee, Bhanu P. Chowdhary Committee Members, Terje Raudsepp Paul B. Samollow Loren C. Skow Penny K. Riggs Head of Department, Evelyn Tiffany-Castiglioni December 2010 Major Subject: Biomedical Sciences iii ABSTRACT Genome-wide Transcriptome Analysis of Laminar Tissue During the Early Stages of Experimentally Induced Equine Laminitis. (December 2010) Jixin Wang, B.S., Tarim University of Agricultural Reclamation; M.S., South China Agricultural University; M.S., Texas A&M University Chair of Advisory Committee: Dr. Bhanu P. Chowdhary Equine laminitis is a debilitating disease that causes extreme sufferring in afflicted horses and often results in a lifetime of chronic pain. The exact sequence of pathophysiological events culminating in laminitis has not yet been characterized, and this is reflected in the lack of any consistently effective therapeutic strategy. For these reasons, we used a newly developed 21,000 element equine-specific whole-genome oligoarray to perform transcriptomic analysis on laminar tissue from horses with experimentally induced models of laminitis: carbohydrate overload (CHO), hyperinsulinaemia (HI), and oligofructose (OF).
    [Show full text]
  • A Systems Approach to Prion Disease
    Molecular Systems Biology 5; Article number 252; doi:10.1038/msb.2009.10 Citation: Molecular Systems Biology 5:252 & 2009 EMBO and Macmillan Publishers Limited All rights reserved 1744-4292/09 www.molecularsystemsbiology.com A systems approach to prion disease Daehee Hwang1,2,8, Inyoul Y Lee1,8, Hyuntae Yoo1,8, Nils Gehlenborg1,3, Ji-Hoon Cho2, Brianne Petritis1, David Baxter1, Rose Pitstick4, Rebecca Young4, Doug Spicer4, Nathan D Price7, John G Hohmann5, Stephen J DeArmond6, George A Carlson4,* and Leroy E Hood1,* 1 Institute for Systems Biology, Seattle, WA, USA, 2 I-Bio Program & Department of Chemical Engineering, POSTECH, Pohang, Republic of Korea, 3 Microarray Team, European Bioinformatics Institute, Wellcome Trust Genome Campus, Cambridge, UK, 4 McLaughlin Research Institute, Great Falls, MT, USA, 5 Allen Brain Institute, Seattle, WA, USA, 6 Department of Pathology, University of California, San Francisco, CA, USA and 7 Department of Chemical and Biomolecular Engineering & Institute for Genomic Biology, University of Illinois, Urbana, IL, USA 8 These authors contributed equally to this work * Corresponding authors. GA Carlson, McLaughlin Research Institute, 1520 23rd Street South, Great Falls, MT 59405, USA. Tel.: þ 1 406 454 6044; Fax: þ 1 406 454 6019; E-mail: [email protected] or LE Hood, Institute for Systems Biology, 1441 North 34th Street, Seattle, WA 98103, USA. Tel.: þ 1 206 732 1201; Fax: þ 1 206 732 1254; E-mail: [email protected] Received 27.11.08; accepted 20.1.09 Prions cause transmissible neurodegenerative diseases and replicate by conformational conversion of normal benign forms of prion protein (PrPC) to disease-causing PrPSc isoforms.
    [Show full text]
  • Rattlesnake Genome Supplemental Materials 1 SUPPLEMENTAL
    Rattlesnake Genome Supplemental Materials 1 1 SUPPLEMENTAL MATERIALS 2 Table of Contents 3 1. Supplementary Methods …… 2 4 2. Supplemental Tables ……….. 23 5 3. Supplemental Figures ………. 37 Rattlesnake Genome Supplemental Materials 2 6 1. SUPPLEMENTARY METHODS 7 Prairie Rattlesnake Genome Sequencing and Assembly 8 A male Prairie Rattlesnake (Crotalus viridis viridis) collected from a wild population in Colorado was 9 used to generate the genome sequence. This specimen was collected and humanely euthanized according 10 to University of Northern Colorado Institutional Animal Care and Use Committee protocols 0901C-SM- 11 MLChick-12 and 1302D-SM-S-16. Colorado Parks and Wildlife scientific collecting license 12HP974 12 issued to S.P. Mackessy authorized collection of the animal. Genomic DNA was extracted using a 13 standard Phenol-Chloroform-Isoamyl alcohol extraction from liver tissue that was snap frozen in liquid 14 nitrogen. Multiple short-read sequencing libraries were prepared and sequenced on various platforms, 15 including 50bp single-end and 150bp paired-end reads on an Illumina GAII, 100bp paired-end reads on an 16 Illumina HiSeq, and 300bp paired-end reads on an Illumina MiSeq. Long insert libraries were also 17 constructed by and sequenced on the PacBio platform. Finally, we constructed two sets of mate-pair 18 libraries using an Illumina Nextera Mate Pair kit, with insert sizes of 3-5 kb and 6-8 kb, respectively. 19 These were sequenced on two Illumina HiSeq lanes with 150bp paired-end sequencing reads. Short and 20 long read data were used to assemble the previous genome assembly version CroVir2.0 (NCBI accession 21 SAMN07738522).
    [Show full text]