Human Histidyl-Trna Synthetase / HARS

AR10151PU-S OriGene Technologies Inc. OriGene EU Acris Antibodies GmbH 9620 Medical Center Drive, Ste 200 Schillerstr. 5 Rockville, MD 20850 32052 Herford UNITED STATES GERMANY Phone: +1-858-888-7900 Phone: +49-5221-34606-0 Fax: +1-858-888-7904 Fax: +49-5221-34606-11 [email protected] [email protected] Human Histidyl-tRNA synthetase / HARS - Purified Alternate names: HRS, HisRS, Histidine-tRNA ligase, JO1, Jo-1 antigen Catalog No.: AR10151PU-S Quantity: 10 µg Concentration: 1.2 mg/ml Background: Aminoacyl-tRNA synthetases are a class of enzymes that charge tRNAs with their cognate amino acids. The protein encoded by this gene is a cytoplasmic enzyme which belongs to the class II family of aminoacyl-tRNA synthetases. The enzyme is responsible for the synthesis of histidyl-transfer RNA, which is essential for the incorporation of histidine into proteins. The gene is located in a head-to-head orientation with HARSL on chromosome five, where the homologous genes share a bidirectional promoter. The gene product is a frequent target of autoantibodies in the human autoimmune disease polymyositis/dermatomyositis. Uniprot ID: P12081 NCBI: NP_002100.2 GeneID: 3035 Species: Human Source: E. coli Format: State: Sterile Filtered clear solution. Purity: >90.0% as determined by both RP-HPLC and SDS-PAGE. Buffer System: 150mM NaCl and 10mM Sodium Phosphate, pH 7.2 Preservatives: 0.09% Sodium Azide Applications: Western Blot: Strongly reactive with Human anti Histidyl-tRNA Synthetase antisera. Other applications not tested. Optimal dilutions are dependent on conditions and should be determined by the user. Description: Histidyl-tRNA Synthetase Human Recombinant produced in E.coli is a single, non- glycosylated, polypeptide chain having a Molecular Mass of 55 kDa. The Histidyl-tRNA Synthetase is purified by proprietary chromatographic techniques. Molecular weight: 55 kDa Add. Information: Protein content: Protein quantitation was carried out by using 0.25-2.0 mg/ml Bra dford assay vs. BSA. Storage: Histidyl-tRNA Synthetase although stable at 2-8°C for 3 weeks, should be stored desiccated below -18°C. Avoid repeated freezing and thawing. Shelf life: one year from despatch. For research and in vitro use only. Not for diagnostic or therapeutic work. MS/20120827 Material Safety Datasheets are available at www.acris-antibodies.com or on request. Acris Antibodies is now part of the OriGene family. Learn more at www.origene.com 1 / 1 Powered by TCPDF (www.tcpdf.org).

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Genomic Correlates of Relationship QTL Involved in Fore- Versus Hind Limb Divergence in Mice
Loyola University Chicago Loyola eCommons Biology: Faculty Publications and Other Works Faculty Publications 2013 Genomic Correlates of Relationship QTL Involved in Fore- Versus Hind Limb Divergence in Mice Mihaela Palicev Gunter P. Wagner James P. Noonan Benedikt Hallgrimsson James M. Cheverud Loyola University Chicago, [email protected] Follow this and additional works at: https://ecommons.luc.edu/biology_facpubs Part of the Biology Commons Recommended Citation Palicev, M, GP Wagner, JP Noonan, B Hallgrimsson, and JM Cheverud. "Genomic Correlates of Relationship QTL Involved in Fore- Versus Hind Limb Divergence in Mice." Genome Biology and Evolution 5(10), 2013. This Article is brought to you for free and open access by the Faculty Publications at Loyola eCommons. It has been accepted for inclusion in Biology: Faculty Publications and Other Works by an authorized administrator of Loyola eCommons. For more information, please contact [email protected]. This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License. © Palicev et al., 2013. GBE Genomic Correlates of Relationship QTL Involved in Fore- versus Hind Limb Divergence in Mice Mihaela Pavlicev1,2,*, Gu¨ nter P. Wagner3, James P. Noonan4, Benedikt Hallgrı´msson5,and James M. Cheverud6 1Konrad Lorenz Institute for Evolution and Cognition Research, Altenberg, Austria 2Department of Pediatrics, Cincinnati Children‘s Hospital Medical Center, Cincinnati, Ohio 3Yale Systems Biology Institute and Department of Ecology and Evolutionary Biology, Yale University 4Department of Genetics, Yale University School of Medicine 5Department of Cell Biology and Anatomy, The McCaig Institute for Bone and Joint Health and the Alberta Children’s Hospital Research Institute for Child and Maternal Health, University of Calgary, Calgary, Canada 6Department of Anatomy and Neurobiology, Washington University *Corresponding author: E-mail: [email protected].
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