Open Data for Differential Network Analysis in Glioma
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Analysis of Trans Esnps Infers Regulatory Network Architecture
Analysis of trans eSNPs infers regulatory network architecture Anat Kreimer Submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Graduate School of Arts and Sciences COLUMBIA UNIVERSITY 2014 © 2014 Anat Kreimer All rights reserved ABSTRACT Analysis of trans eSNPs infers regulatory network architecture Anat Kreimer eSNPs are genetic variants associated with transcript expression levels. The characteristics of such variants highlight their importance and present a unique opportunity for studying gene regulation. eSNPs affect most genes and their cell type specificity can shed light on different processes that are activated in each cell. They can identify functional variants by connecting SNPs that are implicated in disease to a molecular mechanism. Examining eSNPs that are associated with distal genes can provide insights regarding the inference of regulatory networks but also presents challenges due to the high statistical burden of multiple testing. Such association studies allow: simultaneous investigation of many gene expression phenotypes without assuming any prior knowledge and identification of unknown regulators of gene expression while uncovering directionality. This thesis will focus on such distal eSNPs to map regulatory interactions between different loci and expose the architecture of the regulatory network defined by such interactions. We develop novel computational approaches and apply them to genetics-genomics data in human. We go beyond pairwise interactions to define network motifs, including regulatory modules and bi-fan structures, showing them to be prevalent in real data and exposing distinct attributes of such arrangements. We project eSNP associations onto a protein-protein interaction network to expose topological properties of eSNPs and their targets and highlight different modes of distal regulation. -
ACE2 Interaction Networks in COVID-19: a Physiological Framework for Prediction of Outcome in Patients with Cardiovascular Risk Factors
Journal of Clinical Medicine Article ACE2 Interaction Networks in COVID-19: A Physiological Framework for Prediction of Outcome in Patients with Cardiovascular Risk Factors Zofia Wicik 1,2 , Ceren Eyileten 2, Daniel Jakubik 2,Sérgio N. Simões 3, David C. Martins Jr. 1, Rodrigo Pavão 1, Jolanta M. Siller-Matula 2,4,* and Marek Postula 2 1 Centro de Matemática, Computação e Cognição, Universidade Federal do ABC, Santo Andre 09606-045, Brazil; zofi[email protected] (Z.W.); [email protected] (D.C.M.J.); [email protected] (R.P.) 2 Department of Experimental and Clinical Pharmacology, Medical University of Warsaw, Center for Preclinical Research and Technology CEPT, 02-091 Warsaw, Poland; [email protected] (C.E.); [email protected] (D.J.); [email protected] (M.P.) 3 Federal Institute of Education, Science and Technology of Espírito Santo, Serra, Espírito Santo 29056-264, Brazil; [email protected] 4 Department of Internal Medicine II, Division of Cardiology, Medical University of Vienna, 1090 Vienna, Austria * Correspondence: [email protected]; Tel.: +43-1-40400-46140; Fax: +43-1-40400-42160 Received: 9 October 2020; Accepted: 17 November 2020; Published: 21 November 2020 Abstract: Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (coronavirus disease 2019; COVID-19) is associated with adverse outcomes in patients with cardiovascular disease (CVD). The aim of the study was to characterize the interaction between SARS-CoV-2 and Angiotensin-Converting Enzyme 2 (ACE2) functional networks with a focus on CVD. Methods: Using the network medicine approach and publicly available datasets, we investigated ACE2 tissue expression and described ACE2 interaction networks that could be affected by SARS-CoV-2 infection in the heart, lungs and nervous system. -
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. -
Towards a Molecular Understanding of Microrna-Mediated Gene Silencing
REVIEWS NON-CODING RNA Towards a molecular understanding of microRNA-mediated gene silencing Stefanie Jonas and Elisa Izaurralde Abstract | MicroRNAs (miRNAs) are a conserved class of small non-coding RNAs that assemble with Argonaute proteins into miRNA-induced silencing complexes (miRISCs) to direct post-transcriptional silencing of complementary mRNA targets. Silencing is accomplished through a combination of translational repression and mRNA destabilization, with the latter contributing to most of the steady-state repression in animal cell cultures. Degradation of the mRNA target is initiated by deadenylation, which is followed by decapping and 5ʹ‑to‑3ʹ exonucleolytic decay. Recent work has enhanced our understanding of the mechanisms of silencing, making it possible to describe in molecular terms a continuum of direct interactions from miRNA target recognition to mRNA deadenylation, decapping and 5ʹ‑to‑3ʹ degradation. Furthermore, an intricate interplay between translational repression and mRNA degradation is emerging. Deadenylation MicroRNAs (miRNAs) are conserved post-transcriptional recruit additional protein partners to mediate silenc- 5,6 Shortening of mRNA poly(A) regulators of gene expression that are integral to ing . Silencing occurs through a combination of tails. In eukaryotes, this almost all known biological processes, including translational repression, deadenylation, decapping and process is catalysed by the cell growth, proliferation and differentiation, as well 5ʹ‑to‑3ʹ mRNA degradation5,6 (FIG. 1). The GW182 pro- consecutive but partially as organismal metabolism and development1. The teins play a central part in this process and are among redundant action of two 5,6 cytoplasmic deadenylase number of miRNAs encoded within the genomes of the most extensively studied AGO partners . -
1 Canonical BAF Complex in Regulatory T Cells 2 3 Chin
bioRxiv preprint doi: https://doi.org/10.1101/2020.02.26.964981; this version posted February 27, 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. 1 A genome-wide CRISPR screen reveals a role for the BRD9-containing non- 2 canonical BAF complex in regulatory T cells 3 4 Chin-San Loo1,3,#, Jovylyn Gatchalian2,#, Yuqiong Liang1, Mathias Leblanc1, Mingjun 5 Xie1, Josephine Ho2, Bhargav Venkatraghavan1, Diana C. Hargreaves2*, and Ye 6 Zheng1* 7 8 1. NOMIS Center for Immunobiology and Microbial Pathogenesis, Salk Institute for 9 Biological Studies 10 2. Molecular and Cellular Biology Laboratory, Salk Institute for Biological Studies 11 3. Division of Biological Sciences, University of California, San Diego 12 # Co-first authors 13 * Co-corresponding authors 14 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.02.26.964981; this version posted February 27, 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. 15 Summary 16 Regulatory T cells (Tregs) play a pivotal role in suppressing auto-reactive T cells 17 and maintaining immune homeostasis. Treg development and function are 18 dependent on the transcription factor Foxp3. Here we performed a genome-wide 19 CRISPR/Cas9 knockout screen to identify the regulators of Foxp3 in mouse 20 primary Tregs. The results showed that Foxp3 regulators are highly enriched in 21 genes encoding SWI/SNF and SAGA complex subunits. Among the three 22 SWI/SNF-related complexes, the non-canonical or ncBAF (also called GBAF or 23 BRD9-containing BAF) complex promoted the expression of Foxp3, whereas the 24 PBAF complex repressed its expression. -
Requirement for Cyclin D3 in Germinal Center Formation and Function
Cell Research (2010) :1-16. © 2010 IBCB, SIBS, CAS All rights reserved 1001-0602/10 $ 32.00 npg ORIGINAL ARTICLE www.nature.com/cr Requirement for cyclin D3 in germinal center formation and function Jonathan U Peled1, J Jessica Yu1, Jeganathan Venkatesh2, Enguang Bi1, B Belinda Ding1, 5, Melissa Krupski-Downs1, Rita Shaknovich3, Piotr Sicinski4, Betty Diamond2, Matthew D Scharff1, B Hilda Ye1 1Department of Cell Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA; 2The Center for Autoimmune and Musculoskeletal Disease, The Feinstein Institute for Medical Research, Manhasset, NY 11030, USA; 3Depart- ments of Medicine and Pathology, Weill Cornell College of Medicine, New York, NY 10021, USA; 4Department of Cancer Biology, Dana-Farber Cancer Institute, and Department of Pathology, Harvard Medical School, Boston, MA 02115, USA Germinal centers (GC) of secondary lymphoid tissues are critical to mounting a high-affinity humoral immune response. B cells within the GC undergo rapid clonal expansion and selection while diversifying their antibody genes. Although it is generally believed that GC B cells employ a unique proliferative program to accommodate these pro- cesses, little is known about how the GC-associated cell cycle is orchestrated. The D-type cyclins constitute an im- portant component of the cell cycle engine that enables the cells to respond to physiological changes. Cell type- and developmental stage-specific roles of D-type cyclins have been described but the cyclin D requirement during GC reaction has not been addressed. In this study, we report that cyclin D3 is largely dispensable for proliferation and Ig class switching of in vitro activated B cells. -
Genetic and Genomic Analysis of Hyperlipidemia, Obesity and Diabetes Using (C57BL/6J × TALLYHO/Jngj) F2 Mice
University of Tennessee, Knoxville TRACE: Tennessee Research and Creative Exchange Nutrition Publications and Other Works Nutrition 12-19-2010 Genetic and genomic analysis of hyperlipidemia, obesity and diabetes using (C57BL/6J × TALLYHO/JngJ) F2 mice Taryn P. Stewart Marshall University Hyoung Y. Kim University of Tennessee - Knoxville, [email protected] Arnold M. Saxton University of Tennessee - Knoxville, [email protected] Jung H. Kim Marshall University Follow this and additional works at: https://trace.tennessee.edu/utk_nutrpubs Part of the Animal Sciences Commons, and the Nutrition Commons Recommended Citation BMC Genomics 2010, 11:713 doi:10.1186/1471-2164-11-713 This Article is brought to you for free and open access by the Nutrition at TRACE: Tennessee Research and Creative Exchange. It has been accepted for inclusion in Nutrition Publications and Other Works by an authorized administrator of TRACE: Tennessee Research and Creative Exchange. For more information, please contact [email protected]. Stewart et al. BMC Genomics 2010, 11:713 http://www.biomedcentral.com/1471-2164/11/713 RESEARCH ARTICLE Open Access Genetic and genomic analysis of hyperlipidemia, obesity and diabetes using (C57BL/6J × TALLYHO/JngJ) F2 mice Taryn P Stewart1, Hyoung Yon Kim2, Arnold M Saxton3, Jung Han Kim1* Abstract Background: Type 2 diabetes (T2D) is the most common form of diabetes in humans and is closely associated with dyslipidemia and obesity that magnifies the mortality and morbidity related to T2D. The genetic contribution to human T2D and related metabolic disorders is evident, and mostly follows polygenic inheritance. The TALLYHO/ JngJ (TH) mice are a polygenic model for T2D characterized by obesity, hyperinsulinemia, impaired glucose uptake and tolerance, hyperlipidemia, and hyperglycemia. -
Plenary and Platform Abstracts
American Society of Human Genetics 68th Annual Meeting PLENARY AND PLATFORM ABSTRACTS Abstract #'s Tuesday, October 16, 5:30-6:50 pm: 4. Featured Plenary Abstract Session I Hall C #1-#4 Wednesday, October 17, 9:00-10:00 am, Concurrent Platform Session A: 6. Variant Insights from Large Population Datasets Ballroom 20A #5-#8 7. GWAS in Combined Cancer Phenotypes Ballroom 20BC #9-#12 8. Genome-wide Epigenomics and Non-coding Variants Ballroom 20D #13-#16 9. Clonal Mosaicism in Cancer, Alzheimer's Disease, and Healthy Room 6A #17-#20 Tissue 10. Genetics of Behavioral Traits and Diseases Room 6B #21-#24 11. New Frontiers in Computational Genomics Room 6C #25-#28 12. Bone and Muscle: Identifying Causal Genes Room 6D #29-#32 13. Precision Medicine Initiatives: Outcomes and Lessons Learned Room 6E #33-#36 14. Environmental Exposures in Human Traits Room 6F #37-#40 Wednesday, October 17, 4:15-5:45 pm, Concurrent Platform Session B: 24. Variant Interpretation Practices and Resources Ballroom 20A #41-#46 25. Integrated Variant Analysis in Cancer Genomics Ballroom 20BC #47-#52 26. Gene Discovery and Functional Models of Neurological Disorders Ballroom 20D #53-#58 27. Whole Exome and Whole Genome Associations Room 6A #59-#64 28. Sequencing-based Diagnostics for Newborns and Infants Room 6B #65-#70 29. Omics Studies in Alzheimer's Disease Room 6C #71-#76 30. Cardiac, Valvular, and Vascular Disorders Room 6D #77-#82 31. Natural Selection and Human Phenotypes Room 6E #83-#88 32. Genetics of Cardiometabolic Traits Room 6F #89-#94 Wednesday, October 17, 6:00-7:00 pm, Concurrent Platform Session C: 33. -
ARP36414 P050) Data Sheet
SNRNP200 antibody - N-terminal region (ARP36414_P050) Data Sheet Product Number ARP36414_P050 Product Name SNRNP200 antibody - N-terminal region (ARP36414_P050) Size 50ug Gene Symbol SNRNP200 Alias Symbols ASCC3L1; BRR2; FLJ11521; HELIC2; RP33; U5-200KD Nucleotide Accession# NM_014014 Protein Size (# AA) 2136 amino acids Molecular Weight 244kDa Product Format Lyophilized powder NCBI Gene Id 23020 Host Rabbit Clonality Polyclonal Official Gene Full Name Small nuclear ribonucleoprotein 200kDa (U5) This is a rabbit polyclonal antibody against SNRNP200. It was validated on Western Blot by Aviva Systems Biology. At Aviva Systems Biology we manufacture rabbit polyclonal antibodies on a large scale (200-1000 Description products/month) of high throughput manner. Our antibodies are peptide based and protein family oriented. We usually provide antibodies covering each member of a whole protein family of your interest. We also use our best efforts to provide you antibodies recognize various epitopes of a target protein. For availability of antibody needed for your experiment, please inquire (). Peptide Sequence Synthetic peptide located within the following region: GDEDVYGEVREEASDDDMEGDEAVVRCTLSANLVASGELMSSKKKDLHPR Pre-mRNA splicing is catalyzed by the spliceosome, a complex of specialized RNA and protein subunits that removes introns from a transcribed pre-mRNA segment. The spliceosome consists of small nuclear RNA proteins (snRNPs) U1, U2, U4, U5 and U6, together with approximately 80 conserved proteins. U5 snRNP Description of Target contains nine specific proteins. This gene encodes one of the U5 snRNP-specific proteins. This protein belongs to the DEXH-box family of putative RNA helicases. It is a core component of U4/U6-U5 snRNPs and appears to catalyze an ATP-dependent unwinding of U4/U6 RNA duplices. -
Large-Scale Rnai Screening Uncovers New Therapeutic Targets in the Human Parasite
bioRxiv preprint doi: https://doi.org/10.1101/2020.02.05.935833; this version posted February 6, 2020. 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 4.0 International license. 1 Large-scale RNAi screening uncovers new therapeutic targets in the human parasite 2 Schistosoma mansoni 3 4 Jipeng Wang1*, Carlos Paz1*, Gilda Padalino2, Avril Coghlan3, Zhigang Lu3, Irina Gradinaru1, 5 Julie N.R. Collins1, Matthew Berriman3, Karl F. Hoffmann2, James J. Collins III1†. 6 7 8 1Department of Pharmacology, UT Southwestern Medical Center, Dallas, Texas 75390 9 2Institute of Biological, Environmental and Rural Sciences (IBERS), Aberystwyth University, 10 Aberystwyth, Wales, UK. 11 3Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge CB10 1SA, UK 12 *Equal Contribution 13 14 15 16 17 18 19 20 21 22 23 †To whom correspondence should be addressed 24 [email protected] 25 UT Southwestern Medical Center 26 Department of Pharmacology 27 6001 Forest Park. Rd. 28 Dallas, TX 75390 29 United States of America bioRxiv preprint doi: https://doi.org/10.1101/2020.02.05.935833; this version posted February 6, 2020. 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 4.0 International license. 30 ABSTRACT 31 Schistosomes kill 250,000 people every year and are responsible for serious morbidity in 240 32 million of the world’s poorest people. -
Altered Gene Expression Encoding Cytochines, Grow Factors and Cell Cycle Regulators in the Endometrium of Women with Chronic Endometritis
diagnostics Article Altered Gene Expression Encoding Cytochines, Grow Factors and Cell Cycle Regulators in the Endometrium of Women with Chronic Endometritis Ettore Cicinelli 1, Amerigo Vitagliano 2,* , Vera Loizzi 1, Dominique De Ziegler 3, Margherita Fanelli 4 , Stefano Bettocchi 1, Claudia Nardelli 1, Giuseppe Trojano 1, Rossana Cicinelli 1, Crescenzio Francesco Minervini 5 , Daniela Leronni 6 and Luigi Viggiano 7 1 2nd Unit of Obstetrics and Gynecology, Department of Biomedical and Human Oncologic Science, Policlinico University of Bari, 70124 Bari, Italy; [email protected] (E.C.); [email protected] (V.L.); [email protected] (S.B.); [email protected] (C.N.); [email protected] (G.T.); [email protected] (R.C.) 2 Department of Women and Children’s Health, University of Padua, 35128 Padua, Italy 3 Department of Ob Gyn and Reproductive Medicine, Foch Hospital, 92150 Suresnes, France; [email protected] 4 Interdisciplinary Department of Medicine, University of Bari, 70124 Bari, Italy; [email protected] 5 Department of Emergency and Organ Transplantation (D.E.T.O.), Hematology Section, University of Bari, 70124 Bari, Italy; [email protected] 6 Neuroapoptosis Laboratory, Department of Neurological Surgery, University of Pittsburgh, Pittsburgh, PA 15213, USA; [email protected] 7 Department of Biology, University of Bari, 700124 Bari, Italy; [email protected] * Correspondence: [email protected]; Tel.: +39-333-1467105; Fax: +39-049-8211785 Citation: Cicinelli, E.; Vitagliano, A.; Loizzi, V.; De Ziegler, D.; Fanelli, M.; Abstract: To evaluate the expression of genes encoding cytokines, grow factors and cell cycle regula- Bettocchi, S.; Nardelli, C.; Trojano, G.; tors in the proliferative endometrium of women with chronic endometritis (CE) compared to controls. -
A Population-Specific Major Allele Reference Genome from the United
Edith Cowan University Research Online ECU Publications Post 2013 2021 A population-specific major allele efr erence genome from the United Arab Emirates population Gihan Daw Elbait Andreas Henschel Guan K. Tay Edith Cowan University Habiba S. Al Safar Follow this and additional works at: https://ro.ecu.edu.au/ecuworkspost2013 Part of the Life Sciences Commons, and the Medicine and Health Sciences Commons 10.3389/fgene.2021.660428 Elbait, G. D., Henschel, A., Tay, G. K., & Al Safar, H. S. (2021). A population-specific major allele reference genome from the United Arab Emirates population. Frontiers in Genetics, 12, article 660428. https://doi.org/10.3389/ fgene.2021.660428 This Journal Article is posted at Research Online. https://ro.ecu.edu.au/ecuworkspost2013/10373 fgene-12-660428 April 19, 2021 Time: 16:18 # 1 ORIGINAL RESEARCH published: 23 April 2021 doi: 10.3389/fgene.2021.660428 A Population-Specific Major Allele Reference Genome From The United Arab Emirates Population Gihan Daw Elbait1†, Andreas Henschel1,2†, Guan K. Tay1,3,4,5 and Habiba S. Al Safar1,3,6* 1 Center for Biotechnology, Khalifa University of Science and Technology, Abu Dhabi, United Arab Emirates, 2 Department of Electrical Engineering and Computer Science, Khalifa University of Science and Technology, Abu Dhabi, United Arab Emirates, 3 Department of Biomedical Engineering, Khalifa University of Science and Technology, Abu Dhabi, United Arab Emirates, 4 Division of Psychiatry, Faculty of Health and Medical Sciences, The University of Western Australia, Crawley, WA, Australia, 5 School of Medical and Health Sciences, Edith Cowan University, Joondalup, WA, Australia, 6 Department of Genetics and Molecular Biology, College of Medicine and Health Sciences, Khalifa University of Science and Technology, Abu Dhabi, United Arab Emirates The ethnic composition of the population of a country contributes to the uniqueness of each national DNA sequencing project and, ideally, individual reference genomes are required to reduce the confounding nature of ethnic bias.