Search

Your search keyword '"Maharishi Valmiki Hospital"' showing total 2 results
Start Over Author "Maharishi Valmiki Hospital" Topic biology
2 results on '"Maharishi Valmiki Hospital"'

1. La protéine NF-Y contrôle la fidelité de l'initiation de la transcription aux promoteurs de gènes à travers la maintenance de région déplétée en nucléosome

Author

Raja Jothi, Telmo Henriques, Christopher A. Lavender, Dhirendra Kumar, Senthilkumar Cinghu, Karen Adelman, Andrew J. Oldfield, Brian D. Bennett, Adam B. Burkholder, Pengyi Yang, Damien Paulet, Benjamin S. Scruggs, Eric Rivals, Epigenetics and Stem Cell Biology Laboratory [Durham] (ESCBL-NIEHS-NIH), National Institute of Environmental Health Sciences [Durham] (NIEHS-NIH), National Institutes of Health [Bethesda] (NIH)-National Institutes of Health [Bethesda] (NIH), Harvard Medical School [Boston] (HMS), Maharishi Valmiki Hospital, Méthodes et Algorithmes pour la Bioinformatique (MAB), Laboratoire d'Informatique de Robotique et de Microélectronique de Montpellier (LIRMM), Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Institut de Biologie Computationnelle (IBC), Institut National de la Recherche Agronomique (INRA)-Institut National de Recherche en Informatique et en Automatique (Inria)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Marquette University, National Institutes of Health [Bethesda] (NIH), ATGC bioinformatics platform Montpellier. the Institut de Biologie Computationnelle (ANR-11-BINF-0002) Institut Français de Bioinformatique (ANR-11-INBS-0013)GEM Flagship project funded from Labex NUMEV (ANR-10-LABX-0020)France Génomique., ANR-10-LABX-0020/10-LABX-0020,NUMEV,Digital and Hardware Solutions and Modeling for the Environement and Life Sciences(2010), ANR-11-INBS-0013/11-INBS-0013,ReNaBi-IFB,Institut français de bioinformatique(2011), ANR-11-BINF-0002,IBC,Institut de Biologie Computationnelle de Montpellier(2011), ANR-10-INBS-09-01/10-INBS-0009,France-Génomique,Organisation et montée en puissance d'une Infrastructure Nationale de Génomique(2010), Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM), Université de Montpellier (UM)-Institut National de la Recherche Agronomique (INRA)-Institut National de Recherche en Informatique et en Automatique (Inria)-Centre National de la Recherche Scientifique (CNRS), Marquette University [Milwaukee], ANR-10-LABX-0020,NUMEV,Digital and Hardware Solutions and Modeling for the Environement and Life Sciences(2010), ANR-11-INBS-0013,IFB (ex Renabi-IFB),Institut français de bioinformatique(2011), ANR-11-BINF-0002,IBC,Institut de biologie Computationnelle(2011), and ANR-10-INBS-0009,France-Génomique,Organisation et montée en puissance d'une Infrastructure Nationale de Génomique(2010)

Subjects
0301 basic medicine, General Physics and Astronomy, [SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], 02 engineering and technology, Mice, 0302 clinical medicine, Transcription (biology), Gene expression, Gene Knockdown Techniques, RNA, Small Interfering, Promoter Regions, Genetic, lcsh:Science, Transcription Initiation, Genetic, 0303 health sciences, Multidisciplinary, 021001 nanoscience & nanotechnology, [SDV.BIBS]Life Sciences [q-bio]/Quantitative Methods [q-bio.QM], Chromatin, Nucleosomes, 3. Good health, Cell biology, Transcription Initiation Site, 0210 nano-technology, Transcription, Science, Protein domain, Site Transcription Initiation, Genomics, Biology, Small Interfering, Article, General Biochemistry, Genetics and Molecular Biology, Cell Line, Promoter Regions, 03 medical and health sciences, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Animals, Nucleosome, Transcription factor, Embryonic Stem Cells, 030304 developmental biology, Promoter, General Chemistry, Metabolism, 030104 developmental biology, CCAAT-Binding Factor, RNA, lcsh:Q, [INFO.INFO-BI]Computer Science [cs]/Bioinformatics [q-bio.QM], 030217 neurology & neurosurgery
Abstract

Faithful transcription initiation is critical for accurate gene expression, yet the mechanisms underlying specific transcription start site (TSS) selection in mammals remain unclear. Here, we show that the histone-fold domain protein NF-Y, a ubiquitously expressed transcription factor, controls the fidelity of transcription initiation at gene promoters in mouse embryonic stem cells. We report that NF-Y maintains the region upstream of TSSs in a nucleosome-depleted state while simultaneously protecting this accessible region against aberrant and/or ectopic transcription initiation. We find that loss of NF-Y binding in mammalian cells disrupts the promoter chromatin landscape, leading to nucleosomal encroachment over the canonical TSS. Importantly, this chromatin rearrangement is accompanied by upstream relocation of the transcription pre-initiation complex and ectopic transcription initiation. Further, this phenomenon generates aberrant extended transcripts that undergo translation, disrupting gene expression profiles. These results suggest NF-Y is a central player in TSS selection in metazoans and highlight the deleterious consequences of inaccurate transcription initiation., The mechanisms underlying specific TSS selection in mammals remain unclear. Here the authors show that the ubiquitously expressed transcription factor NF-Y regulate fidelity of transcription initiation at gene promoters, maintaining the region upstream of TSSs in a nucleosome-depleted state, while protecting this region from ectopic transcription initiation.

Published
2019

2. Genomic insights into the 2016–2017 cholera epidemic in Yemen

Author

Dhirendra Kumar, Abdullah M. Assiri, Naresh Chand Sharma, Joseph F. Wamala, Samuel Kariuki, Caroline Seguin, Thérèse E. Malliavin, Abdullrahman A. Almesbahi, Nicholas R. Thomson, Samuel M. C. Njoroge, Thandavarayan Ramamurthy, Mona Naji, Daryl Domman, Elisabeth Njamkepo, Samar Saeed Nasher, Jane Y. Carter, Abdinasir Abubakar, Bita Bakhshi, Jean Rauzier, Andrew S. Azman, Christiane Bouchier, John Kiiru, Francisco J. Luquero, François-Xavier Weill, Hayder H.N. Abulmaali, Marie Laure Quilici, Mohammad Reza Pourshafie, Ankur Rakesh, Mamunur Rahman Malik, Bactéries pathogènes entériques (BPE), Institut Pasteur [Paris] (IP), The Wellcome Trust Sanger Institute [Cambridge], Los Alamos National Laboratory (LANL), Ministry of Public Health [Yemen], Epicentre [Paris] [Médecins Sans Frontières], Ministry of Health [Saudi Arabia], Kenya Medical Research Institute (KEMRI), Institut Pasteur d'Iran, Réseau International des Instituts Pasteur (RIIP), WHO - Regional Office for the Eastern Mediterranean [Cairo, Egypt] (EMRO), Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), Amref Health Africa [Kenya], African Medical and Research Foundation (AMREF), Médecins Sans Frontières [Dubai], Génomique (Plate-Forme) - Genomics Platform, Bioinformatique structurale - Structural Bioinformatics, Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Tarbiat Modares University [Tehran], Ministry of Health [Iraq], Maharishi Valmiki Hospital, Translational Health Science and Technology Institute [Faridabad] (THSTI), Johns Hopkins Bloomberg School of Public Health [Baltimore], Johns Hopkins University (JHU), London School of Hygiene and Tropical Medicine (LSHTM), This study was supported by the Institut Pasteur, Santé publique France, the French government’s Investissement d’Avenir programme, Laboratoire d’Excellence ‘Integrative Biology of Emerging Infectious Diseases’ (grant number ANR-10-LABX-62-IBEID), the Wellcome Trust through grant 098051 to the Sanger Institute and the Department of Biotechnology of India. The Institut Pasteur Genomics Platform is a member of the France Génomique consortium (ANR10-INBS-09-08)., ANR-10-LABX-0062,IBEID,Integrative Biology of Emerging Infectious Diseases(2010), Institut Pasteur [Paris], Regional Office for the Eastern Mediterranean [Cairo] (EMRO), and Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS)

Subjects
0301 basic medicine, Serotype, Yemen, 030106 microbiology, Context (language use), Biology, medicine.disease_cause, El Tor, 03 medical and health sciences, Antibiotic resistance, Cholera, Pandemic, medicine, Humans, Vibrio cholerae, Phylogeny, Multidisciplinary, Outbreak, Genomics, biology.organism_classification, medicine.disease, Virology, 3. Good health, 030104 developmental biology, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, Genome, Bacterial
Abstract

International audience; Yemen is currently experiencing, to our knowledge, the largest cholera epidemic in recent history. The first cases were declared in September 2016, and over 1.1 million cases and 2,300 deaths have since been reported1. Here we investigate the phylogenetic relationships, pathogenesis and determinants of antimicrobial resistance by sequencing the genomes of Vibrio cholerae isolates from the epidemic in Yemen and recent isolates from neighbouring regions. These 116 genomic sequences were placed within the phylogenetic context of a global collection of 1,087 isolates of the seventh pandemic V. cholerae serogroups O1 and O139 biotype El Tor2-4. We show that the isolates from Yemen that were collected during the two epidemiological waves of the epidemic1-the first between 28 September 2016 and 23 April 2017 (25,839 suspected cases) and the second beginning on 24 April 2017 (more than 1 million suspected cases)-are V. cholerae serotype Ogawa isolates from a single sublineage of the seventh pandemic V. cholerae O1 El Tor (7PET) lineage. Using genomic approaches, we link the epidemic in Yemen to global radiations of pandemic V. cholerae and show that this sublineage originated from South Asia and that it caused outbreaks in East Africa before appearing in Yemen. Furthermore, we show that the isolates from Yemen are susceptible to several antibiotics that are commonly used to treat cholera and to polymyxin B, resistance to which is used as a marker of the El Tor biotype.

Published
2019

Catalog

Books, media, physical & digital resources
See catalog results