Polyclonal Antibody to APIP (Full Length) - Purified

Total Page:16

File Type:pdf, Size:1020Kb

Polyclonal Antibody to APIP (Full Length) - Purified OriGene Technologies, Inc. OriGene Technologies GmbH 9620 Medical Center Drive, Ste 200 Schillerstr. 5 Rockville, MD 20850 32052 Herford UNITED STATES GERMANY Phone: +1-888-267-4436 Phone: +49-5221-34606-0 Fax: +1-301-340-8606 Fax: +49-5221-34606-11 [email protected] [email protected] AP08426PU-N Polyclonal Antibody to APIP (full length) - Purified Alternate names: APAF1-interacting protein, CGI-29 Quantity: 50 µg Concentration: 0.5 mg/ml Background: The mammalian homologues of the key cell death gene CED-4 in C. elegans has been identified recently from human and mouse and designated Apaf1 (for apoptosis protease activating factor 1). Apaf1 binds to cytochrome c (Apaf2) and caspase 9 (Apaf3), which leads to caspase 9 activation. Activated caspase 9 in turn cleaves and activates caspase 3 that is one of the key proteases, being responsible for the proteolytic cleavage of many key proteins in apoptosis. A new Apaf1 Interacting Protein (APIP) also known as CG129 and MMRP19, has been identified as a negative regulator of ischemic injury. APIP competes with Caspase 9 binding site of Apaf1. APIP is predicted to code for a 204 amino acid. An isoform of APIP, APIP2 encodes a 242 amino acid protein, which is an alternative splicing variant differing in its N terminus from APIP. APIP transcript is ubiquitously expressed in most adult tissue with high expression in skeletal muscle, heart, and kidney. Uniprot ID: Q96GX9 NCBI: NP_057041.2 GeneID: 51074 Host / Isotype: Rabbit / IgG Immunogen: Recombinant protein corresponding to a full-length His-tagged recombinant Human APIP protein Format: State: Liquid purified Ig fraction Purification: Protein G Chromatography Buffer System: PBS containing 0.2% Gelatin as stabilizer and 0.05% Sodium Azide as preservative Applications: Immunohistochemistry on Paraffin Sections: 10 µg/ml. Western Blot: 1 - 2 µg/ml. Other applications not tested. Optimal dilutions are dependent on conditions and should be determined by the user. Specificity: This antibody recognizes APIP. Species Reactivity: Tested: Human Storage: Store the antibody undiluted at 2-8°C for one month or (in aliquots) at -20°C for longer. Avoid repeated freezing and thawing. Shelf life: one year from despatch. For research and in vitro use only. Not for diagnostic or therapeutic work. Material Safety Datasheets are available at www.acris-antibodies.com or on request. OG/20170919 1 / 2 AP08426PU-N: Polyclonal Antibody to APIP (full length) - Purified Pictures: Kidney: Formalin-Fixed Paraffin- Embedded (FFPE) For research and in vitro use only. Not for diagnostic or therapeutic work. Material Safety Datasheets are available at www.acris-antibodies.com or on request. OG/20170919 2 / 2 Powered by TCPDF (www.tcpdf.org).
Recommended publications
  • Genomic Regions Associated with Muscularity in Beef Cattle Differ In
    Doyle et al. Genet Sel Evol (2020) 52:2 https://doi.org/10.1186/s12711-020-0523-1 Genetics Selection Evolution RESEARCH ARTICLE Open Access Genomic regions associated with muscularity in beef cattle difer in fve contrasting cattle breeds Jennifer L. Doyle1,2, Donagh P. Berry1* , Roel F. Veerkamp3, Tara R. Carthy1, Ross D. Evans4, Siobhán W. Walsh2 and Deirdre C. Purfeld1 Abstract Background: Linear type traits, which refect the muscular characteristics of an animal, could provide insight into how, in some cases, morphologically very diferent animals can yield the same carcass weight. Such variability may contribute to diferences in the overall value of the carcass since primal cuts vary greatly in price; such variability may also hinder successful genome-based association studies. Therefore, the objective of our study was to identify genomic regions that are associated with fve muscularity linear type traits and to determine if these signifcant regions are common across fve diferent breeds. Analyses were carried out using linear mixed models on imputed whole-genome sequence data in each of the fve breeds, separately. Then, the results of the within-breed analyses were used to conduct an across-breed meta-analysis per trait. Results: We identifed many quantitative trait loci (QTL) that are located across the whole genome and associated with each trait in each breed. The only commonality among the breeds and traits was a large-efect pleiotropic QTL on BTA2 that contained the MSTN gene, which was associated with all traits in the Charolais and Limousin breeds. Other plausible candidate genes were identifed for muscularity traits including PDE1A, PPP1R1C and multiple col- lagen and HOXD genes.
    [Show full text]
  • APIP (NM 015957) Human Tagged ORF Clone Product Data
    OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for RC203297 APIP (NM_015957) Human Tagged ORF Clone Product data: Product Type: Expression Plasmids Product Name: APIP (NM_015957) Human Tagged ORF Clone Tag: Myc-DDK Symbol: APIP Synonyms: APIP2; CGI-29; CGI29; hAPIP; MMRP19 Vector: pCMV6-Entry (PS100001) E. coli Selection: Kanamycin (25 ug/mL) Cell Selection: Neomycin ORF Nucleotide >RC203297 ORF sequence Sequence: Red=Cloning site Blue=ORF Green=Tags(s) TTTTGTAATACGACTCACTATAGGGCGGCCGGGAATTCGTCGACTGGATCCGGTACCGAGGAGATCTGCC GCCGCGATCGCC ATGTCTGGCTGTGATGCTCGGGAGGGAGACTGTTGTTCCCGGAGATGCGGCGCGCAGGACAAGGAGCGTC CAAGATACCTGATCCCAGAACTTTGCAAACAGTTTTACCATTTAGGCTGGGTCACTGGGACTGGAGGAGG AATTAGCTTGAAGCATGGCGATGAAATCTACATTGCTCCTTCAGGAGTGCAAAAGGAACGAATTCAGCCT GAAGACATGTTTGTTTGTGATATAAATGAAAAGGACATAAGTGGACCTTCGCCATCGAAGAAGCTAAAAA AAAGCCAGTGTACTCCTCTTTTCATGAATGCTTACACAATGAGAGGAGCAGGTGCAGTGATTCATACCCA CTCTAAAGCTGCTGTGATGGCCACACTTCTCTTTCCAGGACGGGAGTTTAAAATTACACATCAAGAGATG ATAAAAGGAATAAAGAAATGTACTTCCGGAGGGTATTATAGATATGATGATATGTTAGTGGTACCCATTA TTGAGAATACACCTGAGGAGAAAGACCTCAAAGATAGAATGGCTCATGCAGTGAATGAATACCCAGACTC CTGTGCAGTACTGGTCAGACGTCATGGAGTATATGTGTGGGGGGAAACATGGGAGAAGGCCAAAACCATG TGTGAGTGTTATGACTATTTATTTGATATTGCCGTATCAATGAAGAAAGTAGGACTTGATCCTTCACAGC TCCCAGTTGGAGAAAATGGAATTGTC ACGCGTACGCGGCCGCTCGAGCAGAAACTCATCTCAGAAGAGGATCTGGCAGCAAATGATATCCTGGATT ACAAGGATGACGACGATAAGGTTTAA This product is to be used for
    [Show full text]
  • NLRP3 and ASC Differentially Affect the Lung Transcriptome During Pneumococcal Pneumonia
    UvA-DARE (Digital Academic Repository) Cell-specific pattern recognition receptor signaling in antibacterial defense van Lieshout, M.H.P. Publication date 2015 Document Version Final published version Link to publication Citation for published version (APA): van Lieshout, M. H. P. (2015). Cell-specific pattern recognition receptor signaling in antibacterial defense. General rights It is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulations If you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: https://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. UvA-DARE is a service provided by the library of the University of Amsterdam (https://dare.uva.nl) Download date:30 Sep 2021 Chapter 7 NLRP3 and ASC differentially affect the lung transcriptome during pneumococcal pneumonia American Journal of Respiratory Cell and Molecular Biology 2014 Apr;50(4):699-712 DOI: 10.1165/rcmb.2013-0015OC Miriam H.P. van Lieshout 1,2 Brendon P. Scicluna 1,2 Sandrine Florquin 3 Tom van der Poll 1,2,4 Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands: 1Center of Infection and Immunity Amsterdam 2Center of Experimental and Molecular Medicine 3Department of Pathology 4Division of Infectious Diseases Chapter 7 Abstract Streptococcus (S.) pneumoniae is the most frequently isolated causative pathogen of community-acquired pneumonia, a leading cause of mortality worldwide.
    [Show full text]
  • Defining Trends in Global Gene Expression in Arabian Horses with Cerebellar Abiotrophy
    Cerebellum DOI 10.1007/s12311-016-0823-8 ORIGINAL PAPER Defining Trends in Global Gene Expression in Arabian Horses with Cerebellar Abiotrophy E. Y. Scott1 & M. C. T. Penedo2,3 & J. D. Murray1,3 & C. J. Finno3 # Springer Science+Business Media New York 2016 Abstract Equine cerebellar abiotrophy (CA) is a hereditary expression (DE) analysis were used (Tophat2/Cuffdiff2, neurodegenerative disease that affects the Purkinje neurons of Kallisto/EdgeR, and Kallisto/Sleuth) with 151 significant the cerebellum and causes ataxia in Arabian foals. Signs of DE genes identified by all three pipelines in CA-affected CA are typically first recognized either at birth to any time up horses. TOE1 (Log2(foldchange) = 0.92, p =0.66)and to 6 months of age. CA is inherited as an autosomal recessive MUTYH (Log2(foldchange) = 1.13, p = 0.66) were not dif- trait and is associated with a single nucleotide polymorphism ferentially expressed. Among the major pathways that were (SNP) on equine chromosome 2 (13074277G>A), located in differentially expressed, genes associated with calcium ho- the fourth exon of TOE1 and in proximity to MUTYH on the meostasis and specifically expressed in Purkinje neurons, antisense strand. We hypothesize that unraveling the func- CALB1 (Log2(foldchange) = −1.7, p < 0.01) and CA8 tional consequences of the CA SNP using RNA-seq will elu- (Log2(foldchange) = −0.97, p < 0.01), were significantly cidate the molecular pathways underlying the CA phenotype. down-regulated, confirming loss of Purkinje neurons. There RNA-seq (100 bp PE strand-specific) was performed in cer- was also a significant up-regulation of markers for microglial ebellar tissue from four CA-affected and five age-matched phagocytosis, TYROBP (Log2(foldchange) = 1.99, p <0.01) unaffected horses.
    [Show full text]
  • Structural and Biochemical Basis for the Inhibition of Cell Death by APIP, a Methionine Salvage Enzyme
    Structural and biochemical basis for the inhibition of cell death by APIP, a methionine salvage enzyme Wonchull Kanga,1, Se Hoon Hongb,1, Hye Min Leea, Na Yeon Kima, Yun Chan Lima, Le Thi My Lea, Bitna Limb, Hyun Chul Kima, Tae Yeon Kima, Hiroki Ashidac, Akiho Yokotac, Sang Soo Hahd, Keun Ho Chuna, Yong-Keun Jungb,2, and Jin Kuk Yanga,2 aDepartment of Chemistry, College of Natural Sciences, Soongsil University, Seoul 156-743, Korea; bSchool of Biological Science/Bio-Max Institute, Seoul National University, Seoul 151-742, Korea; cGraduate School of Biological Sciences, Nara Institute of Science and Technology, 8916-5 Takayama, Ikoma, Nara 630-0192, Japan; and dDepartment of Chemistry and Research Institute for Basic Sciences, Kyung Hee University, Seoul 130-701, Korea Edited by James A. Wells, University of California, San Francisco, CA, and approved December 4, 2013 (received for review May 10, 2013) APIP, Apaf-1 interacting protein, has been known to inhibit two MTA (5-methylthioadenosine) to methionine through six en- main types of programmed cell death, apoptosis and pyropto- zymatic reaction steps, and MtnB is the third enzyme in the sis, and was recently found to be associated with cancers and pathway and catalyzes the dehydration of MTRu-1-P (5-meth- inflammatory diseases. Distinct from its inhibitory role in cell ylthioribulose-1-phosphate) to DK-MTP-1-P (2,3-diketo-5-meth- death, APIP was also shown to act as a 5-methylthioribulose-1- ylthiopentyl-1-phosphate) (Fig. 1B) (4, 5). In the absence of phosphate dehydratase, or MtnB, in the methionine salvage path- methionine, cells supplemented with MTA exhibit decreased way.
    [Show full text]
  • Mining Potentially Actionable Kinase Gene Fusions in Cancer Cell Lines with the Kung FU Database
    www.nature.com/scientificdata OPeN Mining potentially actionable ArTICLe kinase gene fusions in cancer cell lines with the KuNG FU database Alessio Somaschini1,3, Sebastiano Di Bella1,3, Carlo Cusi1, Laura Raddrizzani1, Antonella Leone1, Giovanni Carapezza1, Tommaso Mazza 2, Antonella Isacchi1 & Roberta Bosotti1 ✉ Inhibition of kinase gene fusions (KGFs) has proven successful in cancer treatment and continues to represent an attractive research area, due to kinase druggability and clinical validation. Indeed, literature and public databases report a remarkable number of KGFs as potential drug targets, often identifed by in vitro characterization of tumor cell line models and confrmed also in clinical samples. However, KGF molecular and experimental information can sometimes be sparse and partially overlapping, suggesting the need for a specifc annotation database of KGFs, conveniently condensing all the molecular details that can support targeted drug development pipelines and diagnostic approaches. Here, we describe KuNG FU (KiNase Gene FUsion), a manually curated database collecting detailed annotations on KGFs that were identifed and experimentally validated in human cancer cell lines from multiple sources, exclusively focusing on in-frame KGF events retaining an intact kinase domain, representing potentially active driver kinase targets. To our knowledge, KuNG FU represents to date the largest freely accessible homogeneous and curated database of kinase gene fusions in cell line models. Introduction Genomic instability is one of the
    [Show full text]
  • Genome-Wide Association and Linkage Identify Modifier Loci of Lung Disease Severity in Cystic Fibrosis at 11P13 and 20Q13.2 Fred A
    Genome-wide association and linkage identify modifier loci of lung disease severity in cystic fibrosis at 11p13 and 20q13.2 Fred A. Wright, University of North Carolina Lisa J. Strug, University of Toronto Vishal K. Doshi, Johns Hopkins University Clayton W. Commander, University of North Carolina Scott M. Blackman, Johns Hopkins University Lei Sun, University of Toronto Yves Berthiaume, Centre de recherche Centre Hospitalier de I’Université de Montréal David Cutler, Emory University Andreea Cojocaru, Hospital for Sick Children J. Michael Collaco, Johns Hopkins University Only first 10 authors above; see publication for full author list. Journal Title: Nature Genetics Volume: Volume 43, Number 6 Publisher: Nature Research (part of Springer Nature) | 2011-06-01, Pages 539-U67 Type of Work: Article | Post-print: After Peer Review Publisher DOI: 10.1038/ng.838 Permanent URL: https://pid.emory.edu/ark:/25593/trvrz Final published version: http://dx.doi.org/10.1038/ng.838 Copyright information: © 2011 Nature America, Inc. All rights reserved. Accessed October 9, 2021 8:57 AM EDT HHS Public Access Author manuscript Author Manuscript Author ManuscriptNat Genet Author Manuscript. Author manuscript; Author Manuscript available in PMC 2012 March 07. Published in final edited form as: Nat Genet. 2011 June ; 43(6): 539–546. doi:10.1038/ng.838. Genome-wide association and linkage identify modifier loci of lung disease severity in cystic fibrosis at 11p13 and 20q13.2 Fred A. Wright1, Lisa J. Strug2,3, Vishal K. Doshi4, Clayton W. Commander5, Scott M. Blackman6, Lei Sun3, Yves Berthiaume7, David Cutler8, Andreea Cojocaru2, J. Michael Collaco6, Mary Corey2, Ruslan Dorfman9, Katrina Goddard10, Deanna Green6, Jack W.
    [Show full text]
  • Genome-Wide Association Meta-Analysis Identifies Five
    ARTICLE Received 9 Jan 2015 | Accepted 17 Aug 2015 | Published 29 Sep 2015 DOI: 10.1038/ncomms9382 OPEN Genome-wide association meta-analysis identifies five modifier loci of lung disease severity in cystic fibrosis Harriet Corvol1,2, Scott M. Blackman3, Pierre-Yves Boe¨lle2,4, Paul J. Gallins5, Rhonda G. Pace6, Jaclyn R. Stonebraker6, Frank J. Accurso7,8,9, Annick Clement1,2, Joseph M. Collaco10, Hong Dang6, Anthony T. Dang6, Arianna Franca11, Jiafen Gong12, Loic Guillot1, Katherine Keenan13, Weili Li12, Fan Lin12, Michael V. Patrone6, Karen S. Raraigh11, Lei Sun14,15, Yi-Hui Zhou16, Wanda K. O’Neal6, Marci K. Sontag7,8,9, Hara Levy17, Peter R. Durie13,18, Johanna M. Rommens12,19, Mitchell L. Drumm20, Fred A. Wright21,22, Lisa J. Strug12,15, Garry R. Cutting11,23 & Michael R. Knowles6 The identification of small molecules that target specific CFTR variants has ushered in a new era of treatment for cystic fibrosis (CF), yet optimal, individualized treatment of CF will require identification and targeting of disease modifiers. Here we use genome-wide association analysis to identify genetic modifiers of CF lung disease, the primary cause of mortality. Meta-analysis of 6,365 CF patients identifies five loci that display significant association with variation in lung disease. Regions on chr3q29 (MUC4/MUC20; P ¼ 3.3 Â 10 À 11), chr5p15.3 (SLC9A3; P ¼ 6.8 Â 10 À 12), chr6p21.3 (HLA Class II;P¼ 1.2 Â 10 À 8) and chrXq22-q23 (AGTR2/SLC6A14; P ¼ 1.8 Â 10 À 9) contain genes of high biological relevance to CF patho- physiology.
    [Show full text]
  • UNIVERSITY of CALIFORNIA, SAN DIEGO Measuring
    UNIVERSITY OF CALIFORNIA, SAN DIEGO Measuring and Correlating Blood and Brain Gene Expression Levels: Assays, Inbred Mouse Strain Comparisons, and Applications to Human Disease Assessment A dissertation submitted in partial satisfaction of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences by Mary Elizabeth Winn Committee in charge: Professor Nicholas J Schork, Chair Professor Gene Yeo, Co-Chair Professor Eric Courchesne Professor Ron Kuczenski Professor Sanford Shattil 2011 Copyright Mary Elizabeth Winn, 2011 All rights reserved. 2 The dissertation of Mary Elizabeth Winn is approved, and it is acceptable in quality and form for publication on microfilm and electronically: Co-Chair Chair University of California, San Diego 2011 iii DEDICATION To my parents, Dennis E. Winn II and Ann M. Winn, to my siblings, Jessica A. Winn and Stephen J. Winn, and to all who have supported me throughout this journey. iv TABLE OF CONTENTS Signature Page iii Dedication iv Table of Contents v List of Figures viii List of Tables x Acknowledgements xiii Vita xvi Abstract of Dissertation xix Chapter 1 Introduction and Background 1 INTRODUCTION 2 Translational Genomics, Genome-wide Expression Analysis, and Biomarker Discovery 2 Neuropsychiatric Diseases, Tissue Accessibility and Blood-based Gene Expression 4 Mouse Models of Human Disease 5 Microarray Gene Expression Profiling and Globin Reduction 7 Finding and Accessible Surrogate Tissue for Neural Tissue 9 Genetic Background Effect Analysis 11 SPECIFIC AIMS 12 ENUMERATION OF CHAPTERS
    [Show full text]
  • Finding Modifiers of Known Disease-Related Variants
    Finding Modifiers of Known Disease – Related Variants Cystic Fibrosis: Model of “Monogenic” Recessive Disorder NIH Workshop: Sequencing in Cohort Studies and Large Sample Collections June 29, 2012 Michael R. Knowles, M.D. The University of North Carolina at Chapel Hill CF Gene Modifier Consortium Genetics in Complex vs. Mendelian Genetic Disorders Variability of Lung Function in CF (ΔF508 Homozygotes) Kerem et al., N. Engl. J. Med. 1990;323:1517 Variability of Lung Function Reflects Genetics and Environment • European twin/sib study suggested strong (~50%) genetic contribution to CF phenotype (lung/nutrition)* • U.S. twin/sib study indicates variability of CF lung disease primarily due to genetic factors (0.55-0.86)† Challenge: What are the genes? *Mekus, F. et al. 2000. Twin Res. †Vanscoy et al. 2007. Am. J. Respir. Crit. Care Med. Genetic Modifiers Study (GMS) (Extremes of phenotype) – University of North Carolina • Mike Knowles, Wanda O’Neal • Fred Wright – Case-Western • Mitch Drumm Canadian Consortium for CF Genetic Studies (CGS) – Hospital for Sickkids • Peter Durie, Johanna Rommens CF Twin and Sibling Study (TSS) – Johns Hopkins • Garry Cutting • Scott Blackman Challenge of Lung Disease Phenotype FEV1 (% Pred) vs. Age Toronto “PI” patients; 1357 (ΔF/ΔF = 841) Quantitative Lung Phenotype* • Key for joint analyses (quantitative lung phenotype) • Used multiple measures of FEV1 (3 years), and referenced to Kulich percentiles (age, sex, height adjusted), then survival corrected and z-transformed • Validated; strong correlation (r2 > 0.90) with Schluchter cross-sectional, longitudinal and survival models† • Validated; robust genetic influence (h2 = 0.51)‡ *Taylor, C., et al., Pediatr. Pulmonol. 2011 †Schluchter, M. et al., Am.
    [Show full text]
  • INTRODUCING a NOVEL METHOD for GENETIC ANALYSIS of AUTISM SPECTRUM DISORDER Sepideh Nouri
    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 12-2013 INTRODUCING A NOVEL METHOD FOR GENETIC ANALYSIS OF AUTISM SPECTRUM DISORDER sepideh nouri Follow this and additional works at: https://digitalcommons.library.tmc.edu/utgsbs_dissertations Part of the Bioinformatics Commons, Computational Biology Commons, and the Genomics Commons Recommended Citation nouri, sepideh, "INTRODUCING A NOVEL METHOD FOR GENETIC ANALYSIS OF AUTISM SPECTRUM DISORDER" (2013). The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences Dissertations and Theses (Open Access). 417. https://digitalcommons.library.tmc.edu/utgsbs_dissertations/417 This Thesis (MS) 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]. INTRODUCING A NOVEL METHOD FOR GENETIC ANALYSIS OF AUTISM SPECTRUM DISORDER by Sepideh Nouri, M.S. APPROVED: Eric Boerwinkle, Ph.D., Supervisor Kim-Anh Do, Ph.D. Alanna Morrison, Ph.D. James Hixson, Ph.D. Paul Scheet, Ph.D. APPROVED: Dean, The University of Texas Graduate School of Biomedical Sciences at Houston INTRODUCING A NOVEL METHOD FOR GENETIC ANALYSIS OF AUTISM SPECTRUM DISORDER A THESIS Presented to the Faculty of The University of Texas Health Science Center at Houston and The University of Texas M.
    [Show full text]
  • Minimal Peroxide Exposure of Neuronal Cells Induces Multifaceted Adaptive Responses
    Minimal Peroxide Exposure of Neuronal Cells Induces Multifaceted Adaptive Responses Wayne Chadwick1, Yu Zhou1, Sung-Soo Park1, Liyun Wang1, Nicholas Mitchell2, Matthew D. Stone1, Kevin G. Becker3, Bronwen Martin4, Stuart Maudsley1* 1 Receptor Pharmacology Unit, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America, 2 Department of Biology, Saint Bonaventure University, Saint Bonaventure, New York, United States of America, 3 Gene Expression and Genomics Unit, Research Resources Branch, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America, 4 Metabolism Unit, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America Abstract Oxidative exposure of cells occurs naturally and may be associated with cellular damage and dysfunction. Protracted low level oxidative exposure can induce accumulated cell disruption, affecting multiple cellular functions. Accumulated oxidative exposure has also been proposed as one of the potential hallmarks of the physiological/pathophysiological aging process. We investigated the multifactorial effects of long-term minimal peroxide exposure upon SH-SY5Y neural cells to understand how they respond to the continued presence of oxidative stressors. We show that minimal protracted oxidative stresses induce complex molecular and physiological alterations in cell functionality. Upon chronic exposure to minimal doses of hydrogen peroxide, SH-SY5Y cells displayed a multifactorial response to the stressor. To fully appreciate the peroxide-mediated cellular effects, we assessed these adaptive effects at the genomic, proteomic and cellular signal processing level. Combined analyses of these multiple levels of investigation revealed a complex cellular adaptive response to the protracted peroxide exposure. This adaptive response involved changes in cytoskeletal structure, energy metabolic shifts towards glycolysis and selective alterations in transmembrane receptor activity.
    [Show full text]