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  • 1
    Publication Date: 2001-10-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levine, J A -- Weisell, R -- Chevassus, S -- Martinez, C D -- Burlingame, B -- Coward, W A -- DK 56650/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2001 Oct 26;294(5543):812.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Department of Internal Medicine, Endocrine Research Unit, Mayo Clinic, Rochester, MN 55905, USA. levine.james@mayo.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11679660" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture ; Cote d'Ivoire ; Female ; Humans ; Leisure Activities ; Male ; Nutritional Physiological Phenomena ; Rural Population ; Sex Characteristics ; Sleep ; *Women, Working ; *Work
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2002-05-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levine, James A -- Weisell, Robert -- Chevassus, Simon -- Martinez, Claudio D -- Burlingame, Barbara -- New York, N.Y. -- Science. 2002 May 10;296(5570):1025-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12004902" target="_blank"〉PubMed〈/a〉
    Keywords: Activities of Daily Living ; Adolescent ; Adult ; Child ; *Child Welfare ; Cote d'Ivoire ; Education ; *Employment ; Female ; Humans ; Leisure Activities ; Male ; Poverty ; Sex Characteristics ; Sleep
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-11-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martinez, F -- Poet, T S -- Watson, R R -- New York, N.Y. -- Science. 1990 Nov 23;250(4984):1070.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2251495" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cocaine/metabolism/pharmacokinetics ; Hair/*chemistry/metabolism ; Humans ; Male ; Mice ; Morphine/metabolism/pharmacokinetics ; *Substance Abuse Detection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2009-04-25
    Description: The imprints of domestication and breed development on the genomes of livestock likely differ from those of companion animals. A deep draft sequence assembly of shotgun reads from a single Hereford female and comparative sequences sampled from six additional breeds were used to develop probes to interrogate 37,470 single-nucleotide polymorphisms (SNPs) in 497 cattle from 19 geographically and biologically diverse breeds. These data show that cattle have undergone a rapid recent decrease in effective population size from a very large ancestral population, possibly due to bottlenecks associated with domestication, selection, and breed formation. Domestication and artificial selection appear to have left detectable signatures of selection within the cattle genome, yet the current levels of diversity within breeds are at least as great as exists within humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2735092/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2735092/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bovine HapMap Consortium -- Gibbs, Richard A -- Taylor, Jeremy F -- Van Tassell, Curtis P -- Barendse, William -- Eversole, Kellye A -- Gill, Clare A -- Green, Ronnie D -- Hamernik, Debora L -- Kappes, Steven M -- Lien, Sigbjorn -- Matukumalli, Lakshmi K -- McEwan, John C -- Nazareth, Lynne V -- Schnabel, Robert D -- Weinstock, George M -- Wheeler, David A -- Ajmone-Marsan, Paolo -- Boettcher, Paul J -- Caetano, Alexandre R -- Garcia, Jose Fernando -- Hanotte, Olivier -- Mariani, Paola -- Skow, Loren C -- Sonstegard, Tad S -- Williams, John L -- Diallo, Boubacar -- Hailemariam, Lemecha -- Martinez, Mario L -- Morris, Chris A -- Silva, Luiz O C -- Spelman, Richard J -- Mulatu, Woudyalew -- Zhao, Keyan -- Abbey, Colette A -- Agaba, Morris -- Araujo, Flabio R -- Bunch, Rowan J -- Burton, James -- Gorni, Chiara -- Olivier, Hanotte -- Harrison, Blair E -- Luff, Bill -- Machado, Marco A -- Mwakaya, Joel -- Plastow, Graham -- Sim, Warren -- Smith, Timothy -- Thomas, Merle B -- Valentini, Alessio -- Williams, Paul -- Womack, James -- Woolliams, John A -- Liu, Yue -- Qin, Xiang -- Worley, Kim C -- Gao, Chuan -- Jiang, Huaiyang -- Moore, Stephen S -- Ren, Yanru -- Song, Xing-Zhi -- Bustamante, Carlos D -- Hernandez, Ryan D -- Muzny, Donna M -- Patil, Shobha -- San Lucas, Anthony -- Fu, Qing -- Kent, Matthew P -- Vega, Richard -- Matukumalli, Aruna -- McWilliam, Sean -- Sclep, Gert -- Bryc, Katarzyna -- Choi, Jungwoo -- Gao, Hong -- Grefenstette, John J -- Murdoch, Brenda -- Stella, Alessandra -- Villa-Angulo, Rafael -- Wright, Mark -- Aerts, Jan -- Jann, Oliver -- Negrini, Riccardo -- Goddard, Mike E -- Hayes, Ben J -- Bradley, Daniel G -- Barbosa da Silva, Marcos -- Lau, Lilian P L -- Liu, George E -- Lynn, David J -- Panzitta, Francesca -- Dodds, Ken G -- R01 GM083606/GM/NIGMS NIH HHS/ -- R01 GM083606-02/GM/NIGMS NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2009 Apr 24;324(5926):528-32. doi: 10.1126/science.1167936.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19390050" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breeding ; Cattle/*genetics ; Female ; Gene Frequency ; *Genetic Variation ; *Genome ; Male ; Molecular Sequence Data ; Mutation ; *Polymorphism, Single Nucleotide ; Population Density
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 1997-08-22
    Description: It has been suggested that European Middle Pleistocene humans, Neandertals, and prehistoric modern humans had a greater sexual dimorphism than modern humans. Analysis of body size variation and cranial capacity variation in the large sample from the Sima de los Huesos site in Spain showed instead that the sexual dimorphism is comparable in Middle Pleistocene and modern populations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arsuaga, J L -- Carretero, J M -- Lorenzo, C -- Gracia, A -- Martinez, I -- Bermudez de Castro, J M -- Carbonell, E -- New York, N.Y. -- Science. 1997 Aug 22;277(5329):1086-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departamento de Paleontologia, Instituto de Geologia Economica, Facultad de Ciencias Geologicas, Universidad Complutense de Madrid, Ciudad Universitaria 28040 Madrid, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9262474" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Body Constitution ; Female ; *Fossils ; Hominidae/*anatomy & histology ; Humans ; Male ; *Sex Characteristics ; Skull/*anatomy & histology ; Spain
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2013-03-12
    Description: CLP1 was the first mammalian RNA kinase to be identified. However, determining its in vivo function has been elusive. Here we generated kinase-dead Clp1 (Clp1(K/K)) mice that show a progressive loss of spinal motor neurons associated with axonal degeneration in the peripheral nerves and denervation of neuromuscular junctions, resulting in impaired motor function, muscle weakness, paralysis and fatal respiratory failure. Transgenic rescue experiments show that CLP1 functions in motor neurons. Mechanistically, loss of CLP1 activity results in accumulation of a novel set of small RNA fragments, derived from aberrant processing of tyrosine pre-transfer RNA. These tRNA fragments sensitize cells to oxidative-stress-induced p53 (also known as TRP53) activation and p53-dependent cell death. Genetic inactivation of p53 rescues Clp1(K/K) mice from the motor neuron loss, muscle denervation and respiratory failure. Our experiments uncover a mechanistic link between tRNA processing, formation of a new RNA species and progressive loss of lower motor neurons regulated by p53.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3674495/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3674495/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanada, Toshikatsu -- Weitzer, Stefan -- Mair, Barbara -- Bernreuther, Christian -- Wainger, Brian J -- Ichida, Justin -- Hanada, Reiko -- Orthofer, Michael -- Cronin, Shane J -- Komnenovic, Vukoslav -- Minis, Adi -- Sato, Fuminori -- Mimata, Hiromitsu -- Yoshimura, Akihiko -- Tamir, Ido -- Rainer, Johannes -- Kofler, Reinhard -- Yaron, Avraham -- Eggan, Kevin C -- Woolf, Clifford J -- Glatzel, Markus -- Herbst, Ruth -- Martinez, Javier -- Penninger, Josef M -- K99NS077435-01A1/NS/NINDS NIH HHS/ -- NS038253/NS/NINDS NIH HHS/ -- P 19223/Austrian Science Fund FWF/Austria -- P 21667/Austrian Science Fund FWF/Austria -- R00 NS077435/NS/NINDS NIH HHS/ -- R01 NS038253/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Mar 28;495(7442):474-80. doi: 10.1038/nature11923. Epub 2013 Mar 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉IMBA, Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Vienna 1030, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23474986" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis ; Animals ; Animals, Newborn ; Axons/metabolism/pathology ; Cell Death ; Diaphragm/innervation ; Embryo Loss ; Embryo, Mammalian/metabolism/pathology ; Exons/genetics ; Female ; Fibroblasts ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Motor Neurons/*metabolism/*pathology ; Muscular Atrophy, Spinal ; Neuromuscular Diseases/metabolism/pathology ; Oxidative Stress ; RNA Processing, Post-Transcriptional ; RNA, Transfer, Tyr/genetics/*metabolism ; Respiration ; Spinal Nerves/cytology ; Transcription Factors/deficiency/*metabolism ; Tumor Suppressor Protein p53/metabolism ; Tyrosine/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2013-09-13
    Description: Reprogramming of adult cells to generate induced pluripotent stem cells (iPS cells) has opened new therapeutic opportunities; however, little is known about the possibility of in vivo reprogramming within tissues. Here we show that transitory induction of the four factors Oct4, Sox2, Klf4 and c-Myc in mice results in teratomas emerging from multiple organs, implying that full reprogramming can occur in vivo. Analyses of the stomach, intestine, pancreas and kidney reveal groups of dedifferentiated cells that express the pluripotency marker NANOG, indicative of in situ reprogramming. By bone marrow transplantation, we demonstrate that haematopoietic cells can also be reprogrammed in vivo. Notably, reprogrammable mice present circulating iPS cells in the blood and, at the transcriptome level, these in vivo generated iPS cells are closer to embryonic stem cells (ES cells) than standard in vitro generated iPS cells. Moreover, in vivo iPS cells efficiently contribute to the trophectoderm lineage, suggesting that they achieve a more plastic or primitive state than ES cells. Finally, intraperitoneal injection of in vivo iPS cells generates embryo-like structures that express embryonic and extraembryonic markers. We conclude that reprogramming in vivo is feasible and confers totipotency features absent in standard iPS or ES cells. These discoveries could be relevant for future applications of reprogramming in regenerative medicine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abad, Maria -- Mosteiro, Lluc -- Pantoja, Cristina -- Canamero, Marta -- Rayon, Teresa -- Ors, Inmaculada -- Grana, Osvaldo -- Megias, Diego -- Dominguez, Orlando -- Martinez, Dolores -- Manzanares, Miguel -- Ortega, Sagrario -- Serrano, Manuel -- England -- Nature. 2013 Oct 17;502(7471):340-5. doi: 10.1038/nature12586. Epub 2013 Sep 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tumour Suppression Group, Spanish National Cancer Research Centre (CNIO), Madrid E-28029, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24025773" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Cells/cytology/metabolism ; Cell Dedifferentiation ; Cell Separation ; Cells, Cultured ; *Cellular Reprogramming/genetics ; Ectoderm/cytology ; Embryoid Bodies/cytology/metabolism ; Embryonic Stem Cells/cytology/metabolism ; Female ; Fibroblasts/cytology ; Gene Expression Profiling ; Induced Pluripotent Stem Cells/*cytology/metabolism ; Intestines/cytology ; Kidney/cytology ; Kruppel-Like Transcription Factors/genetics/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Octamer Transcription Factor-3/genetics/metabolism ; Organ Specificity ; Pancreas/cytology ; Proto-Oncogene Proteins c-myc/genetics/metabolism ; SOXB1 Transcription Factors/genetics/metabolism ; Stomach/cytology ; Teratoma/genetics/*metabolism/pathology ; Totipotent Stem Cells/*cytology/metabolism ; Transcriptome/genetics ; Trophoblasts/cytology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2013-02-05
    Description: Cancer control by adaptive immunity involves a number of defined death and clearance mechanisms. However, efficient inhibition of exponential cancer growth by T cells and interferon-gamma (IFN-gamma) requires additional undefined mechanisms that arrest cancer cell proliferation. Here we show that the combined action of the T-helper-1-cell cytokines IFN-gamma and tumour necrosis factor (TNF) directly induces permanent growth arrest in cancers. To safely separate senescence induced by tumour immunity from oncogene-induced senescence, we used a mouse model in which the Simian virus 40 large T antigen (Tag) expressed under the control of the rat insulin promoter creates tumours by attenuating p53- and Rb-mediated cell cycle control. When combined, IFN-gamma and TNF drive Tag-expressing cancers into senescence by inducing permanent growth arrest in G1/G0, activation of p16INK4a (also known as CDKN2A), and downstream Rb hypophosphorylation at serine 795. This cytokine-induced senescence strictly requires STAT1 and TNFR1 (also known as TNFRSF1A) signalling in addition to p16INK4a. In vivo, Tag-specific T-helper 1 cells permanently arrest Tag-expressing cancers by inducing IFN-gamma- and TNFR1-dependent senescence. Conversely, Tnfr1(-/-)Tag-expressing cancers resist cytokine-induced senescence and grow aggressively, even in TNFR1-expressing hosts. Finally, as IFN-gamma and TNF induce senescence in numerous murine and human cancers, this may be a general mechanism for arresting cancer progression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Braumuller, Heidi -- Wieder, Thomas -- Brenner, Ellen -- Assmann, Sonja -- Hahn, Matthias -- Alkhaled, Mohammed -- Schilbach, Karin -- Essmann, Frank -- Kneilling, Manfred -- Griessinger, Christoph -- Ranta, Felicia -- Ullrich, Susanne -- Mocikat, Ralph -- Braungart, Kilian -- Mehra, Tarun -- Fehrenbacher, Birgit -- Berdel, Julia -- Niessner, Heike -- Meier, Friedegund -- van den Broek, Maries -- Haring, Hans-Ulrich -- Handgretinger, Rupert -- Quintanilla-Martinez, Leticia -- Fend, Falko -- Pesic, Marina -- Bauer, Jurgen -- Zender, Lars -- Schaller, Martin -- Schulze-Osthoff, Klaus -- Rocken, Martin -- England -- Nature. 2013 Feb 21;494(7437):361-5. doi: 10.1038/nature11824. Epub 2013 Feb 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Dermatology, Eberhard Karls University, Liebermeister Strasse 25, 72076 Tubingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23376950" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Polyomavirus Transforming/genetics/metabolism ; Cell Aging/*immunology ; Cell Cycle ; Cell Proliferation ; Cyclin-Dependent Kinase Inhibitor p16/deficiency/genetics/metabolism ; Cytokines/*immunology ; Disease Models, Animal ; Disease Progression ; Female ; Humans ; Interferon-gamma/immunology ; Male ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Mice, Transgenic ; Neoplasms/*immunology/*pathology ; Oncogenes/genetics ; Phosphoserine/metabolism ; Receptors, Tumor Necrosis Factor, Type I/metabolism ; Retinoblastoma Protein/chemistry/metabolism ; STAT1 Transcription Factor/metabolism ; Th1 Cells/*immunology ; Time Factors ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha/immunology ; Tumor Suppressor Protein p53/metabolism
    Print ISSN: 0028-0836
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  • 9
    Publication Date: 2014-01-28
    Description: Ancient genomic sequences have started to reveal the origin and the demographic impact of farmers from the Neolithic period spreading into Europe. The adoption of farming, stock breeding and sedentary societies during the Neolithic may have resulted in adaptive changes in genes associated with immunity and diet. However, the limited data available from earlier hunter-gatherers preclude an understanding of the selective processes associated with this crucial transition to agriculture in recent human evolution. Here we sequence an approximately 7,000-year-old Mesolithic skeleton discovered at the La Brana-Arintero site in Leon, Spain, to retrieve a complete pre-agricultural European human genome. Analysis of this genome in the context of other ancient samples suggests the existence of a common ancient genomic signature across western and central Eurasia from the Upper Paleolithic to the Mesolithic. The La Brana individual carries ancestral alleles in several skin pigmentation genes, suggesting that the light skin of modern Europeans was not yet ubiquitous in Mesolithic times. Moreover, we provide evidence that a significant number of derived, putatively adaptive variants associated with pathogen resistance in modern Europeans were already present in this hunter-gatherer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4269527/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4269527/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olalde, Inigo -- Allentoft, Morten E -- Sanchez-Quinto, Federico -- Santpere, Gabriel -- Chiang, Charleston W K -- DeGiorgio, Michael -- Prado-Martinez, Javier -- Rodriguez, Juan Antonio -- Rasmussen, Simon -- Quilez, Javier -- Ramirez, Oscar -- Marigorta, Urko M -- Fernandez-Callejo, Marcos -- Prada, Maria Encina -- Encinas, Julio Manuel Vidal -- Nielsen, Rasmus -- Netea, Mihai G -- Novembre, John -- Sturm, Richard A -- Sabeti, Pardis -- Marques-Bonet, Tomas -- Navarro, Arcadi -- Willerslev, Eske -- Lalueza-Fox, Carles -- F32 GM106656/GM/NIGMS NIH HHS/ -- F32GM106656/GM/NIGMS NIH HHS/ -- R01 HG007089/HG/NHGRI NIH HHS/ -- R01-HG007089/HG/NHGRI NIH HHS/ -- England -- Nature. 2014 Mar 13;507(7491):225-8. doi: 10.1038/nature12960. Epub 2014 Jan 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Institut de Biologia Evolutiva, CSIC-UPF, Barcelona 08003, Spain [2]. ; 1] Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, DK-1350 Copenhagen K, Denmark [2]. ; Institut de Biologia Evolutiva, CSIC-UPF, Barcelona 08003, Spain. ; Department of Ecology and Evolutionary Biology, University of California, Los Angeles, California 90095, USA. ; 1] Department of Integrative Biology, University of California, Berkeley, California 94720, USA [2] Department of Biology, Pennsylvania State University, 502 Wartik Laboratory, University Park, Pennsylvania 16802, USA. ; Center for Biological Sequence Analysis, Technical University of Denmark, DK-2800 Kongens Lyngby, Denmark. ; I.E.S.O. 'Los Salados', Junta de Castilla y Leon, E-49600 Benavente, Spain. ; Junta de Castilla y Leon, Servicio de Cultura de Leon, E-24071 Leon, Spain. ; Center for Theoretical Evolutionary Genomics, University of California, Berkeley, California 94720, USA. ; Department of Medicine and Nijmegen Institute for Infection, Inflammation and Immunity, Radboud University Nijmegen Medical Centre, 6500 Nijmegen, The Netherlands. ; Department of Human Genetics, University of Chicago, Illinois 60637, USA. ; Institute for Molecular Bioscience, Melanogenix Group, The University of Queensland, Brisbane, Queensland 4072, Australia. ; 1] Center for Systems Biology, Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, Massachusetts 02138, USA [2] Broad Institute of the Massachusetts Institute of Technology and Harvard, Cambridge, Massachusetts 02142, USA. ; 1] Institut de Biologia Evolutiva, CSIC-UPF, Barcelona 08003, Spain [2] Institucio Catalana de Recerca i Estudis Avancats (ICREA), 08010 Barcelona, Catalonia, Spain. ; 1] Institut de Biologia Evolutiva, CSIC-UPF, Barcelona 08003, Spain [2] Institucio Catalana de Recerca i Estudis Avancats (ICREA), 08010 Barcelona, Catalonia, Spain [3] Centre de Regulacio Genomica (CRG), Barcelona 08003, Catalonia, Spain [4] National Institute for Bioinformatics (INB), Barcelona 08003, Catalonia, Spain. ; Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, DK-1350 Copenhagen K, Denmark.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24463515" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture/history ; *Alleles ; Biological Evolution ; Caves ; European Continental Ancestry Group/*genetics ; Eye Color/genetics ; *Fossils ; Genome, Human/genetics ; Genomics ; History, Ancient ; Humans ; Immunity/*genetics ; Lactose Intolerance/genetics ; Male ; Pigmentation/*genetics ; Polymorphism, Single Nucleotide/genetics ; Principal Component Analysis ; Skeleton ; Skin Pigmentation/genetics ; Spain/ethnology
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2014-08-01
    Description: Self-renewal is the hallmark feature both of normal stem cells and cancer stem cells. Since the regenerative capacity of normal haematopoietic stem cells is limited by the accumulation of reactive oxygen species and DNA double-strand breaks, we speculated that DNA damage might also constrain leukaemic self-renewal and malignant haematopoiesis. Here we show that the histone methyl-transferase MLL4, a suppressor of B-cell lymphoma, is required for stem-cell activity and an aggressive form of acute myeloid leukaemia harbouring the MLL-AF9 oncogene. Deletion of MLL4 enhances myelopoiesis and myeloid differentiation of leukaemic blasts, which protects mice from death related to acute myeloid leukaemia. MLL4 exerts its function by regulating transcriptional programs associated with the antioxidant response. Addition of reactive oxygen species scavengers or ectopic expression of FOXO3 protects MLL4(-/-) MLL-AF9 cells from DNA damage and inhibits myeloid maturation. Similar to MLL4 deficiency, loss of ATM or BRCA1 sensitizes transformed cells to differentiation, suggesting that myeloid differentiation is promoted by loss of genome integrity. Indeed, we show that restriction-enzyme-induced double-strand breaks are sufficient to induce differentiation of MLL-AF9 blasts, which requires cyclin-dependent kinase inhibitor p21(Cip1) (Cdkn1a) activity. In summary, we have uncovered an unexpected tumour-promoting role of genome guardians in enforcing the oncogene-induced differentiation blockade in acute myeloid leukaemia.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4410707/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4410707/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Santos, Margarida A -- Faryabi, Robert B -- Ergen, Aysegul V -- Day, Amanda M -- Malhowski, Amy -- Canela, Andres -- Onozawa, Masahiro -- Lee, Ji-Eun -- Callen, Elsa -- Gutierrez-Martinez, Paula -- Chen, Hua-Tang -- Wong, Nancy -- Finkel, Nadia -- Deshpande, Aniruddha -- Sharrow, Susan -- Rossi, Derrick J -- Ito, Keisuke -- Ge, Kai -- Aplan, Peter D -- Armstrong, Scott A -- Nussenzweig, Andre -- CA140575/CA/NCI NIH HHS/ -- CA66996/CA/NCI NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- R00 CA139009/CA/NCI NIH HHS/ -- R01 DK098263/DK/NIDDK NIH HHS/ -- R01 DK100689/DK/NIDDK NIH HHS/ -- Intramural NIH HHS/ -- England -- Nature. 2014 Oct 2;514(7520):107-11. doi: 10.1038/nature13483. Epub 2014 Jul 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genome Integrity, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. ; 1] Laboratory of Genome Integrity, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA [2]. ; The Genetics Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. ; Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. ; 1] Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, Massachusetts 02115, USA [2] Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, Massachusetts 02138, USA. ; Human Oncology and Pathogenesis Program and Department of Pediatrics, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA. ; Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. ; Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research, Departments of Cell Biology and Medicine, Albert Einstein Cancer Center, Albert Einstein College of Medicine, Bronx, New York 10461, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25079327" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxia Telangiectasia Mutated Proteins/metabolism ; BRCA1 Protein/genetics/metabolism ; Cell Transformation, Neoplastic ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; DNA Breaks, Double-Stranded ; *DNA Damage ; DNA Repair ; Female ; Gene Expression Regulation, Neoplastic ; Genes, BRCA1 ; Hematopoietic Stem Cells/cytology/metabolism/pathology ; Histone-Lysine N-Methyltransferase/deficiency/genetics/metabolism ; Leukemia, Myeloid, Acute/*enzymology/*pathology ; Male ; Mice ; *Myelopoiesis ; Oncogene Proteins, Fusion/genetics/metabolism ; Reactive Oxygen Species/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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