Supplementary Table S5 A: ALCL Characteristic Genes
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An Interactive Web Application to Explore Regeneration-Associated Gene Expression and Chromatin Accessibility
Supplementary Materials Regeneration Rosetta: An interactive web application to explore regeneration-associated gene expression and chromatin accessibility Andrea Rau, Sumona P. Dhara, Ava J. Udvadia, Paul L. Auer 1. Table S1. List of cholesterol metabolic genes from MGI database 2. Table S2. List of differentially expressed transcripts during optic nerve regeneration in zebrafish using the MGI cholesterol metabolic gene queries in the Regeneration Rosetta app 3. Table S3. List of transcription factor encoding genes from brain cell bodies following spinal cord injury in lamprey over a course of 12 weeKs 4. Table S4. List of transcription factor encoding genes from spinal cell bodies following spinal cord injury in lamprey over a course of 12 weeks Ensembl ID MGI Gene ID Symbol Name ENSMUSG00000015243 MGI:99607 Abca1 ATP-binding cassette, sub-family A (ABC1), member 1 ENSMUSG00000026944 MGI:99606 Abca2 ATP-binding cassette, sub-family A (ABC1), member 2 ENSMUSG00000024030 MGI:107704 Abcg1 ATP binding cassette subfamily G member 1 ENSMUSG00000026003 MGI:87866 Acadl acyl-Coenzyme A dehydrogenase, long-chain ENSMUSG00000018574 MGI:895149 Acadvl acyl-Coenzyme A dehydrogenase, very long chain ENSMUSG00000038641 MGI:2384785 Akr1d1 aldo-keto reductase family 1, member D1 ENSMUSG00000028553 MGI:1353627 Angptl3 angiopoietin-like 3 ENSMUSG00000031996 MGI:88047 Aplp2 amyloid beta (A4) precursor-like protein 2 ENSMUSG00000032083 MGI:88049 Apoa1 apolipoprotein A-I ENSMUSG00000005681 MGI:88050 Apoa2 apolipoprotein A-II ENSMUSG00000032080 MGI:88051 Apoa4 -
SUPPLEMENTARY FIGURES LEGENDS Figure S1. (A) Gene
Supplementary material Gut SUPPLEMENTARY FIGURES LEGENDS Figure S1. (A) Gene Ontology enrichment analysis of biological processes in which selected TS/ONC identified by proteomic analysis are involved. Inter-connections between biological processes and genes involved are represented in B. Figure S2. mRNA expression of TSs/ONCs in constitutive hepatocytes-specific PTEN knockout mice. (A) qRT-PCR analyses of TS/ONC in liver tissues (4 controls and 5 LPTENKO mice) from 4-months-old control and constitutive hepatocyte-specific PTEN knockout (LPTENKO) mice. Cyclophilin-A was used to normalize qRT-PCR analyses. Data represent the mean+/-SD. (B) The mRNA level of TS/ONCO candidates identified in the proteomic analysis were investigated in a transcriptomic dataset from the Gene Expression Omnibus Database (GSE70681, LPTENKO 3-months old. For each candidate, Log2-Fold Change between Control and LPTENKO mice were calculated and represented in a heatmap. ***P<0.001, **P<0.01, and *P<0.05 (t-test). Figure S3. Hepatic steatosis and AKT phosphorylation in inducible hepatocytes-specific PTEN knockout mice (LIPTENKO). A. Hematoxylin/Eosin (H&E) staining of histological sections from 5-month old control and LIPTENKO mice treated with tamoxifen for 3 months. The protein level of PTEN, pAKTser473, pAKTthr308 and AKT were analyzed by Western Blot (B). Corresponding quantifications are reported in C. Data represent the mean +/- SD. *P<0.05, **P<0.01, ***P<0.001 compared with controls (t-test). Figure S4. Hepatic steatosis in ob/ob and db/db mice and analysis of TS/ONC mRNA expression in ob/ob mice. (A) Hematoxylin/Eosin (H&E) staining of histological sections from 2-month old Control, ob/ob and db/db (n=5-6 mice/group) mice. -
` Probing the Epigenome Andrea Huston1, Cheryl H Arrowsmith1,2
` Probing the Epigenome Andrea Huston1, Cheryl H Arrowsmith1,2, Stefan Knapp3,4,*, Matthieu Schapira1,5,* 1. Structural Genomics Consortium, University of Toronto, Toronto, ON M5G 1L7, Canada 2. Princess Margaret Cancer Centre and Department of Medical Biophysics, University of Toronto , Toronto, ON M5G 1L7, Canada 3. Nuffield Department of Clinical Medicine, Target Discovery Institute, and Structural Genomic Consortium, University of Oxford, Headington, Oxford OX3 7DQ, United Kingdom 4. Institute for Pharmaceutical Chemistry, Johann Wolfgang Goethe University, D-60438 Frankfurt am Main, Germany 5. Department of Pharmacology and Toxicology, University of Toronto, Toronto, ON M5S 1A8, Canada * Correspondence: [email protected], [email protected] Epigenetic chemical probes are having a strong impact on biological discovery and target validation. Systematic coverage of emerging epigenetic target classes with these potent, selective, cell-active chemical tools will profoundly influence our understanding of the human biology and pathology of chromatin-templated mechanisms. ` Chemical probes are research-enablers Advances in genomics and proteomics methodologies in recent years have made it possible to associate thousands of genes and proteins with specific diseases, biological processes, molecular networks and pathways. However, data from these large scale initiatives alone has not translated widely into new studies on these disease-associated proteins, and the biomedical research community still tends to focus on proteins that were already known before the sequencing of the human genome1. The human kinome for instance, a target class of direct relevance to cancer and other disease areas, is a telling example: based on the number of research articles indexed in pubmed in 2011, 75% of the research activity focused on only 10% of the 518 human kinases – largely the same kinases that were the focus of research before sequencing of the human genome - while 60% of the kinome, some 300 enzymes, was virtually ignored by the community2. -
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. -
Protein Kinase A-Mediated Septin7 Phosphorylation Disrupts Septin Filaments and Ciliogenesis
cells Article Protein Kinase A-Mediated Septin7 Phosphorylation Disrupts Septin Filaments and Ciliogenesis Han-Yu Wang 1,2, Chun-Hsiang Lin 1, Yi-Ru Shen 1, Ting-Yu Chen 2,3, Chia-Yih Wang 2,3,* and Pao-Lin Kuo 1,2,4,* 1 Department of Obstetrics and Gynecology, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan; [email protected] (H.-Y.W.); [email protected] (C.-H.L.); [email protected] (Y.-R.S.) 2 Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan; [email protected] 3 Department of Cell Biology and Anatomy, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan 4 Department of Obstetrics and Gynecology, National Cheng-Kung University Hospital, Tainan 704, Taiwan * Correspondence: [email protected] (C.-Y.W.); [email protected] (P.-L.K.); Tel.: +886-6-2353535 (ext. 5338); (C.-Y.W.)+886-6-2353535 (ext. 5262) (P.-L.K.) Abstract: Septins are GTP-binding proteins that form heteromeric filaments for proper cell growth and migration. Among the septins, septin7 (SEPT7) is an important component of all septin filaments. Here we show that protein kinase A (PKA) phosphorylates SEPT7 at Thr197, thus disrupting septin filament dynamics and ciliogenesis. The Thr197 residue of SEPT7, a PKA phosphorylating site, was conserved among different species. Treatment with cAMP or overexpression of PKA catalytic subunit (PKACA2) induced SEPT7 phosphorylation, followed by disruption of septin filament formation. Constitutive phosphorylation of SEPT7 at Thr197 reduced SEPT7-SEPT7 interaction, but did not affect SEPT7-SEPT6-SEPT2 or SEPT4 interaction. -
Rage (Receptor for Advanced Glycation End Products) in Melanoma
RAGE (RECEPTOR FOR ADVANCED GLYCATION END PRODUCTS) IN MELANOMA PROGRESSION A Dissertation Submitted to the Graduate Faculty of the North Dakota State University of Agriculture and Applied Science By Varsha Meghnani In Partial Fulfillment for the Degree of DOCTOR OF PHILOSOPHY Major Department: Pharmaceutical Sciences May 2014 Fargo, North Dakota North Dakota State University Graduate School Title RAGE (RECEPTOR FOR ADVANCED GLYCATION END PRODUCTS) IN MELANOMA PROGRESSION By VARSHA MEGHNANI The Supervisory Committee certifies that this disquisition complies with North Dakota State University’s regulations and meets the accepted standards for the degree of DOCTOR OF PHILOSOPHY SUPERVISORY COMMITTEE: ESTELLE LECLERC Chair BIN GUO STEPHEN O’ROURKE JANE SCHUH Approved: 5/22/2014 JAGDISH SINGH Date Department Chair ABSTRACT The Receptor for Advanced Glycation End Products (RAGE) and its ligands are expressed in multiple cancer types and are implicated in cancer progression. Our lab has previously reported higher transcript levels of RAGE and S100B in advanced staged melanoma patients. The contribution of RAGE in the pathophysiology of melanoma has not been well studied. Based on previous reports, we hypothesized that RAGE, when over-expressed in melanoma cells, promotes melanoma progression. To study the pathogenic role of RAGE in melanoma, a primary melanoma cell line, WM115, was selected and stably transfected with full length RAGE (FL_RAGE) to generate a model cell line over-expressing RAGE (WM115_RAGE). WM266, a sister cell line of WM115, originated from a metastatic tumor of the same patient was used as a metastatic control cell line in the study. After assessing the expression levels of RAGE in the transfected cells, the influence of RAGE on their cellular properties was examined. -
Toxicogenomics Applications of New Functional Genomics Technologies in Toxicology
\-\w j Toxicogenomics Applications of new functional genomics technologies in toxicology Wilbert H.M. Heijne Proefschrift ter verkrijging vand egraa dva n doctor opgeza gva nd e rector magnificus vanWageninge n Universiteit, Prof.dr.ir. L. Speelman, in netopenbaa r te verdedigen op maandag6 decembe r200 4 des namiddagst e half twee ind eAul a - Table of contents Abstract Chapter I. page 1 General introduction [1] Chapter II page 21 Toxicogenomics of bromobenzene hepatotoxicity: a combined transcriptomics and proteomics approach[2] Chapter III page 48 Bromobenzene-induced hepatotoxicity atth etranscriptom e level PI Chapter IV page 67 Profiles of metabolites and gene expression in rats with chemically induced hepatic necrosis[4] Chapter V page 88 Liver gene expression profiles in relation to subacute toxicity in rats exposed to benzene[5] Chapter VI page 115 Toxicogenomics analysis of liver gene expression in relation to subacute toxicity in rats exposed totrichloroethylen e [6] Chapter VII page 135 Toxicogenomics analysis ofjoin t effects of benzene and trichloroethylene mixtures in rats m Chapter VII page 159 Discussion and conclusions References page 171 Appendices page 187 Samenvatting page 199 Dankwoord About the author Glossary Abbreviations List of genes Chapter I General introduction Parts of this introduction were publishedin : Molecular Biology in Medicinal Chemistry, Heijne etal., 2003 m NATO Advanced Research Workshop proceedings, Heijne eral., 2003 81 Chapter I 1. General introduction 1.1 Background /.1.1 Toxicologicalrisk -
8296.Full.Pdf
Inflammation-Induced Chondrocyte Hypertrophy Is Driven by Receptor for Advanced Glycation End Products This information is current as Denise L. Cecil, Kristen Johnson, John Rediske, Martin of September 28, 2021. Lotz, Ann Marie Schmidt and Robert Terkeltaub J Immunol 2005; 175:8296-8302; ; doi: 10.4049/jimmunol.175.12.8296 http://www.jimmunol.org/content/175/12/8296 Downloaded from References This article cites 43 articles, 13 of which you can access for free at: http://www.jimmunol.org/content/175/12/8296.full#ref-list-1 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 September 28, 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 Copyright © 2005 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Inflammation-Induced Chondrocyte Hypertrophy Is Driven by Receptor for Advanced Glycation End Products1 Denise L. Cecil,* Kristen Johnson,* John Rediske,‡ Martin Lotz,§ Ann Marie Schmidt,† and Robert Terkeltaub2* The multiligand receptor for advanced glycation end products (RAGE) mediates certain chronic vascular and neurologic degen- erative diseases accompanied by low-grade inflammation. -
(Rage) in Progression of Pancreatic Cancer
The Texas Medical Center Library DigitalCommons@TMC The University of Texas MD Anderson Cancer Center UTHealth Graduate School of The University of Texas MD Anderson Cancer Biomedical Sciences Dissertations and Theses Center UTHealth Graduate School of (Open Access) Biomedical Sciences 8-2017 INVOLVEMENT OF THE RECEPTOR FOR ADVANCED GLYCATION END PRODUCTS (RAGE) IN PROGRESSION OF PANCREATIC CANCER Nancy Azizian MS Follow this and additional works at: https://digitalcommons.library.tmc.edu/utgsbs_dissertations Part of the Biology Commons, and the Medicine and Health Sciences Commons Recommended Citation Azizian, Nancy MS, "INVOLVEMENT OF THE RECEPTOR FOR ADVANCED GLYCATION END PRODUCTS (RAGE) IN PROGRESSION OF PANCREATIC CANCER" (2017). The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences Dissertations and Theses (Open Access). 748. https://digitalcommons.library.tmc.edu/utgsbs_dissertations/748 This Dissertation (PhD) is brought to you for free and open access by the The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences at DigitalCommons@TMC. It has been accepted for inclusion in The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences Dissertations and Theses (Open Access) by an authorized administrator of DigitalCommons@TMC. For more information, please contact [email protected]. INVOLVEMENT OF THE RECEPTOR FOR ADVANCED GLYCATION END PRODUCTS (RAGE) IN PROGRESSION OF PANCREATIC CANCER by Nancy -
Tudor Staphylococcal Nuclease Drives Chemoresistance of Non-Small Cell
www.impactjournals.com/oncotarget/ Oncotarget, Vol. 6, No. 14 Tudor staphylococcal nuclease drives chemoresistance of non-small cell lung carcinoma cells by regulating S100A11 Anna Zagryazhskaya1, Olga Surova1,2, Nadeem S. Akbar1, Giulia Allavena1,3, Katarina Gyuraszova1,4, Irina B. Zborovskaya5,6, Elena M. Tchevkina5,6, Boris Zhivotovsky1,6 1Institute of Environmental Medicine, Division of Toxicology, Stockholm, Sweden 2Ludwig Institute for Cancer Research Ltd, Karolinska Institutet, Stockholm, Sweden 3Department of Molecular and Developmental Medicine, University of Siena, Siena, Italy 4Institute of Biology and Ecology, Faculty of Science, Pavol Jozef Šafárik University in Košice, Košice, Slovakia 5NN Blokhin Russian Cancer Research Center, Moscow, Russia 6Faculty of Fundamental Medicine, ML Lomonosov State University, Moscow, Russia Correspondence to: Boris Zhivotovsky, e-mail: [email protected] Keywords: tudor staphylococcal nuclease, S100A11, phospholipase A2, non-small cell lung cancer, apoptosis Received: December 19, 2014 Accepted: March 07, 2015 Published: March 26, 2015 ABSTRACT Lung cancer is the leading cause of cancer-related deaths worldwide. Non-small cell lung cancer (NSCLC), the major lung cancer subtype, is characterized by high resistance to chemotherapy. Here we demonstrate that Tudor staphylococcal nuclease (SND1 or TSN) is overexpressed in NSCLC cell lines and tissues, and is important for maintaining NSCLC chemoresistance. Downregulation of TSN by RNAi in NSCLC cells led to strong potentiation of cell death in response to cisplatin. Silencing of TSN was accompanied by a significant decrease in S100A11 expression at both mRNA and protein level. Downregulation of S100A11 by RNAi resulted in enhanced sensitivity of NSCLC cells to cisplatin, oxaliplatin and 5-fluouracil. AACOCF3, a phospholipase A2 (PLA2) inhibitor, strongly abrogated chemosensitization upon silencing of S100A11 suggesting that PLA2 inhibition by S100A11 governs the chemoresistance of NSCLC. -
Supplementary Table S4. FGA Co-Expressed Gene List in LUAD
Supplementary Table S4. FGA co-expressed gene list in LUAD tumors Symbol R Locus Description FGG 0.919 4q28 fibrinogen gamma chain FGL1 0.635 8p22 fibrinogen-like 1 SLC7A2 0.536 8p22 solute carrier family 7 (cationic amino acid transporter, y+ system), member 2 DUSP4 0.521 8p12-p11 dual specificity phosphatase 4 HAL 0.51 12q22-q24.1histidine ammonia-lyase PDE4D 0.499 5q12 phosphodiesterase 4D, cAMP-specific FURIN 0.497 15q26.1 furin (paired basic amino acid cleaving enzyme) CPS1 0.49 2q35 carbamoyl-phosphate synthase 1, mitochondrial TESC 0.478 12q24.22 tescalcin INHA 0.465 2q35 inhibin, alpha S100P 0.461 4p16 S100 calcium binding protein P VPS37A 0.447 8p22 vacuolar protein sorting 37 homolog A (S. cerevisiae) SLC16A14 0.447 2q36.3 solute carrier family 16, member 14 PPARGC1A 0.443 4p15.1 peroxisome proliferator-activated receptor gamma, coactivator 1 alpha SIK1 0.435 21q22.3 salt-inducible kinase 1 IRS2 0.434 13q34 insulin receptor substrate 2 RND1 0.433 12q12 Rho family GTPase 1 HGD 0.433 3q13.33 homogentisate 1,2-dioxygenase PTP4A1 0.432 6q12 protein tyrosine phosphatase type IVA, member 1 C8orf4 0.428 8p11.2 chromosome 8 open reading frame 4 DDC 0.427 7p12.2 dopa decarboxylase (aromatic L-amino acid decarboxylase) TACC2 0.427 10q26 transforming, acidic coiled-coil containing protein 2 MUC13 0.422 3q21.2 mucin 13, cell surface associated C5 0.412 9q33-q34 complement component 5 NR4A2 0.412 2q22-q23 nuclear receptor subfamily 4, group A, member 2 EYS 0.411 6q12 eyes shut homolog (Drosophila) GPX2 0.406 14q24.1 glutathione peroxidase -
PHF16 Antibody (C-Term) Affinity Purified Rabbit Polyclonal Antibody (Pab) Catalog # Ap17166b
10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 PHF16 Antibody (C-term) Affinity Purified Rabbit Polyclonal Antibody (Pab) Catalog # AP17166b Specification PHF16 Antibody (C-term) - Product Information Application WB, IHC-P,E Primary Accession Q92613 Other Accession NP_001070913.1, NP_055550.1 Reactivity Human Host Rabbit Clonality Polyclonal Isotype Rabbit Ig Calculated MW 93808 Antigen Region 779-806 PHF16 Antibody (C-term) - Additional Information PHF16 Antibody (C-term) (Cat. #AP17166b) Gene ID 9767 western blot analysis in 293 cell line lysates (35ug/lane).This demonstrates the PHF16 Other Names antibody detected the PHF16 protein (arrow). Protein Jade-3, Jade family PHD finger protein 3, PHD finger protein 16, JADE3, KIAA0215, PHF16 Target/Specificity This PHF16 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 779-806 amino acids from the C-terminal region of human PHF16. Dilution WB~~1:1000 IHC-P~~1:10~50 Format Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity PHF16 Antibody (C-term) purification. (AP17166b)immunohistochemistry analysis in formalin fixed and paraffin embedded human Storage uterus tissue followed by peroxidase Maintain refrigerated at 2-8°C for up to 2 conjugation of the secondary antibody and weeks. For long term storage store at -20°C DAB staining.This data demonstrates the use in small aliquots to prevent freeze-thaw of PHF16 Antibody (C-term) for cycles. immunohistochemistry. Clinical relevance has not been evaluated. Precautions Page 1/2 10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 PHF16 Antibody (C-term) is for research use PHF16 Antibody (C-term) - Background only and not for use in diagnostic or therapeutic procedures.