Supplementary Data- Figure Legends S1: Transfection of SH-SY5Y

Total Page:16

File Type:pdf, Size:1020Kb

Supplementary Data- Figure Legends S1: Transfection of SH-SY5Y Supplementary Data- Figure legends S1: Transfection of SH-SY5Y neuroblastoma cells with LSD1-directed siRNA resulted in reproducible knock-down of LSD1 mRNA expression. mRNA levels were measured by quantitative real-time PCR. S2: TaqMan quantitative RT-PCR confirmed the expression changes detected via microarray analysis for LSD1, DNAL4, DNM2, TNS1 and TPM1. * p < 0.1,** p < 0.5 S3: As TNS1 is induced upon siRNA mediated LSD1 knock-down in vitro, we analyzed TNS1 expression in vivo. TNS1 was significantly down-regulated in primary tumors with low LSD1 expression, and in ganglioneuroma and ganglioneuroblastoma. S4: Treatment of NB69, SKNAS and Kelly neuroblastoma cells with tranylcypromine, resulted in extensive reduction of cell numbers. Western blot analysis confirmed an accumulation of H3K4 dimethylation upon treatment with tranylcypromine. β-actin served as the loading control. Supplementary Table 1: Genes annotated with ‚neuronal differentiation’ were analyzed for their correlation with LSD1 expression and differential expression between poorly differentiated neuroblastoma, differentiating neuroblastoma and ganglioneuroma / ganglioneuroblastoma by ANOVA in 110 primary neuroblastic tumors using Affymatrix microarrays. Most genes that showed differential expression between NBpd, NBdiff and GNB/GN were also correlated with LSD1 expression. Supplementary Table 2: Genes correlating with LSD1 were annotated according to gene ontology. These genes were compared to all genes which have been considered expressed in at least 1 of the 110 samples (the reference) to determine if any GO class was enriched in the genes which correlated with LSD1. P-Values were calculated to evaluate if any go class was significantly overrepresented, and the 5 most significant classes were displayed in table 2. Supplementary Table 3: Patients were categorized according to known molecular and clinical risk factors. ANOVA was used to analyse if LSD1 is differentially expressed between patients of different groups. While differential expression of LSD1 did not reached significance between patients grouped according to stage, NMYC or LOH1p36, a week difference was observed between patients grouped according to age. Supplementary Table 4 Annotation of genes differentially expressed between cells treated with siRNA against LSD1 and control siRNA. (Probe-IDs correspond to Affymetrix U133v2 microarrays, a=mean expression in control cells, b=mean expression upon siRNA mediated knock down, FC=Fold change, tt=P-Value T-test) Supplementary data S2: Materials and Methods LSD1, DNAL4, DNM2, TNS1, TPM1 expression was quantitatively measured using the ABI 7900HT TaqMan instrument (Applied Biosystems, Foster City, CA). TaqMan reactions were done in 384-well plates according to the instructions of the manufacturer. Expression of LSD1, DNAL4, DNM2, TNS1, TPM were measured in duplicates and normalized to 18S RNA. Primers were labelled with 5'-FAM as a reporter and 3'-NFQ-1 as a quencher and purchased from Applied Biosystems. .
Recommended publications
  • A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
    Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated.
    [Show full text]
  • To Study Mutant P53 Gain of Function, Various Tumor-Derived P53 Mutants
    Differential effects of mutant TAp63γ on transactivation of p53 and/or p63 responsive genes and their effects on global gene expression. A thesis submitted in partial fulfillment of the requirements for the degree of Master of Science By Shama K Khokhar M.Sc., Bilaspur University, 2004 B.Sc., Bhopal University, 2002 2007 1 COPYRIGHT SHAMA K KHOKHAR 2007 2 WRIGHT STATE UNIVERSITY SCHOOL OF GRADUATE STUDIES Date of Defense: 12-03-07 I HEREBY RECOMMEND THAT THE THESIS PREPARED UNDER MY SUPERVISION BY SHAMA KHAN KHOKHAR ENTITLED Differential effects of mutant TAp63γ on transactivation of p53 and/or p63 responsive genes and their effects on global gene expression BE ACCEPTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF Master of Science Madhavi P. Kadakia, Ph.D. Thesis Director Daniel Organisciak , Ph.D. Department Chair Committee on Final Examination Madhavi P. Kadakia, Ph.D. Steven J. Berberich, Ph.D. Michael Leffak, Ph.D. Joseph F. Thomas, Jr., Ph.D. Dean, School of Graduate Studies 3 Abstract Khokhar, Shama K. M.S., Department of Biochemistry and Molecular Biology, Wright State University, 2007 Differential effect of TAp63γ mutants on transactivation of p53 and/or p63 responsive genes and their effects on global gene expression. p63, a member of the p53 gene family, known to play a role in development, has more recently also been implicated in cancer progression. Mice lacking p63 exhibit severe developmental defects such as limb truncations, abnormal skin, and absence of hair follicles, teeth, and mammary glands. Germline missense mutations of p63 have been shown to be responsible for several human developmental syndromes including SHFM, EEC and ADULT syndromes and are associated with anomalies in the development of organs of epithelial origin.
    [Show full text]
  • UNIVERSITY of CALIFORNIA, IRVINE Combinatorial Regulation By
    UNIVERSITY OF CALIFORNIA, IRVINE Combinatorial regulation by maternal transcription factors during activation of the endoderm gene regulatory network DISSERTATION submitted in partial satisfaction of the requirements for the degree of DOCTOR OF PHILOSOPHY in Biological Sciences by Kitt D. Paraiso Dissertation Committee: Professor Ken W.Y. Cho, Chair Associate Professor Olivier Cinquin Professor Thomas Schilling 2018 Chapter 4 © 2017 Elsevier Ltd. © 2018 Kitt D. Paraiso DEDICATION To the incredibly intelligent and talented people, who in one way or another, helped complete this thesis. ii TABLE OF CONTENTS Page LIST OF FIGURES vii LIST OF TABLES ix LIST OF ABBREVIATIONS X ACKNOWLEDGEMENTS xi CURRICULUM VITAE xii ABSTRACT OF THE DISSERTATION xiv CHAPTER 1: Maternal transcription factors during early endoderm formation in 1 Xenopus Transcription factors co-regulate in a cell type-specific manner 2 Otx1 is expressed in a variety of cell lineages 4 Maternal otx1 in the endodermal conteXt 5 Establishment of enhancers by maternal transcription factors 9 Uncovering the endodermal gene regulatory network 12 Zygotic genome activation and temporal control of gene eXpression 14 The role of maternal transcription factors in early development 18 References 19 CHAPTER 2: Assembly of maternal transcription factors initiates the emergence 26 of tissue-specific zygotic cis-regulatory regions Introduction 28 Identification of maternal vegetally-localized transcription factors 31 Vegt and OtX1 combinatorially regulate the endodermal 33 transcriptome iii
    [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]
  • S1 Table Analyzed Transcriptomics Parameters of Lung Tissue of Chronic
    S1 Table Analyzed transcriptomics parameters of lung tissue of chronic obstructive pulmonary disease rats p- FCAbsolute regulation(B_v GeneSymbo GenbankAcces ProbeName value(B (B vs A) s_A) l sion vs A) A_44_P4095 0.0079 1.2996 down Gmpr NM_057188 18 A_44_P2605 NM_0011067 0.0378 1.2427 up Klhl28 80 35 A_44_P1052 0.0018 2.0900 up Hnrpll XM_233805 387 A_43_P1546 0.0365 1.3240 up Pde5a NM_133584 6 A_44_P7283 0.0035 1.2634 up AW915320 87 A_42_P8435 0.0143 1.1393 up 92 A_44_P4310 0.0124 1.3434 down Cyp2d4 U48220 92 A_44_P3056 0.0496 1.1467 up BP465973 36 A_44_P1779 0.0311 1.1157 down Rccd1 XM_218819 07 A_44_P9133 0.0129 1.2963 up 60 A_44_P3412 0.0167 1.3108 up AA997107 04 A_44_P9971 NM_0011057 0.0033 1.2820 up Atrx 74 57 A_42_P7763 0.0310 1.1275 up BF556698 00 A_44_P4634 0.0180 1.3210 up BQ210920 20 A_44_P5212 0.0101 1.2583 up AA925252 64 A_44_P8855 0.0469 1.2051 down 48 A_44_P6998 0.0151 1.5168 up 21 A_44_P1414 0.0236 1.2774 up AI575641 75 A_44_P4922 NM_0011064 0.0041 1.6816 down Eps8l3 14 63 A_43_P2202 0.0488 1.2176 up Setx XM_342400 0 A_44_P2066 0.0205 1.2767 up BF417274 31 A_44_P6213 0.0007 2.0237 up 04 A_44_P3775 0.0068 1.2952 up 20 A_44_P6058 0.0365 1.1240 up 38 A_44_P2861 0.0022 1.4896 up XM_226020 58 A_44_P9139 0.0108 1.5661 up 62 A_43_P1214 0.0058 1.9100 up Hnf4a NM_022180 6 A_44_P6525 NM_0011300 0.0036 1.1586 down Kdm1 85 98 A_44_P3541 0.0061 1.3319 down Cep250 XR_009560 50 A_44_P5160 RGD131055 NM_0011068 0.0293 1.2854 down 73 2 38 A_44_P2237 0.0192 1.3087 up AW142694 41 A_43_P1552 0.0096 1.2036 up Ccnd3 NM_012766 4 A_44_P4098 0.0479
    [Show full text]
  • Supplemental Table 1 List of Genes Differentially Expressed In
    Supplemental Table 1 List of genes differentially expressed in normal nasopharyngeal epithelium (N), metaplastic and displastic lesions (R), and carcinoma (T). Parametric Permutation Geom Geom Geom Unique Description Clone UG Gene symbol Map p-value p-value mean mean mean id cluster of of of ratios ratios ratios in in in class class class 1 : N 2 : R 3 : T 1 p < 1e-07 0 0.061 0.123 2.708 169329 secretory leukocyte protease IncytePD:2510171 Hs.251754 SLPI 20q12 inhibitor (antileukoproteinase) 2 p < 1e-07 0 0.125 0.394 1.863 163628 sodium channel, nonvoltage-gated IncytePD:1453049 Hs.446415 SCNN1A 12p13 1 alpha 3 p < 1e-07 0 0.122 0.046 1.497 160401 carcinoembryonic antigen-related IncytePD:2060355 Hs.73848 CEACAM6 19q13.2 cell adhesion molecule 6 (non- specific cross reacting antigen) 4 p < 1e-07 0 0.675 1.64 5.594 165101 monoglyceride lipase IncytePD:2174920 Hs.6721 MGLL 3q21.3 5 p < 1e-07 0 0.182 0.487 0.998 166827 nei endonuclease VIII-like 1 (E. IncytePD:1926409 Hs.28355 NEIL1 15q22.33 coli) 6 p < 1e-07 0 0.194 0.339 0.915 162931 hypothetical protein FLJ22418 IncytePD:2816379 Hs.36563 FLJ22418 1p11.1 7 p < 1e-07 0 1.313 0.645 13.593 162399 S100 calcium binding protein P IncytePD:2060823 Hs.2962 S100P 4p16 8 p < 1e-07 0 0.157 1.445 2.563 169315 selenium binding protein 1 IncytePD:2591494 Hs.334841 SELENBP1 1q21-q22 9 p < 1e-07 0 0.046 0.738 1.213 160115 prominin-like 1 (mouse) IncytePD:2070568 Hs.112360 PROML1 4p15.33 10 p < 1e-07 0 0.787 2.264 3.013 167294 HRAS-like suppressor 3 IncytePD:1969263 Hs.37189 HRASLS3 11q12.3 11 p < 1e-07 0 0.292 0.539 1.493 168221 Homo sapiens cDNA FLJ13510 IncytePD:64451 Hs.37896 2 fis, clone PLACE1005146.
    [Show full text]
  • Genome-Wide Screening Identifies Genes and Biological Processes
    Louisiana State University LSU Digital Commons LSU Doctoral Dissertations Graduate School 10-12-2018 Genome-Wide Screening Identifies Genes and Biological Processes Implicated in Chemoresistance and Oncogene-Induced Apoptosis Tengyu Ko Louisiana State University and Agricultural and Mechanical College, [email protected] Follow this and additional works at: https://digitalcommons.lsu.edu/gradschool_dissertations Part of the Cancer Biology Commons, Cell Biology Commons, and the Genomics Commons Recommended Citation Ko, Tengyu, "Genome-Wide Screening Identifies Genes and Biological Processes Implicated in Chemoresistance and Oncogene- Induced Apoptosis" (2018). LSU Doctoral Dissertations. 4715. https://digitalcommons.lsu.edu/gradschool_dissertations/4715 This Dissertation is brought to you for free and open access by the Graduate School at LSU Digital Commons. It has been accepted for inclusion in LSU Doctoral Dissertations by an authorized graduate school editor of LSU Digital Commons. For more information, please [email protected]. GENOME-WIDE SCREENING IDENTIFIES GENES AND BIOLOGICAL PROCESSES IMPLICATED IN CHEMORESISTANCE AND ONCOGENE- INDUCED APOPTOSIS A Dissertation Submitted to the Graduate Faculty of the Louisiana State University and Agricultural and Mechanical College in partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical and Veterinary Medical Sciences through the Department of Comparative Biomedical Sciences by Tengyu Ko B.S., University of California, Santa Barbara 2010 December 2018 ACKNOWLEDGEMENTS I would like to express my sincerest gratitude to my major supervisor Dr. Shisheng Li for giving me the opportunity to join his team and the freedom to pursue projects. I appreciate all of his thoughts and efforts. Truly, none of these findings would be possible without his supervisions, supports, insightful discussions, and patience.
    [Show full text]
  • LOXL2-Mediated H3K4 Oxidation Reduces Chromatin Accessibility in Triple-Negative Breast Cancer Cells
    Oncogene (2020) 39:79–121 https://doi.org/10.1038/s41388-019-0969-1 ARTICLE LOXL2-mediated H3K4 oxidation reduces chromatin accessibility in triple-negative breast cancer cells 1 1 2 1 1 1 J. P. Cebrià-Costa ● L. Pascual-Reguant ● A. Gonzalez-Perez ● G. Serra-Bardenys ● J. Querol ● M. Cosín ● 1,3 4 4 2 5 6 G. Verde ● R. A. Cigliano ● W. Sanseverino ● S. Segura-Bayona ● A. Iturbide ● D. Andreu ● 1 1,7 1 1,7,8,9 10 6,10 P. Nuciforo ● C. Bernado-Morales ● V. Rodilla ● J. Arribas ● J. Yelamos ● A. Garcia de Herreros ● 2 1 T. H. Stracker ● S. Peiró Received: 28 January 2019 / Revised: 8 July 2019 / Accepted: 9 August 2019 / Published online: 28 August 2019 © The Author(s) 2019. This article is published with open access Abstract Oxidation of H3 at lysine 4 (H3K4ox) by lysyl oxidase-like 2 (LOXL2) generates an H3 modification with an unknown physiological function. We find that LOXL2 and H3K4ox are higher in triple-negative breast cancer (TNBC) cell lines and patient-derived xenografts (PDXs) than those from other breast cancer subtypes. ChIP-seq revealed that H3K4ox is located primarily in heterochromatin, where it is involved in chromatin compaction. Knocking down LOXL2 reduces H3K4ox levels 1234567890();,: 1234567890();,: and causes chromatin decompaction, resulting in a sustained activation of the DNA damage response (DDR) and increased susceptibility to anticancer agents. This critical role that LOXL2 and oxidized H3 play in chromatin compaction and DDR suggests that functionally targeting LOXL2 could be a way to sensitize TNBC cells to conventional therapy.
    [Show full text]
  • (B6;129.Cg-Gt(ROSA)26Sor Tm20(CAG-Ctgf-GFP)Jsd) Were Crossed with Female Foxd1cre/+ Heterozygote Mice 1, and Experimental Mice Were Selected As Foxd1cre/+; Rs26cig/+
    Supplemental Information SI Methods Animal studies Heterozygote mice (B6;129.Cg-Gt(ROSA)26Sor tm20(CAG-Ctgf-GFP)Jsd) were crossed with female Foxd1Cre/+ heterozygote mice 1, and experimental mice were selected as Foxd1Cre/+; Rs26CIG/+. In some studies Coll-GFPTg or TCF/Lef:H2B-GFPTg mice or Foxd1Cre/+; Rs26tdTomatoR/+ mice were used as described 2; 3. Left kidneys were subjected to ureteral obstruction using a posterior surgical approach as described 2. In some experiments recombinant mouse DKK1 (0.5mg/kg) or an equal volume of vehicle was administered by daily IP injection. In the in vivo ASO experiment, either specific Lrp6 (TACCTCAATGCGATTT) or scrambled negative control ASO (AACACGTCTATACGC) (30mg/kg) (Exiqon, LNA gapmers) was administered by IP injection on d-1, d1, d4, and d7. In other experiments anti-CTGF domain-IV antibodies (5mg/kg) or control IgG were administered d-1, d1 and d6. All animal experiments were performed under approved IACUC protocols held at the University of Washington and Biogen. Recombinant protein and antibody generation and characterization Human CTGF domain I (sequence Met1 CPDEPAPRCPAGVSLVLDGCGCCRVCAKQLGELCTERDPCDPHKGLFC), domain I+II (sequence Met1CPDEPAPRCPAGVSLVLDGCGCCRVCAKQLGELCTERDPCDPHKGLFCCIFGGT VYRSGESFQSSCKYQCTCLDGAVGCMPLCSMDVRLPSPDCPFPRRVKLPGKCCEE) were cloned and expressed in 293 cells, and purified by Chelating SFF(Ni) Column, tested for single band by SEC and PAGE, and tested for absence of contamination. Domain-IV (sequence GKKCIRTPKISKPIKFELSGCTSMKTYRAKFCGVCTDGRCCTPHRTTTLPVEFKCPDGE VMKKNMMFIKTCACHYNCPGDNDIFESLYYRKMY) was purchased from Peprotech. Mouse or human DKK1 was generated from the coding sequence with some modifications and a tag. Secreted protein was harvested from 293 cells, and purified by nickel column, and tested for activity in a supertopflash (STF) assay 4. DKK1 showed EC50 of 0.69nM for WNT3a-induced WNT signaling in STF cells.
    [Show full text]
  • Deep RNA Sequencing Analysis of Readthrough Gene Fusions in Human
    Nacu et al. BMC Medical Genomics 2011, 4:11 http://www.biomedcentral.com/1755-8794/4/11 RESEARCHARTICLE Open Access Deep RNA sequencing analysis of readthrough gene fusions in human prostate adenocarcinoma and reference samples Serban Nacu, Wenlin Yuan, Zhengyan Kan, Deepali Bhatt, Celina Sanchez Rivers, Jeremy Stinson, Brock A Peters, Zora Modrusan, Kenneth Jung, Somasekar Seshagiri*, Thomas D Wu* Abstract Background: Readthrough fusions across adjacent genes in the genome, or transcription-induced chimeras (TICs), have been estimated using expressed sequence tag (EST) libraries to involve 4-6% of all genes. Deep transcriptional sequencing (RNA-Seq) now makes it possible to study the occurrence and expression levels of TICs in individual samples across the genome. Methods: We performed single-end RNA-Seq on three human prostate adenocarcinoma samples and their corresponding normal tissues, as well as brain and universal reference samples. We developed two bioinformatics methods to specifically identify TIC events: a targeted alignment method using artificial exon-exon junctions within 200,000 bp from adjacent genes, and genomic alignment allowing splicing within individual reads. We performed further experimental verification and characterization of selected TIC and fusion events using quantitative RT-PCR and comparative genomic hybridization microarrays. Results: Targeted alignment against artificial exon-exon junctions yielded 339 distinct TIC events, including 32 gene pairs with multiple isoforms. The false discovery rate was estimated to be 1.5%. Spliced alignment to the genome was less sensitive, finding only 18% of those found by targeted alignment in 33-nt reads and 59% of those in 50-nt reads. However, spliced alignment revealed 30 cases of TICs with intervening exons, in addition to distant inversions, scrambled genes, and translocations.
    [Show full text]
  • Mrna Expression in Human Leiomyoma and Eker Rats As Measured by Microarray Analysis
    Table 3S: mRNA Expression in Human Leiomyoma and Eker Rats as Measured by Microarray Analysis Human_avg Rat_avg_ PENG_ Entrez. Human_ log2_ log2_ RAPAMYCIN Gene.Symbol Gene.ID Gene Description avg_tstat Human_FDR foldChange Rat_avg_tstat Rat_FDR foldChange _DN A1BG 1 alpha-1-B glycoprotein 4.982 9.52E-05 0.68 -0.8346 0.4639 -0.38 A1CF 29974 APOBEC1 complementation factor -0.08024 0.9541 -0.02 0.9141 0.421 0.10 A2BP1 54715 ataxin 2-binding protein 1 2.811 0.01093 0.65 0.07114 0.954 -0.01 A2LD1 87769 AIG2-like domain 1 -0.3033 0.8056 -0.09 -3.365 0.005704 -0.42 A2M 2 alpha-2-macroglobulin -0.8113 0.4691 -0.03 6.02 0 1.75 A4GALT 53947 alpha 1,4-galactosyltransferase 0.4383 0.7128 0.11 6.304 0 2.30 AACS 65985 acetoacetyl-CoA synthetase 0.3595 0.7664 0.03 3.534 0.00388 0.38 AADAC 13 arylacetamide deacetylase (esterase) 0.569 0.6216 0.16 0.005588 0.9968 0.00 AADAT 51166 aminoadipate aminotransferase -0.9577 0.3876 -0.11 0.8123 0.4752 0.24 AAK1 22848 AP2 associated kinase 1 -1.261 0.2505 -0.25 0.8232 0.4689 0.12 AAMP 14 angio-associated, migratory cell protein 0.873 0.4351 0.07 1.656 0.1476 0.06 AANAT 15 arylalkylamine N-acetyltransferase -0.3998 0.7394 -0.08 0.8486 0.456 0.18 AARS 16 alanyl-tRNA synthetase 5.517 0 0.34 8.616 0 0.69 AARS2 57505 alanyl-tRNA synthetase 2, mitochondrial (putative) 1.701 0.1158 0.35 0.5011 0.6622 0.07 AARSD1 80755 alanyl-tRNA synthetase domain containing 1 4.403 9.52E-05 0.52 1.279 0.2609 0.13 AASDH 132949 aminoadipate-semialdehyde dehydrogenase -0.8921 0.4247 -0.12 -2.564 0.02993 -0.32 AASDHPPT 60496 aminoadipate-semialdehyde
    [Show full text]
  • Knockdown of Hnrnpa0, a Del(5Q) Gene, Alters Myeloid Cell Fate In
    Myelodysplastic Syndromes SUPPLEMENTARY APPENDIX Knockdown of Hnrnpa0 , a del(5q) gene, alters myeloid cell fate in murine cells through regulation of AU-rich transcripts David J. Young, 1 Angela Stoddart, 2 Joy Nakitandwe, 3 Shann-Ching Chen, 3 Zhijian Qian, 4 James R. Downing, 3 and Michelle M. Le Beau 2 1Department of Pediatrics, Division of Oncology, Johns Hopkins University, Baltimora, MD; 2Department of Medicine and the Compre - hensive Cancer Center, University of Chicago, IL; 3St. Jude Children's Research Hospital, Memphis, Tennessee; and 4University of Illi - nois Cancer Center, Chicago, IL, USA DJY and AS equally contributed to this work. ©2014 Ferrata Storti Foundation. This is an open-access paper. doi:10.3324/haematol.2013.098657 Manuscript received on September 25, 2013. Manuscript accepted on February 13, 2014. Correspondence: [email protected] Supplementary Materials for D. Young et al. Purification of hematopoietic populations from mice. Cells from the spleens, thymi, and bone marrow of C57BL/6J mice were harvested as appropriate for each population. For primitive populations including Lin–Sca-1+Kit+ (LSK), common lymphoid (CLP) and myeloid (CMP) progenitors, and granulocyte- monocyte progenitors (GMP), the cells were depleted of mature cells using the Mouse Hematopoietic Progenitor Cell Enrichment Kit (StemCell Technologies). The cells were stained for appropriate lineage markers, as described in Supplementary Figure S1, and sorted using a FACSAria fluorescence activated cell sorter (BD Biosciences). Real-time RT-PCR analysis Total RNA was purified from cells using Stat-60 (Tel-Test), according to the manufacturer’s protocols. First-strand cDNA was synthesized using SuperScript III SuperMix for qRT-PCR (Invitrogen) containing both random hexamers and oligo(dT)20 for priming.
    [Show full text]