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  • Humans  (819)
  • Animals  (796)
  • EARTH RESOURCES AND REMOTE SENSING
  • Life and Medical Sciences
  • Nature Publishing Group (NPG)  (1,252)
  • 2010-2014  (1,252)
  • 1990-1994
  • 1980-1984
  • 2013  (1,252)
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  • 2010-2014  (1,252)
  • 1990-1994
  • 1980-1984
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  • 1
    Publication Date: 2013-12-07
    Description: The objective of science is to advance knowledge, primarily in two interlinked ways: circulating ideas, and defending or criticizing the ideas of others. Peer review acts as the gatekeeper to these mechanisms. Given the increasing concern surrounding the reproducibility of much published research, it is critical to understand whether peer review is intrinsically susceptible to failure, or whether other extrinsic factors are responsible that distort scientists' decisions. Here we show that even when scientists are motivated to promote the truth, their behaviour may be influenced, and even dominated, by information gleaned from their peers' behaviour, rather than by their personal dispositions. This phenomenon, known as herding, subjects the scientific community to an inherent risk of converging on an incorrect answer and raises the possibility that, under certain conditions, science may not be self-correcting. We further demonstrate that exercising some subjectivity in reviewer decisions, which serves to curb the herding process, can be beneficial for the scientific community in processing available information to estimate truth more accurately. By examining the impact of different models of reviewer decisions on the dynamic process of publication, and thereby on eventual aggregation of knowledge, we provide a new perspective on the ongoing discussion of how the peer-review process may be improved.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Park, In-Uck -- Peacey, Mike W -- Munafo, Marcus R -- MC_UU_12013/6/Medical Research Council/United Kingdom -- Cancer Research UK/United Kingdom -- British Heart Foundation/United Kingdom -- Medical Research Council/United Kingdom -- England -- Nature. 2014 Feb 6;506(7486):93-6. doi: 10.1038/nature12786. Epub 2013 Dec 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Economics, University of Bristol, Bristol BS8 1TN, UK [2] Department of Economics, Sungkyunkwan University, Seoul 110-745, South Korea. ; 1] Department of Economics, University of Bristol, Bristol BS8 1TN, UK [2] Department of Economics, University of Bath, Bath BA2 7AY, UK. ; 1] MRC Integrative Epidemiology Unit (IEU), University of Bristol, Bristol BS8 1BN, UK [2] UK Centre for Tobacco and Alcohol Studies, University of Bristol, Bristol BS8 1TU, UK [3] School of Experimental Psychology, University of Bristol, Bristol BS8 1TU, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24305052" target="_blank"〉PubMed〈/a〉
    Keywords: *Bias (Epidemiology) ; *Decision Making ; Empirical Research ; Humans ; *Models, Theoretical ; Peer Group ; *Peer Review, Research/standards ; Research Personnel/*psychology/standards
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  • 2
    Publication Date: 2013-12-10
    Description: Evolution drives, and is driven by, demography. A genotype moulds its phenotype's age patterns of mortality and fertility in an environment; these two patterns in turn determine the genotype's fitness in that environment. Hence, to understand the evolution of ageing, age patterns of mortality and reproduction need to be compared for species across the tree of life. However, few studies have done so and only for a limited range of taxa. Here we contrast standardized patterns over age for 11 mammals, 12 other vertebrates, 10 invertebrates, 12 vascular plants and a green alga. Although it has been predicted that evolution should inevitably lead to increasing mortality and declining fertility with age after maturity, there is great variation among these species, including increasing, constant, decreasing, humped and bowed trajectories for both long- and short-lived species. This diversity challenges theoreticians to develop broader perspectives on the evolution of ageing and empiricists to study the demography of more species.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4157354/" 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/PMC4157354/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, Owen R -- Scheuerlein, Alexander -- Salguero-Gomez, Roberto -- Camarda, Carlo Giovanni -- Schaible, Ralf -- Casper, Brenda B -- Dahlgren, Johan P -- Ehrlen, Johan -- Garcia, Maria B -- Menges, Eric S -- Quintana-Ascencio, Pedro F -- Caswell, Hal -- Baudisch, Annette -- Vaupel, James W -- P01 AG-031719/AG/NIA NIH HHS/ -- P01 AG031719/AG/NIA NIH HHS/ -- England -- Nature. 2014 Jan 9;505(7482):169-73. doi: 10.1038/nature12789. Epub 2013 Dec 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Max-Planck Odense Center on the Biodemography of Aging, Campusvej 55, 5230 Odense M, Denmark [2] Department of Biology, University of Southern Denmark, Campusvej 55, 5230 Odense M, Denmark [3]. ; 1] Max Planck Institute for Demographic Research, Konrad-Zuse-Strasse 1, 18057 Rostock, Germany [2]. ; 1] Max Planck Institute for Demographic Research, Konrad-Zuse-Strasse 1, 18057 Rostock, Germany [2] School of Biological Sciences, Centre for Biodiversity and Conservation Science, University of Queensland, Brisbane QLD 4072, Australia. ; Institut National d'Etudes Demographiques, 133 Boulevard Davout, 75980 Paris Cedex 20, France. ; Max Planck Institute for Demographic Research, Konrad-Zuse-Strasse 1, 18057 Rostock, Germany. ; Department of Biology, University of Pennsylvania, 433 South University Avenue, Philadelphia, Pennsylvania 19104-6018, USA. ; 1] Max-Planck Odense Center on the Biodemography of Aging, Campusvej 55, 5230 Odense M, Denmark [2] Department of Biology, University of Southern Denmark, Campusvej 55, 5230 Odense M, Denmark. ; Department of Ecology, Environment and Plant Sciences, Stockholm University, Lilla Frescativagen 5, 10691 Stockholm, Sweden. ; Pyrenean Institute of Ecology (CSIC), Avenida Montanana 1005, 50059 Zaragoza, Spain. ; Archbold Biological Station, 123 Main Drive, Venus, Florida 33960, USA. ; Department of Biology, University of Central Florida, 4110 Libra Drive, Orlando, Florida 32816-2368, USA. ; 1] Department of Biology, University of Southern Denmark, Campusvej 55, 5230 Odense M, Denmark [2] Max Planck Institute for Demographic Research, Konrad-Zuse-Strasse 1, 18057 Rostock, Germany [3] Woods Hole Oceanographic Institution, Biology Department MS-34, Woods Hole, Massachusetts 02543 USA [4] Institute for Biodiversity and Ecosystem Dynamics, University of Amsterdam, PO Box 94248, 1090GE Amsterdam, The Netherlands. ; 1] Max-Planck Odense Center on the Biodemography of Aging, Campusvej 55, 5230 Odense M, Denmark [2] Max Planck Institute for Demographic Research, Konrad-Zuse-Strasse 1, 18057 Rostock, Germany [3] Duke Population Research Institute, Duke University, Durham, North Carolina 27705, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24317695" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; Biological Evolution ; Chlorophyta ; Fertility/*physiology ; Longevity/*physiology ; *Phylogeny ; Plants ; Reproduction/physiology
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  • 3
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    Nature Publishing Group (NPG)
    Publication Date: 2013-01-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dusheck, Jennie -- England -- Nature. 2012 Nov 22;491(7425):S50-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23320286" target="_blank"〉PubMed〈/a〉
    Keywords: Biomechanical Phenomena ; Biomedical Research/economics/*trends ; Europe ; Humans ; Interdisciplinary Studies/*trends ; *Medical Oncology ; *Neoplasms/drug therapy/mortality/pathology ; *Physics ; United States
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  • 4
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    Nature Publishing Group (NPG)
    Publication Date: 2013-01-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2012 Dec 20;492(7429):311-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23281498" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Child ; Child Mortality ; Evidence-Based Medicine/methods ; Global Health/*statistics & numerical data/trends ; Health Care Surveys ; Health Policy/*trends ; *Health Status ; *Health Surveys ; Humans ; Life Expectancy ; Malaria/mortality ; Maternal Mortality
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  • 5
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    Nature Publishing Group (NPG)
    Publication Date: 2013-01-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2012 Dec 20;492(7429):311.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23281497" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Pyridinylmethylsulfinylbenzimidazoles ; Clinical Trials as Topic/statistics & numerical data ; Drug Approval/legislation & jurisprudence ; Drug Industry/economics/ethics/*legislation & jurisprudence ; Drug Prescriptions/standards ; *Freedom ; Humans ; Marketing/*ethics/*legislation & jurisprudence ; Off-Label Use/*ethics/*legislation & jurisprudence ; Patient Advocacy/legislation & jurisprudence ; Reproducibility of Results ; Sodium Oxybate ; United States ; United States Food and Drug Administration/legislation & jurisprudence
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  • 6
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    Nature Publishing Group (NPG)
    Publication Date: 2013-01-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gatenby, Robert -- England -- Nature. 2012 Nov 22;491(7425):S55.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Radiology andIntegrated Mathematical Oncology at the H. Lee Moffitt CancerCenter in Tampa, Florida, USA.robert.gatenby@moffitt.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23320287" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Biomedical Research/*methods ; Caves ; Fishes/genetics/physiology ; Humans ; *Models, Biological ; Molecular Biology ; Molecular Targeted Therapy ; *Neoplasms/genetics/metabolism/pathology ; Physics/*methods
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  • 7
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    Nature Publishing Group (NPG)
    Publication Date: 2013-01-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bourzac, Katherine -- England -- Nature. 2012 Nov 22;491(7425):S58-60.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23320289" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/*administration & dosage/adverse effects/*pharmacokinetics ; Cisplatin/adverse effects/pharmacokinetics ; Clinical Trials as Topic ; Doxorubicin/administration & dosage/pharmacokinetics ; Drug Carriers/administration & dosage/*chemistry/*pharmacokinetics ; Drug Resistance, Neoplasm ; Humans ; Leukemia/drug therapy/metabolism ; Logic ; Nanomedicine/*methods ; Nanoparticles/administration & dosage/*chemistry ; Neoplasm Metastasis ; Neoplasms/*drug therapy/genetics ; Pancreatic Neoplasms/drug therapy ; RNA Interference ; RNA, Small Interfering/administration & dosage/genetics/pharmacokinetics ; Robotics ; Substrate Specificity
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  • 8
    Publication Date: 2013-05-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weinberger, Daniel R -- England -- Nature. 2013 May 30;497(7451):565. doi: 10.1038/497565d.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23719455" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; Mental Disorders/*diagnosis/drug therapy/genetics/physiopathology
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  • 9
    Publication Date: 2013-02-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, Peter -- England -- Nature. 2013 Feb 21;494(7437):316-7. doi: 10.1038/494316a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23426319" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthropology ; Australia ; Chromosomes, Human, Y/genetics ; Continental Population Groups/genetics ; DNA, Mitochondrial/genetics ; *Dogs/genetics ; Female ; Gene Flow/genetics ; History, Ancient ; Human Migration/*history ; Humans ; India ; Paleontology ; Papua New Guinea ; Phylogeny
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  • 10
    Publication Date: 2013-03-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kosik, Kenneth S -- England -- Nature. 2013 Mar 21;495(7441):322-4. doi: 10.1038/nature11956. Epub 2013 Feb 27.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23446351" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; *Gene Expression Regulation ; Humans ; Male ; MicroRNAs/*metabolism ; RNA/*metabolism
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  • 11
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    Nature Publishing Group (NPG)
    Publication Date: 2013-01-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gravitz, Lauren -- England -- Nature. 2012 Nov 22;491(7425):S49.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23320284" target="_blank"〉PubMed〈/a〉
    Keywords: *Biology ; Biomedical Research/manpower/*trends ; Humans ; Interdisciplinary Studies/*trends ; *Neoplasms/diagnosis/drug therapy/genetics/pathology ; *Physics
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  • 12
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    Nature Publishing Group (NPG)
    Publication Date: 2013-01-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Agus, David B -- Gell-Mann, Murray -- England -- Nature. 2012 Nov 22;491(7425):S61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Southern California's Center for Applied Molecular Medicine in Beverly Hills, USA. agus@usc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23320291" target="_blank"〉PubMed〈/a〉
    Keywords: Biomedical Research/*methods ; *Concept Formation ; DNA/genetics ; Genetic Code ; Humans ; Medical Oncology ; Metagenome ; *Models, Biological ; Neoplasms/therapy ; Physics/*methods
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  • 13
    Publication Date: 2013-03-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sleeboom-Faulkner, Margaret -- England -- Nature. 2013 Mar 7;495(7439):47. doi: 10.1038/495047b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23467160" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; Medical Tourism/*legislation & jurisprudence ; Patient Safety/*legislation & jurisprudence ; Stem Cell Transplantation/*legislation & jurisprudence
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  • 14
    Publication Date: 2013-01-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dessai, Suraje -- Afionis, Stavros -- Van Alstine, James -- England -- Nature. 2013 Jan 3;493(7430):26. doi: 10.1038/493026d.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23282356" target="_blank"〉PubMed〈/a〉
    Keywords: Conservation of Natural Resources/*legislation & jurisprudence/*methods ; Environmental Policy/*legislation & jurisprudence ; *Goals ; Humans ; *International Cooperation ; Science/*methods
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  • 15
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    Nature Publishing Group (NPG)
    Publication Date: 2013-01-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hamre, Kristin -- England -- Nature. 2013 Jan 24;493(7433):480. doi: 10.1038/493480c.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23344351" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; Obesity/*physiopathology ; Research/*trends
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  • 16
    Publication Date: 2013-10-25
    Description: Mutations in SHANK3 and large duplications of the region spanning SHANK3 both cause a spectrum of neuropsychiatric disorders, indicating that proper SHANK3 dosage is critical for normal brain function. However, SHANK3 overexpression per se has not been established as a cause of human disorders because 22q13 duplications involve several genes. Here we report that Shank3 transgenic mice modelling a human SHANK3 duplication exhibit manic-like behaviour and seizures consistent with synaptic excitatory/inhibitory imbalance. We also identified two patients with hyperkinetic disorders carrying the smallest SHANK3-spanning duplications reported so far. These findings indicate that SHANK3 overexpression causes a hyperkinetic neuropsychiatric disorder. To probe the mechanism underlying the phenotype, we generated a Shank3 in vivo interactome and found that Shank3 directly interacts with the Arp2/3 complex to increase F-actin levels in Shank3 transgenic mice. The mood-stabilizing drug valproate, but not lithium, rescues the manic-like behaviour of Shank3 transgenic mice raising the possibility that this hyperkinetic disorder has a unique pharmacogenetic profile.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3923348/" 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/PMC3923348/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Han, Kihoon -- Holder, J Lloyd Jr -- Schaaf, Christian P -- Lu, Hui -- Chen, Hongmei -- Kang, Hyojin -- Tang, Jianrong -- Wu, Zhenyu -- Hao, Shuang -- Cheung, Sau Wai -- Yu, Peng -- Sun, Hao -- Breman, Amy M -- Patel, Ankita -- Lu, Hui-Chen -- Zoghbi, Huda Y -- 1R01NS070302/NS/NINDS NIH HHS/ -- 2T32NS043124/NS/NINDS NIH HHS/ -- P30HD024064/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Nov 7;503(7474):72-7. doi: 10.1038/nature12630. Epub 2013 Oct 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030, USA [2] Howard Hughes Medical Institute, Baylor College of Medicine, Houston, Texas 77030, USA [3] Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24153177" target="_blank"〉PubMed〈/a〉
    Keywords: Actin-Related Protein 2-3 Complex/metabolism ; Actins/metabolism ; Adult ; Animals ; Behavior, Animal ; Bipolar Disorder/*drug therapy/genetics/*physiopathology ; Chromosomes, Human, Pair 22/genetics ; Disease Models, Animal ; Excitatory Postsynaptic Potentials ; Female ; Gene Dosage/genetics ; Gene Expression/genetics ; Genes, Duplicate/genetics ; Humans ; Hyperkinesis/genetics/physiopathology ; Inhibitory Postsynaptic Potentials ; Lithium/pharmacology ; Male ; Mice ; Mice, Transgenic ; Nerve Tissue Proteins/*genetics/*metabolism ; Seizures/genetics ; Valproic Acid/pharmacology/therapeutic use
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  • 17
    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
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  • 18
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    Nature Publishing Group (NPG)
    Publication Date: 2013-07-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mole, Beth -- England -- Nature. 2013 Jul 25;499(7459):398-400. doi: 10.1038/499398a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23887415" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture ; Animals ; Animals, Domestic/*microbiology/virology ; Anti-Bacterial Agents/pharmacology/supply & distribution ; European Union ; Fomites/microbiology/statistics & numerical data ; Humans ; Iowa/epidemiology ; Meat/*microbiology ; Methicillin Resistance ; Methicillin-Resistant Staphylococcus aureus/classification/genetics/*isolation & ; purification/pathogenicity ; Staphylococcal Infections/epidemiology/microbiology/*transmission/*veterinary ; Swine/microbiology/virology ; Swine Diseases/microbiology/transmission/virology ; Zoonoses/epidemiology/*microbiology/*transmission/virology
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  • 19
    Publication Date: 2013-08-24
    Description: The RAG1/RAG2 endonuclease (RAG) initiates the V(D)J recombination reaction that assembles immunoglobulin heavy (IgH) and light (IgL) chain variable region exons from germline gene segments to generate primary antibody repertoires. IgH V(D)J assembly occurs in progenitor (pro-) B cells followed by that of IgL in precursor (pre-) B cells. Expression of IgH mu and IgL (Igkappa or Iglambda) chains generates IgM, which is expressed on immature B cells as the B-cell antigen-binding receptor (BCR). Rag expression can continue in immature B cells, allowing continued Igkappa V(D)J recombination that replaces the initial VkappaJkappa exon with one that generates a new specificity. This 'receptor editing' process, which can also lead to Iglambda V(D)J recombination and expression, provides a mechanism whereby antigen encounter at the Rag-expressing immature B-cell stage helps shape pre-immune BCR repertoires. As the major site of postnatal B-cell development, the bone marrow is the principal location of primary immunoglobulin repertoire diversification in mice. Here we report that early B-cell development also occurs within the mouse intestinal lamina propria (LP), where the associated V(D)J recombination/receptor editing processes modulate primary LP immunoglobulin repertoires. At weanling age in normally housed mice, the LP contains a population of Rag-expressing B-lineage cells that harbour intermediates indicative of ongoing V(D)J recombination and which contain cells with pro-B, pre-B and editing phenotypes. Consistent with LP-specific receptor editing, Rag-expressing LP B-lineage cells have similar VH repertoires, but significantly different Vkappa repertoires, compared to those of Rag2-expressing bone marrow counterparts. Moreover, colonization of germ-free mice leads to an increased ratio of Iglambda-expressing versus Igkappa-expressing B cells specifically in the LP. We conclude that B-cell development occurs in the intestinal mucosa, where it is regulated by extracellular signals from commensal microbes that influence gut immunoglobulin repertoires.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3807868/" 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/PMC3807868/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wesemann, Duane R -- Portuguese, Andrew J -- Meyers, Robin M -- Gallagher, Michael P -- Cluff-Jones, Kendra -- Magee, Jennifer M -- Panchakshari, Rohit A -- Rodig, Scott J -- Kepler, Thomas B -- Alt, Frederick W -- AI020047/AI/NIAID NIH HHS/ -- AI89972/AI/NIAID NIH HHS/ -- HHSN272201000053C/PHS HHS/ -- K08 AI089972/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Sep 5;501(7465):112-5. doi: 10.1038/nature12496. Epub 2013 Aug 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Cellular and Molecular Medicine and Department of Medicine, Children's Hospital Boston, Boston, Massachusetts 02115, USA. dwesemann@research.bwh.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23965619" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*cytology/*immunology/metabolism ; Bone Marrow Cells/cytology/immunology ; *Cell Lineage ; DNA-Binding Proteins/genetics/metabolism ; Gene Rearrangement, B-Lymphocyte/genetics ; Germ-Free Life ; Immunoglobulins/genetics/immunology ; Intestinal Mucosa/*cytology/*immunology ; Mice ; Precursor Cells, B-Lymphoid/cytology/metabolism ; Symbiosis ; Weaning
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  • 20
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    Nature Publishing Group (NPG)
    Publication Date: 2013-10-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉DeWeerdt, Sarah -- England -- Nature. 2013 Oct 10;502(7470):S8-9. doi: 10.1038/502S8a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24108081" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; BCG Vaccine/immunology ; Clinical Trials as Topic ; Humans ; Immunity, Cellular ; Immunity, Humoral ; Tuberculosis Vaccines/administration & dosage/*immunology/*standards ; Tuberculosis, Pulmonary/immunology/*prevention & control
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  • 21
    Publication Date: 2013-09-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rathinam, Vijay A K -- Fitzgerald, Katherine A -- England -- Nature. 2013 Sep 12;501(7466):173-5. doi: 10.1038/nature12556. Epub 2013 Sep 4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24005321" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caspases/metabolism ; Cytoplasm/immunology/*metabolism ; Gram-Negative Bacteria/*immunology ; Humans ; Immunity, Innate ; Inflammasomes/immunology/metabolism ; Lipopolysaccharides/analysis/*immunology ; Mice ; Toll-Like Receptor 4
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  • 22
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    Nature Publishing Group (NPG)
    Publication Date: 2013-07-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, Caitlin -- England -- Nature. 2013 Jul 25;499(7459):505-8. doi: 10.1038/499505a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23887432" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Movement/drug effects ; Cell Separation/instrumentation/methods ; Cell Shape ; Drug Resistance, Neoplasm/*drug effects/genetics ; Humans ; Melanoma/pathology ; Microscopy, Confocal/methods ; Neoplasm Metastasis/drug therapy/pathology ; Neoplasms/*drug therapy/genetics/*pathology ; RNA, Messenger/analysis ; RNA, Neoplasm/analysis ; Secondary Prevention ; Single-Cell Analysis
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  • 23
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    Nature Publishing Group (NPG)
    Publication Date: 2013-12-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Westly, Erica -- England -- Nature. 2013 Dec 5;504(7478):22-3. doi: 10.1038/504022a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24305135" target="_blank"〉PubMed〈/a〉
    Keywords: *Cause of Death ; Female ; Global Health/*statistics & numerical data ; Humans ; India/epidemiology ; Interviews as Topic ; Male ; Rural Population ; Urban Population
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  • 24
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    Nature Publishing Group (NPG)
    Publication Date: 2013-03-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2013 Mar 14;495(7440):142.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23495394" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomedical Research/economics ; Budgets ; *Goals ; Health Education/*economics/organization & administration ; Humans ; National Cancer Institute (U.S.)/*economics/*organization & administration ; *Neoplasms/economics/epidemiology/prevention & control/therapy ; United States
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  • 25
    Publication Date: 2013-09-13
    Description: Established infections with the human and simian immunodeficiency viruses (HIV and SIV, respectively) are thought to be permanent with even the most effective immune responses and antiretroviral therapies only able to control, but not clear, these infections. Whether the residual virus that maintains these infections is vulnerable to clearance is a question of central importance to the future management of millions of HIV-infected individuals. We recently reported that approximately 50% of rhesus macaques (RM; Macaca mulatta) vaccinated with SIV protein-expressing rhesus cytomegalovirus (RhCMV/SIV) vectors manifest durable, aviraemic control of infection with the highly pathogenic strain SIVmac239 (ref. 5). Here we show that regardless of the route of challenge, RhCMV/SIV vector-elicited immune responses control SIVmac239 after demonstrable lymphatic and haematogenous viral dissemination, and that replication-competent SIV persists in several sites for weeks to months. Over time, however, protected RM lost signs of SIV infection, showing a consistent lack of measurable plasma- or tissue-associated virus using ultrasensitive assays, and a loss of T-cell reactivity to SIV determinants not in the vaccine. Extensive ultrasensitive quantitative PCR and quantitative PCR with reverse transcription analyses of tissues from RhCMV/SIV vector-protected RM necropsied 69-172 weeks after challenge did not detect SIV RNA or DNA sequences above background levels, and replication-competent SIV was not detected in these RM by extensive co-culture analysis of tissues or by adoptive transfer of 60 million haematolymphoid cells to naive RM. These data provide compelling evidence for progressive clearance of a pathogenic lentiviral infection, and suggest that some lentiviral reservoirs may be susceptible to the continuous effector memory T-cell-mediated immune surveillance elicited and maintained by cytomegalovirus vectors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3849456/" 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/PMC3849456/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hansen, Scott G -- Piatak, Michael Jr -- Ventura, Abigail B -- Hughes, Colette M -- Gilbride, Roxanne M -- Ford, Julia C -- Oswald, Kelli -- Shoemaker, Rebecca -- Li, Yuan -- Lewis, Matthew S -- Gilliam, Awbrey N -- Xu, Guangwu -- Whizin, Nathan -- Burwitz, Benjamin J -- Planer, Shannon L -- Turner, John M -- Legasse, Alfred W -- Axthelm, Michael K -- Nelson, Jay A -- Fruh, Klaus -- Sacha, Jonah B -- Estes, Jacob D -- Keele, Brandon F -- Edlefsen, Paul T -- Lifson, Jeffrey D -- Picker, Louis J -- HHSN261200800001E/PHS HHS/ -- P01 AI094417/AI/NIAID NIH HHS/ -- P51OD011092/OD/NIH HHS/ -- R01 AI060392/AI/NIAID NIH HHS/ -- R01 DE021291/DE/NIDCR NIH HHS/ -- R37 AI054292/AI/NIAID NIH HHS/ -- U19 AI095985/AI/NIAID NIH HHS/ -- U19 AI096109/AI/NIAID NIH HHS/ -- U24 OD010850/OD/NIH HHS/ -- U42 OD010426/OD/NIH HHS/ -- England -- Nature. 2013 Oct 3;502(7469):100-4. doi: 10.1038/nature12519. Epub 2013 Sep 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vaccine and Gene Therapy Institute and Oregon National Primate Research Center, Oregon Health & Science University, Beaverton, Oregon 97006, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24025770" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytomegalovirus/genetics/immunology ; Female ; Macaca mulatta ; Male ; Molecular Sequence Data ; SAIDS Vaccines/*immunology ; Simian Acquired Immunodeficiency Syndrome/*prevention & control/virology ; Simian Immunodeficiency Virus/*immunology ; Time Factors ; Vaccines, Attenuated/immunology ; Viral Load ; Virus Replication/physiology
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  • 26
    Publication Date: 2013-04-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wheeler, Quentin -- Assis, Leandro -- Rieppel, Olivier -- England -- Nature. 2013 Apr 18;496(7445):295-6. doi: 10.1038/496295a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Schools of Sustainability and Life Sciences, Arizona State University, Tempe, Arizona, USA. quentin.wheeler@asu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23598324" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Animals ; Classification/*methods ; Entomology/history ; Evolution, Molecular ; Germany ; History, 20th Century ; Paleontology ; *Phylogeny ; Species Specificity
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  • 27
    Publication Date: 2013-08-27
    Description: Early sensory experience instructs the maturation of neural circuitry in the cortex. This has been studied extensively in the primary visual cortex, in which loss of vision to one eye permanently degrades cortical responsiveness to that eye, a phenomenon known as ocular dominance plasticity (ODP). Cortical inhibition mediates this process, but the precise role of specific classes of inhibitory neurons in ODP is controversial. Here we report that evoked firing rates of binocular excitatory neurons in the primary visual cortex immediately drop by half when vision is restricted to one eye, but gradually return to normal over the following twenty-four hours, despite the fact that vision remains restricted to one eye. This restoration of binocular-like excitatory firing rates after monocular deprivation results from a rapid, although transient, reduction in the firing rates of fast-spiking, parvalbumin-positive (PV) interneurons, which in turn can be attributed to a decrease in local excitatory circuit input onto PV interneurons. This reduction in PV-cell-evoked responses after monocular lid suture is restricted to the critical period for ODP and appears to be necessary for subsequent shifts in excitatory ODP. Pharmacologically enhancing inhibition at the time of sight deprivation blocks ODP and, conversely, pharmacogenetic reduction of PV cell firing rates can extend the critical period for ODP. These findings define the microcircuit changes initiating competitive plasticity during critical periods of cortical development. Moreover, they show that the restoration of evoked firing rates of layer 2/3 pyramidal neurons by PV-specific disinhibition is a key step in the progression of ODP.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3962838/" 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/PMC3962838/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuhlman, Sandra J -- Olivas, Nicholas D -- Tring, Elaine -- Ikrar, Taruna -- Xu, Xiangmin -- Trachtenberg, Joshua T -- EY016052/EY/NEI NIH HHS/ -- NS078434/NS/NINDS NIH HHS/ -- R00 DA023700/DA/NIDA NIH HHS/ -- R01 EY023871/EY/NEI NIH HHS/ -- R01 NS078434/NS/NINDS NIH HHS/ -- England -- Nature. 2013 Sep 26;501(7468):543-6. doi: 10.1038/nature12485. Epub 2013 Aug 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, David Geffen School of Medicine, University of California, Los Angeles, California 90048, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23975100" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Critical Period (Psychology) ; Dominance, Ocular/drug effects/*physiology ; Female ; Interneurons/cytology/drug effects ; Lasers ; Male ; Mice ; *Neural Inhibition/drug effects ; Neuronal Plasticity/drug effects/*physiology ; Parvalbumins/metabolism ; Photic Stimulation ; Sensory Deprivation/physiology ; Vision, Binocular/drug effects/physiology ; Vision, Monocular/drug effects/*physiology ; Visual Cortex/cytology/drug effects/*physiology
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  • 28
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    Publication Date: 2013-03-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2013 Mar 7;495(7439):5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23472264" target="_blank"〉PubMed〈/a〉
    Keywords: Child ; Child Care ; Education, Graduate/statistics & numerical data ; Europe ; Foundations/economics/organization & administration ; Germany ; Humans ; Internet ; Periodicals as Topic ; Research Personnel/economics/education/*statistics & numerical data ; Science/*manpower ; Sex Distribution ; Sexism/*statistics & numerical data ; United States ; Women's Rights/*statistics & numerical data
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  • 29
    Publication Date: 2013-10-11
    Description: DNA methylation was first described almost a century ago; however, the rules governing its establishment and maintenance remain elusive. Here we present data demonstrating that active transcription regulates levels of genomic methylation. We identify a novel RNA arising from the CEBPA gene locus that is critical in regulating the local DNA methylation profile. This RNA binds to DNMT1 and prevents CEBPA gene locus methylation. Deep sequencing of transcripts associated with DNMT1 combined with genome-scale methylation and expression profiling extend the generality of this finding to numerous gene loci. Collectively, these results delineate the nature of DNMT1-RNA interactions and suggest strategies for gene-selective demethylation of therapeutic targets in human diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3870304/" 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/PMC3870304/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Di Ruscio, Annalisa -- Ebralidze, Alexander K -- Benoukraf, Touati -- Amabile, Giovanni -- Goff, Loyal A -- Terragni, Jolyon -- Figueroa, Maria Eugenia -- De Figueiredo Pontes, Lorena Lobo -- Alberich-Jorda, Meritxell -- Zhang, Pu -- Wu, Mengchu -- D'Alo, Francesco -- Melnick, Ari -- Leone, Giuseppe -- Ebralidze, Konstantin K -- Pradhan, Sriharsa -- Rinn, John L -- Tenen, Daniel G -- CA118316/CA/NCI NIH HHS/ -- CA66996/CA/NCI NIH HHS/ -- HL56745/HL/NHLBI NIH HHS/ -- P01 CA066996/CA/NCI NIH HHS/ -- R01 CA118316/CA/NCI NIH HHS/ -- R01 HL056745/HL/NHLBI NIH HHS/ -- R01 HL112719/HL/NHLBI NIH HHS/ -- T32 HL007917-11A1/HL/NHLBI NIH HHS/ -- England -- Nature. 2013 Nov 21;503(7476):371-6. doi: 10.1038/nature12598. Epub 2013 Oct 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Harvard Stem Cell Institute, Harvard Medical School, Boston, Massachusetts 02115, USA [2] Beth Israel Deaconess Medical Center, Boston, Massachusetts 02115, USA [3] Universita Cattolica del Sacro Cuore, Institute of Hematology, L.go A. Gemelli 8, Rome 00168, Italy [4].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24107992" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; CCAAT-Enhancer-Binding Proteins/*genetics ; Cell Line ; DNA/genetics/metabolism ; DNA (Cytosine-5-)-Methyltransferase/*metabolism ; DNA Methylation/*genetics ; Gene Expression Profiling ; Gene Expression Regulation/*genetics ; Genome, Human/genetics ; Humans ; RNA, Messenger/genetics/metabolism ; RNA, Untranslated/genetics/*metabolism ; RNA-Binding Proteins/metabolism ; Substrate Specificity ; Transcription, Genetic/genetics
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  • 30
    Publication Date: 2013-11-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Westwick, Peter -- England -- Nature. 2013 Nov 21;503(7476):341. doi: 10.1038/503341a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24256794" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Athletes ; Athletic Performance ; Diving ; Forecasting ; Global Warming ; Research ; *Research Personnel ; *Sports ; *Water Movements
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  • 31
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    Nature Publishing Group (NPG)
    Publication Date: 2013-05-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, Kerri -- England -- Nature. 2013 May 30;497(7451):550-2. doi: 10.1038/497550a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23719444" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anxiety/drug therapy/metabolism ; Brain Mapping/instrumentation/*methods ; Child ; Child Development Disorders, Pervasive/pathology ; Cocaine-Related Disorders/prevention & control ; Depression/metabolism ; Dopamine/metabolism ; History, 21st Century ; Humans ; Imaging, Three-Dimensional/instrumentation/*methods ; Male ; Mice ; Microscopy ; Neural Pathways/physiology ; Neurosciences/instrumentation/*methods ; Opsins/metabolism/radiation effects ; Optogenetics/history ; Rats
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  • 32
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    Nature Publishing Group (NPG)
    Publication Date: 2013-05-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Monastersky, Richard -- England -- Nature. 2013 May 30;497(7451):545-6. doi: 10.1038/497545a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23719440" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Animals ; Birds/physiology ; Entomology ; Female ; Hemiptera/classification/genetics/growth & development/*physiology ; Larva/genetics/growth & development/physiology ; Life Cycle Stages/*physiology ; Male ; *Periodicity ; Plant Roots/metabolism ; Population Dynamics ; Predatory Behavior/physiology ; Research Personnel ; Sexual Behavior, Animal/physiology ; Survival Rate ; Time Factors ; United States ; Vocalization, Animal/physiology
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  • 33
    Publication Date: 2013-03-01
    Description: The rapid cell turnover of the intestinal epithelium is achieved from small numbers of stem cells located in the base of glandular crypts. These stem cells have been variously described as rapidly cycling or quiescent. A functional arrangement of stem cells that reconciles both of these behaviours has so far been difficult to obtain. Alternative explanations for quiescent cells have been that they act as a parallel or reserve population that replace rapidly cycling stem cells periodically or after injury; their exact nature remains unknown. Here we show mouse intestinal quiescent cells to be precursors that are committed to mature into differentiated secretory cells of the Paneth and enteroendocrine lineage. However, crucially we find that after intestinal injury they are capable of extensive proliferation and can give rise to clones comprising the main epithelial cell types. Thus, quiescent cells can be recalled to the stem-cell state. These findings establish quiescent cells as an effective clonogenic reserve and provide a motivation for investigating their role in pathologies such as colorectal cancers and intestinal inflammation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buczacki, Simon J A -- Zecchini, Heather Ireland -- Nicholson, Anna M -- Russell, Roslin -- Vermeulen, Louis -- Kemp, Richard -- Winton, Douglas J -- Cancer Research UK/United Kingdom -- England -- Nature. 2013 Mar 7;495(7439):65-9. doi: 10.1038/nature11965. Epub 2013 Feb 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research UK Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23446353" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers/analysis/metabolism ; Cell Differentiation ; Cell Division ; *Cell Lineage ; Cell Separation ; Clone Cells/cytology/metabolism ; Intestinal Neoplasms/pathology ; Intestines/cytology/injuries/pathology ; Mice ; Multipotent Stem Cells/*cytology/metabolism/*secretion ; Paneth Cells/*cytology/*metabolism ; Receptors, G-Protein-Coupled/*metabolism ; Regeneration ; Staining and Labeling ; Stem Cell Niche
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  • 34
    Publication Date: 2013-07-13
    Description: RNA-binding proteins are key regulators of gene expression, yet only a small fraction have been functionally characterized. Here we report a systematic analysis of the RNA motifs recognized by RNA-binding proteins, encompassing 205 distinct genes from 24 diverse eukaryotes. The sequence specificities of RNA-binding proteins display deep evolutionary conservation, and the recognition preferences for a large fraction of metazoan RNA-binding proteins can thus be inferred from their RNA-binding domain sequence. The motifs that we identify in vitro correlate well with in vivo RNA-binding data. Moreover, we can associate them with distinct functional roles in diverse types of post-transcriptional regulation, enabling new insights into the functions of RNA-binding proteins both in normal physiology and in human disease. These data provide an unprecedented overview of RNA-binding proteins and their targets, and constitute an invaluable resource for determining post-transcriptional regulatory mechanisms in eukaryotes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3929597/" 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/PMC3929597/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ray, Debashish -- Kazan, Hilal -- Cook, Kate B -- Weirauch, Matthew T -- Najafabadi, Hamed S -- Li, Xiao -- Gueroussov, Serge -- Albu, Mihai -- Zheng, Hong -- Yang, Ally -- Na, Hong -- Irimia, Manuel -- Matzat, Leah H -- Dale, Ryan K -- Smith, Sarah A -- Yarosh, Christopher A -- Kelly, Seth M -- Nabet, Behnam -- Mecenas, Desirea -- Li, Weimin -- Laishram, Rakesh S -- Qiao, Mei -- Lipshitz, Howard D -- Piano, Fabio -- Corbett, Anita H -- Carstens, Russ P -- Frey, Brendan J -- Anderson, Richard A -- Lynch, Kristen W -- Penalva, Luiz O F -- Lei, Elissa P -- Fraser, Andrew G -- Blencowe, Benjamin J -- Morris, Quaid D -- Hughes, Timothy R -- 1R01HG00570/HG/NHGRI NIH HHS/ -- DK015602-05/DK/NIDDK NIH HHS/ -- MOP-125894/Canadian Institutes of Health Research/Canada -- MOP-14409/Canadian Institutes of Health Research/Canada -- MOP-49451/Canadian Institutes of Health Research/Canada -- MOP-67011/Canadian Institutes of Health Research/Canada -- MOP-93671/Canadian Institutes of Health Research/Canada -- P30 CA014520/CA/NCI NIH HHS/ -- R01 CA104708/CA/NCI NIH HHS/ -- R01 GM051968/GM/NIGMS NIH HHS/ -- R01 GM084034/GM/NIGMS NIH HHS/ -- R01 HG005700/HG/NHGRI NIH HHS/ -- R01GM084034/GM/NIGMS NIH HHS/ -- T32 GM008061/GM/NIGMS NIH HHS/ -- Z01 DK015602-01/Intramural NIH HHS/ -- England -- Nature. 2013 Jul 11;499(7457):172-7. doi: 10.1038/nature12311.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Donnelly Centre, University of Toronto, Toronto M5S 3E1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23846655" target="_blank"〉PubMed〈/a〉
    Keywords: Autistic Disorder/genetics ; Base Sequence ; Binding Sites/genetics ; Conserved Sequence/genetics ; Eukaryotic Cells/metabolism ; Gene Expression Regulation/*genetics ; Humans ; Molecular Sequence Data ; Nucleotide Motifs/*genetics ; Protein Structure, Tertiary/genetics ; RNA Stability/genetics ; RNA-Binding Proteins/chemistry/genetics/*metabolism
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  • 35
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    Nature Publishing Group (NPG)
    Publication Date: 2013-05-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, Kerri -- England -- Nature. 2013 May 23;497(7450):S4-5. doi: 10.1038/497S4a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23698506" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cats ; Female ; Hippocampus/physiology ; Humans ; Infant ; Memory/*physiology ; Models, Neurological ; Neuronal Plasticity/physiology ; Rats ; Sleep/*physiology ; Sleep, REM/physiology ; Wakefulness/physiology
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  • 36
    Publication Date: 2013-02-22
    Description: Pathogens often infect hosts through collective actions: they secrete growth-promoting compounds or virulence factors, or evoke host reactions that fuel the colonization of the host. Such behaviours are vulnerable to the rise of mutants that benefit from the collective action without contributing to it; how these behaviours can be evolutionarily stable is not well understood. We address this question using the intestinal pathogen Salmonella enterica serovar Typhimurium (hereafter termed S. typhimurium), which manipulates its host to induce inflammation, and thereby outcompetes the commensal microbiota. Notably, the virulence factors needed for host manipulation are expressed in a bistable fashion, leading to a slow-growing subpopulation that expresses virulence genes, and a fast-growing subpopulation that is phenotypically avirulent. Here we show that the expression of the genetically identical but phenotypically avirulent subpopulation is essential for the evolutionary stability of virulence in this pathogen. Using a combination of mathematical modelling, experimental evolution and competition experiments we found that within-host evolution leads to the emergence of mutants that are genetically avirulent and fast-growing. These mutants are defectors that exploit inflammation without contributing to it. In infection experiments initiated with wild-type S. typhimurium, defectors increase only slowly in frequency. In a genetically modified S. typhimurium strain in which the phenotypically avirulent subpopulation is reduced in size, defectors rise more rapidly, inflammation ceases prematurely, and S. typhimurium is quickly cleared from the gut. Our results establish that host manipulation by S. typhimurium is a cooperative trait that is vulnerable to the rise of avirulent defectors; the expression of a phenotypically avirulent subpopulation that grows as fast as defectors slows down this process, and thereby promotes the evolutionary stability of virulence. This points to a key role of bistable virulence gene expression in stabilizing cooperative virulence and may lead the way to new approaches for controlling pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diard, Mederic -- Garcia, Victor -- Maier, Lisa -- Remus-Emsermann, Mitja N P -- Regoes, Roland R -- Ackermann, Martin -- Hardt, Wolf-Dietrich -- England -- Nature. 2013 Feb 21;494(7437):353-6. doi: 10.1038/nature11913.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Microbiology, ETH Zurich, Wolfgang-Pauli-Str. 10, 8093 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23426324" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Host-Pathogen Interactions ; Inflammation/microbiology/pathology ; Intestines/microbiology ; Mice ; Mice, Inbred C57BL ; Mutation ; *Phenotype ; Salmonella Infections/microbiology/prevention & control/transmission ; Salmonella typhimurium/genetics/growth & development/*pathogenicity ; Virulence/genetics/physiology ; Virulence Factors/genetics/metabolism
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  • 37
    Publication Date: 2013-06-28
    Description: The activation-induced cytidine deaminase (AID; also known as AICDA) enzyme is required for somatic hypermutation and class switch recombination at the immunoglobulin locus. In germinal-centre B cells, AID is highly expressed, and has an inherent mutator activity that helps generate antibody diversity. However, AID may also regulate gene expression epigenetically by directly deaminating 5-methylcytosine in concert with base-excision repair to exchange cytosine. This pathway promotes gene demethylation, thereby removing epigenetic memory. For example, AID promotes active demethylation of the genome in primordial germ cells. However, different studies have suggested either a requirement or a lack of function for AID in promoting pluripotency in somatic nuclei after fusion with embryonic stem cells. Here we tested directly whether AID regulates epigenetic memory by comparing the relative ability of cells lacking AID to reprogram from a differentiated murine cell type to an induced pluripotent stem cell. We show that Aid-null cells are transiently hyper-responsive to the reprogramming process. Although they initiate expression of pluripotency genes, they fail to stabilize in the pluripotent state. The genome of Aid-null cells remains hypermethylated in reprogramming cells, and hypermethylated genes associated with pluripotency fail to be stably upregulated, including many MYC target genes. Recent studies identified a late step of reprogramming associated with methylation status, and implicated a secondary set of pluripotency network components. AID regulates this late step, removing epigenetic memory to stabilize the pluripotent state.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3762466/" 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/PMC3762466/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kumar, Ritu -- DiMenna, Lauren -- Schrode, Nadine -- Liu, Ting-Chun -- Franck, Philipp -- Munoz-Descalzo, Silvia -- Hadjantonakis, Anna-Katerina -- Zarrin, Ali A -- Chaudhuri, Jayanta -- Elemento, Olivier -- Evans, Todd -- AI072194/AI/NIAID NIH HHS/ -- HL056182/HL/NHLBI NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- R01 HD052115/HD/NICHD NIH HHS/ -- R37 HL056182/HL/NHLBI NIH HHS/ -- T32 AI007621/AI/NIAID NIH HHS/ -- England -- Nature. 2013 Aug 1;500(7460):89-92. doi: 10.1038/nature12299. Epub 2013 Jun 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Weill Cornell Medical College, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23803762" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Dedifferentiation/genetics ; Cellular Reprogramming/genetics ; Cytidine Deaminase/genetics/*metabolism ; Epigenesis, Genetic/*genetics ; Female ; Fibroblasts/cytology/metabolism ; Gene Expression Regulation ; HEK293 Cells ; Humans ; Male ; Mice ; Pluripotent Stem Cells/*cytology/enzymology/*metabolism ; Transcription Factors/metabolism
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  • 38
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    Unknown
    Nature Publishing Group (NPG)
    Publication Date: 2013-05-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harris, Henry -- England -- Nature. 2013 May 9;497(7448):188. doi: 10.1038/497188d.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23657339" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Genome/*genetics ; Humans ; Molecular Biology/*manpower/*trends ; RNA, Long Noncoding/*genetics ; *Research Personnel
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  • 39
    Publication Date: 2013-10-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kunin, William E -- England -- Nature. 2013 Oct 17;502(7471):303. doi: 10.1038/502303a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24132279" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; *Policy Making ; Research/*standards ; Research Design/*standards
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  • 40
    Publication Date: 2013-01-22
    Description: The intestinal microbiota has a critical role in immune system and metabolic homeostasis, but it must be tolerated by the host to avoid inflammatory responses that can damage the epithelial barrier separating the host from the luminal contents. Breakdown of this regulation and the resulting inappropriate immune response to commensals are thought to lead to the development of inflammatory bowel diseases such as Crohn's disease and ulcerative colitis. We proposed that the intestinal immune system is instructed by the microbiota to limit responses to luminal antigens. Here we demonstrate in mice that, at steady state, the microbiota inhibits the transport of both commensal and pathogenic bacteria from the lumen to a key immune inductive site, the mesenteric lymph nodes (MLNs). However, in the absence of Myd88 or under conditions of antibiotic-induced dysbiosis, non-invasive bacteria were trafficked to the MLNs in a CCR7-dependent manner, and induced both T-cell responses and IgA production. Trafficking was carried out by CX(3)CR1(hi) mononuclear phagocytes, an intestinal-cell population previously reported to be non-migratory. These findings define a central role for commensals in regulating the migration to the MLNs of CX(3)CR1(hi) mononuclear phagocytes endowed with the ability to capture luminal bacteria, thereby compartmentalizing the intestinal immune response to avoid inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3711636/" 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/PMC3711636/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diehl, Gretchen E -- Longman, Randy S -- Zhang, Jing-Xin -- Breart, Beatrice -- Galan, Carolina -- Cuesta, Adolfo -- Schwab, Susan R -- Littman, Dan R -- 5P30CA016087-32/CA/NCI NIH HHS/ -- R01 AI085166/AI/NIAID NIH HHS/ -- R01AI085166/AI/NIAID NIH HHS/ -- T32 CA009161/CA/NCI NIH HHS/ -- T32 DK083256/DK/NIDDK NIH HHS/ -- T32 DK083256-02/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Feb 7;494(7435):116-20. doi: 10.1038/nature11809. Epub 2013 Jan 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Pathogenesis Program, The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, New York 10016, USA. Gretchen.Diehl@med.nyu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23334413" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/pharmacology ; Antigens, Bacterial/immunology ; Cell Movement ; Dendritic Cells/cytology/immunology ; Immunity, Mucosal/drug effects/*immunology ; Immunoglobulin A/immunology ; Inflammation/immunology ; Intestinal Mucosa/cytology/immunology/microbiology ; Lymph Nodes/*immunology/*microbiology ; Mesentery/*immunology ; Metagenome/immunology/*physiology ; Mice ; Mice, Inbred C57BL ; Myeloid Differentiation Factor 88/deficiency/metabolism ; Phagocytes/cytology/immunology/*metabolism/microbiology ; Phagocytosis ; Receptors, CCR7/deficiency/genetics/metabolism ; Receptors, Chemokine/*metabolism ; Salmonella/cytology/drug effects/immunology ; T-Lymphocytes/immunology
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  • 41
    Publication Date: 2013-10-11
    Description: Cell cycle quiescence is a critical feature contributing to haematopoietic stem cell (HSC) maintenance. Although various candidate stromal cells have been identified as potential HSC niches, the spatial localization of quiescent HSCs in the bone marrow remains unclear. Here, using a novel approach that combines whole-mount confocal immunofluorescence imaging techniques and computational modelling to analyse significant three-dimensional associations in the mouse bone marrow among vascular structures, stromal cells and HSCs, we show that quiescent HSCs associate specifically with small arterioles that are preferentially found in endosteal bone marrow. These arterioles are ensheathed exclusively by rare NG2 (also known as CSPG4)(+) pericytes, distinct from sinusoid-associated leptin receptor (LEPR)(+) cells. Pharmacological or genetic activation of the HSC cell cycle alters the distribution of HSCs from NG2(+) periarteriolar niches to LEPR(+) perisinusoidal niches. Conditional depletion of NG2(+) cells induces HSC cycling and reduces functional long-term repopulating HSCs in the bone marrow. These results thus indicate that arteriolar niches are indispensable for maintaining HSC quiescence.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3821873/" 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/PMC3821873/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kunisaki, Yuya -- Bruns, Ingmar -- Scheiermann, Christoph -- Ahmed, Jalal -- Pinho, Sandra -- Zhang, Dachuan -- Mizoguchi, Toshihide -- Wei, Qiaozhi -- Lucas, Daniel -- Ito, Keisuke -- Mar, Jessica C -- Bergman, Aviv -- Frenette, Paul S -- HL069438/HL/NHLBI NIH HHS/ -- HL097700/HL/NHLBI NIH HHS/ -- R00 CA139009/CA/NCI NIH HHS/ -- R01 DK056638/DK/NIDDK NIH HHS/ -- R01 DK098263/DK/NIDDK NIH HHS/ -- R01 DK100689/DK/NIDDK NIH HHS/ -- R01 HL069438/HL/NHLBI NIH HHS/ -- R01 HL097700/HL/NHLBI NIH HHS/ -- R01 HL116340/HL/NHLBI NIH HHS/ -- T32 063754/PHS HHS/ -- England -- Nature. 2013 Oct 31;502(7473):637-43. doi: 10.1038/nature12612. Epub 2013 Oct 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research, Albert Einstein College of Medicine, Bronx, New York 10461, USA [2] Department of Cell Biology, 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/24107994" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arterioles/*cytology ; Bone Marrow/blood supply ; Cell Division ; Cell Separation ; Female ; Flow Cytometry ; Hematopoietic Stem Cells/*cytology/metabolism ; Male ; Mesenchymal Stromal Cells/cytology ; Mice ; Mice, Inbred C57BL ; Nestin/metabolism ; *Stem Cell Niche
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  • 42
    Publication Date: 2013-06-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Whiten, Andrew -- England -- Nature. 2013 Jun 20;498(7454):303-5. doi: 10.1038/498303a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23783622" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Archaeology ; Cebus/*physiology ; Humans ; Nuts ; *Tool Use Behavior
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  • 43
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    Unknown
    Nature Publishing Group (NPG)
    Publication Date: 2013-11-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moody, Alan -- England -- Nature. 2013 Oct 31;502(7473):S95.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24187705" target="_blank"〉PubMed〈/a〉
    Keywords: Archives ; Biomedical Research/*methods/*trends ; Confidentiality/ethics ; Humans ; Image Interpretation, Computer-Assisted/*utilization ; *Information Dissemination/ethics ; Information Storage and Retrieval/trends
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  • 44
    Publication Date: 2013-06-07
    Description: G-protein-gated inward rectifier K(+) (GIRK) channels allow neurotransmitters, through G-protein-coupled receptor stimulation, to control cellular electrical excitability. In cardiac and neuronal cells this control regulates heart rate and neural circuit activity, respectively. Here we present the 3.5 A resolution crystal structure of the mammalian GIRK2 channel in complex with betagamma G-protein subunits, the central signalling complex that links G-protein-coupled receptor stimulation to K(+) channel activity. Short-range atomic and long-range electrostatic interactions stabilize four betagamma G-protein subunits at the interfaces between four K(+) channel subunits, inducing a pre-open state of the channel. The pre-open state exhibits a conformation that is intermediate between the closed conformation and the open conformation of the constitutively active mutant. The resultant structural picture is compatible with 'membrane delimited' activation of GIRK channels by G proteins and the characteristic burst kinetics of channel gating. The structures also permit a conceptual understanding of how the signalling lipid phosphatidylinositol-4,5-bisphosphate (PIP2) and intracellular Na(+) ions participate in multi-ligand regulation of GIRK channels.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4654628/" 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/PMC4654628/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Whorton, Matthew R -- MacKinnon, Roderick -- 1S10RR022321-01/RR/NCRR NIH HHS/ -- 1S10RR027037-01/RR/NCRR NIH HHS/ -- S10 RR027037/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Jun 13;498(7453):190-7. doi: 10.1038/nature12241. Epub 2013 Jun 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Neurobiology and Biophysics, The Rockefeller University, 1230 York Avenue, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23739333" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Crystallography, X-Ray ; G Protein-Coupled Inwardly-Rectifying Potassium ; Channels/*chemistry/genetics/metabolism ; Heterotrimeric GTP-Binding Proteins/*chemistry/genetics/metabolism ; Humans ; Ion Channel Gating ; Models, Biological ; Models, Molecular ; Phosphatidylinositol 4,5-Diphosphate/metabolism ; Protein Conformation ; Protein Interaction Domains and Motifs ; Protein Subunits/chemistry/metabolism ; Sodium/metabolism ; Static Electricity
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  • 45
    Publication Date: 2013-03-29
    Description: Protein N-myristoylation is a 14-carbon fatty-acid modification that is conserved across eukaryotic species and occurs on nearly 1% of the cellular proteome. The ability of the myristoyl group to facilitate dynamic protein-protein and protein-membrane interactions (known as the myristoyl switch) makes it an essential feature of many signal transduction systems. Thus pathogenic strategies that facilitate protein demyristoylation would markedly alter the signalling landscape of infected host cells. Here we describe an irreversible mechanism of protein demyristoylation catalysed by invasion plasmid antigen J (IpaJ), a previously uncharacterized Shigella flexneri type III effector protein with cysteine protease activity. A yeast genetic screen for IpaJ substrates identified ADP-ribosylation factor (ARF)1p and ARF2p, small molecular mass GTPases that regulate cargo transport through the Golgi apparatus. Mass spectrometry showed that IpaJ cleaved the peptide bond between N-myristoylated glycine-2 and asparagine-3 of human ARF1, thereby providing a new mechanism for host secretory inhibition by a bacterial pathogen. We further demonstrate that IpaJ cleaves an array of N-myristoylated proteins involved in cellular growth, signal transduction, autophagasome maturation and organelle function. Taken together, these findings show a previously unrecognized pathogenic mechanism for the site-specific elimination of N-myristoyl protein modification.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3722872/" 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/PMC3722872/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burnaevskiy, Nikolay -- Fox, Thomas G -- Plymire, Daniel A -- Ertelt, James M -- Weigele, Bethany A -- Selyunin, Andrey S -- Way, Sing Sing -- Patrie, Steven M -- Alto, Neal M -- 5T32AI007520/AI/NIAID NIH HHS/ -- R01 AI083359/AI/NIAID NIH HHS/ -- R01 AI087830/AI/NIAID NIH HHS/ -- R01 AI100934/AI/NIAID NIH HHS/ -- R01 GM100486/GM/NIGMS NIH HHS/ -- R01AI083359/AI/NIAID NIH HHS/ -- R01GM100486/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Apr 4;496(7443):106-9. doi: 10.1038/nature12004. Epub 2013 Mar 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-8816, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23535599" target="_blank"〉PubMed〈/a〉
    Keywords: ADP-Ribosylation Factor 1/chemistry/metabolism ; ADP-Ribosylation Factors/metabolism ; Amino Acid Sequence ; Animals ; Antigens, Bacterial/*metabolism ; Asparagine/metabolism ; Autophagy ; Biocatalysis ; Cysteine Proteases/metabolism ; Dysentery, Bacillary ; Female ; Glycine/metabolism ; Golgi Apparatus/metabolism/pathology ; HEK293 Cells ; HeLa Cells ; Humans ; Listeria monocytogenes/physiology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Myristic Acid/*metabolism ; Phagosomes/metabolism ; *Protein Processing, Post-Translational ; *Proteolysis ; Saccharomyces cerevisiae ; Saccharomyces cerevisiae Proteins/metabolism ; Sequence Alignment ; Shigella flexneri/enzymology/*metabolism ; Signal Transduction ; Substrate Specificity ; Virulence ; Virulence Factors/*metabolism
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  • 46
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    Nature Publishing Group (NPG)
    Publication Date: 2013-02-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2013 Feb 21;494(7437):282. doi: 10.1038/494282a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23426286" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conservation of Natural Resources/*methods ; Ecology/methods ; *Ecosystem ; Fisheries/economics/methods/standards/*statistics & numerical data ; Fishes/growth & development/*physiology ; Marine Biology/methods ; Oceans and Seas ; Population Dynamics ; Uncertainty
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  • 47
    Publication Date: 2013-11-05
    Description: Hepatitis C virus (HCV) and classical swine fever virus (CSFV) messenger RNAs contain related (HCV-like) internal ribosome entry sites (IRESs) that promote 5'-end independent initiation of translation, requiring only a subset of the eukaryotic initiation factors (eIFs) needed for canonical initiation on cellular mRNAs. Initiation on HCV-like IRESs relies on their specific interaction with the 40S subunit, which places the initiation codon into the P site, where it directly base-pairs with eIF2-bound initiator methionyl transfer RNA to form a 48S initiation complex. However, all HCV-like IRESs also specifically interact with eIF3 (refs 2, 5-7, 9-12), but the role of this interaction in IRES-mediated initiation has remained unknown. During canonical initiation, eIF3 binds to the 40S subunit as a component of the 43S pre-initiation complex, and comparison of the ribosomal positions of eIF3 and the HCV IRES revealed that they overlap, so that their rearrangement would be required for formation of ribosomal complexes containing both components. Here we present a cryo-electron microscopy reconstruction of a 40S ribosomal complex containing eIF3 and the CSFV IRES. Remarkably, although the position and interactions of the CSFV IRES with the 40S subunit in this complex are similar to those of the HCV IRES in the 40S-IRES binary complex, eIF3 is completely displaced from its ribosomal position in the 43S complex, and instead interacts through its ribosome-binding surface exclusively with the apical region of domain III of the IRES. Our results suggest a role for the specific interaction of HCV-like IRESs with eIF3 in preventing ribosomal association of eIF3, which could serve two purposes: relieving the competition between the IRES and eIF3 for a common binding site on the 40S subunit, and reducing formation of 43S complexes, thereby favouring translation of viral mRNAs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4106463/" 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/PMC4106463/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hashem, Yaser -- des Georges, Amedee -- Dhote, Vidya -- Langlois, Robert -- Liao, Hstau Y -- Grassucci, Robert A -- Pestova, Tatyana V -- Hellen, Christopher U T -- Frank, Joachim -- R01 AI51340/AI/NIAID NIH HHS/ -- R01 GM029169/GM/NIGMS NIH HHS/ -- R01 GM59660/GM/NIGMS NIH HHS/ -- R01GM29169/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Nov 28;503(7477):539-43. doi: 10.1038/nature12658. Epub 2013 Nov 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Howard Hughes Medical Institute (HHMI), Department of Biochemistry and Molecular Biophysics, Columbia University, New York City, New York 10032, USA [2] Department of Biochemistry and Molecular Biophysics, Columbia University, New York City, New York 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24185006" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding, Competitive ; Classical swine fever virus/*genetics ; Cryoelectron Microscopy ; Eukaryotic Initiation Factor-3/chemistry/*metabolism/ultrastructure ; Humans ; Models, Molecular ; Protein Biosynthesis ; RNA, Viral/*genetics/*metabolism ; Rabbits ; Regulatory Sequences, Ribonucleic Acid/*genetics ; Ribosome Subunits, Small, Eukaryotic/chemistry/*metabolism/ultrastructure ; Ribosomes/chemistry/*metabolism/ultrastructure
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  • 48
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    Nature Publishing Group (NPG)
    Publication Date: 2013-10-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moore, David D -- England -- Nature. 2013 Oct 24;502(7472):454-5. doi: 10.1038/502454a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24153294" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Circadian Rhythm ; Fatty Acids/*metabolism ; Lipids/*blood ; *Lipogenesis ; Liver/*metabolism ; Male
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  • 49
    Publication Date: 2013-02-08
    Description: Several mutations are required for cancer development, and genome sequencing has revealed that many cancers, including breast cancer, have somatic mutation spectra dominated by C-to-T transitions. Most of these mutations occur at hydrolytically disfavoured non-methylated cytosines throughout the genome, and are sometimes clustered. Here we show that the DNA cytosine deaminase APOBEC3B is a probable source of these mutations. APOBEC3B messenger RNA is upregulated in most primary breast tumours and breast cancer cell lines. Tumours that express high levels of APOBEC3B have twice as many mutations as those that express low levels and are more likely to have mutations in TP53. Endogenous APOBEC3B protein is predominantly nuclear and the only detectable source of DNA C-to-U editing activity in breast cancer cell-line extracts. Knockdown experiments show that endogenous APOBEC3B correlates with increased levels of genomic uracil, increased mutation frequencies, and C-to-T transitions. Furthermore, induced APOBEC3B overexpression causes cell cycle deviations, cell death, DNA fragmentation, gamma-H2AX accumulation and C-to-T mutations. Our data suggest a model in which APOBEC3B-catalysed deamination provides a chronic source of DNA damage in breast cancers that could select TP53 inactivation and explain how some tumours evolve rapidly and manifest heterogeneity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3907282/" 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/PMC3907282/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burns, Michael B -- Lackey, Lela -- Carpenter, Michael A -- Rathore, Anurag -- Land, Allison M -- Leonard, Brandon -- Refsland, Eric W -- Kotandeniya, Delshanee -- Tretyakova, Natalia -- Nikas, Jason B -- Yee, Douglas -- Temiz, Nuri A -- Donohue, Duncan E -- McDougle, Rebecca M -- Brown, William L -- Law, Emily K -- Harris, Reuben S -- 1UL1RR033183/RR/NCRR NIH HHS/ -- F31 DA033186/DA/NIDA NIH HHS/ -- F32 GM095219/GM/NIGMS NIH HHS/ -- KL2 RR033182/RR/NCRR NIH HHS/ -- P01 GM091743/GM/NIGMS NIH HHS/ -- P30 CA77598/CA/NCI NIH HHS/ -- P50 CA101955/CA/NCI NIH HHS/ -- R01 AI064046/AI/NIAID NIH HHS/ -- T32 AI083196/AI/NIAID NIH HHS/ -- T32 CA009138/CA/NCI NIH HHS/ -- UL1 TR000114/TR/NCATS NIH HHS/ -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2013 Feb 21;494(7437):366-70. doi: 10.1038/nature11881. Epub 2013 Feb 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biochemistry, Molecular Biology and Biophysics Department, University of Minnesota, Minneapolis, Minnesota 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23389445" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Biocatalysis ; Breast Neoplasms/*enzymology/*genetics/pathology ; Cell Death ; Cell Line, Tumor ; Cytidine Deaminase/genetics/*metabolism ; DNA Damage/genetics ; DNA Fragmentation ; DNA, Neoplasm/genetics/metabolism ; Deamination ; Gene Expression Regulation, Enzymologic ; Gene Expression Regulation, Neoplastic ; Histones/metabolism ; Humans ; *Mutagenesis/genetics ; Phenotype ; *Point Mutation/genetics ; Tumor Suppressor Protein p53/genetics/metabolism ; Up-Regulation ; Uracil/metabolism
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  • 50
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    Nature Publishing Group (NPG)
    Publication Date: 2013-10-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Witze, Alexandra -- England -- Nature. 2013 Oct 24;502(7472):422-3. doi: 10.1038/502422a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24153274" target="_blank"〉PubMed〈/a〉
    Keywords: Accidents, Aviation/*prevention & control ; Aircraft/*instrumentation ; Atmosphere/chemistry ; Environmental Monitoring/*instrumentation ; Evaluation Studies as Topic ; France ; Humans ; Iceland ; Norway ; Volcanic Eruptions/*analysis
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  • 51
    Publication Date: 2013-03-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Butler, Jason M -- Rafii, Shahin -- England -- Nature. 2013 Mar 21;495(7441):317-8. doi: 10.1038/nature12085. Epub 2013 Mar 13.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23485972" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dinoprostone/*metabolism ; Hematopoietic Stem Cells/*cytology ; Humans ; Stem Cells/*cytology
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  • 52
    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
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  • 53
    Publication Date: 2013-07-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steinhauer, David A -- England -- Nature. 2013 Jul 25;499(7459):412-3. doi: 10.1038/nature12455. Epub 2013 Jul 17.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23863929" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Influenza A virus/*metabolism/*physiology ; Influenza in Birds/*virology ; Influenza, Human/*virology ; N-Acetylneuraminic Acid/*metabolism ; Receptors, Virus/*metabolism
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  • 54
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    Nature Publishing Group (NPG)
    Publication Date: 2013-10-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Witze, Alexandra -- England -- Nature. 2013 Oct 3;502(7469):14-5. doi: 10.1038/502014a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24091958" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arizona ; Ecosystem ; Fossils ; Geologic Sediments/*analysis ; *Geology
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  • 55
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    Nature Publishing Group (NPG)
    Publication Date: 2013-10-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dufour, Heloise D -- Carroll, Sean B -- England -- Nature. 2013 Oct 3;502(7469):32-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Wisconsin-Madison, 1525 Linden Drive, Madison, Wisconsin 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24137644" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biography as Topic ; *Famous Persons ; France ; History, 20th Century ; Humans ; *Mythology ; Rabies Vaccines/history
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  • 56
    Publication Date: 2013-01-22
    Description: Interferon-induced proteins with tetratricopeptide repeats (IFITs) are innate immune effector molecules that are thought to confer antiviral defence through disruption of protein-protein interactions in the host translation-initiation machinery. However, it was recently discovered that IFITs can directly recognize viral RNA bearing a 5'-triphosphate group (PPP-RNA), which is a molecular signature that distinguishes it from host RNA. Here we report crystal structures of human IFIT5, its complex with PPP-RNAs, and an amino-terminal fragment of IFIT1. The structures reveal a new helical domain that houses a positively charged cavity designed to specifically engage only single-stranded PPP-RNA, thus distinguishing it from the canonical cytosolic sensor of double-stranded viral PPP-RNA, retinoic acid-inducible gene I (RIG-I, also known as DDX58). Mutational analysis, proteolysis and gel-shift assays reveal that PPP-RNA is bound in a non-sequence-specific manner and requires a 5'-overhang of approximately three nucleotides. Abrogation of PPP-RNA binding in IFIT1 and IFIT5 was found to cause a defect in the antiviral response by human embryonic kidney cells. These results demonstrate the mechanism by which IFIT proteins selectively recognize viral RNA, and lend insight into their downstream effector function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abbas, Yazan M -- Pichlmair, Andreas -- Gorna, Maria W -- Superti-Furga, Giulio -- Nagar, Bhushan -- MOP-82929/Canadian Institutes of Health Research/Canada -- England -- Nature. 2013 Feb 7;494(7435):60-4. doi: 10.1038/nature11783. Epub 2013 Jan 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Groupe de Recherche Axe sur la Structure des Proteines, McGill University, Montreal, Quebec H3G 0B1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23334420" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Binding Sites ; Carrier Proteins/*chemistry/*metabolism ; Humans ; Immunity, Innate/immunology ; Models, Molecular ; Neoplasm Proteins/*chemistry/*metabolism ; Phosphorylation ; Protein Conformation ; RNA, Viral/*chemistry/genetics/*metabolism ; Reproducibility of Results ; Substrate Specificity
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  • 57
    Publication Date: 2013-06-19
    Description: Major international projects are underway that are aimed at creating a comprehensive catalogue of all the genes responsible for the initiation and progression of cancer. These studies involve the sequencing of matched tumour-normal samples followed by mathematical analysis to identify those genes in which mutations occur more frequently than expected by random chance. Here we describe a fundamental problem with cancer genome studies: as the sample size increases, the list of putatively significant genes produced by current analytical methods burgeons into the hundreds. The list includes many implausible genes (such as those encoding olfactory receptors and the muscle protein titin), suggesting extensive false-positive findings that overshadow true driver events. We show that this problem stems largely from mutational heterogeneity and provide a novel analytical methodology, MutSigCV, for resolving the problem. We apply MutSigCV to exome sequences from 3,083 tumour-normal pairs and discover extraordinary variation in mutation frequency and spectrum within cancer types, which sheds light on mutational processes and disease aetiology, and in mutation frequency across the genome, which is strongly correlated with DNA replication timing and also with transcriptional activity. By incorporating mutational heterogeneity into the analyses, MutSigCV is able to eliminate most of the apparent artefactual findings and enable the identification of genes truly associated with cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3919509/" 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/PMC3919509/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lawrence, Michael S -- Stojanov, Petar -- Polak, Paz -- Kryukov, Gregory V -- Cibulskis, Kristian -- Sivachenko, Andrey -- Carter, Scott L -- Stewart, Chip -- Mermel, Craig H -- Roberts, Steven A -- Kiezun, Adam -- Hammerman, Peter S -- McKenna, Aaron -- Drier, Yotam -- Zou, Lihua -- Ramos, Alex H -- Pugh, Trevor J -- Stransky, Nicolas -- Helman, Elena -- Kim, Jaegil -- Sougnez, Carrie -- Ambrogio, Lauren -- Nickerson, Elizabeth -- Shefler, Erica -- Cortes, Maria L -- Auclair, Daniel -- Saksena, Gordon -- Voet, Douglas -- Noble, Michael -- DiCara, Daniel -- Lin, Pei -- Lichtenstein, Lee -- Heiman, David I -- Fennell, Timothy -- Imielinski, Marcin -- Hernandez, Bryan -- Hodis, Eran -- Baca, Sylvan -- Dulak, Austin M -- Lohr, Jens -- Landau, Dan-Avi -- Wu, Catherine J -- Melendez-Zajgla, Jorge -- Hidalgo-Miranda, Alfredo -- Koren, Amnon -- McCarroll, Steven A -- Mora, Jaume -- Lee, Ryan S -- Crompton, Brian -- Onofrio, Robert -- Parkin, Melissa -- Winckler, Wendy -- Ardlie, Kristin -- Gabriel, Stacey B -- Roberts, Charles W M -- Biegel, Jaclyn A -- Stegmaier, Kimberly -- Bass, Adam J -- Garraway, Levi A -- Meyerson, Matthew -- Golub, Todd R -- Gordenin, Dmitry A -- Sunyaev, Shamil -- Lander, Eric S -- Getz, Gad -- ES065073/ES/NIEHS NIH HHS/ -- T32 CA009172/CA/NCI NIH HHS/ -- T32 CA009216/CA/NCI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- U24 CA143845/CA/NCI NIH HHS/ -- U54 HG003067/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- England -- Nature. 2013 Jul 11;499(7457):214-8. doi: 10.1038/nature12213. Epub 2013 Jun 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02141, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23770567" target="_blank"〉PubMed〈/a〉
    Keywords: Artifacts ; DNA Replication Timing ; Exome/genetics ; False Positive Reactions ; Gene Expression ; *Genetic Heterogeneity ; Genome, Human/genetics ; Humans ; Lung Neoplasms/genetics ; Mutation/*genetics ; Mutation Rate ; Neoplasms/classification/*genetics/pathology ; Neoplasms, Squamous Cell/genetics ; Oncogenes/*genetics ; Reproducibility of Results ; Sample Size
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  • 58
    Publication Date: 2013-05-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buzsaki, Gyorgy -- England -- Nature. 2013 May 30;497(7451):568-9. doi: 10.1038/497568a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23719456" target="_blank"〉PubMed〈/a〉
    Keywords: Cognition/*physiology ; Hippocampus/*cytology/*physiology ; Humans ; *Memory, Episodic ; Space Perception/*physiology ; *Time ; Time Factors
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  • 59
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    Nature Publishing Group (NPG)
    Publication Date: 2013-06-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moyer, Melinda Wenner -- England -- Nature. 2013 Jun 27;498(7455):S16. doi: 10.1038/498S16a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23803945" target="_blank"〉PubMed〈/a〉
    Keywords: *Blood Banks ; *Cord Blood Stem Cell Transplantation/adverse effects ; Female ; *Graft vs Leukemia Effect/immunology ; Health Education ; Humans ; Infant, Newborn ; Interleukin-7/immunology/therapeutic use ; Leukemia/immunology/pathology/*therapy ; Leukemia, Myeloid, Acute/immunology/pathology/therapy ; Male ; Pregnancy ; Umbilical Cord/*cytology
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  • 60
    Publication Date: 2013-08-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lawrence, Robert S -- Nachman, Keeve E -- Smith, Tyler J -- England -- Nature. 2013 Aug 22;500(7463):400. doi: 10.1038/500400b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23969450" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Domestic/*microbiology ; Humans ; Meat/*microbiology ; Methicillin-Resistant Staphylococcus aureus/*isolation & purification ; Staphylococcal Infections/*transmission/*veterinary ; Zoonoses/*microbiology/*transmission
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  • 61
    Publication Date: 2013-08-24
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3819120/" 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/PMC3819120/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Djulbegovic, Benjamin -- Kumar, Ambuj -- Glasziou, Paul -- Miladinovic, Branko -- Chalmers, Iain -- R01 CA133594/CA/NCI NIH HHS/ -- R01 CA140408/CA/NCI NIH HHS/ -- R01 NS044417/NS/NINDS NIH HHS/ -- R01 NS052956/NS/NINDS NIH HHS/ -- England -- Nature. 2013 Aug 22;500(7463):395-6. doi: 10.1038/500395a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, University of South Florida, Tampa, Florida, USA. bdjulbeg@health.usf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23969443" target="_blank"〉PubMed〈/a〉
    Keywords: Biomedical Research/*statistics & numerical data ; *Comparative Effectiveness Research ; Drug Discovery/*statistics & numerical data ; Humans ; Randomized Controlled Trials as Topic/*statistics & numerical data ; *Therapeutic Equipoise ; Treatment Outcome ; Uncertainty
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  • 62
    Publication Date: 2013-09-21
    Description: Recent studies have revealed extensive genetic diversity both between and within tumours. This heterogeneity affects key cancer pathways, driving phenotypic variation, and poses a significant challenge to personalized cancer medicine. A major cause of genetic heterogeneity in cancer is genomic instability. This instability leads to an increased mutation rate and can shape the evolution of the cancer genome through a plethora of mechanisms. By understanding these mechanisms we can gain insight into the common pathways of tumour evolution that could support the development of future therapeutic strategies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burrell, Rebecca A -- McGranahan, Nicholas -- Bartek, Jiri -- Swanton, Charles -- Cancer Research UK/United Kingdom -- Medical Research Council/United Kingdom -- England -- Nature. 2013 Sep 19;501(7467):338-45. doi: 10.1038/nature12625.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Translational Cancer Therapeutics Laboratory, Cancer Research UK London Research Institute, 44 Lincoln's Inn Fields, London WC2A 3LY, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24048066" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Disease Progression ; *Genetic Heterogeneity ; Genomic Instability/genetics ; Humans ; Neoplasms/*genetics/metabolism/*pathology
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  • 63
    Publication Date: 2013-08-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sokolov, Konstantin -- England -- Nature. 2013 Aug 1;500(7460):36-7. doi: 10.1038/500036b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23903745" target="_blank"〉PubMed〈/a〉
    Keywords: Fibroblasts/*cytology ; Humans ; Metal Nanoparticles/*chemistry ; Nanodiamonds/*chemistry ; *Thermometers ; Thermometry/*instrumentation/*methods
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  • 64
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    Nature Publishing Group (NPG)
    Publication Date: 2013-10-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abbott, Alison -- England -- Nature. 2013 Oct 10;502(7470):153-4. doi: 10.1038/502153a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24108029" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drug Industry/*trends ; Humans ; Nervous System Diseases/drug therapy/genetics/*therapy ; Research/*trends
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  • 65
    Publication Date: 2013-06-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dupont, Sam -- Portner, Hans -- England -- Nature. 2013 Jun 27;498(7455):429. doi: 10.1038/498429a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Gothenburg, Kristineberg, Sweden. sam.dupont@bioenv.gu.se〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23803827" target="_blank"〉PubMed〈/a〉
    Keywords: Acclimatization/*drug effects ; Animals ; Carbon Dioxide/*adverse effects ; Climate Change/statistics & numerical data ; *Ecosystem ; Hydrogen-Ion Concentration/drug effects ; Marine Biology ; Oceans and Seas ; Seawater/*chemistry
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  • 66
    Publication Date: 2013-05-17
    Description: High latitudes contain nearly half of global soil carbon, prompting interest in understanding how the Arctic terrestrial carbon balance will respond to rising temperatures. Low temperatures suppress the activity of soil biota, retarding decomposition and nitrogen release, which limits plant and microbial growth. Warming initially accelerates decomposition, increasing nitrogen availability, productivity and woody-plant dominance. However, these responses may be transitory, because coupled abiotic-biotic feedback loops that alter soil-temperature dynamics and change the structure and activity of soil communities, can develop. Here we report the results of a two-decade summer warming experiment in an Alaskan tundra ecosystem. Warming increased plant biomass and woody dominance, indirectly increased winter soil temperature, homogenized the soil trophic structure across horizons and suppressed surface-soil-decomposer activity, but did not change total soil carbon or nitrogen stocks, thereby increasing net ecosystem carbon storage. Notably, the strongest effects were in the mineral horizon, where warming increased decomposer activity and carbon stock: a 'biotic awakening' at depth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sistla, Seeta A -- Moore, John C -- Simpson, Rodney T -- Gough, Laura -- Shaver, Gaius R -- Schimel, Joshua P -- England -- Nature. 2013 May 30;497(7451):615-8. doi: 10.1038/nature12129. Epub 2013 May 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology, Evolution and Marine Biology, University of California Santa Barbara, Santa Barbara, California 93108, USA. sistla@lifesci.ucsb.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23676669" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arctic Regions ; Biomass ; Carbon/*analysis ; *Carbon Cycle ; *Cold Climate ; Discriminant Analysis ; *Ecosystem ; Food Chain ; Global Warming/*statistics & numerical data ; History, 20th Century ; History, 21st Century ; Nitrogen/metabolism ; Photosynthesis ; Plants/metabolism ; Rain ; Soil/analysis/*chemistry/parasitology ; Soil Microbiology ; *Temperature ; Time Factors ; Uncertainty
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  • 67
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    Nature Publishing Group (NPG)
    Publication Date: 2013-11-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rachman, Stanley -- England -- Nature. 2013 Nov 7;503(7474):7. doi: 10.1038/503007a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24201246" target="_blank"〉PubMed〈/a〉
    Keywords: Clinical Trials as Topic ; Cognitive Therapy ; Conditioning (Psychology) ; Fear/psychology ; Female ; Humans ; Obsessive-Compulsive Disorder/*psychology/*therapy ; Rape/psychology/rehabilitation
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  • 68
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    Nature Publishing Group (NPG)
    Publication Date: 2013-02-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hall, Stephen S -- England -- Nature. 2013 Feb 21;494(7437):296-9. doi: 10.1038/494296a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23426306" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal, Humanized ; Caenorhabditis elegans/*genetics/*physiology ; Caenorhabditis elegans Proteins/genetics/metabolism ; Copulation ; Eating/genetics ; Exploratory Behavior ; Female ; *Genetics, Behavioral ; Humans ; Male ; Neuropeptides/genetics/metabolism ; *Neurosciences ; Receptors, Neuropeptide Y/genetics/metabolism ; Smell/genetics ; Social Behavior ; Taste/genetics ; Trastuzumab
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  • 69
    Publication Date: 2013-05-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mirkin, Sergei M -- England -- Nature. 2013 May 23;497(7450):449-50. doi: 10.1038/nature12244. Epub 2013 May 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Tufts University, Medford, Massachusetts 02155, USA. sergei.mirkin@tufts.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23657255" target="_blank"〉PubMed〈/a〉
    Keywords: DNA Helicases/*metabolism ; *G-Quadruplexes ; *Genomic Instability ; Humans ; Saccharomyces cerevisiae/*genetics/*metabolism
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  • 70
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    Nature Publishing Group (NPG)
    Publication Date: 2013-02-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2013 Feb 7;494(7435):6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23393657" target="_blank"〉PubMed〈/a〉
    Keywords: DNA, Mitochondrial/genetics ; *Exhumation ; Famous Persons ; Forensic Anthropology/*standards ; Great Britain ; Humans ; Male ; *Skeleton
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  • 71
    Publication Date: 2013-02-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mulder, David T -- Coombes, Brian K -- England -- Nature. 2013 Feb 21;494(7437):321-2. doi: 10.1038/494321a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23426321" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; *Phenotype ; Salmonella typhimurium/*pathogenicity
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  • 72
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    Nature Publishing Group (NPG)
    Publication Date: 2013-12-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Callaway, Ewen -- England -- Nature. 2013 Dec 5;504(7478):16-7. doi: 10.1038/504016a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24305130" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA, Mitochondrial/*genetics ; *Fossils ; Hominidae/*classification/*genetics ; Humans ; Phylogeny
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  • 73
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    Publication Date: 2013-08-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Witze, Alexandra -- England -- Nature. 2013 Aug 29;500(7464):509-10. doi: 10.1038/500509a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23985849" target="_blank"〉PubMed〈/a〉
    Keywords: Carcinogens/chemistry/toxicity ; *Green Chemistry Technology ; Humans ; Hydrazines/*chemistry/toxicity ; *Spacecraft ; United States ; United States National Aeronautics and Space Administration
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  • 74
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    Publication Date: 2013-11-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hede, Karyn -- England -- Nature. 2013 Nov 14;503(7475):S14-5. doi: 10.1038/503S14a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24227001" target="_blank"〉PubMed〈/a〉
    Keywords: Emergency Medicine/education ; Emergency Service, Hospital/*standards ; Humans ; Spinal Cord Injuries/diagnosis/surgery/*therapy ; *Time
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  • 75
    Publication Date: 2013-05-07
    Description: MicroRNAs (miRNAs) show differential expression across breast cancer subtypes, and have both oncogenic and tumour-suppressive roles. Here we report the miRNA expression profiles of 1,302 breast tumours with matching detailed clinical annotation, long-term follow-up and genomic and messenger RNA expression data. This provides a comprehensive overview of the quantity, distribution and variation of the miRNA population and provides information on the extent to which genomic, transcriptional and post-transcriptional events contribute to miRNA expression architecture, suggesting an important role for post-transcriptional regulation. The key clinical parameters and cellular pathways related to the miRNA landscape are characterized, revealing context-dependent interactions, for example with regards to cell adhesion and Wnt signalling. Notably, only prognostic miRNA signatures derived from breast tumours devoid of somatic copy-number aberrations (CNA-devoid) are consistently prognostic across several other subtypes and can be validated in external cohorts. We then use a data-driven approach to seek the effects of miRNAs associated with differential co-expression of mRNAs, and find that miRNAs act as modulators of mRNA-mRNA interactions rather than as on-off molecular switches. We demonstrate such an important modulatory role for miRNAs in the biology of CNA-devoid breast cancers, a common subtype in which the immune response is prominent. These findings represent a new framework for studying the biology of miRNAs in human breast cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dvinge, Heidi -- Git, Anna -- Graf, Stefan -- Salmon-Divon, Mali -- Curtis, Christina -- Sottoriva, Andrea -- Zhao, Yongjun -- Hirst, Martin -- Armisen, Javier -- Miska, Eric A -- Chin, Suet-Feung -- Provenzano, Elena -- Turashvili, Gulisa -- Green, Andrew -- Ellis, Ian -- Aparicio, Sam -- Caldas, Carlos -- 11832/Cancer Research UK/United Kingdom -- Cancer Research UK/United Kingdom -- England -- Nature. 2013 May 16;497(7449):378-82. doi: 10.1038/nature12108. Epub 2013 May 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research UK Cambridge Institute and Department of Oncology, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23644459" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Breast Neoplasms/*genetics/pathology ; DNA Copy Number Variations ; Female ; Follow-Up Studies ; Gene Expression Profiling ; *Gene Expression Regulation, Neoplastic ; Genome, Human/genetics ; Humans ; Kaplan-Meier Estimate ; MicroRNAs/*genetics/metabolism ; Prognosis ; Proportional Hazards Models ; RNA, Messenger/genetics/metabolism ; RNA, Neoplasm/genetics/metabolism
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    Publication Date: 2013-12-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leach, Jeff -- England -- Nature. 2013 Dec 5;504(7478):33. doi: 10.1038/504033c.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Food Project, New Orleans, USA, and London School of Hygiene & Tropical Medicine, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24305143" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biodiversity ; Environmental Microbiology ; Gastrointestinal Tract/*microbiology ; Humans ; Tanzania
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  • 77
    Publication Date: 2013-05-17
    Description: Apes and Old World monkeys are prominent components of modern African and Asian ecosystems, yet the earliest phases of their evolutionary history have remained largely undocumented. The absence of crown catarrhine fossils older than approximately 20 million years (Myr) has stood in stark contrast to molecular divergence estimates of approximately 25-30 Myr for the split between Cercopithecoidea (Old World monkeys) and Hominoidea (apes), implying long ghost lineages for both clades. Here we describe the oldest known fossil 'ape', represented by a partial mandible preserving dental features that place it with 'nyanzapithecine' stem hominoids. Additionally, we report the oldest stem member of the Old World monkey clade, represented by a lower third molar. Both specimens were recovered from a precisely dated 25.2-Myr-old stratum in the Rukwa Rift, a segment of the western branch of the East African Rift in Tanzania. These finds extend the fossil record of apes and Old World monkeys well into the Oligocene epoch of Africa, suggesting a possible link between diversification of crown catarrhines and changes in the African landscape brought about by previously unrecognized tectonic activity in the East African rift system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stevens, Nancy J -- Seiffert, Erik R -- O'Connor, Patrick M -- Roberts, Eric M -- Schmitz, Mark D -- Krause, Cornelia -- Gorscak, Eric -- Ngasala, Sifa -- Hieronymus, Tobin L -- Temu, Joseph -- England -- Nature. 2013 May 30;497(7451):611-4. doi: 10.1038/nature12161. Epub 2013 May 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, Ohio 45701, USA. stevensn@ohio.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23676680" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cercopithecidae/anatomy & histology/*classification ; *Fossils ; History, Ancient ; Hominidae/anatomy & histology/*classification ; Mandible/anatomy & histology ; *Phylogeny ; Tanzania ; Tooth/anatomy & histology
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  • 78
    Publication Date: 2013-06-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mummery, Christine L -- Roelen, Bernard A J -- England -- Nature. 2013 Jun 13;498(7453):174-5. doi: 10.1038/498174a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23765489" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/cytology ; Cellular Reprogramming ; *Cloning, Organism ; Embryo, Mammalian/*cytology/embryology ; Embryonic Stem Cells/*cytology/metabolism ; Genes, Mitochondrial/genetics ; Humans ; Induced Pluripotent Stem Cells/cytology/metabolism ; *Nuclear Transfer Techniques ; Research Design ; Sheep
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  • 79
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    Nature Publishing Group (NPG)
    Publication Date: 2013-09-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abbott, Alison -- England -- Nature. 2013 Sep 5;501(7465):18. doi: 10.1038/501018a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24005397" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Aging/physiology ; Biomedical Enhancement/*methods ; Computers ; Female ; Humans ; Middle Aged ; Mild Cognitive Impairment/*prevention & control ; Neuronal Plasticity/physiology ; Neuropsychological Tests ; Psychomotor Performance ; *Task Performance and Analysis ; Time Factors ; *Video Games
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  • 80
    Publication Date: 2013-09-21
    Description: Somatic cells can be inefficiently and stochastically reprogrammed into induced pluripotent stem (iPS) cells by exogenous expression of Oct4 (also called Pou5f1), Sox2, Klf4 and Myc (hereafter referred to as OSKM). The nature of the predominant rate-limiting barrier(s) preventing the majority of cells to successfully and synchronously reprogram remains to be defined. Here we show that depleting Mbd3, a core member of the Mbd3/NuRD (nucleosome remodelling and deacetylation) repressor complex, together with OSKM transduction and reprogramming in naive pluripotency promoting conditions, result in deterministic and synchronized iPS cell reprogramming (near 100% efficiency within seven days from mouse and human cells). Our findings uncover a dichotomous molecular function for the reprogramming factors, serving to reactivate endogenous pluripotency networks while simultaneously directly recruiting the Mbd3/NuRD repressor complex that potently restrains the reactivation of OSKM downstream target genes. Subsequently, the latter interactions, which are largely depleted during early pre-implantation development in vivo, lead to a stochastic and protracted reprogramming trajectory towards pluripotency in vitro. The deterministic reprogramming approach devised here offers a novel platform for the dissection of molecular dynamics leading to establishing pluripotency at unprecedented flexibility and resolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rais, Yoach -- Zviran, Asaf -- Geula, Shay -- Gafni, Ohad -- Chomsky, Elad -- Viukov, Sergey -- Mansour, Abed AlFatah -- Caspi, Inbal -- Krupalnik, Vladislav -- Zerbib, Mirie -- Maza, Itay -- Mor, Nofar -- Baran, Dror -- Weinberger, Leehee -- Jaitin, Diego A -- Lara-Astiaso, David -- Blecher-Gonen, Ronnie -- Shipony, Zohar -- Mukamel, Zohar -- Hagai, Tzachi -- Gilad, Shlomit -- Amann-Zalcenstein, Daniela -- Tanay, Amos -- Amit, Ido -- Novershtern, Noa -- Hanna, Jacob H -- England -- Nature. 2013 Oct 3;502(7469):65-70. doi: 10.1038/nature12587. Epub 2013 Sep 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Department of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24048479" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cells, Cultured ; Cellular Reprogramming/genetics/*physiology ; DNA-Binding Proteins/genetics ; Embryonic Stem Cells ; Female ; Gene Expression Regulation ; HEK293 Cells ; Humans ; Induced Pluripotent Stem Cells/*physiology ; Male ; Mice ; *Models, Biological ; Transcription Factors/genetics
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  • 81
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    Nature Publishing Group (NPG)
    Publication Date: 2013-11-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kosik, Kenneth S -- England -- Nature. 2013 Nov 7;503(7474):31-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24218661" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/diagnosis/drug therapy/*pathology/*physiopathology ; Biomarkers/analysis ; Diagnostic Imaging ; Humans ; Nerve Net/*pathology/*physiopathology ; Neurons/*pathology ; Neuropsychological Tests ; Plaque, Amyloid/drug therapy/pathology ; tau Proteins/metabolism
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  • 82
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    Nature Publishing Group (NPG)
    Publication Date: 2013-05-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morange, Michel -- England -- Nature. 2013 May 23;497(7450):440. doi: 10.1038/497440a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cavailles Centre, CIRPHLES, USR 3308 for the History and Philosophy of Science, Ecole Normale Superieure, Paris, France. morange@biologie.ens.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23698437" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conjugation, Genetic ; France ; History, 20th Century ; Humans ; Mice ; Molecular Biology/*history ; Nobel Prize ; Operon/genetics
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  • 83
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    Nature Publishing Group (NPG)
    Publication Date: 2013-02-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2013 Feb 7;494(7435):5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23393655" target="_blank"〉PubMed〈/a〉
    Keywords: Guidelines as Topic ; Humans ; Japan ; Medical Tourism/*legislation & jurisprudence/statistics & numerical data ; Patient Safety/*legislation & jurisprudence/standards ; Stem Cell Transplantation/*legislation & jurisprudence/standards ; United States ; United States Food and Drug Administration/legislation & jurisprudence
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  • 84
    Publication Date: 2013-01-29
    Description: Insulin resistance is a fundamental pathogenic factor present in various metabolic disorders including obesity and type 2 diabetes. Although skeletal muscle accounts for 70-90% of insulin-stimulated glucose disposal, the mechanism underlying muscle insulin resistance is poorly understood. Here we show in mice that muscle-specific mitsugumin 53 (MG53; also called TRIM72) mediates the degradation of the insulin receptor and insulin receptor substrate 1 (IRS1), and when upregulated, causes metabolic syndrome featuring insulin resistance, obesity, hypertension and dyslipidaemia. MG53 expression is markedly elevated in models of insulin resistance, and MG53 overexpression suffices to trigger muscle insulin resistance and metabolic syndrome sequentially. Conversely, ablation of MG53 prevents diet-induced metabolic syndrome by preserving the insulin receptor, IRS1 and insulin signalling integrity. Mechanistically, MG53 acts as an E3 ligase targeting the insulin receptor and IRS1 for ubiquitin-dependent degradation, comprising a central mechanism controlling insulin signal strength in skeletal muscle. These findings define MG53 as a novel therapeutic target for treating metabolic disorders and associated cardiovascular complications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Song, Ruisheng -- Peng, Wei -- Zhang, Yan -- Lv, Fengxiang -- Wu, Hong-Kun -- Guo, Jiaojiao -- Cao, Yongxing -- Pi, Yanbin -- Zhang, Xin -- Jin, Li -- Zhang, Mao -- Jiang, Peng -- Liu, Fenghua -- Meng, Shaoshuai -- Zhang, Xiuqin -- Jiang, Ping -- Cao, Chun-Mei -- Xiao, Rui-Ping -- England -- Nature. 2013 Feb 21;494(7437):375-9. doi: 10.1038/nature11834. Epub 2013 Jan 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Medicine, State Key Laboratory of Biomembrane and Membrane Biotechnology, Peking University, Beijing 100871, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23354051" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/genetics/*metabolism ; Diabetes Mellitus, Type 2 ; Diet, High-Fat ; Dyslipidemias/metabolism ; Gene Deletion ; Hypertension/metabolism ; *Insulin/metabolism ; Insulin Receptor Substrate Proteins/metabolism ; Insulin Resistance/genetics/*physiology ; Male ; Metabolic Syndrome X/enzymology/genetics/*metabolism/prevention & control ; Mice ; Obesity/chemically induced/metabolism ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Receptor, Insulin/metabolism ; Signal Transduction ; Ubiquitin-Protein Ligases/*metabolism ; Ubiquitination
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  • 85
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    Nature Publishing Group (NPG)
    Publication Date: 2013-02-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2013 Feb 7;494(7435):35.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23393651" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Research/*standards ; Research Personnel/*education ; *Statistics as Topic
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  • 86
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    Nature Publishing Group (NPG)
    Publication Date: 2013-11-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Butler, Declan -- England -- Nature. 2013 Nov 7;503(7474):19. doi: 10.1038/503019a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24201262" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Warfare/legislation & jurisprudence/*prevention & control ; Biomedical Research/*legislation & jurisprudence ; Communicable Disease Control/*legislation & jurisprudence ; Communicable Diseases/transmission/*virology ; *European Union/organization & administration ; Humans ; Influenza A Virus, H5N1 Subtype/genetics/pathogenicity ; Orthomyxoviridae Infections/prevention & control/transmission/virology ; Publishing/legislation & jurisprudence ; Virology/*legislation & jurisprudence ; Zoonoses/prevention & control/transmission/virology
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  • 87
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    Nature Publishing Group (NPG)
    Publication Date: 2013-07-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abbott, Alison -- England -- Nature. 2013 Jul 25;499(7459):390. doi: 10.1038/499390a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23887410" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Separation ; *Cell Size ; Embryo, Mammalian/cytology ; Humans ; Mice ; Reproducibility of Results ; Stem Cell Transplantation ; Stem Cells/*cytology ; *Uncertainty
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  • 88
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    Nature Publishing Group (NPG)
    Publication Date: 2013-10-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Callaway, Ewen -- MR/K006584/1/Medical Research Council/United Kingdom -- England -- Nature. 2013 Oct 17;502(7471):283. doi: 10.1038/502283a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24132268" target="_blank"〉PubMed〈/a〉
    Keywords: *Confidentiality/psychology ; *Data Mining ; Databases, Factual ; *Electronic Health Records/statistics & numerical data ; *Federal Government ; Great Britain ; Humans ; *Medical Record Linkage ; *National Health Programs
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  • 89
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    Nature Publishing Group (NPG)
    Publication Date: 2013-11-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Callaway, Ewen -- England -- Nature. 2013 Nov 7;503(7474):18-9. doi: 10.1038/503018a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24201261" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Archaeology/methods ; Collagen/analysis/genetics ; Elephants/*classification/metabolism ; Evolution, Molecular ; Fossils ; Humans ; Mass Spectrometry ; Phylogeny ; Proteomics/*methods ; Reproducibility of Results ; Sequence Analysis, DNA
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  • 90
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    Nature Publishing Group (NPG)
    Publication Date: 2013-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ledford, Heidi -- England -- Nature. 2013 Dec 12;504(7479):198. doi: 10.1038/504198a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24336264" target="_blank"〉PubMed〈/a〉
    Keywords: Benzhydryl Compounds ; Blood Glucose/analysis ; Clinical Trials as Topic ; Diabetes Mellitus/*drug therapy/epidemiology ; Glucosides/adverse effects/pharmacology/therapeutic use ; Heart Diseases/chemically induced ; Humans ; Hypoglycemic Agents/*adverse effects/pharmacology/therapeutic use ; Sodium-Glucose Transporter 2/*antagonists & inhibitors/metabolism ; Weight Loss/drug effects
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  • 91
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    Nature Publishing Group (NPG)
    Publication Date: 2013-07-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abbott, Alison -- England -- Nature. 2013 Jul 18;499(7458):272-4. doi: 10.1038/499272a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23868244" target="_blank"〉PubMed〈/a〉
    Keywords: Brain/*physiology ; Brain Mapping ; Europe ; Humans ; Research/trends ; United States
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  • 92
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    Nature Publishing Group (NPG)
    Publication Date: 2013-10-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Callaway, Ewen -- England -- Nature. 2013 Oct 10;502(7470):S16-7. doi: 10.1038/502S16a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24108077" target="_blank"〉PubMed〈/a〉
    Keywords: Drug Resistance, Bacterial ; Genome, Bacterial ; Humans ; Latent Tuberculosis/drug therapy/epidemiology ; Mycobacterium tuberculosis/genetics ; Tuberculosis/drug therapy/microbiology/*prevention & control/*transmission
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  • 93
    Publication Date: 2013-06-19
    Description: Rett syndrome (RTT) is an X-linked human neurodevelopmental disorder with features of autism and severe neurological dysfunction in females. RTT is caused by mutations in methyl-CpG-binding protein 2 (MeCP2), a nuclear protein that, in neurons, regulates transcription, is expressed at high levels similar to that of histones, and binds to methylated cytosines broadly across the genome. By phosphotryptic mapping, we identify three sites (S86, S274 and T308) of activity-dependent MeCP2 phosphorylation. Phosphorylation of these sites is differentially induced by neuronal activity, brain-derived neurotrophic factor, or agents that elevate the intracellular level of 3',5'-cyclic AMP (cAMP), indicating that MeCP2 may function as an epigenetic regulator of gene expression that integrates diverse signals from the environment. Here we show that the phosphorylation of T308 blocks the interaction of the repressor domain of MeCP2 with the nuclear receptor co-repressor (NCoR) complex and suppresses the ability of MeCP2 to repress transcription. In knock-in mice bearing the common human RTT missense mutation R306C, neuronal activity fails to induce MeCP2 T308 phosphorylation, suggesting that the loss of T308 phosphorylation might contribute to RTT. Consistent with this possibility, the mutation of MeCP2 T308A in mice leads to a decrease in the induction of a subset of activity-regulated genes and to RTT-like symptoms. These findings indicate that the activity-dependent phosphorylation of MeCP2 at T308 regulates the interaction of MeCP2 with the NCoR complex, and that RTT in humans may be due, in part, to the loss of activity-dependent MeCP2 T308 phosphorylation and a disruption of the phosphorylation-regulated interaction of MeCP2 with the NCoR complex.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3922283/" 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/PMC3922283/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ebert, Daniel H -- Gabel, Harrison W -- Robinson, Nathaniel D -- Kastan, Nathaniel R -- Hu, Linda S -- Cohen, Sonia -- Navarro, Adrija J -- Lyst, Matthew J -- Ekiert, Robert -- Bird, Adrian P -- Greenberg, Michael E -- 092076/Wellcome Trust/United Kingdom -- K08 MH090306/MH/NIMH NIH HHS/ -- K08MH90306/MH/NIMH NIH HHS/ -- P30 HD018655/HD/NICHD NIH HHS/ -- P30-HD 18655/HD/NICHD NIH HHS/ -- R01 NS048276/NS/NINDS NIH HHS/ -- R01NS048276/NS/NINDS NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- England -- Nature. 2013 Jul 18;499(7458):341-5. doi: 10.1038/nature12348.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, and Department of Psychiatry, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23770587" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Co-Repressor Proteins/*metabolism ; Humans ; Methyl-CpG-Binding Protein 2/chemistry/genetics/*metabolism ; Mice ; Mutation ; Neurons/metabolism ; Phosphorylation ; Rett Syndrome/genetics ; Threonine/*metabolism ; Transcription, Genetic
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  • 94
    Publication Date: 2013-10-18
    Description: Conodonts are an extinct group of jawless vertebrates whose tooth-like elements are the earliest instance of a mineralized skeleton in the vertebrate lineage, inspiring the 'inside-out' hypothesis that teeth evolved independently of the vertebrate dermal skeleton and before the origin of jaws. However, these propositions have been based on evidence from derived euconodonts. Here we test hypotheses of a paraconodont ancestry of euconodonts using synchrotron radiation X-ray tomographic microscopy to characterize and compare the microstructure of morphologically similar euconodont and paraconodont elements. Paraconodonts exhibit a range of grades of structural differentiation, including tissues and a pattern of growth common to euconodont basal bodies. The different grades of structural differentiation exhibited by paraconodonts demonstrate the stepwise acquisition of euconodont characters, resolving debate over the relationship between these two groups. By implication, the putative homology of euconodont crown tissue and vertebrate enamel must be rejected as these tissues have evolved independently and convergently. Thus, the precise ontogenetic, structural and topological similarities between conodont elements and vertebrate odontodes appear to be a remarkable instance of convergence. The last common ancestor of conodonts and jawed vertebrates probably lacked mineralized skeletal tissues. The hypothesis that teeth evolved before jaws and the inside-out hypothesis of dental evolution must be rejected; teeth seem to have evolved through the extension of odontogenic competence from the external dermis to internal epithelium soon after the origin of jaws.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murdock, Duncan J E -- Dong, Xi-Ping -- Repetski, John E -- Marone, Federica -- Stampanoni, Marco -- Donoghue, Philip C J -- England -- Nature. 2013 Oct 24;502(7472):546-9. doi: 10.1038/nature12645. Epub 2013 Oct 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Earth Sciences, University of Bristol, Wills Memorial Building, Queen's Road, Bristol BS8 1RJ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24132236" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; *Fossils ; Jaw ; Nevada ; Phylogeny ; Skeleton ; Synchrotrons ; Tomography, X-Ray ; Tooth/*anatomy & histology ; Vertebrates/*anatomy & histology/*classification ; Wyoming
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  • 95
    Publication Date: 2013-04-13
    Description: Fossil dinosaur embryos are surprisingly rare, being almost entirely restricted to Upper Cretaceous strata that record the late stages of non-avian dinosaur evolution. Notable exceptions are the oldest known embryos from the Early Jurassic South African sauropodomorph Massospondylus and Late Jurassic embryos of a theropod from Portugal. The fact that dinosaur embryos are rare and typically enclosed in eggshells limits their availability for tissue and cellular level investigations of development. Consequently, little is known about growth patterns in dinosaur embryos, even though post-hatching ontogeny has been studied in several taxa. Here we report the discovery of an embryonic dinosaur bone bed from the Lower Jurassic of China, the oldest such occurrence in the fossil record. The embryos are similar in geological age to those of Massospondylus and are also assignable to a sauropodomorph dinosaur, probably Lufengosaurus. The preservation of numerous disarticulated skeletal elements and eggshells in this monotaxic bone bed, representing different stages of incubation and therefore derived from different nests, provides opportunities for new investigations of dinosaur embryology in a clade noted for gigantism. For example, comparisons among embryonic femora of different sizes and developmental stages reveal a consistently rapid rate of growth throughout development, possibly indicating that short incubation times were characteristic of sauropodomorphs. In addition, asymmetric radial growth of the femoral shaft and rapid expansion of the fourth trochanter suggest that embryonic muscle activation played an important role in the pre-hatching ontogeny of these dinosaurs. This discovery also provides the oldest evidence of in situ preservation of complex organic remains in a terrestrial vertebrate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reisz, Robert R -- Huang, Timothy D -- Roberts, Eric M -- Peng, ShinRung -- Sullivan, Corwin -- Stein, Koen -- LeBlanc, Aaron R H -- Shieh, DarBin -- Chang, RongSeng -- Chiang, ChengCheng -- Yang, Chuanwei -- Zhong, Shiming -- England -- Nature. 2013 Apr 11;496(7444):210-4. doi: 10.1038/nature11978.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Toronto Mississauga, Mississauga, Ontario L5L 1C6, Canada. robert.reisz@utoronto.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23579680" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; China ; Dinosaurs/*anatomy & histology/*embryology ; Femur/anatomy & histology/embryology ; *Fossils ; Spectroscopy, Fourier Transform Infrared ; Synchrotrons
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 96
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    Unknown
    Nature Publishing Group (NPG)
    Publication Date: 2013-09-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Butler, Declan -- England -- Nature. 2013 Sep 19;501(7467):294-5. doi: 10.1038/501294a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24048048" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Camels/virology ; Coronavirus/*isolation & purification ; Coronavirus Infections/epidemiology/*transmission/*virology ; Humans ; Middle East/epidemiology ; Severe Acute Respiratory Syndrome/epidemiology/virology ; Zoonoses/transmission/virology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 97
    Publication Date: 2013-06-04
    Description: Rev-Erb-alpha and Rev-Erb-beta are nuclear receptors that regulate the expression of genes involved in the control of circadian rhythm, metabolism and inflammatory responses. Rev-Erbs function as transcriptional repressors by recruiting nuclear receptor co-repressor (NCoR)-HDAC3 complexes to Rev-Erb response elements in enhancers and promoters of target genes, but the molecular basis for cell-specific programs of repression is not known. Here we present evidence that in mouse macrophages Rev-Erbs regulate target gene expression by inhibiting the functions of distal enhancers that are selected by macrophage-lineage-determining factors, thereby establishing a macrophage-specific program of repression. Remarkably, the repressive functions of Rev-Erbs are associated with their ability to inhibit the transcription of enhancer-derived RNAs (eRNAs). Furthermore, targeted degradation of eRNAs at two enhancers subject to negative regulation by Rev-Erbs resulted in reduced expression of nearby messenger RNAs, suggesting a direct role of these eRNAs in enhancer function. By precisely defining eRNA start sites using a modified form of global run-on sequencing that quantifies nascent 5' ends, we show that transfer of full enhancer activity to a target promoter requires both the sequences mediating transcription-factor binding and the specific sequences encoding the eRNA transcript. These studies provide evidence for a direct role of eRNAs in contributing to enhancer functions and suggest that Rev-Erbs act to suppress gene expression at a distance by repressing eRNA transcription.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3839578/" 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/PMC3839578/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lam, Michael T Y -- Cho, Han -- Lesch, Hanna P -- Gosselin, David -- Heinz, Sven -- Tanaka-Oishi, Yumiko -- Benner, Christopher -- Kaikkonen, Minna U -- Kim, Aneeza S -- Kosaka, Mika -- Lee, Cindy Y -- Watt, Andy -- Grossman, Tamar R -- Rosenfeld, Michael G -- Evans, Ronald M -- Glass, Christopher K -- CA014195/CA/NCI NIH HHS/ -- CA17390/CA/NCI NIH HHS/ -- CA52599/CA/NCI NIH HHS/ -- DK057978/DK/NIDDK NIH HHS/ -- DK063491/DK/NIDDK NIH HHS/ -- DK091183/DK/NIDDK NIH HHS/ -- HL088093/HL/NHLBI NIH HHS/ -- HL105278/HL/NHLBI NIH HHS/ -- P01 DK074868/DK/NIDDK NIH HHS/ -- P01 HL088093/HL/NHLBI NIH HHS/ -- P30 CA014195/CA/NCI NIH HHS/ -- P30 DK063491/DK/NIDDK NIH HHS/ -- R01 CA052599/CA/NCI NIH HHS/ -- R01 CA173903/CA/NCI NIH HHS/ -- R01 DK018477/DK/NIDDK NIH HHS/ -- R01 DK091183/DK/NIDDK NIH HHS/ -- R01 HL105278/HL/NHLBI NIH HHS/ -- R37 DK057978/DK/NIDDK NIH HHS/ -- T32 GM007198-37/GM/NIGMS NIH HHS/ -- T32 GM008666/GM/NIGMS NIH HHS/ -- U19 DK062434/DK/NIDDK NIH HHS/ -- U19DK62434/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Jun 27;498(7455):511-5. doi: 10.1038/nature12209. Epub 2013 Jun 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23728303" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Base Sequence ; Binding Sites ; Down-Regulation/*genetics ; Enhancer Elements, Genetic/*genetics ; Gene Knockdown Techniques ; Macrophages/*metabolism ; Mice ; Nuclear Receptor Subfamily 1, Group D, Member 1/deficiency/genetics/*metabolism ; Organ Specificity ; Promoter Regions, Genetic/genetics ; RNA, Messenger/genetics/metabolism ; Response Elements/genetics ; Transcription, Genetic/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 98
    Publication Date: 2013-05-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abbott, Alison -- England -- Nature. 2013 May 2;497(7447):16. doi: 10.1038/497016a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23636371" target="_blank"〉PubMed〈/a〉
    Keywords: *Cues ; Humans ; *Intelligence Tests ; Psychology/standards ; Reproducibility of Results ; Scientific Misconduct ; Sociology/standards ; *Unconscious (Psychology)
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 99
    facet.materialart.
    Unknown
    Nature Publishing Group (NPG)
    Publication Date: 2013-08-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hayden, Erika Check -- England -- Nature. 2013 Aug 29;500(7464):514. doi: 10.1038/500514a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23985853" target="_blank"〉PubMed〈/a〉
    Keywords: Africa/ethnology ; Archaeology ; Genetics, Population/*methods ; Genome, Human/*genetics ; History, Ancient ; Human Migration/*history ; Humans ; Linguistics ; Oligonucleotide Array Sequence Analysis
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 100
    Publication Date: 2013-07-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Donnelly, Christl -- MR/K010174/1/Medical Research Council/United Kingdom -- England -- Nature. 2013 Jul 11;499(7457):154. doi: 10.1038/499154d.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23846648" target="_blank"〉PubMed〈/a〉
    Keywords: *Animal Rights ; Animals ; *Dissent and Disputes ; *Mustelidae ; *Policy Making ; Tuberculosis, Bovine/*epidemiology/*prevention & control
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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