Gene % HDV Positive Cells % Infection Compared to Sictrl P-Value FDR
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The G Protein-Coupled Receptor Subset of the Dog Genome Is More Similar
BMC Genomics BioMed Central Research article Open Access The G protein-coupled receptor subset of the dog genome is more similar to that in humans than rodents Tatjana Haitina1, Robert Fredriksson1, Steven M Foord2, Helgi B Schiöth*1 and David E Gloriam*2 Address: 1Department of Neuroscience, Functional Pharmacology, Uppsala University, BMC, Box 593, 751 24, Uppsala, Sweden and 2GlaxoSmithKline Pharmaceuticals, New Frontiers Science Park, 3rd Avenue, Harlow CM19 5AW, UK Email: Tatjana Haitina - [email protected]; Robert Fredriksson - [email protected]; Steven M Foord - [email protected]; Helgi B Schiöth* - [email protected]; David E Gloriam* - [email protected] * Corresponding authors Published: 15 January 2009 Received: 20 August 2008 Accepted: 15 January 2009 BMC Genomics 2009, 10:24 doi:10.1186/1471-2164-10-24 This article is available from: http://www.biomedcentral.com/1471-2164/10/24 © 2009 Haitina et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background: The dog is an important model organism and it is considered to be closer to humans than rodents regarding metabolism and responses to drugs. The close relationship between humans and dogs over many centuries has lead to the diversity of the canine species, important genetic discoveries and an appreciation of the effects of old age in another species. The superfamily of G protein-coupled receptors (GPCRs) is one of the largest gene families in most mammals and the most exploited in terms of drug discovery. -
Database Tool the Systematic Annotation of the Three Main GPCR
Database, Vol. 2010, Article ID baq018, doi:10.1093/database/baq018 ............................................................................................................................................................................................................................................................................................. Database tool The systematic annotation of the three main Downloaded from https://academic.oup.com/database/article-abstract/doi/10.1093/database/baq018/406672 by guest on 15 January 2019 GPCR families in Reactome Bijay Jassal1, Steven Jupe1, Michael Caudy2, Ewan Birney1, Lincoln Stein2, Henning Hermjakob1 and Peter D’Eustachio3,* 1European Bioinformatics Institute, Hinxton, Cambridge, CB10 1SD, UK, 2Ontario Institute for Cancer Research, Toronto, ON M5G 0A3, Canada and 3New York University School of Medicine, New York, NY 10016, USA *Corresponding author: Tel: +212 263 5779; Fax: +212 263 8166; Email: [email protected] Submitted 14 April 2010; Revised 14 June 2010; Accepted 13 July 2010 ............................................................................................................................................................................................................................................................................................. Reactome is an open-source, freely available database of human biological pathways and processes. A major goal of our work is to provide an integrated view of cellular signalling processes that spans from ligand–receptor -
The Attenuated Secretion of Hyaluronan by UVA
International Journal of Molecular Sciences Article The Attenuated Secretion of Hyaluronan by UVA-Exposed Human Fibroblasts Is Associated with Up- and Downregulation of HYBID and HAS2 Expression via Activated and Inactivated Signaling of the p38/ATF2 and JAK2/STAT3 Cascades Shuko Terazawa 1,†, Mariko Takada 1,†, Yoriko Sato 1, Hiroaki Nakajima 2 and Genji Imokawa 1,* 1 Center for Bioscience Research & Education, Utsunomiya University, Tochigi 321-8505, Japan; [email protected] (S.T.); [email protected] (M.T.); [email protected] (Y.S.) 2 School of Bioscience and Biotechnology, Tokyo University of Technology, Tokyo 192-0982, Japan; [email protected] * Correspondence: [email protected]; Tel.: +81-28-649-5282 † These authors contributed equally to this work. Abstract: Little is known about the effects on hyaluronan (HA) metabolism of UVA radiation. This study demonstrates that the secretion of HA by human dermal fibroblasts (HDFs) is down- Citation: Terazawa, S.; Takada, M.; regulated by UVA, accompanied by the down- and upregulation of mRNA and protein levels of Sato, Y.; Nakajima, H.; Imokawa, G. the HA-synthesizing enzyme (HAS2) and the HA-degrading protein, HYaluronan Binding protein The Attenuated Secretion of Involved in HA Depolymerization(HYBID), respectively. Signaling analysis revealed that the ex- Hyaluronan by UVA-Exposed posure distinctly elicits activation of the p38/MSK1/CREB/c-Fos/AP-1 axis, the JNK/c-Jun axis, Human Fibroblasts Is Associated and the p38/ATF-2 axis, but downregulates the phosphorylation of NF-kB and JAK/STAT3. A signal with Up- and Downregulation of inhibition study demonstrated that the inhibition of p38 significantly abrogates the UVA-accentuated HYBID and HAS2 Expression via mRNA level of HYBID. -
The Genetics of Normal and Defective Color Vision
Vision Research xxx (2011) xxx–xxx Contents lists available at ScienceDirect Vision Research journal homepage: www.elsevier.com/locate/visres Review The genetics of normal and defective color vision Jay Neitz ⇑, Maureen Neitz University of Washington, Dept. of Ophthalmology, Seattle, WA 98195, United States article info a b s t r a c t Article history: The contributions of genetics research to the science of normal and defective color vision over the previ- Received 3 July 2010 ous few decades are reviewed emphasizing the developments in the 25 years since the last anniversary Received in revised form 25 November 2010 issue of Vision Research. Understanding of the biology underlying color vision has been vaulted forward Available online xxxx through the application of the tools of molecular genetics. For all their complexity, the biological pro- cesses responsible for color vision are more accessible than for many other neural systems. This is partly Keywords: because of the wealth of genetic variations that affect color perception, both within and across species, Color vision and because components of the color vision system lend themselves to genetic manipulation. Mutations Cone photoreceptor and rearrangements in the genes encoding the long, middle, and short wavelength sensitive cone pig- Colorblindness Cone mosaic ments are responsible for color vision deficiencies and mutations have been identified that affect the Opsin genes number of cone types, the absorption spectra of the pigments, the functionality and viability of the cones, Evolution and the topography of the cone mosaic. The addition of an opsin gene, as occurred in the evolution of pri- Comparative color vision mate color vision, and has been done in experimental animals can produce expanded color vision capac- Cone photopigments ities and this has provided insight into the underlying neural circuitry. -
Splicing-Correcting Therapeutic Approaches for Retinal Dystrophies: Where Endogenous Gene Regulation and Specificity Matter
New Developments Splicing-Correcting Therapeutic Approaches for Retinal Dystrophies: Where Endogenous Gene Regulation and Specificity Matter Niccolo` Bacchi,1 Simona Casarosa,1,2 and Michela A. Denti1,3 1Centre for Integrative Biology (CIBIO) - University of Trento, Trento, Italy 2Neuroscience Institute - National Research Council (CNR), Pisa, Italy 3Neuroscience Institute - National Research Council (CNR), Padova, Italy Correspondence: Simona Casarosa, Splicing is an important and highly regulated step in gene expression. The ability to modulate Centre for Integrative Biology it can offer a therapeutic option for many genetic disorders. Antisense-mediated splicing- (CIBIO) - University of Trento, Via correction approaches have recently been successfully exploited for some genetic diseases, Sommarive 9, 38123 Trento, Italy; and are currently demonstrating safety and efficacy in different clinical trials. Their [email protected]. application for the treatment of retinal dystrophies could potentially solve a vast panel of Michela A. Denti, Centre for Inte- grative Biology (CIBIO) - University cases, as illustrated by the abundance of mutations that could be targeted and the versatility of ofTrento,ViaSommarive9,38123 the technique. In this review, we will give an insight of the different therapeutic strategies, Trento, Italy; focusing on the current status of their application for retinal dystrophies. [email protected]. Keywords: splicing correction, antisense oligonucleotides, retinal dystrophy, gene therapy SC and MAD contributed equally to the work presented here and should therefore be regarded as equivalent authors. Submitted: April 8, 2014 Accepted: April 11, 2014 Citation: Bacchi N, Casarosa S, Denti MA. Splicing-correcting therapeutic approaches for retinal dystrophies: where endogenous gene regulation and specificity matter. Invest Oph- thalmol Vis Sci. -
Transcriptomic Analysis of Native Versus Cultured Human and Mouse Dorsal Root Ganglia Focused on Pharmacological Targets Short
bioRxiv preprint doi: https://doi.org/10.1101/766865; this version posted September 12, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-ND 4.0 International license. Transcriptomic analysis of native versus cultured human and mouse dorsal root ganglia focused on pharmacological targets Short title: Comparative transcriptomics of acutely dissected versus cultured DRGs Andi Wangzhou1, Lisa A. McIlvried2, Candler Paige1, Paulino Barragan-Iglesias1, Carolyn A. Guzman1, Gregory Dussor1, Pradipta R. Ray1,#, Robert W. Gereau IV2, # and Theodore J. Price1, # 1The University of Texas at Dallas, School of Behavioral and Brain Sciences and Center for Advanced Pain Studies, 800 W Campbell Rd. Richardson, TX, 75080, USA 2Washington University Pain Center and Department of Anesthesiology, Washington University School of Medicine # corresponding authors [email protected], [email protected] and [email protected] Funding: NIH grants T32DA007261 (LM); NS065926 and NS102161 (TJP); NS106953 and NS042595 (RWG). The authors declare no conflicts of interest Author Contributions Conceived of the Project: PRR, RWG IV and TJP Performed Experiments: AW, LAM, CP, PB-I Supervised Experiments: GD, RWG IV, TJP Analyzed Data: AW, LAM, CP, CAG, PRR Supervised Bioinformatics Analysis: PRR Drew Figures: AW, PRR Wrote and Edited Manuscript: AW, LAM, CP, GD, PRR, RWG IV, TJP All authors approved the final version of the manuscript. 1 bioRxiv preprint doi: https://doi.org/10.1101/766865; this version posted September 12, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. -
Detecting Substrate Glycans of Fucosyltransferases on Glycoproteins with Fluorescent Fucose
bioRxiv preprint doi: https://doi.org/10.1101/2020.01.28.919860; this version posted January 29, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Detecting substrate glycans of fucosyltransferases on glycoproteins with fluorescent fucose Key words: Fucose/Fucosylation/fucosyltransferase/core-fucose/glycosylation Supplementary Data Included: Supplemental Fig.1 to Fig. 2 Zhengliang L Wu1*, Mark Whitaker, Anthony D Person1, Vassili Kalabokis1 1Bio-techne, R&D Systems, Inc. 614 McKinley Place N.E. Minneapolis, MN, 55413, USA *Correspondence: Phone: 612-656-4544. Email: [email protected], bioRxiv preprint doi: https://doi.org/10.1101/2020.01.28.919860; this version posted January 29, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Abstract Like sialylation, fucose usually locates at the non-reducing ends of various glycans on glycoproteins and constitutes important glycan epitopes. Detecting the substrate glycans of fucosyltransferases is important for understanding how these glycan epitopes are regulated in response to different growth conditions and external stimuli. Here we report the detection of these glycans via enzymatic incorporation of fluorescent tagged fucose using fucosyltransferases including FUT2, FUT6, FUT7, and FUT8 and FUT9. More specifically, we describe the detection of substrate glycans of FUT8 and FUT9 on therapeutic antibodies and the detection of high mannose glycans on glycoproteins by enzymatic conversion of high mannose glycans to the substrate glycans of FUT8. -
Ablation of EYS in Zebrafish Causes Mislocalisation of Outer Segment
www.nature.com/scientificreports OPEN Ablation of EYS in zebrafish causes mislocalisation of outer segment proteins, F-actin disruption and Received: 02 November 2016 Accepted: 10 March 2017 cone-rod dystrophy Published: 05 April 2017 Zhaojing Lu1,*, Xuebin Hu1,*, Fei Liu1, Dinesh C. Soares2, Xiliang Liu1, Shanshan Yu1, Meng Gao1, Shanshan Han1, Yayun Qin1, Chang Li1, Tao Jiang1, Daji Luo3, An-Yuan Guo4, Zhaohui Tang1 & Mugen Liu1 Mutations in EYS are associated with autosomal recessive retinitis pigmentosa (arRP) and autosomal recessive cone-rod dystrophy (arCRD) however, the function of EYS and the molecular mechanisms of how these mutations cause retinal degeneration are still unclear. Because EYS is absent in mouse and rat, and the structure of the retina differs substantially between humans andDrosophila , we utilised zebrafish as a model organism to study the function ofEYS in the retina. We constructed an EYS-knockout zebrafish-line by TALEN technology which showed visual impairment at an early age, while the histological and immunofluorescence assays indicated the presence of progressive retinal degeneration with a cone predominately affected pattern. These phenotypes recapitulate the clinical manifestations of arCRD patients. Furthermore, the EYS−/− zebrafish also showed mislocalisation of certain outer segment proteins (rhodopsin, opn1lw, opn1sw1, GNB3 and PRPH2), and disruption of actin filaments in photoreceptors. Protein mislocalisation may, therefore, disrupt the function of cones and rods in these zebrafish and cause photoreceptor death. Collectively, these results point to a novel role for EYS in maintaining the morphological structure of F-actin and in protein transport, loss of this function might be the trigger for the resultant cellular events that ultimately lead to photoreceptor death. -
(12) Patent Application Publication (10) Pub. No.: US 2003/0082511 A1 Brown Et Al
US 20030082511A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2003/0082511 A1 Brown et al. (43) Pub. Date: May 1, 2003 (54) IDENTIFICATION OF MODULATORY Publication Classification MOLECULES USING INDUCIBLE PROMOTERS (51) Int. Cl." ............................... C12O 1/00; C12O 1/68 (52) U.S. Cl. ..................................................... 435/4; 435/6 (76) Inventors: Steven J. Brown, San Diego, CA (US); Damien J. Dunnington, San Diego, CA (US); Imran Clark, San Diego, CA (57) ABSTRACT (US) Correspondence Address: Methods for identifying an ion channel modulator, a target David B. Waller & Associates membrane receptor modulator molecule, and other modula 5677 Oberlin Drive tory molecules are disclosed, as well as cells and vectors for Suit 214 use in those methods. A polynucleotide encoding target is San Diego, CA 92121 (US) provided in a cell under control of an inducible promoter, and candidate modulatory molecules are contacted with the (21) Appl. No.: 09/965,201 cell after induction of the promoter to ascertain whether a change in a measurable physiological parameter occurs as a (22) Filed: Sep. 25, 2001 result of the candidate modulatory molecule. Patent Application Publication May 1, 2003 Sheet 1 of 8 US 2003/0082511 A1 KCNC1 cDNA F.G. 1 Patent Application Publication May 1, 2003 Sheet 2 of 8 US 2003/0082511 A1 49 - -9 G C EH H EH N t R M h so as se W M M MP N FIG.2 Patent Application Publication May 1, 2003 Sheet 3 of 8 US 2003/0082511 A1 FG. 3 Patent Application Publication May 1, 2003 Sheet 4 of 8 US 2003/0082511 A1 KCNC1 ITREXCHO KC 150 mM KC 2000000 so 100 mM induced Uninduced Steady state O 100 200 300 400 500 600 700 Time (seconds) FIG. -
Cldn19 Clic2 Clmp Cln3
NewbornDx™ Advanced Sequencing Evaluation When time to diagnosis matters, the NewbornDx™ Advanced Sequencing Evaluation from Athena Diagnostics delivers rapid, 5- to 7-day results on a targeted 1,722-genes. A2ML1 ALAD ATM CAV1 CLDN19 CTNS DOCK7 ETFB FOXC2 GLUL HOXC13 JAK3 AAAS ALAS2 ATP1A2 CBL CLIC2 CTRC DOCK8 ETFDH FOXE1 GLYCTK HOXD13 JUP AARS2 ALDH18A1 ATP1A3 CBS CLMP CTSA DOK7 ETHE1 FOXE3 GM2A HPD KANK1 AASS ALDH1A2 ATP2B3 CC2D2A CLN3 CTSD DOLK EVC FOXF1 GMPPA HPGD K ANSL1 ABAT ALDH3A2 ATP5A1 CCDC103 CLN5 CTSK DPAGT1 EVC2 FOXG1 GMPPB HPRT1 KAT6B ABCA12 ALDH4A1 ATP5E CCDC114 CLN6 CUBN DPM1 EXOC4 FOXH1 GNA11 HPSE2 KCNA2 ABCA3 ALDH5A1 ATP6AP2 CCDC151 CLN8 CUL4B DPM2 EXOSC3 FOXI1 GNAI3 HRAS KCNB1 ABCA4 ALDH7A1 ATP6V0A2 CCDC22 CLP1 CUL7 DPM3 EXPH5 FOXL2 GNAO1 HSD17B10 KCND2 ABCB11 ALDOA ATP6V1B1 CCDC39 CLPB CXCR4 DPP6 EYA1 FOXP1 GNAS HSD17B4 KCNE1 ABCB4 ALDOB ATP7A CCDC40 CLPP CYB5R3 DPYD EZH2 FOXP2 GNE HSD3B2 KCNE2 ABCB6 ALG1 ATP8A2 CCDC65 CNNM2 CYC1 DPYS F10 FOXP3 GNMT HSD3B7 KCNH2 ABCB7 ALG11 ATP8B1 CCDC78 CNTN1 CYP11B1 DRC1 F11 FOXRED1 GNPAT HSPD1 KCNH5 ABCC2 ALG12 ATPAF2 CCDC8 CNTNAP1 CYP11B2 DSC2 F13A1 FRAS1 GNPTAB HSPG2 KCNJ10 ABCC8 ALG13 ATR CCDC88C CNTNAP2 CYP17A1 DSG1 F13B FREM1 GNPTG HUWE1 KCNJ11 ABCC9 ALG14 ATRX CCND2 COA5 CYP1B1 DSP F2 FREM2 GNS HYDIN KCNJ13 ABCD3 ALG2 AUH CCNO COG1 CYP24A1 DST F5 FRMD7 GORAB HYLS1 KCNJ2 ABCD4 ALG3 B3GALNT2 CCS COG4 CYP26C1 DSTYK F7 FTCD GP1BA IBA57 KCNJ5 ABHD5 ALG6 B3GAT3 CCT5 COG5 CYP27A1 DTNA F8 FTO GP1BB ICK KCNJ8 ACAD8 ALG8 B3GLCT CD151 COG6 CYP27B1 DUOX2 F9 FUCA1 GP6 ICOS KCNK3 ACAD9 ALG9 -
GJB4 (NM 153212) 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 RC204406 GJB4 (NM_153212) Human Tagged ORF Clone Product data: Product Type: Expression Plasmids Product Name: GJB4 (NM_153212) Human Tagged ORF Clone Tag: Myc-DDK Symbol: GJB4 Synonyms: CX30.3; EKV; EKVP2 Vector: pCMV6-Entry (PS100001) E. coli Selection: Kanamycin (25 ug/mL) Cell Selection: Neomycin ORF Nucleotide >RC204406 ORF sequence Sequence: Red=Cloning site Blue=ORF Green=Tags(s) TTTTGTAATACGACTCACTATAGGGCGGCCGGGAATTCGTCGACTGGATCCGGTACCGAGGAGATCTGCC GCCGCGATCGCC ATGAACTGGGCATTTCTGCAGGGCCTGCTGAGTGGCGTGAACAAGTACTCCACAGTGCTGAGCCGCATCT GGCTGTCTGTGGTGTTCATCTTTCGTGTGCTGGTGTACGTGGTGGCAGCGGAGGAGGTGTGGGACGATGA GCAGAAGGACTTTGTCTGCAACACCAAGCAGCCCGGCTGCCCCAACGTCTGCTATGACGAGTTCTTCCCC GTGTCCCACGTGCGCCTCTGGGCCCTACAGCTCATCCTGGTCACGTGCCCCTCACTGCTCGTGGTCATGC ACGTGGCCTACCGCGAGGAACGCGAGCGCAAGCACCACCTGAAACACGGGCCCAATGCCCCGTCCCTGTA CGACAACCTGAGCAAGAAGCGGGGCGGACTGTGGTGGACGTACTTGCTGAGCCTCATCTTCAAGGCCGCC GTGGATGCTGGCTTCCTCTATATCTTCCACCGCCTCTACAAGGATTATGACATGCCCCGCGTGGTGGCCT GCTCCGTGGAGCCTTGCCCCCACACTGTGGACTGTTACATCTCCCGGCCCACGGAGAAGAAGGTCTTCAC CTACTTCATGGTGACCACAGCTGCCATCTGCATCCTGCTCAACCTCAGTGAAGTCTTCTACCTGGTGGGC AAGAGGTGCATGGAGATCTTCGGCCCCAGGCACCGGCGGCCTCGGTGCCGGGAATGCCTACCCGATACGT GCCCACCATATGTCCTCTCCCAGGGAGGGCACCCTGAGGATGGGAACTCTGTCCTAATGAAGGCTGGGTC GGCCCCAGTGGATGCAGGTGGGTATCCA ACGCGTACGCGGCCGCTCGAGCAGAAACTCATCTCAGAAGAGGATCTGGCAGCAAATGATATCCTGGATT -
Ion Channels
UC Davis UC Davis Previously Published Works Title THE CONCISE GUIDE TO PHARMACOLOGY 2019/20: Ion channels. Permalink https://escholarship.org/uc/item/1442g5hg Journal British journal of pharmacology, 176 Suppl 1(S1) ISSN 0007-1188 Authors Alexander, Stephen PH Mathie, Alistair Peters, John A et al. Publication Date 2019-12-01 DOI 10.1111/bph.14749 License https://creativecommons.org/licenses/by/4.0/ 4.0 Peer reviewed eScholarship.org Powered by the California Digital Library University of California S.P.H. Alexander et al. The Concise Guide to PHARMACOLOGY 2019/20: Ion channels. British Journal of Pharmacology (2019) 176, S142–S228 THE CONCISE GUIDE TO PHARMACOLOGY 2019/20: Ion channels Stephen PH Alexander1 , Alistair Mathie2 ,JohnAPeters3 , Emma L Veale2 , Jörg Striessnig4 , Eamonn Kelly5, Jane F Armstrong6 , Elena Faccenda6 ,SimonDHarding6 ,AdamJPawson6 , Joanna L Sharman6 , Christopher Southan6 , Jamie A Davies6 and CGTP Collaborators 1School of Life Sciences, University of Nottingham Medical School, Nottingham, NG7 2UH, UK 2Medway School of Pharmacy, The Universities of Greenwich and Kent at Medway, Anson Building, Central Avenue, Chatham Maritime, Chatham, Kent, ME4 4TB, UK 3Neuroscience Division, Medical Education Institute, Ninewells Hospital and Medical School, University of Dundee, Dundee, DD1 9SY, UK 4Pharmacology and Toxicology, Institute of Pharmacy, University of Innsbruck, A-6020 Innsbruck, Austria 5School of Physiology, Pharmacology and Neuroscience, University of Bristol, Bristol, BS8 1TD, UK 6Centre for Discovery Brain Science, University of Edinburgh, Edinburgh, EH8 9XD, UK Abstract The Concise Guide to PHARMACOLOGY 2019/20 is the fourth in this series of biennial publications. The Concise Guide provides concise overviews of the key properties of nearly 1800 human drug targets with an emphasis on selective pharmacology (where available), plus links to the open access knowledgebase source of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties.