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The RNA Response to DNA Damage
ÔØ ÅÒÙ×Ö ÔØ The RNA response to DNA damage Luciana E. Giono, Nicol´as Nieto Moreno, Adri´an E. Cambindo Botto, Gwendal Dujardin, Manuel J. Mu˜noz, Alberto R. Kornblihtt PII: S0022-2836(16)00177-7 DOI: doi: 10.1016/j.jmb.2016.03.004 Reference: YJMBI 65022 To appear in: Journal of Molecular Biology Received date: 10 December 2015 Revised date: 1 March 2016 Accepted date: 7 March 2016 Please cite this article as: Giono, L.E., Moreno, N.N., Botto, A.E.C., Dujardin, G., Mu˜noz, M.J. & Kornblihtt, A.R., The RNA response to DNA damage, Journal of Molec- ular Biology (2016), doi: 10.1016/j.jmb.2016.03.004 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. ACCEPTED MANUSCRIPT The RNA response to DNA damage Luciana E. Giono1, Nicolás Nieto Moreno1, Adrián E. Cambindo Botto1, Gwendal Dujardin1,2, Manuel J. Muñoz1, and Alberto R. Kornblihtt1* 1Instituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE-UBA-CONICET) and Departamento de Fisiología, Biología Molecular y Celular, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Ciudad Universitaria, Pabellón 2, C1428EHA Buenos Aires, Argentina 2Centre for GenomicACCEPTED Regulation. Dr. -
The Rise and Fall of the Bovine Corpus Luteum
University of Nebraska Medical Center DigitalCommons@UNMC Theses & Dissertations Graduate Studies Spring 5-6-2017 The Rise and Fall of the Bovine Corpus Luteum Heather Talbott University of Nebraska Medical Center Follow this and additional works at: https://digitalcommons.unmc.edu/etd Part of the Biochemistry Commons, Molecular Biology Commons, and the Obstetrics and Gynecology Commons Recommended Citation Talbott, Heather, "The Rise and Fall of the Bovine Corpus Luteum" (2017). Theses & Dissertations. 207. https://digitalcommons.unmc.edu/etd/207 This Dissertation is brought to you for free and open access by the Graduate Studies at DigitalCommons@UNMC. It has been accepted for inclusion in Theses & Dissertations by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. THE RISE AND FALL OF THE BOVINE CORPUS LUTEUM by Heather Talbott A DISSERTATION Presented to the Faculty of the University of Nebraska Graduate College in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy Biochemistry and Molecular Biology Graduate Program Under the Supervision of Professor John S. Davis University of Nebraska Medical Center Omaha, Nebraska May, 2017 Supervisory Committee: Carol A. Casey, Ph.D. Andrea S. Cupp, Ph.D. Parmender P. Mehta, Ph.D. Justin L. Mott, Ph.D. i ACKNOWLEDGEMENTS This dissertation was supported by the Agriculture and Food Research Initiative from the USDA National Institute of Food and Agriculture (NIFA) Pre-doctoral award; University of Nebraska Medical Center Graduate Student Assistantship; University of Nebraska Medical Center Exceptional Incoming Graduate Student Award; the VA Nebraska-Western Iowa Health Care System Department of Veterans Affairs; and The Olson Center for Women’s Health, Department of Obstetrics and Gynecology, Nebraska Medical Center. -
Discovery of Progenitor Cell Signatures by Time-Series Synexpression Analysis During Drosophila Embryonic Cell Immortalization
Correction DEVELOPMENTAL BIOLOGY Correction for “Discovery of progenitor cell signatures by time- series synexpression analysis during Drosophila embryonic cell immortalization,” by Mary-Lee Dequéant, Delphine Fagegaltier, Yanhui Hu, Kerstin Spirohn, Amanda Simcox, Gregory J. Hannon, and Norbert Perrimon, which appeared in issue 42, October 20, 2015, of Proc Natl Acad Sci USA (112:12974–12979; first published October 5, 2015; 10.1073/pnas.1517729112). The authors note that Delphine Fagegaltier should be credited for designing research and performing research. The authors also note that Delphine Fagegaltier, Amanda Simcox, and Gregory J. Hannon should be credited for contributing to the writing of the paper. The corrected author contributions footnote appears below. Author contributions: M.-L.D., D.F., A.S., G.J.H., and N.P. designed research; M.-L.D., D.F., K.S., and A.S. performed research; M.-L.D., D.F., and Y.H. analyzed data; and M.-L.D. and N.P. wrote the paper with contributions from D.F., A.S., and G.J.H. www.pnas.org/cgi/doi/10.1073/pnas.1520482112 E6408 | PNAS | November 17, 2015 | vol. 112 | no. 46 www.pnas.org Downloaded by guest on September 25, 2021 Discovery of progenitor cell signatures by time-series synexpression analysis during Drosophila embryonic cell immortalization Mary-Lee Dequéanta,1, Delphine Fagegaltierb, Yanhui Hua, Kerstin Spirohna, Amanda Simcoxc, Gregory J. Hannond, and Norbert Perrimona,e,1 aDepartment of Genetics, Harvard Medical School, Boston, MA 02115, bCold Spring Harbor Laboratories, Cold Spring Harbor, NY 11724; cDepartment of Molecular Genetics, The Ohio State University, Columbus, OH 43210; dHoward Hughes Medical Institute, Cold Spring Harbor Laboratories, Cold Spring Harbor, NY 11724; and eHoward Hughes Medical Institute, Harvard Medical School, Boston, MA 02115 Contributed by Norbert Perrimon, September 10, 2015 (sent for review May 18, 2015; reviewed by Peter Cherbas, Gary Karpen, and Renato Paro) The use of time series profiling to identify groups of functionally population contributing to adult muscles (4–7). -
Association of Gene Ontology Categories with Decay Rate for Hepg2 Experiments These Tables Show Details for All Gene Ontology Categories
Supplementary Table 1: Association of Gene Ontology Categories with Decay Rate for HepG2 Experiments These tables show details for all Gene Ontology categories. Inferences for manual classification scheme shown at the bottom. Those categories used in Figure 1A are highlighted in bold. Standard Deviations are shown in parentheses. P-values less than 1E-20 are indicated with a "0". Rate r (hour^-1) Half-life < 2hr. Decay % GO Number Category Name Probe Sets Group Non-Group Distribution p-value In-Group Non-Group Representation p-value GO:0006350 transcription 1523 0.221 (0.009) 0.127 (0.002) FASTER 0 13.1 (0.4) 4.5 (0.1) OVER 0 GO:0006351 transcription, DNA-dependent 1498 0.220 (0.009) 0.127 (0.002) FASTER 0 13.0 (0.4) 4.5 (0.1) OVER 0 GO:0006355 regulation of transcription, DNA-dependent 1163 0.230 (0.011) 0.128 (0.002) FASTER 5.00E-21 14.2 (0.5) 4.6 (0.1) OVER 0 GO:0006366 transcription from Pol II promoter 845 0.225 (0.012) 0.130 (0.002) FASTER 1.88E-14 13.0 (0.5) 4.8 (0.1) OVER 0 GO:0006139 nucleobase, nucleoside, nucleotide and nucleic acid metabolism3004 0.173 (0.006) 0.127 (0.002) FASTER 1.28E-12 8.4 (0.2) 4.5 (0.1) OVER 0 GO:0006357 regulation of transcription from Pol II promoter 487 0.231 (0.016) 0.132 (0.002) FASTER 6.05E-10 13.5 (0.6) 4.9 (0.1) OVER 0 GO:0008283 cell proliferation 625 0.189 (0.014) 0.132 (0.002) FASTER 1.95E-05 10.1 (0.6) 5.0 (0.1) OVER 1.50E-20 GO:0006513 monoubiquitination 36 0.305 (0.049) 0.134 (0.002) FASTER 2.69E-04 25.4 (4.4) 5.1 (0.1) OVER 2.04E-06 GO:0007050 cell cycle arrest 57 0.311 (0.054) 0.133 (0.002) -
Technical Note, Appendix: an Analysis of Blood Processing Methods to Prepare Samples for Genechip® Expression Profiling (Pdf, 1
Appendix 1: Signature genes for different blood cell types. Blood Cell Type Source Probe Set Description Symbol Blood Cell Type Source Probe Set Description Symbol Fraction ID Fraction ID Mono- Lympho- GSK 203547_at CD4 antigen (p55) CD4 Whitney et al. 209813_x_at T cell receptor TRG nuclear cytes gamma locus cells Whitney et al. 209995_s_at T-cell leukemia/ TCL1A Whitney et al. 203104_at colony stimulating CSF1R lymphoma 1A factor 1 receptor, Whitney et al. 210164_at granzyme B GZMB formerly McDonough (granzyme 2, feline sarcoma viral cytotoxic T-lymphocyte- (v-fms) oncogene associated serine homolog esterase 1) Whitney et al. 203290_at major histocompatibility HLA-DQA1 Whitney et al. 210321_at similar to granzyme B CTLA1 complex, class II, (granzyme 2, cytotoxic DQ alpha 1 T-lymphocyte-associated Whitney et al. 203413_at NEL-like 2 (chicken) NELL2 serine esterase 1) Whitney et al. 203828_s_at natural killer cell NK4 (H. sapiens) transcript 4 Whitney et al. 212827_at immunoglobulin heavy IGHM Whitney et al. 203932_at major histocompatibility HLA-DMB constant mu complex, class II, Whitney et al. 212998_x_at major histocompatibility HLA-DQB1 DM beta complex, class II, Whitney et al. 204655_at chemokine (C-C motif) CCL5 DQ beta 1 ligand 5 Whitney et al. 212999_x_at major histocompatibility HLA-DQB Whitney et al. 204661_at CDW52 antigen CDW52 complex, class II, (CAMPATH-1 antigen) DQ beta 1 Whitney et al. 205049_s_at CD79A antigen CD79A Whitney et al. 213193_x_at T cell receptor beta locus TRB (immunoglobulin- Whitney et al. 213425_at Homo sapiens cDNA associated alpha) FLJ11441 fis, clone Whitney et al. 205291_at interleukin 2 receptor, IL2RB HEMBA1001323, beta mRNA sequence Whitney et al. -
Genome-Wide Transcriptional Sequencing Identifies Novel Mutations in Metabolic Genes in Human Hepatocellular Carcinoma DAOUD M
CANCER GENOMICS & PROTEOMICS 11 : 1-12 (2014) Genome-wide Transcriptional Sequencing Identifies Novel Mutations in Metabolic Genes in Human Hepatocellular Carcinoma DAOUD M. MEERZAMAN 1,2 , CHUNHUA YAN 1, QING-RONG CHEN 1, MICHAEL N. EDMONSON 1, CARL F. SCHAEFER 1, ROBERT J. CLIFFORD 2, BARBARA K. DUNN 3, LI DONG 2, RICHARD P. FINNEY 1, CONSTANCE M. CULTRARO 2, YING HU1, ZHIHUI YANG 2, CU V. NGUYEN 1, JENNY M. KELLEY 2, SHUANG CAI 2, HONGEN ZHANG 2, JINGHUI ZHANG 1,4 , REBECCA WILSON 2, LAUREN MESSMER 2, YOUNG-HWA CHUNG 5, JEONG A. KIM 5, NEUNG HWA PARK 6, MYUNG-SOO LYU 6, IL HAN SONG 7, GEORGE KOMATSOULIS 1 and KENNETH H. BUETOW 1,2 1Center for Bioinformatics and Information Technology, National Cancer Institute, Rockville, MD, U.S.A.; 2Laboratory of Population Genetics, National Cancer Institute, National Cancer Institute, Bethesda, MD, U.S.A.; 3Basic Prevention Science Research Group, Division of Cancer Prevention, National Cancer Institute, Bethesda, MD, U.S.A; 4Department of Biotechnology/Computational Biology, St. Jude Children’s Research Hospital, Memphis, TN, U.S.A.; 5Department of Internal Medicine, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea; 6Department of Internal Medicine, University of Ulsan College of Medicine, Ulsan University Hospital, Ulsan, Korea; 7Department of Internal Medicine, College of Medicine, Dankook University, Cheon-An, Korea Abstract . We report on next-generation transcriptome Worldwide, liver cancer is the fifth most common cancer and sequencing results of three human hepatocellular carcinoma the third most common cause of cancer-related mortality (1). tumor/tumor-adjacent pairs. -
Inhibition of Mitochondrial Complex II in Neuronal Cells Triggers Unique
www.nature.com/scientificreports OPEN Inhibition of mitochondrial complex II in neuronal cells triggers unique pathways culminating in autophagy with implications for neurodegeneration Sathyanarayanan Ranganayaki1, Neema Jamshidi2, Mohamad Aiyaz3, Santhosh‑Kumar Rashmi4, Narayanappa Gayathri4, Pulleri Kandi Harsha5, Balasundaram Padmanabhan6 & Muchukunte Mukunda Srinivas Bharath7* Mitochondrial dysfunction and neurodegeneration underlie movement disorders such as Parkinson’s disease, Huntington’s disease and Manganism among others. As a corollary, inhibition of mitochondrial complex I (CI) and complex II (CII) by toxins 1‑methyl‑4‑phenylpyridinium (MPP+) and 3‑nitropropionic acid (3‑NPA) respectively, induced degenerative changes noted in such neurodegenerative diseases. We aimed to unravel the down‑stream pathways associated with CII inhibition and compared with CI inhibition and the Manganese (Mn) neurotoxicity. Genome‑wide transcriptomics of N27 neuronal cells exposed to 3‑NPA, compared with MPP+ and Mn revealed varied transcriptomic profle. Along with mitochondrial and synaptic pathways, Autophagy was the predominant pathway diferentially regulated in the 3‑NPA model with implications for neuronal survival. This pathway was unique to 3‑NPA, as substantiated by in silico modelling of the three toxins. Morphological and biochemical validation of autophagy markers in the cell model of 3‑NPA revealed incomplete autophagy mediated by mechanistic Target of Rapamycin Complex 2 (mTORC2) pathway. Interestingly, Brain Derived Neurotrophic Factor -
Appendix 2. Significantly Differentially Regulated Genes in Term Compared with Second Trimester Amniotic Fluid Supernatant
Appendix 2. Significantly Differentially Regulated Genes in Term Compared With Second Trimester Amniotic Fluid Supernatant Fold Change in term vs second trimester Amniotic Affymetrix Duplicate Fluid Probe ID probes Symbol Entrez Gene Name 1019.9 217059_at D MUC7 mucin 7, secreted 424.5 211735_x_at D SFTPC surfactant protein C 416.2 206835_at STATH statherin 363.4 214387_x_at D SFTPC surfactant protein C 295.5 205982_x_at D SFTPC surfactant protein C 288.7 1553454_at RPTN repetin solute carrier family 34 (sodium 251.3 204124_at SLC34A2 phosphate), member 2 238.9 206786_at HTN3 histatin 3 161.5 220191_at GKN1 gastrokine 1 152.7 223678_s_at D SFTPA2 surfactant protein A2 130.9 207430_s_at D MSMB microseminoprotein, beta- 99.0 214199_at SFTPD surfactant protein D major histocompatibility complex, class II, 96.5 210982_s_at D HLA-DRA DR alpha 96.5 221133_s_at D CLDN18 claudin 18 94.4 238222_at GKN2 gastrokine 2 93.7 1557961_s_at D LOC100127983 uncharacterized LOC100127983 93.1 229584_at LRRK2 leucine-rich repeat kinase 2 HOXD cluster antisense RNA 1 (non- 88.6 242042_s_at D HOXD-AS1 protein coding) 86.0 205569_at LAMP3 lysosomal-associated membrane protein 3 85.4 232698_at BPIFB2 BPI fold containing family B, member 2 84.4 205979_at SCGB2A1 secretoglobin, family 2A, member 1 84.3 230469_at RTKN2 rhotekin 2 82.2 204130_at HSD11B2 hydroxysteroid (11-beta) dehydrogenase 2 81.9 222242_s_at KLK5 kallikrein-related peptidase 5 77.0 237281_at AKAP14 A kinase (PRKA) anchor protein 14 76.7 1553602_at MUCL1 mucin-like 1 76.3 216359_at D MUC7 mucin 7, -
Functional Characterization of TBR1 Variants in Neurodevelopmental Disorder Received: 14 May 2018 Joery Den Hoed1, Elliot Sollis1, Hanka Venselaar2, Sara B
www.nature.com/scientificreports OPEN Functional characterization of TBR1 variants in neurodevelopmental disorder Received: 14 May 2018 Joery den Hoed1, Elliot Sollis1, Hanka Venselaar2, Sara B. Estruch1, Pelagia Deriziotis1 & Accepted: 31 August 2018 Simon E. Fisher 1,3 Published: xx xx xxxx Recurrent de novo variants in the TBR1 transcription factor are implicated in the etiology of sporadic autism spectrum disorders (ASD). Disruptions include missense variants located in the T-box DNA- binding domain and previous work has demonstrated that they disrupt TBR1 protein function. Recent screens of thousands of simplex families with sporadic ASD cases uncovered additional T-box variants in TBR1 but their etiological relevance is unclear. We performed detailed functional analyses of de novo missense TBR1 variants found in the T-box of ASD cases, assessing many aspects of protein function, including subcellular localization, transcriptional activity and protein-interactions. Only two of the three tested variants severely disrupted TBR1 protein function, despite in silico predictions that all would be deleterious. Furthermore, we characterized a putative interaction with BCL11A, a transcription factor that was recently implicated in a neurodevelopmental syndrome involving developmental delay and language defcits. Our fndings enhance understanding of molecular functions of TBR1, as well as highlighting the importance of functional testing of variants that emerge from next-generation sequencing, to decipher their contributions to neurodevelopmental disorders like ASD. TBR1 (T-box brain, 1; OMIM *604616) encodes a neuron-specifc transcription factor of the T-box family1. Te TBR1 protein is highly expressed in the deep layers of the cortex, where it is involved in diferentiation of subsets of projection neurons2–4. -
Reduction of BCL11A in Hematopoietic Stem Cells Through
Science Bulletin 64 (2019) 1562–1564 Contents lists available at ScienceDirect Science Bulletin journal homepage: www.elsevier.com/locate/scib Research Highlight Reduction of BCL11A in hematopoietic stem cells through gene editing: new strategy to ameliorate the severe b-globin disorders sickle cell disease ⇑ Weiqi Hong, Mengyuan Huang, Yuquan Wei, Xiawei Wei Laboratory of Aging Research and Cancer Drug Target, State Key Laboratory of Biotherapy, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu 610041, China Site-specific gene editing is of great importance in precise Sickle-cell anemia is a prototypical monogenic disorder caused medicine. Two conventional genome editing methods, Zine finger by mutation of b-globin subunit. It is a promising therapy strategy nucleases (ZFNs) and transcription activator-like effector nucleases to induct fetal hemoglobin (HbF, a2c2) by re-expressing the paral- (TALENs), are based on protein-DNA recognition, with tedious ogous c-globin genes (HBG1/2) for severe b-globin disorders sickle work in constructing target protein [1,2]. Developed from immune cell disease (SCD) and b-thalassemia [9]. Researches in the past response of bacteria, CRISPR/Cas9 has been widely investigated as have shown that the core of the +58 erythroid enhancer of BCL11A a promising tool for therapeutic genome editing in clinical settings was crucial for repression of HBF in adult stage erythroid. Wu et al nowadays [3,4]. This system succeeds in gene deletion, insertion found that chemically modified synthetic sgRNAs (MS-sgRNAs) and frameshift mutations with higher efficiency, less cost, was more efficient than in vitro transcribed sgRNAs. Targeting improved flexibility and simplified designing process [5]. -
Transcriptome Alterations of Vascular Smooth Muscle Cells in Aortic Wall of Myocardial Infarction Patients
This document is downloaded from DR‑NTU (https://dr.ntu.edu.sg) Nanyang Technological University, Singapore. Transcriptome alterations of vascular smooth muscle cells in aortic wall of myocardial infarction patients Wongsurawat, Thidathip; Woo, Chin Cheng; Giannakakis, Antonis; Lin, Xiao Yun; Cheow, Esther Sok Hwee; Lee, Chuen Neng; Richards, Mark; Sze, Siu Kwan; Nookaew, Intawat; Sorokin, Vitaly; Kuznetsov, Vladimir Andreevich 2018 Wongsurawat, T., Woo, C. C., Giannakakis, A., Lin, X. Y., Cheow, E. S. H., Lee, C. N., et al. (2018). Transcriptome alterations of vascular smooth muscle cells in aortic wall of myocardial infarction patients. Data in Brief, 17, 1112‑1135. https://hdl.handle.net/10356/85590 https://doi.org/10.1016/j.dib.2018.01.108 © 2018 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/). Downloaded on 09 Oct 2021 06:21:01 SGT Data in Brief 17 (2018) 1112–1135 Contents lists available at ScienceDirect Data in Brief journal homepage: www.elsevier.com/locate/dib Data Article Transcriptome alterations of vascular smooth muscle cells in aortic wall of myocardial infarction patients Thidathip Wongsurawat a,b, Chin Cheng Woo c, Antonis Giannakakis a, Xiao Yun Lin d, Esther Sok Hwee Cheow e, Chuen Neng Lee c,d, Mark Richards f,g, Siu Kwan Sze e, Intawat Nookaew b, Vladimir A. Kuznetsov a,h, Vitaly Sorokin c,d,⁎ a Department of Genome and Gene Expression Data Analysis, Bioinformatics Institute, Agency for Science, Technology and Research (A*STAR), -
Characterization of Transcription Factor Networks Involved in Umbilical Cord Blood CD34+ Stem Cells-Derived Erythropoiesis
Characterization of Transcription Factor Networks Involved in Umbilical Cord Blood CD34+ Stem Cells-Derived Erythropoiesis Biaoru Li1, Lianghao Ding2, Chinrang Yang2, Baolin Kang1, Li Liu3, Michael D. Story2, Betty S. Pace1* 1 Department of Pediatrics, Hematology/Oncology Division, Georgia Regents University, Augusta, Georgia, United States of America, 2 Department of Radiation Oncology and Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, Texas, United States of America, 3 Department of Molecular and Cell Biology, University of Texas at Dallas, Richardson, Texas, United States of America Abstract Fetal stem cells isolated from umbilical cord blood (UCB) possess a great capacity for proliferation and differentiation and serve as a valuable model system to study gene regulation. Expanded knowledge of the molecular control of hemoglobin synthesis will provide a basis for rational design of therapies for b-hemoglobinopathies. Transcriptome data are available for erythroid progenitors derived from adult stem cells, however studies to define molecular mechanisms controlling globin gene regulation during fetal erythropoiesis are limited. Here, we utilize UCB-CD34+ stem cells induced to undergo erythroid differentiation to characterize the transcriptome and transcription factor networks (TFNs) associated with the c/b-globin switch during fetal erythropoiesis. UCB-CD34+ stem cells grown in the one-phase liquid culture system displayed a higher proliferative capacity than adult CD34+ stem cells. The c/b-globin switch was observed after day 42 during fetal erythropoiesis in contrast to adult progenitors where the switch occurred around day 21. To gain insights into transcription factors involved in globin gene regulation, microarray analysis was performed on RNA isolated from UCB-CD34+ cell-derived erythroid progenitors harvested on day 21, 42, 49 and 56 using the HumanHT-12 Expression BeadChip.