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Whole Brain and Brain Regional Coexpression Network Interactions Associated with Predisposition to Alcohol Consumption Lauren A
Virginia Commonwealth University VCU Scholars Compass Study of Biological Complexity Publications Center for the Study of Biological Complexity 2013 Whole Brain and Brain Regional Coexpression Network Interactions Associated with Predisposition to Alcohol Consumption Lauren A. Vanderlinden University of Colorado at Aurora Laura M. Saba University of Colorado at Aurora Katerina Kechris University of Colorado at Aurora See next page for additional authors Follow this and additional works at: http://scholarscompass.vcu.edu/csbc_pubs Part of the Life Sciences Commons © 2013 Vanderlinden et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Downloaded from http://scholarscompass.vcu.edu/csbc_pubs/24 This Article is brought to you for free and open access by the Center for the Study of Biological Complexity at VCU Scholars Compass. It has been accepted for inclusion in Study of Biological Complexity Publications by an authorized administrator of VCU Scholars Compass. For more information, please contact [email protected]. Authors Lauren A. Vanderlinden, Laura M. Saba, Katerina Kechris, Michael F. Miles, Paula L. Hoffman, and Boris Tabakoff This article is available at VCU Scholars Compass: http://scholarscompass.vcu.edu/csbc_pubs/24 Whole Brain and Brain Regional Coexpression Network Interactions Associated with Predisposition to Alcohol Consumption Lauren -
Exceptional Conservation of Horse–Human Gene Order on X Chromosome Revealed by High-Resolution Radiation Hybrid Mapping
Exceptional conservation of horse–human gene order on X chromosome revealed by high-resolution radiation hybrid mapping Terje Raudsepp*†, Eun-Joon Lee*†, Srinivas R. Kata‡, Candice Brinkmeyer*, James R. Mickelson§, Loren C. Skow*, James E. Womack‡, and Bhanu P. Chowdhary*¶ʈ *Department of Veterinary Anatomy and Public Health, ‡Department of Veterinary Pathobiology, College of Veterinary Medicine, and ¶Department of Animal Science, College of Agriculture and Life Science, Texas A&M University, College Station, TX 77843; and §Department of Veterinary Pathobiology, University of Minnesota, 295f AS͞VM, St. Paul, MN 55108 Contributed by James E. Womack, December 30, 2003 Development of a dense map of the horse genome is key to efforts ciated with the traits, once they are mapped by genetic linkage aimed at identifying genes controlling health, reproduction, and analyses with highly polymorphic markers. performance. We herein report a high-resolution gene map of the The X chromosome is the most conserved mammalian chro- horse (Equus caballus) X chromosome (ECAX) generated by devel- mosome (18, 19). Extensive comparisons of structure, organi- oping and typing 116 gene-specific and 12 short tandem repeat zation, and gene content of this chromosome in evolutionarily -markers on the 5,000-rad horse ؋ hamster whole-genome radia- diverse mammals have revealed a remarkable degree of conser tion hybrid panel and mapping 29 gene loci by fluorescence in situ vation (20–22). Until now, the chromosome has been best hybridization. The human X chromosome sequence was used as a studied in humans and mice, where the focus of research has template to select genes at 1-Mb intervals to develop equine been the intriguing patterns of X inactivation and the involve- orthologs. -
In-Depth Analysis of Genetic Variation Associated with Severe West Nile Viral Disease
Article In-Depth Analysis of Genetic Variation Associated with Severe West Nile Viral Disease Megan E. Cahill 1, Mark Loeb 2, Andrew T. Dewan 1 and Ruth R. Montgomery 3,* 1 Center for Perinatal, Pediatric and Environmental Epidemiology, Department of Chronic Disease Epidemiology, Yale School of Public Health, 1 Church Street, New Haven, CT 06510, USA; [email protected] (M.E.C.); [email protected] (A.T.D.) 2 3208 Michael DeGroote Centre for Learning & Discovery, Division of Clinical Pathology, McMaster University, Hamilton, ON L8S 4L8, Canada; [email protected] 3 Department of Internal Medicine, Yale School of Medicine, 300 Cedar Street, New Haven, CT 06520, USA * Correspondence: [email protected] Received: 30 October 2020; Accepted: 3 December 2020; Published: 8 December 2020 Abstract: West Nile virus (WNV) is a mosquito-borne virus which causes symptomatic disease in a minority of infected humans. To identify novel genetic variants associated with severe disease, we utilized data from an existing case-control study of WNV and included population controls for an expanded analysis. We conducted imputation and gene-gene interaction analysis in the largest and most comprehensive genetic study conducted to date for West Nile neuroinvasive disease (WNND). Within the imputed West Nile virus dataset (severe cases n = 381 and asymptomatic/mild controls = 441), we found novel loci within the MCF.2 Cell Line Derived Transforming Sequence Like (MCF2L) gene (rs9549655 and rs2297192) through the individual loci analyses, although none reached statistical significance. Incorporating population controls from the Wisconsin Longitudinal Study on Aging (n = 9012) did not identify additional novel variants, a possible reflection of the cohort’s inclusion of individuals who could develop mild or severe WNV disease upon infection. -
Proteomic Analysis of the Venom of Jellyfishes Rhopilema Esculentum and Sanderia Malayensis
marine drugs Article Proteomic Analysis of the Venom of Jellyfishes Rhopilema esculentum and Sanderia malayensis 1, 2, 2 2, Thomas C. N. Leung y , Zhe Qu y , Wenyan Nong , Jerome H. L. Hui * and Sai Ming Ngai 1,* 1 State Key Laboratory of Agrobiotechnology, School of Life Sciences, The Chinese University of Hong Kong, Hong Kong, China; [email protected] 2 Simon F.S. Li Marine Science Laboratory, State Key Laboratory of Agrobiotechnology, School of Life Sciences, The Chinese University of Hong Kong, Hong Kong, China; [email protected] (Z.Q.); [email protected] (W.N.) * Correspondence: [email protected] (J.H.L.H.); [email protected] (S.M.N.) Contributed equally. y Received: 27 November 2020; Accepted: 17 December 2020; Published: 18 December 2020 Abstract: Venomics, the study of biological venoms, could potentially provide a new source of therapeutic compounds, yet information on the venoms from marine organisms, including cnidarians (sea anemones, corals, and jellyfish), is limited. This study identified the putative toxins of two species of jellyfish—edible jellyfish Rhopilema esculentum Kishinouye, 1891, also known as flame jellyfish, and Amuska jellyfish Sanderia malayensis Goette, 1886. Utilizing nano-flow liquid chromatography tandem mass spectrometry (nLC–MS/MS), 3000 proteins were identified from the nematocysts in each of the above two jellyfish species. Forty and fifty-one putative toxins were identified in R. esculentum and S. malayensis, respectively, which were further classified into eight toxin families according to their predicted functions. Amongst the identified putative toxins, hemostasis-impairing toxins and proteases were found to be the most dominant members (>60%). -
PDF Datasheet
Product Datasheet C9orf85 Overexpression Lysate NBL1-08604 Unit Size: 0.1 mg Store at -80C. Avoid freeze-thaw cycles. Protocols, Publications, Related Products, Reviews, Research Tools and Images at: www.novusbio.com/NBL1-08604 Updated 3/17/2020 v.20.1 Earn rewards for product reviews and publications. Submit a publication at www.novusbio.com/publications Submit a review at www.novusbio.com/reviews/destination/NBL1-08604 Page 1 of 2 v.20.1 Updated 3/17/2020 NBL1-08604 C9orf85 Overexpression Lysate Product Information Unit Size 0.1 mg Concentration The exact concentration of the protein of interest cannot be determined for overexpression lysates. Please contact technical support for more information. Storage Store at -80C. Avoid freeze-thaw cycles. Buffer RIPA buffer Target Molecular Weight 18.1 kDa Product Description Description Transient overexpression lysate of chromosome 9 open reading frame 85 (C9orf85) The lysate was created in HEK293T cells, using Plasmid ID RC208807 and based on accession number NM_182505. The protein contains a C- MYC/DDK Tag. Gene ID 138241 Gene Symbol C9ORF85 Species Human Notes HEK293T cells in 10-cm dishes were transiently transfected with a non-lipid polymer transfection reagent specially designed and manufactured for large volume DNA transfection. Transfected cells were cultured for 48hrs before collection. The cells were lysed in modified RIPA buffer (25mM Tris-HCl pH7.6, 150mM NaCl, 1% NP-40, 1mM EDTA, 1xProteinase inhibitor cocktail mix, 1mM PMSF and 1mM Na3VO4, and then centrifuged to clarify the lysate. Protein concentration was measured by BCA protein assay kit.This product is manufactured by and sold under license from OriGene Technologies and its use is limited solely for research purposes. -
Product Name: C9orf78 Polyclonal Antibody, ALEXA FLUOR® 647 Conjugated Catalog No
Product Name: C9orf78 Polyclonal Antibody, ALEXA FLUOR® 647 Conjugated Catalog No. : TAP01-84658R-A647 Intended Use: For Research Use Only. Not for used in diagnostic procedures. Size 100ul Concentration 1ug/ul Gene ID 51759 ISO Type Rabbit IgG Clone N/A Immunogen Range Conjugation ALEXA FLUOR® 647 Subcellular Locations Applications IF(IHC-P) Cross Reactive Species Human, Mouse, Rat Source KLH conjugated synthetic peptide derived from human C9orf78 Applications with IF(IHC-P)(1:50-200) Dilutions Purification Purified by Protein A. Background Chromosome 9 consists of about 145 million bases and 4% of the human genome and encodes nearly 900 genes. Considered to play a role in gender determination, deletion of the distal portion of 9p can lead to development of male to female sex reversal, the phenotype of a female with a male X,Y genotype. Hereditary hemorrhagic telangiectasia, which is characterized by harmful vascular defects, is associated with the chromosome 9 gene encoding endoglin protein, ENG. Familial dysautonomia is also associated with chromosome 9 though through the gene IKBKAP. Notably, chromosome 9 encompasses the largest interferon family gene cluster. Chromosome 9 is partnered with chromosome 22 in the translocation leading to the aberrant production of BCR-ABL fusion protein often found in leukemias. The C9orf78 gene product has been provisionally designated C9orf78 pending further characterization. Synonyms bA409K20.3; C9orf78; Chromosome 9 open reading frame 78; CI078_HUMAN; HCA59; Hepatocellular carcinoma associated antigen 59; Hepatocellular carcinoma-associated antigen 59; HSPC220; Uncharacterized protein C9orf78. Storage Aqueous buffered solution containing 1% BSA, 50% glycerol and 0.09% sodium azide. Store at 4°C for 12 months. -
Dual Proteome-Scale Networks Reveal Cell-Specific Remodeling of the Human Interactome
bioRxiv preprint doi: https://doi.org/10.1101/2020.01.19.905109; this version posted January 19, 2020. 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. Dual Proteome-scale Networks Reveal Cell-specific Remodeling of the Human Interactome Edward L. Huttlin1*, Raphael J. Bruckner1,3, Jose Navarrete-Perea1, Joe R. Cannon1,4, Kurt Baltier1,5, Fana Gebreab1, Melanie P. Gygi1, Alexandra Thornock1, Gabriela Zarraga1,6, Stanley Tam1,7, John Szpyt1, Alexandra Panov1, Hannah Parzen1,8, Sipei Fu1, Arvene Golbazi1, Eila Maenpaa1, Keegan Stricker1, Sanjukta Guha Thakurta1, Ramin Rad1, Joshua Pan2, David P. Nusinow1, Joao A. Paulo1, Devin K. Schweppe1, Laura Pontano Vaites1, J. Wade Harper1*, Steven P. Gygi1*# 1Department of Cell Biology, Harvard Medical School, Boston, MA, 02115, USA. 2Broad Institute, Cambridge, MA, 02142, USA. 3Present address: ICCB-Longwood Screening Facility, Harvard Medical School, Boston, MA, 02115, USA. 4Present address: Merck, West Point, PA, 19486, USA. 5Present address: IQ Proteomics, Cambridge, MA, 02139, USA. 6Present address: Vor Biopharma, Cambridge, MA, 02142, USA. 7Present address: Rubius Therapeutics, Cambridge, MA, 02139, USA. 8Present address: RPS North America, South Kingstown, RI, 02879, USA. *Correspondence: [email protected] (E.L.H.), [email protected] (J.W.H.), [email protected] (S.P.G.) #Lead Contact: [email protected] bioRxiv preprint doi: https://doi.org/10.1101/2020.01.19.905109; this version posted January 19, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. -
A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated. -
Screening of a Clinically and Biochemically Diagnosed SOD Patient Using Exome Sequencing: a Case Report with a Mutations/Variations Analysis Approach
The Egyptian Journal of Medical Human Genetics (2016) 17, 131–136 HOSTED BY Ain Shams University The Egyptian Journal of Medical Human Genetics www.ejmhg.eg.net www.sciencedirect.com CASE REPORT Screening of a clinically and biochemically diagnosed SOD patient using exome sequencing: A case report with a mutations/variations analysis approach Mohamad-Reza Aghanoori a,b,1, Ghazaleh Mohammadzadeh Shahriary c,2, Mahdi Safarpour d,3, Ahmad Ebrahimi d,* a Department of Medical Genetics, Shiraz University of Medical Sciences, Shiraz, Iran b Research and Development Division, RoyaBioGene Co., Tehran, Iran c Department of Genetics, Shahid Chamran University of Ahvaz, Ahvaz, Iran d Cellular and Molecular Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran Received 12 May 2015; accepted 15 June 2015 Available online 22 July 2015 KEYWORDS Abstract Background: Sulfite oxidase deficiency (SOD) is a rare neurometabolic inherited disor- Sulfite oxidase deficiency; der causing severe delay in developmental stages and premature death. The disease follows an auto- Case report; somal recessive pattern of inheritance and causes deficiency in the activity of sulfite oxidase, an Exome sequencing enzyme that normally catalyzes conversion of sulfite to sulfate. Aim of the study: SOD is an underdiagnosed disorder and its diagnosis can be difficult in young infants as early clinical features and neuroimaging changes may imitate some common diseases. Since the prognosis of the disease is poor, using exome sequencing as a powerful and efficient strat- egy for identifying the genes underlying rare mendelian disorders can provide important knowledge about early diagnosis, disease mechanisms, biological pathways, and potential therapeutic targets. -
Transcriptional Profiling of Breast Cancer Cells in Response to Mevinolin: Evidence of Cell Cycle Arrest, DNA Degradation and Apoptosis
1886 INTERNATIONAL JOURNAL OF ONCOLOGY 48: 1886-1894, 2016 Transcriptional profiling of breast cancer cells in response to mevinolin: Evidence of cell cycle arrest, DNA degradation and apoptosis ALI M. MAHMOUD1,2, MOURAD A.M. ABOUL-SOUD1,3, JUNKYU HAN4,5, YAZEED A. AL-SHEIKH3, AHMED M. AL-ABD6 and HANY A. EL-SHEMY1 1Department of Biochemistry, Faculty of Agriculture, Cairo University, Giza 12613; 2Centre for Aging and Associated Diseases, Helmy Institute for Medical Sciences, Zewail City of Science and Technology, Giza 12588, Egypt; 3Chair of Medical and Molecular Genetics Research, Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Saud University, Riyadh 11433, Kingdom of Saudi Arabia; 4Graduate School of Life and Environmental Sciences; 5Alliance for Research on North Africa (ARENA), University of Tsukuba, Tsukuba, Ibaraki 305-8572, Japan; 6Department of Pharmacology, Medical Division, National Research Centre, Cairo 21622, Egypt Received January 29, 2015; Accepted March 3, 2016 DOI: 10.3892/ijo.2016.3418 Abstract. The merging of high-throughput gene expression lines. In addition, MVN‑induced transcript abundance profiles techniques, such as microarray, in the screening of natural inferred from microarrays showed significant changes in some products as anticancer agents, is considered the optimal solu- key cell processes. The changes were predicted to induce cell tion for gaining a better understanding of the intervention cycle arrest and reactive oxygen species generation but inhibit mechanism. Red yeast rice (RYR), a Chinese dietary product, DNA repair and cell proliferation. This MVN-mediated contains a mixture of hypocholesterolemia agents such as multi‑factorial stress triggered specific programmed cell death statins. -
1) (As of December 2018) and the Latest GWAS of AD (2
SUPPLEMENTARY FIGURES downstream intergenic ncRNA_exonic upstream ●936 ●918 group downstream intergenic ncRNA_exonic upstream group exonic exonicintronicintronic ncRNA_intronic ncRNA_intronicUTR3 UTR3 3.8% 1.2%1.5%1.9% 3.8% 5.4%5.4% 750 0.3% 3.8%1.2%1.5%1.9% ●700 5.4% ●670 0.3% 500 45.8% 40.240.2% % 45.8% ●329 ●274 250 ●223 Number (GWAS SNPs/studies) Number (GWAS ●128 ●105 45.8% ●54 ●57 ●58 ●48 ●42 ●46 ●50 ●30 ●3740.2% ● ●17 ●25 ●4 ●6 ●12 0 ● 2007 2008 2009 2010 2011 2012 2013 2014 2015 2016 2017 2018 2019 Year Supplementary Figure S1. GWAS of AD since 2007. The figure is based on data from the GWAS Catalog (1) (as of December 2018) and the latest GWAS of AD (2). The green area shows the total number of AD-associated SNPs, and the purple area shows the total number of GWAS of AD. The insert chart shows the proportions of different types of all 936 AD-associated SNPs. 1 100 200 RPS27A TGFB2 BIN1 C4BPB MSH2 PROC UGT1A1 RAB1A TTN DISC1 50 PDCL3 COL4A3 CD55 ERCC3 100 USP21 C4BPA ITSN2 PTPRF MPZ FMN2 INPP5D CEP85 FNBP1L CSF1 CD46 ADAMTS4 PRKRA SPRED2 0 CTNNA2 DGKD ADCY10 ZAP70 LIMS2 PDE1A PROX1 0 CHRNB2 CR1 HSPG2 SH3BGRL3 DAB1 CTBS FCER1G MAP3K2 AD risk score or log10(P value) IL6R CDC73 CD34 AD risk score or log10(P value) −50 B4GALT3 IL19 0 50 100 150 200 250 0 50 100 150 200 Chromosome 1 (Mb) Chromosome 2 (Mb) ATP2B2 LTF ARF4 MECOM PAK2 EPHB1 40 VHL PRSS42 ARL6IP5 150 COL25A1 TDGF1 RPSA CCR2 CCR1 IL1RAP IRAK2 20 PTPRG 100 FLNB TF CX3CR1 IL17RD SH3RF1 FGG FANCD2 LIMD1 CCR5 50 0 WDR1 PDGFRA EIF4E FGB AD risk score or log10(P value) AD risk -
Myopia in African Americans Is Significantly Linked to Chromosome 7P15.2-14.2
Genetics Myopia in African Americans Is Significantly Linked to Chromosome 7p15.2-14.2 Claire L. Simpson,1,2,* Anthony M. Musolf,2,* Roberto Y. Cordero,1 Jennifer B. Cordero,1 Laura Portas,2 Federico Murgia,2 Deyana D. Lewis,2 Candace D. Middlebrooks,2 Elise B. Ciner,3 Joan E. Bailey-Wilson,1,† and Dwight Stambolian4,† 1Department of Genetics, Genomics and Informatics and Department of Ophthalmology, University of Tennessee Health Science Center, Memphis, Tennessee, United States 2Computational and Statistical Genomics Branch, National Human Genome Research Institute, National Institutes of Health, Baltimore, Maryland, United States 3The Pennsylvania College of Optometry at Salus University, Elkins Park, Pennsylvania, United States 4Department of Ophthalmology, University of Pennsylvania, Philadelphia, Pennsylvania, United States Correspondence: Joan E. PURPOSE. The purpose of this study was to perform genetic linkage analysis and associ- Bailey-Wilson, NIH/NHGRI, 333 ation analysis on exome genotyping from highly aggregated African American families Cassell Drive, Suite 1200, Baltimore, with nonpathogenic myopia. African Americans are a particularly understudied popula- MD 21131, USA; tion with respect to myopia. [email protected]. METHODS. One hundred six African American families from the Philadelphia area with a CLS and AMM contributed equally to family history of myopia were genotyped using an Illumina ExomePlus array and merged this work and should be considered co-first authors. with previous microsatellite data. Myopia was initially measured in mean spherical equiv- JEB-W and DS contributed equally alent (MSE) and converted to a binary phenotype where individuals were identified as to this work and should be affected, unaffected, or unknown.