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Anthropoid Primate–Specific Retroviral Element THE1B Controls Expression of CRH in Placenta and Alters Gestation Length
SHORT REPORTS Anthropoid primate±specific retroviral element THE1B controls expression of CRH in placenta and alters gestation length 1 1 1 2 Caitlin E. Dunn-FletcherID *, Lisa M. Muglia , Mihaela Pavlicev , Gernot Wolf , Ming- An Sun2, Yueh-Chiang Hu3, Elizabeth Huffman1, Shivani Tumukuntala1, Katri Thiele1, Amrita Mukherjee1, Sandra Zoubovsky1, Xuzhe Zhang1, Kayleigh A. Swaggart1, Katherine Y. Bezold Lamm1, Helen Jones4, Todd S. Macfarlan2, Louis J. Muglia1* a1111111111 1 Division of Human Genetics, Center for Prevention of Preterm Birth, Perinatal Institute, Cincinnati a1111111111 Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, a1111111111 Cincinnati, Ohio, United States of America, 2 The Eunice Kennedy Shriver National Institute of Child Health a1111111111 and Human Development, The National Institutes of Health, Bethesda, Maryland, United States of America, 3 Division of Developmental Biology, Cincinnati Children's Hospital Medical Center, Department of a1111111111 Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio, United States of America, 4 Division of Pediatric Surgery, Cincinnati Children's Hospital Medical Center, Department of Surgery, University of Cincinnati College of Medicine, Cincinnati, Ohio, United States of America * [email protected] (CED); [email protected] (LJM) OPEN ACCESS Citation: Dunn-Fletcher CE, Muglia LM, Pavlicev M, Wolf G, Sun M-A, Hu Y-C, et al. (2018) Anthropoid Abstract primate±specific retroviral element THE1B controls expression of CRH in placenta and alters gestation Pregnancy and parturition are intricately regulated to ensure successful reproductive out- length. PLoS Biol 16(9): e2006337. https://doi.org/ comes. However, the factors that control gestational length in humans and other anthropoid 10.1371/journal.pbio.2006337 primates remain poorly defined. -
The Expression of Human Endogenous Retroviruses Is Modulated by the Tat Protein of HIV‐1
The Expression of Human Endogenous Retroviruses is modulated by the Tat protein of HIV‐1 by Marta Jeannette Gonzalez‐Hernandez A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy (Immunology) in The University of Michigan 2012 Doctoral Committee Professor David M. Markovitz, Chair Professor Gary Huffnagle Professor Michael J. Imperiale Associate Professor David J. Miller Assistant Professor Akira Ono Assistant Professor Christiane E. Wobus © Marta Jeannette Gonzalez‐Hernandez 2012 For my family and friends, the most fantastic teachers I have ever had. ii Acknowledgements First, and foremost, I would like to thank David Markovitz for his patience and his scientific and mentoring endeavor. My time in the laboratory has been an honor and a pleasure. Special thanks are also due to all the members of the Markovitz laboratory, past and present. It has been a privilege, and a lot of fun, to work near such excellent scientists and friends. You all have a special place in my heart. I would like to thank all the members of my thesis committee for all the valuable advice, help and jokes whenever needed. Our collaborators from the Bioinformatics Core, particularly James Cavalcoli, Fan Meng, Manhong Dai, Maureen Sartor and Gil Omenn gave generous support, technical expertise and scientific insight to a very important part of this project. Thank you. Thanks also go to Mariana Kaplan’s and Akira Ono’s laboratory for help with experimental designs and for being especially generous with time and reagents. iii Table of Contents Dedication ............................................................................................................................ ii Acknowledgements ............................................................................................................. iii List of Figures ................................................................................................................... -
Figure S1. Representative Report Generated by the Ion Torrent System Server for Each of the KCC71 Panel Analysis and Pcafusion Analysis
Figure S1. Representative report generated by the Ion Torrent system server for each of the KCC71 panel analysis and PCaFusion analysis. (A) Details of the run summary report followed by the alignment summary report for the KCC71 panel analysis sequencing. (B) Details of the run summary report for the PCaFusion panel analysis. A Figure S1. Continued. Representative report generated by the Ion Torrent system server for each of the KCC71 panel analysis and PCaFusion analysis. (A) Details of the run summary report followed by the alignment summary report for the KCC71 panel analysis sequencing. (B) Details of the run summary report for the PCaFusion panel analysis. B Figure S2. Comparative analysis of the variant frequency found by the KCC71 panel and calculated from publicly available cBioPortal datasets. For each of the 71 genes in the KCC71 panel, the frequency of variants was calculated as the variant number found in the examined cases. Datasets marked with different colors and sample numbers of prostate cancer are presented in the upper right. *Significantly high in the present study. Figure S3. Seven subnetworks extracted from each of seven public prostate cancer gene networks in TCNG (Table SVI). Blue dots represent genes that include initial seed genes (parent nodes), and parent‑child and child‑grandchild genes in the network. Graphical representation of node‑to‑node associations and subnetwork structures that differed among and were unique to each of the seven subnetworks. TCNG, The Cancer Network Galaxy. Figure S4. REVIGO tree map showing the predicted biological processes of prostate cancer in the Japanese. Each rectangle represents a biological function in terms of a Gene Ontology (GO) term, with the size adjusted to represent the P‑value of the GO term in the underlying GO term database. -
Loss of the Tectorial Membrane Protein CEACAM16 Enhances Spontaneous, Stimulus-Frequency, and Transiently Evoked Otoacoustic Emissions
The Journal of Neuroscience, July 30, 2014 • 34(31):10325–10338 • 10325 Cellular/Molecular Loss of the Tectorial Membrane Protein CEACAM16 Enhances Spontaneous, Stimulus-Frequency, and Transiently Evoked Otoacoustic Emissions Mary Ann Cheatham,1 Richard J. Goodyear,3 Kazuaki Homma,4 P. Kevin Legan,3 Julia Korchagina,3 Souvik Naskar,3 Jonathan H. Siegel,1 X Peter Dallos,1,2 Jing Zheng,4 and Guy P. Richardson3 1Roxelyn and Richard Pepper Department of Communication Sciences and Disorders, The Knowles Hearing Center, and 2Department of Neurobiology, Northwestern University, Evanston, Illinois 60208, 3Sussex Neuroscience, School of Life Sciences, University of Sussex, Falmer, Brighton, BN1 9QG, United Kingdom, and 4Department of Otolaryngology-Head and Neck Surgery, The Knowles Hearing Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611 ␣-Tectorin (TECTA), -tectorin (TECTB), and carcinoembryonic antigen-related cell adhesion molecule 16 (CEACAM) are secreted glycoproteins that are present in the tectorial membrane (TM), an extracellular structure overlying the hearing organ of the inner ear, the organ of Corti. Previous studies have shown that TECTA and TECTB are both required for formation of the striated-sheet matrix within which collagen fibrils of the TM are imbedded and that CEACAM16 interacts with TECTA. To learn more about the structural and functional significance of CEACAM16, we created a Ceacam16-null mutant mouse. In the absence of CEACAM16, TECTB levels are reduced, a clearly defined striated-sheet matrix does not develop, and Hensen’s stripe, a prominent feature in the basal two-thirds of the TM in WT mice, is absent. CEACAM16 is also shown to interact with TECTB, indicating that it may stabilize interactions between TECTA and TECTB. -
Role of Amylase in Ovarian Cancer Mai Mohamed University of South Florida, [email protected]
University of South Florida Scholar Commons Graduate Theses and Dissertations Graduate School July 2017 Role of Amylase in Ovarian Cancer Mai Mohamed University of South Florida, [email protected] Follow this and additional works at: http://scholarcommons.usf.edu/etd Part of the Pathology Commons Scholar Commons Citation Mohamed, Mai, "Role of Amylase in Ovarian Cancer" (2017). Graduate Theses and Dissertations. http://scholarcommons.usf.edu/etd/6907 This Dissertation is brought to you for free and open access by the Graduate School at Scholar Commons. It has been accepted for inclusion in Graduate Theses and Dissertations by an authorized administrator of Scholar Commons. For more information, please contact [email protected]. Role of Amylase in Ovarian Cancer by Mai Mohamed A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy Department of Pathology and Cell Biology Morsani College of Medicine University of South Florida Major Professor: Patricia Kruk, Ph.D. Paula C. Bickford, Ph.D. Meera Nanjundan, Ph.D. Marzenna Wiranowska, Ph.D. Lauri Wright, Ph.D. Date of Approval: June 29, 2017 Keywords: ovarian cancer, amylase, computational analyses, glycocalyx, cellular invasion Copyright © 2017, Mai Mohamed Dedication This dissertation is dedicated to my parents, Ahmed and Fatma, who have always stressed the importance of education, and, throughout my education, have been my strongest source of encouragement and support. They always believed in me and I am eternally grateful to them. I would also like to thank my brothers, Mohamed and Hussien, and my sister, Mariam. I would also like to thank my husband, Ahmed. -
Distinct Energy Metabolism of Auditory and Vestibular Sensory Epithelia
Distinct energy metabolism of auditory and vestibular PNAS PLUS sensory epithelia revealed by quantitative mass spectrometry using MS2 intensity Kateri J. Spinellia,b,1, John E. Klimekc,1, Phillip A. Wilmarthc, Jung-Bum Shina,b,2, Dongseok Choid, Larry L. Davidc,e, and Peter G. Gillespiea,b,3 aOregon Hearing Research Center, bVollum Institute, cProteomics Shared Resource, dDepartment of Public Health and Preventive Medicine, and eDepartment of Biochemistry and Molecular Biology, Oregon Health and Science University, Portland OR 97239 Edited by David P. Corey, Harvard Medical School, Boston, MA, and accepted by the Editorial Board December 14, 2011 (received for review September 26, 2011) Measuring the abundance of many proteins over a broad dynamic In our experiments, we desired an accurate quantitation method range requires accurate quantitation. We show empirically that, in for relative comparisons. Because varying peptide ionization, MS2 MS experiments, relative quantitation using summed dissociation- selection, and MS2 signal render the relationship between ion-cur- product ion-current intensities is accurate, albeit variable from rent intensity and peptide abundance uncertain, we sought to em- protein to protein, and outperforms spectral counting. By apply- pirically determine the suitability of MS2 intensity for protein ing intensities to quantify proteins in two complex but related quantitation under conditions of high protein complexity. Moreover, tissues, chick auditory and vestibular sensory epithelia, we find to verify our MS2 intensity quantitation methods, we sought a direct that glycolytic enzymes are enriched threefold in auditory epithe- comparison of the molecular composition of two related but distinct lia, whereas enzymes responsible for oxidative phosphorylation biological tissues. -
Proteomic Analysis of the Organ of Corti Using Nanoscale Liquid Chromatography Coupled with Tandem Mass Spectrometry
Int. J. Mol. Sci. 2012, 13, 8171-8188; doi:10.3390/ijms13078171 OPEN ACCESS International Journal of Molecular Sciences ISSN 1422-0067 www.mdpi.com/journal/ijms Article Proteomic Analysis of the Organ of Corti Using Nanoscale Liquid Chromatography Coupled with Tandem Mass Spectrometry Hong Peng 1,2, Miao Liu 1, Jason Pecka 3, Kirk W. Beisel 3,* and Shi-Jian Ding 1,4,* 1 Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198, USA; E-Mails: [email protected] (H.P.); [email protected] (M.L.) 2 Department of Environmental, Agricultural & Occupational Health, University of Nebraska Medical Center, Omaha, NE 68198, USA 3 Department of Biomedical Sciences, Creighton University, Omaha, NE 68178, USA; E-Mail: [email protected] 4 Mass Spectrometry and Proteomics Core Facility, University of Nebraska Medical Center, Omaha, NE 68198, USA * Authors to whom correspondence should be addressed; E-Mails: [email protected] (K.W.B.); [email protected] (S.-J.D.); Tel.: +1-402-280-4069 (K.W.B.); +1-402-559-4183 (S.-J.D.); Fax: +1-402-280-2690 (K.W.B.); +1-402-559-4651 (S.-J.D.). Received: 27 May 2012; in revised form: 5 June 2012 / Accepted: 25 June 2012 / Published: 2 July 2012 Abstract: The organ of Corti (OC) in the cochlea plays an essential role in auditory signal transduction in the inner ear. For its minute size and trace amount of proteins, the identification of the molecules in pathophysiologic processes in the bone-encapsulated OC requires both delicate separation and a highly sensitive analytical tool. -
Supplemental Table 3 Site ID Intron Poly(A) Site Type NM/KG Inum
Supplemental Table 3 Site ID Intron Poly(A) site Type NM/KG Inum Region Gene ID Gene Symbol Gene Annotation Hs.120277.1.10 chr3:170997234:170996860 170996950 b NM_153353 7 CDS 151827 LRRC34 leucine rich repeat containing 34 Hs.134470.1.27 chr17:53059664:53084458 53065543 b NM_138962 10 CDS 124540 MSI2 musashi homolog 2 (Drosophila) Hs.162889.1.18 chr14:80367239:80329208 80366262 b NM_152446 12 CDS 145508 C14orf145 chromosome 14 open reading frame 145 Hs.187898.1.27 chr22:28403623:28415294 28404458 b NM_181832 16 3UTR 4771 NF2 neurofibromin 2 (bilateral acoustic neuroma) Hs.228320.1.6 chr10:115527009:115530350 115527470 b BC036365 5 CDS 79949 C10orf81 chromosome 10 open reading frame 81 Hs.266308.1.2 chr11:117279579:117278191 117278967 b NM_032046 12 CDS 84000 TMPRSS13 transmembrane protease, serine 13 Hs.266308.1.4 chr11:117284536:117281662 117283722 b NM_032046 9 CDS 84000 TMPRSS13 transmembrane protease, serine 13 Hs.2689.1.4 chr10:53492398:53563605 53492622 b NM_006258 7 CDS 5592 PRKG1 protein kinase, cGMP-dependent, type I Hs.280781.1.6 chr18:64715646:64829150 64715837 b NM_024781 4 CDS 79839 C18orf14 chromosome 18 open reading frame 14 Hs.305985.2.25 chr12:8983686:8984438 8983942 b BX640639 17 3UTR NA NA NA Hs.312098.1.36 chr1:151843991:151844258 151844232 b NM_003815 15 CDS 8751 ADAM15 a disintegrin and metalloproteinase domain 15 (metargidin) Hs.314338.1.11 chr21:39490293:39481214 39487623 b NM_018963 41 CDS 54014 BRWD1 bromodomain and WD repeat domain containing 1 Hs.33368.1.3 chr15:92685158:92689361 92688314 b NM_018349 6 CDS 55784 MCTP2 multiple C2-domains with two transmembrane regions 2 Hs.346736.1.21 chr2:99270738:99281614 99272414 b AK126402 10 3UTR 51263 MRPL30 mitochondrial ribosomal protein L30 Hs.445061.1.19 chr16:69322898:69290216 69322712 b NM_018052 14 CDS 55697 VAC14 Vac14 homolog (S. -
Expression of Placental Regulatory Genes Is Associated with Fetal Growth
City University of New York (CUNY) CUNY Academic Works Publications and Research Queens College 2017 Expression of Placental Regulatory Genes Is Associated with Fetal Growth Maya A. Deyssenroth Icahn School of Medicine at Mount Sinai Qian Li Icahn School of Medicine at Mount Sinai Marina Lacasaña Andalusian School of Public Health Yoko Nomura CUNY Queens College Carmen Marsit Emory University See next page for additional authors How does access to this work benefit ou?y Let us know! More information about this work at: https://academicworks.cuny.edu/qc_pubs/189 Discover additional works at: https://academicworks.cuny.edu This work is made publicly available by the City University of New York (CUNY). Contact: [email protected] Authors Maya A. Deyssenroth, Qian Li, Marina Lacasaña, Yoko Nomura, Carmen Marsit, and Jia Chen This article is available at CUNY Academic Works: https://academicworks.cuny.edu/qc_pubs/189 J. Perinat. Med. 2017; aop Maya A. Deyssenrotha, Qian Lia, Marina Lacasaña, Yoko Nomura, Carmen Marsit and Jia Chen* Expression of placental regulatory genes is associated with fetal growth DOI 10.1515/jpm-2017-0064 independent cohort (n = 306). Given that aberrant fetal Received February 25, 2017. Accepted May 31, 2017. growth may have long-lasting effects, our results suggest the potential utility of placental gene expression profiles as Abstract: The placenta is the principal organ regulating potential early markers of disease onset later in life. respiratory, nutritional, endocrine and metabolic functions on behalf of the developing fetus. Changes in gene expres- Keywords: Birth weight; gene expression, placenta. sion patterns of placenta-specific genes may influence fetal growth. -
Supplementary Material Computational Prediction of SARS
Supplementary_Material Computational prediction of SARS-CoV-2 encoded miRNAs and their putative host targets Sheet_1 List of potential stem-loop structures in SARS-CoV-2 genome as predicted by VMir. Rank Name Start Apex Size Score Window Count (Absolute) Direct Orientation 1 MD13 2801 2864 125 243.8 61 2 MD62 11234 11286 101 211.4 49 4 MD136 27666 27721 104 205.6 119 5 MD108 21131 21184 110 204.7 210 9 MD132 26743 26801 119 188.9 252 19 MD56 9797 9858 128 179.1 59 26 MD139 28196 28233 72 170.4 133 28 MD16 2934 2974 76 169.9 71 43 MD103 20002 20042 80 159.3 403 46 MD6 1489 1531 86 156.7 171 51 MD17 2981 3047 131 152.8 38 87 MD4 651 692 75 140.3 46 95 MD7 1810 1872 121 137.4 58 116 MD140 28217 28252 72 133.8 62 122 MD55 9712 9758 96 132.5 49 135 MD70 13171 13219 93 130.2 131 164 MD95 18782 18820 79 124.7 184 173 MD121 24086 24135 99 123.1 45 176 MD96 19046 19086 75 123.1 179 196 MD19 3197 3236 76 120.4 49 200 MD86 17048 17083 73 119.8 428 223 MD75 14534 14600 137 117 51 228 MD50 8824 8870 94 115.8 79 234 MD129 25598 25642 89 115.6 354 Reverse Orientation 6 MR61 19088 19132 88 197.8 271 10 MR72 23563 23636 148 188.8 286 11 MR11 3775 3844 136 185.1 116 12 MR94 29532 29582 94 184.6 271 15 MR43 14973 15028 109 183.9 226 27 MR14 4160 4206 89 170 241 34 MR35 11734 11792 111 164.2 37 52 MR5 1603 1652 89 152.7 118 53 MR57 18089 18132 101 152.7 139 94 MR8 2804 2864 122 137.4 38 107 MR58 18474 18508 72 134.9 237 117 MR16 4506 4540 72 133.8 311 120 MR34 10010 10048 82 132.7 245 133 MR7 2534 2578 90 130.4 75 146 MR79 24766 24808 75 127.9 59 150 MR65 21528 21576 99 127.4 83 180 MR60 19016 19049 70 122.5 72 187 MR51 16450 16482 75 121 363 190 MR80 25687 25734 96 120.6 75 198 MR64 21507 21544 70 120.3 35 206 MR41 14500 14542 84 119.2 94 218 MR84 26840 26894 108 117.6 94 Sheet_2 List of stable stem-loop structures based on MFE. -
Supplementary Table 1
Supplementary Table 1. 492 genes are unique to 0 h post-heat timepoint. The name, p-value, fold change, location and family of each gene are indicated. Genes were filtered for an absolute value log2 ration 1.5 and a significance value of p ≤ 0.05. Symbol p-value Log Gene Name Location Family Ratio ABCA13 1.87E-02 3.292 ATP-binding cassette, sub-family unknown transporter A (ABC1), member 13 ABCB1 1.93E-02 −1.819 ATP-binding cassette, sub-family Plasma transporter B (MDR/TAP), member 1 Membrane ABCC3 2.83E-02 2.016 ATP-binding cassette, sub-family Plasma transporter C (CFTR/MRP), member 3 Membrane ABHD6 7.79E-03 −2.717 abhydrolase domain containing 6 Cytoplasm enzyme ACAT1 4.10E-02 3.009 acetyl-CoA acetyltransferase 1 Cytoplasm enzyme ACBD4 2.66E-03 1.722 acyl-CoA binding domain unknown other containing 4 ACSL5 1.86E-02 −2.876 acyl-CoA synthetase long-chain Cytoplasm enzyme family member 5 ADAM23 3.33E-02 −3.008 ADAM metallopeptidase domain Plasma peptidase 23 Membrane ADAM29 5.58E-03 3.463 ADAM metallopeptidase domain Plasma peptidase 29 Membrane ADAMTS17 2.67E-04 3.051 ADAM metallopeptidase with Extracellular other thrombospondin type 1 motif, 17 Space ADCYAP1R1 1.20E-02 1.848 adenylate cyclase activating Plasma G-protein polypeptide 1 (pituitary) receptor Membrane coupled type I receptor ADH6 (includes 4.02E-02 −1.845 alcohol dehydrogenase 6 (class Cytoplasm enzyme EG:130) V) AHSA2 1.54E-04 −1.6 AHA1, activator of heat shock unknown other 90kDa protein ATPase homolog 2 (yeast) AK5 3.32E-02 1.658 adenylate kinase 5 Cytoplasm kinase AK7 -
Whole Exome Sequencing to Investigate Genetic Variants of Non-Syndromic Hearing Impairment in a Population of African Ancestry
Whole exome sequencing to investigate genetic variants of non-syndromic hearing impairment in a population of African Ancestry By Noluthando Manyisa MNYNOL006 Submitted to the University of Cape Town in fulfilment of requirements of the degree MSc Med in Human UniversityGenetics of Cape Town University of Cape Town, Faculty of Health Sciences, Department of Pathology, Faculty of Human Genetics Supervisor: Professor Ambroise Wonkam Co-Supervisors: Professor Collet Dandara and Dr Emile Chimusa Word Count: 18 772 Date of Submission: February 2018 1 The copyright of this thesis vests in the author. No quotation from it or information derived from it is to be published without full acknowledgement of the source. The thesis is to be used for private study or non- commercial research purposes only. Published by the University of Cape Town (UCT) in terms of the non-exclusive license granted to UCT by the author. University of Cape Town Table of Contents Plagiarism declaration ................................................................................................................ I Acknowledgments..................................................................................................................... II List of Figures and Tables........................................................................................................ III Figures.................................................................................................................................. III Tables ..................................................................................................................................