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  • Mice  (1,423)
  • Female  (1,332)
  • Models, Molecular  (403)
  • American Association for the Advancement of Science (AAAS)  (2,918)
  • 2010-2014  (1,703)
  • 1990-1994  (1,215)
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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-03-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gregersen, Peter K -- New York, N.Y. -- Science. 2014 Mar 7;343(6175):1087-8. doi: 10.1126/science.1251426.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Robert S. Boas Center for Genomics and Human Genetics, The Feinstein Institute for Medical Research, North Shore LIJ Health System, 350 Community Drive, Manhasset, NY 110430, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24604188" target="_blank"〉PubMed〈/a〉
    Keywords: Crohn Disease/*genetics ; Dendritic Cells/*immunology ; Female ; Gene Expression Regulation/*immunology ; *Gene-Environment Interaction ; *Genetic Predisposition to Disease ; Host-Pathogen Interactions/*genetics ; Humans ; Immunity, Innate/*genetics ; Interferon Regulatory Factor-7/*genetics ; Male ; Monocytes/*immunology ; STAT Transcription Factors/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2014-08-26
    Description: Aging-associated cognitive decline is affected by factors produced inside and outside the brain. By using multiorgan genome-wide analysis of aged mice, we found that the choroid plexus, an interface between the brain and the circulation, shows a type I interferon (IFN-I)-dependent gene expression profile that was also found in aged human brains. In aged mice, this response was induced by brain-derived signals, present in the cerebrospinal fluid. Blocking IFN-I signaling within the aged brain partially restored cognitive function and hippocampal neurogenesis and reestablished IFN-II-dependent choroid plexus activity, which is lost in aging. Our data identify a chronic aging-induced IFN-I signature, often associated with antiviral response, at the brain's choroid plexus and demonstrate its negative influence on brain function, thereby suggesting a target for ameliorating cognitive decline in aging.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baruch, Kuti -- Deczkowska, Aleksandra -- David, Eyal -- Castellano, Joseph M -- Miller, Omer -- Kertser, Alexander -- Berkutzki, Tamara -- Barnett-Itzhaki, Zohar -- Bezalel, Dana -- Wyss-Coray, Tony -- Amit, Ido -- Schwartz, Michal -- AG045034/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2014 Oct 3;346(6205):89-93. doi: 10.1126/science.1252945. Epub 2014 Aug 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Weizmann Institute of Science, Rehovot 76100, Israel. ; Department of Immunology, Weizmann Institute of Science, Rehovot 76100, Israel. ; Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA. ; Department of Immunology, Weizmann Institute of Science, Rehovot 76100, Israel. michal.schwartz@weizmann.ac.il ido.amit@weizmann.ac.il. ; Department of Neurobiology, Weizmann Institute of Science, Rehovot 76100, Israel. michal.schwartz@weizmann.ac.il ido.amit@weizmann.ac.il.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25147279" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/genetics/*pathology ; Animals ; Brain/*physiology ; Choroid Plexus/*metabolism ; *Cognition ; *Gene Expression Regulation ; Hippocampus/cytology ; Interferon Regulatory Factors/*genetics ; Interferon Type I/*physiology ; Mice ; Mice, Transgenic ; Neurogenesis ; Receptors, Interferon/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2014-05-17
    Description: A switchlike response in nuclear factor-kappaB (NF-kappaB) activity implies the existence of a threshold in the NF-kappaB signaling module. We show that the CARD-containing MAGUK protein 1 (CARMA1, also called CARD11)-TAK1 (MAP3K7)-inhibitor of NF-kappaB (IkappaB) kinase-beta (IKKbeta) module is a switch mechanism for NF-kappaB activation in B cell receptor (BCR) signaling. Experimental and mathematical modeling analyses showed that IKK activity is regulated by positive feedback from IKKbeta to TAK1, generating a steep dose response to BCR stimulation. Mutation of the scaffolding protein CARMA1 at serine-578, an IKKbeta target, abrogated not only late TAK1 activity, but also the switchlike activation of NF-kappaB in single cells, suggesting that phosphorylation of this residue accounts for the feedback.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shinohara, Hisaaki -- Behar, Marcelo -- Inoue, Kentaro -- Hiroshima, Michio -- Yasuda, Tomoharu -- Nagashima, Takeshi -- Kimura, Shuhei -- Sanjo, Hideki -- Maeda, Shiori -- Yumoto, Noriko -- Ki, Sewon -- Akira, Shizuo -- Sako, Yasushi -- Hoffmann, Alexander -- Kurosaki, Tomohiro -- Okada-Hatakeyama, Mariko -- 5R01CA141722/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2014 May 16;344(6185):760-4. doi: 10.1126/science.1250020.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Integrated Cellular Systems, RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan. ; Signaling Systems Laboratory, Department of Chemistry and Biochemistry, University of California, San Diego, La Jolla, CA 92093, USA. Institute for Quantitative and Computational Biosciences (QC Bio) and Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90025, USA. ; Laboratory for Cell Signaling Dynamics, RIKEN Quantitative Biology Center (QBiC), 6-2-3, Furuedai, Suita, Osaka 565-0874, Japan. Cellular Informatics Laboratory, RIKEN, 2-1 Hirosawa, Wako 351-0198, Japan. ; Laboratory for Lymphocyte Differentiation, RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan. ; Graduate School of Engineering, Tottori University 4-101, Koyama-minami, Tottori 680-8552, Japan. ; Laboratory of Host Defense, WPI Immunology Frontier Research Center, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan. ; Cellular Informatics Laboratory, RIKEN, 2-1 Hirosawa, Wako 351-0198, Japan. ; Signaling Systems Laboratory, Department of Chemistry and Biochemistry, University of California, San Diego, La Jolla, CA 92093, USA. Institute for Quantitative and Computational Biosciences (QC Bio) and Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90025, USA. ahoffmann@ucla.edu kurosaki@rcai.riken.jp marikoh@rcai.riken.jp. ; Laboratory for Lymphocyte Differentiation, RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan. Laboratory for Lymphocyte Differentiation, WPI Immunology Frontier Research Center, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan. ahoffmann@ucla.edu kurosaki@rcai.riken.jp marikoh@rcai.riken.jp. ; Laboratory for Integrated Cellular Systems, RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan. ahoffmann@ucla.edu kurosaki@rcai.riken.jp marikoh@rcai.riken.jp.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24833394" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/metabolism ; CARD Signaling Adaptor Proteins/genetics/*metabolism ; Cell Line ; Chickens ; Feedback, Physiological ; Guanylate Cyclase/genetics/*metabolism ; I-kappa B Kinase/*metabolism ; MAP Kinase Kinase Kinases/genetics/*metabolism ; Mice ; Mice, Knockout ; Mutation ; NF-kappa B/*agonists ; Phosphorylation ; Receptors, Antigen, B-Cell/genetics/*metabolism ; Serine/genetics/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-10-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, Ann -- New York, N.Y. -- Science. 2014 Oct 24;346(6208):405-6. doi: 10.1126/science.346.6208.405.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25342776" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Domestic/*psychology ; *Biological Evolution ; *Cooperative Behavior ; Female ; Hominidae/anatomy & histology/psychology ; Humans ; Male ; Skull/*anatomy & histology ; Testosterone/metabolism ; Tooth/anatomy & histology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2014-06-14
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4340075/" 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/PMC4340075/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Churcher, Thomas S -- Cohen, Justin M -- Novotny, Joseph -- Ntshalintshali, Nyasatu -- Kunene, Simon -- Cauchemez, Simon -- MR/K010174/1/Medical Research Council/United Kingdom -- U54 GM088491/GM/NIGMS NIH HHS/ -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2014 Jun 13;344(6189):1230-2. doi: 10.1126/science.1251449.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Infectious Disease Epidemiology, Imperial College London, London, UK. ; Clinton Health Access Initiative, Boston, MA 02127, USA. ; Clinton Health Access Initiative, Boston, MA 02127, USA. Global Health Group, University of California, San Francisco, CA 94143, USA. ; National Malaria Control Program, Manzini, Swaziland. ; Department of Infectious Disease Epidemiology, Imperial College London, London, UK. Mathematical Modelling of Infectious Diseases Unit, Institut Pasteur, Paris, France. simon.cauchemez@pasteur.fr.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24926005" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Culicidae/parasitology ; Disease Eradication/*methods/*trends ; Endemic Diseases/*prevention & control ; Female ; *Global Health ; Humans ; Insect Vectors/parasitology ; Malaria/epidemiology/*prevention & control/transmission ; Mosquito Control/methods ; Seasons
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2014-09-23
    Description: The neuromuscular junction (NMJ) is the synapse between a motor neuron and skeletal muscle. Defects in NMJ transmission cause muscle weakness, termed myasthenia. The muscle protein Dok-7 is essential for activation of the receptor kinase MuSK, which governs NMJ formation, and DOK7 mutations underlie familial limb-girdle myasthenia (DOK7 myasthenia), a neuromuscular disease characterized by small NMJs. Here, we show in a mouse model of DOK7 myasthenia that therapeutic administration of an adeno-associated virus (AAV) vector encoding the human DOK7 gene resulted in an enlargement of NMJs and substantial increases in muscle strength and life span. When applied to model mice of another neuromuscular disorder, autosomal dominant Emery-Dreifuss muscular dystrophy, DOK7 gene therapy likewise resulted in enlargement of NMJs as well as positive effects on motor activity and life span. These results suggest that therapies aimed at enlarging the NMJ may be useful for a range of neuromuscular disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arimura, Sumimasa -- Okada, Takashi -- Tezuka, Tohru -- Chiyo, Tomoko -- Kasahara, Yuko -- Yoshimura, Toshiro -- Motomura, Masakatsu -- Yoshida, Nobuaki -- Beeson, David -- Takeda, Shin'ichi -- Yamanashi, Yuji -- G0701521/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2014 Sep 19;345(6203):1505-8. doi: 10.1126/science.1250744.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Genetics, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan. ; Department of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan. ; Department of Occupational Therapy, Nagasaki University School of Health Sciences, Nagasaki, Japan. ; Department of Electrical and Electronics Engineering, Faculty of Engineering, Nagasaki Institute of Applied Science, Nagasaki, Japan. ; Laboratory of Developmental Genetics, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan. ; Neurosciences Group, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK. ; Division of Genetics, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan. yyamanas@ims.u-tokyo.ac.jp.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25237101" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dependovirus ; Disease Models, Animal ; Female ; Genetic Therapy/*methods ; Genetic Vectors/administration & dosage ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle Proteins/*genetics ; Muscle, Skeletal/*innervation/physiopathology ; Muscular Dystrophies, Limb-Girdle/genetics/*pathology/*therapy ; Neuromuscular Junction/*pathology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2014-03-29
    Description: The field of optogenetics uses channelrhodopsins (ChRs) for light-induced neuronal activation. However, optimized tools for cellular inhibition at moderate light levels are lacking. We found that replacement of E90 in the central gate of ChR with positively charged residues produces chloride-conducting ChRs (ChloCs) with only negligible cation conductance. Molecular dynamics modeling unveiled that a high-affinity Cl(-)-binding site had been generated near the gate. Stabilizing the open state dramatically increased the operational light sensitivity of expressing cells (slow ChloC). In CA1 pyramidal cells, ChloCs completely inhibited action potentials triggered by depolarizing current injections or synaptic stimulation. Thus, by inverting the charge of the selectivity filter, we have created a class of directly light-gated anion channels that can be used to block neuronal output in a fully reversible fashion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wietek, Jonas -- Wiegert, J Simon -- Adeishvili, Nona -- Schneider, Franziska -- Watanabe, Hiroshi -- Tsunoda, Satoshi P -- Vogt, Arend -- Elstner, Marcus -- Oertner, Thomas G -- Hegemann, Peter -- New York, N.Y. -- Science. 2014 Apr 25;344(6182):409-12. doi: 10.1126/science.1249375. Epub 2014 Mar 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Biology, Experimental Biophysics, Humboldt Universitat zu Berlin, D-10115 Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24674867" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Binding Sites ; CA1 Region, Hippocampal/cytology ; Chloride Channels/*chemistry/*metabolism ; Chlorides/*metabolism ; HEK293 Cells ; Humans ; Hydrogen Bonding ; Ion Channel Gating ; Light ; Models, Molecular ; Molecular Dynamics Simulation ; Mutation ; Patch-Clamp Techniques ; Protein Conformation ; Protein Engineering ; Pyramidal Cells/metabolism ; Rats ; Recombinant Fusion Proteins/chemistry ; Rhodopsin/*chemistry/genetics/*metabolism ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-03-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2014 Mar 28;343(6178):1460-1. doi: 10.1126/science.343.6178.1460.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24675951" target="_blank"〉PubMed〈/a〉
    Keywords: Biomedical Research/*economics ; *Breast Neoplasms ; Female ; Humans ; *Patient Advocacy ; United States
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2014-10-04
    Description: After an infection, pathogen-specific tissue-resident memory T cells (T(RM) cells) persist in nonlymphoid tissues to provide rapid control upon reinfection, and vaccination strategies that create T(RM) cell pools at sites of pathogen entry are therefore attractive. However, it is not well understood how T(RM) cells provide such pathogen protection. Here, we demonstrate that activated T(RM) cells in mouse skin profoundly alter the local tissue environment by inducing a number of broadly active antiviral and antibacterial genes. This "pathogen alert" allows skin T(RM) cells to protect against an antigenically unrelated virus. These data describe a mechanism by which tissue-resident memory CD8(+) T cells protect previously infected sites that is rapid, amplifies the activation of a small number of cells into an organ-wide response, and has the capacity to control escape variants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ariotti, Silvia -- Hogenbirk, Marc A -- Dijkgraaf, Feline E -- Visser, Lindy L -- Hoekstra, Mirjam E -- Song, Ji-Ying -- Jacobs, Heinz -- Haanen, John B -- Schumacher, Ton N -- New York, N.Y. -- Science. 2014 Oct 3;346(6205):101-5. doi: 10.1126/science.1254803. Epub 2014 Aug 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunology, Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands. ; Division of Biological Stress Response, Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands. ; Experimental Animal Pathology, Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands. ; Division of Immunology, Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands. t.schumacher@nki.nl.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25278612" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD8-Positive T-Lymphocytes/*immunology ; Female ; Immunologic Memory/genetics/*immunology ; Male ; Mice ; Skin/*immunology/microbiology/virology ; Transcriptome
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  • 10
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-04-05
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4143233/" 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/PMC4143233/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mann, Richard S -- R01 NS070644/NS/NINDS NIH HHS/ -- R01NS070644/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2014 Apr 4;344(6179):48-9. doi: 10.1126/science.1252431.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biophysics, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24700848" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drosophila/*physiology ; Female ; Male ; Neurons/*physiology
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  • 11
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-06-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, Ann -- New York, N.Y. -- Science. 2014 Jun 13;344(6189):1213-4. doi: 10.1126/science.344.6189.1213.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24925995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Horses/*genetics/*physiology ; *Inbreeding ; Male ; *Physical Conditioning, Animal ; *Running ; Selection, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-02-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2014 Jan 31;343(6170):477. doi: 10.1126/science.343.6170.477.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24482460" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcysteine/administration & dosage/*adverse effects ; Animals ; Antioxidants/administration & dosage/*adverse effects ; Carcinogens/toxicity ; DNA Damage ; Dietary Supplements/adverse effects ; Genes, Neoplasm/*drug effects ; Humans ; Lung Neoplasms/*chemically induced/prevention & control ; Mice ; Smoking/adverse effects ; Tumor Suppressor Protein p53/genetics/metabolism ; Vitamin E/administration & dosage/*adverse effects ; Vitamins/administration & dosage/*adverse effects
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  • 13
    Publication Date: 2014-03-15
    Description: Vertebrate limbs first emerge as small buds at specific locations along the trunk. Although a fair amount is known about the molecular regulation of limb initiation and outgrowth, the cellular events underlying these processes have remained less clear. We show that the mesenchymal limb progenitors arise through localized epithelial-to-mesenchymal transition (EMT) of the coelomic epithelium specifically within the presumptive limb fields. This EMT is regulated at least in part by Tbx5 and Fgf10, two genes known to control limb initiation. This work shows that limb buds initiate earlier than previously thought, as a result of localized EMT rather than differential proliferation rates.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4097009/" 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/PMC4097009/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gros, Jerome -- Tabin, Clifford J -- R01 HD045499/HD/NICHD NIH HHS/ -- R01-HD045499/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2014 Mar 14;343(6176):1253-6. doi: 10.1126/science.1248228.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24626928" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cadherins/metabolism ; Chick Embryo ; *Epithelial-Mesenchymal Transition ; Extremities/*embryology ; Fibroblast Growth Factor 10/genetics/metabolism ; Limb Buds/*cytology/metabolism ; Mice ; Mice, Mutant Strains ; Protein Kinase C/metabolism ; T-Box Domain Proteins/genetics/metabolism ; Vimentin/metabolism ; beta Catenin/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
    Publication Date: 2014-05-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin-Frankel, Jennifer -- New York, N.Y. -- Science. 2014 May 16;344(6185):679. doi: 10.1126/science.344.6185.679.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24833367" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Experimentation/*standards ; Animals ; Biomedical Research/*standards ; Cells ; Female ; Male ; Mice ; National Institutes of Health (U.S.) ; Sex Factors ; United States ; X Chromosome ; Y Chromosome
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  • 15
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-02-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, Ann -- New York, N.Y. -- Science. 2014 Jan 31;343(6170):471-2. doi: 10.1126/science.343.6170.471.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24482455" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Crohn Disease/genetics ; DNA/genetics ; Diabetes Mellitus, Type 2/genetics ; Disease/*genetics ; *Evolution, Molecular ; Female ; Genome, Human/*genetics ; Humans ; Interleukin-18/genetics ; Keratins/genetics ; Liver Cirrhosis, Biliary/genetics ; Male ; Neanderthals/*genetics ; Optic Disk/anatomy & histology ; Sequence Analysis, DNA ; Smoking/genetics
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-10-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clery, Daniel -- New York, N.Y. -- Science. 2014 Oct 17;346(6207):290-1. doi: 10.1126/science.346.6207.290.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25324365" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chemistry ; Mice ; Microscopy, Fluorescence/*methods ; *Nobel Prize ; Organelles/ultrastructure ; United States
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  • 17
    Publication Date: 2014-04-15
    Description: Myelination of the central nervous system requires the generation of functionally mature oligodendrocytes from oligodendrocyte precursor cells (OPCs). Electrically active neurons may influence OPC function and selectively instruct myelination of an active neural circuit. In this work, we use optogenetic stimulation of the premotor cortex in awake, behaving mice to demonstrate that neuronal activity elicits a mitogenic response of neural progenitor cells and OPCs, promotes oligodendrogenesis, and increases myelination within the deep layers of the premotor cortex and subcortical white matter. We further show that this neuronal activity-regulated oligodendrogenesis and myelination is associated with improved motor function of the corresponding limb. Oligodendrogenesis and myelination appear necessary for the observed functional improvement, as epigenetic blockade of oligodendrocyte differentiation and myelin changes prevents the activity-regulated behavioral improvement.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4096908/" 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/PMC4096908/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibson, Erin M -- Purger, David -- Mount, Christopher W -- Goldstein, Andrea K -- Lin, Grant L -- Wood, Lauren S -- Inema, Ingrid -- Miller, Sarah E -- Bieri, Gregor -- Zuchero, J Bradley -- Barres, Ben A -- Woo, Pamelyn J -- Vogel, Hannes -- Monje, Michelle -- 1S10RR02678001/RR/NCRR NIH HHS/ -- K08 NS070926/NS/NINDS NIH HHS/ -- K08NS070926/NS/NINDS NIH HHS/ -- R01 EY10257/EY/NEI NIH HHS/ -- T32 MH020016/MH/NIMH NIH HHS/ -- UL1 RR025744/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 May 2;344(6183):1252304. doi: 10.1126/science.1252304. Epub 2014 Apr 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Neurology, Neurosurgery, and Pediatrics, Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24727982" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Thy-1/genetics ; Behavior, Animal/physiology ; *Cell Differentiation ; Cell Lineage ; Cell Proliferation ; Corpus Callosum/cytology/physiology ; Mice ; Mice, Mutant Strains ; Motor Activity/physiology ; Motor Cortex/cytology/*physiology ; Myelin Sheath/*metabolism ; Nerve Fibers, Myelinated/*metabolism ; Neural Stem Cells/*physiology ; Neurons/*physiology ; Oligodendroglia/*cytology ; Rhodopsin/genetics
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  • 18
    Publication Date: 2014-01-25
    Description: Episodic memory requires associations of temporally discontiguous events. In the entorhinal-hippocampal network, temporal associations are driven by a direct pathway from layer III of the medial entorhinal cortex (MECIII) to the hippocampal CA1 region. However, the identification of neural circuits that regulate this association has remained unknown. In layer II of entorhinal cortex (ECII), we report clusters of excitatory neurons called island cells, which appear in a curvilinear matrix of bulblike structures, directly project to CA1, and activate interneurons that target the distal dendrites of CA1 pyramidal neurons. Island cells suppress the excitatory MECIII input through the feed-forward inhibition to control the strength and duration of temporal association in trace fear memory. Together, the two EC inputs compose a control circuit for temporal association memory.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kitamura, Takashi -- Pignatelli, Michele -- Suh, Junghyup -- Kohara, Keigo -- Yoshiki, Atsushi -- Abe, Kuniya -- Tonegawa, Susumu -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Feb 21;343(6173):896-901. doi: 10.1126/science.1244634. Epub 2014 Jan 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉RIKEN-MIT Center for Neural Circuit Genetics at the Picower Institute for Learning and Memory, Department of Biology and Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24457215" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Association ; CA1 Region, Hippocampal/cytology/*physiology ; Entorhinal Cortex/cytology/*physiology ; GABAergic Neurons/physiology ; Interneurons/physiology ; Membrane Proteins/genetics ; *Memory, Episodic ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Nerve Net ; Neurons/*physiology
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  • 19
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-03-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Silvente-Poirot, Sandrine -- Poirot, Marc -- New York, N.Y. -- Science. 2014 Mar 28;343(6178):1445-6. doi: 10.1126/science.1252787.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉UMR 1037 INSERM-University Toulouse III, Cancer Research Center of Toulouse, and Institut Claudius Regaud, 31052 Toulouse, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24675946" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/*metabolism/*pathology ; Cholesterol/*metabolism ; Cholesterol, Dietary/administration & dosage/metabolism ; Disease Models, Animal ; Female ; Humans ; Hypercholesterolemia/metabolism ; Metabolic Networks and Pathways ; Mice
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  • 20
    Publication Date: 2014-11-15
    Description: Activators of innate immunity may have the potential to combat a broad range of infectious agents. We report that treatment with bacterial flagellin prevented rotavirus (RV) infection in mice and cured chronically RV-infected mice. Protection was independent of adaptive immunity and interferon (IFN, type I and II) and required flagellin receptors Toll-like receptor 5 (TLR5) and NOD-like receptor C4 (NLRC4). Flagellin-induced activation of TLR5 on dendritic cells elicited production of the cytokine interleukin-22 (IL-22), which induced a protective gene expression program in intestinal epithelial cells. Flagellin also induced NLRC4-dependent production of IL-18 and immediate elimination of RV-infected cells. Administration of IL-22 and IL-18 to mice fully recapitulated the capacity of flagellin to prevent or eliminate RV infection and thus holds promise as a broad-spectrum antiviral agent.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Benyue -- Chassaing, Benoit -- Shi, Zhenda -- Uchiyama, Robin -- Zhang, Zhan -- Denning, Timothy L -- Crawford, Sue E -- Pruijssers, Andrea J -- Iskarpatyoti, Jason A -- Estes, Mary K -- Dermody, Terence S -- Ouyang, Wenjun -- Williams, Ifor R -- Vijay-Kumar, Matam -- Gewirtz, Andrew T -- AI038296/AI/NIAID NIH HHS/ -- AI080656/AI/NIAID NIH HHS/ -- AI107943/AI/NIAID NIH HHS/ -- DK061417/DK/NIDDK NIH HHS/ -- DK064730/DK/NIDDK NIH HHS/ -- DK56338/DK/NIDDK NIH HHS/ -- R01 AI038296/AI/NIAID NIH HHS/ -- R37 AI038296/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2014 Nov 14;346(6211):861-5. doi: 10.1126/science.1256999.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA, USA. ; Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA, USA. Department of Pathology, Emory University School of Medicine, Atlanta, GA, USA. ; Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX, USA. ; Elizabeth B. Lamb Center for Pediatric Research, Vanderbilt University School of Medicine, Nashville, TN, USA. ; Elizabeth B. Lamb Center for Pediatric Research, Vanderbilt University School of Medicine, Nashville, TN, USA. Departments of Pediatrics, Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, TN, USA. ; Department of Immunology, Genentech, South San Francisco, CA, USA. ; Department of Pathology, Emory University School of Medicine, Atlanta, GA, USA. ; Department of Nutritional Sciences and Medicine, Pennsylvania State University, University Park, PA 16802, USA. ; Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA, USA. Department of Pathology, Emory University School of Medicine, Atlanta, GA, USA. agewirtz@gsu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25395539" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Diarrhea/immunology/therapy/virology ; Disease Models, Animal ; Feces/virology ; Flagellin/*administration & dosage/immunology ; Homeodomain Proteins/genetics ; *Immunity, Innate ; Interleukin-18/administration & dosage/genetics/*immunology ; Interleukins/administration & dosage/genetics/*immunology ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Mutation ; Rotavirus Infections/immunology/*prevention & control/therapy ; Toll-Like Receptor 5/genetics/*physiology ; Virus Shedding
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  • 21
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-10-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2014 Oct 17;346(6207):292-5. doi: 10.1126/science.346.6207.292.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25324367" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Child ; Female ; Health ; Humans ; Infant ; Longevity ; Male ; Papio/*physiology/*psychology ; Reproduction ; Starvation/epidemiology/physiopathology ; Stress, Psychological/epidemiology/*physiopathology
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  • 22
    Publication Date: 2014-12-17
    Description: Birds are the most species-rich class of tetrapod vertebrates and have wide relevance across many research fields. We explored bird macroevolution using full genomes from 48 avian species representing all major extant clades. The avian genome is principally characterized by its constrained size, which predominantly arose because of lineage-specific erosion of repetitive elements, large segmental deletions, and gene loss. Avian genomes furthermore show a remarkably high degree of evolutionary stasis at the levels of nucleotide sequence, gene synteny, and chromosomal structure. Despite this pattern of conservation, we detected many non-neutral evolutionary changes in protein-coding genes and noncoding regions. These analyses reveal that pan-avian genomic diversity covaries with adaptations to different lifestyles and convergent evolution of traits.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4390078/" 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/PMC4390078/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Guojie -- Li, Cai -- Li, Qiye -- Li, Bo -- Larkin, Denis M -- Lee, Chul -- Storz, Jay F -- Antunes, Agostinho -- Greenwold, Matthew J -- Meredith, Robert W -- Odeen, Anders -- Cui, Jie -- Zhou, Qi -- Xu, Luohao -- Pan, Hailin -- Wang, Zongji -- Jin, Lijun -- Zhang, Pei -- Hu, Haofu -- Yang, Wei -- Hu, Jiang -- Xiao, Jin -- Yang, Zhikai -- Liu, Yang -- Xie, Qiaolin -- Yu, Hao -- Lian, Jinmin -- Wen, Ping -- Zhang, Fang -- Li, Hui -- Zeng, Yongli -- Xiong, Zijun -- Liu, Shiping -- Zhou, Long -- Huang, Zhiyong -- An, Na -- Wang, Jie -- Zheng, Qiumei -- Xiong, Yingqi -- Wang, Guangbiao -- Wang, Bo -- Wang, Jingjing -- Fan, Yu -- da Fonseca, Rute R -- Alfaro-Nunez, Alonzo -- Schubert, Mikkel -- Orlando, Ludovic -- Mourier, Tobias -- Howard, Jason T -- Ganapathy, Ganeshkumar -- Pfenning, Andreas -- Whitney, Osceola -- Rivas, Miriam V -- Hara, Erina -- Smith, Julia -- Farre, Marta -- Narayan, Jitendra -- Slavov, Gancho -- Romanov, Michael N -- Borges, Rui -- Machado, Joao Paulo -- Khan, Imran -- Springer, Mark S -- Gatesy, John -- Hoffmann, Federico G -- Opazo, Juan C -- Hastad, Olle -- Sawyer, Roger H -- Kim, Heebal -- Kim, Kyu-Won -- Kim, Hyeon Jeong -- Cho, Seoae -- Li, Ning -- Huang, Yinhua -- Bruford, Michael W -- Zhan, Xiangjiang -- Dixon, Andrew -- Bertelsen, Mads F -- Derryberry, Elizabeth -- Warren, Wesley -- Wilson, Richard K -- Li, Shengbin -- Ray, David A -- Green, Richard E -- O'Brien, Stephen J -- Griffin, Darren -- Johnson, Warren E -- Haussler, David -- Ryder, Oliver A -- Willerslev, Eske -- Graves, Gary R -- Alstrom, Per -- Fjeldsa, Jon -- Mindell, David P -- Edwards, Scott V -- Braun, Edward L -- Rahbek, Carsten -- Burt, David W -- Houde, Peter -- Zhang, Yong -- Yang, Huanming -- Wang, Jian -- Avian Genome Consortium -- Jarvis, Erich D -- Gilbert, M Thomas P -- Wang, Jun -- DP1 OD000448/OD/NIH HHS/ -- DP1OD000448/OD/NIH HHS/ -- R01 HL087216/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Dec 12;346(6215):1311-20. doi: 10.1126/science.1251385. Epub 2014 Dec 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. Centre for Social Evolution, Department of Biology, Universitetsparken 15, University of Copenhagen, DK-2100 Copenhagen, Denmark. zhanggj@genomics.cn jarvis@neuro.duke.edu mtpgilbert@gmail.com wangj@genomics.cn. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, Oster Voldgade 5-7, 1350 Copenhagen, Denmark. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. ; Royal Veterinary College, University of London, London, UK. ; Interdisciplinary Program in Bioinformatics, Seoul National University, Seoul 151-742, Republic of Korea. Cho and Kim Genomics, Seoul National University Research Park, Seoul 151-919, Republic of Korea. ; School of Biological Sciences, University of Nebraska, Lincoln, NE 68588, USA. ; Centro de Investigacion en Ciencias del Mar y Limnologia (CIMAR)/Centro Interdisciplinar de Investigacao Marinha e Ambiental (CIIMAR), Universidade do Porto, Rua dos Bragas, 177, 4050-123 Porto, Portugal. Departamento de Biologia, Faculdade de Ciencias, Universidade do Porto, Rua do Campo Alegre, 4169-007 Porto, Portugal. ; Department of Biological Sciences, University of South Carolina, Columbia, SC, USA. ; Department of Biology and Molecular Biology, Montclair State University, Montclair, NJ 07043, USA. ; Department of Animal Ecology, Uppsala University, Norbyvagen 18D, S-752 36 Uppsala, Sweden. ; Marie Bashir Institute for Infectious Diseases and Biosecurity, Charles Perkins Centre, School of Biological Sciences and Sydney Medical School, The University of Sydney, Sydney, NSW 2006, Australia. Program in Emerging Infectious Diseases, Duke-NUS Graduate Medical School, Singapore 169857, Singapore. ; Department of Integrative Biology University of California, Berkeley, CA 94720, USA. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. College of Life Sciences, Wuhan University, Wuhan 430072, China. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. School of Bioscience and Bioengineering, South China University of Technology, Guangzhou 510006, China. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. BGI Education Center,University of Chinese Academy of Sciences,Shenzhen, 518083, China. ; Key Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Kunming, Yunnan 650223, China. ; Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, Oster Voldgade 5-7, 1350 Copenhagen, Denmark. ; Department of Neurobiology, Howard Hughes Medical Institute, Duke University Medical Center, Durham, NC 27710, USA. ; Institute of Biological, Environmental and Rural Sciences, Aberystwyth University, Aberystwyth, UK. ; School of Biosciences, University of Kent, Canterbury CT2 7NJ, UK. ; Centro de Investigacion en Ciencias del Mar y Limnologia (CIMAR)/Centro Interdisciplinar de Investigacao Marinha e Ambiental (CIIMAR), Universidade do Porto, Rua dos Bragas, 177, 4050-123 Porto, Portugal. Instituto de Ciencias Biomedicas Abel Salazar (ICBAS), Universidade do Porto, Portugal. ; Department of Biology, University of California Riverside, Riverside, CA 92521, USA. ; Department of Biochemistry, Molecular Biology, Entomology and Plant Pathology, Mississippi State University, Mississippi State, MS 39762, USA. Institute for Genomics, Biocomputing and Biotechnology, Mississippi State University, Mississippi State, MS 39762, USA. ; Instituto de Ciencias Ambientales y Evolutivas, Facultad de Ciencias, Universidad Austral de Chile, Valdivia, Chile. ; Department of Anatomy, Physiology and Biochemistry, Swedish University of Agricultural Sciences, Post Office Box 7011, S-750 07, Uppsala, Sweden. ; Interdisciplinary Program in Bioinformatics, Seoul National University, Seoul 151-742, Republic of Korea. Cho and Kim Genomics, Seoul National University Research Park, Seoul 151-919, Republic of Korea. Department of Agricultural Biotechnology and Research Institute for Agriculture and Life Sciences, Seoul National University, Seoul 151-742, Republic of Korea. ; Interdisciplinary Program in Bioinformatics, Seoul National University, Seoul 151-742, Republic of Korea. ; Cho and Kim Genomics, Seoul National University Research Park, Seoul 151-919, Republic of Korea. ; State Key Laboratory for Agrobiotechnology, China Agricultural University, Beijing 100094, China. ; State Key Laboratory for Agrobiotechnology, China Agricultural University, Beijing 100094, China. College of Animal Science and Technology, China Agricultural University, Beijing 100094, China. ; Organisms and Environment Division, Cardiff School of Biosciences, Cardiff University, Cardiff CF10 3AX, Wales, UK. ; Organisms and Environment Division, Cardiff School of Biosciences, Cardiff University, Cardiff CF10 3AX, Wales, UK. Key Lab of Animal Ecology and Conservation Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101 China. ; International Wildlife Consultants, Carmarthen SA33 5YL, Wales, UK. ; Centre for Zoo and Wild Animal Health, Copenhagen Zoo, Roskildevej 38, DK-2000 Frederiksberg, Denmark. ; Department of Ecology and Evolutionary Biology, Tulane University, New Orleans, LA, USA. Museum of Natural Science, Louisiana State University, Baton Rouge, LA 70803, USA. ; The Genome Institute at Washington University, St. Louis, MO 63108, USA. ; College of Medicine and Forensics, Xi'an Jiaotong University, Xi'an, 710061, China. ; Institute for Genomics, Biocomputing and Biotechnology, Mississippi State University, Mississippi State, MS 39762, USA. ; Department of Biomolecular Engineering, University of California, Santa Cruz, CA 95064, USA. ; Theodosius Dobzhansky Center for Genome Bioinformatics, St. Petersburg State University, St. Petersburg, Russia. Nova Southeastern University Oceanographic Center 8000 N Ocean Drive, Dania, FL 33004, USA. ; Smithsonian Conservation Biology Institute, National Zoological Park, 1500 Remount Road, Front Royal, VA 22630, USA. ; Genetics Division, San Diego Zoo Institute for Conservation Research, 15600 San Pasqual Valley Road, Escondido, CA 92027, USA. ; Department of Vertebrate Zoology, MRC-116, National Museum of Natural History, Smithsonian Institution, Post Office Box 37012, Washington, DC 20013-7012, USA. Center for Macroecology, Evolution and Climate, the Natural History Museum of Denmark, University of Copenhagen, Universitetsparken 15, DK-2100 Copenhagen O, Denmark. ; Key Laboratory of Zoological Systematics and Evolution, Institute of Zoology, Chinese Academy of Sciences, 1 Beichen West Road, Chaoyang District, Beijing 100101, China. Swedish Species Information Centre, Swedish University of Agricultural Sciences, Box 7007, SE-750 07 Uppsala, Sweden. ; Center for Macroecology, Evolution and Climate, the Natural History Museum of Denmark, University of Copenhagen, Universitetsparken 15, DK-2100 Copenhagen O, Denmark. ; Department of Biochemistry & Biophysics, University of California, San Francisco, CA 94158, USA. ; Department of Organismic and Evolutionary Biology and Museum of Comparative Zoology, Harvard University, 26 Oxford Street, Cambridge, MA 02138, USA. ; Department of Biology and Genetics Institute, University of Florida, Gainesville, FL 32611, USA. ; Center for Macroecology, Evolution and Climate, the Natural History Museum of Denmark, University of Copenhagen, Universitetsparken 15, DK-2100 Copenhagen O, Denmark. Imperial College London, Grand Challenges in Ecosystems and the Environment Initiative, Silwood Park Campus, Ascot, Berkshire SL5 7PY, UK. ; Division of Genetics and Genomics, The Roslin Institute and Royal (Dick) School of Veterinary Studies, The Roslin Institute Building, University of Edinburgh, Easter Bush Campus, Midlothian EH25 9RG, UK. ; Department of Biology, New Mexico State University, Box 30001 MSC 3AF, Las Cruces, NM 88003, USA. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. Macau University of Science and Technology, Avenida Wai long, Taipa, Macau 999078, China. ; Department of Neurobiology, Howard Hughes Medical Institute, Duke University Medical Center, Durham, NC 27710, USA. zhanggj@genomics.cn jarvis@neuro.duke.edu mtpgilbert@gmail.com wangj@genomics.cn. ; Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, Oster Voldgade 5-7, 1350 Copenhagen, Denmark. Trace and Environmental DNA Laboratory, Department of Environment and Agriculture, Curtin University, Perth, Western Australia, 6102, Australia. zhanggj@genomics.cn jarvis@neuro.duke.edu mtpgilbert@gmail.com wangj@genomics.cn. ; China National GeneBank, Beijing Genomics Institute (BGI)-Shenzhen, Shenzhen, 518083, China. Macau University of Science and Technology, Avenida Wai long, Taipa, Macau 999078, China. Department of Biology, University of Copenhagen, Ole Maaloes Vej 5, 2200 Copenhagen, Denmark. Princess Al Jawhara Center of Excellence in the Research of Hereditary Disorders, King Abdulaziz University, Jeddah 21589, Saudi Arabia. Department of Medicine, University of Hong Kong, Hong Kong. zhanggj@genomics.cn jarvis@neuro.duke.edu mtpgilbert@gmail.com wangj@genomics.cn.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25504712" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Animals ; Biodiversity ; *Biological Evolution ; Birds/classification/*genetics/physiology ; Conserved Sequence ; Diet ; *Evolution, Molecular ; Female ; Flight, Animal ; Genes ; Genetic Variation ; *Genome ; Genomics ; Male ; Molecular Sequence Annotation ; Phylogeny ; Reproduction/genetics ; Selection, Genetic ; Sequence Analysis, DNA ; Synteny ; Vision, Ocular/genetics ; Vocalization, Animal
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  • 23
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-07-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stone, Richard -- New York, N.Y. -- Science. 2014 Jul 11;345(6193):130-1, 133. doi: 10.1126/science.345.6193.130.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25013042" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Communicable Diseases, Emerging/*epidemiology/*prevention & control ; Encephalitis Viruses, Tick-Borne/isolation & purification ; Female ; Haplorhini ; Humans ; India/epidemiology ; Kyasanur Forest Disease/*epidemiology/*prevention & control ; Male ; Ticks/virology ; Trees
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 24
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-03-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benderly, Beryl Lieff -- New York, N.Y. -- Science. 2014 Mar 14;343(6176):1200. doi: 10.1126/science.343.6176.1200-b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Science Careers Columnist.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24626915" target="_blank"〉PubMed〈/a〉
    Keywords: *Career Choice ; Female ; Humans ; *Leadership ; Physicians, Women/*psychology ; *Sexism
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  • 25
    Publication Date: 2014-05-07
    Description: Parabiosis experiments indicate that impaired regeneration in aged mice is reversible by exposure to a young circulation, suggesting that young blood contains humoral "rejuvenating" factors that can restore regenerative function. Here, we demonstrate that the circulating protein growth differentiation factor 11 (GDF11) is a rejuvenating factor for skeletal muscle. Supplementation of systemic GDF11 levels, which normally decline with age, by heterochronic parabiosis or systemic delivery of recombinant protein, reversed functional impairments and restored genomic integrity in aged muscle stem cells (satellite cells). Increased GDF11 levels in aged mice also improved muscle structural and functional features and increased strength and endurance exercise capacity. These data indicate that GDF11 systemically regulates muscle aging and may be therapeutically useful for reversing age-related skeletal muscle and stem cell dysfunction.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4104429/" 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/PMC4104429/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sinha, Manisha -- Jang, Young C -- Oh, Juhyun -- Khong, Danika -- Wu, Elizabeth Y -- Manohar, Rohan -- Miller, Christine -- Regalado, Samuel G -- Loffredo, Francesco S -- Pancoast, James R -- Hirshman, Michael F -- Lebowitz, Jessica -- Shadrach, Jennifer L -- Cerletti, Massimiliano -- Kim, Mi-Jeong -- Serwold, Thomas -- Goodyear, Laurie J -- Rosner, Bernard -- Lee, Richard T -- Wagers, Amy J -- 1DP2 OD004345/OD/NIH HHS/ -- 1R01 AG033053/AG/NIA NIH HHS/ -- 1R01 AG040019/AG/NIA NIH HHS/ -- 5U01 HL100402/HL/NHLBI NIH HHS/ -- DP2 OD004345/OD/NIH HHS/ -- P30 AG038072/AG/NIA NIH HHS/ -- R01 AG032977/AG/NIA NIH HHS/ -- R01 AG033053/AG/NIA NIH HHS/ -- R01 AG040019/AG/NIA NIH HHS/ -- R01 AR042238/AR/NIAMS NIH HHS/ -- R01 AR42238/AR/NIAMS NIH HHS/ -- T32 DE007057/DE/NIDCR NIH HHS/ -- U01 HL100402/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 May 9;344(6184):649-52. doi: 10.1126/science.1251152. Epub 2014 May 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Harvard Stem Cell Institute and Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24797481" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Aging/blood/drug effects/*physiology ; Animals ; Bone Morphogenetic Proteins/administration & dosage/blood/*physiology ; Growth Differentiation Factors/administration & dosage/blood/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal/*blood supply/drug effects/*physiology ; Myoblasts, Skeletal/drug effects/*physiology ; Parabiosis ; *Regeneration ; *Rejuvenation
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  • 26
    Publication Date: 2014-02-08
    Description: Neuronal intracellular chloride concentration [Cl(-)](i) is an important determinant of gamma-aminobutyric acid type A (GABA(A)) receptor (GABA(A)R)-mediated inhibition and cytoplasmic volume regulation. Equilibrative cation-chloride cotransporters (CCCs) move Cl(-) across the membrane, but accumulating evidence suggests factors other than the bulk concentrations of transported ions determine [Cl(-)](i). Measurement of [Cl(-)](i) in murine brain slice preparations expressing the transgenic fluorophore Clomeleon demonstrated that cytoplasmic impermeant anions ([A](i)) and polyanionic extracellular matrix glycoproteins ([A](o)) constrain the local [Cl(-)]. CCC inhibition had modest effects on [Cl(-)](i) and neuronal volume, but substantial changes were produced by alterations of the balance between [A](i) and [A](o). Therefore, CCCs are important elements of Cl(-) homeostasis, but local impermeant anions determine the homeostatic set point for [Cl(-)], and hence, neuronal volume and the polarity of local GABA(A)R signaling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4220679/" 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/PMC4220679/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Glykys, J -- Dzhala, V -- Egawa, K -- Balena, T -- Saponjian, Y -- Kuchibhotla, K V -- Bacskai, B J -- Kahle, K T -- Zeuthen, T -- Staley, K J -- NS 40109-06/NS/NINDS NIH HHS/ -- R01 EB000768/EB/NIBIB NIH HHS/ -- R01 NS040109/NS/NINDS NIH HHS/ -- R01 NS074772/NS/NINDS NIH HHS/ -- R25 NS065743/NS/NINDS NIH HHS/ -- S10 RR025645/RR/NCRR NIH HHS/ -- U41 RR019703/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2014 Feb 7;343(6171):670-5. doi: 10.1126/science.1245423.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24503855" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; Cell Membrane Permeability ; Cell Polarity ; Chloride Channels/*metabolism ; Chlorides/*metabolism ; Cytoplasm/metabolism ; Extracellular Matrix Proteins/metabolism ; Glycoproteins/metabolism ; Mice ; Mice, Transgenic ; Neurons/*metabolism ; Receptors, GABA-A/*metabolism ; Recombinant Fusion Proteins/genetics/metabolism ; Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 27
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-06-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2014 Jun 6;344(6188):1072. doi: 10.1126/science.344.6188.1072.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24904133" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Nucleus/metabolism ; Cells/*metabolism ; Humans ; Inflammation ; Mice ; Mice, Knockout ; Neoplasms ; Pain ; RNA, Long Noncoding/genetics/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 28
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-03-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kean, Sam -- New York, N.Y. -- Science. 2014 Mar 28;343(6178):1457-9. doi: 10.1126/science.343.6178.1457.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24675950" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*genetics ; Checkpoint Kinase 2/genetics ; Female ; Genes, BRCA1 ; Genes, BRCA2 ; *Genetic Predisposition to Disease ; Humans ; Mutation ; Nuclear Proteins/genetics ; *Oncogenes ; Tumor Suppressor Proteins/genetics
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  • 29
    Publication Date: 2014-08-26
    Description: Riboswitches are ligand-binding elements contained within the 5' untranslated regions of bacterial transcripts, which generally regulate expression of downstream open reading frames. Here, we show that in Listeria monocytogenes, a riboswitch that binds vitamin B12 controls expression of a noncoding regulatory RNA, Rli55. Rli55, in turn, controls expression of the eut genes, whose products enable ethanolamine utilization and require B12 as a cofactor. Defects in ethanolamine utilization, or in its regulation by Rli55, significantly attenuate Listeria virulence in mice. Rli55 functions by sequestering the two-component response regulator EutV by means of a EutV-binding site contained within the RNA. Thus, Rli55 is a riboswitch-regulated member of the small group of regulatory RNAs that function by sequestering a protein and reveals a distinctive mechanism of signal integration in bacterial gene regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mellin, J R -- Koutero, Mikael -- Dar, Daniel -- Nahori, Marie-Anne -- Sorek, Rotem -- Cossart, Pascale -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Aug 22;345(6199):940-3. doi: 10.1126/science.1255083.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite des Interactions Bacteries-Cellules, Institut Pasteur, F-75015 Paris, France. INSERM, U604, Paris, F-75015 France. INRA, USC2020, F-75015 Paris, France. ; Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel. ; Unite des Interactions Bacteries-Cellules, Institut Pasteur, F-75015 Paris, France. INSERM, U604, Paris, F-75015 France. INRA, USC2020, F-75015 Paris, France. pcossart@pasteur.fr.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25146292" target="_blank"〉PubMed〈/a〉
    Keywords: 5' Untranslated Regions ; Animals ; Ethanolamine/*metabolism ; *Gene Expression Regulation, Bacterial ; Listeria monocytogenes/*genetics/metabolism/virology ; Mice ; Mice, Inbred BALB C ; Operon ; RNA, Untranslated/*metabolism ; Response Elements ; *Riboswitch ; Vitamin B 12/*metabolism
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  • 30
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-02-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Promislow, Daniel E L -- Kaeberlein, Matt -- R01 AG031108/AG/NIA NIH HHS/ -- R01 AG033598/AG/NIA NIH HHS/ -- R01 GM102279/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Jan 31;343(6170):491-2. doi: 10.1126/science.1250174.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Washington, Seattle, WA 98195 USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24482469" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*physiology ; Drosophila melanogaster/*physiology ; Female ; Longevity/*physiology ; Male ; Pheromones/*physiology ; *Reward ; Sexual Behavior, Animal/*physiology ; Spermatozoa/*physiology ; *Taste Perception
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  • 31
    Publication Date: 2014-03-08
    Description: The excitatory neurotransmitter glutamate induces modulatory actions via the metabotropic glutamate receptors (mGlus), which are class C G protein-coupled receptors (GPCRs). We determined the structure of the human mGlu1 receptor seven-transmembrane (7TM) domain bound to a negative allosteric modulator, FITM, at a resolution of 2.8 angstroms. The modulator binding site partially overlaps with the orthosteric binding sites of class A GPCRs but is more restricted than most other GPCRs. We observed a parallel 7TM dimer mediated by cholesterols, which suggests that signaling initiated by glutamate's interaction with the extracellular domain might be mediated via 7TM interactions within the full-length receptor dimer. A combination of crystallography, structure-activity relationships, mutagenesis, and full-length dimer modeling provides insights about the allosteric modulation and activation mechanism of class C GPCRs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3991565/" 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/PMC3991565/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Huixian -- Wang, Chong -- Gregory, Karen J -- Han, Gye Won -- Cho, Hyekyung P -- Xia, Yan -- Niswender, Colleen M -- Katritch, Vsevolod -- Meiler, Jens -- Cherezov, Vadim -- Conn, P Jeffrey -- Stevens, Raymond C -- P50 GM073197/GM/NIGMS NIH HHS/ -- R01 DK097376/DK/NIDDK NIH HHS/ -- R01 GM080403/GM/NIGMS NIH HHS/ -- R01 GM099842/GM/NIGMS NIH HHS/ -- R01 MH062646/MH/NIMH NIH HHS/ -- R01 MH090192/MH/NIMH NIH HHS/ -- R01 NS031373/NS/NINDS NIH HHS/ -- R21 NS078262/NS/NINDS NIH HHS/ -- R37 NS031373/NS/NINDS NIH HHS/ -- U54 GM094618/GM/NIGMS NIH HHS/ -- Y1-CO-1020/CO/NCI NIH HHS/ -- Y1-GM-1104/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Apr 4;344(6179):58-64. doi: 10.1126/science.1249489. Epub 2014 Mar 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Integrative Structural and Computational Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24603153" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Regulation ; Allosteric Site ; Amino Acid Sequence ; Benzamides/*chemistry/*metabolism ; Binding Sites ; Cholesterol ; Crystallography, X-Ray ; Humans ; Hydrophobic and Hydrophilic Interactions ; Ligands ; Models, Molecular ; Molecular Sequence Data ; Mutation ; Protein Conformation ; Protein Multimerization ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Receptors, Metabotropic Glutamate/*chemistry/*metabolism ; Structure-Activity Relationship ; Thiazoles/*chemistry/*metabolism
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  • 32
    Publication Date: 2014-02-18
    Description: The human neocortex has numerous specialized functional areas whose formation is poorly understood. Here, we describe a 15-base pair deletion mutation in a regulatory element of GPR56 that selectively disrupts human cortex surrounding the Sylvian fissure bilaterally including "Broca's area," the primary language area, by disrupting regional GPR56 expression and blocking RFX transcription factor binding. GPR56 encodes a heterotrimeric guanine nucleotide-binding protein (G protein)-coupled receptor required for normal cortical development and is expressed in cortical progenitor cells. GPR56 expression levels regulate progenitor proliferation. GPR56 splice forms are highly variable between mice and humans, and the regulatory element of gyrencephalic mammals directs restricted lateral cortical expression. Our data reveal a mechanism by which control of GPR56 expression pattern by multiple alternative promoters can influence stem cell proliferation, gyral patterning, and, potentially, neocortex evolution.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4480613/" 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/PMC4480613/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bae, Byoung-Il -- Tietjen, Ian -- Atabay, Kutay D -- Evrony, Gilad D -- Johnson, Matthew B -- Asare, Ebenezer -- Wang, Peter P -- Murayama, Ayako Y -- Im, Kiho -- Lisgo, Steven N -- Overman, Lynne -- Sestan, Nenad -- Chang, Bernard S -- Barkovich, A James -- Grant, P Ellen -- Topcu, Meral -- Politsky, Jeffrey -- Okano, Hideyuki -- Piao, Xianhua -- Walsh, Christopher A -- 2R01NS035129/NS/NINDS NIH HHS/ -- G0700089/Medical Research Council/United Kingdom -- GR082557/Wellcome Trust/United Kingdom -- HHSN275200900011C/PHS HHS/ -- N01-HD-9-0011/HD/NICHD NIH HHS/ -- R01 NS035129/NS/NINDS NIH HHS/ -- U01 MH081896/MH/NIMH NIH HHS/ -- U01MH081896/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Feb 14;343(6172):764-8. doi: 10.1126/science.1244392.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Genetics and Genomics, Manton Center for Orphan Disease, and Howard Hughes Medical Institute, Boston Children's Hospital, Broad Institute of MIT and Harvard, and Departments of Pediatrics and Neurology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24531968" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Animals ; Base Sequence ; Biological Evolution ; Body Patterning/*genetics ; Cats ; Cell Proliferation ; Cerebral Cortex/anatomy & histology/cytology/*embryology ; Codon, Nonsense ; Frontal Lobe/anatomy & histology/cytology/embryology ; Genetic Variation ; Haplotypes ; Humans ; Mice ; Molecular Sequence Data ; Neural Stem Cells/cytology/*physiology ; Pedigree ; Promoter Regions, Genetic/genetics ; Receptors, G-Protein-Coupled/*genetics ; Sequence Deletion
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  • 33
    Publication Date: 2014-01-25
    Description: Comparative genomic analyses have revealed that genes may arise from ancestrally nongenic sequence. However, the origin and spread of these de novo genes within populations remain obscure. We identified 142 segregating and 106 fixed testis-expressed de novo genes in a population sample of Drosophila melanogaster. These genes appear to derive primarily from ancestral intergenic, unexpressed open reading frames, with natural selection playing a significant role in their spread. These results reveal a heretofore unappreciated dynamism of gene content.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4391638/" 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/PMC4391638/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhao, Li -- Saelao, Perot -- Jones, Corbin D -- Begun, David J -- GM084056/GM/NIGMS NIH HHS/ -- R01 GM084056/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Feb 14;343(6172):769-72. doi: 10.1126/science.1248286. Epub 2014 Jan 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Evolution and Ecology, University of California, Davis, CA 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24457212" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drosophila melanogaster/*genetics ; *Evolution, Molecular ; Female ; Gene Expression ; Gene Expression Regulation ; *Genes, Insect ; Genetic Association Studies ; Male ; Open Reading Frames ; Selection, Genetic ; Testis/metabolism
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  • 34
    Publication Date: 2014-04-05
    Description: Most land animals normally walk forward but switch to backward walking upon sensing an obstacle or danger in the path ahead. A change in walking direction is likely to be triggered by descending "command" neurons from the brain that act upon local motor circuits to alter the timing of leg muscle activation. Here we identify descending neurons for backward walking in Drosophila--the MDN neurons. MDN activity is required for flies to walk backward when they encounter an impassable barrier and is sufficient to trigger backward walking under conditions in which flies would otherwise walk forward. We also identify ascending neurons, MAN, that promote persistent backward walking, possibly by inhibiting forward walking. These findings provide an initial glimpse into the circuits and logic that control walking direction in Drosophila.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bidaye, Salil S -- Machacek, Christian -- Wu, Yang -- Dickson, Barry J -- New York, N.Y. -- Science. 2014 Apr 4;344(6179):97-101. doi: 10.1126/science.1249964.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Institute of Molecular Pathology (IMP), Dr. Bohrgasse 7, A-1030 Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24700860" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/cytology ; Drosophila/*physiology ; Extremities/physiology ; Female ; Gait ; Ganglia, Invertebrate/cytology ; Male ; Neurons/*physiology ; Walking/physiology
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  • 35
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-01-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2014 Jan 17;343(6168):239. doi: 10.1126/science.343.6168.239.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24436399" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ants/*microbiology/physiology ; Brain/metabolism/microbiology ; Fat Body/virology ; Female ; Gryllidae/physiology/*virology ; Guanidines/analysis/metabolism ; *Host-Pathogen Interactions ; Hypocreales/*physiology ; Insect Viruses/*physiology ; Lizards/virology ; Male ; Rats ; Sexual Behavior, Animal/*physiology ; Sphingosine/analysis/metabolism ; Virus Replication
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  • 36
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-04-26
    Description: How we attend to objects and their features that cannot be separated by location is not understood. We presented two temporally and spatially overlapping streams of objects, faces versus houses, and used magnetoencephalography and functional magnetic resonance imaging to separate neuronal responses to attended and unattended objects. Attention to faces versus houses enhanced the sensory responses in the fusiform face area (FFA) and parahippocampal place area (PPA), respectively. The increases in sensory responses were accompanied by induced gamma synchrony between the inferior frontal junction, IFJ, and either FFA or PPA, depending on which object was attended. The IFJ appeared to be the driver of the synchrony, as gamma phases were advanced by 20 ms in IFJ compared to FFA or PPA. Thus, the IFJ may direct the flow of visual processing during object-based attention, at least in part through coupled oscillations with specialized areas such as FFA and PPA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baldauf, Daniel -- Desimone, Robert -- P30EY2621/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2014 Apr 25;344(6182):424-7. doi: 10.1126/science.1247003. Epub 2014 Apr 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉McGovern Institute for Brain Research, Massachusetts Institute of Technology, Cambridge, 02139 MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24763592" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; *Attention ; Brain/*physiology ; Brain Mapping ; Diffusion Tensor Imaging ; Female ; Frontal Lobe/*physiology ; Functional Laterality ; Humans ; Magnetic Resonance Imaging ; Magnetoencephalography ; Male ; Temporal Lobe/*physiology ; Visual Cortex/physiology ; Visual Perception ; Young Adult
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  • 37
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-04-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- New York, N.Y. -- Science. 2014 Apr 18;344(6181):244-5. doi: 10.1126/science.344.6181.244.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24744351" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antiviral Agents/administration & dosage/*toxicity ; Arabinofuranosyluracil/administration & dosage/*analogs & derivatives/toxicity ; Chimera ; Hepatocytes/drug effects/metabolism/transplantation ; Humans ; Liver/cytology/*drug effects/metabolism ; Liver Transplantation ; Mice ; Mice, Transgenic ; *Models, Animal ; Toxicity Tests/*methods
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  • 38
    Publication Date: 2014-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- Kaiser, Jocelyn -- Service, Robert F -- Gibbons, Ann -- Vogel, Gretchen -- Underwood, Emily -- Hand, Eric -- New York, N.Y. -- Science. 2014 Dec 19;346(6216):1444-9. doi: 10.1126/science.346.6216.1444. Epub 2014 Dec 18.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25525224" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomedical Research/*trends ; Humans ; Mice
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  • 39
    Publication Date: 2014-05-31
    Description: Netrins are secreted proteins that regulate axon guidance and neuronal migration. Deleted in colorectal cancer (DCC) is a well-established netrin-1 receptor mediating attractive responses. We provide evidence that its close relative neogenin is also a functional netrin-1 receptor that acts with DCC to mediate guidance in vivo. We determined the structures of a functional netrin-1 region, alone and in complexes with neogenin or DCC. Netrin-1 has a rigid elongated structure containing two receptor-binding sites at opposite ends through which it brings together receptor molecules. The ligand/receptor complexes reveal two distinct architectures: a 2:2 heterotetramer and a continuous ligand/receptor assembly. The differences result from different lengths of the linker connecting receptor domains fibronectin type III domain 4 (FN4) and FN5, which differs among DCC and neogenin splice variants, providing a basis for diverse signaling outcomes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4369087/" 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/PMC4369087/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, Kai -- Wu, Zhuhao -- Renier, Nicolas -- Antipenko, Alexander -- Tzvetkova-Robev, Dorothea -- Xu, Yan -- Minchenko, Maria -- Nardi-Dei, Vincenzo -- Rajashankar, Kanagalaghatta R -- Himanen, Juha -- Tessier-Lavigne, Marc -- Nikolov, Dimitar B -- P41 GM103403/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Jun 13;344(6189):1275-9. doi: 10.1126/science.1255149. Epub 2014 May 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Structural Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA. ; Laboratory of Brain Development and Repair, Rockefeller University, New York, NY 10065, USA. ; Department of Chemistry and Chemical Biology, Cornell University and Northeastern Collaborative Access Team, Advanced Photon Source, Argonne, IL 60439, USA. ; Laboratory of Brain Development and Repair, Rockefeller University, New York, NY 10065, USA. nikolovd@mskcc.org marctl@mail.rockefeller.edu. ; Structural Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA. nikolovd@mskcc.org marctl@mail.rockefeller.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24876346" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Cell Movement ; Fibronectins/chemistry ; Ligands ; Membrane Proteins/*chemistry/genetics/ultrastructure ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Nerve Growth Factors/*chemistry/genetics/ultrastructure ; Neurons/physiology ; Protein Multimerization ; Protein Structure, Tertiary ; Receptors, Cell Surface/*chemistry/genetics/ultrastructure ; Tumor Suppressor Proteins/*chemistry/genetics/ultrastructure
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  • 40
    Publication Date: 2014-08-26
    Description: Sensory systems define an animal's capacity for perception and can evolve to promote survival in new environmental niches. We have uncovered a noncanonical mechanism for sweet taste perception that evolved in hummingbirds since their divergence from insectivorous swifts, their closest relatives. We observed the widespread absence in birds of an essential subunit (T1R2) of the only known vertebrate sweet receptor, raising questions about how specialized nectar feeders such as hummingbirds sense sugars. Receptor expression studies revealed that the ancestral umami receptor (the T1R1-T1R3 heterodimer) was repurposed in hummingbirds to function as a carbohydrate receptor. Furthermore, the molecular recognition properties of T1R1-T1R3 guided taste behavior in captive and wild hummingbirds. We propose that changing taste receptor function enabled hummingbirds to perceive and use nectar, facilitating the massive radiation of hummingbird species.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4302410/" 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/PMC4302410/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baldwin, Maude W -- Toda, Yasuka -- Nakagita, Tomoya -- O'Connell, Mary J -- Klasing, Kirk C -- Misaka, Takumi -- Edwards, Scott V -- Liberles, Stephen D -- R01 DC013289/DC/NIDCD NIH HHS/ -- R01DC013289/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 2014 Aug 22;345(6199):929-33. doi: 10.1126/science.1255097.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Organismic and Evolutionary Biology, Harvard University, and Museum of Comparative Zoology, Cambridge, MA 02138, USA. maudebaldwin@gmail.com stephen_liberles@hms.harvard.edu. ; Department of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo, Japan. ; Bioinformatics and Molecular Evolution Group, School of Biotechnology, Dublin City University, Glasnevin, Dublin 9, Ireland. ; Department of Animal Science, University of California, Davis, Davis, CA 95616, USA. ; Department of Organismic and Evolutionary Biology, Harvard University, and Museum of Comparative Zoology, Cambridge, MA 02138, USA. ; Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA. maudebaldwin@gmail.com stephen_liberles@hms.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25146290" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Evolution, Molecular ; Mice ; Molecular Sequence Data ; Plant Nectar ; Protein Structure, Tertiary ; Receptors, G-Protein-Coupled/chemistry/classification/*genetics ; Taste/*physiology ; Taste Perception/genetics/*physiology
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  • 41
    Publication Date: 2014-04-26
    Description: The hierarchical packaging of eukaryotic chromatin plays a central role in transcriptional regulation and other DNA-related biological processes. Here, we report the 11-angstrom-resolution cryogenic electron microscopy (cryo-EM) structures of 30-nanometer chromatin fibers reconstituted in the presence of linker histone H1 and with different nucleosome repeat lengths. The structures show a histone H1-dependent left-handed twist of the repeating tetranucleosomal structural units, within which the four nucleosomes zigzag back and forth with a straight linker DNA. The asymmetric binding and the location of histone H1 in chromatin play a role in the formation of the 30-nanometer fiber. Our results provide mechanistic insights into how nucleosomes compact into higher-order chromatin fibers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Song, Feng -- Chen, Ping -- Sun, Dapeng -- Wang, Mingzhu -- Dong, Liping -- Liang, Dan -- Xu, Rui-Ming -- Zhu, Ping -- Li, Guohong -- New York, N.Y. -- Science. 2014 Apr 25;344(6182):376-80. doi: 10.1126/science.1251413.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24763583" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Chromatin/chemistry/metabolism/*ultrastructure ; Cryoelectron Microscopy ; DNA/chemistry/*ultrastructure ; Histones/*chemistry/metabolism ; Imaging, Three-Dimensional ; Models, Molecular ; Molecular Sequence Data ; Nucleic Acid Conformation ; Nucleosomes/*ultrastructure ; Protein Conformation ; Recombinant Proteins/chemistry/metabolism ; Xenopus Proteins/chemistry ; Xenopus laevis
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  • 42
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-09-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hall, Stephen S -- New York, N.Y. -- Science. 2014 Sep 12;345(6202):1234-7. doi: 10.1126/science.345.6202.1234.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25214587" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Animals ; *Blood ; Bone Morphogenetic Proteins/administration & dosage/physiology ; Brain/physiology ; Growth Differentiation Factors/administration & dosage/physiology ; Heart/drug effects/physiology ; Humans ; Liver/physiology ; Mice ; Muscle, Skeletal/physiology ; Rejuvenation/*physiology
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  • 43
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-02-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blair, H T -- New York, N.Y. -- Science. 2014 Feb 21;343(6173):846-7. doi: 10.1126/science.1251252.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Psychology Department and Brain Research Institute, University of California, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24558150" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Association ; CA1 Region, Hippocampal/*physiology ; Entorhinal Cortex/*cytology/*physiology ; Female ; Male ; *Memory, Episodic ; *Nerve Net ; Neurons/*physiology ; Pyramidal Cells/*physiology/*ultrastructure ; *Theta Rhythm
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  • 44
    Publication Date: 2014-09-13
    Description: Fucosylation of intestinal epithelial cells, catalyzed by fucosyltransferase 2 (Fut2), is a major glycosylation mechanism of host-microbiota symbiosis. Commensal bacteria induce epithelial fucosylation, and epithelial fucose is used as a dietary carbohydrate by many of these bacteria. However, the molecular and cellular mechanisms that regulate the induction of epithelial fucosylation are unknown. Here, we show that type 3 innate lymphoid cells (ILC3) induced intestinal epithelial Fut2 expression and fucosylation in mice. This induction required the cytokines interleukin-22 and lymphotoxin in a commensal bacteria-dependent and -independent manner, respectively. Disruption of intestinal fucosylation led to increased susceptibility to infection by Salmonella typhimurium. Our data reveal a role for ILC3 in shaping the gut microenvironment through the regulation of epithelial glycosylation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4774895/" 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/PMC4774895/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goto, Yoshiyuki -- Obata, Takashi -- Kunisawa, Jun -- Sato, Shintaro -- Ivanov, Ivaylo I -- Lamichhane, Aayam -- Takeyama, Natsumi -- Kamioka, Mariko -- Sakamoto, Mitsuo -- Matsuki, Takahiro -- Setoyama, Hiromi -- Imaoka, Akemi -- Uematsu, Satoshi -- Akira, Shizuo -- Domino, Steven E -- Kulig, Paulina -- Becher, Burkhard -- Renauld, Jean-Christophe -- Sasakawa, Chihiro -- Umesaki, Yoshinori -- Benno, Yoshimi -- Kiyono, Hiroshi -- 1R01DK098378/DK/NIDDK NIH HHS/ -- R01 DK098378/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2014 Sep 12;345(6202):1254009. doi: 10.1126/science.1254009. Epub 2014 Aug 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Mucosal Immunology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan. Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Saitama 332-0012, Japan. Microbe Division/Japan Collection of Microorganisms, RIKEN BioResource Center, Tsukuba 305-0074, Japan. ; Division of Mucosal Immunology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan. Microbe Division/Japan Collection of Microorganisms, RIKEN BioResource Center, Tsukuba 305-0074, Japan. ; Division of Mucosal Immunology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan. Laboratory of Vaccine Materials, National Institute of Biomedical Innovation, Osaka 567-0085, Japan. Division of Mucosal Immunology, International Research and Development Center for Mucosal Vaccines, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan. ; Division of Mucosal Immunology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan. Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Saitama 332-0012, Japan. ; Department of Microbiology and Immunology, Columbia University Medical Center, New York, NY 10032, USA. ; Division of Mucosal Immunology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan. ; Division of Mucosal Immunology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan. Nippon Institute for Biological Science, Tokyo 198-0024, Japan. ; Microbe Division/Japan Collection of Microorganisms, RIKEN BioResource Center, Tsukuba 305-0074, Japan. ; Yakult Central Institute, Tokyo 186-8650, Japan. ; Division of Innate Immune Regulation, International Research and Development Center for Mucosal Vaccines, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan. Department of Mucosal Immunology, School of Medicine, Chiba University, 1-8-1 Inohana, Chuou-ku, Chiba, 260-8670, Japan. ; Laboratory of Host Defense, WPI Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan. ; Department of Obstetrics and Gynecology, Cellular and Molecular Biology Program, University of Michigan Medical Center, Ann Arbor, MI 48109-5617, USA. ; Institute of Experimental Immunology, University of Zurich, Winterthurerstrasse 190, Zurich CH-8057, Switzerland. ; Ludwig Institute for Cancer Research and Universite Catholique de Louvain, Brussels B-1200, Belgium. ; Nippon Institute for Biological Science, Tokyo 198-0024, Japan. Division of Bacterial Infection, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan. Medical Mycology Research Center, Chiba University, Chiba 260-8673, Japan. ; Benno Laboratory, Innovation Center, RIKEN, Wako, Saitama 351-0198, Japan. ; Division of Mucosal Immunology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan. Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Saitama 332-0012, Japan. Division of Mucosal Immunology, International Research and Development Center for Mucosal Vaccines, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25214634" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Disease Models, Animal ; Fucose/*metabolism ; Fucosyltransferases/genetics/metabolism ; Germ-Free Life ; Glycosylation ; Goblet Cells/enzymology/immunology/microbiology ; Ileum/enzymology/immunology/microbiology ; *Immunity, Innate ; Interleukins/immunology ; Intestinal Mucosa/enzymology/*immunology/microbiology ; Lymphocytes/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Microbiota/*immunology ; Molecular Sequence Data ; Paneth Cells/enzymology/immunology/microbiology ; Salmonella Infections/*immunology/microbiology ; *Salmonella typhimurium
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  • 45
    Publication Date: 2014-04-12
    Description: Many neurologic and psychiatric disorders are marked by imbalances between neural excitation and inhibition. In the cerebral cortex, inhibition is mediated largely by GABAergic (gamma-aminobutyric acid-secreting) interneurons, a cell type that originates in the embryonic ventral telencephalon and populates the cortex through long-distance tangential migration. Remarkably, when transplanted from embryos or in vitro culture preparations, immature interneurons disperse and integrate into host brain circuits, both in the cerebral cortex and in other regions of the central nervous system. These features make interneuron transplantation a powerful tool for the study of neurodevelopmental processes such as cell specification, cell death, and cortical plasticity. Moreover, interneuron transplantation provides a novel strategy for modifying neural circuits in rodent models of epilepsy, Parkinson's disease, mood disorders, and chronic pain.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4056344/" 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/PMC4056344/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Southwell, Derek G -- Nicholas, Cory R -- Basbaum, Allan I -- Stryker, Michael P -- Kriegstein, Arnold R -- Rubenstein, John L -- Alvarez-Buylla, Arturo -- HD032116/HD/NICHD NIH HHS/ -- MH049428/MH/NIMH NIH HHS/ -- NS14627/NS/NINDS NIH HHS/ -- NS28478/NS/NINDS NIH HHS/ -- NS78326/NS/NINDS NIH HHS/ -- R01 EY002874/EY/NEI NIH HHS/ -- R01 MH049428/MH/NIMH NIH HHS/ -- R01 NS014627/NS/NINDS NIH HHS/ -- R01 NS028478/NS/NINDS NIH HHS/ -- R01 NS078326/NS/NINDS NIH HHS/ -- R01-EY02874/EY/NEI NIH HHS/ -- R37 HD032116/HD/NICHD NIH HHS/ -- T32 GM008568/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Apr 11;344(6180):1240622. doi: 10.1126/science.1240622.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurological Surgery, University of California, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24723614" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Count ; Cell Separation ; *Cell- and Tissue-Based Therapy ; Cerebral Cortex/cytology/growth & development/physiology ; *Embryonic Development ; Humans ; Interneurons/*physiology/*transplantation ; Mental Disorders/*therapy ; Mice ; Nervous System Diseases/*therapy
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  • 46
    Publication Date: 2014-12-17
    Description: Some HIV-infected individuals develop broadly neutralizing antibodies (bNAbs), whereas most develop antibodies that neutralize only a narrow range of viruses (nNAbs). bNAbs, but not nNAbs, protect animals from experimental infection and are likely a key component of an effective vaccine. nNAbs and bNAbs target the same regions of the viral envelope glycoprotein (Env), but for reasons that remain unclear only nNAbs are elicited by Env immunization. We show that in contrast to germline-reverted (gl) bNAbs, glnNAbs recognized diverse recombinant Envs. Moreover, owing to binding affinity differences, nNAb B cell progenitors had an advantage in becoming activated and internalizing Env compared with bNAb B cell progenitors. We then identified an Env modification strategy that minimized the activation of nNAb B cells targeting epitopes that overlap those of bNAbs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4290850/" 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/PMC4290850/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McGuire, Andrew T -- Dreyer, Anita M -- Carbonetti, Sara -- Lippy, Adriana -- Glenn, Jolene -- Scheid, Johannes F -- Mouquet, Hugo -- Stamatatos, Leonidas -- P01 AI094419/AI/NIAID NIH HHS/ -- P01 AI094419-01/AI/NIAID NIH HHS/ -- U19 19AI109632-01/AI/NIAID NIH HHS/ -- U19 AI109632/AI/NIAID NIH HHS/ -- Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2014 Dec 12;346(6215):1380-3. doi: 10.1126/science.1259206.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Seattle Biomedical Research Institute, Seattle, WA 98109, USA. ; Laboratory of Molecular Immunology, The Rockefeller University, New York, NY 10065, USA. ; Laboratory of Humoral Response to Pathogens, Department of Immunology, Institut Pasteur and CNRS-URA 1961, 75015 Paris, France. ; Seattle Biomedical Research Institute, Seattle, WA 98109, USA. Department of Global Health, University of Washington, Seattle, WA 98109, USA. lstamata@fhcrc.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25504724" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/immunology ; Antibodies, Neutralizing/*immunology ; Antibody Affinity ; B-Lymphocytes/immunology ; Binding, Competitive ; Epitopes/immunology ; HIV Antibodies/genetics/*immunology ; HIV-1/*immunology ; Humans ; Lymphocyte Activation ; Models, Molecular ; Receptors, Antigen, B-Cell/genetics/immunology ; Recombinant Proteins/immunology ; env Gene Products, Human Immunodeficiency Virus/chemistry/genetics/*immunology
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  • 47
    Publication Date: 2014-12-17
    Description: Sex-specific chromosomes, like the W of most female birds and the Y of male mammals, usually have lost most genes owing to a lack of recombination. We analyze newly available genomes of 17 bird species representing the avian phylogenetic range, and find that more than half of them do not have as fully degenerated W chromosomes as that of chicken. We show that avian sex chromosomes harbor tremendous diversity among species in their composition of pseudoautosomal regions and degree of Z/W differentiation. Punctuated events of shared or lineage-specific recombination suppression have produced a gradient of "evolutionary strata" along the Z chromosome, which initiates from the putative avian sex-determining gene DMRT1 and ends at the pseudoautosomal region. W-linked genes are subject to ongoing functional decay after recombination was suppressed, and the tempo of degeneration slows down in older strata. Overall, we unveil a complex history of avian sex chromosome evolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Qi -- Zhang, Jilin -- Bachtrog, Doris -- An, Na -- Huang, Quanfei -- Jarvis, Erich D -- Gilbert, M Thomas P -- Zhang, Guojie -- GM076007/GM/NIGMS NIH HHS/ -- GM093182/GM/NIGMS NIH HHS/ -- R01 GM076007/GM/NIGMS NIH HHS/ -- R01 GM093182/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Dec 12;346(6215):1246338. doi: 10.1126/science.1246338. Epub 2014 Dec 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Integrative Biology, University of California, Berkeley, CA94720, USA. zhouqi@berkeley.edu zhanggj@genomics.org.cn. ; China National Genebank, BGI-Shenzhen, Shenzhen, 518083. China. ; Department of Integrative Biology, University of California, Berkeley, CA94720, USA. ; Department of Neurobiology, Howard Hughes Medical Institute, Duke University Medical Center, Durham, NC 27710, USA. ; Centre for GeoGenetics, Natural History Museum of Denmark, University of Copenhagen, Oster Voldgade 5-7, 1350 Copenhagen, Denmark. Trace and Environmental DNA laboratory, Department of Environment and Agriculture, Curtin University, Perth, Western Australia 6102, Australia. ; China National Genebank, BGI-Shenzhen, Shenzhen, 518083. China. Centre for Social Evolution, Department of Biology, Universitetsparken 15, University of Copenhagen, DK-2100 Copenhagen, Denmark. zhouqi@berkeley.edu zhanggj@genomics.org.cn.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25504727" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avian Proteins/genetics ; *Biological Evolution ; Birds/classification/*genetics ; Chickens/genetics ; Chromosome Inversion ; Chromosome Mapping ; *Evolution, Molecular ; Female ; Male ; Phylogeny ; Recombination, Genetic ; Sex Chromosomes/*genetics ; Species Specificity ; Struthioniformes/genetics ; Synteny ; Transcription Factors/genetics
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  • 48
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-02-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blanton, Richard E -- New York, N.Y. -- Science. 2014 Jan 31;343(6170):485-6. doi: 10.1126/science.343.6170.485-b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anthropology, Purdue University, West Lafayette, IN 47907, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24482466" target="_blank"〉PubMed〈/a〉
    Keywords: *Capitalism ; Family/*history ; Female ; *Fertility ; Humans ; Plague/*history ; Women/*history ; Work/*history
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  • 49
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-02-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zimmerman, Andrew W -- Connors, Susan L -- New York, N.Y. -- Science. 2014 Feb 7;343(6171):620-1. doi: 10.1126/science.1250214.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics (Neurology), Center for Autism and Neurodevelopmental Disorders, University of Massachusetts Medical School, Worcester, MA 01655, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24503843" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/*chemically induced/*genetics ; *Cytoprotection ; Female ; Oxytocin/*metabolism ; Pregnancy ; gamma-Aminobutyric Acid/*metabolism
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  • 50
    Publication Date: 2014-03-01
    Description: Epigenetic gene silencing is seen in several repeat-expansion diseases. In fragile X syndrome, the most common genetic form of mental retardation, a CGG trinucleotide-repeat expansion adjacent to the fragile X mental retardation 1 (FMR1) gene promoter results in its epigenetic silencing. Here, we show that FMR1 silencing is mediated by the FMR1 mRNA. The FMR1 mRNA contains the transcribed CGG-repeat tract as part of the 5' untranslated region, which hybridizes to the complementary CGG-repeat portion of the FMR1 gene to form an RNA.DNA duplex. Disrupting the interaction of the mRNA with the CGG-repeat portion of the FMR1 gene prevents promoter silencing. Thus, our data link trinucleotide-repeat expansion to a form of RNA-directed gene silencing mediated by direct interactions of the trinucleotide-repeat RNA and DNA.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4357282/" 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/PMC4357282/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Colak, Dilek -- Zaninovic, Nikica -- Cohen, Michael S -- Rosenwaks, Zev -- Yang, Wang-Yong -- Gerhardt, Jeannine -- Disney, Matthew D -- Jaffrey, Samie R -- R01 GM079235/GM/NIGMS NIH HHS/ -- R01 MH80420/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2014 Feb 28;343(6174):1002-5. doi: 10.1126/science.1245831.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Weill Cornell Medical College, Cornell University, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24578575" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; DNA Methylation ; Embryonic Stem Cells/metabolism ; Fragile X Mental Retardation Protein/*genetics ; Fragile X Syndrome/*genetics ; *Gene Silencing ; Humans ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Neurons/metabolism ; Nuclear Proteins/genetics ; Promoter Regions, Genetic/genetics ; RNA, Messenger/*genetics ; RNA, Small Interfering/genetics ; Trinucleotide Repeats/*genetics
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 51
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-08-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Susiarjo, Martha -- Bartolomei, Marisa S -- P30 ES013508/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 2014 Aug 15;345(6198):733-4. doi: 10.1126/science.1258654.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. bartolom@mail.med.upenn.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25124413" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *DNA Methylation ; Female ; Fetal Nutrition Disorders/*metabolism ; Male ; Pregnancy ; *Prenatal Exposure Delayed Effects ; Spermatozoa/*metabolism
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  • 52
    Publication Date: 2014-06-07
    Description: How sleep helps learning and memory remains unknown. We report in mouse motor cortex that sleep after motor learning promotes the formation of postsynaptic dendritic spines on a subset of branches of individual layer V pyramidal neurons. New spines are formed on different sets of dendritic branches in response to different learning tasks and are protected from being eliminated when multiple tasks are learned. Neurons activated during learning of a motor task are reactivated during subsequent non-rapid eye movement sleep, and disrupting this neuronal reactivation prevents branch-specific spine formation. These findings indicate that sleep has a key role in promoting learning-dependent synapse formation and maintenance on selected dendritic branches, which contribute to memory storage.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4447313/" 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/PMC4447313/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Guang -- Lai, Cora Sau Wan -- Cichon, Joseph -- Ma, Lei -- Li, Wei -- Gan, Wen-Biao -- P01 NS074972/NS/NINDS NIH HHS/ -- R01 NS047325/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2014 Jun 6;344(6188):1173-8. doi: 10.1126/science.1249098.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skirball Institute, Department of Neuroscience and Physiology, New York University School of Medicine, New York, NY 10016, USA. Department of Anesthesiology, New York University School of Medicine, New York, NY 10016, USA. ; Skirball Institute, Department of Neuroscience and Physiology, New York University School of Medicine, New York, NY 10016, USA. ; Skirball Institute, Department of Neuroscience and Physiology, New York University School of Medicine, New York, NY 10016, USA. Drug Discovery Center, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, 518055, China. ; Drug Discovery Center, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, 518055, China. ; Skirball Institute, Department of Neuroscience and Physiology, New York University School of Medicine, New York, NY 10016, USA. gan@saturn.med.nyu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24904169" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dendritic Spines/*physiology ; Female ; Learning/*physiology ; Male ; Mice ; Mice, Mutant Strains ; Motor Cortex/*physiology ; Sleep, REM/*physiology
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  • 53
    Publication Date: 2014-10-18
    Description: Myelin-forming oligodendrocytes (OLs) are formed continuously in the healthy adult brain. In this work, we study the function of these late-forming cells and the myelin they produce. Learning a new motor skill (such as juggling) alters the structure of the brain's white matter, which contains many OLs, suggesting that late-born OLs might contribute to motor learning. Consistent with this idea, we show that production of newly formed OLs is briefly accelerated in mice that learn a new skill (running on a "complex wheel" with irregularly spaced rungs). By genetically manipulating the transcription factor myelin regulatory factor in OL precursors, we blocked production of new OLs during adulthood without affecting preexisting OLs or myelin. This prevented the mice from mastering the complex wheel. Thus, generation of new OLs and myelin is important for learning motor skills.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McKenzie, Ian A -- Ohayon, David -- Li, Huiliang -- de Faria, Joana Paes -- Emery, Ben -- Tohyama, Koujiro -- Richardson, William D -- 100269/Wellcome Trust/United Kingdom -- G0800575/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2014 Oct 17;346(6207):318-22. doi: 10.1126/science.1254960.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Wolfson Institute for Biomedical Research, University College London, Gower Street, London WC1E 6BT, UK. ; Department of Anatomy and Neuroscience and the Florey Institute for Neuroscience and Mental Health, University of Melbourne, Melbourne, Victoria 3010, Australia. ; The Center for Electron Microscopy and Bio-Imaging Research, Iwate Medical University, 19-1 Uchimuru, Morioka, Iwate 020-8505, Japan. ; The Wolfson Institute for Biomedical Research, University College London, Gower Street, London WC1E 6BT, UK. w.richardson@ucl.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25324381" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*cytology/metabolism ; *Cell Proliferation ; Gene Deletion ; Humans ; *Learning ; Male ; Mental Recall ; Mice ; Mice, Transgenic ; Motor Skills/*physiology ; Myelin Sheath/genetics/*metabolism ; Oligodendroglia/cytology/metabolism/*physiology ; Synaptic Transmission ; Transcription Factors/genetics/metabolism
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  • 54
    Publication Date: 2014-05-17
    Description: Environmental exposures affect gamete function and fertility, but the mechanisms are poorly understood. Here, we show that pheromones sensed by ciliated neurons in the Caenorhabditis elegans nose alter the lipid microenvironment within the oviduct, thereby affecting sperm motility. In favorable environments, pheromone-responsive sensory neurons secrete a transforming growth factor-beta ligand called DAF-7, which acts as a neuroendocrine factor that stimulates prostaglandin-endoperoxide synthase [cyclooxygenase (Cox)]-independent prostaglandin synthesis in the ovary. Oocytes secrete F-class prostaglandins that guide sperm toward them. These prostaglandins are also synthesized in Cox knockout mice, raising the possibility that similar mechanisms exist in other animals. Our data indicate that environmental cues perceived by the female nervous system affect sperm function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4094289/" 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/PMC4094289/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McKnight, Katherine -- Hoang, Hieu D -- Prasain, Jeevan K -- Brown, Naoko -- Vibbert, Jack -- Hollister, Kyle A -- Moore, Ray -- Ragains, Justin R -- Reese, Jeff -- Miller, Michael A -- GM085105/GM/NIGMS NIH HHS/ -- HL096967/HL/NHLBI NIH HHS/ -- HL109199/HL/NHLBI NIH HHS/ -- HL110950/HL/NHLBI NIH HHS/ -- HL114439/HL/NHLBI NIH HHS/ -- P30 AR050948/AR/NIAMS NIH HHS/ -- P30 DK079337/DK/NIDDK NIH HHS/ -- P40 OD010440/OD/NIH HHS/ -- R01 GM085105/GM/NIGMS NIH HHS/ -- R01 HL096967/HL/NHLBI NIH HHS/ -- R01 HL109199/HL/NHLBI NIH HHS/ -- S10 RR19261/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2014 May 16;344(6185):754-7. doi: 10.1126/science.1250598.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University of Alabama at Birmingham, Birmingham, AL 35294, USA. ; Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA. ; Department of Pharmacology and Toxicology, University of Alabama at Birmingham, Birmingham, AL 35294, USA. ; Department of Pediatrics, Vanderbilt University, Nashville, TN 37232, USA. ; Department of Chemistry, Louisiana State University, Baton Rouge, LA 70803, USA. ; Department of Pediatrics, Vanderbilt University, Nashville, TN 37232, USA. Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN 37232, USA. ; Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA. mamiller@uab.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24833393" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/genetics/metabolism/*physiology ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Environmental Exposure ; Female ; *Fertilization ; Male ; Neurons, Afferent/*physiology ; Neurosecretory Systems/physiology ; Oocytes/metabolism/physiology ; Ovum/metabolism/physiology ; Perception ; Pheromones/*physiology ; Prostaglandin-Endoperoxide Synthases/metabolism ; Prostaglandins/biosynthesis ; *Sperm Motility ; Spermatozoa/*physiology ; Transforming Growth Factor beta/genetics/*metabolism
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  • 55
    Publication Date: 2014-02-08
    Description: Cellular responses elicited by cell surface receptors differ according to stimulus strength. We investigated how the high-affinity receptor for immunoglobulin E (IgE) modulates the response of mast cells to a high- or low-affinity stimulus. Both high- and low-affinity stimuli elicited similar receptor phosphorylation; however, differences were observed in receptor cluster size, mobility, distribution, and the cells' effector responses. Low-affinity stimulation increased receptor association with the Src family kinase Fgr and shifted signals from the adapter LAT1 to the related adapter LAT2. LAT1-dependent calcium signals required for mast cell degranulation were dampened, but the role of LAT2 in chemokine production was enhanced, altering immune cell recruitment at the site of inflammation. These findings uncover how receptor discrimination of stimulus strength can be interpreted as distinct in vivo outcomes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4188507/" 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/PMC4188507/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suzuki, Ryo -- Leach, Sarah -- Liu, Wenhua -- Ralston, Evelyn -- Scheffel, Jorg -- Zhang, Weiguo -- Lowell, Clifford A -- Rivera, Juan -- R01 AI065495/AI/NIAID NIH HHS/ -- R01 AI068150/AI/NIAID NIH HHS/ -- ZIA AR041101-20/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2014 Feb 28;343(6174):1021-5. doi: 10.1126/science.1246976. Epub 2014 Feb 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunogenetics, National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24505132" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; Amino Acid Transport System y+/metabolism ; Animals ; Antigens, CD98 Light Chains/metabolism ; Cattle ; Cell Movement ; Chemokines/metabolism ; Dinitrophenols ; Immunoglobulin E/*metabolism ; Inflammation/immunology ; Mast Cells/*immunology ; Membrane Proteins/metabolism ; Mice ; Phosphoproteins/metabolism ; Proto-Oncogene Proteins/metabolism ; Receptors, IgE/*metabolism ; src-Family Kinases/metabolism
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  • 56
    Publication Date: 2014-12-06
    Description: Immune and inflammatory responses require leukocytes to migrate within and through the vasculature, a process that is facilitated by their capacity to switch to a polarized morphology with an asymmetric distribution of receptors. We report that neutrophil polarization within activated venules served to organize a protruding domain that engaged activated platelets present in the bloodstream. The selectin ligand PSGL-1 transduced signals emanating from these interactions, resulting in the redistribution of receptors that drive neutrophil migration. Consequently, neutrophils unable to polarize or to transduce signals through PSGL-1 displayed aberrant crawling, and blockade of this domain protected mice against thromboinflammatory injury. These results reveal that recruited neutrophils scan for activated platelets, and they suggest that the neutrophils' bipolarity allows the integration of signals present at both the endothelium and the circulation before inflammation proceeds.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4280847/" 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/PMC4280847/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sreeramkumar, Vinatha -- Adrover, Jose M -- Ballesteros, Ivan -- Cuartero, Maria Isabel -- Rossaint, Jan -- Bilbao, Izaskun -- Nacher, Maria -- Pitaval, Christophe -- Radovanovic, Irena -- Fukui, Yoshinori -- McEver, Rodger P -- Filippi, Marie-Dominique -- Lizasoain, Ignacio -- Ruiz-Cabello, Jesus -- Zarbock, Alexander -- Moro, Maria A -- Hidalgo, Andres -- HL03463/HL/NHLBI NIH HHS/ -- HL085607/HL/NHLBI NIH HHS/ -- HL090676/HL/NHLBI NIH HHS/ -- P01 HL085607/HL/NHLBI NIH HHS/ -- R01 HL034363/HL/NHLBI NIH HHS/ -- R01 HL090676/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2014 Dec 5;346(6214):1234-8. doi: 10.1126/science.1256478. Epub 2014 Dec 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Atherothrombosis, Imaging and Epidemiology, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain. ; Unidad de Investigacion Neurovascular, Department of Pharmacology, Faculty of Medicine, Universidad Complutense and Instituto de Investigacion Hospital 12 de Octubre (i+12), Madrid, Spain. ; Department of Anesthesiology and Critical Care Medicine, University of Munster and Max Planck Institute Munster, Munster, Germany. ; Department of Atherothrombosis, Imaging and Epidemiology, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain. Ciber de Enfermedades Respiratorias (CIBERES), Madrid, Spain. ; Department of Atherothrombosis, Imaging and Epidemiology, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain. Faculty of Science, Medicine and Health, University of Wollongong, New South Wales, Australia. ; Division of Immunogenetics, Department of Immunobiology and Neuroscience, Kyushu University, Japan. ; Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA. ; Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Research Foundation, University of Cincinnati College of Medicine, Cincinnati, OH, USA. ; Department of Atherothrombosis, Imaging and Epidemiology, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain. Institute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany. ahidalgo@cnic.es.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25477463" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Circulation ; Blood Platelets/*immunology ; Cell Movement ; Cell Polarity ; Endothelium, Vascular/immunology ; Inflammation/blood/*immunology ; Male ; Membrane Glycoproteins ; Mice ; Mice, Inbred C57BL ; Neutrophils/*immunology ; *Platelet Activation ; Signal Transduction ; Thrombosis/*immunology ; Venules/immunology
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  • 57
    Publication Date: 2014-10-11
    Description: Tyzio et al. (Reports, 7 February 2014, p. 675) reported that bumetanide restored the impaired oxytocin-mediated gamma-aminobutyric acid (GABA) excitatory-inhibitory shift during delivery in animal models of autism, ameliorating some autistic-like characteristics in the offspring. However, standard practices in the study of these models, such as the use of sex-dimorphic or males-only analyses and implementation of tests measuring social behavior, are lacking to definitely associate their findings to autism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bambini-Junior, Victorio -- Nunes, Gustavo Della Flora -- Schneider, Tomasz -- Gottfried, Carmem -- New York, N.Y. -- Science. 2014 Oct 10;346(6206):176. doi: 10.1126/science.1255679.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Federal University of Rio Grande do Sul, Research Group in Neuroglial Plasticity at the Department of Biochemistry, Institute of Health's Basic Science, Porto Alegre, Rio Grande do Sul, Brazil. Federal University of Rio Grande do Sul, Translational Research Group in Autism Spectrum Disorders (GETTEA), Porto Alegre, RS, Brazil. victoriobambini@gmail.com. ; Federal University of Rio Grande do Sul, Research Group in Neuroglial Plasticity at the Department of Biochemistry, Institute of Health's Basic Science, Porto Alegre, Rio Grande do Sul, Brazil. Federal University of Rio Grande do Sul, Translational Research Group in Autism Spectrum Disorders (GETTEA), Porto Alegre, RS, Brazil. ; School of Medicine, Pharmacy and Health, TS17 6BH, Durham University, Durham, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25301610" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/*chemically induced/*genetics ; *Cytoprotection ; Female ; Oxytocin/*metabolism ; Pregnancy ; gamma-Aminobutyric Acid/*metabolism
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  • 58
    Publication Date: 2014-10-25
    Description: During cell entry, capsids of incoming influenza A viruses (IAVs) must be uncoated before viral ribonucleoproteins (vRNPs) can enter the nucleus for replication. After hemagglutinin-mediated membrane fusion in late endocytic vacuoles, the vRNPs and the matrix proteins dissociate from each other and disperse within the cytosol. Here, we found that for capsid disassembly, IAV takes advantage of the host cell's aggresome formation and disassembly machinery. The capsids mimicked misfolded protein aggregates by carrying unanchored ubiquitin chains that activated a histone deacetylase 6 (HDAC6)-dependent pathway. The ubiquitin-binding domain was essential for recruitment of HDAC6 to viral fusion sites and for efficient uncoating and infection. That other components of the aggresome processing machinery, including dynein, dynactin, and myosin II, were also required suggested that physical forces generated by microtubule- and actin-associated motors are essential for IAV entry.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Banerjee, Indranil -- Miyake, Yasuyuki -- Nobs, Samuel Philip -- Schneider, Christoph -- Horvath, Peter -- Kopf, Manfred -- Matthias, Patrick -- Helenius, Ari -- Yamauchi, Yohei -- New York, N.Y. -- Science. 2014 Oct 24;346(6208):473-7. doi: 10.1126/science.1257037.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Biochemistry, Eidgenossische Technische Hochschule (ETH) Zurich, Switzerland. ; Epigenetics, Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland. ; Institute of Molecular Health Sciences, ETH Zurich, Switzerland. ; Synthetic and Systems Biology Unit, Biological Research Center, Szeged, Hungary. ; Epigenetics, Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland. Faculty of Sciences, University of Basel, Basel, Switzerland. ; Institute of Biochemistry, Eidgenossische Technische Hochschule (ETH) Zurich, Switzerland. ari.helenius@bc.biol.ethz.ch yohei.yamauchi@bc.biol.ethz.ch.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25342804" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Capsid/*metabolism ; Cell Line, Tumor ; Cell Nucleus/virology ; Dyneins/metabolism ; Gene Knockout Techniques ; Histone Deacetylases/genetics/*physiology ; Host-Pathogen Interactions ; Humans ; Influenza A virus/*physiology ; Influenza, Human/genetics/metabolism/*virology ; Membrane Fusion/genetics/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Microtubule-Associated Proteins/metabolism ; Microtubules/metabolism ; Myosin Type II/metabolism ; Protein Binding ; Protein Folding ; Protein Structure, Tertiary ; RNA Interference ; Ribonucleoproteins/metabolism ; Ubiquitin/chemistry/metabolism ; *Virus Internalization ; Virus Replication
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  • 59
    Publication Date: 2014-05-24
    Description: Novel vaccines are urgently needed to reduce the burden of severe malaria. Using a differential whole-proteome screening method, we identified Plasmodium falciparum schizont egress antigen-1 (PfSEA-1), a 244-kilodalton parasite antigen expressed in schizont-infected red blood cells (RBCs). Antibodies to PfSEA-1 decreased parasite replication by arresting schizont rupture, and conditional disruption of PfSEA-1 resulted in a profound parasite replication defect. Vaccination of mice with recombinant Plasmodium berghei PbSEA-1 significantly reduced parasitemia and delayed mortality after lethal challenge with the Plasmodium berghei strain ANKA. Tanzanian children with antibodies to recombinant PfSEA-1A (rPfSEA-1A) did not experience severe malaria, and Kenyan adolescents and adults with antibodies to rPfSEA-1A had significantly lower parasite densities than individuals without these antibodies. By blocking schizont egress, PfSEA-1 may synergize with other vaccines targeting hepatocyte and RBC invasion.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4184151/" 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/PMC4184151/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raj, Dipak K -- Nixon, Christian P -- Nixon, Christina E -- Dvorin, Jeffrey D -- DiPetrillo, Christen G -- Pond-Tor, Sunthorn -- Wu, Hai-Wei -- Jolly, Grant -- Pischel, Lauren -- Lu, Ailin -- Michelow, Ian C -- Cheng, Ling -- Conteh, Solomon -- McDonald, Emily A -- Absalon, Sabrina -- Holte, Sarah E -- Friedman, Jennifer F -- Fried, Michal -- Duffy, Patrick E -- Kurtis, Jonathan D -- 1K08AI100997-01A1/AI/NIAID NIH HHS/ -- DP2 AI112219/AI/NIAID NIH HHS/ -- DP2-AI112219/AI/NIAID NIH HHS/ -- K08 AI100997/AI/NIAID NIH HHS/ -- P20GM103421/GM/NIGMS NIH HHS/ -- P30 AI042853/AI/NIAID NIH HHS/ -- P30AI042853/AI/NIAID NIH HHS/ -- R01 AI102907/AI/NIAID NIH HHS/ -- R01-AI076353/AI/NIAID NIH HHS/ -- R01-AI102907/AI/NIAID NIH HHS/ -- R01-AI52059/AI/NIAID NIH HHS/ -- T32-DA013911/DA/NIDA NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2014 May 23;344(6186):871-7. doi: 10.1126/science.1254417.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for International Health Research, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02903, USA. ; Division of Infectious Diseases, Boston Children's Hospital and Harvard Medical School, Boston, MA 02115, USA. ; Center for International Health Research, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02903, USA. Department of Pediatrics, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02903, USA. ; Department of Pathology and Laboratory Medicine, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02906, USA. ; Laboratory of Malaria Immunology and Vaccinology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20892, USA. ; Fred Hutchinson Cancer Research Center Program in Biostatistics and Biomathematics, Department of Biostatistics and Global Health, University of Washington, Seattle, WA 98109, USA. ; Center for International Health Research, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02903, USA. Department of Pathology and Laboratory Medicine, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02906, USA. jonathan_kurtis@brown.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24855263" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Animals ; Antibodies, Protozoan/blood/*immunology ; Antigens, Protozoan/*immunology ; Child ; Erythrocytes/*parasitology ; Hepatocytes/immunology/parasitology ; Humans ; Immunoglobulin G/blood/immunology ; Kenya ; Malaria/prevention & control ; Malaria Vaccines/*immunology ; Malaria, Falciparum/*prevention & control ; Mice ; Plasmodium berghei/immunology ; Plasmodium falciparum/*growth & development/immunology ; Protozoan Proteins/*immunology ; Recombinant Proteins/immunology ; Schizonts/*growth & development ; Young Adult
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  • 60
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-01-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Vrieze, Jop -- New York, N.Y. -- Science. 2014 Jan 17;343(6168):241-3. doi: 10.1126/science.343.6168.241.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24436401" target="_blank"〉PubMed〈/a〉
    Keywords: Anthropology ; Diabetes Mellitus, Type 1/immunology/microbiology ; Feces/microbiology ; Female ; Gastrointestinal Tract/*microbiology ; Germ-Free Life ; Health ; Humans ; *Life Style ; Male ; Meat/microbiology ; *Microbiota ; Tanzania
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  • 61
    Publication Date: 2014-05-09
    Description: Cross-cultural psychologists have mostly contrasted East Asia with the West. However, this study shows that there are major psychological differences within China. We propose that a history of farming rice makes cultures more interdependent, whereas farming wheat makes cultures more independent, and these agricultural legacies continue to affect people in the modern world. We tested 1162 Han Chinese participants in six sites and found that rice-growing southern China is more interdependent and holistic-thinking than the wheat-growing north. To control for confounds like climate, we tested people from neighboring counties along the rice-wheat border and found differences that were just as large. We also find that modernization and pathogen prevalence theories do not fit the data.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Talhelm, T -- Zhang, X -- Oishi, S -- Shimin, C -- Duan, D -- Lan, X -- Kitayama, S -- New York, N.Y. -- Science. 2014 May 9;344(6184):603-8. doi: 10.1126/science.1246850.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University of Virginia, Charlottesville, VA 22904, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24812395" target="_blank"〉PubMed〈/a〉
    Keywords: *Agriculture ; Asian Continental Ancestry Group/*psychology ; China ; Female ; Humans ; *Individuation ; Male ; *Oryza ; *Triticum
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  • 62
    Publication Date: 2014-08-02
    Description: During limb development, digits emerge from the undifferentiated mesenchymal tissue that constitutes the limb bud. It has been proposed that this process is controlled by a self-organizing Turing mechanism, whereby diffusible molecules interact to produce a periodic pattern of digital and interdigital fates. However, the identities of the molecules remain unknown. By combining experiments and modeling, we reveal evidence that a Turing network implemented by Bmp, Sox9, and Wnt drives digit specification. We develop a realistic two-dimensional simulation of digit patterning and show that this network, when modulated by morphogen gradients, recapitulates the expression patterns of Sox9 in the wild type and in perturbation experiments. Our systems biology approach reveals how a combination of growth, morphogen gradients, and a self-organizing Turing network can achieve robust and reproducible pattern formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raspopovic, J -- Marcon, L -- Russo, L -- Sharpe, J -- New York, N.Y. -- Science. 2014 Aug 1;345(6196):566-70. doi: 10.1126/science.1252960.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Systems Biology Program, Centre for Genomic Regulation (CRG), and Universitat Pompeu Fabra (UPF), Dr. Aiguader 88, 08003 Barcelona, Spain. ; Systems Biology Program, Centre for Genomic Regulation (CRG), and Universitat Pompeu Fabra (UPF), Dr. Aiguader 88, 08003 Barcelona, Spain. Institucio Catalana de Recerca i Estudis Avancats (ICREA), Passeig Lluis Companys 23, 08010 Barcelona, Spain. james.sharpe@crg.eu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25082703" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Patterning/*genetics ; Bone Morphogenetic Proteins/*metabolism ; Computer Simulation ; Extremities/*embryology ; Female ; *Gene Expression Regulation, Developmental ; Gene Knockdown Techniques ; Green Fluorescent Proteins/genetics/metabolism ; Limb Buds/*embryology ; Mice ; Mice, Inbred Strains ; Models, Biological ; Oligonucleotide Array Sequence Analysis ; SOX9 Transcription Factor/genetics/*metabolism ; Wnt Proteins/*metabolism
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  • 63
    Publication Date: 2014-02-01
    Description: Genetic errors in meiosis can lead to birth defects and spontaneous abortions. Checkpoint mechanisms of hitherto unknown nature eliminate oocytes with unrepaired DNA damage, causing recombination-defective mutant mice to be sterile. Here, we report that checkpoint kinase 2 (Chk2 or Chek2), is essential for culling mouse oocytes bearing unrepaired meiotic or induced DNA double-strand breaks (DSBs). Female infertility caused by a meiotic recombination mutation or irradiation was reversed by mutation of Chk2. Both meiotically programmed and induced DSBs trigger CHK2-dependent activation of TRP53 (p53) and TRP63 (p63), effecting oocyte elimination. These data establish CHK2 as essential for DNA damage surveillance in female meiosis and indicate that the oocyte DSB damage response primarily involves a pathway hierarchy in which ataxia telangiectasia and Rad3-related (ATR) signals to CHK2, which then activates p53 and p63.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4048839/" 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/PMC4048839/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bolcun-Filas, Ewelina -- Rinaldi, Vera D -- White, Michelle E -- Schimenti, John C -- GM45415/GM/NIGMS NIH HHS/ -- R01 GM045415/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Jan 31;343(6170):533-6. doi: 10.1126/science.1247671.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biomedical Sciences, Cornell University, Ithaca, NY 14850, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24482479" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/genetics/metabolism ; Animals ; Cell Cycle Proteins/genetics/metabolism ; Checkpoint Kinase 2/genetics/*physiology ; *DNA Breaks, Double-Stranded ; Female ; HeLa Cells ; Humans ; Infertility, Female/*genetics/pathology ; Meiosis/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Oocytes/*metabolism/pathology ; Phosphoproteins/*metabolism ; Trans-Activators/*metabolism ; Tumor Suppressor Protein p53/*metabolism
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  • 64
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-08-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McNutt, Marcia -- New York, N.Y. -- Science. 2014 Aug 15;345(6198):739. doi: 10.1126/science.345.6198.739-b. Epub 2014 Aug 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Editor-in-Chief.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25124417" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; *HIV Infections ; Humans ; Male ; *Periodicals as Topic ; *Sex Workers ; *Transgender Persons
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  • 65
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-03-29
    Description: The existence of BRCA1 was proven in 1990 by mapping predisposition to young-onset breast cancer in families to chromosome 17q21. Knowing that such a gene existed and approximately where it lay triggered efforts by public and private groups to clone and sequence it. The press baptized the competition "the race" and reported on it in detail for the next 4 years. BRCA1 was positionally cloned in September 1994. Twenty years later, I reflect on "the race" and its consequences for breast cancer prevention and treatment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉King, Mary-Claire -- R01 CA157744/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2014 Mar 28;343(6178):1462-5. doi: 10.1126/science.1251900.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine and Department of Genome Sciences, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24675952" target="_blank"〉PubMed〈/a〉
    Keywords: BRCA1 Protein/*genetics/history ; Breast Neoplasms/*genetics/history ; Chromosome Mapping ; Chromosomes, Human, Pair 17/*genetics ; Cloning, Molecular ; Female ; Genetic Linkage ; History, 20th Century ; Humans
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  • 66
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-09-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉You, Jia -- New York, N.Y. -- Science. 2014 Sep 19;345(6203):1440-1. doi: 10.1126/science.345.6203.1440.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25237081" target="_blank"〉PubMed〈/a〉
    Keywords: *Communication ; Female ; Humans ; Male ; Research Personnel/*classification/*psychology ; *Science ; Sex Factors ; *Social Media
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  • 67
    Publication Date: 2014-08-12
    Description: Phospholipids (PLs) with polyunsaturated acyl chains are extremely abundant in a few specialized cellular organelles such as synaptic vesicles and photoreceptor discs, but their effect on membrane properties is poorly understood. Here, we found that polyunsaturated PLs increased the ability of dynamin and endophilin to deform and vesiculate synthetic membranes. When cells incorporated polyunsaturated fatty acids into PLs, the plasma membrane became more amenable to deformation by a pulling force and the rate of endocytosis was accelerated, in particular, under conditions in which cholesterol was limiting. Molecular dynamics simulations and biochemical measurements indicated that polyunsaturated PLs adapted their conformation to membrane curvature. Thus, by reducing the energetic cost of membrane bending and fission, polyunsaturated PLs may help to support rapid endocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pinot, Mathieu -- Vanni, Stefano -- Pagnotta, Sophie -- Lacas-Gervais, Sandra -- Payet, Laurie-Anne -- Ferreira, Thierry -- Gautier, Romain -- Goud, Bruno -- Antonny, Bruno -- Barelli, Helene -- New York, N.Y. -- Science. 2014 Aug 8;345(6197):693-7. doi: 10.1126/science.1255288.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Pharmacologie Moleculaire et Cellulaire, Universite Nice Sophia Antipolis and CNRS, 06560 Valbonne, France. Unite Mixte de Recherche 144, Institut Curie and CNRS, F-75248 Paris, France. ; Institut de Pharmacologie Moleculaire et Cellulaire, Universite Nice Sophia Antipolis and CNRS, 06560 Valbonne, France. ; Centre Commun de Microscopie Appliquee, Universite Nice Sophia Antipolis, Parc Valrose, 06000 Nice, France. ; Signalisation et Transports Ioniques Membranaires, Universite de Poitiers and CNRS, Poitiers, France. ; Unite Mixte de Recherche 144, Institut Curie and CNRS, F-75248 Paris, France. ; Institut de Pharmacologie Moleculaire et Cellulaire, Universite Nice Sophia Antipolis and CNRS, 06560 Valbonne, France. antonny@ipmc.cnrs.fr.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25104391" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/chemistry/metabolism ; Animals ; Cell Line, Tumor ; Cell Membrane/chemistry/*physiology ; Dynamins/chemistry/metabolism ; *Endocytosis ; Fatty Acids, Unsaturated/chemistry/*physiology ; Humans ; Membranes, Artificial ; Mice ; Molecular Dynamics Simulation
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  • 68
    Publication Date: 2014-05-24
    Description: Cushing's syndrome is caused by excess cortisol production from the adrenocortical gland. In corticotropin-independent Cushing's syndrome, the excess cortisol production is primarily attributed to an adrenocortical adenoma, in which the underlying molecular pathogenesis has been poorly understood. We report a hotspot mutation (L206R) in PRKACA, which encodes the catalytic subunit of cyclic adenosine monophosphate (cAMP)-dependent protein kinase (PKA), in more than 50% of cases with adrenocortical adenomas associated with corticotropin-independent Cushing's syndrome. The L206R PRKACA mutant abolished its binding to the regulatory subunit of PKA (PRKAR1A) that inhibits catalytic activity of PRKACA, leading to constitutive, cAMP-independent PKA activation. These results highlight the major role of cAMP-independent activation of cAMP/PKA signaling by somatic mutations in corticotropin-independent Cushing's syndrome, providing insights into the diagnosis and therapeutics of this syndrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sato, Yusuke -- Maekawa, Shigekatsu -- Ishii, Ryohei -- Sanada, Masashi -- Morikawa, Teppei -- Shiraishi, Yuichi -- Yoshida, Kenichi -- Nagata, Yasunobu -- Sato-Otsubo, Aiko -- Yoshizato, Tetsuichi -- Suzuki, Hiromichi -- Shiozawa, Yusuke -- Kataoka, Keisuke -- Kon, Ayana -- Aoki, Kosuke -- Chiba, Kenichi -- Tanaka, Hiroko -- Kume, Haruki -- Miyano, Satoru -- Fukayama, Masashi -- Nureki, Osamu -- Homma, Yukio -- Ogawa, Seishi -- New York, N.Y. -- Science. 2014 May 23;344(6186):917-20. doi: 10.1126/science.1252328.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan. Department of Urology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. ; Department of Urology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. ; Department of Biophysics and Biochemistry, Graduate School of Science, The University of Tokyo, Tokyo, Japan. ; Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan. ; Department of Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. ; Laboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan. ; Laboratory of Sequence Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan. ; Laboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan. Laboratory of Sequence Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan. ; Department of Urology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. sogawa-tky@umin.ac.jp homma-uro@umin.ac.jp. ; Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan. sogawa-tky@umin.ac.jp homma-uro@umin.ac.jp.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24855271" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Cortex Neoplasms/*genetics ; Adrenocortical Adenoma/*genetics ; Adrenocorticotropic Hormone/metabolism ; Animals ; Catalytic Domain/genetics ; Cushing Syndrome/*genetics/metabolism ; Cyclic AMP-Dependent Protein Kinase Catalytic Subunits/*genetics/metabolism ; DNA Mutational Analysis ; GTP-Binding Protein alpha Subunits/genetics ; HEK293 Cells ; Humans ; Mice ; Mutation ; NIH 3T3 Cells ; PC12 Cells ; Rats
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  • 69
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-03-29
    Description: Germline mutations in BRCA1 and BRCA2 predispose to common human malignancies, most notably tumors of the breast and ovaries. The proteins encoded by these genes have been implicated in a plethora of biochemical interactions and biological functions, confounding attempts to coherently explain how their inactivation promotes carcinogenesis. Here, I argue that tumor suppression by BRCA1 and BRCA2 originates from their fundamental role in controlling the assembly and activity of macromolecular complexes that monitor chromosome duplication, maintenance, and segregation across the cell cycle. A tumor-suppressive role for the BRCA proteins as "chromosome custodians" helps to explain the clinical features of cancer susceptibility after their inactivation, provides foundations for the rational therapy of BRCA-deficient cancers, and offers general insights into the mechanisms opposing early steps in human carcinogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Venkitaraman, Ashok R -- G1001521/Medical Research Council/United Kingdom -- G1001522/Medical Research Council/United Kingdom -- MC_U105359877/Medical Research Council/United Kingdom -- MC_UU_12022/1/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2014 Mar 28;343(6178):1470-5. doi: 10.1126/science.1252230.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Cancer Unit, University of Cambridge, Hills Road, Cambridge CB2 0XZ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24675954" target="_blank"〉PubMed〈/a〉
    Keywords: BRCA1 Protein/genetics/*physiology ; BRCA2 Protein/genetics/*physiology ; Breast Neoplasms/*genetics/pathology ; Carcinogenesis/genetics ; Chromosomal Instability ; Chromosome Aberrations ; Female ; Genes, Tumor Suppressor/*physiology ; Germ-Line Mutation ; Humans ; Models, Genetic ; Organ Specificity/genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 70
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-08-16
    Description: Parental care, including feeding and protection of young, is essential for the survival as well as mental and physical well-being of the offspring. A large variety of parental behaviors has been described across species and sexes, raising fascinating questions about how animals identify the young and how brain circuits drive and modulate parental displays in males and females. Recent studies have begun to uncover a striking antagonistic interplay between brain systems underlying parental care and infant-directed aggression in both males and females, as well as a large range of intrinsic and environmentally driven neural modulation and plasticity. Improved understanding of the neural control of parental interactions in animals should provide novel insights into the complex issue of human parental care in both health and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4230532/" 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/PMC4230532/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dulac, Catherine -- O'Connell, Lauren A -- Wu, Zheng -- R01 DC009019/DC/NIDCD NIH HHS/ -- R01 DC013087/DC/NIDCD NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Aug 15;345(6198):765-70. doi: 10.1126/science.1253291. Epub 2014 Aug 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular and Cellular Biology, Center for Brain Science, Harvard University, Cambridge, MA 02138, USA. dulac@fas.harvard.edu. ; FAS Center for System Biology, Harvard University, Cambridge, MA 02138, USA. ; Howard Hughes Medical Institute, Department of Molecular and Cellular Biology, Center for Brain Science, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25124430" target="_blank"〉PubMed〈/a〉
    Keywords: Aggression ; Animals ; Biological Evolution ; Brain/*physiology ; Cues ; Female ; Humans ; Male ; Maternal Behavior/*physiology ; Models, Neurological ; Neural Pathways/physiology ; Neurons/physiology ; *Parenting ; Paternal Behavior/*physiology ; Sensation/*physiology
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  • 71
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-03-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nilsen, Timothy W -- New York, N.Y. -- Science. 2014 Mar 14;343(6176):1207-8. doi: 10.1126/science.1249340.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for RNA Molecular Biology, Case Western Reserve University School of Medicine, 10900 Euclid Avenue, Cleveland, OH 44106, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24626918" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/*metabolism ; Animals ; Cell Nucleus/enzymology ; Cytoplasm/enzymology ; Dioxygenases/genetics/metabolism ; Gene Knockdown Techniques ; Humans ; Membrane Proteins/genetics/metabolism ; Methylation ; Methyltransferases/genetics/metabolism ; Mice ; Proteins/genetics/metabolism ; *RNA Stability ; RNA, Messenger/*metabolism ; RNA-Binding Proteins/genetics/metabolism ; *Transcription, Genetic
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  • 72
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-06-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morell, Virginia -- New York, N.Y. -- Science. 2014 Jun 20;344(6190):1334-7. doi: 10.1126/science.344.6190.1334.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24948718" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chiroptera/*physiology ; Female ; Humans ; Male ; Sexual Behavior, Animal/*physiology ; Speech/physiology/radiation effects ; *Vocalization, Animal
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  • 73
    Publication Date: 2014-12-06
    Description: The prevention of fertilization through self-pollination (or pollination by a close relative) in the Brassicaceae plant family is determined by the genotype of the plant at the self-incompatibility locus (S locus). The many alleles at this locus exhibit a dominance hierarchy that determines which of the two allelic specificities of a heterozygous genotype is expressed at the phenotypic level. Here, we uncover the evolution of how at least 17 small RNA (sRNA)-producing loci and their multiple target sites collectively control the dominance hierarchy among alleles within the gene controlling the pollen S-locus phenotype in a self-incompatible Arabidopsis species. Selection has created a dynamic repertoire of sRNA-target interactions by jointly acting on sRNA genes and their target sites, which has resulted in a complex system of regulation among alleles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Durand, Eleonore -- Meheust, Raphael -- Soucaze, Marion -- Goubet, Pauline M -- Gallina, Sophie -- Poux, Celine -- Fobis-Loisy, Isabelle -- Guillon, Eline -- Gaude, Thierry -- Sarazin, Alexis -- Figeac, Martin -- Prat, Elisa -- Marande, William -- Berges, Helene -- Vekemans, Xavier -- Billiard, Sylvain -- Castric, Vincent -- New York, N.Y. -- Science. 2014 Dec 5;346(6214):1200-5. doi: 10.1126/science.1259442.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire Genetique et Evolution des Populations Vegetales, CNRS UMR 8198, Universite Lille 1, F-59655 Villeneuve d'Ascq cedex, France. ; Reproduction et Developpement des Plantes, Institut Federatif de Recherche 128, Centre National de la Recherche Scientifique, Institut National de la Recherche Agronomique, Universite Claude Bernard Lyon I, Ecole Normale Superieure de Lyon, F-69364 Lyon, Cedex 07, France. ; Department of Biology, Swiss Federal Institute of Technology Zurich, CH-8093 Zurich, Switzerland. ; UDSL Universite Lille 2 Droit et Sante, and Plate-forme de genomique fonctionnelle et structurale IFR-114, F-59000 Lille, France. ; Centre National des Ressources Genomiques Vegetales, INRA UPR 1258, Castanet-Tolosan, France. ; Laboratoire Genetique et Evolution des Populations Vegetales, CNRS UMR 8198, Universite Lille 1, F-59655 Villeneuve d'Ascq cedex, France. vincent.castric@univ-lille1.fr.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25477454" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Arabidopsis/*genetics ; *Biological Evolution ; *Gene Expression Regulation, Plant ; *Gene Regulatory Networks ; *Genes, Dominant ; *Genes, Recessive ; Genetic Loci ; Models, Molecular ; Phylogeny ; Pollination ; RNA, Small Untranslated/classification/*genetics ; Selection, Genetic
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  • 74
    Publication Date: 2014-06-14
    Description: The peripheral autonomic nervous system reaches far throughout the body and includes neurons of diverse functions, such as sympathetic and parasympathetic. We show that the parasympathetic system in mice--including trunk ganglia and the cranial ciliary, pterygopalatine, lingual, submandibular, and otic ganglia--arise from glial cells in nerves, not neural crest cells. The parasympathetic fate is induced in nerve-associated Schwann cell precursors at distal peripheral sites. We used multicolor Cre-reporter lineage tracing to show that most of these neurons arise from bi-potent progenitors that generate both glia and neurons. This nerve origin places cellular elements for generating parasympathetic neurons in diverse tissues and organs, which may enable wiring of the developing parasympathetic nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dyachuk, Vyacheslav -- Furlan, Alessandro -- Shahidi, Maryam Khatibi -- Giovenco, Marcela -- Kaukua, Nina -- Konstantinidou, Chrysoula -- Pachnis, Vassilis -- Memic, Fatima -- Marklund, Ulrika -- Muller, Thomas -- Birchmeier, Carmen -- Fried, Kaj -- Ernfors, Patrik -- Adameyko, Igor -- MC_U117537087/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2014 Jul 4;345(6192):82-7. doi: 10.1126/science.1253281. Epub 2014 Jun 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unit of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden. A.V. Zhirmunsky Institute of Marine Biology of the Far Eastern Branch of the Russian Academy of Sciences, Vladivostok, Russia. ; Unit of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden. ; Department of Dental Medicine, Karolinska Institutet, Stockholm, Sweden. ; Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden. ; Division of Molecular Neurobiology, Medical Research Council (MRC) National Institute for Medical Research, London, UK. ; Department of Neuroscience, The Max Delbruck Center for Molecular Medicine, Berlin-Buch, Germany. ; Unit of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden. igor.adameyko@ki.se patrik.ernfors@ki.se. ; Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden. igor.adameyko@ki.se patrik.ernfors@ki.se.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24925909" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism ; Ganglia, Parasympathetic/cytology/embryology ; Mice ; Mice, Mutant Strains ; Neural Stem Cells/*cytology/metabolism ; Neuroanatomical Tract-Tracing Techniques/methods ; *Neurogenesis ; Neuroglia/*cytology/metabolism ; Neurons/*cytology/metabolism ; Parasympathetic Nervous System/cytology/*embryology ; SOXE Transcription Factors/genetics/metabolism ; Schwann Cells/cytology/metabolism
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  • 75
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-08-16
    Description: Preterm birth is associated with 5 to 18% of pregnancies and is a leading cause of infant morbidity and mortality. Spontaneous preterm labor, a syndrome caused by multiple pathologic processes, leads to 70% of preterm births. The prevention and the treatment of preterm labor have been long-standing challenges. We summarize the current understanding of the mechanisms of disease implicated in this condition and review advances relevant to intra-amniotic infection, decidual senescence, and breakdown of maternal-fetal tolerance. The success of progestogen treatment to prevent preterm birth in a subset of patients at risk is a cause for optimism. Solving the mystery of preterm labor, which compromises the health of future generations, is a formidable scientific challenge worthy of investment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4191866/" 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/PMC4191866/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Romero, Roberto -- Dey, Sudhansu K -- Fisher, Susan J -- DA06668/DA/NIDA NIH HHS/ -- HD068524/HD/NICHD NIH HHS/ -- P50 HD055764/HD/NICHD NIH HHS/ -- R01 HD068524/HD/NICHD NIH HHS/ -- R37 HD076253/HD/NICHD NIH HHS/ -- U54 HD055764/HD/NICHD NIH HHS/ -- ZIA HD002400-23/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2014 Aug 15;345(6198):760-5. doi: 10.1126/science.1251816. Epub 2014 Aug 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Perinatology Research Branch, Program for Perinatal Research and Obstetrics, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health, Bethesda, MD, Wayne State University/the Detroit Medical Center, Detroit, MI, USA. Department of Obstetrics and Gynecology, University of Michigan, Ann Arbor, MI, USA. Department of Epidemiology and Biostatistics, Michigan State University, East Lansing, MI, USA. romeror@mail.nih.gov. ; Division of Reproductive Sciences, Perinatal Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA. ; Department of Obstetrics, Gynecology and Reproductive Sciences, Department of Anatomy, and Center for Reproductive Sciences, University of California San Francisco, San Francisco, CA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25124429" target="_blank"〉PubMed〈/a〉
    Keywords: Decidua/physiopathology ; Female ; Fetus/immunology ; Humans ; Immune Tolerance ; Infection/complications/physiopathology ; Inflammation/complications/physiopathology ; Obstetric Labor, Premature/*etiology/physiopathology/*prevention & control ; Placenta/immunology ; Pregnancy ; Syndrome ; Vascular Diseases/complications/physiopathology
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  • 76
    Publication Date: 2014-03-15
    Description: The intestinal microbiota and tissue-resident myeloid cells promote immune responses that maintain intestinal homeostasis in the host. However, the cellular cues that translate microbial signals into intestinal homeostasis remain unclear. Here, we show that deficient granulocyte-macrophage colony-stimulating factor (GM-CSF) production altered mononuclear phagocyte effector functions and led to reduced regulatory T cell (T(reg)) numbers and impaired oral tolerance. We observed that RORgammat(+) innate lymphoid cells (ILCs) are the primary source of GM-CSF in the gut and that ILC-driven GM-CSF production was dependent on the ability of macrophages to sense microbial signals and produce interleukin-1beta. Our findings reveal that commensal microbes promote a crosstalk between innate myeloid and lymphoid cells that leads to immune homeostasis in the intestine.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4291125/" 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/PMC4291125/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mortha, Arthur -- Chudnovskiy, Aleksey -- Hashimoto, Daigo -- Bogunovic, Milena -- Spencer, Sean P -- Belkaid, Yasmine -- Merad, Miriam -- F30 DK094708/DK/NIDDK NIH HHS/ -- R01 CA154947/CA/NCI NIH HHS/ -- R01 CA154947A/CA/NCI NIH HHS/ -- R01 CA173861/CA/NCI NIH HHS/ -- U01 AI095611/AI/NIAID NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2014 Mar 28;343(6178):1249288. doi: 10.1126/science.1249288. Epub 2014 Mar 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncological Sciences, 1470 Madison Avenue, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24625929" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/immunology ; Eating ; Granulocyte-Macrophage Colony-Stimulating Factor/genetics/*metabolism ; Homeostasis ; *Immune Tolerance ; Immunity, Innate ; Interleukin-1beta/immunology ; Intestines/*immunology/*microbiology ; Macrophages/*immunology/*microbiology ; Mice ; Mice, Mutant Strains ; Microbiota/*immunology ; Mouth/immunology ; Nuclear Receptor Subfamily 1, Group F, Member 3/metabolism ; T-Lymphocytes, Regulatory/immunology
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  • 77
    Publication Date: 2014-04-26
    Description: Tissue-resident macrophages are heterogeneous as a consequence of anatomical niche-specific functions. Many populations self-renew independently of bone marrow in the adult, but the molecular mechanisms of this are poorly understood. We determined a transcriptional profile for the major self-renewing population of peritoneal macrophages in mice. These cells specifically expressed the transcription factor Gata6. Selective deficiency of Gata6 in myeloid cells caused substantial alterations in the transcriptome of peritoneal macrophages. Gata6 deficiency also resulted in dysregulated peritoneal macrophage proliferative renewal during homeostasis and in response to inflammation, which was associated with delays in the resolution of inflammation. Our investigations reveal that the tissue macrophage phenotype is under discrete tissue-selective transcriptional control and that this is fundamentally linked to the regulation of their proliferation renewal.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4185421/" 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/PMC4185421/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosas, Marcela -- Davies, Luke C -- Giles, Peter J -- Liao, Chia-Te -- Kharfan, Bashar -- Stone, Timothy C -- O'Donnell, Valerie B -- Fraser, Donald J -- Jones, Simon A -- Taylor, Philip R -- 094143/Wellcome Trust/United Kingdom -- G0601617/Medical Research Council/United Kingdom -- MR/J002151/1/Medical Research Council/United Kingdom -- MR/K02003X/1/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2014 May 9;344(6184):645-8. doi: 10.1126/science.1251414. Epub 2014 Apr 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiff Institute of Infection and Immunity, Cardiff University School of Medicine, Heath Park, Cardiff CF14 4XN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24762537" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Proliferation ; GATA6 Transcription Factor/genetics/*physiology ; Inflammation/immunology ; Macrophages, Peritoneal/*immunology ; Mice ; Mice, Knockout ; Myeloid Cells/immunology ; Phenotype
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  • 78
    Publication Date: 2014-02-08
    Description: We report that the oxytocin-mediated neuroprotective gamma-aminobutyric acid (GABA) excitatory-inhibitory shift during delivery is abolished in the valproate and fragile X rodent models of autism. During delivery and subsequently, hippocampal neurons in these models have elevated intracellular chloride levels, increased excitatory GABA, enhanced glutamatergic activity, and elevated gamma oscillations. Maternal pretreatment with bumetanide restored in offspring control electrophysiological and behavioral phenotypes. Conversely, blocking oxytocin signaling in naive mothers produced offspring having electrophysiological and behavioral autistic-like features. Our results suggest a chronic deficient chloride regulation in these rodent models of autism and stress the importance of oxytocin-mediated GABAergic inhibition during the delivery process. Our data validate the amelioration observed with bumetanide and oxytocin and point to common pathways in a drug-induced and a genetic rodent model of autism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tyzio, Roman -- Nardou, Romain -- Ferrari, Diana C -- Tsintsadze, Timur -- Shahrokhi, Amene -- Eftekhari, Sanaz -- Khalilov, Ilgam -- Tsintsadze, Vera -- Brouchoud, Corinne -- Chazal, Genevieve -- Lemonnier, Eric -- Lozovaya, Natalia -- Burnashev, Nail -- Ben-Ari, Yehezkel -- New York, N.Y. -- Science. 2014 Feb 7;343(6171):675-9. doi: 10.1126/science.1247190.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mediterranean Institute of Neurobiology (INMED), U901, INSERM, Marseille, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24503856" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/*chemically induced/*genetics/metabolism ; Behavior, Animal ; Bumetanide/administration & dosage ; Chlorides/metabolism ; *Cytoprotection ; Disease Models, Animal ; Female ; Fragile X Mental Retardation Protein/genetics ; Maternal-Fetal Exchange ; Mice ; Oxytocin/*metabolism ; Parturition ; Pregnancy ; Rats ; Valproic Acid/pharmacology ; gamma-Aminobutyric Acid/*metabolism
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  • 79
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-08-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Underwood, Emily -- New York, N.Y. -- Science. 2014 Aug 15;345(6198):750-1. doi: 10.1126/science.345.6198.750.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25124425" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Diet ; Female ; Fetus/*physiology ; *Food Preferences ; Humans ; Infant ; Infant, Newborn/*physiology ; Mice ; *Mothers ; Olfactory Receptor Neurons/physiology ; Pregnancy ; *Taste ; Taste Perception
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  • 80
    Publication Date: 2014-03-22
    Description: Humans can discriminate several million different colors and almost half a million different tones, but the number of discriminable olfactory stimuli remains unknown. The lay and scientific literature typically claims that humans can discriminate 10,000 odors, but this number has never been empirically validated. We determined the resolution of the human sense of smell by testing the capacity of humans to discriminate odor mixtures with varying numbers of shared components. On the basis of the results of psychophysical testing, we calculated that humans can discriminate at least 1 trillion olfactory stimuli. This is far more than previous estimates of distinguishable olfactory stimuli. It demonstrates that the human olfactory system, with its hundreds of different olfactory receptors, far outperforms the other senses in the number of physically different stimuli it can discriminate.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4483192/" 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/PMC4483192/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bushdid, C -- Magnasco, M O -- Vosshall, L B -- Keller, A -- UL1 TR000043/TR/NCATS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Mar 21;343(6177):1370-2. doi: 10.1126/science.1249168.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Neurogenetics and Behavior, The Rockefeller University, 1230 York Avenue, Box 63, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24653035" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Female ; Humans ; Male ; Middle Aged ; *Odors ; *Olfactory Perception ; Smell/*physiology ; Young Adult
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  • 81
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-01-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caldecott, Keith W -- MR/J006750/1/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2014 Jan 17;343(6168):260-1. doi: 10.1126/science.1248234.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genome Damage and Stability Centre, University of Sussex, Falmer, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24436412" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/metabolism ; DNA/biosynthesis/*chemistry ; *DNA Repair ; *DNA Replication ; DNA-Directed DNA Polymerase/chemistry ; *Genomic Instability ; Humans ; Mice ; RNA/*chemistry ; Ribonucleases/chemistry ; Ribonucleotides/*chemistry ; Ribose/*chemistry
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  • 82
    Publication Date: 2014-10-11
    Description: Longer lives and fertility far below the replacement level of 2.1 births per woman are leading to rapid population aging in many countries. Many observers are concerned that aging will adversely affect public finances and standards of living. Analysis of newly available National Transfer Accounts data for 40 countries shows that fertility well above replacement would typically be most beneficial for government budgets. However, fertility near replacement would be most beneficial for standards of living when the analysis includes the effects of age structure on families as well as governments. And fertility below replacement would maximize per capita consumption when the cost of providing capital for a growing labor force is taken into account. Although low fertility will indeed challenge government programs and very low fertility undermines living standards, we find that moderately low fertility and population decline favor the broader material standard of living.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4545628/" 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/PMC4545628/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Ronald -- Mason, Andrew -- members of the NTA Network -- R37 AG025247/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2014 Oct 10;346(6206):229-34. doi: 10.1126/science.1250542.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Demography and Department of Economics, University of California, 2232 Piedmont Avenue, Berkeley, CA 94720, USA. rlee@demog.berkeley.edu amason@hawaii.edu. ; Department of Economics, University of Hawaii at Manoa, 2424 Maile Way, Honolulu, HI 96821, USA. East-West Center, 1601 East-West Road, Honolulu, HI 96848-1601, USA. rlee@demog.berkeley.edu amason@hawaii.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25301626" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; *Aging ; Birth Rate/*trends ; Economics ; Female ; *Fertility ; Humans ; Income ; Income Tax ; *Population Growth ; Socioeconomic Factors
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 83
    Publication Date: 2014-10-04
    Description: Colloidal nanoparticle biosensors have received intense scientific attention and offer promising applications in both research and medicine. We review the state of the art in nanoparticle development, surface chemistry, and biosensing mechanisms, discussing how a range of technologies are contributing toward commercial and clinical translation. Recent examples of success include the ultrasensitive detection of cancer biomarkers in human serum and in vivo sensing of methyl mercury. We identify five key materials challenges, including the development of robust mass-scale nanoparticle synthesis methods, and five broader challenges, including the use of simulations and bioinformatics-driven experimental approaches for predictive modeling of biosensor performance. The resultant generation of nanoparticle biosensors will form the basis of high-performance analytical assays, effective multiplexed intracellular sensors, and sophisticated in vivo probes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Howes, Philip D -- Chandrawati, Rona -- Stevens, Molly M -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2014 Oct 3;346(6205):1247390. doi: 10.1126/science.1247390. Epub 2014 Oct 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Materials, Department of Bioengineering, and Institute of Biomedical Engineering, Imperial College London, Exhibition Road, London SW7 2AZ, UK. ; Department of Materials, Department of Bioengineering, and Institute of Biomedical Engineering, Imperial College London, Exhibition Road, London SW7 2AZ, UK. m.stevens@imperial.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25278614" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biosensing Techniques ; *Chemistry Techniques, Analytical ; Colloids ; Humans ; Mice ; *Molecular Diagnostic Techniques ; Nanoparticles/*chemistry ; Sensitivity and Specificity ; Surface Properties
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  • 84
    Publication Date: 2014-09-23
    Description: The small number of hematopoietic stem and progenitor cells in cord blood units limits their widespread use in human transplant protocols. We identified a family of chemically related small molecules that stimulates the expansion ex vivo of human cord blood cells capable of reconstituting human hematopoiesis for at least 6 months in immunocompromised mice. The potent activity of these newly identified compounds, UM171 being the prototype, is independent of suppression of the aryl hydrocarbon receptor, which targets cells with more-limited regenerative potential. The properties of UM171 make it a potential candidate for hematopoietic stem cell transplantation and gene therapy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4372335/" 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/PMC4372335/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fares, Iman -- Chagraoui, Jalila -- Gareau, Yves -- Gingras, Stephane -- Ruel, Rejean -- Mayotte, Nadine -- Csaszar, Elizabeth -- Knapp, David J H F -- Miller, Paul -- Ngom, Mor -- Imren, Suzan -- Roy, Denis-Claude -- Watts, Kori L -- Kiem, Hans-Peter -- Herrington, Robert -- Iscove, Norman N -- Humphries, R Keith -- Eaves, Connie J -- Cohen, Sandra -- Marinier, Anne -- Zandstra, Peter W -- Sauvageau, Guy -- HL84345/HL/NHLBI NIH HHS/ -- R01 HL084345/HL/NHLBI NIH HHS/ -- Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2014 Sep 19;345(6203):1509-12. doi: 10.1126/science.1256337.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Genetics of Stem Cells Laboratory, Institute of Research in Immunology and Cancer (IRIC), University of Montreal, Montreal, QC, Canada. ; Medicinal Chemistry, IRIC, University of Montreal, Montreal, QC, Canada. ; Terrence Donnelly Centre for Cellular and Biomolecular Research, University of Toronto, Toronto, ON, Canada. ; Terry Fox Laboratory, British Columbia Cancer Agency and University of British Columbia, Vancouver, BC, Canada. ; Division of Hematology, Maisonneuve-Rosemont Hospital, Montreal, QC, Canada. Department of Medicine, Faculty of Medicine, Universite de Montreal, Montreal, QC, Canada. ; Clinical Research Division, Fred Hutchinson Cancer Research Center and University of Washington, Seattle, WA, USA. ; Clinical Research Division, Fred Hutchinson Cancer Research Center and University of Washington, Seattle, WA, USA. Department of Medicine and Pathology, University of Washington, Seattle, WA, USA. ; Ontario Cancer Institute, University Health Network, Toronto, ON, Canada. ; Ontario Cancer Institute, University Health Network, Toronto, ON, Canada. Department of Immunology, University of Toronto, Toronto, ON, Canada. ; Molecular Genetics of Stem Cells Laboratory, Institute of Research in Immunology and Cancer (IRIC), University of Montreal, Montreal, QC, Canada. Division of Hematology, Maisonneuve-Rosemont Hospital, Montreal, QC, Canada. Department of Medicine, Faculty of Medicine, Universite de Montreal, Montreal, QC, Canada. guy.sauvageau@umontreal.ca.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25237102" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Culture Techniques ; Fetal Blood/cytology/*drug effects/physiology ; Genetic Therapy/methods ; Hematopoiesis/*drug effects/physiology ; Hematopoietic Stem Cell Transplantation/methods ; Hematopoietic Stem Cells/*drug effects/physiology ; Humans ; Immunocompromised Host ; Indoles/chemistry/*pharmacology ; Mice ; Pyrimidines/chemistry/*pharmacology ; Receptors, Aryl Hydrocarbon/*antagonists & inhibitors ; Regeneration/*drug effects ; Small Molecule Libraries/chemistry/pharmacology
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  • 85
    Publication Date: 2014-07-12
    Description: Heterosexual transmission of HIV-1 typically results in one genetic variant establishing systemic infection. We compared, for 137 linked transmission pairs, the amino acid sequences encoded by non-envelope genes of viruses in both partners and demonstrate a selection bias for transmission of residues that are predicted to confer increased in vivo fitness on viruses in the newly infected, immunologically naive recipient. Although tempered by transmission risk factors, such as donor viral load, genital inflammation, and recipient gender, this selection bias provides an overall transmission advantage for viral quasispecies that are dominated by viruses with high in vivo fitness. Thus, preventative or therapeutic approaches that even marginally reduce viral fitness may lower the overall transmission rates and offer long-term benefits even upon successful transmission.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4289910/" 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/PMC4289910/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carlson, Jonathan M -- Schaefer, Malinda -- Monaco, Daniela C -- Batorsky, Rebecca -- Claiborne, Daniel T -- Prince, Jessica -- Deymier, Martin J -- Ende, Zachary S -- Klatt, Nichole R -- DeZiel, Charles E -- Lin, Tien-Ho -- Peng, Jian -- Seese, Aaron M -- Shapiro, Roger -- Frater, John -- Ndung'u, Thumbi -- Tang, Jianming -- Goepfert, Paul -- Gilmour, Jill -- Price, Matt A -- Kilembe, William -- Heckerman, David -- Goulder, Philip J R -- Allen, Todd M -- Allen, Susan -- Hunter, Eric -- 2P51RR000165-51/RR/NCRR NIH HHS/ -- G108/626/Medical Research Council/United Kingdom -- OD P51OD11132/OD/NIH HHS/ -- P01-AI074415/AI/NIAID NIH HHS/ -- P30 AI050409/AI/NIAID NIH HHS/ -- P51 OD010425/OD/NIH HHS/ -- P51 OD011132/OD/NIH HHS/ -- P51RR165/RR/NCRR NIH HHS/ -- R01 AI064060/AI/NIAID NIH HHS/ -- R01 AI64060/AI/NIAID NIH HHS/ -- R37 AI051231/AI/NIAID NIH HHS/ -- R37 AI51231/AI/NIAID NIH HHS/ -- T32 AI007387/AI/NIAID NIH HHS/ -- T32-AI007387/AI/NIAID NIH HHS/ -- U01 AI 66454/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Jul 11;345(6193):1254031. doi: 10.1126/science.1254031. Epub 2014 Jul 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Microsoft Research, Redmond, WA 98052, USA. carlson@microsoft.com ehunte4@emory.edu. ; Emory Vaccine Center at Yerkes National Primate Research Center, Emory University, Atlanta, GA 30329, USA. ; Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02114, USA. ; Microsoft Research, Redmond, WA 98052, USA. ; Division of Infectious Diseases, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. ; Nuffield Department of Clinical Medicine, University of Oxford, Oxford OX1 7BN, UK. National Institute of Health Research, Oxford Biomedical Research Centre, Oxford OX3 7LE, UK. Oxford Martin School, University of Oxford, Oxford OX1 3BD, UK. ; Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02114, USA. HIV Pathogenesis Programme, Doris Duke Medical Research Institute, Nelson R. Mandela School of Medicine, University of KwaZulu-Natal, Durban 4013, South Africa. KwaZulu-Natal Research Institute for Tuberculosis and HIV (K-RITH), Nelson R. Mandela School of Medicine, University of KwaZulu-Natal, Durban 4001, South Africa. Max Planck Institute for Infection Biology, D-10117 Berlin, Germany. ; Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA. ; International AIDS Vaccine Initiative, London SW10 9NH, UK. Imperial College of Science Technology and Medicine, London SW10 9NH, UK. ; International AIDS Vaccine Initiative, San Francisco, CA 94105, USA. Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, CA 94105, USA. ; Rwanda-Zambia HIV Research Group: Zambia-Emory HIV Research Project, Lusaka, Zambia. ; Microsoft Research, Los Angeles, CA 98117, USA. ; HIV Pathogenesis Programme, Doris Duke Medical Research Institute, Nelson R. Mandela School of Medicine, University of KwaZulu-Natal, Durban 4013, South Africa. Department of Paediatrics, University of Oxford, Oxford OX1 3SY, UK. ; Rwanda-Zambia HIV Research Group: Zambia-Emory HIV Research Project, Lusaka, Zambia. Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA 30322, USA. Department of Global Health, Rollins School of Public Health, Emory University, Atlanta, GA 30322, USA. ; International AIDS Vaccine Initiative, San Francisco, CA 94105, USA. Microsoft Research, Los Angeles, CA 98117, USA. Department of Paediatrics, University of Oxford, Oxford OX1 3SY, UK. ; Emory Vaccine Center at Yerkes National Primate Research Center, Emory University, Atlanta, GA 30329, USA. Rwanda-Zambia HIV Research Group: Zambia-Emory HIV Research Project, Lusaka, Zambia. Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA 30322, USA. carlson@microsoft.com ehunte4@emory.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25013080" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Consensus Sequence ; DNA Mutational Analysis ; Disease Transmission, Infectious/statistics & numerical data ; Female ; HIV Infections/*transmission ; HIV-1/*genetics ; *Heterosexuality ; High-Throughput Nucleotide Sequencing ; Human Immunodeficiency Virus Proteins/genetics ; Humans ; Male ; Models, Statistical ; Molecular Sequence Data ; Point Mutation ; Risk Factors ; *Selection, Genetic ; Viral Load
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  • 86
    Publication Date: 2014-01-18
    Description: A major evolutionary transition to eusociality with reproductive division of labor between queens and workers has arisen independently at least 10 times in the ants, bees, and wasps. Pheromones produced by queens are thought to play a key role in regulating this complex social system, but their evolutionary history remains unknown. Here, we identify the first sterility-inducing queen pheromones in a wasp, bumblebee, and desert ant and synthesize existing data on compounds that characterize female fecundity in 64 species of social insects. Our results show that queen pheromones are strikingly conserved across at least three independent origins of eusociality, with wasps, ants, and some bees all appearing to use nonvolatile, saturated hydrocarbons to advertise fecundity and/or suppress worker reproduction. These results suggest that queen pheromones evolved from conserved signals of solitary ancestors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Van Oystaeyen, Annette -- Oliveira, Ricardo Caliari -- Holman, Luke -- van Zweden, Jelle S -- Romero, Carmen -- Oi, Cintia A -- d'Ettorre, Patrizia -- Khalesi, Mohammadreza -- Billen, Johan -- Wackers, Felix -- Millar, Jocelyn G -- Wenseleers, Tom -- New York, N.Y. -- Science. 2014 Jan 17;343(6168):287-90. doi: 10.1126/science.1244899.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Socioecology and Social Evolution, Zoological Institute, University of Leuven, Naamsestraat 59-Box 2466, 3000 Leuven, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24436417" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ants/*physiology ; Bees/*physiology ; Biological Assay ; *Biological Evolution ; Female ; Fertility/drug effects/*physiology ; Male ; Pheromones/classification/pharmacology/*physiology ; Reproduction/drug effects/physiology ; Wasps/*physiology
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  • 87
    Publication Date: 2014-04-05
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4414116/" 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/PMC4414116/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fauci, Anthony S -- Marovich, Mary A -- Dieffenbach, Carl W -- Hunter, Eric -- Buchbinder, Susan P -- P51 OD011132/OD/NIH HHS/ -- P51 RR000165/RR/NCRR NIH HHS/ -- U19 AI096187/AI/NIAID NIH HHS/ -- UM1 AI068614/AI/NIAID NIH HHS/ -- Z01 AI000390-25/Intramural NIH HHS/ -- Z01 AI000677-15/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2014 Apr 4;344(6179):49-51. doi: 10.1126/science.1250672.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24700849" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/*administration & dosage/*immunology/*therapeutic use ; Female ; HIV Antigens/*immunology ; HIV Infections/*immunology/*prevention & control ; HIV-1/*immunology ; Humans ; Male ; T-Lymphocytes/*immunology
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  • 88
    Publication Date: 2014-04-12
    Description: The olfactory system remains plastic throughout life because of continuous neurogenesis of sensory neurons in the nose and inhibitory interneurons in the olfactory bulb. Here, we reveal that transgenic expression of an odorant receptor has non-cell autonomous effects on axons expressing this receptor from the endogenous gene. Perinatal expression of transgenic odorant receptor causes rerouting of like axons to new glomeruli, whereas expression after the sensory map is established does not lead to rerouting. Further, chemical ablation of the map after rerouting does not restore the normal map, even when the transgenic receptor is no longer expressed. Our results reveal that glomeruli are designated as targets for sensory neurons expressing specific odorant receptors during a critical period in the formation of the olfactory sensory map.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4104295/" 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/PMC4104295/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsai, Lulu -- Barnea, Gilad -- 5R01MH086920/MH/NIMH NIH HHS/ -- P30 GM103410/GM/NIGMS NIH HHS/ -- R01 MH086920/MH/NIMH NIH HHS/ -- T32 GM007601/GM/NIGMS NIH HHS/ -- T32GM007601/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Apr 11;344(6180):197-200. doi: 10.1126/science.1248806.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Brown University, Providence, RI 02912, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24723611" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/metabolism/*physiology ; Gene Expression Regulation, Developmental ; Mice ; Mice, Transgenic ; Neuropil/metabolism ; Olfactory Bulb/*growth & development/metabolism ; Receptors, Odorant/*biosynthesis/genetics ; Transcriptional Activation
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  • 89
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-06-21
    Description: It is not just a manner of speaking: "Mind reading," or working out what others are thinking and feeling, is markedly similar to print reading. Both of these distinctly human skills recover meaning from signs, depend on dedicated cortical areas, are subject to genetically heritable disorders, show cultural variation around a universal core, and regulate how people behave. But when it comes to development, the evidence is conflicting. Some studies show that, like learning to read print, learning to read minds is a long, hard process that depends on tuition. Others indicate that even very young, nonliterate infants are already capable of mind reading. Here, we propose a resolution to this conflict. We suggest that infants are equipped with neurocognitive mechanisms that yield accurate expectations about behavior ("automatic" or "implicit" mind reading), whereas "explicit" mind reading, like literacy, is a culturally inherited skill; it is passed from one generation to the next by verbal instruction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heyes, Cecilia M -- Frith, Chris D -- 091593/Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2014 Jun 20;344(6190):1243091. doi: 10.1126/science.1243091.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉All Souls College and Department of Experimental Psychology, University of Oxford, Oxford OX1 4AL, UK. cecilia.heyes@all-souls.ox.ac.uk. ; Wellcome Trust Centre for Neuroimaging, University College London, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24948740" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Autistic Disorder/psychology ; Brain/physiology ; Child, Preschool ; Cognition ; *Cultural Evolution ; Dyslexia/psychology ; Female ; Humans ; Learning ; Male ; *Nonverbal Communication ; *Telepathy ; *Theory of Mind
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  • 90
    Publication Date: 2014-04-05
    Description: Damage to the central nervous system caused by traumatic injury or neurological disorders can lead to permanent loss of voluntary motor function and muscle paralysis. Here, we describe an approach that circumvents central motor circuit pathology to restore specific skeletal muscle function. We generated murine embryonic stem cell-derived motor neurons that express the light-sensitive ion channel channelrhodopsin-2, which we then engrafted into partially denervated branches of the sciatic nerve of adult mice. These engrafted motor neurons not only reinnervated lower hind-limb muscles but also enabled their function to be restored in a controllable manner using optogenetic stimulation. This synthesis of regenerative medicine and optogenetics may be a successful strategy to restore muscle function after traumatic injury or disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bryson, J Barney -- Machado, Carolina Barcellos -- Crossley, Martin -- Stevenson, Danielle -- Bros-Facer, Virginie -- Burrone, Juan -- Greensmith, Linda -- Lieberam, Ivo -- 095589/Wellcome Trust/United Kingdom -- G0900585/Medical Research Council/United Kingdom -- G1001234/Biotechnology and Biological Sciences Research Council/United Kingdom -- MR/K000608/1/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2014 Apr 4;344(6179):94-7. doi: 10.1126/science.1248523.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sobell Department of Motor Neuroscience and Movement Disorders, University College London (UCL) Institute of Neurology, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24700859" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Cell Line ; Electric Stimulation ; Embryonic Stem Cells/cytology/physiology ; Female ; Hindlimb ; Isometric Contraction ; *Light ; Mice ; Mice, Inbred C57BL ; Motor Neurons/cytology/*physiology/*transplantation ; Muscle Denervation ; Muscle Fibers, Skeletal/physiology ; Muscle, Skeletal/*innervation/*physiology ; Nerve Regeneration ; *Optogenetics ; Rhodopsin/genetics/metabolism ; Sciatic Nerve/physiology ; Transfection ; Transgenes
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  • 91
    Publication Date: 2014-05-17
    Description: Neural circuits are shaped by elimination of early-formed redundant synapses during postnatal development. Retrograde signaling from postsynaptic cells regulates synapse elimination. In this work, we identified semaphorins, a family of versatile cell recognition molecules, as retrograde signals for elimination of redundant climbing fiber to Purkinje cell synapses in developing mouse cerebellum. Knockdown of Sema3A, a secreted semaphorin, in Purkinje cells or its receptor in climbing fibers accelerated synapse elimination during postnatal day 8 (P8) to P18. Conversely, knockdown of Sema7A, a membrane-anchored semaphorin, in Purkinje cells or either of its two receptors in climbing fibers impaired synapse elimination after P15. The effect of Sema7A involves signaling by metabotropic glutamate receptor 1, a canonical pathway for climbing fiber synapse elimination. These findings define how semaphorins retrogradely regulate multiple processes of synapse elimination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Uesaka, Naofumi -- Uchigashima, Motokazu -- Mikuni, Takayasu -- Nakazawa, Takanobu -- Nakao, Harumi -- Hirai, Hirokazu -- Aiba, Atsu -- Watanabe, Masahiko -- Kano, Masanobu -- New York, N.Y. -- Science. 2014 May 30;344(6187):1020-3. doi: 10.1126/science.1252514. Epub 2014 May 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurophysiology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan. ; Department of Anatomy, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan. ; Laboratory of Animal Resources, Center for Disease Biology and Integrated Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan. ; Department of Neurophysiology, Gunma University Graduate School of Medicine, Maebashi, Gunma 371-8511, Japan. ; Department of Neurophysiology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan. mkano-tky@m.u-tokyo.ac.jp.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24831527" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/genetics/*metabolism ; Brain/*growth & development/metabolism ; Gene Knockdown Techniques ; Mice ; Mice, Inbred C57BL ; Purkinje Cells/metabolism/*physiology ; RNA Interference ; Rats ; Rats, Sprague-Dawley ; Receptors, Metabotropic Glutamate/genetics/metabolism ; Semaphorin-3A/genetics/*metabolism ; Semaphorins/genetics/*metabolism ; Signal Transduction ; Synapses/genetics/*physiology
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  • 92
    Publication Date: 2014-04-26
    Description: Mutations in the mitochondrial genome are associated with multiple diseases and biological processes; however, little is known about the extent of sequence variation in the mitochondrial transcriptome. By ultra-deeply sequencing mitochondrial RNA (〉6000x) from the whole blood of ~1000 individuals from the CARTaGENE project, we identified remarkable levels of sequence variation within and across individuals, as well as sites that show consistent patterns of posttranscriptional modification. Using a genome-wide association study, we find that posttranscriptional modification of functionally important sites in mitochondrial transfer RNAs (tRNAs) is under strong genetic control, largely driven by a missense mutation in MRPP3 that explains ~22% of the variance. These results reveal a major nuclear genetic determinant of posttranscriptional modification in mitochondria and suggest that tRNA posttranscriptional modification may affect cellular energy production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hodgkinson, Alan -- Idaghdour, Youssef -- Gbeha, Elias -- Grenier, Jean-Christophe -- Hip-Ki, Elodie -- Bruat, Vanessa -- Goulet, Jean-Philippe -- de Malliard, Thibault -- Awadalla, Philip -- New York, N.Y. -- Science. 2014 Apr 25;344(6182):413-5. doi: 10.1126/science.1251110.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CHU Sainte-Justine Research Centre, Department of Pediatrics, Faculty of Medicine, Universite de Montreal, 3175 Chemin de la Cote-Sainte-Catherine, Montreal, Quebec H3T 1C5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24763589" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Base Sequence ; DNA, Mitochondrial/chemistry/genetics ; Female ; *Genetic Variation ; *Genome, Mitochondrial ; Genome-Wide Association Study ; High-Throughput Nucleotide Sequencing ; Humans ; Male ; Methylation ; Middle Aged ; Mutation, Missense ; Polymorphism, Single Nucleotide ; RNA/chemistry/*genetics/metabolism ; RNA Processing, Post-Transcriptional ; RNA, Transfer/chemistry/*genetics/metabolism ; Ribonuclease P/*genetics/metabolism ; Sequence Analysis, DNA ; Sequence Analysis, RNA ; Transcriptome
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 93
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-09-13
    Description: The science of morality has drawn heavily on well-controlled but artificial laboratory settings. To study everyday morality, we repeatedly assessed moral or immoral acts and experiences in a large (N = 1252) sample using ecological momentary assessment. Moral experiences were surprisingly frequent and manifold. Liberals and conservatives emphasized somewhat different moral dimensions. Religious and nonreligious participants did not differ in the likelihood or quality of committed moral and immoral acts. Being the target of moral or immoral deeds had the strongest impact on happiness, whereas committing moral or immoral deeds had the strongest impact on sense of purpose. Analyses of daily dynamics revealed evidence for both moral contagion and moral licensing. In sum, morality science may benefit from a closer look at the antecedents, dynamics, and consequences of everyday moral experience.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hofmann, Wilhelm -- Wisneski, Daniel C -- Brandt, Mark J -- Skitka, Linda J -- New York, N.Y. -- Science. 2014 Sep 12;345(6202):1340-3. doi: 10.1126/science.1251560. Epub 2014 Sep 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University of Cologne, 50931 Cologne, Germany. wilhelm.hofmann@uni-koeln.de. ; Department of Psychology, University of Illinois, Chicago, IL 60607, USA. ; Department of Social Psychology, Tilburg University, 5000, Tilburg, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25214626" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Employee Discipline ; Female ; Happiness ; Humans ; Male ; Middle Aged ; *Morals ; Personnel Loyalty ; Young Adult
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  • 94
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-05-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Underwood, Emily -- New York, N.Y. -- Science. 2014 May 23;344(6186):829-31. doi: 10.1126/science.344.6186.829.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24855255" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Cardiovascular Diseases/mortality ; Cause of Death/*trends ; Female ; Great Britain/epidemiology ; Health/statistics & numerical data/*trends ; *Hierarchy, Social ; Humans ; Male ; Poverty/statistics & numerical data/trends ; Risk Factors ; *Social Class ; Socioeconomic Factors ; Stress, Psychological/etiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 95
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-08-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leslie, Mitch -- New York, N.Y. -- Science. 2014 Aug 1;345(6196):506-7. doi: 10.1126/science.345.6196.506.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25082681" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/*pharmacology/therapeutic use ; Benzothiazoles/*pharmacology/therapeutic use ; Cell Nucleolus/*drug effects/physiology/ultrastructure ; Clinical Trials, Phase I as Topic ; Colonic Neoplasms/pathology ; Humans ; Mice ; Naphthyridines/*pharmacology/therapeutic use ; Neoplasms/*drug therapy ; RNA Polymerase I/*antagonists & inhibitors/*drug effects/physiology ; Therapies, Investigational
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  • 96
    Publication Date: 2014-03-08
    Description: To systematically investigate the impact of immune stimulation upon regulatory variant activity, we exposed primary monocytes from 432 healthy Europeans to interferon-gamma (IFN-gamma) or differing durations of lipopolysaccharide and mapped expression quantitative trait loci (eQTLs). More than half of cis-eQTLs identified, involving hundreds of genes and associated pathways, are detected specifically in stimulated monocytes. Induced innate immune activity reveals multiple master regulatory trans-eQTLs including the major histocompatibility complex (MHC), coding variants altering enzyme and receptor function, an IFN-beta cytokine network showing temporal specificity, and an interferon regulatory factor 2 (IRF2) transcription factor-modulated network. Induced eQTL are significantly enriched for genome-wide association study loci, identifying context-specific associations to putative causal genes including CARD9, ATM, and IRF8. Thus, applying pathophysiologically relevant immune stimuli assists resolution of functional genetic variants.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4064786/" 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/PMC4064786/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fairfax, Benjamin P -- Humburg, Peter -- Makino, Seiko -- Naranbhai, Vivek -- Wong, Daniel -- Lau, Evelyn -- Jostins, Luke -- Plant, Katharine -- Andrews, Robert -- McGee, Chris -- Knight, Julian C -- 074318/Wellcome Trust/United Kingdom -- 088891/Wellcome Trust/United Kingdom -- 090532/Wellcome Trust/United Kingdom -- 090532/Z/09/Z/Wellcome Trust/United Kingdom -- 281824/European Research Council/International -- 98082/Medical Research Council/United Kingdom -- G1001708/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2014 Mar 7;343(6175):1246949. doi: 10.1126/science.1246949.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Centre for Human Genetics, University of Oxford, Roosevelt Drive, Oxford OX3 7BN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24604202" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Antigens, CD14/immunology ; Aryl Hydrocarbon Hydroxylases/genetics ; Basic-Leucine Zipper Transcription Factors/genetics ; CARD Signaling Adaptor Proteins/genetics ; Chromosome Mapping ; Crohn Disease/epidemiology/*genetics ; Cytochrome P-450 CYP1B1 ; Female ; Gene Expression Regulation/*immunology ; *Genetic Predisposition to Disease ; Genetic Variation ; Genome-Wide Association Study ; Humans ; Immunity, Innate/*genetics ; Indoleamine-Pyrrole 2,3,-Dioxygenase/genetics ; Interferon Regulatory Factor-2/genetics ; Interferon Regulatory Factors/genetics ; Interferon-gamma/pharmacology ; Male ; Middle Aged ; Monocytes/drug effects/*immunology ; Polymorphism, Single Nucleotide ; Quantitative Trait Loci ; Receptors, Purinergic P2/genetics ; Young Adult
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  • 97
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-01-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Capel, Blanche -- R37 HD039963/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2014 Jan 3;343(6166):32-3. doi: 10.1126/science.1248486.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24385621" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Eukaryotic Initiation Factor-2/*physiology ; Female ; Humans ; Male ; *Reproductive Techniques, Assisted ; Sex Determination Processes/*genetics ; Sex-Determining Region Y Protein/*physiology ; Y Chromosome/*genetics
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  • 98
    Publication Date: 2014-02-22
    Description: Receptor-interacting protein kinase 1 (RIPK1) and RIPK3 trigger pro-inflammatory cell death termed "necroptosis." Studies with RIPK3-deficient mice or the RIPK1 inhibitor necrostatin-1 suggest that necroptosis exacerbates pathology in many disease models. We engineered mice expressing catalytically inactive RIPK3 D161N or RIPK1 D138N to determine the need for the active kinase in the whole animal. Unexpectedly, RIPK3 D161N promoted lethal RIPK1- and caspase-8-dependent apoptosis. In contrast, mice expressing RIPK1 D138N were viable and, like RIPK3-deficient mice, resistant to tumor necrosis factor (TNF)-induced hypothermia. Cells expressing RIPK1 D138N were resistant to TNF-induced necroptosis, whereas TNF-induced signaling pathways promoting gene transcription were unperturbed. Our data indicate that the kinase activity of RIPK3 is essential for necroptosis but also governs whether a cell activates caspase-8 and dies by apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Newton, Kim -- Dugger, Debra L -- Wickliffe, Katherine E -- Kapoor, Neeraj -- de Almagro, M Cristina -- Vucic, Domagoj -- Komuves, Laszlo -- Ferrando, Ronald E -- French, Dorothy M -- Webster, Joshua -- Roose-Girma, Merone -- Warming, Soren -- Dixit, Vishva M -- New York, N.Y. -- Science. 2014 Mar 21;343(6177):1357-60. doi: 10.1126/science.1249361. Epub 2014 Feb 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiological Chemistry, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24557836" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Caspase 8/genetics/metabolism ; Cell Survival ; Embryo Loss ; Embryonic Development ; Enteritis/pathology ; Fas-Associated Death Domain Protein/metabolism ; Gene Knock-In Techniques ; Intestine, Large/pathology ; Intestine, Small/pathology ; Mice ; *Necrosis ; Receptor-Interacting Protein Serine-Threonine Kinases/antagonists & ; inhibitors/genetics/*metabolism ; Tumor Necrosis Factor-alpha/pharmacology
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  • 99
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2014-10-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carbone, Francis R -- Gebhardt, Thomas -- New York, N.Y. -- Science. 2014 Oct 3;346(6205):40-1. doi: 10.1126/science.1259925. Epub 2014 Oct 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, The University of Melbourne at The Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Parkville, VIC 3010, Australia. f.carbone@microbiology.unimelb.edu.au. ; Department of Microbiology and Immunology, The University of Melbourne at The Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Parkville, VIC 3010, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25278601" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity/*immunology ; Animals ; CD4-Positive T-Lymphocytes/*immunology ; CD8-Positive T-Lymphocytes/*immunology ; Chemokines/*immunology ; Female ; Herpes Genitalis/*immunology ; *Herpesvirus 2, Human ; Immunity, Innate/*immunology ; Immunologic Memory/*immunology ; Macrophages/*immunology ; Male ; Skin/*immunology ; Vagina/*immunology ; Virus Diseases/*immunology
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  • 100
    Publication Date: 2014-02-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moss-Racusin, Corinne A -- van der Toorn, Jojanneke -- Dovidio, John F -- Brescoll, Victoria L -- Graham, Mark J -- Handelsman, Jo -- 1R13GM090574-01/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Feb 7;343(6171):615-6. doi: 10.1126/science.1245936.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skidmore College, Saratoga Springs, NY 12866, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24503840" target="_blank"〉PubMed〈/a〉
    Keywords: *Cultural Diversity ; Female ; Humans ; Male ; *Racism ; Research Design ; Science/ethics/*manpower ; *Sexism
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