Table S3: Analysis of Genes Induced in BAHD1 Knockdown HEK213 Cells
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Whole-Genome Microarray Detects Deletions and Loss of Heterozygosity of Chromosome 3 Occurring Exclusively in Metastasizing Uveal Melanoma
Anatomy and Pathology Whole-Genome Microarray Detects Deletions and Loss of Heterozygosity of Chromosome 3 Occurring Exclusively in Metastasizing Uveal Melanoma Sarah L. Lake,1 Sarah E. Coupland,1 Azzam F. G. Taktak,2 and Bertil E. Damato3 PURPOSE. To detect deletions and loss of heterozygosity of disease is fatal in 92% of patients within 2 years of diagnosis. chromosome 3 in a rare subset of fatal, disomy 3 uveal mela- Clinical and histopathologic risk factors for UM metastasis noma (UM), undetectable by fluorescence in situ hybridization include large basal tumor diameter (LBD), ciliary body involve- (FISH). ment, epithelioid cytomorphology, extracellular matrix peri- ϩ ETHODS odic acid-Schiff-positive (PAS ) loops, and high mitotic M . Multiplex ligation-dependent probe amplification 3,4 5 (MLPA) with the P027 UM assay was performed on formalin- count. Prescher et al. showed that a nonrandom genetic fixed, paraffin-embedded (FFPE) whole tumor sections from 19 change, monosomy 3, correlates strongly with metastatic death, and the correlation has since been confirmed by several disomy 3 metastasizing UMs. Whole-genome microarray analy- 3,6–10 ses using a single-nucleotide polymorphism microarray (aSNP) groups. Consequently, fluorescence in situ hybridization were performed on frozen tissue samples from four fatal dis- (FISH) detection of chromosome 3 using a centromeric probe omy 3 metastasizing UMs and three disomy 3 tumors with Ͼ5 became routine practice for UM prognostication; however, 5% years’ metastasis-free survival. to 20% of disomy 3 UM patients unexpectedly develop metas- tases.11 Attempts have therefore been made to identify the RESULTS. Two metastasizing UMs that had been classified as minimal region(s) of deletion on chromosome 3.12–15 Despite disomy 3 by FISH analysis of a small tumor sample were found these studies, little progress has been made in defining the key on MLPA analysis to show monosomy 3. -
Primepcr™Assay Validation Report
PrimePCR™Assay Validation Report Gene Information Gene Name epithelial membrane protein 2 Gene Symbol Emp2 Organism Rat Gene Summary Description Not Available Gene Aliases Not Available RefSeq Accession No. Not Available UniGene ID Rn.21730 Ensembl Gene ID ENSRNOG00000002664 Entrez Gene ID 360468 Assay Information Unique Assay ID qRnoCIP0024746 Assay Type Probe - Validation information is for the primer pair using SYBR® Green detection Detected Coding Transcript(s) ENSRNOT00000003615 Amplicon Context Sequence CCTGCTGCCTTCGCTGCCCTGTGAACATGTTGGTGATTCTTGCCTTCATCATCGT CTTCCACATCGTGTCTACGGCACTCTTGTTCATTTCAACCATTGACAATGCCTGG TGGGTAGGAGATGGCTTCTCAGCT Amplicon Length (bp) 104 Chromosome Location 10:4276703-4281842 Assay Design Intron-spanning Purification Desalted Validation Results Efficiency (%) 99 R2 0.9989 cDNA Cq 20.98 cDNA Tm (Celsius) 82.5 gDNA Cq Specificity (%) 100 Information to assist with data interpretation is provided at the end of this report. Page 1/4 PrimePCR™Assay Validation Report Emp2, Rat Amplification Plot Amplification of cDNA generated from 25 ng of universal reference RNA Melt Peak Melt curve analysis of above amplification Standard Curve Standard curve generated using 20 million copies of template diluted 10-fold to 20 copies Page 2/4 PrimePCR™Assay Validation Report Products used to generate validation data Real-Time PCR Instrument CFX384 Real-Time PCR Detection System Reverse Transcription Reagent iScript™ Advanced cDNA Synthesis Kit for RT-qPCR Real-Time PCR Supermix SsoAdvanced™ SYBR® Green Supermix Experimental Sample qPCR Reference Total RNA Data Interpretation Unique Assay ID This is a unique identifier that can be used to identify the assay in the literature and online. Detected Coding Transcript(s) This is a list of the Ensembl transcript ID(s) that this assay will detect. -
A Study of Chemotherapy Resistance in Acute Myeloid Leukemia
A Study of Chemotherapy Resistance in Acute Myeloid Leukemia A DISSERTATION SUBMITTED TO THE FACULTY OF THE GRADUATE SCHOOL OF THE UNIVERSITY OF MINNESOTA BY Susan Kay Rathe IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY David A. Largaespada October, 2013 © Susan Kay Rathe 2013 Acknowledgements Funding: The leukemia research was funded by The Leukemia & Lymphoma Society (grant 7019-04). The MMuFLR workflow was funded by The Children's Cancer Research Fund. University of Minnesota Resources: The BioMedical Genomics Center provided services for gene expression microarray, RNA sequencing, oligo preparation, and Sanger sequencing. The Minnesota Supercomputing Institute maintains the Galaxy Software, as well as provides data management services and training. The Masonic Cancer Center Bioinformatics Core provided guidance in the analysis of the RNA-seq data. The FDA Drug Screen was performed at the Institute for Therapeutics Discovery and Development. Colleagues: First and foremost, I would like to recognize Dr. David Largaespada for his mentorship and the opportunity to continue research he started while a postdoc in Dr. Neal Copeland’s lab. I would also like to thank the many members of the Largaespada lab who provided direct or indirect assistance to my research. Dr. Bin Yin continued Dr. Largaespada’s work on the BXH-2 AML cell lines by making drug resistant derivatives and provided training in cell culture and drug assay techniques. Dr. Won-Il Kim developed the TNM mouse model and provided training in mouse related experimental techniques. Miechaleen Diers did all of the tail vein injections for the AML transplants and assisted with necropsies. -
DDEF1 Monoclonal Antibody (M01), Clone 2G7
Produktinformation Diagnostik & molekulare Diagnostik Laborgeräte & Service Zellkultur & Verbrauchsmaterial Forschungsprodukte & Biochemikalien Weitere Information auf den folgenden Seiten! See the following pages for more information! Lieferung & Zahlungsart Lieferung: frei Haus Bestellung auf Rechnung SZABO-SCANDIC Lieferung: € 10,- HandelsgmbH & Co KG Erstbestellung Vorauskassa Quellenstraße 110, A-1100 Wien T. +43(0)1 489 3961-0 Zuschläge F. +43(0)1 489 3961-7 [email protected] • Mindermengenzuschlag www.szabo-scandic.com • Trockeneiszuschlag • Gefahrgutzuschlag linkedin.com/company/szaboscandic • Expressversand facebook.com/szaboscandic DDEF1 monoclonal antibody (M01), clone 2G7 Catalog # : H00050807-M01 規格 : [ 100 ug ] List All Specification Application Image Product Mouse monoclonal antibody raised against a partial recombinant Western Blot (Cell lysate) Description: DDEF1. Immunogen: DDEF1 (NP_060952, 1030 a.a. ~ 1129 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa. Sequence: VQSRDAIQKQASEDSNDLTPTLPETPVPLPRKINTGKNKVRRVKTIYDCQ ADNDDELTFIEGEVIIVTGEEDQEWWIGHIEGQPERKGVFPVSFVHILSD enlarge Western Blot (Cell lysate) Host: Mouse Reactivity: Human, Rat Isotype: IgG2a Kappa Quality Control Antibody Reactive Against Recombinant Protein. enlarge Testing: Western Blot (Recombinant protein) Immunofluorescence enlarge Sandwich ELISA (Recombinant Western Blot detection against Immunogen (36.74 KDa) . protein) Storage Buffer: In 1x PBS, pH 7.4 Storage Store at -20°C or lower. Aliquot to avoid repeated freezing -
Human Lectins, Their Carbohydrate Affinities and Where to Find Them
biomolecules Review Human Lectins, Their Carbohydrate Affinities and Where to Review HumanFind Them Lectins, Their Carbohydrate Affinities and Where to FindCláudia ThemD. Raposo 1,*, André B. Canelas 2 and M. Teresa Barros 1 1, 2 1 Cláudia D. Raposo * , Andr1 é LAQVB. Canelas‐Requimte,and Department M. Teresa of Chemistry, Barros NOVA School of Science and Technology, Universidade NOVA de Lisboa, 2829‐516 Caparica, Portugal; [email protected] 12 GlanbiaLAQV-Requimte,‐AgriChemWhey, Department Lisheen of Chemistry, Mine, Killoran, NOVA Moyne, School E41 of ScienceR622 Co. and Tipperary, Technology, Ireland; canelas‐ [email protected] NOVA de Lisboa, 2829-516 Caparica, Portugal; [email protected] 2* Correspondence:Glanbia-AgriChemWhey, [email protected]; Lisheen Mine, Tel.: Killoran, +351‐212948550 Moyne, E41 R622 Tipperary, Ireland; [email protected] * Correspondence: [email protected]; Tel.: +351-212948550 Abstract: Lectins are a class of proteins responsible for several biological roles such as cell‐cell in‐ Abstract:teractions,Lectins signaling are pathways, a class of and proteins several responsible innate immune for several responses biological against roles pathogens. such as Since cell-cell lec‐ interactions,tins are able signalingto bind to pathways, carbohydrates, and several they can innate be a immuneviable target responses for targeted against drug pathogens. delivery Since sys‐ lectinstems. In are fact, able several to bind lectins to carbohydrates, were approved they by canFood be and a viable Drug targetAdministration for targeted for drugthat purpose. delivery systems.Information In fact, about several specific lectins carbohydrate were approved recognition by Food by andlectin Drug receptors Administration was gathered for that herein, purpose. plus Informationthe specific organs about specific where those carbohydrate lectins can recognition be found by within lectin the receptors human was body. -
Integrative Analysis of Genomic Amplification-Dependent Expression
Oncogene (2020) 39:4118–4131 https://doi.org/10.1038/s41388-020-1279-3 ARTICLE Integrative analysis of genomic amplification-dependent expression and loss-of-function screen identifies ASAP1 as a driver gene in triple-negative breast cancer progression 1 1 1 2 2 Jichao He ● Ronan P. McLaughlin ● Lambert van der Beek ● Sander Canisius ● Lodewyk Wessels ● 3 3 3 1 1 Marcel Smid ● John W. M. Martens ● John A. Foekens ● Yinghui Zhang ● Bob van de Water Received: 26 September 2019 / Revised: 14 March 2020 / Accepted: 17 March 2020 / Published online: 31 March 2020 © The Author(s) 2020. This article is published with open access Abstract The genetically heterogeneous triple-negative breast cancer (TNBC) continues to be an intractable disease, due to lack of effective targeted therapies. Gene amplification is a major event in tumorigenesis. Genes with amplification-dependent expression are being explored as therapeutic targets for cancer treatment. In this study, we have applied Analytical Multi- scale Identification of Recurring Events analysis and transcript quantification in the TNBC genome across 222 TNBC tumors and identified 138 candidate genes with positive correlation in copy number gain (CNG) and gene expression. siRNA-based 1234567890();,: 1234567890();,: loss-of-function screen of the candidate genes has validated EGFR, MYC, ASAP1, IRF2BP2, and CCT5 genes as drivers promoting proliferation in different TNBC cells. MYC, ASAP1, IRF2BP2, and CCT5 display frequent CNG and concurrent expression over 2173 breast cancer tumors (cBioPortal dataset). More frequently are MYC and ASAP1 amplified in TNBC tumors (>30%, n = 320). In particular, high expression of ASAP1, the ADP-ribosylation factor GTPase-activating protein, is significantly related to poor metastatic relapse-free survival of TNBC patients (n = 257, bc-GenExMiner). -
(12) United States Patent (10) Patent No.: US 7.873,482 B2 Stefanon Et Al
US007873482B2 (12) United States Patent (10) Patent No.: US 7.873,482 B2 Stefanon et al. (45) Date of Patent: Jan. 18, 2011 (54) DIAGNOSTIC SYSTEM FOR SELECTING 6,358,546 B1 3/2002 Bebiak et al. NUTRITION AND PHARMACOLOGICAL 6,493,641 B1 12/2002 Singh et al. PRODUCTS FOR ANIMALS 6,537,213 B2 3/2003 Dodds (76) Inventors: Bruno Stefanon, via Zilli, 51/A/3, Martignacco (IT) 33035: W. Jean Dodds, 938 Stanford St., Santa Monica, (Continued) CA (US) 90403 FOREIGN PATENT DOCUMENTS (*) Notice: Subject to any disclaimer, the term of this patent is extended or adjusted under 35 WO WO99-67642 A2 12/1999 U.S.C. 154(b) by 158 days. (21)21) Appl. NoNo.: 12/316,8249 (Continued) (65) Prior Publication Data Swanson, et al., “Nutritional Genomics: Implication for Companion Animals'. The American Society for Nutritional Sciences, (2003).J. US 2010/O15301.6 A1 Jun. 17, 2010 Nutr. 133:3033-3040 (18 pages). (51) Int. Cl. (Continued) G06F 9/00 (2006.01) (52) U.S. Cl. ........................................................ 702/19 Primary Examiner—Edward Raymond (58) Field of Classification Search ................... 702/19 (74) Attorney, Agent, or Firm Greenberg Traurig, LLP 702/23, 182–185 See application file for complete search history. (57) ABSTRACT (56) References Cited An analysis of the profile of a non-human animal comprises: U.S. PATENT DOCUMENTS a) providing a genotypic database to the species of the non 3,995,019 A 1 1/1976 Jerome human animal Subject or a selected group of the species; b) 5,691,157 A 1 1/1997 Gong et al. -
Identification of Novel Genes in Human Airway Epithelial Cells Associated with Chronic Obstructive Pulmonary Disease (COPD) Usin
www.nature.com/scientificreports OPEN Identifcation of Novel Genes in Human Airway Epithelial Cells associated with Chronic Obstructive Received: 6 July 2018 Accepted: 7 October 2018 Pulmonary Disease (COPD) using Published: xx xx xxxx Machine-Based Learning Algorithms Shayan Mostafaei1, Anoshirvan Kazemnejad1, Sadegh Azimzadeh Jamalkandi2, Soroush Amirhashchi 3, Seamas C. Donnelly4,5, Michelle E. Armstrong4 & Mohammad Doroudian4 The aim of this project was to identify candidate novel therapeutic targets to facilitate the treatment of COPD using machine-based learning (ML) algorithms and penalized regression models. In this study, 59 healthy smokers, 53 healthy non-smokers and 21 COPD smokers (9 GOLD stage I and 12 GOLD stage II) were included (n = 133). 20,097 probes were generated from a small airway epithelium (SAE) microarray dataset obtained from these subjects previously. Subsequently, the association between gene expression levels and smoking and COPD, respectively, was assessed using: AdaBoost Classifcation Trees, Decision Tree, Gradient Boosting Machines, Naive Bayes, Neural Network, Random Forest, Support Vector Machine and adaptive LASSO, Elastic-Net, and Ridge logistic regression analyses. Using this methodology, we identifed 44 candidate genes, 27 of these genes had been previously been reported as important factors in the pathogenesis of COPD or regulation of lung function. Here, we also identifed 17 genes, which have not been previously identifed to be associated with the pathogenesis of COPD or the regulation of lung function. The most signifcantly regulated of these genes included: PRKAR2B, GAD1, LINC00930 and SLITRK6. These novel genes may provide the basis for the future development of novel therapeutics in COPD and its associated morbidities. -
Download Validation Data
PrimePCR™Assay Validation Report Gene Information Gene Name ArfGAP with SH3 domain, ankyrin repeat and PH domain 1 Gene Symbol ASAP1 Organism Human Gene Summary This gene encodes an ADP-ribosylation factor (ARF) GTPase-activating protein. The GTPase-activating activity is stimulated by phosphatidylinositol 45-biphosphate (PIP2) and is greater towards ARF1 and ARF5 and lesser for ARF6. This gene maybe involved in regulation of membrane trafficking and cytoskeleton remodeling. Alternatively spliced transcript variants encoding different isoforms have been found for this gene. Gene Aliases AMAP1, CENTB4, DDEF1, KIAA1249, PAG2, PAP, ZG14P RefSeq Accession No. NC_000008.10, NT_008046.16 UniGene ID Hs.655552 Ensembl Gene ID ENSG00000153317 Entrez Gene ID 50807 Assay Information Unique Assay ID qHsaCIP0028499 Assay Type Probe - Validation information is for the primer pair using SYBR® Green detection Detected Coding Transcript(s) ENST00000518721, ENST00000343135, ENST00000357668, ENST00000524124 Amplicon Context Sequence AAGGTTCTGCGTTTTGCTAGTCAGACAGGATATGAACAAAGGACACTGGAAAGA CCCCCTTCCTTTCAGGCTGTCCTTCGATGTGGCCAATCCACCACTCCTGGTCCTC TTCCCCTGTGACGATAATCACTTCTCCCTCGATGAATGTGAGCTCGTCATCGTTG TCTGCCTGG Amplicon Length (bp) 143 Chromosome Location 8:131066961-131070281 Assay Design Intron-spanning Purification Desalted Validation Results Efficiency (%) 94 R2 0.9994 cDNA Cq 20.2 cDNA Tm (Celsius) 84 Page 1/5 PrimePCR™Assay Validation Report gDNA Cq 38.05 Specificity (%) 100 Information to assist with data interpretation is provided at the end of this report. -
Comparative Analyses of Gene Copy Number and Mrna Expression in GBM Tumors And
Title page Comparative analyses of gene copy number and mRNA expression in GBM tumors and GBM xenografts J. Graeme Hodgson # *, Ru-Fang Yeh #, Amrita Ray, Nicholas J Wang, Ivan Smirnov, Mamie Yu, Sujatmi Hariono, Joachim Silber, Heidi S. Feiler, Joe W. Gray, Paul T. Spellman, Scott R. Vandenberg, Mitchel S. Berger, C. David James Departments of Neurological Surgery (JGH, IS, MY, SH, JS, SRV, MSB, CDJ), Pathology (SRV), and Epidemiology and Biostatistics (RY) University of California, San Francisco, CA 94143. Life Sciences Division, Lawrence Berkeley National Lab, Berkeley, CA 94720 (AR, NJW, HSF, JWG, PTS) # These authors contributed equally to this work Running title: Genomic analyses of a GBM xenograft tumor panel * Corresponding Author J. Graeme Hodgson Dept. Neurological Surgery UC San Francisco San Francisco, CA 94143-0808 Phone: 415-476-3630 Fax: 415-476-8218 e-mail: [email protected] Abstract Development of model systems that recapitulate the molecular heterogeneity observed amongst GBM tumors will expedite the testing of targeted molecular therapeutic strategies for GBM treatment. In this study, we profiled DNA copy number and mRNA expression in 21 independent GBM tumor lines maintained as subcutaneous xenografts (GBMX), and compared GBMX molecular signatures to those observed in GBM clinical specimens derived from The Cancer Genome Atlas (TCGA). The predominant copy number signature in both tumor groups was defined by chromosome-7-gain/chromosome-10-loss, a poor prognosis genetic signature. We also observed, at frequencies similar to that detected in TCGA GBMs genomic amplification and overexpression of known GBM oncogenes such as EGFR, MDM2, CDK6 and MYCN, and novel genes including NUP107, SLC35E3, MMP1, MMP13 and DDX1. -
Detailed Characterization of Human Induced Pluripotent Stem Cells Manufactured for Therapeutic Applications
Stem Cell Rev and Rep DOI 10.1007/s12015-016-9662-8 Detailed Characterization of Human Induced Pluripotent Stem Cells Manufactured for Therapeutic Applications Behnam Ahmadian Baghbaderani 1 & Adhikarla Syama2 & Renuka Sivapatham3 & Ying Pei4 & Odity Mukherjee2 & Thomas Fellner1 & Xianmin Zeng3,4 & Mahendra S. Rao5,6 # The Author(s) 2016. This article is published with open access at Springerlink.com Abstract We have recently described manufacturing of hu- help determine which set of tests will be most useful in mon- man induced pluripotent stem cells (iPSC) master cell banks itoring the cells and establishing criteria for discarding a line. (MCB) generated by a clinically compliant process using cord blood as a starting material (Baghbaderani et al. in Stem Cell Keywords Induced pluripotent stem cells . Embryonic stem Reports, 5(4), 647–659, 2015). In this manuscript, we de- cells . Manufacturing . cGMP . Consent . Markers scribe the detailed characterization of the two iPSC clones generated using this process, including whole genome se- quencing (WGS), microarray, and comparative genomic hy- Introduction bridization (aCGH) single nucleotide polymorphism (SNP) analysis. We compare their profiles with a proposed calibra- Induced pluripotent stem cells (iPSCs) are akin to embryonic tion material and with a reporter subclone and lines made by a stem cells (ESC) [2] in their developmental potential, but dif- similar process from different donors. We believe that iPSCs fer from ESC in the starting cell used and the requirement of a are likely to be used to make multiple clinical products. We set of proteins to induce pluripotency [3]. Although function- further believe that the lines used as input material will be used ally identical, iPSCs may differ from ESC in subtle ways, at different sites and, given their immortal status, will be used including in their epigenetic profile, exposure to the environ- for many years or even decades. -
Immune-Related Genes: Potential Regulators and Drug Therapeutic Targets in Hypertrophic Cardiomyopathy
Hindawi Journal of Nanomaterials Volume 2021, Article ID 5528347, 14 pages https://doi.org/10.1155/2021/5528347 Research Article Immune-Related Genes: Potential Regulators and Drug Therapeutic Targets in Hypertrophic Cardiomyopathy Wei Liu ,1 Ju Ye,2 Jinqiang Cai ,3 Feng Xie,4 Mengjie Tang,5 and QinJing Yang 1 1Department of Pharmacy, The Third Xiangya Hospital, Central South University, Changsha 410013, China 2Department of Pharmacy, Zunyi Medical University, Zunyi 563000, China 3Department of Pharmacy, Xiangya Medical College, Central South University, Changsha 410013, China 4Department of Pharmacy, The Nanshan District Maternity & Child Healthcare Hospital of Shenzhen, Shenzhen 518052, China 5Hunan Cancer Hospital, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha 410013, China Correspondence should be addressed to QinJing Yang; [email protected] Received 29 January 2021; Revised 5 February 2021; Accepted 9 February 2021; Published 3 March 2021 Academic Editor: Tingting Hong Copyright © 2021 Wei Liu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background. Accumulating evidence shows that the innate immune system is a key player in cardiovascular repair and regeneration, but little is known about the role of immune-related genes (IRGs) in hypertrophic cardiomyopathy (HCM). Methods. The differential mRNA expression profiles of HCM samples were downloaded from the Gene Expression Omnibus (GEO) dataset (GSE89714), and the IRG expression profile was obtained from the ImmPort database. The regulatory pathways of IRGs in HCM were screened out through discrepantly expressive genes (DEGs) analysis, enrichment of gene function/pathway analysis, and protein-protein interaction (PPI) network.