Anti-Interferon-Α Monoclonal Antibody, Clone NU5 (DMAB8011) This Product Is for Research Use Only and Is Not Intended for Diagnostic Use

Total Page：16

File Type：pdf, Size：1020Kb

Anti-Interferon-α monoclonal antibody, clone NU5 (DMAB8011) This product is for research use only and is not intended for diagnostic use. PRODUCT INFORMATION Product Overview Mouse Anti-Human Interferon-α Monoclonal Antibody Specificity Native and recombinant human IFN-α. MT4 in combination with antibody MT3 binds subtypes 8, 10, 14 and 17. The antibody combination shows weak reactivity with subtypes 2, 6 and 7. Immunogen Human recombinant Interferon-α 17 Isotype IgG1 Source/Host Mouse Species Reactivity Human Clone NU5 Purification Purified from in vitro cultures by protein G affinity chromatography. Conjugate Unconjugated Applications ELISA, ELISPOT Concentration Supplied at 1 mg/ml in sterile filtered (0.2 μm) PBS with 0.02% sodium azide. Size 250 μg Preservative 0.2% Sodium Azide Storage Store product at 4-8°C or frozen at -20°C or below. Avoid repeated freezing/thawing. BACKGROUND Introduction Human type I interferons comprise a vast and growing group of IFN proteins. All type I IFNs bind to a specific cell surface receptor complex known as the IFN-α receptor (IFNAR) that consists of IFNAR1 and IFNAR2 chains. Homologous molecules to type I IFNs are found in many species, including all mammals, and some have been identified in birds, reptiles, amphibians and fish species. The IFN-α proteins are produced by leukocytes. They are mainly involved in innate immune response against viral infection. They come in 14 subtypes that are called IFNA1, 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 1 © Creative Diagnostics All Rights Reserved IFNA2, IFNA4, IFNA5, IFNA6, IFNA7, IFNA8, IFNA10, IFNA13, IFNA14, IFNA16, IFNA17, IFNA21. These genes for these IFN-α molecules are found together in a cluster on chromosome 9. Keywords Interferon-α; IFN-α; IFNAR; IFNA2; Pegylated interferon alfa-2a; Pegylated interferon alfa-2b; IFN-alphaA; MGC125764; MGC125765 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 2 © Creative Diagnostics All Rights Reserved.

Copy Link

Recommended publications

Supplemental Materials ZNF281 Enhances Cardiac Reprogramming
Supplemental Materials ZNF281 enhances cardiac reprogramming by modulating cardiac and inflammatory gene expression Huanyu Zhou, Maria Gabriela Morales, Hisayuki Hashimoto, Matthew E. Dickson, Kunhua Song, Wenduo Ye, Min S. Kim, Hanspeter Niederstrasser, Zhaoning Wang, Beibei Chen, Bruce A. Posner, Rhonda Bassel-Duby and Eric N. Olson Supplemental Table 1; related to Figure 1. Supplemental Table 2; related to Figure 1. Supplemental Table 3; related to the “quantitative mRNA measurement” in Materials and Methods section. Supplemental Table 4; related to the “ChIP-seq, gene ontology and pathway analysis” and “RNA-seq” and gene ontology analysis” in Materials and Methods section. Supplemental Figure S1; related to Figure 1. Supplemental Figure S2; related to Figure 2. Supplemental Figure S3; related to Figure 3. Supplemental Figure S4; related to Figure 4. Supplemental Figure S5; related to Figure 6. Supplemental Table S1. Genes included in human retroviral ORF cDNA library. Gene Gene Gene Gene Gene Gene Gene Gene Symbol Symbol Symbol Symbol Symbol Symbol Symbol Symbol AATF BMP8A CEBPE CTNNB1 ESR2 GDF3 HOXA5 IL17D ADIPOQ BRPF1 CEBPG CUX1 ESRRA GDF6 HOXA6 IL17F ADNP BRPF3 CERS1 CX3CL1 ETS1 GIN1 HOXA7 IL18 AEBP1 BUD31 CERS2 CXCL10 ETS2 GLIS3 HOXB1 IL19 AFF4 C17ORF77 CERS4 CXCL11 ETV3 GMEB1 HOXB13 IL1A AHR C1QTNF4 CFL2 CXCL12 ETV7 GPBP1 HOXB5 IL1B AIMP1 C21ORF66 CHIA CXCL13 FAM3B GPER HOXB6 IL1F3 ALS2CR8 CBFA2T2 CIR1 CXCL14 FAM3D GPI HOXB7 IL1F5 ALX1 CBFA2T3 CITED1 CXCL16 FASLG GREM1 HOXB9 IL1F6 ARGFX CBFB CITED2 CXCL3 FBLN1 GREM2 HOXC4 IL1F7
[Show full text]
Recombinant Human IFN-Α6 Mammalian Cell-Expressed Human Interferon Alpha 6 (Alpha K) with HSA Cat
Recombinant human IFN-α6 Mammalian cell-expressed human interferon alpha 6 (alpha K) with HSA Cat. code: rcyc-hifna6 https://www.invivogen.com/human-ifna6 For research use only, not for diagnostic or therapeutic use Version 18I12-NJ PRODUCT INFORMATION BACKGROUND Contents Type I interferons (IFN) include the IFN-α family, IFN-β, IFN-ε, IFN-κ • 1 µg of lyophilized recombinant human IFN-α6 and IFN-ω. IFN-αs are important anti-viral cytokines that also play Note: This product is sterile filtered prior to lyophilization. anti-proliferative and immuno-modulatory functions. The human IFN-α • 1.5 ml endotoxin-free water family comprises 13 genes encoding 12 proteins, IFN-α13 being identical to IFN-α1. All IFN-αs bind to a common heterodimer receptor IFNAR1/ Storage and stability IFNAR2. The ternary complex signals through the Janus kinase (JAK) • Recombinant human IFN-α6 is shipped at room temperature. Upon and signal transducer and activator of transcription (STAT) signaling receipt it should be immediately stored at -20 °C. Lyophilized product is stable for 6 months at -20°C. pathway, inducing the formation of the ISGF3 transcriptional complex • Upon resuspension, prepare aliquots of recombinant human IFN-α6 and (STAT1/STAT2/IRF9). ISGF3 binds to IFN-stimulated response elements 2 store at -80 °C for 4 months. (ISRE) in the promoters of numerous IFN-stimulated genes (ISGs) . Note: Avoid repeated freeze-thaw cycles. Quality control IFN-α IFN-α • Purity: ≥ 95% (SDS-PAGE) Low affinity High affinity • Endotoxin: ≤ 1 EU/µg • The biological activity has been confirmed using HEK-Blue™ IFN-α/β IFNAR1 IFNAR2 cells (see validation data sheet available on our website).
[Show full text]
Jimmunol.0903453.Full.Pdf
Antiviral Response Dictated by Choreographed Cascade of Transcription Factors This information is current as Elena Zaslavsky, Uri Hershberg, Jeremy Seto, Alissa M. of October 2, 2021. Pham, Susanna Marquez, Jamie L. Duke, James G. Wetmur, Benjamin R. tenOever, Stuart C. Sealfon and Steven H. Kleinstein J Immunol published online 17 February 2010 http://www.jimmunol.org/content/early/2010/02/17/jimmun ol.0903453 Downloaded from Supplementary http://www.jimmunol.org/content/suppl/2010/02/15/jimmunol.090345 Material 3.DC1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication by guest on October 2, 2021 *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published February 17, 2010, doi:10.4049/jimmunol.0903453 The Journal of Immunology Antiviral Response Dictated by Choreographed Cascade of Transcription Factors Elena Zaslavsky,*,†,1 Uri Hershberg,‡,1 Jeremy Seto,*,† Alissa M. Pham,x Susanna Marquez,‡ Jamie L. Duke,{ James G. Wetmur,x Benjamin R. tenOever,x Stuart C. Sealfon,*,† and Steven H.
[Show full text]
Diverse Functional Autoantibodies in Patients with COVID-19
medRxiv preprint doi: https://doi.org/10.1101/2020.12.10.20247205; this version posted December 11, 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. It is made available under a CC-BY-NC-ND 4.0 International license . Diverse Functional Autoantibodies in Patients with COVID-19 Eric Y. Wang1,*, Tianyang Mao1,*, Jon Klein1,*, Yile Dai1,*, John D. Huck1, Feimei Liu1, Neil S. Zheng1, Ting Zhou1, Benjamin Israelow1, Patrick Wong1, Carolina Lucas1, Julio Silva1, Ji Eun Oh1, Eric Song1, Emily S. Perotti1, Suzanne Fischer1, Melissa Campbell5, John B. Fournier5, Anne L. Wyllie3, Chantal B. F. Vogels3, Isabel M. Ott3, Chaney C. Kalinich3, Mary E. Petrone3, Anne E. Watkins3, Yale IMPACT Team¶, Charles Dela Cruz4, Shelli F. Farhadian5, Wade L. Schulz6,7, Nathan D. Grubaugh3, Albert I. Ko3,5, Akiko Iwasaki1,3,8,#, Aaron M. Ring1,2,# 1 Department of Immunobiology, Yale School of Medicine, New Haven, CT, USA 2 Department of Pharmacology, Yale School of Medicine, New Haven, CT, USA 3 Department of Epidemiology of Microbial Diseases, Yale School of Public Health, New Haven, CT, USA 4 Department of Medicine, Section of Pulmonary and Critical Care Medicine, Yale School of Medicine, New Haven, CT, USA 5 Department of Internal Medicine (Infectious Diseases), Yale School of Medicine, New Haven, CT, USA 6 Department of Laboratory Medicine, Yale School of Medicine, New Haven, CT, USA 7 Center for Outcomes Research and Evaluation, Yale-New Haven Hospital, New Haven, CT, USA 8 Howard Hughes Medical Institute, Chevy Chase, MD, USA * These authors contributed equally to this work ¶ A list of authors and their affiliations appears at the end of the paper # Correspondence: [email protected] (A.M.R.); [email protected] (A.I.) 1 NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice.
[Show full text]
Supplementary Material DNA Methylation in Inflammatory Pathways Modifies the Association Between BMI and Adult-Onset Non- Atopic
Supplementary Material DNA Methylation in Inflammatory Pathways Modifies the Association between BMI and Adult-Onset Non- Atopic Asthma Ayoung Jeong 1,2, Medea Imboden 1,2, Akram Ghantous 3, Alexei Novoloaca 3, Anne-Elie Carsin 4,5,6, Manolis Kogevinas 4,5,6, Christian Schindler 1,2, Gianfranco Lovison 7, Zdenko Herceg 3, Cyrille Cuenin 3, Roel Vermeulen 8, Deborah Jarvis 9, André F. S. Amaral 9, Florian Kronenberg 10, Paolo Vineis 11,12 and Nicole Probst-Hensch 1,2,* 1 Swiss Tropical and Public Health Institute, 4051 Basel, Switzerland; [email protected] (A.J.); [email protected] (M.I.); [email protected] (C.S.) 2 Department of Public Health, University of Basel, 4001 Basel, Switzerland 3 International Agency for Research on Cancer, 69372 Lyon, France; [email protected] (A.G.); [email protected] (A.N.); [email protected] (Z.H.); [email protected] (C.C.) 4 ISGlobal, Barcelona Institute for Global Health, 08003 Barcelona, Spain; [email protected] (A.-E.C.); [email protected] (M.K.) 5 Universitat Pompeu Fabra (UPF), 08002 Barcelona, Spain 6 CIBER Epidemiología y Salud Pública (CIBERESP), 08005 Barcelona, Spain 7 Department of Economics, Business and Statistics, University of Palermo, 90128 Palermo, Italy; [email protected] 8 Environmental Epidemiology Division, Utrecht University, Institute for Risk Assessment Sciences, 3584CM Utrecht, Netherlands; [email protected] 9 Population Health and Occupational Disease, National Heart and Lung Institute, Imperial College, SW3 6LR London, UK; [email protected] (D.J.); [email protected] (A.F.S.A.) 10 Division of Genetic Epidemiology, Medical University of Innsbruck, 6020 Innsbruck, Austria; [email protected] 11 MRC-PHE Centre for Environment and Health, School of Public Health, Imperial College London, W2 1PG London, UK; [email protected] 12 Italian Institute for Genomic Medicine (IIGM), 10126 Turin, Italy * Correspondence: [email protected]; Tel.: +41-61-284-8378 Int.
[Show full text]
And IRAK1 Knock-In Mice Production Defined by the Study of IRAK2 Two
Two Phases of Inflammatory Mediator Production Defined by the Study of IRAK2 and IRAK1 Knock-in Mice This information is current as Eduardo Pauls, Sambit K. Nanda, Hilary Smith, Rachel of September 29, 2021. Toth, J. Simon C. Arthur and Philip Cohen J Immunol 2013; 191:2717-2730; Prepublished online 5 August 2013; doi: 10.4049/jimmunol.1203268 http://www.jimmunol.org/content/191/5/2717 Downloaded from Supplementary http://www.jimmunol.org/content/suppl/2013/08/06/jimmunol.120326 Material 8.DC1 http://www.jimmunol.org/ References This article cites 55 articles, 33 of which you can access for free at: http://www.jimmunol.org/content/191/5/2717.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision by guest on September 29, 2021 • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts Errata An erratum has been published regarding this article. Please see next page or: /content/191/10/5317.full.pdf The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2013 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606.
[Show full text]
Prevalent Homozygous Deletions of Type I Interferon and Defensin Genes in Human Cancers Associate with Immunotherapy Resistance
Author Manuscript Published OnlineFirst on April 4, 2018; DOI: 10.1158/1078-0432.CCR-17-3008 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Prevalent Homozygous Deletions of Type I Interferon and Defensin Genes in Human Cancers Associate with Immunotherapy Resistance Zhenqing Ye1; Haidong Dong2,3; Ying Li1; Tao Ma1,4; Haojie Huang4; Hon-Sing Leong4; Jeanette Eckel-Passow1; Jean-Pierre A. Kocher1; Han Liang5; LiguoWang1,4,* 1Division of Biomedical Statistics and Informatics, Department of Health Sciences, Mayo Clinic, Rochester, Minnesota 55905, United States of America 2Department of Immunology, College of Medicine, Mayo Clinic, Rochester, Minnesota 55905, United States of America 3Department of Urology, Mayo Clinic, Rochester, Minnesota 55905, United States of America 4Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota 55905, United States of America 5Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, United States of America Running title: Pervasive Deletion of Interferon/Defensin in Human Cancers Keywords: Homozygous deletion, Type-I interferon, Defensin, immunotherapy resistance, cancer * Correspondence to: Liguo Wang, Ph.D. Associate Professor Division of Biomedical Statistics and Informatics, Mayo Clinic 200 1st St SW Rochester, MN 55905, USA Phone: +1-507-284-8728 Fax: +1-507-284-0745 Email: [email protected] The authors declare no potential conflicts of interest. 1 Downloaded from clincancerres.aacrjournals.org on September 29, 2021. © 2018 American Association for Cancer Research. Author Manuscript Published OnlineFirst on April 4, 2018; DOI: 10.1158/1078-0432.CCR-17-3008 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited.
[Show full text]
( 12 ) United States Patent
US010428349B2 (12 ) United States Patent ( 10 ) Patent No. : US 10 , 428 ,349 B2 DeRosa et al . (45 ) Date of Patent: Oct . 1 , 2019 ( 54 ) MULTIMERIC CODING NUCLEIC ACID C12N 2830 / 50 ; C12N 9 / 1018 ; A61K AND USES THEREOF 38 / 1816 ; A61K 38 /45 ; A61K 38/ 44 ; ( 71 ) Applicant: Translate Bio , Inc ., Lexington , MA A61K 38 / 177 ; A61K 48 /005 (US ) See application file for complete search history . (72 ) Inventors : Frank DeRosa , Lexington , MA (US ) ; Michael Heartlein , Lexington , MA (56 ) References Cited (US ) ; Daniel Crawford , Lexington , U . S . PATENT DOCUMENTS MA (US ) ; Shrirang Karve , Lexington , 5 , 705 , 385 A 1 / 1998 Bally et al. MA (US ) 5 ,976 , 567 A 11/ 1999 Wheeler ( 73 ) Assignee : Translate Bio , Inc ., Lexington , MA 5 , 981, 501 A 11/ 1999 Wheeler et al. 6 ,489 ,464 B1 12 /2002 Agrawal et al. (US ) 6 ,534 ,484 B13 / 2003 Wheeler et al. ( * ) Notice : Subject to any disclaimer , the term of this 6 , 815 ,432 B2 11/ 2004 Wheeler et al. patent is extended or adjusted under 35 7 , 422 , 902 B1 9 /2008 Wheeler et al . 7 , 745 ,651 B2 6 / 2010 Heyes et al . U . S . C . 154 ( b ) by 0 days. 7 , 799 , 565 B2 9 / 2010 MacLachlan et al. (21 ) Appl. No. : 16 / 280, 772 7 , 803 , 397 B2 9 / 2010 Heyes et al . 7 , 901, 708 B2 3 / 2011 MacLachlan et al. ( 22 ) Filed : Feb . 20 , 2019 8 , 101 ,741 B2 1 / 2012 MacLachlan et al . 8 , 188 , 263 B2 5 /2012 MacLachlan et al . (65 ) Prior Publication Data 8 , 236 , 943 B2 8 /2012 Lee et al .
[Show full text]
Identification of 42 Genes Linked to Stage II Colorectal Cancer Metastatic Relapse
Int. J. Mol. Sci. 2016, 17, 598; doi:10.3390/ijms17040598 S1 of S16 Supplementary Materials: Identification of 42 Genes Linked to Stage II Colorectal Cancer Metastatic Relapse Rabeah A. Al-Temaimi, Tuan Zea Tan, Makia J. Marafie, Jean Paul Thiery, Philip Quirke and Fahd Al-Mulla Figure S1. Cont. Int. J. Mol. Sci. 2016, 17, 598; doi:10.3390/ijms17040598 S2 of S16 Figure S1. Mean expression levels of fourteen genes of significant association with CRC DFS and OS that are differentially expressed in normal colon compared to CRC tissues. Each dot represents a sample. Table S1. Copy number aberrations associated with poor disease-free survival and metastasis in early stage II CRC as predicted by STAC and SPPS combined methodologies with resident gene symbols. CN stands for copy number, whereas CNV is copy number variation. Region Cytoband % of CNV Count of Region Event Gene Symbols Length Location Overlap Genes chr1:113,025,076–113,199,133 174,057 p13.2 CN Loss 0.0 2 AKR7A2P1, SLC16A1 chr1:141,465,960–141,822,265 356,305 q12–q21.1 CN Gain 95.9 1 SRGAP2B MIR5087, LOC10013000 0, FLJ39739, LOC10028679 3, PPIAL4G, PPIAL4A, NBPF14, chr1:144,911,564–146,242,907 1,331,343 q21.1 CN Gain 99.6 16 NBPF15, NBPF16, PPIAL4E, NBPF16, PPIAL4D, PPIAL4F, LOC645166, LOC388692, FCGR1C chr1:177,209,428–177,226,812 17,384 q25.3 CN Gain 0.0 0 chr1:197,652,888–197,676,831 23,943 q32.1 CN Gain 0.0 1 KIF21B chr1:201,015,278–201,033,308 18,030 q32.1 CN Gain 0.0 1 PLEKHA6 chr1:201,289,154–201,298,247 9093 q32.1 CN Gain 0.0 0 chr1:216,820,186–217,043,421 223,235 q41 CN
[Show full text]
Gene Set Size Count Z-Score P-Value Q-Value List of Genes
Supplementary Data 2-1 Results from competitive pathway enrichment analysis based on genome-wide summary-level data of hsGWAS. Gene Set Size Count z-score p-value q-value List of Genes KEGG_ALLOGRAFT_ 38 36 12.6476 0.00E+00 0.00E+00 HLA-DRB5(4.11028); IL2(3.62922); HLA-E(3.27708); HLA-G(3.2749); HLA- REJECTION DQA2(3.16347); HLA-DRA(3.14994); HLA-DOB(3.11438); HLA-DMB(3.09917); HLA-DMA(3.09615); TNF(3.09414); HLA-DPB1(3.03922); HLA-DPA1(3.0355); HLA-A(3.02312); HLA-C(2.98835); HLA-DQB1(2.97025); HLA-B(2.95626); HLA- DQA1(2.94591); HLA-F(2.83254); HLA-DRB1(2.76738); HLA-DOA(2.72508); IFNG(1.74523); PRF1(1.46483); FASLG(1.10083); FAS(0.923795); HLA- DRB3(0.760622); CD80(0.436654); IL4(0.324564); CD40(0.271072); HLA- DRB4(0.0708609); IL12A(0.0685942); IL5(0.0659333); CD86(0.049911); CD28(- 0.16103); IL10(-0.165903); IL12B(-0.245281); GZMB(-0.268581); KEGG_GRAFT_VERSUS_HOS 42 37 12.6129 0.00E+00 0.00E+00 HLA-DRB5(4.11028); IL2(3.62922); HLA-E(3.27708); HLA-G(3.2749); HLA- T_DISEASE DQA2(3.16347); HLA-DRA(3.14994); HLA-DOB(3.11438); HLA-DMB(3.09917); HLA-DMA(3.09615); TNF(3.09414); HLA-DPB1(3.03922); HLA-DPA1(3.0355); HLA-A(3.02312); HLA-C(2.98835); HLA-DQB1(2.97025); HLA-B(2.95626); HLA- DQA1(2.94591); HLA-F(2.83254); HLA-DRB1(2.76738); HLA-DOA(2.72508); IL6(1.94139); IFNG(1.74523); PRF1(1.46483); FASLG(1.10083); FAS(0.923795); HLA-DRB3(0.760622); CD80(0.436654); IL1A(0.402186); KLRD1(0.29064); KIR3DL1(0.157683); HLA-DRB4(0.0708609); CD86(0.049911); CD28(-0.16103); GZMB(-0.268581); IL1B(-0.388308); KLRC1(-0.466394); KIR3DL2(-0.786806); KEGG_TYPE_I_DIABETES_ME
[Show full text]
Single Cell Derived Clonal Analysis of Human Glioblastoma Links
SUPPLEMENTARY INFORMATION: Single cell derived clonal analysis of human glioblastoma links functional and genomic heterogeneity ! Mona Meyer*, Jüri Reimand*, Xiaoyang Lan, Renee Head, Xueming Zhu, Michelle Kushida, Jane Bayani, Jessica C. Pressey, Anath Lionel, Ian D. Clarke, Michael Cusimano, Jeremy Squire, Stephen Scherer, Mark Bernstein, Melanie A. Woodin, Gary D. Bader**, and Peter B. Dirks**! ! * These authors contributed equally to this work.! ** Correspondence: [email protected] or [email protected]! ! Supplementary information - Meyer, Reimand et al. Supplementary methods" 4" Patient samples and ﬂuorescence activated cell sorting (FACS)! 4! Differentiation! 4! Immunocytochemistry and EdU Imaging! 4! Proliferation! 5! Western blotting ! 5! Temozolomide treatment! 5! NCI drug library screen! 6! Orthotopic injections! 6! Immunohistochemistry on tumor sections! 6! Promoter methylation of MGMT! 6! Fluorescence in situ Hybridization (FISH)! 7! SNP6 microarray analysis and genome segmentation! 7! Calling copy number alterations! 8! Mapping altered genome segments to genes! 8! Recurrently altered genes with clonal variability! 9! Global analyses of copy number alterations! 9! Phylogenetic analysis of copy number alterations! 10! Microarray analysis! 10! Gene expression differences of TMZ resistant and sensitive clones of GBM-482! 10! Reverse transcription-PCR analyses! 11! Tumor subtype analysis of TMZ-sensitive and resistant clones! 11! Pathway analysis of gene expression in the TMZ-sensitive clone of GBM-482! 11! Supplementary ﬁgures and tables" 13" "2 Supplementary information - Meyer, Reimand et al. Table S1: Individual clones from all patient tumors are tumorigenic. ! 14! Fig. S1: clonal tumorigenicity.! 15! Fig. S2: clonal heterogeneity of EGFR and PTEN expression.! 20! Fig. S3: clonal heterogeneity of proliferation.! 21! Fig.
[Show full text]
Specialized Interferon Ligand Action in COVID19
medRxiv preprint doi: https://doi.org/10.1101/2021.07.29.21261325; this version posted August 1, 2021. 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. It is made available under a CC-BY 4.0 International license . Specialized interferon ligand action in COVID19 Matthew D. Galbraith1,2, Kohl T. Kinning1, Kelly D. Sullivan1,3, Paula Araya1, Keith P. Smith1, Ross E. Granrath1, Jessica R. Shaw1, Ryan Baxter4, Kimberly R. Jordan4, Seth Russell5, Monika Dzieciatkowska6, Julie A. Reisz6, Fabia Gamboni6, Francesca CenDali6, Tusharkanti Ghosh7, AnDrew A. Monte8, Tellen D. Bennett9, Kirk C. Hansen6, Elena W.Y. Hsieh4,10, Angelo D’AlessanDro6, and Joaquin M. Espinosa1,2* Affiliations: 1Linda Crnic Institute for Down SynDrome, University of ColoraDo Anschutz MeDical Campus; Aurora, CO, USA. 2Department of Pharmacology, University of ColoraDo Anschutz MeDical Campus; Aurora, CO, USA. 3Department of PeDiatrics, Section of Developmental Biology, University of ColoraDo Anschutz MeDical Campus; Aurora, CO, USA. 4Department of Immunology anD Microbiology, University of ColoraDo Anschutz MeDical Campus; Aurora, CO, USA. 5Data Science to Patient Value, University of Colorado Anschutz Medical Campus; Aurora, CO, USA. 6Department of Biochemistry anD Molecular Genetics, University of ColoraDo Anschutz MeDical Campus; Aurora, CO, USA. 7Department of Biostatistics anD Informatics, ColoraDo School of Public Health; Aurora, CO, USA. 8Department of Emergency MeDicine, University of ColoraDo Anschutz MeDical Campus; Aurora, CO, USA. 9Department of PeDiatrics, Sections of Informatics anD Data Science anD Critical Care MeDicine, University of ColoraDo Anschutz Medical Campus; Aurora, CO, USA.
[Show full text]