Rabbit Anti-GOLGA8H/FITC Conjugated Antibody-SL16258R

Total Page:16

File Type:pdf, Size:1020Kb

Rabbit Anti-GOLGA8H/FITC Conjugated Antibody-SL16258R SunLong Biotech Co.,LTD Tel: 0086-571- 56623320 Fax:0086-571- 56623318 E-mail:[email protected] www.sunlongbiotech.com Rabbit Anti-GOLGA8H/FITC Conjugated antibody SL16258R-FITC Product Name: Anti-GOLGA8H/FITC Chinese Name: FITC标记的高尔基体自身蛋白8H抗体 GOLGA6L11; GOG8H_HUMAN; Golgin A8 family, member H; Golgin subfamily A Alias: member 8H. Organism Species: Rabbit Clonality: Polyclonal React Species: Human, ICC=1:50-200IF=1:50-200 Applications: not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. Molecular weight: 71kDa Form: Lyophilized or Liquid Concentration: 1mg/ml immunogen: KLH conjugated synthetic peptide derived from human GOLGA8H Lsotype: IgG Purification: affinity purified by Protein A Storage Buffer: 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. Storewww.sunlongbiotech.com at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year Storage: when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. background: The Golgi complex plays an essential role in the post-translational modification and sorting of proteins transported from the endoplasmic reticulum (ER). The Golgi stack consists of a distinct cis face, or entry face, and a trans face, or exit face, which are Product Detail: connected via the cis, medial and trans Golgi networks. GOLGA8H (putative golgin subfamily A member 8I) is a 632 amino acid protein that belongs to the GOLGA8 family. Localizing to Golgi apparatus, GOLGA8H may play a role in Golgi structure maintenance. The gene encoding GOLGA8H maps to human chromosome 15, which houses over 700 genes and comprises nearly 3% of the human genome. Angelman syndrome, Prader-Willi syndrome, Tay-Sachs disease and Marfan syndrome are all associated with defects in chromosome 15-localized genes. Subcellular Location: Golgi Apparatus Similarity: Belongs to the GOLGA8 family. Database links: Entrez Gene: 728498 Human SwissProt: P0CJ92 Human Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. www.sunlongbiotech.com.
Recommended publications
  • Gene Expression Profiles Complement the Analysis of Genomic Modifiers of the Clinical Onset of Huntington Disease
    bioRxiv preprint doi: https://doi.org/10.1101/699033; this version posted July 11, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 1 Gene expression profiles complement the analysis of genomic modifiers of the clinical onset of Huntington disease Galen E.B. Wright1,2,3; Nicholas S. Caron1,2,3; Bernard Ng1,2,4; Lorenzo Casal1,2,3; Xiaohong Xu5; Jolene Ooi5; Mahmoud A. Pouladi5,6,7; Sara Mostafavi1,2,4; Colin J.D. Ross3,7 and Michael R. Hayden1,2,3* 1Centre for Molecular Medicine and Therapeutics, Vancouver, British Columbia, Canada; 2Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada; 3BC Children’s Hospital Research Institute, Vancouver, British Columbia, Canada; 4Department of Statistics, University of British Columbia, Vancouver, British Columbia, Canada; 5Translational Laboratory in Genetic Medicine (TLGM), Agency for Science, Technology and Research (A*STAR), Singapore; 6Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore; 7Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore; 8Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, British Columbia, Canada; *Corresponding author ABSTRACT Huntington disease (HD) is a neurodegenerative disorder that is caused by a CAG repeat expansion in the HTT gene. In an attempt to identify genomic modifiers that contribute towards the age of onset of HD, we performed a transcriptome wide association study assessing heritable differences in genetically determined expression in diverse tissues, employing genome wide data from over 4,000 patients.
    [Show full text]
  • Improving the Detection of Genomic Rearrangements in Short Read Sequencing Data
    Improving the detection of genomic rearrangements in short read sequencing data Daniel Lee Cameron orcid.org/0000-0002-0951-7116 Doctor of Philosophy July 2017 Department of Medical Biology, University of Melbourne Bioinformatics Division, Walter and Eliza Hall Institute of Medical Research Submitted in total fulfilment of the requirements of the degree of Doctor of Philosophy Produced on archival quality paper Page i Abstract Genomic rearrangements, also known as structural variants, play a significant role in the development of cancer and in genetic disorders. With the bulk of genetic studies focusing on single nucleotide variants and small insertions and deletions, structural variants are often overlooked. In part this is due to the increased complexity of analysis required, but is also due to the increased difficulty of detection. The identification of genomic rearrangements using massively parallel sequencing remains a major challenge. To address this, I have developed the Genome Rearrangement Identification Software Suite (GRIDSS). In this thesis, I show that high sensitivity and specificity can be achieved by performing reference-guided assembly prior to variant calling and incorporating the results of this assembly into the variant calling process itself. Utilising a novel genome-wide break-end assembly approach, GRIDSS halves the false discovery rate compared to other recent methods on human cell line data. A comparison of assembly approaches reveals that incorporating read alignment information into a positional de Bruijn graph improves assembly quality compared to traditional de Bruijn graph assembly. To characterise the performance of structural variant calling software, I have performed the most comprehensive benchmarking of structural variant calling software to date.
    [Show full text]
  • SUPPLEMENTARY APPENDIX MLL Partial Tandem Duplication Leukemia Cells Are Sensitive to Small Molecule DOT1L Inhibition
    SUPPLEMENTARY APPENDIX MLL partial tandem duplication leukemia cells are sensitive to small molecule DOT1L inhibition Michael W.M. Kühn, 1* Michael J. Hadler, 1* Scott R. Daigle, 2 Richard P. Koche, 1 Andrei V. Krivtsov, 1 Edward J. Olhava, 2 Michael A. Caligiuri, 3 Gang Huang, 4 James E. Bradner, 5 Roy M. Pollock, 2 and Scott A. Armstrong 1,6 1Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY; 2Epizyme, Inc., Cambridge, MA; 3The Compre - hensive Cancer Center, The Ohio State University, Columbus, OH; 4Divisions of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH; 5Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA; 6Department of Pe - diatrics, Memorial Sloan Kettering Cancer Center, New York, NY, USA Correspondence: [email protected] doi:10.3324/haematol.2014.115337 SUPPLEMENTAL METHODS, TABLES, RESULTS, AND FIGURE LEGENDS MLL-PTD leukemia cells are sensitive to small molecule DOT1L inhibition Michael J. Hadler1,*, Michael W.M. Kühn1,*, Scott R. Daigle3, Richard P. Koche1, Andrei V. Krivtsov1, Edward J. Olhava3, Michael A. Caligiuri4, Gang Huang5, James E. Bradner6, Roy M. Pollock3, and Scott A. Armstrong1,2 1Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA; 2Department of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, NY, USA; 3Epizyme, Inc., Cambridge, MA, USA; 4The Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA; 5Divisions of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA; 6Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
    [Show full text]
  • Identification of Genetic Factors Underpinning Phenotypic Heterogeneity in Huntington’S Disease and Other Neurodegenerative Disorders
    Identification of genetic factors underpinning phenotypic heterogeneity in Huntington’s disease and other neurodegenerative disorders. By Dr Davina J Hensman Moss A thesis submitted to University College London for the degree of Doctor of Philosophy Department of Neurodegenerative Disease Institute of Neurology University College London (UCL) 2020 1 I, Davina Hensman Moss confirm that the work presented in this thesis is my own. Where information has been derived from other sources, I confirm that this has been indicated in the thesis. Collaborative work is also indicated in this thesis. Signature: Date: 2 Abstract Neurodegenerative diseases including Huntington’s disease (HD), the spinocerebellar ataxias and C9orf72 associated Amyotrophic Lateral Sclerosis / Frontotemporal dementia (ALS/FTD) do not present and progress in the same way in all patients. Instead there is phenotypic variability in age at onset, progression and symptoms. Understanding this variability is not only clinically valuable, but identification of the genetic factors underpinning this variability has the potential to highlight genes and pathways which may be amenable to therapeutic manipulation, hence help find drugs for these devastating and currently incurable diseases. Identification of genetic modifiers of neurodegenerative diseases is the overarching aim of this thesis. To identify genetic variants which modify disease progression it is first necessary to have a detailed characterization of the disease and its trajectory over time. In this thesis clinical data from the TRACK-HD studies, for which I collected data as a clinical fellow, was used to study disease progression over time in HD, and give subjects a progression score for subsequent analysis. In this thesis I show blood transcriptomic signatures of HD status and stage which parallel HD brain and overlap with Alzheimer’s disease brain.
    [Show full text]
  • Characterizing Genomic Duplication in Autism Spectrum Disorder by Edward James Higginbotham a Thesis Submitted in Conformity
    Characterizing Genomic Duplication in Autism Spectrum Disorder by Edward James Higginbotham A thesis submitted in conformity with the requirements for the degree of Master of Science Graduate Department of Molecular Genetics University of Toronto © Copyright by Edward James Higginbotham 2020 i Abstract Characterizing Genomic Duplication in Autism Spectrum Disorder Edward James Higginbotham Master of Science Graduate Department of Molecular Genetics University of Toronto 2020 Duplication, the gain of additional copies of genomic material relative to its ancestral diploid state is yet to achieve full appreciation for its role in human traits and disease. Challenges include accurately genotyping, annotating, and characterizing the properties of duplications, and resolving duplication mechanisms. Whole genome sequencing, in principle, should enable accurate detection of duplications in a single experiment. This thesis makes use of the technology to catalogue disease relevant duplications in the genomes of 2,739 individuals with Autism Spectrum Disorder (ASD) who enrolled in the Autism Speaks MSSNG Project. Fine-mapping the breakpoint junctions of 259 ASD-relevant duplications identified 34 (13.1%) variants with complex genomic structures as well as tandem (193/259, 74.5%) and NAHR- mediated (6/259, 2.3%) duplications. As whole genome sequencing-based studies expand in scale and reach, a continued focus on generating high-quality, standardized duplication data will be prerequisite to addressing their associated biological mechanisms. ii Acknowledgements I thank Dr. Stephen Scherer for his leadership par excellence, his generosity, and for giving me a chance. I am grateful for his investment and the opportunities afforded me, from which I have learned and benefited. I would next thank Drs.
    [Show full text]
  • Ülevaade Põhimõtetest Ning Teise Põlvkonna Sekveneerimise Võimalike Artefaktsete Snvde Annoteerimine
    TARTU ÜLIKOOL LOODUS- JA TÄPPISTEADUSTE VALDKOND MOLEKULAAR- JA RAKUBIOLOOGIA INSTITUUT BIOINFORMAATIKA ÕPPETOOL Anna Smertina Inimgenoomi ühenukleotiidiliste variatsioonide annotatsioon – ülevaade põhimõtetest ning teise põlvkonna sekveneerimise võimalike artefaktsete SNVde annoteerimine Bakalaureusetöö Maht: 12 EAP Juhendaja PhD Ulvi Gerst Talas TARTU 2016 Inimgenoomi ühenukleotiidiliste variatsioonide annotatsioon – ülevaade põhimõtetest ning teise põlvkonna sekveneerimise võimalike artefaktsete SNVde annoteerimine Teise põlvkonna sekveneerimine võimaldab tänu oma kiirusele ja suhtelisele odavusele järjestada kiiresti palju genoome, mille baasil on võimalik läbi viia nii ülegenoomseid assotsiatsiooniuuringuid kui ka kasutada andmeid kliinilises praktikas. Mõlemad lähenemised sõltuvad tugevalt SNVde ja teiste variatsioonide õigest tuvastamisest ning täpsest annotatsioonist. Antud töös tutvustatakse SNVde annoteerimise protsessi ja selle eripärasid, tuuakse välja annotatsiooni tõlgendamise erinevused lähtuvalt erinevatest tööriistadest ning andmebaasidest. Töö praktilises pooles näidatakse, et valepositiivselt tuvastatud SNVd võivad annoteerimise ja tulemuste tõlgendamise põhjal olla näiliselt füsioloogiliselt olulised. Artefaktsete SNVde tuvastamisega arvestamine võimaldab vältida vigaste andmete põhjal tehtud ekslikke järeldusi. Märksõnad: teise põlvkonna sekveneerimine, annoteerimine, SNV, bioinformaatika CERCS: B110 Bioinformaatika, meditsiiniinformaatika Annotation of single nucleotide variants in human genome: an overview and annotation
    [Show full text]
  • The Small RNA Content of Human Sperm Reveals Pseudogene-Derived Pirnas Complementary to Protein-Coding Genes
    Downloaded from rnajournal.cshlp.org on October 2, 2021 - Published by Cold Spring Harbor Laboratory Press BIOINFORMATICS The small RNA content of human sperm reveals pseudogene-derived piRNAs complementary to protein-coding genes LORENA PANTANO,1 MERITXELL JODAR,2 MADS BAK,3,4 JOSEP LLUÍS BALLESCÀ,5 NIELS TOMMERUP,3,4 RAFAEL OLIVA,2 and TANYA VAVOURI1,6 1Institute of Predictive and Personalized Medicine of Cancer (IMPPC), Can Ruti Campus, Badalona, Barcelona 08916, Spain 2Genetics Unit, Department of Physiological Sciences, University of Barcelona, Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Biochemistry and Molecular Genetics Service, Hospital Clinic, 08036 Barcelona, Spain 3Center for non-coding RNA in Technology and Health (RTH), University of Copenhagen, DK-2200 Copenhagen, Denmark 4Wilhelm Johannsen Centre for Functional Genome Research, Department of Cellular and Molecular Medicine, Faculty of Health Science, University of Copenhagen, DK-2200 Copenhagen, Denmark 5Andrology Unit, Institut Clínic de Ginecologia, Obstetricia i Neonatologia, Hospital Clínic, 08036 Barcelona, Spain 6Josep Carreras Leukaemia Research Institute (IJC), ICO-Hospital GermansTrias i Pujol, Badalona, Barcelona 08916, Spain ABSTRACT At the end of mammalian sperm development, sperm cells expel most of their cytoplasm and dispose of the majority of their RNA. Yet, hundreds of RNA molecules remain in mature sperm. The biological significance of the vast majority of these molecules is unclear. To better understand the processes that generate sperm small RNAs and what roles they may have, we sequenced and characterized the small RNA content of sperm samples from two human fertile individuals. We detected 182 microRNAs, some of which are highly abundant. The most abundant microRNA in sperm is miR-1246 with predicted targets among sperm- specific genes.
    [Show full text]
  • Table S2 A375P Vs SK-MEL-2
    Supplemental Data: Table S2 tracking_id A375P SK-MEL2 Fold change des ZEB2-AS1 1.35E-286 0.315166 2.3284E+285 ZEB2 antisense RNA 1 PCDHGC5 5.45E-242 0.284138 5.2132E+240 protocadherin gamma subfamily C, 5 APOBEC3B-AS1 3.98E-240 0.130813 3.2873E+238 APOBEC3B antisense RNA 1 C6orf201 1.14E-227 0.15186 1.3345E+226 chromosome 6 open reading frame 201 LRRC24 1.93E-168 0.459062 2.3783E+167 leucine rich repeat containing 24 ZACN 3.22E-158 0.0670639 2.0857E+156 zinc activated ligand-gated ion channel LOC100506071 1.62E-144 3.33E-38 2.0564E+106 uncharacterized LOC100506071 EGFR-AS1 4.29E-101 0.0771076 1.7966E+99 EGFR antisense RNA 1 PRR5-ARHGAP8 3.44E-103 3.89E-10 1.13143E+93 PRR5-ARHGAP8 readthrough LOC100129148 8.77E-284 2.60E-214 2.96023E+69 uncharacterized LOC100129148 VLDLR-AS1 3.00E-65 0.0959249 3.20259E+63 VLDLR antisense RNA 1 ZASP 4.04E-72 4.00E-16 9.91857E+55 ZO-2 associated speckle protein SYNE1-AS1 7.86E-57 0.166307 2.11625E+55 SYNE1 antisense RNA 1 MED4-AS1 8.51E-47 0.193771 2.27656E+45 MED4 antisense RNA 1 MSTO2P 2.80E-42 0.111398 3.97942E+40 misato family member 2, pseudogene CABP7 2.99E-36 0.0263724 8.82596E+33 calcium binding protein 7 KCTD14 1.36E-151 3.05E-121 2.23303E+30 potassium channel tetramerization domain containing 14 RAET1E-AS1 1.26E-31 0.215175 1.71406E+30 RAET1E antisense RNA 1 ST7-OT3 2.06E-30 0.0817968 3.98019E+28 ST7 overlapping transcript 3 PKLR 3.86E-28 0.0268357 6.9509E+25 pyruvate kinase, liver and RBC LY75-CD302 2.64E-26 0.184984 7.01824E+24 LY75-CD302 readthrough TMEM189-UBE2V1 7.87E-23 0.322541 4.09933E+21
    [Show full text]
  • Identification and Replication of RNA-Seq Gene Network Modules
    University of Nebraska - Lincoln DigitalCommons@University of Nebraska - Lincoln Educational Psychology Papers and Publications Educational Psychology, Department of 2018 Identification and eplicationr of RNA-Seq gene network modules associated with depression severity Trang T. Le Jonathan Savitz Hideo Suzuki Masaya Misaki T. Kent Teague See next page for additional authors Follow this and additional works at: https://digitalcommons.unl.edu/edpsychpapers Part of the Child Psychology Commons, Cognitive Psychology Commons, Developmental Psychology Commons, and the School Psychology Commons This Article is brought to you for free and open access by the Educational Psychology, Department of at DigitalCommons@University of Nebraska - Lincoln. It has been accepted for inclusion in Educational Psychology Papers and Publications by an authorized administrator of DigitalCommons@University of Nebraska - Lincoln. Authors Trang T. Le, Jonathan Savitz, Hideo Suzuki, Masaya Misaki, T. Kent Teague, Bill C. White, Julie H. Marino, Graham Wiley, Patrick M. Gaffney, Wayne C. Drevets, Brett A. McKinney, and Jerzy Bodurka Le et al. Translational Psychiatry (2018) 8:180 DOI 10.1038/s41398-018-0234-3 Translational Psychiatry ARTICLE Open Access Identification and replication of RNA-Seq gene network modules associated with depression severity Trang T. Le1,2, Jonathan Savitz2,3, Hideo Suzuki2,4, Masaya Misaki2,T.KentTeague5,6,7, Bill C. White 8, Julie H. Marino9, Graham Wiley10, Patrick M. Gaffney10, Wayne C. Drevets11, Brett A. McKinney1,8 and Jerzy Bodurka2,12 Abstract Genomic variation underlying major depressive disorder (MDD) likely involves the interaction and regulation of multiple genes in a network. Data-driven co-expression network module inference has the potential to account for variation within regulatory networks, reduce the dimensionality of RNA-Seq data, and detect significant gene- expression modules associated with depression severity.
    [Show full text]
  • Runs of Homozygosity in Sub-Saharan African Populations Provide Insights Into a Complex
    bioRxiv preprint doi: https://doi.org/10.1101/470583; this version posted November 14, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 1 Runs of Homozygosity in sub-Saharan African populations provide insights into a complex 2 demographic and health history 3 Francisco C. Ceballos1, Scott Hazelhurst1,3 and Michele Ramsay1,2 4 Affiliations 5 1. Sydney Brenner Institute for Molecular Bioscience, Faculty of Health Sciences, University of the 6 Witwatersrand, Johannesburg, South Africa. 7 2. Division of Human Genetics, School of Pathology, Faculty of Health Sciences, University of the 8 Witwatersrand, Johannesburg, South Africa. 9 3. School of Electrical & Information Engineering, University of the Witwatersrand, Johannesburg, South 10 Africa. 11 Correspondence Author: [email protected] 12 Abstract 13 The study of runs of homozygosity (ROH), contiguous regions in the genome where an individual is 14 homozygous across all sites, can shed light on the demographic history and cultural practices. We present 15 a fine-scale ROH analysis of 1679 individuals from 28 sub-Saharan African (SSA) populations along with 16 1384 individuals from 17 world-wide populations. Using high-density SNP coverage, we could accurately 17 obtain ROH as low as 300Kb using PLINK software. The analyses showed a heterogeneous distribution of 18 autozygosity across SSA, revealing a complex demographic history. They highlight differences between 19 African groups and can differentiate between the impact of consanguineous practices (e.g. among the 20 Somali) and endogamy (e.g. among several Khoe-San groups1).
    [Show full text]
  • Supplementary Figure 1. the TLR4/NF-Κb Signalling Axis Was Activated In
    Supplementary Figure 1. The TLR4/NF-κB signalling axis was activated in sarcopenia patient samples Three-paired muscle tissues from healthy controls and sarcopenia patients were subjected to total protein extraction and isolation of the cytoplasmic and nuclear protein fractions. (A and B) The protein levels of TLR4, MyD88, TRAF4, p50 and p65 in total cell extracts. Total cell extracts were subjected to immunoblot analyses to determine protein levels of TLR4, MyD88, TRAF4, p50 and p65. GAPDH was used as a loading control (A). (B) The quantified protein levels in (A). ** P < 0.01. (C and D) The protein levels of p50 and p65 in the cytoplasmic and nuclear protein fractions. The purified cytoplasmic and nuclear fractions were subjected to immunoblot analyses to determine protein levels of p50 and p65. β-actin and HDAC1 were used as loading controls. (D) The quantified protein levels in (C). ** P < 0.01. Supplementary Figure 2. The effects of LPS and IL-1β on miR-532-3p and its downstream molecules (A) The relative protein levels of BAK1 and Caspases in sarcopenia samples. The protein signals in Figure 5B were quantified using Image J software. The protein levels of BAK1 in Control-1 was defined as one-fold. The protein levels of C-Caspase3 and C-caspase-9 in sarcopenia-1 were defined as one-fold. *** P < 0.001. (B) The effects of different concentrations of LPS and IL-1β on the expression of miR-532-3p and BAK1. The HSMM-1 cells were treated with different concentrations of LPS (0, 50, 100 and 200 ng/mL) and IL-1β (0, 1, 5 and 25 ng/mL), followed by qRT-PCR analyses to examine the expression of miR-532-3p and BAK1.
    [Show full text]
  • W O 2014/074847 a L 1 5 May 2014 (15.05.2014) P O P C T
    (12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date W O 2014/074847 A l 1 5 May 2014 (15.05.2014) P O P C T (51) International Patent Classification: (81) Designated States (unless otherwise indicated, for every C12Q 1/68 (2006.01) G01N 33/48 (2006.01) kind of national protection available): AE, AG, AL, AM, C12N 15/11 (2006.01) AO, AT, AU, AZ, BA, BB, BG, BH, BN, BR, BW, BY, BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, (21) International Application Number: DO, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, PCT/US20 13/069 192 HN, HR, HU, ID, IL, IN, IR, IS, JP, KE, KG, KN, KP, KR, (22) International Filing Date: KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, ME, 8 November 2013 (08.1 1.2013) MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, OM, PA, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SA, (25) Filing Language: English SC, SD, SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, (26) Publication Language: English TN, TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. (30) Priority Data: 61/724,707 ' November 2012 (09. 11.2012) US (84) Designated States (unless otherwise indicated, for every kind of regional protection available): ARIPO (BW, GH, (71) Applicant: THE JOHNS HOPKINS UNIVERSITY GM, KE, LR, LS, MW, MZ, NA, RW, SD, SL, SZ, TZ, [US/US]; 3400 N.
    [Show full text]