OPCD05726) Data Sheet

Total Page:16

File Type:pdf, Size:1020Kb

OPCD05726) Data Sheet 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 NOS1AP Recombinant Protein (OPCD05726) Data Sheet Product Number OPCD05726 Product Page http://www.avivasysbio.com/nos1ap-recombinant-protein-opcd05726.html Product Name NOS1AP Recombinant Protein (OPCD05726) Size 10 ug Gene Symbol NOS1AP Alias Symbols 6330408P19Rik, CAPON, Carboxyl-terminal PDZ ligand of neuronal nitric oxide synthase protein, C-terminal PDZ ligand of neuronal nitric oxide synt hase protein, KIAA0464, MGC138500, Nitric oxide synthase 1 adaptor protein Molecular Weight 28 kDa Product Format Lyophilized Tag N-terminal His Tag Conjugation Unconjugated NCBI Gene Id 9722 Host E.coli Purity > 95% Source Prokaryotic Expressed Recombinant Official Gene Full Name nitric oxide synthase 1 adaptor protein Description of Target Adapter protein involved in neuronal nitric-oxide (NO) synthesis regulation via its association with nNOS/NOS1. The complex formed with NOS1 and synapsins is necessary for specific NO and synapsin functions at a presynaptic level. Mediates an indirect interaction between NOS1 and RASD1 l eading to enhance the ability of NOS1 to activate RASD1. Competes with DLG4 for interaction with NOS1, possibly affecting NOS1 activity by regul ating the interaction between NOS1 and DLG4. Reconstitution and Storage Reconstitute in PBS or others. Store at 2-8C for one month. Aliquot and store at -80C for 12 months. Avoid repeated freeze/thaw cycles. Additional Information Endotoxin Level: < 1.0 EU per 1 ug (determined by the LAL method) Additional Information Residues: Thr285 - Val506 Lead Time Domestic: within 1-2 weeks delivery International: 1-3 weeks Formulation Lyophilized in PBS, pH7.4, containing 0.01% SKL, 1mM DTT, 5% Trehalose and Proclin300. Tissue Tool Find tissues and cell lines supported by DNA array analysis to express NOS1AP. Swissprot Id O75052 Protein Name Carboxyl-terminal PDZ ligand of neuronal nitric oxide synthase protein Protein Accession # NP_001119532.2 RNA Seq Find tissues and cell lines supported by RNA-seq analysis to express NOS1AP. Nucleotide Accession # NM_001126060.1 Species Reactivity Human Application SDS-PAGE, WB, ELISA, IP Image 1 SDS-PAGE NOS1AP Recombinant Protein (OPCD05726) using SDS-PAGE AVIVA SYSTEMS BIOLOGY manufactures and sells quality antibody products covering genome wide proteins. This product is for Research Use Only. Not for diagnostic, human, or veterinary use. Optimal conditions of its use should be determined by end users. AVIVA SYSTEMS BIOLOGY 5754 Pacific Center Blvd., Suite 201 San Diego, CA 92121 USA | Tel: (858)552-6979 | [email protected].
Recommended publications
  • 1 Evidence for Gliadin Antibodies As Causative Agents in Schizophrenia
    1 Evidence for gliadin antibodies as causative agents in schizophrenia. C.J.Carter PolygenicPathways, 20 Upper Maze Hill, Saint-Leonard’s on Sea, East Sussex, TN37 0LG [email protected] Tel: 0044 (0)1424 422201 I have no fax Abstract Antibodies to gliadin, a component of gluten, have frequently been reported in schizophrenia patients, and in some cases remission has been noted following the instigation of a gluten free diet. Gliadin is a highly immunogenic protein, and B cell epitopes along its entire immunogenic length are homologous to the products of numerous proteins relevant to schizophrenia (p = 0.012 to 3e-25). These include members of the DISC1 interactome, of glutamate, dopamine and neuregulin signalling networks, and of pathways involved in plasticity, dendritic growth or myelination. Antibodies to gliadin are likely to cross react with these key proteins, as has already been observed with synapsin 1 and calreticulin. Gliadin may thus be a causative agent in schizophrenia, under certain genetic and immunological conditions, producing its effects via antibody mediated knockdown of multiple proteins relevant to the disease process. Because of such homology, an autoimmune response may be sustained by the human antigens that resemble gliadin itself, a scenario supported by many reports of immune activation both in the brain and in lymphocytes in schizophrenia. Gluten free diets and removal of such antibodies may be of therapeutic benefit in certain cases of schizophrenia. 2 Introduction A number of studies from China, Norway, and the USA have reported the presence of gliadin antibodies in schizophrenia 1-5. Gliadin is a component of gluten, intolerance to which is implicated in coeliac disease 6.
    [Show full text]
  • The Genetic Variation Rs12143842 in NOS1AP Increases Idiopathic
    www.nature.com/scientificreports OPEN The genetic variation rs12143842 in NOS1AP increases idiopathic ventricular tachycardia risk in Received: 21 December 2016 Accepted: 14 July 2017 Chinese Han populations Published: xx xx xxxx Ronfeng Zhang, Feifei Chen, Honjiu Yu, Lianjun Gao, Xiaomeng Yin, Yingxue Dong, Yanzong Yang & Yunlong Xia Genome-wide association studies identified that the common T of rs12143842 in NOS1AP is associated with a QT/QTc interval in European populations. In this study, we test the association between the variation rs12143842 in NOS1AP and idiopathic ventricular tachycardia (IVT). A case-control association study examining rs12143842 was performed in two independent cohorts. The Northern cohort enrolled 277 IVT patients and 728 controls from a Chinese Gene ID population. The Central cohort enrolled 301 IVT patients and 803 matched controls. Genotyping was performed using high-resolution melt analysis. The minor T allele of the rs12143842 SNP was significantly associated with decreased IVT risk in the Northern cohort (adjusted P = 0.024, OR 0.71(0.52~0.96)), and this association was replicated in an independent Central Gene ID cohort (adjusted P = 0.029, OR 0.78 (0.62~0.97)). The association was more significant in the combined population (adjustedP = 0.001, OR 0.76 (0.64~0.90)). The P values for the genotypic association were significant for the dominant (P < 0.001) and additive (P = 0.001) models. The minor T allele for the SNP rs12143842 in NOS1AP is significantly associated with IVT.NOS1AP might be a novel gene affecting IVT, and further functional studies should be performed.
    [Show full text]
  • NOS1AP Regulates Dendrite Patterning of Hippocampal Neurons Through a Carboxypeptidase E-Mediated Pathway
    8248 • The Journal of Neuroscience, June 24, 2009 • 29(25):8248–8258 Cellular/Molecular NOS1AP Regulates Dendrite Patterning of Hippocampal Neurons through a Carboxypeptidase E-Mediated Pathway Damien Carrel,1* Yangzhou Du,1* Daniel Komlos,1,2 Norell M. Hadzimichalis,1 Munjin Kwon,1,3 Bo Wang,1 Linda M. Brzustowicz,4 and Bonnie L. Firestein1 1Department of Cell Biology and Neuroscience, 2Neuroscience Graduate Program, 3Molecular Biosciences Graduate Program, and 4Department of Genetics, Rutgers University, Piscataway, New Jersey 08854-8082 During neuronal development, neurons form elaborate dendritic arbors that receive signals from axons. Additional studies are needed to elucidate the factors regulating the establishment of dendritic patterns. Our work explored possible roles played by nitric oxide synthase 1 adaptor protein (NOS1AP; also known as C-terminal PDZ ligand of neuronal nitric oxide synthase or CAPON) in dendritic patterning of cultured hippocampal neurons. Here we report that the long isoform of NOS1AP (NOS1AP-L) plays a novel role in regulating dendrite outgrowth and branching. NOS1AP-L decreases dendrite number when overexpressed at any interval between day in vitro (DIV) 0 and DIV 12, and knockdown of NOS1AP-L results in increased dendrite number. In contrast, the short isoform of NOS1AP (NOS1AP-S) decreases dendrite number only when overexpressed during DIV 5–7. Using mutants of NOS1AP-L, we show that neither the PDZ- binding domain nor the PTB domain is necessary for the effects of NOS1AP-L. We have functionally narrowed the region of NOS1AP-L that mediates this effect to the middle amino acids 181–307, a region that is not present in NOS1AP-S.
    [Show full text]
  • Single-Nucleotide Variations in Cardiac Arrhythmias: Prospects for Genomics and Proteomics Based Biomarker Discovery and Diagnostics
    Genes 2014, 5, 254-269; doi:10.3390/genes5020254 OPEN ACCESS genes ISSN 2073-4425 www.mdpi.com/journal/genes Article Single-Nucleotide Variations in Cardiac Arrhythmias: Prospects for Genomics and Proteomics Based Biomarker Discovery and Diagnostics Ayman Abunimer 1, Krista Smith 1, Tsung-Jung Wu 1, Phuc Lam 2, Vahan Simonyan 2 and Raja Mazumder 1,3,* 1 Department of Biochemistry and Molecular Medicine, George Washington University, Washington, DC 20037, USA; E-Mails: [email protected] (A.A.); [email protected] (K.S.); [email protected] (T.-J.W.) 2 Center for Biologics Evaluation and Research, Food and Drug Administration, Rockville, MD 20852, USA; E-Mails: [email protected] (P.L.); [email protected] (V.S.) 3 McCormick Genomic and Proteomic Center, George Washington University, Washington, DC 20037, USA * Author to whom correspondence should be addressed; E-Mail: [email protected]; Tel.: +1-202-994-5004; Fax: +1-202-994-8974. Received: 21 November 2013; in revised form: 19 February 2014 / Accepted: 19 February 2014 / Published: 27 March 2014 Abstract: Cardiovascular diseases are a large contributor to causes of early death in developed countries. Some of these conditions, such as sudden cardiac death and atrial fibrillation, stem from arrhythmias—a spectrum of conditions with abnormal electrical activity in the heart. Genome-wide association studies can identify single nucleotide variations (SNVs) that may predispose individuals to developing acquired forms of arrhythmias. Through manual curation of published genome-wide association studies, we have collected a comprehensive list of 75 SNVs associated with cardiac arrhythmias. Ten of the SNVs result in amino acid changes and can be used in proteomic-based detection methods.
    [Show full text]
  • Clinical, Molecular, and Immune Analysis of Dabrafenib-Trametinib
    Supplementary Online Content Chen G, McQuade JL, Panka DJ, et al. Clinical, molecular and immune analysis of dabrafenib-trametinib combination treatment for metastatic melanoma that progressed during BRAF inhibitor monotherapy: a phase 2 clinical trial. JAMA Oncology. Published online April 28, 2016. doi:10.1001/jamaoncol.2016.0509. eMethods. eReferences. eTable 1. Clinical efficacy eTable 2. Adverse events eTable 3. Correlation of baseline patient characteristics with treatment outcomes eTable 4. Patient responses and baseline IHC results eFigure 1. Kaplan-Meier analysis of overall survival eFigure 2. Correlation between IHC and RNAseq results eFigure 3. pPRAS40 expression and PFS eFigure 4. Baseline and treatment-induced changes in immune infiltrates eFigure 5. PD-L1 expression eTable 5. Nonsynonymous mutations detected by WES in baseline tumors This supplementary material has been provided by the authors to give readers additional information about their work. © 2016 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/30/2021 eMethods Whole exome sequencing Whole exome capture libraries for both tumor and normal samples were constructed using 100ng genomic DNA input and following the protocol as described by Fisher et al.,3 with the following adapter modification: Illumina paired end adapters were replaced with palindromic forked adapters with unique 8 base index sequences embedded within the adapter. In-solution hybrid selection was performed using the Illumina Rapid Capture Exome enrichment kit with 38Mb target territory (29Mb baited). The targeted region includes 98.3% of the intervals in the Refseq exome database. Dual-indexed libraries were pooled into groups of up to 96 samples prior to hybridization.
    [Show full text]
  • Overexpression of Isoforms of Nitric Oxide Synthase 1 Adaptor Protein, Encoded by a Risk Gene for Schizophrenia, Alters Actin Dynamics and Synaptic Function
    ORIGINAL RESEARCH published: 02 February 2016 doi: 10.3389/fncel.2016.00006 Overexpression of Isoforms of Nitric Oxide Synthase 1 Adaptor Protein, Encoded by a Risk Gene for Schizophrenia, Alters Actin Dynamics and Synaptic Function Kristina Hernandez 1, Przemyslaw Swiatkowski 2, Mihir V. Patel 2, Chen Liang 2, Natasha R. Dudzinski 2, Linda M. Brzustowicz 3 and Bonnie L. Firestein 1* 1 Department of Cell Biology and Neuroscience, Human Genetics Institute of New Jersey, Rutgers—The State University of New Jersey, Piscataway, NJ, USA, 2 Department of Cell Biology and Neuroscience, Rutgers—The State University of New Jersey, Piscataway, NJ, USA, 3 Department of Genetics, Human Genetics Institute of New Jersey, Rutgers—The State University of New Jersey, Piscataway, NJ, USA Proper communication between neurons depends upon appropriate patterning of dendrites and correct distribution and structure of spines. Schizophrenia is a neuropsychiatric disorder characterized by alterations in dendrite branching and spine density. Nitric oxide synthase 1 adaptor protein (NOS1AP), a risk gene for schizophrenia, encodes proteins that are upregulated in the dorsolateral prefrontal cortex (DLPFC) of individuals with schizophrenia. To elucidate the effects of NOS1AP overexpression observed in individuals with schizophrenia, we investigated changes in actin dynamics Edited by: and spine development when a long (NOS1AP-L) or short (NOS1AP-S) isoform of Gerald W. Zamponi, NOS1AP is overexpressed. Increased NOS1AP-L protein promotes the formation University of Calgary, Canada of immature spines when overexpressed in rat cortical neurons from day in vitro Reviewed by: Stephen Ferguson, (DIV) 14 to DIV 17 and reduces the amplitude of miniature excitatory postsynaptic University of Western Ontario, Canada currents (mEPSCs).
    [Show full text]
  • Nos1-Adaptor Protein Dysfunction in the Nucleus Tractus Solitarii Contributes to the Neurogenic Heart Damage and Qt Interval Prolongation
    NOS1-ADAPTOR PROTEIN DYSFUNCTION IN THE NUCLEUS TRACTUS SOLITARII CONTRIBUTES TO THE NEUROGENIC HEART DAMAGE AND QT INTERVAL PROLONGATION A Dissertation Submitted to the Graduate Faculty of the North Dakota State University of Agriculture and Applied Science By Neha Singh In Partial Fulfillment of the Requirements for the Degree of DOCTOR OF PHILOSOPHY Major Department: Cellular and Molecular Biology November 2014 Fargo, North Dakota North Dakota State University Graduate School Title NOS1-ADAPTOR PROTEIN DYSFUNCTION IN THE NUCLEUS TRACTUS SOLITARII CONTRIBUTES TO THE NEUROGENIC HEART DAMAGE AND QT INTERVAL PROLONGATION By Neha Singh The Supervisory Committee certifies that this disquisition complies with North Dakota State University’s regulations and meets the accepted standards for the degree of DOCTOR OF PHILOSOPHY SUPERVISORY COMMITTEE: Chengwen Sun, M.D., Ph.D. Chair Stephen T. O’Rourke, Ph.D. Jagdish Singh, Ph.D. Mark Sheridan, Ph.D. Approved: 4/20/15 Jane Schuh, Ph.D. Date Department Chair ABSTRACT Variants of the Nitric Oxide Synthase 1 Adaptor Protein (NOS1AP) locus are strongly related to QT interval prolongation and sudden cardiac death (SCD) in human. Neurogenic cardiac damage due to subarachnoid hemorrhage, stroke, epilepsy and myocardial infarction is known to contribute to sudden death in most cases. Our aim was to study the role of NOS1AP in the neurogenic cardiac damage by silencing NOS1AP expression in the Nucleus Tractus Solitarii (NTS) area of the brainstem using lentiviral vector-mediated NOS1AP shRNA (Lv-NOS1AP- shRNA). Real time PCR data showed NOS1AP mRNA levels were expressed in the NTS 3-fold higher than other organs such as kidney and heart in Sprague Dawley (SD) rats.
    [Show full text]
  • Genetic Factors of Nitric Oxide's System in Psychoneurologic Disorders
    Preprints (www.preprints.org) | NOT PEER-REVIEWED | Posted: 4 February 2020 doi:10.20944/preprints202002.0048.v1 Peer-reviewed version available at Int. J. Mol. Sci. 2020, 21, 1604; doi:10.3390/ijms21051604 Review Genetic factors of nitric oxide’s system in psychoneurologic disorders Regina F. Nasyrova 1,2*, Polina V. Moskaleva1, Elena E. Vaiman1, Natalya A. Shnayder1, Nataliya L. Blatt 2,3, Albert A. Rizvanov 2,3 1 Federal State Budget-funded Institution “V.M. Bekhterev National Medical Research Center for Psychiatry and Neurology” of the Russian Ministry of Health, Saint-Petersburg, Russian Federation”. Address: Bekhterev Street, 3, Saint-Petersburg, 192019, Russian Federation, [email protected], [email protected], [email protected], [email protected], [email protected] 2 Federal State Autonomous Educational Institution of Higher Professional Learning “Kazan (Volga Region) Federal University”. Address: Kremlyovskaya Street, 18, Kazan, 420008, Russian Federation, [email protected] 3 Faculty of Medicine and Health Sciences, University of Nottingham, Nottingham, United Kingdom, [email protected] * Correspondence: [email protected]; +7(812)6700220 Abstract. According to the recent data, nitric oxide (NO) is a chemical messenger that mediates functions such as vasodilation and neurotransmission, it also possesses antimicrobial and antitumoral activities. Nitric oxide has been implicated in neurotoxicity associated with stroke and neurodegenerative diseases, neural regulation of smooth muscle, including peristalsis, and penile erection. We searched for full-text English publications in Pubmed and SNPedia databases using keywords and combined word searches (nitric oxide, single nucleotide variants, single nucleotide polymorphisms, genes) over the past 15 years. In addition, earlier publications of historical interest were included in the review.
    [Show full text]
  • The Development and Pilot of a Quality Assurance Program for Proficiency
    Page 1 of 39 ins RCPAQAP Molecular Genetics Quality Use of Pathology Program Final Report Agreement id: 4-ALD5HVH July 2020 Title The development of a quality assurance pilot program for proficiency testing in cardiovascular disease Final Report A project funded under the Australian Government’s Quality Use of Pathology Program 1 Page 2 of 39 Contents List of Abbreviations 4 1. Executive Summary 5 2. Aims and Outcomes of the Study 8 2.1 Aims 8 2.2 Outcome 9 3. Background 10 4. Addressing Essential Needs 12 5. Benefits 13 6. Reference Samples 14 7. Methods 15 7.1 Laboratories 15 7.2 Reference testing of samples 15 7.3 Homogeneity and stability of the reference DNA 15 7.4 Whole genome DNA sequencing 15 7.5 Clinical data 15 7.6 Proficiency testing 16 8. Results and Discussion 17 8.1 Laboratories 17 8.2 Reference testing of samples 17 8.3 Homogeneity and stability 17 8.4 Whole genome DNA sequencing 18 8.5 Proficiency testing data 18 9. Project Findings 31 10. Problems Encountered 32 11. Future Diagnostics 33 12. Project Assessment 34 12.1 Short term 34 12.2 Intermediate term 34 12.3 Long term 34 12.3.1 Economy 34 12.3.2 Efficiency 35 12.3.3 Effectiveness 35 2 Page 3 of 39 13. Project Sustainability 36 14. Appendix 37 15. References 38 3 Page 4 of 39 List of abbreviations: CVD Cardiovascular disease DIN DNA Integrity Number EQA External quality assurance FH Familial hypercholesterolemia LDL Low-density lipoproteins NGS Next generation sequencing RCPAQAP Royal College of Pathologists of Australasia Quality Assurance Programs RPAH Royal Prince Alfred Hospital SNP Single nucleotide polymorphism 4 Page 5 of 39 1.
    [Show full text]
  • Polymorphisms in the NOS1AP Gene Modulate QT Interval Duration and Risk of Arrhythmias in the Long QT Syndrome
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Journal of the American College of Cardiology Vol. 55, No. 24, 2010 © 2010 by the American College of Cardiology Foundation ISSN 0735-1097/$36.00 Published by Elsevier Inc. doi:10.1016/j.jacc.2009.12.065 Heart Rhythm Disorders Polymorphisms in the NOS1AP Gene Modulate QT Interval Duration and Risk of Arrhythmias in the Long QT Syndrome Marta Toma´s, PHD,*† Carlo Napolitano, MD, PHD,*‡ Luciana De Giuli, PHD,* Raffaella Bloise, MD,* Isaac Subirana, MS,†§ Alberto Malovini, MS,ʈ# Riccardo Bellazzi, PHD,ʈ Dan E. Arking, PHD,** Eduardo Marban, MD, PHD,‡‡ Aravinda Chakravarti, PHD,** Peter M. Spooner, PHD,†† Silvia G. Priori, MD, PHD*‡¶ Pavia and Milan, Italy; Barcelona, Spain; New York, New York; Baltimore, Maryland; and Los Angeles, California Objectives We investigated the role of nitric oxide 1 adaptor protein (NOS1AP) as a genetic modifier of long QT syndrome (LQTS). Background LQTS risk stratification is complicated by the phenotype variability that limits prediction of life-threatening ar- rhythmic events based on available metrics. Thus, the identification of new markers is desirable. Recent studies have shown that NOS1AP variations in the gene modulate QT interval in healthy and 1 LQTS kindred, and occur- rence of cardiac events in healthy subjects. Methods The study included 901 patients enrolled in a prospective LQTS registry. Three NOS1AP marker SNPs (rs4657139, rs16847548, and rs10494366) were genotyped to assess the effect of variant alleles on QTc and on the incidence of cardiac events. We quantified the association between variant alleles, QTc, and outcomes to assess whether NOS1AP is a useful risk stratifier in LQTS.
    [Show full text]
  • CHARACTERIZATION of a NOVEL ISOFORM of NOS1AP: Nos1apc
    CHARACTERIZATION OF A NOVEL ISOFORM OF NOS1AP: NOS1APc by Michael O’Brien Submitted in partial fulfilment of the requirements for the degree of Master of Science at Dalhousie University Halifax, Nova Scotia March 2011 © Copyright by Michael O’Brien, 2011 DALHOUSIE UNIVERSITY DEPARTMENT OF PHARMACOLOGY The undersigned hereby certify that they have read and recommend to the Faculty of Graduate Studies for acceptance a thesis entitled “CHARACTERIZATION OF A NOVEL ISOFORM OF NOS1AP: NOS1APc” by Michael O’Brien in partial fulfillment of the requirements for the degree of Master of Science. Dated: March 29, 2011 Supervisor: _________________________________ Readers: _________________________________ _________________________________ _________________________________ ii DALHOUSIE UNIVERSITY DATE: March 29, 2011 AUTHOR: Michael O’Brien TITLE: CHARACTERIZATION OF A NOVEL ISOFORM OF NOS1AP: NOS1APc DEPARTMENT OR SCHOOL: Department of Pharmacology DEGREE: MSc CONVOCATION: May YEAR: 2011 Permission is herewith granted to Dalhousie University to circulate and to have copied for non-commercial purposes, at its discretion, the above title upon the request of individuals or institutions. I understand that my thesis will be electronically available to the public. The author reserves other publication rights, and neither the thesis nor extensive extracts from it may be printed or otherwise reproduced without the author’s written permission. The author attests that permission has been obtained for the use of any copyrighted material appearing in the thesis (other than the brief excerpts requiring only proper acknowledgement in scholarly writing), and that all such use is clearly acknowledged. _______________________________ Signature of Author iii TABLE OF CONTENTS LIST OF FIGURES…………………………………………………………………….. viii ABSTRACT……………………………………………………………………………... ix LIST OF ABREVIATIONS AND SYMBOLS USED………………………………...
    [Show full text]
  • Powerful Gene-Based Testing by Integrating Long-Range Chromatin Interactions and Knockoff Genotypes
    medRxiv preprint doi: https://doi.org/10.1101/2021.07.14.21260405; this version posted July 18, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license . Powerful gene-based testing by integrating long-range chromatin interactions and knockoff genotypes Shiyang Ma1, James L. Dalgleish1, Justin Lee2, Chen Wang1, Linxi Liu3, Richard Gill4;5, Joseph D. Buxbaum6, Wendy Chung7, Hugues Aschard8, Edwin K. Silverman9, Michael H. Cho9, Zihuai He2;10, Iuliana Ionita-Laza1;# 1 Department of Biostatistics, Columbia University, New York, NY, 10032, USA 2 Quantitative Sciences Unit, Department of Medicine, Stanford University, Stanford, CA, 94305, USA 3 Department of Statistics, University of Pittsburgh, Pittsburgh, PA, 15260, USA 4 Department of Human Genetics, Genentech, South San Francisco, CA, 94080, USA 5 Department of Epidemiology, Columbia University, New York, NY, 10032, USA 6 Departments of Psychiatry, Neuroscience, and Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA 7 Department of Pediatrics and Medicine, Herbert Irving Comprehensive Cancer Center, Columbia Uni- versity Irving Medical Center, New York, NY, 10032, USA 8 Department of Computational Biology, Institut Pasteur, Paris, France 9 Channing Division of Network Medicine and Division of Pulmonary and Critical Care Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115, USA 10 Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94305, USA # e-mail: [email protected] Abstract Gene-based tests are valuable techniques for identifying genetic factors in complex traits.
    [Show full text]