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Produktinformation Diagnostik & molekulare Diagnostik Laborgeräte & Service Zellkultur & Verbrauchsmaterial Forschungsprodukte & Biochemikalien Weitere Information auf den folgenden Seiten! See the following pages for more information! Lieferung & Zahlungsart Lieferung: frei Haus Bestellung auf Rechnung SZABO-SCANDIC Lieferung: € 10,- HandelsgmbH & Co KG Erstbestellung Vorauskassa Quellenstraße 110, A-1100 Wien T. +43(0)1 489 3961-0 Zuschläge F. +43(0)1 489 3961-7 [email protected] • Mindermengenzuschlag www.szabo-scandic.com • Trockeneiszuschlag • Gefahrgutzuschlag linkedin.com/company/szaboscandic • Expressversand facebook.com/szaboscandic ANKRD17 monoclonal antibody (M01A), clone 1D8 Catalog # : H00026057-M01A 規格 : [ 200 uL ] List All Specification Application Image Product Mouse monoclonal antibody raised against a partial recombinant ELISA Description: ANKRD17. Immunogen: ANKRD17 (NP_115593, 2501 a.a. ~ 2603 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa. Sequence: ERDSTGIVTPSGTFHQHVPAGYMDFPKVGGMPFSVYGNAMIPPVAPIPD GAGGPIFNGPHAADPSWNSLIKMVSSSTENNGPQTVWTGPWAPHMNSV HMNQLG Host: Mouse Reactivity: Human Isotype: IgG1 Kappa Quality Control Antibody Reactive Against Recombinant Protein. Testing: Storage Buffer: In ascites fluid Storage Store at -20°C or lower. Aliquot to avoid repeated freezing and thawing. Instruction: MSDS: Download Datasheet: Download Applications ELISA Gene Information Entrez GeneID: 26057 GeneBank NM_032217 Accession#: Protein NP_115593 Accession#: Gene Name: ANKRD17 Gene Alias: FLJ22206,GTAR,KIAA0697,NY-BR-16 Gene ankyrin repeat domain 17 Description: Gene Ontology: Hyperlink Page 1 of 2 2020/6/25 Gene Summary: This gene encodes a protein with ankyrin repeats, which are associated with protein-protein interactions. Studies in mice suggest that this protein is involved in liver development. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq Other ankyrin repeat domain protein 17,gene trap ankyrin repeat,serologically Designations: defined breast cancer antigen NY-BR-16 Related Disease Osteoporosis Tobacco Use Disorder 服務條款 | 隱私權政策 | 著作及商標 | 網站地圖 ©2020 亞諾法生技股份有限公司 Abnova Corporation. 版權所有. Page 2 of 2 2020/6/25.

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Supplemental information Dissection of the genomic structure of the miR-183/96/182 gene. Previously, we showed that the miR-183/96/182 cluster is an intergenic miRNA cluster, located in a ~60-kb interval between the genes encoding nuclear respiratory factor-1 (Nrf1) and ubiquitin-conjugating enzyme E2H (Ube2h) on mouse chr6qA3.3 (1). To start to uncover the genomic structure of the miR- 183/96/182 gene, we first studied genomic features around miR-183/96/182 in the UCSC genome browser (http://genome.UCSC.edu/), and identified two CpG islands 3.4-6.5 kb 5’ of pre-miR-183, the most 5’ miRNA of the cluster (Fig. 1A; Fig. S1 and Seq. S1). A cDNA clone, AK044220, located at 3.2-4.6 kb 5’ to pre-miR-183, encompasses the second CpG island (Fig. 1A; Fig. S1). We hypothesized that this cDNA clone was derived from 5’ exon(s) of the primary transcript of the miR-183/96/182 gene, as CpG islands are often associated with promoters (2). Supporting this hypothesis, multiple expressed sequences detected by gene-trap clones, including clone D016D06 (3, 4), were co-localized with the cDNA clone AK044220 (Fig. 1A; Fig. S1). Clone D016D06, deposited by the German GeneTrap Consortium (GGTC) (http://tikus.gsf.de) (3, 4), was derived from insertion of a retroviral construct, rFlpROSAβgeo in 129S2 ES cells (Fig. 1A and C). The rFlpROSAβgeo construct carries a promoterless reporter gene, the β−geo cassette - an in-frame fusion of the β-galactosidase and neomycin resistance (Neor) gene (5), with a splicing acceptor (SA) immediately upstream, and a polyA signal downstream of the β−geo cassette (Fig.
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Twin Study of Early-Onset Major Depression Finds DNA Methylation
bioRxiv preprint doi: https://doi.org/10.1101/422345; this version posted September 20, 2018. 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. Twin Study of Early-Onset Major Depression Finds DNA Methylation Enrichment for Neurodevelopmental Genes Roxann Roberson-Nay1,2, Aaron R. Wolen4, Dana M. Lapato2,4, Eva E. Lancaster2,4, Bradley T. Webb1,2,4, Bradley Verhulst3, John M. Hettema1,2, Timothy P. YorK2,4 1. Virginia Commonwealth University, Department of Psychiatry, Richmond, VA. 2. Virginia Commonwealth University, Virginia Institute for Psychiatric and Behavioral Genetics, Richmond, VA. 3. Department of Psychology, Michigan State University, East Lansing, MI. 4. Virginia Commonwealth University, Department of Human and Molecular Genetics, Richmond, VA. Correspondence: Roxann Roberson-Nay, Ph.D., Virginia Commonwealth University, Depart- ment of Psychiatry, Virginia Institute for Psychiatric and Behavioral Genetics, P.O. Box 980489, Richmond, VA 23298, Fax (804) 828-0245, email: roxann.roberson- [email protected]. bioRxiv preprint doi: https://doi.org/10.1101/422345; this version posted September 20, 2018. 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 Major depression (MD) is a debilitating mental health condition with peak prevalence occurring early in life. Genome-wide examination of DNA methylation (DNAm) offers an attractive comple- ment to studies of allelic risk given it can reflect the combined influence of genes and environment.
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Human Proteins That Interact with RNA/DNA Hybrids
Downloaded from genome.cshlp.org on October 4, 2021 - Published by Cold Spring Harbor Laboratory Press Resource Human proteins that interact with RNA/DNA hybrids Isabel X. Wang,1,2 Christopher Grunseich,3 Jennifer Fox,1,2 Joshua Burdick,1,2 Zhengwei Zhu,2,4 Niema Ravazian,1 Markus Hafner,5 and Vivian G. Cheung1,2,4 1Howard Hughes Medical Institute, Chevy Chase, Maryland 20815, USA; 2Life Sciences Institute, University of Michigan, Ann Arbor, Michigan 48109, USA; 3Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, Maryland 20892, USA; 4Department of Pediatrics, University of Michigan, Ann Arbor, Michigan 48109, USA; 5Laboratory of Muscle Stem Cells and Gene Regulation, National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, Maryland 20892, USA RNA/DNA hybrids form when RNA hybridizes with its template DNA generating a three-stranded structure known as the R-loop. Knowledge of how they form and resolve, as well as their functional roles, is limited. Here, by pull-down assays followed by mass spectrometry, we identified 803 proteins that bind to RNA/DNA hybrids. Because these proteins were identified using in vitro assays, we confirmed that they bind to R-loops in vivo. They include proteins that are involved in a variety of functions, including most steps of RNA processing. The proteins are enriched for K homology (KH) and helicase domains. Among them, more than 300 proteins preferred binding to hybrids than double-stranded DNA. These proteins serve as starting points for mechanistic studies to elucidate what RNA/DNA hybrids regulate and how they are regulated.
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A Case Report of Familial 4Q13.3 Microdeletion in Three Individuals with Syndromic Intellectual Disability Živilė Maldžienė1* , Evelina M
Maldžienė et al. BMC Medical Genomics (2020) 13:63 https://doi.org/10.1186/s12920-020-0711-4 CASE REPORT Open Access A case report of familial 4q13.3 microdeletion in three individuals with syndromic intellectual disability Živilė Maldžienė1* , Evelina M. Vaitėnienė2, Beata Aleksiūnienė1, Algirdas Utkus1 and Eglė Preikšaitienė1 Abstract Background: Interstitial 4q deletions are rare chromosomal alterations. Most of the previously reported deletions involving the 4q13.3 region are large chromosomal alterations with a common loss of band 4q21 resulting in marked growth restriction, severe intellectual disability, and absent or severely delayed speech. A microdeletion of 4q13.3 hasn’t been previously reported. We discuss the involvement of genes and the observed phenotype, comparing it with that of previously reported patients. Case presentation: We report on a 4q13.3 microdeletion detected in three affected individuals of a Lithuanian family. The clinical features of two affected children and their affected mother are very similar and include short stature, congenital heart defect, skeletal anomalies, minor facial anomalies, delayed puberty, and intellectual disability. Whole genome SNP microarray analysis of one child revealed an interstitial 4q13.3 microdeletion, 1.56 Mb in size. FISH analysis confirmed the deletion in the proband and identified the same deletion in her affected sib and mother, while it was not detected in a healthy sib. Deletion includes ADAMTS3, ANKRD17, COX18, GC, and NPFFR2 protein-coding genes. Conclusions: Our findings suggest that 4q13.3 microdeletion is a cause of a recognizable phenotype of three affected individuals. The detected microdeletion is the smallest interstitial deletion in 4q13. We highlight ADAMTS3, ANKRD17 and RNU4ATAC9P as candidate genes for intellectual disability, growth retardation and congenital heart defect.
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A Strategy to Identify Housekeeping Genes Suitable for Analysis in Breast Cancer Diseases Tatiana M
Tilli et al. BMC Genomics (2016) 17:639 DOI 10.1186/s12864-016-2946-1 RESEARCH ARTICLE Open Access A strategy to identify housekeeping genes suitable for analysis in breast cancer diseases Tatiana M. Tilli1, Cláudio da Silva Castro2, Jack A. Tuszynski3,4 and Nicolas Carels1* Abstract Background: The selection of suitable internal control genes is crucial for proper interpretation of real-time PCR data. Here we outline a strategy to identify housekeeping genes that could serve as suitable internal control for comparative analyses of gene expression data in breast cancer cell lines and tissues obtained by high throughput sequencing and quantitative real-time PCR (qRT-PCR). Methods: The strategy proposed includes the large-scale screening of potential candidate reference genes from RNA-seq data as well as their validation by qRT-PCR, and careful examination of reference data from the International Cancer Genome Consortium, The Cancer Genome Atlas and Gene Expression Omnibus repositories. Results: The identified set of reference genes, also called novel housekeeping genes that includes CCSER2, SYMPK, ANKRD17 and PUM1, proved to be less variable and thus potentially more accurate for research and clinical analyses of breast cell lines and tissue samples compared to the traditional housekeeping genes used to this end. Discussion: These results highlight the importance of a massive evaluation of housekeeping genes for their relevance as internal control for optimized intra- and inter-assay comparison of gene expression. Conclusion: We developed a strategy to identify and evaluate the significance of housekeeping genes as internal control for the intra- and inter-assay comparison of gene expression in breast cancer that could be applied to other tumor types and diseases.
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Quantitative Trait Loci Mapping of Macrophage Atherogenic Phenotypes
QUANTITATIVE TRAIT LOCI MAPPING OF MACROPHAGE ATHEROGENIC PHENOTYPES BRIAN RITCHEY Bachelor of Science Biochemistry John Carroll University May 2009 submitted in partial fulfillment of requirements for the degree DOCTOR OF PHILOSOPHY IN CLINICAL AND BIOANALYTICAL CHEMISTRY at the CLEVELAND STATE UNIVERSITY December 2017 We hereby approve this thesis/dissertation for Brian Ritchey Candidate for the Doctor of Philosophy in Clinical-Bioanalytical Chemistry degree for the Department of Chemistry and the CLEVELAND STATE UNIVERSITY College of Graduate Studies by ______________________________ Date: _________ Dissertation Chairperson, Johnathan D. Smith, PhD Department of Cellular and Molecular Medicine, Cleveland Clinic ______________________________ Date: _________ Dissertation Committee member, David J. Anderson, PhD Department of Chemistry, Cleveland State University ______________________________ Date: _________ Dissertation Committee member, Baochuan Guo, PhD Department of Chemistry, Cleveland State University ______________________________ Date: _________ Dissertation Committee member, Stanley L. Hazen, MD PhD Department of Cellular and Molecular Medicine, Cleveland Clinic ______________________________ Date: _________ Dissertation Committee member, Renliang Zhang, MD PhD Department of Cellular and Molecular Medicine, Cleveland Clinic ______________________________ Date: _________ Dissertation Committee member, Aimin Zhou, PhD Department of Chemistry, Cleveland State University Date of Defense: October 23, 2017 DEDICATION I dedicate this work to my entire family. In particular, my brother Greg Ritchey, and most especially my father Dr. Michael Ritchey, without whose support none of this work would be possible. I am forever grateful to you for your devotion to me and our family. You are an eternal inspiration that will fuel me for the remainder of my life. I am extraordinarily lucky to have grown up in the family I did, which I will never forget.
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Genome-Wide Haplotypic Testing in a Finnish Cohort Identifies a Novel
European Journal of Human Genetics (2015) 23, 672–677 & 2015 Macmillan Publishers Limited All rights reserved 1018-4813/15 www.nature.com/ejhg ARTICLE Genome-wide haplotypic testing in a Finnish cohort identifies a novel association with low-density lipoprotein cholesterol Qian S Zhang*,1,2, Brian L Browning2,3,4 and Sharon R Browning*,2,4 We performed genome-wide tests for association between haplotype clusters and each of 9 metabolic traits in a cohort of 5402 Northern Finnish individuals genotyped for 330 000 single-nucleotide polymorphisms. The metabolic traits were body mass index, C-reactive protein, diastolic blood pressure, glucose, high-density lipoprotein (HDL), insulin, low-density lipoprotein (LDL), systolic blood pressure, and triglycerides. Haplotype clusters were determined using Beagle. There were LDL-associated clusters in the chromosome 4q13.3-q21.1 region containing the albumin (ALB) and platelet factor 4 (PF4) genes. This region has not been associated with LDL in previous genome-wide association studies. The most significant haplotype cluster in this region was associated with 0.488 mmol/l higher LDL (95% CI: 0.361–0.615 mmol/l, P-value: 6.4 Â 10 À14). We also observed three previously reported associations: Chromosome 16q13 with HDL, chromosome 1p32.3-p32.2 with LDL and chromosome 19q13.31-q13.32 with LDL. The chromosome 1 and chromosome 4 LDL associations do not reach genome-wide significance in single-marker analyses of these data, illustrating the power of haplotypic association testing. European Journal of Human Genetics (2015) 23, 672–677; doi:10.1038/ejhg.2014.105; published online 4 June 2014 INTRODUCTION cannot be imputed, unless there exists a reference panel drawn from The identification of genetic factors that influence quantitative traits that population.
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Pattern Discovery and Cancer Gene Identification in Integrated Cancer
Pattern discovery and cancer gene identiﬁcation in integrated cancer genomic data Qianxing Moa,b, Sijian Wangc, Venkatraman E. Seshana, Adam B. Olshend, Nikolaus Schultze, Chris Sandere, R. Scott Powersf, Marc Ladanyig, and Ronglai Shena,1 aDepartment of Epidemiology and Biostatistics, eComputational Biology Program, and gDepartment of Pathology and Human Oncology and Pathogenesis Program, Memorial Sloan–Kettering Cancer Center, New York, NY 10065; bDepartment of Medicine and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030; cDepartment of Biostatistics and Medical Informatics, University of Wisconsin, Madison, WI 53792; dDepartment of Epidemiology and Biostatistics, University of California, San Francisco, CA 94107; and fCancer Genome Center, Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11797 Edited by Peter J. Bickel, University of California, Berkeley, CA, and approved December 19, 2012 (received for review May 27, 2012) Large-scale integrated cancer genome characterization efforts in- integrates the information to extract biological principles from the cluding the cancer genome atlas and the cancer cell line encyclo- massive amount of data to provide useful insights for advancing pedia have created unprecedented opportunities to study cancer diagnostic, prognostic, and therapeutic strategies. biology in the context of knowing the entire catalog of genetic In a previous publication (8), we proposed an integrative alterations. A clinically important challenge is to discover cancer clustering framework
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Pan-Cancer Network Analysis Identifies Combinations of Rare Somatic Mutations Across Pathways and Protein Complexes
Pan-Cancer Network Analysis Identifies Combinations of Rare Somatic Mutations across Pathways and Protein Complexes The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Leiserson, M. D., F. Vandin, H. Wu, J. R. Dobson, J. V. Eldridge, J. L. Thomas, A. Papoutsaki, et al. 2014. “Pan-Cancer Network Analysis Identifies Combinations of Rare Somatic Mutations across Pathways and Protein Complexes.” Nature genetics 47 (2): 106-114. doi:10.1038/ng.3168. http://dx.doi.org/10.1038/ng.3168. Published Version doi:10.1038/ng.3168 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:21462211 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA HHS Public Access Author manuscript Author Manuscript Author ManuscriptNat Genet Author Manuscript. Author manuscript; Author Manuscript available in PMC 2015 August 01. Published in final edited form as: Nat Genet. 2015 February ; 47(2): 106–114. doi:10.1038/ng.3168. Pan-Cancer Network Analysis Identifies Combinations of Rare Somatic Mutations across Pathways and Protein Complexes Mark D.M. Leiserson1,2,*, Fabio Vandin1,2,3,*, Hsin-Ta Wu1,2, Jason R. Dobson1,2,4, Jonathan V. Eldridge1, Jacob L. Thomas1, Alexandra Papoutsaki1, Younhun Kim1, Beifang Niu5, Michael McLellan5, Michael S. Lawrence6, Abel Gonzalez-Perez7, David Tamborero7, Yuwei Cheng8, Gregory A. Ryslik9, Nuria Lopez-Bigas7,10, Gad Getz6,11, Li Ding5,12,13, and Benjamin J.
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Autocrine IFN Signaling Inducing Profibrotic Fibroblast Responses By
Downloaded from http://www.jimmunol.org/ by guest on September 23, 2021 Inducing is online at: average * The Journal of Immunology , 11 of which you can access for free at: 2013; 191:2956-2966; Prepublished online 16 from submission to initial decision 4 weeks from acceptance to publication August 2013; doi: 10.4049/jimmunol.1300376 http://www.jimmunol.org/content/191/6/2956 A Synthetic TLR3 Ligand Mitigates Profibrotic Fibroblast Responses by Autocrine IFN Signaling Feng Fang, Kohtaro Ooka, Xiaoyong Sun, Ruchi Shah, Swati Bhattacharyya, Jun Wei and John Varga J Immunol cites 49 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html http://www.jimmunol.org/content/suppl/2013/08/20/jimmunol.130037 6.DC1 This article http://www.jimmunol.org/content/191/6/2956.full#ref-list-1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material References Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2013 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 23, 2021. The Journal of Immunology A Synthetic TLR3 Ligand Mitigates Proﬁbrotic Fibroblast Responses by Inducing Autocrine IFN Signaling Feng Fang,* Kohtaro Ooka,* Xiaoyong Sun,† Ruchi Shah,* Swati Bhattacharyya,* Jun Wei,* and John Varga* Activation of TLR3 by exogenous microbial ligands or endogenous injury-associated ligands leads to production of type I IFN.
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Downloadable KEGG Pathways with the R Package GSA As Was Done with the Functional Modules
bioRxiv preprint doi: https://doi.org/10.1101/091280; this version posted December 2, 2016. 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. Characterizing Xenopus tropicalis endurance capacities with multilevel transcriptomics Adam J. Richards∗;1, Anthony Herrel2;3, Mathieu Videlier2, Konrad Paszkiewicz4, Nicolas Pollet5 and Camille Bonneaud∗;1;6 1 Station d’Ecologie Expérimentale du CNRS, USR 2936, 09200, Moulis, France 2 Département d’Ecologie et de Gestion de la Biodiversité, UMR 7179 CNRS/MNHN, 75231 Paris, France 3 Department of Evolutionary Morphology of Vertebrates, Ghent University, B-9000 Gent, Belgium 4 Exeter Sequencing Service, College of Life and Environmental Sciences, University of Exeter, Exeter EX4 4QD, UK 5 Laboratoire Evolution Genomes Comportement Ecologie, CNRS, F-91198 Gif-sur-Yvette, France 6 Centre for Ecology & Conservation, College of Life and Environmental Sciences, University of Exeter Cornwall Campus, Penryn TR10 9EZ, UK Keywords: RNA-sequencing, Gene set enrichment analysis Abstract Vertebrate endurance capacity is a phenotype with considerable genetic heterogeneity. RNA-Seq technologies are an ideal tool to investigate the involved genes and processes, but several challenges exist when the phenotype of interest has a complex genetic background. Diﬃculties manifest at the level of results interpretation because commonly used statistical methods are designed to identify strongly associated genes. If an observed phenotype can be achieved though multiple distinct genetic mechanisms then typical gene-centric methods come with the attached risk that signal may be lost or misconstrued. Gene set analysis (GSA) methods are now widely accepted as a means to address some of the shortcomings of gene-by-gene analysis methods.
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Identification of Germ Cell-Specific Genes in Mammalian Meiotic Prophase Yunfei Li1, Debjit Ray1,2 and Ping Ye1,3*
Li et al. BMC Bioinformatics 2013, 14:72 http://www.biomedcentral.com/1471-2105/14/72 RESEARCH ARTICLE Open Access Identification of germ cell-specific genes in mammalian meiotic prophase Yunfei Li1, Debjit Ray1,2 and Ping Ye1,3* Abstract Background: Mammalian germ cells undergo meiosis to produce sperm or eggs, haploid cells that are primed to meet and propagate life. Meiosis is initiated by retinoic acid and meiotic prophase is the first and most complex stage of meiosis when homologous chromosomes pair to exchange genetic information. Errors in meiosis can lead to infertility and birth defects. However, despite the importance of this process, germ cell-specific gene expression patterns during meiosis remain undefined due to difficulty in obtaining pure germ cell samples, especially in females, where prophase occurs in the embryonic ovary. Indeed, mixed signals from both germ cells and somatic cells complicate gonadal transcriptome studies. Results: We developed a machine-learning method for identifying germ cell-specific patterns of gene expression in microarray data from mammalian gonads, specifically during meiotic initiation and prophase. At 10% recall, the method detected spermatocyte genes and oocyte genes with 90% and 94% precision, respectively. Our method outperformed gonadal expression levels and gonadal expression correlations in predicting germ cell-specific expression. Top-predicted spermatocyte and oocyte genes were both preferentially localized to the X chromosome and significantly enriched for essential genes. Also identified were transcription factors and microRNAs that might regulate germ cell-specific expression. Finally, we experimentally validated Rps6ka3, a top-predicted X-linked spermatocyte gene. Protein localization studies in the mouse testis revealed germ cell-specific expression of RPS6KA3, mainly detected in the cytoplasm of spermatogonia and prophase spermatocytes.
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