A Meta-Analysis of the Effects of High-LET Ionizing Radiations in Human Gene Expression
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Original Article Upregulation of HOXA13 As a Potential Tumorigenesis and Progression Promoter of LUSC Based on Qrt-PCR and Bioinformatics
Int J Clin Exp Pathol 2017;10(10):10650-10665 www.ijcep.com /ISSN:1936-2625/IJCEP0065149 Original Article Upregulation of HOXA13 as a potential tumorigenesis and progression promoter of LUSC based on qRT-PCR and bioinformatics Rui Zhang1*, Yun Deng1*, Yu Zhang1, Gao-Qiang Zhai1, Rong-Quan He2, Xiao-Hua Hu2, Dan-Ming Wei1, Zhen-Bo Feng1, Gang Chen1 Departments of 1Pathology, 2Medical Oncology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, China. *Equal contributors. Received September 7, 2017; Accepted September 29, 2017; Epub October 1, 2017; Published October 15, 2017 Abstract: In this study, we investigated the levels of homeobox A13 (HOXA13) and the mechanisms underlying the co-expressed genes of HOXA13 in lung squamous cancer (LUSC), the signaling pathways in which the co-ex- pressed genes of HOXA13 are involved and their functional roles in LUSC. The clinical significance of 23 paired LUSC tissues and adjacent non-tumor tissues were gathered. HOXA13 levels in LUSC were detected by quantita- tive real-time polymerase chain reaction (qRT-PCR). HOXA13 levels in LUSC from The Cancer Genome Atlas (TCGA) and Oncomine were analyzed. We performed receiver operator characteristic (ROC) curves of various clinicopath- ological features of LUSC. Co-expressed of HOXA13 were collected from MEM, cBioPortal and GEPIA. The func- tions and pathways of the most reliable overlapped genes were achieved from the Gene Otology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases, respectively. The protein-protein interaction (PPI) net- works were mapped using STRING. HOXA13 in LUSC were markedly upregulated compared with those in the non- cancerous controls as demonstrated by qRT-PCR (LUSC: 0.330±0.360; CONTROLS: 0.155±0.142; P=0.021). -
C8cc08685k1.Pdf
Electronic Supplementary Material (ESI) for ChemComm. This journal is © The Royal Society of Chemistry 2018 Supporting Information Minimalist Linkers Suitable for Irreversible Inhibitors in Simultaneous Proteome Profiling, Live-Cell Imaging and Drug Screening Cuiping Guo,Yu Chang, Xin Wang, Chengqian Zhang, Piliang Hao*, Ke Ding and Zhengqiu Li* School of Pharmacy, Jinan University, Guangzhou, China 510632 *Corresponding author ([email protected]) 1. General Information All chemicals were purchased from commercial vendors and used without further purification, unless indicated otherwise. All reactions requiring anhydrous conditions were carried out under argon or nitrogen atmosphere using oven-dried glassware. AR-grade solvents were used for all reactions. Reaction progress was monitored by TLC on pre-coated silica plates (Merck 60 F254 nm, 0.25 µm) and spots were visualized by UV, iodine or other suitable stains. Flash column chromatography was carried out using silica gel (Qingdao Ocean). All NMR spectra (1H-NMR, 13C-NMR) were recorded on Bruker 300 MHz/400 MHz NMR spectrometers. Chemical shifts were reported in parts per million (ppm) referenced with respect to appropriate internal standards or residual solvent peaks (CDCl3 = 7.26 ppm, DMSO-d6 = 2.50 ppm). The following abbreviations were used in reporting spectra, br s (broad singlet), s (singlet), d (doublet), t (triplet), q (quartet), m (multiplet), dd (doublet of doublets). Mass spectra were obtained on Agilent LC-ESI-MS system. All analytical HPLC were carried out on Agilent system. Water with 0.1% TFA and acetonitrile with 0.1% TFA were used as eluents and the flow rate was 0.5 mL/min. -
Reprogramming of Trna Modifications Controls the Oxidative Stress Response by Codon-Biased Translation of Proteins
Reprogramming of tRNA modifications controls the oxidative stress response by codon-biased translation of proteins The MIT Faculty has made this article openly available. Please share how this access benefits you. Your story matters. Citation Chan, Clement T.Y. et al. “Reprogramming of tRNA Modifications Controls the Oxidative Stress Response by Codon-biased Translation of Proteins.” Nature Communications 3 (2012): 937. As Published http://dx.doi.org/10.1038/ncomms1938 Publisher Nature Publishing Group Version Author's final manuscript Citable link http://hdl.handle.net/1721.1/76775 Terms of Use Article is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use. Reprogramming of tRNA modifications controls the oxidative stress response by codon-biased translation of proteins Clement T.Y. Chan,1,2 Yan Ling Joy Pang,1 Wenjun Deng,1 I. Ramesh Babu,1 Madhu Dyavaiah,3 Thomas J. Begley3 and Peter C. Dedon1,4* 1Department of Biological Engineering, 2Department of Chemistry and 4Center for Environmental Health Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139; 3College of Nanoscale Science and Engineering, University at Albany, SUNY, Albany, NY 12203 * Corresponding author: PCD, Department of Biological Engineering, NE47-277, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139; tel 617-253-8017; fax 617-324-7554; email [email protected] 2 ABSTRACT Selective translation of survival proteins is an important facet of cellular stress response. We recently demonstrated that this translational control involves a stress-specific reprogramming of modified ribonucleosides in tRNA. -
C19) United States C12) Patent Application Publication C10) Pub
1111111111111111 IIIIII IIIII 1111111111 11111 11111 111111111111111 1111111111 1111111111 11111111 US 20200081016Al c19) United States c12) Patent Application Publication c10) Pub. No.: US 2020/0081016 Al Talaat et al. (43) Pub. Date: Mar. 12, 2020 (54) BIOMARKERS FOR EARLY DIAGNOSIS Publication Classification AND DIFFERENTIATION OF (51) Int. Cl. MYCOBACTERIAL INFECTION GOIN 33/68 (2006.01) C12Q 116851 (2006.01) (71) Applicant: Wisconsin Alumni Research GOIN 33/569 (2006.01) Foundation, Madison, WI (US) (52) U.S. Cl. (72) Inventors: Adel Mohamed Talaat, Madison, WI CPC ......... GOIN 33/6854 (2013.01); GOIN 33/68 (US); Chia-wei Wu, Madison, WI (US) (2013.01); GOIN 2800/50 (2013.01); GOIN 33/5695 (2013.01); GOIN 2800/26 (2013.01); (21) Appl. No.: 16/555,819 C12Q 116851 (2013.01) (22) Filed: Aug. 29, 2019 (57) ABSTRACT Mycobacterial-specific biomarkers and methods of using Related U.S. Application Data such biomarkers for diagnosis of mycobacterial infection in (60) Provisional application No. 62/728,387, filed on Sep. a mammal are disclosed. 7, 2018. Specification includes a Sequence Listing. Patent Application Publication Mar. 12, 2020 Sheet 1 of 10 US 2020/0081016 Al FIG. 1 ·~{:: -{t i * !lpNbiNi$ 1 !lpN p~ra 111:111111 llillllll: 111!11,111llltllllll~ 11111 ■111 ~; C,,Nmnsus KR.IGINMTKX L.lC(X.AXXXXG AXXXXMPXTX RXO-GXVXXVG VKVXPWIPTX ® • ® l I I iipN lK>V(S ~Hl!lli!Wiofflij 1!11.llofJiillj mllB~lijftlt flol=fiolill ••t-il-~MM ~9 llpN p~ra HfHJoffit:torti ilffllGNillm miJllt~ttiollf ~•01:101111 llm:l:l1IA@~ iOO C,,nstmsus XXRXLXXGRS Vt IOGNT.LDP i LOt.MLSXXR XXGXOG.I...XVO ODXXXSR:AXM t2:;: i-/4~~ ! l 1 I~~~~b;:: llllil~l:1:1 llil 111111:1~:111~ 1111111::;1 1lllilllll: ~:~ C,,nimnsus XXXXXXXPGP QtHVDVXXI...X XPGPAGXIPA RHYRPXGGXX QXPt.l...VFYHG Consl:lrvat,ofl -:§;::. -
Implications in Parkinson's Disease
Journal of Clinical Medicine Review Lysosomal Ceramide Metabolism Disorders: Implications in Parkinson’s Disease Silvia Paciotti 1,2 , Elisabetta Albi 3 , Lucilla Parnetti 1 and Tommaso Beccari 3,* 1 Laboratory of Clinical Neurochemistry, Department of Medicine, University of Perugia, Sant’Andrea delle Fratte, 06132 Perugia, Italy; [email protected] (S.P.); [email protected] (L.P.) 2 Section of Physiology and Biochemistry, Department of Experimental Medicine, University of Perugia, Sant’Andrea delle Fratte, 06132 Perugia, Italy 3 Department of Pharmaceutical Sciences, University of Perugia, Via Fabretti, 06123 Perugia, Italy; [email protected] * Correspondence: [email protected] Received: 29 January 2020; Accepted: 20 February 2020; Published: 21 February 2020 Abstract: Ceramides are a family of bioactive lipids belonging to the class of sphingolipids. Sphingolipidoses are a group of inherited genetic diseases characterized by the unmetabolized sphingolipids and the consequent reduction of ceramide pool in lysosomes. Sphingolipidoses include several disorders as Sandhoff disease, Fabry disease, Gaucher disease, metachromatic leukodystrophy, Krabbe disease, Niemann Pick disease, Farber disease, and GM2 gangliosidosis. In sphingolipidosis, lysosomal lipid storage occurs in both the central nervous system and visceral tissues, and central nervous system pathology is a common hallmark for all of them. Parkinson’s disease, the most common neurodegenerative movement disorder, is characterized by the accumulation and aggregation of misfolded α-synuclein that seem associated to some lysosomal disorders, in particular Gaucher disease. This review provides evidence into the role of ceramide metabolism in the pathophysiology of lysosomes, highlighting the more recent findings on its involvement in Parkinson’s disease. Keywords: ceramide metabolism; Parkinson’s disease; α-synuclein; GBA; GLA; HEX A-B; GALC; ASAH1; SMPD1; ARSA * Correspondence [email protected] 1. -
Datasheet PB1029 Anti-AEBP2 Antibody
Product datasheet Anti-AEBP2 Antibody Catalog Number: PB1029 BOSTER BIOLOGICAL TECHNOLOGY Special NO.1, International Enterprise Center, 2nd Guanshan Road, Wuhan, China Web: www.boster.com.cn Phone: +86 27 67845390 Fax: +86 27 67845390 Email: [email protected] Basic Information Product Name Anti-AEBP2 Antibody Gene Name AEBP2 Source Rabbit IgG Species Reactivity human,mouse,rat Tested Application WB,IHC-P,ICC/IF,FCM Contents 500ug/ml antibody with PBS ,0.02% NaN3 , 1mg BSA and 50% glycerol. Immunogen E.coli-derived human AEBP2 recombinant protein (Position: K424-Q517). Human AEBP2 shares 98.8% amino acid (aa) sequence identity with mouse AEBP2. Purification Immunogen affinity purified. Observed MW 54KD Dilution Ratios Western blot: 1:500-2000 Immunohistochemistry(Paraffin-embedded Section): 1:50-400 Immunocytochemistry/Immunofluorescence (ICC/IF): 1:50-400 Flow cytometry (FCM): 1-3μg/1x106 cells Storage 12 months from date of receipt,-20℃ as supplied.6 months 2 to 8℃ after reconstitution. Avoid repeated freezing and thawing Background Information Adipocyte Enhancer-Binding Protein is a zinc finger protein that in humans is encoded by the evolutionarily well-conserved gene AEBP2. This gene is mapped to 12p12.3. AEBP2 is a DNA-binding transcriptional repressor. It may regulate the migration and development of the neural crest cells through the PRC2-mediated epigenetic mechanism and is most likely a targeting protein for the mammalian PRC2 complex. Reference Anti-AEBP2 Antibody被引用在0文献中。 暂无引用 FOR RESEARCH USE ONLY. NOT FOR DIAGNOSTIC AND CLINICAL USE. 1 Product datasheet Anti-AEBP2 Antibody Catalog Number: PB1029 BOSTER BIOLOGICAL TECHNOLOGY Special NO.1, International Enterprise Center, 2nd Guanshan Road, Wuhan, China Web: www.boster.com.cn Phone: +86 27 67845390 Fax: +86 27 67845390 Email: [email protected] Selected Validation Data Figure 1. -
Protein Interaction Network of Alternatively Spliced Isoforms from Brain Links Genetic Risk Factors for Autism
ARTICLE Received 24 Aug 2013 | Accepted 14 Mar 2014 | Published 11 Apr 2014 DOI: 10.1038/ncomms4650 OPEN Protein interaction network of alternatively spliced isoforms from brain links genetic risk factors for autism Roser Corominas1,*, Xinping Yang2,3,*, Guan Ning Lin1,*, Shuli Kang1,*, Yun Shen2,3, Lila Ghamsari2,3,w, Martin Broly2,3, Maria Rodriguez2,3, Stanley Tam2,3, Shelly A. Trigg2,3,w, Changyu Fan2,3, Song Yi2,3, Murat Tasan4, Irma Lemmens5, Xingyan Kuang6, Nan Zhao6, Dheeraj Malhotra7, Jacob J. Michaelson7,w, Vladimir Vacic8, Michael A. Calderwood2,3, Frederick P. Roth2,3,4, Jan Tavernier5, Steve Horvath9, Kourosh Salehi-Ashtiani2,3,w, Dmitry Korkin6, Jonathan Sebat7, David E. Hill2,3, Tong Hao2,3, Marc Vidal2,3 & Lilia M. Iakoucheva1 Increased risk for autism spectrum disorders (ASD) is attributed to hundreds of genetic loci. The convergence of ASD variants have been investigated using various approaches, including protein interactions extracted from the published literature. However, these datasets are frequently incomplete, carry biases and are limited to interactions of a single splicing isoform, which may not be expressed in the disease-relevant tissue. Here we introduce a new interactome mapping approach by experimentally identifying interactions between brain-expressed alternatively spliced variants of ASD risk factors. The Autism Spliceform Interaction Network reveals that almost half of the detected interactions and about 30% of the newly identified interacting partners represent contribution from splicing variants, emphasizing the importance of isoform networks. Isoform interactions greatly contribute to establishing direct physical connections between proteins from the de novo autism CNVs. Our findings demonstrate the critical role of spliceform networks for translating genetic knowledge into a better understanding of human diseases. -
Supplementary Table 3 Complete List of RNA-Sequencing Analysis of Gene Expression Changed by ≥ Tenfold Between Xenograft and Cells Cultured in 10%O2
Supplementary Table 3 Complete list of RNA-Sequencing analysis of gene expression changed by ≥ tenfold between xenograft and cells cultured in 10%O2 Expr Log2 Ratio Symbol Entrez Gene Name (culture/xenograft) -7.182 PGM5 phosphoglucomutase 5 -6.883 GPBAR1 G protein-coupled bile acid receptor 1 -6.683 CPVL carboxypeptidase, vitellogenic like -6.398 MTMR9LP myotubularin related protein 9-like, pseudogene -6.131 SCN7A sodium voltage-gated channel alpha subunit 7 -6.115 POPDC2 popeye domain containing 2 -6.014 LGI1 leucine rich glioma inactivated 1 -5.86 SCN1A sodium voltage-gated channel alpha subunit 1 -5.713 C6 complement C6 -5.365 ANGPTL1 angiopoietin like 1 -5.327 TNN tenascin N -5.228 DHRS2 dehydrogenase/reductase 2 leucine rich repeat and fibronectin type III domain -5.115 LRFN2 containing 2 -5.076 FOXO6 forkhead box O6 -5.035 ETNPPL ethanolamine-phosphate phospho-lyase -4.993 MYO15A myosin XVA -4.972 IGF1 insulin like growth factor 1 -4.956 DLG2 discs large MAGUK scaffold protein 2 -4.86 SCML4 sex comb on midleg like 4 (Drosophila) Src homology 2 domain containing transforming -4.816 SHD protein D -4.764 PLP1 proteolipid protein 1 -4.764 TSPAN32 tetraspanin 32 -4.713 N4BP3 NEDD4 binding protein 3 -4.705 MYOC myocilin -4.646 CLEC3B C-type lectin domain family 3 member B -4.646 C7 complement C7 -4.62 TGM2 transglutaminase 2 -4.562 COL9A1 collagen type IX alpha 1 chain -4.55 SOSTDC1 sclerostin domain containing 1 -4.55 OGN osteoglycin -4.505 DAPL1 death associated protein like 1 -4.491 C10orf105 chromosome 10 open reading frame 105 -4.491 -
Primate Specific Retrotransposons, Svas, in the Evolution of Networks That Alter Brain Function
Title: Primate specific retrotransposons, SVAs, in the evolution of networks that alter brain function. Olga Vasieva1*, Sultan Cetiner1, Abigail Savage2, Gerald G. Schumann3, Vivien J Bubb2, John P Quinn2*, 1 Institute of Integrative Biology, University of Liverpool, Liverpool, L69 7ZB, U.K 2 Department of Molecular and Clinical Pharmacology, Institute of Translational Medicine, The University of Liverpool, Liverpool L69 3BX, UK 3 Division of Medical Biotechnology, Paul-Ehrlich-Institut, Langen, D-63225 Germany *. Corresponding author Olga Vasieva: Institute of Integrative Biology, Department of Comparative genomics, University of Liverpool, Liverpool, L69 7ZB, [email protected] ; Tel: (+44) 151 795 4456; FAX:(+44) 151 795 4406 John Quinn: Department of Molecular and Clinical Pharmacology, Institute of Translational Medicine, The University of Liverpool, Liverpool L69 3BX, UK, [email protected]; Tel: (+44) 151 794 5498. Key words: SVA, trans-mobilisation, behaviour, brain, evolution, psychiatric disorders 1 Abstract The hominid-specific non-LTR retrotransposon termed SINE–VNTR–Alu (SVA) is the youngest of the transposable elements in the human genome. The propagation of the most ancient SVA type A took place about 13.5 Myrs ago, and the youngest SVA types appeared in the human genome after the chimpanzee divergence. Functional enrichment analysis of genes associated with SVA insertions demonstrated their strong link to multiple ontological categories attributed to brain function and the disorders. SVA types that expanded their presence in the human genome at different stages of hominoid life history were also associated with progressively evolving behavioural features that indicated a potential impact of SVA propagation on a cognitive ability of a modern human. -
Understanding the Molecular Pathobiology of Acid Ceramidase Deficiency
Understanding the Molecular Pathobiology of Acid Ceramidase Deficiency By Fabian Yu A thesis submitted in conformity with the requirements for the degree of Doctor of Philosophy Institute of Medical Science University of Toronto © Copyright by Fabian PS Yu 2018 Understanding the Molecular Pathobiology of Acid Ceramidase Deficiency Fabian Yu Doctor of Philosophy Institute of Medical Science University of Toronto 2018 Abstract Farber disease (FD) is a devastating Lysosomal Storage Disorder (LSD) caused by mutations in ASAH1, resulting in acid ceramidase (ACDase) deficiency. ACDase deficiency manifests along a broad spectrum but in its classical form patients die during early childhood. Due to the scarcity of cases FD has largely been understudied. To circumvent this, our lab previously generated a mouse model that recapitulates FD. In some case reports, patients have shown signs of visceral involvement, retinopathy and respiratory distress that may lead to death. Beyond superficial descriptions in case reports, there have been no in-depth studies performed to address these conditions. To improve the understanding of FD and gain insights for evaluating future therapies, we performed comprehensive studies on the ACDase deficient mouse. In the visual system, we reported presence of progressive uveitis. Further tests revealed cellular infiltration, lipid buildup and extensive retinal pathology. Mice developed retinal dysplasia, impaired retinal response and decreased visual acuity. Within the pulmonary system, lung function tests revealed a decrease in lung compliance. Mice developed chronic lung injury that was contributed by cellular recruitment, and vascular leakage. Additionally, we report impairment to lipid homeostasis in the lungs. ii To understand the liver involvement in FD, we characterized the pathology and performed transcriptome analysis to identify gene and pathway changes. -
ADAMTSL3 As a Candidate Gene for Schizophrenia: Gene Sequencing and Ultra-High Density Association Analysis by Imputation
Schizophrenia Research 127 (2011) 28–34 Contents lists available at ScienceDirect Schizophrenia Research journal homepage: www.elsevier.com/locate/schres ADAMTSL3 as a candidate gene for schizophrenia: Gene sequencing and ultra-high density association analysis by imputation David J. Dow a, Julie Huxley-Jones b, Jamie M. Hall a, Clyde Francks b, Peter R. Maycox a, James N.C. Kew a, Israel S. Gloger a, Nalini A.L. Mehta a, Fiona M. Kelly a, Pierandrea Muglia b, Gerome Breen c, Sarah Jugurnauth c, Inti Pederoso c, David St.Clair d, Dan Rujescu e, Michael R. Barnes b,c,⁎ a Molecular Discovery Research, GlaxoSmithKline Pharmaceuticals, New Frontiers Science Park (North), Third Avenue, Harlow, CM19 5AW, UK b Computational Biology and Genetics, Quantitative Sciences, Drug Discovery, GlaxoSmithKline Pharmaceuticals, Gunnels Wood Road, Stevenage, SG1 2NY, UK c Division of Psychological Medicine and Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King's College, London, UK d Department of Mental Health, University of Aberdeen, Aberdeen, United Kingdom e Division of Molecular and Clinical Neurobiology, Department of Psychiatry, Ludwig-Maximilians-University, Munich, Germany article info abstract Article history: We previously reported an association with a putative functional variant in the ADAMTSL3 gene, just below Received 27 July 2010 genome-wide significance in a genome-wide association study of schizophrenia. As variants impacting the Received in revised form 29 November 2010 function of ADAMTSL3 (a disintegrin-like and metalloprotease domain with thrombospondin type I motifs- Accepted 11 December 2010 like-3) could illuminate a novel disease mechanism and a potentially specific target, we have used Available online 15 January 2011 complementary approaches to further evaluate the association. -
Hras Intracellular Trafficking and Signal Transduction Jodi Ho-Jung Mckay Iowa State University
Iowa State University Capstones, Theses and Retrospective Theses and Dissertations Dissertations 2007 HRas intracellular trafficking and signal transduction Jodi Ho-Jung McKay Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/rtd Part of the Biological Phenomena, Cell Phenomena, and Immunity Commons, Cancer Biology Commons, Cell Biology Commons, Genetics and Genomics Commons, and the Medical Cell Biology Commons Recommended Citation McKay, Jodi Ho-Jung, "HRas intracellular trafficking and signal transduction" (2007). Retrospective Theses and Dissertations. 13946. https://lib.dr.iastate.edu/rtd/13946 This Dissertation is brought to you for free and open access by the Iowa State University Capstones, Theses and Dissertations at Iowa State University Digital Repository. It has been accepted for inclusion in Retrospective Theses and Dissertations by an authorized administrator of Iowa State University Digital Repository. For more information, please contact [email protected]. HRas intracellular trafficking and signal transduction by Jodi Ho-Jung McKay A dissertation submitted to the graduate faculty in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY Major: Genetics Program of Study Committee: Janice E. Buss, Co-major Professor Linda Ambrosio, Co-major Professor Diane Bassham Drena Dobbs Ted Huiatt Iowa State University Ames, Iowa 2007 Copyright © Jodi Ho-Jung McKay, 2007. All rights reserved. UMI Number: 3274881 Copyright 2007 by McKay, Jodi Ho-Jung All rights reserved. UMI Microform 3274881 Copyright 2008 by ProQuest Information and Learning Company. All rights reserved. This microform edition is protected against unauthorized copying under Title 17, United States Code. ProQuest Information and Learning Company 300 North Zeeb Road P.O.