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  • Mice  (169)
  • *Conservation of Natural Resources
  • Cell & Developmental Biology
  • Chemical Engineering
  • Inorganic Chemistry
  • SPACE SCIENCES
  • American Association for the Advancement of Science (AAAS)  (192)
  • 2010-2014  (192)
  • 2011  (192)
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  • 2010-2014  (192)
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  • 1
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    Conservation. Boosting CITES (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-01-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Phelps, Jacob -- Webb, Edward L -- Bickford, David -- Nijman, Vincent -- Sodhi, Navjot S -- New York, N.Y. -- Science. 2010 Dec 24;330(6012):1752-3. doi: 10.1126/science.1195558.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, National University of Singapore, Singapore, 117543, Singapore. jacob.phelps@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21205655" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Animals, Wild ; *Commerce ; *Conservation of Natural Resources ; Data Collection ; *Endangered Species ; *International Cooperation ; Peer Review ; *Plants
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Predicting a human gut microbiota's response to diet in gnotobiotic mice (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-05-21
    Description: The interrelationships between our diets and the structure and operations of our gut microbial communities are poorly understood. A model community of 10 sequenced human gut bacteria was introduced into gnotobiotic mice, and changes in species abundance and microbial gene expression were measured in response to randomized perturbations of four defined ingredients in the host diet. From the responses, we developed a statistical model that predicted over 60% of the variation in species abundance evoked by diet perturbations, and we were able to identify which factors in the diet best explained changes seen for each community member. The approach is generally applicable, as shown by a follow-up study involving diets containing various mixtures of pureed human baby foods.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3303606/" 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/PMC3303606/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Faith, Jeremiah J -- McNulty, Nathan P -- Rey, Federico E -- Gordon, Jeffrey I -- DK30292/DK/NIDDK NIH HHS/ -- DK70977/DK/NIDDK NIH HHS/ -- R01 DK070977/DK/NIDDK NIH HHS/ -- R01 DK070977-08/DK/NIDDK NIH HHS/ -- R37 DK030292/DK/NIDDK NIH HHS/ -- R37 DK030292-31/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2011 Jul 1;333(6038):101-4. doi: 10.1126/science.1206025. Epub 2011 May 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Genome Sciences and Systems Biology, Washington University School of Medicine, St. Louis, MO 63108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21596954" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteroides/genetics/physiology ; Biomass ; Caseins/administration & dosage ; Desulfovibrio/genetics/physiology ; *Diet ; Dietary Carbohydrates/administration & dosage ; Dietary Fats, Unsaturated/administration & dosage ; Dietary Proteins/administration & dosage ; Dietary Sucrose/administration & dosage ; Escherichia coli/genetics/physiology ; Feces/*microbiology ; Gastrointestinal Tract/*microbiology ; Gene Expression Profiling ; Gene Expression Regulation, Bacterial ; *Germ-Free Life ; Gram-Negative Bacteria/*physiology ; Gram-Positive Bacteria/genetics/*physiology ; Humans ; Infant ; Infant Food ; Linear Models ; Male ; *Metagenome ; Mice ; Mice, Inbred C57BL ; Models, Animal
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Interconversion between intestinal stem cell populations in distinct niches (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-11-15
    Description: Intestinal epithelial stem cell identity and location have been the subject of substantial research. Cells in the +4 niche are slow-cycling and label-retaining, whereas a different stem cell niche located at the crypt base is occupied by crypt base columnar (CBC) cells. CBCs are distinct from +4 cells, and the relationship between them is unknown, though both give rise to all intestinal epithelial lineages. We demonstrate that Hopx, an atypical homeobox protein, is a specific marker of +4 cells. Hopx-expressing cells give rise to CBCs and all mature intestinal epithelial lineages. Conversely, CBCs can give rise to +4 Hopx-positive cells. These findings demonstrate a bidirectional lineage relationship between active and quiescent stem cells in their niches.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3705713/" 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/PMC3705713/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takeda, Norifumi -- Jain, Rajan -- LeBoeuf, Matthew R -- Wang, Qiaohong -- Lu, Min Min -- Epstein, Jonathan A -- R01 HL071546/HL/NHLBI NIH HHS/ -- U01 HL100405/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2011 Dec 9;334(6061):1420-4. doi: 10.1126/science.1213214. Epub 2011 Nov 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22075725" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle ; Cell Differentiation ; Cell Lineage ; Cell Proliferation ; Cells, Cultured ; Epithelial Cells/*cytology ; Homeodomain Proteins/analysis/genetics ; Intestinal Mucosa/*cytology/drug effects ; Intestine, Small/*cytology/drug effects ; Mice ; Models, Biological ; Multipotent Stem Cells/*cytology/physiology ; Paneth Cells/cytology ; *Stem Cell Niche ; Tamoxifen/pharmacology
    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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    Cerebellum shapes hippocampal spatial code (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-10-25
    Description: Spatial representation is an active process that requires complex multimodal integration from a large interacting network of cortical and subcortical structures. We sought to determine the role of cerebellar protein kinase C (PKC)-dependent plasticity in spatial navigation by recording the activity of hippocampal place cells in transgenic L7PKCI mice with selective disruption of PKC-dependent plasticity at parallel fiber-Purkinje cell synapses. Place cell properties were exclusively impaired when L7PKCI mice had to rely on self-motion cues. The behavioral consequence of such a deficit is evidenced here by selectively impaired navigation capabilities during a path integration task. Together, these results suggest that cerebellar PKC-dependent mechanisms are involved in processing self-motion signals essential to the shaping of hippocampal spatial representation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rochefort, Christelle -- Arabo, Arnaud -- Andre, Marion -- Poucet, Bruno -- Save, Etienne -- Rondi-Reig, Laure -- New York, N.Y. -- Science. 2011 Oct 21;334(6054):385-9. doi: 10.1126/science.1207403.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurobiologie des Processus Adaptatifs (UMR 7102), Navigation, Memory, and Aging (ENMVI) Team, Universite Pierre et Marie Curie-Centre National de la Recherche Scientifique (CNRS), F-75005 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22021859" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CA1 Region, Hippocampal/cytology/*physiology ; Cerebellum/enzymology/*physiology ; Cues ; Darkness ; *Long-Term Synaptic Depression ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; *Motor Activity ; *Orientation ; Protein Kinase C/antagonists & inhibitors/metabolism ; Purkinje Cells/physiology ; Pyramidal Cells/*physiology ; *Space Perception
    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
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    Molecular biology. Demystifying DNA demethylation (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-09-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nabel, Christopher S -- Kohli, Rahul M -- New York, N.Y. -- Science. 2011 Sep 2;333(6047):1229-30. doi: 10.1126/science.1211917.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21885763" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine/*metabolism ; Animals ; Cytosine/*analogs & derivatives/metabolism ; DNA/*metabolism ; DNA Methylation ; DNA-Binding Proteins/genetics/*metabolism ; Embryonic Stem Cells/metabolism ; Mice ; Oxidation-Reduction ; Proto-Oncogene Proteins/genetics/*metabolism ; Thymine DNA Glycosylase/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Embryological evidence identifies wing digits in birds as digits 1, 2, and 3 (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-02-12
    Description: The identities of the digits of the avian forelimb are disputed. Whereas paleontological findings support the position that the digits correspond to digits one, two, and three, embryological evidence points to digit two, three, and four identities. By using transplantation and cell-labeling experiments, we found that the posteriormost digit in the wing does not correspond to digit four in the hindlimb; its progenitor segregates early from the zone of polarizing activity, placing it in the domain of digit three specification. We suggest that an avian-specific shift uncouples the digit anlagen from the molecular mechanisms that pattern them, resulting in the imposition of digit one, two, and three identities on the second, third, and fourth anlagens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tamura, Koji -- Nomura, Naoki -- Seki, Ryohei -- Yonei-Tamura, Sayuri -- Yokoyama, Hitoshi -- New York, N.Y. -- Science. 2011 Feb 11;331(6018):753-7. doi: 10.1126/science.1198229.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology and Neurosciences, Graduate School of Life Sciences, Tohoku University, Aobayama, Aoba-ku, Sendai 980-8578, Japan. tam@m.tohoku.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21311019" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Chick Embryo/*embryology ; Coturnix/*embryology ; Forelimb/embryology/transplantation ; Hedgehog Proteins/metabolism ; Hindlimb/embryology/transplantation ; Limb Buds/embryology ; Mice ; Signal Transduction ; Toes/embryology ; Wings, Animal/*embryology
    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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  • 7
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    Noncanonical TGFbeta signaling contributes to aortic aneurysm progression in Marfan syndrome mice (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-04-16
    Description: Transforming growth factor-beta (TGFbeta) signaling drives aneurysm progression in multiple disorders, including Marfan syndrome (MFS), and therapies that inhibit this signaling cascade are in clinical trials. TGFbeta can stimulate multiple intracellular signaling pathways, but it is unclear which of these pathways drives aortic disease and, when inhibited, which result in disease amelioration. Here we show that extracellular signal-regulated kinase (ERK) 1 and 2 and Smad2 are activated in a mouse model of MFS, and both are inhibited by therapies directed against TGFbeta. Whereas selective inhibition of ERK1/2 activation ameliorated aortic growth, Smad4 deficiency exacerbated aortic disease and caused premature death in MFS mice. Smad4-deficient MFS mice uniquely showed activation of Jun N-terminal kinase-1 (JNK1), and a JNK antagonist ameliorated aortic growth in MFS mice that lacked or retained full Smad4 expression. Thus, noncanonical (Smad-independent) TGFbeta signaling is a prominent driver of aortic disease in MFS mice, and inhibition of the ERK1/2 or JNK1 pathways is a potential therapeutic strategy for the disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3111087/" 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/PMC3111087/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holm, Tammy M -- Habashi, Jennifer P -- Doyle, Jefferson J -- Bedja, Djahida -- Chen, YiChun -- van Erp, Christel -- Lindsay, Mark E -- Kim, David -- Schoenhoff, Florian -- Cohn, Ronald D -- Loeys, Bart L -- Thomas, Craig J -- Patnaik, Samarjit -- Marugan, Juan J -- Judge, Daniel P -- Dietz, Harry C -- P01 AR049698/AR/NIAMS NIH HHS/ -- P01 AR049698-07/AR/NIAMS NIH HHS/ -- R01 AR041135/AR/NIAMS NIH HHS/ -- R01 AR041135-12/AR/NIAMS NIH HHS/ -- R01 AR041135-17/AR/NIAMS NIH HHS/ -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2011 Apr 15;332(6027):358-61. doi: 10.1126/science.1192149.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21493862" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthracenes/pharmacology/therapeutic use ; Aorta/pathology ; Aortic Aneurysm/*metabolism/pathology/physiopathology/prevention & control ; Diphenylamine/analogs & derivatives/pharmacology/therapeutic use ; Disease Models, Animal ; Disease Progression ; Enzyme Activation ; Losartan/pharmacology/therapeutic use ; *MAP Kinase Signaling System ; Marfan Syndrome/drug therapy/*metabolism/pathology ; Mice ; Mitogen-Activated Protein Kinase 1/antagonists & inhibitors/*metabolism ; Mitogen-Activated Protein Kinase 3/antagonists & inhibitors/*metabolism ; Mitogen-Activated Protein Kinase 8/antagonists & inhibitors/metabolism ; Protein Kinase Inhibitors/pharmacology/therapeutic use ; Smad2 Protein/metabolism ; Smad4 Protein/deficiency/genetics ; Sulfonamides/pharmacology/therapeutic use ; Transforming Growth Factor beta/antagonists & inhibitors/immunology/*metabolism
    Print ISSN: 0036-8075
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  • 8
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    Molecular biology. Time-lapse transcription (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-04-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nair, Gautham -- Raj, Arjun -- New York, N.Y. -- Science. 2011 Apr 22;332(6028):431-2. doi: 10.1126/science.1205995.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21512026" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA-Directed RNA Polymerases/metabolism ; Fibroblasts ; *Gene Expression ; *Gene Silencing ; Genes, Fungal ; Kinetics ; Mice ; Models, Genetic ; RNA, Messenger/*genetics/metabolism ; Signal Processing, Computer-Assisted ; Stochastic Processes ; *Transcription, Genetic ; *Transcriptional Activation ; Yeasts/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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  • 9
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    The growth factor progranulin binds to TNF receptors and is therapeutic against inflammatory arthritis in mice (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-03-12
    Description: The growth factor progranulin (PGRN) has been implicated in embryonic development, tissue repair, tumorigenesis, and inflammation, but its receptors remain unidentified. We report that PGRN bound directly to tumor necrosis factor receptors (TNFRs) and disturbed the TNFalpha-TNFR interaction. PGRN-deficient mice were susceptible to collagen-induced arthritis, and administration of PGRN reversed inflammatory arthritis. Atsttrin, an engineered protein composed of three PGRN fragments, exhibited selective TNFR binding. PGRN and Atsttrin prevented inflammation in multiple arthritis mouse models and inhibited TNFalpha-activated intracellular signaling. Collectively, these findings demonstrate that PGRN is a ligand of TNFR, an antagonist of TNFalpha signaling, and plays a critical role in the pathogenesis of inflammatory arthritis in mice. They also suggest new potential therapeutic interventions for various TNFalpha-mediated pathologies and conditions, including rheumatoid arthritis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3104397/" 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/PMC3104397/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tang, Wei -- Lu, Yi -- Tian, Qing-Yun -- Zhang, Yan -- Guo, Feng-Jin -- Liu, Guang-Yi -- Syed, Nabeel Muzaffar -- Lai, Yongjie -- Lin, Edward Alan -- Kong, Li -- Su, Jeffrey -- Yin, Fangfang -- Ding, Ai-Hao -- Zanin-Zhorov, Alexandra -- Dustin, Michael L -- Tao, Jian -- Craft, Joseph -- Yin, Zhinan -- Feng, Jian Q -- Abramson, Steven B -- Yu, Xiu-Ping -- Liu, Chuan-ju -- AI43542/AI/NIAID NIH HHS/ -- AR040072/AR/NIAMS NIH HHS/ -- AR050620/AR/NIAMS NIH HHS/ -- AR053210/AR/NIAMS NIH HHS/ -- GM061710/GM/NIGMS NIH HHS/ -- R01 AI030165/AI/NIAID NIH HHS/ -- R01 AI030165-20/AI/NIAID NIH HHS/ -- R01 GM061710/GM/NIGMS NIH HHS/ -- R01 GM061710-08/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Apr 22;332(6028):478-84. doi: 10.1126/science.1199214. Epub 2011 Mar 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Orthopaedic Surgery, New York University School of Medicine and NYU Hospital for Joint Diseases, New York, NY 10003, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21393509" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/metabolism/pharmacology/therapeutic use ; Arthritis, Experimental/*drug therapy/*immunology/pathology/physiopathology ; Cartilage, Articular/metabolism/pathology ; Female ; Humans ; Intercellular Signaling Peptides and ; Proteins/chemistry/genetics/*metabolism/therapeutic use ; Ligands ; Male ; Mice ; Mice, Inbred Strains ; Mice, Knockout ; Mice, Transgenic ; Middle Aged ; Protein Interaction Domains and Motifs ; Receptors, Tumor Necrosis Factor, Type I/genetics/*metabolism ; Receptors, Tumor Necrosis Factor, Type II/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism/pharmacology/therapeutic use ; Recombinant Proteins/therapeutic use ; Signal Transduction ; T-Lymphocytes, Regulatory/immunology/physiology ; Tumor Necrosis Factor-alpha/*metabolism ; Young Adult
    Print ISSN: 0036-8075
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  • 10
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    A circadian rhythm orchestrated by histone deacetylase 3 controls hepatic lipid metabolism (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-03-12
    Description: Disruption of the circadian clock exacerbates metabolic diseases, including obesity and diabetes. We show that histone deacetylase 3 (HDAC3) recruitment to the genome displays a circadian rhythm in mouse liver. Histone acetylation is inversely related to HDAC3 binding, and this rhythm is lost when HDAC3 is absent. Although amounts of HDAC3 are constant, its genomic recruitment in liver corresponds to the expression pattern of the circadian nuclear receptor Rev-erbalpha. Rev-erbalpha colocalizes with HDAC3 near genes regulating lipid metabolism, and deletion of HDAC3 or Rev-erbalpha in mouse liver causes hepatic steatosis. Thus, genomic recruitment of HDAC3 by Rev-erbalpha directs a circadian rhythm of histone acetylation and gene expression required for normal hepatic lipid homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3389392/" 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/PMC3389392/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feng, Dan -- Liu, Tao -- Sun, Zheng -- Bugge, Anne -- Mullican, Shannon E -- Alenghat, Theresa -- Liu, X Shirley -- Lazar, Mitchell A -- DK19525/DK/NIDDK NIH HHS/ -- DK43806/DK/NIDDK NIH HHS/ -- DK45586/DK/NIDDK NIH HHS/ -- DK49210/DK/NIDDK NIH HHS/ -- HG4069/HG/NHGRI NIH HHS/ -- P30 DK019525/DK/NIDDK NIH HHS/ -- R01 DK045586/DK/NIDDK NIH HHS/ -- R37 DK043806/DK/NIDDK NIH HHS/ -- R37 DK043806-20/DK/NIDDK NIH HHS/ -- RC1 DK086239/DK/NIDDK NIH HHS/ -- RC1DK08623/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2011 Mar 11;331(6022):1315-9. doi: 10.1126/science.1198125.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21393543" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Chromatin Immunoprecipitation ; Chronobiology Disorders/genetics/metabolism ; *Circadian Clocks ; *Circadian Rhythm ; DNA/metabolism ; Epigenesis, Genetic ; Fatty Liver/*metabolism ; Gene Expression Regulation ; *Genome ; Histone Deacetylases/*metabolism ; Histones/metabolism ; Homeostasis ; *Lipid Metabolism ; Lipogenesis/genetics ; Liver/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; Nuclear Receptor Co-Repressor 1/metabolism ; Nuclear Receptor Subfamily 1, Group D, Member 1/genetics/metabolism ; RNA Polymerase II/metabolism ; Up-Regulation
    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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  • 11
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    Acetylcholine-synthesizing T cells relay neural signals in a vagus nerve circuit (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-09-17
    Description: Neural circuits regulate cytokine production to prevent potentially damaging inflammation. A prototypical vagus nerve circuit, the inflammatory reflex, inhibits tumor necrosis factor-alpha production in spleen by a mechanism requiring acetylcholine signaling through the alpha7 nicotinic acetylcholine receptor expressed on cytokine-producing macrophages. Nerve fibers in spleen lack the enzymatic machinery necessary for acetylcholine production; therefore, how does this neural circuit terminate in cholinergic signaling? We identified an acetylcholine-producing, memory phenotype T cell population in mice that is integral to the inflammatory reflex. These acetylcholine-producing T cells are required for inhibition of cytokine production by vagus nerve stimulation. Thus, action potentials originating in the vagus nerve regulate T cells, which in turn produce the neurotransmitter, acetylcholine, required to control innate immune responses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4548937/" 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/PMC4548937/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosas-Ballina, Mauricio -- Olofsson, Peder S -- Ochani, Mahendar -- Valdes-Ferrer, Sergio I -- Levine, Yaakov A -- Reardon, Colin -- Tusche, Michael W -- Pavlov, Valentin A -- Andersson, Ulf -- Chavan, Sangeeta -- Mak, Tak W -- Tracey, Kevin J -- R01 GM057226/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Oct 7;334(6052):98-101. doi: 10.1126/science.1209985. Epub 2011 Sep 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, New York 11030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21921156" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/*biosynthesis ; Action Potentials ; Animals ; CD4-Positive T-Lymphocytes/*immunology/*metabolism ; Choline O-Acetyltransferase/metabolism ; Cholinergic Agents/metabolism ; Female ; *Immunity, Innate ; Immunologic Memory ; Inflammation ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; *Neuroimmunomodulation ; Norepinephrine/pharmacology ; Receptors, Nicotinic/metabolism ; Signal Transduction ; Spleen/immunology/innervation/metabolism ; T-Lymphocyte Subsets/immunology/metabolism ; Tumor Necrosis Factor-alpha/blood ; Vagus Nerve/*physiology ; Vagus Nerve Stimulation ; alpha7 Nicotinic Acetylcholine Receptor
    Print ISSN: 0036-8075
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  • 12
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    Spatial coupling of mTOR and autophagy augments secretory phenotypes (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-04-23
    Description: Protein synthesis and autophagic degradation are regulated in an opposite manner by mammalian target of rapamycin (mTOR), whereas under certain conditions it would be beneficial if they occurred in unison to handle rapid protein turnover. We observed a distinct cellular compartment at the trans side of the Golgi apparatus, the TOR-autophagy spatial coupling compartment (TASCC), where (auto)lysosomes and mTOR accumulated during Ras-induced senescence. mTOR recruitment to the TASCC was amino acid- and Rag guanosine triphosphatase-dependent, and disruption of mTOR localization to the TASCC suppressed interleukin-6/8 synthesis. TASCC formation was observed during macrophage differentiation and in glomerular podocytes; both displayed increased protein secretion. The spatial coupling of cells' catabolic and anabolic machinery could augment their respective functions and facilitate the mass synthesis of secretory proteins.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3426290/" 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/PMC3426290/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Narita, Masako -- Young, Andrew R J -- Arakawa, Satoko -- Samarajiwa, Shamith A -- Nakashima, Takayuki -- Yoshida, Sei -- Hong, Sungki -- Berry, Lorraine S -- Reichelt, Stefanie -- Ferreira, Manuela -- Tavare, Simon -- Inoki, Ken -- Shimizu, Shigeomi -- Narita, Masashi -- DK083491/DK/NIDDK NIH HHS/ -- R01 DK083491/DK/NIDDK NIH HHS/ -- R01 DK083491-03/DK/NIDDK NIH HHS/ -- Cancer Research UK/United Kingdom -- New York, N.Y. -- Science. 2011 May 20;332(6032):966-70. doi: 10.1126/science.1205407. Epub 2011 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research UK Cambridge Research Institute (CRI), Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21512002" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/metabolism ; Animals ; *Autophagy ; *Cell Aging ; Cell Line ; Cytoplasm/metabolism ; Cytoplasmic Vesicles/*metabolism/ultrastructure ; Endoplasmic Reticulum, Rough/ultrastructure ; Genes, ras ; Golgi Apparatus/ultrastructure ; HL-60 Cells ; Humans ; Interleukin-6/metabolism ; Interleukin-8/metabolism ; Lysosomes/metabolism/ultrastructure ; Mice ; Monomeric GTP-Binding Proteins/genetics/metabolism ; Nocodazole/pharmacology ; Phagosomes/metabolism/ultrastructure ; Phenotype ; Podocytes/metabolism/ultrastructure ; Protein Biosynthesis ; Proteins/*secretion ; TOR Serine-Threonine Kinases/*metabolism ; Vacuoles/ultrastructure ; trans-Golgi Network/metabolism/ultrastructure
    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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  • 13
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    Tet proteins can convert 5-methylcytosine to 5-formylcytosine and 5-carboxylcytosine (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-07-23
    Description: 5-methylcytosine (5mC) in DNA plays an important role in gene expression, genomic imprinting, and suppression of transposable elements. 5mC can be converted to 5-hydroxymethylcytosine (5hmC) by the Tet (ten eleven translocation) proteins. Here, we show that, in addition to 5hmC, the Tet proteins can generate 5-formylcytosine (5fC) and 5-carboxylcytosine (5caC) from 5mC in an enzymatic activity-dependent manner. Furthermore, we reveal the presence of 5fC and 5caC in genomic DNA of mouse embryonic stem cells and mouse organs. The genomic content of 5hmC, 5fC, and 5caC can be increased or reduced through overexpression or depletion of Tet proteins. Thus, we identify two previously unknown cytosine derivatives in genomic DNA as the products of Tet proteins. Our study raises the possibility that DNA demethylation may occur through Tet-catalyzed oxidation followed by decarboxylation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3495246/" 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/PMC3495246/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ito, Shinsuke -- Shen, Li -- Dai, Qing -- Wu, Susan C -- Collins, Leonard B -- Swenberg, James A -- He, Chuan -- Zhang, Yi -- GM071440/GM/NIGMS NIH HHS/ -- GM68804/GM/NIGMS NIH HHS/ -- P30 ES010126/ES/NIEHS NIH HHS/ -- P30 ES010126-11/ES/NIEHS NIH HHS/ -- P30ES10126/ES/NIEHS NIH HHS/ -- P42 ES005948/ES/NIEHS NIH HHS/ -- P42 ES005948-17/ES/NIEHS NIH HHS/ -- P42ES5948/ES/NIEHS NIH HHS/ -- R01 GM068804/GM/NIGMS NIH HHS/ -- U01 DK089565/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Sep 2;333(6047):1300-3. doi: 10.1126/science.1210597. Epub 2011 Jul 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry and Biophysics, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7295, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21778364" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine/*metabolism ; Animals ; Cell Line ; Cytosine/*analogs & derivatives/metabolism ; DNA/*metabolism ; DNA Methylation ; DNA-Binding Proteins/genetics/*metabolism ; Embryonic Stem Cells/metabolism ; Humans ; Mice ; Oxidation-Reduction ; Proto-Oncogene Proteins/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism
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  • 14
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    Leishmania RNA virus controls the severity of mucocutaneous leishmaniasis (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-02-12
    Description: Mucocutaneous leishmaniasis is caused by infections with intracellular parasites of the Leishmania Viannia subgenus, including Leishmania guyanensis. The pathology develops after parasite dissemination to nasopharyngeal tissues, where destructive metastatic lesions form with chronic inflammation. Currently, the mechanisms involved in lesion development are poorly understood. Here we show that metastasizing parasites have a high Leishmania RNA virus-1 (LRV1) burden that is recognized by the host Toll-like receptor 3 (TLR3) to induce proinflammatory cytokines and chemokines. Paradoxically, these TLR3-mediated immune responses rendered mice more susceptible to infection, and the animals developed an increased footpad swelling and parasitemia. Thus, LRV1 in the metastasizing parasites subverted the host immune response to Leishmania and promoted parasite persistence.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3253482/" 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/PMC3253482/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ives, Annette -- Ronet, Catherine -- Prevel, Florence -- Ruzzante, Giulia -- Fuertes-Marraco, Silvia -- Schutz, Frederic -- Zangger, Haroun -- Revaz-Breton, Melanie -- Lye, Lon-Fye -- Hickerson, Suzanne M -- Beverley, Stephen M -- Acha-Orbea, Hans -- Launois, Pascal -- Fasel, Nicolas -- Masina, Slavica -- A129646/PHS HHS/ -- R01 AI029646/AI/NIAID NIH HHS/ -- R01 AI029646-23/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2011 Feb 11;331(6018):775-8. doi: 10.1126/science.1199326.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Lausanne, 1066 Epalinges, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21311023" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chemokines/*metabolism ; Cytokines/*metabolism ; Inflammation Mediators/metabolism ; Leishmania guyanensis/*pathogenicity/*virology ; Leishmaniasis, Mucocutaneous/*immunology/parasitology ; Leishmaniavirus/*immunology/physiology ; Macrophages/immunology/parasitology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Parasitemia ; Phagosomes/parasitology ; RNA, Double-Stranded/immunology ; RNA, Viral/immunology ; Toll-Like Receptor 3/*immunology ; Toll-Like Receptors/immunology
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  • 15
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    The intraepithelial T cell response to NKG2D-ligands links lymphoid stress surveillance to atopy (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-12-07
    Description: Epithelial cells respond to physicochemical damage with up-regulation of major histocompatibility complex-like ligands that can activate the cytolytic potential of neighboring intraepithelial T cells by binding the activating receptor, NKG2D. The systemic implications of this lymphoid stress-surveillance response, however, are unknown. We found that antigens encountered at the same time as cutaneous epithelial stress induced strong primary and secondary systemic, T helper 2 (T(H)2)-associated atopic responses in mice. These responses required NKG2D-dependent communication between dysregulated epithelial cells and tissue-associated lymphoid cells. These data are germane to uncertainty over the afferent induction of T(H)2 responses and provide a molecular framework for considering atopy as an important component of the response to tissue damage and carcinogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3842529/" 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/PMC3842529/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strid, Jessica -- Sobolev, Olga -- Zafirova, Biljana -- Polic, Bojan -- Hayday, Adrian -- 085780/Wellcome Trust/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2011 Dec 2;334(6060):1293-7. doi: 10.1126/science.1211250.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉London Research Institute, Cancer Research UK, London WC2A 3LY, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22144628" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Epidermis/*immunology ; Hypersensitivity, Immediate/*immunology ; Ligands ; Lymphoid Tissue/*immunology ; Membrane Proteins/immunology/metabolism ; Mice ; Mice, Transgenic ; NK Cell Lectin-Like Receptor Subfamily K/immunology/*metabolism ; Receptors, Antigen, T-Cell, gamma-delta/immunology ; Stress, Physiological ; T-Lymphocyte Subsets/*immunology ; Th2 Cells/*immunology ; Up-Regulation
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  • 16
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    Genetics and disease. Growth defect blocks cancer and diabetes (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-02-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leslie, Mitch -- New York, N.Y. -- Science. 2011 Feb 18;331(6019):837. doi: 10.1126/science.331.6019.837.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21330503" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Diabetes Mellitus, Type 2/*genetics/prevention & control ; Genetic Predisposition to Disease ; Human Growth Hormone/metabolism ; Humans ; Immunity, Innate/genetics ; Insulin-Like Growth Factor I/metabolism ; Laron Syndrome/*genetics ; Mice ; Neoplasms/*genetics/prevention & control ; *Point Mutation ; Receptors, Somatotropin/*genetics
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  • 17
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    A gustotopic map of taste qualities in the mammalian brain (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-09-03
    Description: The taste system is one of our fundamental senses, responsible for detecting and responding to sweet, bitter, umami, salty, and sour stimuli. In the tongue, the five basic tastes are mediated by separate classes of taste receptor cells each finely tuned to a single taste quality. We explored the logic of taste coding in the brain by examining how sweet, bitter, umami, and salty qualities are represented in the primary taste cortex of mice. We used in vivo two-photon calcium imaging to demonstrate topographic segregation in the functional architecture of the gustatory cortex. Each taste quality is represented in its own separate cortical field, revealing the existence of a gustotopic map in the brain. These results expose the basic logic for the central representation of taste.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3523322/" 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/PMC3523322/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Xiaoke -- Gabitto, Mariano -- Peng, Yueqing -- Ryba, Nicholas J P -- Zuker, Charles S -- Z01 DE000561-15/Intramural NIH HHS/ -- Z01 DE000561-16/Intramural NIH HHS/ -- ZIA DE000561-17/Intramural NIH HHS/ -- ZIA DE000561-18/Intramural NIH HHS/ -- ZIA DE000561-19/Intramural NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Sep 2;333(6047):1262-6. doi: 10.1126/science.1204076.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biochemistry and Molecular Biophysics, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21885776" target="_blank"〉PubMed〈/a〉
    Keywords: Afferent Pathways ; Animals ; *Brain Mapping ; Cerebral Cortex/cytology/*physiology ; Cycloheximide ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Imaging ; Neurons/*physiology ; Sodium Chloride ; Sodium Glutamate ; Sweetening Agents ; Taste/*physiology ; Taste Buds/physiology
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  • 18
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    De-AMPylation of the small GTPase Rab1 by the pathogen Legionella pneumophila (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-06-18
    Description: The bacterial pathogen Legionella pneumophila exploits host cell vesicle transport by transiently manipulating the activity of the small guanosine triphosphatase (GTPase) Rab1. The effector protein SidM recruits Rab1 to the Legionella-containing vacuole (LCV), where it activates Rab1 and then AMPylates it by covalently adding adenosine monophosphate (AMP). L. pneumophila GTPase-activating protein LepB inactivates Rab1 before its removal from LCVs. Because LepB cannot bind AMPylated Rab1, the molecular events leading to Rab1 inactivation are unknown. We found that the effector protein SidD from L. pneumophila catalyzed AMP release from Rab1, generating de-AMPylated Rab1 accessible for inactivation by LepB. L. pneumophila mutants lacking SidD were defective for Rab1 removal from LCVs, identifying SidD as the missing link connecting the processes of early Rab1 accumulation and subsequent Rab1 removal during infection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3209958/" 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/PMC3209958/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Neunuebel, M Ramona -- Chen, Yang -- Gaspar, Andrew H -- Backlund, Peter S Jr -- Yergey, Alfred -- Machner, Matthias P -- ZIA HD008893-01/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2011 Jul 22;333(6041):453-6. doi: 10.1126/science.1207193. Epub 2011 Jun 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Program, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21680813" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Monophosphate/*metabolism ; Animals ; Bacterial Proteins/genetics/*metabolism ; COS Cells ; Cercopithecus aethiops ; Golgi Apparatus/metabolism ; Guanine Nucleotide Exchange Factors/metabolism ; Guanosine Monophosphate/metabolism ; Guanosine Triphosphate/metabolism ; Humans ; Legionella pneumophila/*metabolism/pathogenicity ; Ligands ; Macrophages/metabolism/microbiology ; Mice ; Mice, Inbred A ; Models, Biological ; Mutant Proteins/metabolism ; U937 Cells ; Vacuoles/metabolism/*microbiology ; rab1 GTP-Binding Proteins/*metabolism
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  • 19
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    Conservation: limits of land sparing (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-11-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fischer, Joern -- Batary, Peter -- Bawa, Kamaljit S -- Brussaard, Lijbert -- Chappell, M Jahi -- Clough, Yann -- Daily, Gretchen C -- Dorrough, Josh -- Hartel, Tibor -- Jackson, Louise E -- Klein, Alexandra M -- Kremen, Claire -- Kuemmerle, Tobias -- Lindenmayer, David B -- Mooney, Harold A -- Perfecto, Ivette -- Philpott, Stacy M -- Tscharntke, Teja -- Vandermeer, John -- Wanger, Thomas Cherico -- Von Wehrden, Henrik -- New York, N.Y. -- Science. 2011 Nov 4;334(6056):593; author reply 594-5. doi: 10.1126/science.334.6056.593-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22053026" target="_blank"〉PubMed〈/a〉
    Keywords: *Agriculture ; Animals ; *Biodiversity ; *Conservation of Natural Resources ; Crops, Agricultural/*growth & development ; *Ecosystem ; *Food
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 20
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    Invasives: classify with care (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-08-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moore, Christopher -- New York, N.Y. -- Science. 2011 Aug 19;333(6045):936. doi: 10.1126/science.333.6045.936-b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21852471" target="_blank"〉PubMed〈/a〉
    Keywords: Biodiversity ; *Conservation of Natural Resources ; *Ecosystem ; *Introduced Species
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    The Toll-like receptor 2 pathway establishes colonization by a commensal of the human microbiota (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-04-23
    Description: Mucosal surfaces constantly encounter microbes. Toll-like receptors (TLRs) mediate recognition of microbial patterns to eliminate pathogens. By contrast, we demonstrate that the prominent gut commensal Bacteroides fragilis activates the TLR pathway to establish host-microbial symbiosis. TLR2 on CD4(+) T cells is required for B. fragilis colonization of a unique mucosal niche in mice during homeostasis. A symbiosis factor (PSA, polysaccharide A) of B. fragilis signals through TLR2 directly on Foxp3(+) regulatory T cells to promote immunologic tolerance. B. fragilis lacking PSA is unable to restrain T helper 17 cell responses and is defective in niche-specific mucosal colonization. Therefore, commensal bacteria exploit the TLR pathway to actively suppress immunity. We propose that the immune system can discriminate between pathogens and the microbiota through recognition of symbiotic bacterial molecules in a process that engenders commensal colonization.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3164325/" 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/PMC3164325/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Round, June L -- Lee, S Melanie -- Li, Jennifer -- Tran, Gloria -- Jabri, Bana -- Chatila, Talal A -- Mazmanian, Sarkis K -- AI 080002/AI/NIAID NIH HHS/ -- AI 088626/AI/NIAID NIH HHS/ -- DK 078938/DK/NIDDK NIH HHS/ -- DK 083633/DK/NIDDK NIH HHS/ -- R01 AI085090/AI/NIAID NIH HHS/ -- R01 AI085090-01/AI/NIAID NIH HHS/ -- R01 AI085090-01S1/AI/NIAID NIH HHS/ -- R01 AI085090-02/AI/NIAID NIH HHS/ -- R01 AI085090-03/AI/NIAID NIH HHS/ -- R01 DK078938/DK/NIDDK NIH HHS/ -- R01 DK078938-01A2/DK/NIDDK NIH HHS/ -- R01 DK078938-02/DK/NIDDK NIH HHS/ -- R01 DK078938-03/DK/NIDDK NIH HHS/ -- R01 DK078938-04/DK/NIDDK NIH HHS/ -- R21 AI080002/AI/NIAID NIH HHS/ -- R21 AI080002-01/AI/NIAID NIH HHS/ -- R21 AI080002-02/AI/NIAID NIH HHS/ -- R21 AI088626/AI/NIAID NIH HHS/ -- R21 AI088626-01/AI/NIAID NIH HHS/ -- R21 AI088626-02/AI/NIAID NIH HHS/ -- R21 DK083633/DK/NIDDK NIH HHS/ -- R21 DK083633-01A1/DK/NIDDK NIH HHS/ -- R21 DK083633-02/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2011 May 20;332(6032):974-7. doi: 10.1126/science.1206095. Epub 2011 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA. jround@caltech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21512004" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteroides fragilis/*growth & development/*immunology ; Colon/immunology/microbiology ; Germ-Free Life ; Homeostasis ; Humans ; *Immune Tolerance ; Immunity, Mucosal ; Interleukin-10/metabolism ; Intestinal Mucosa/*immunology/*microbiology ; Metagenome ; Mice ; Mice, Inbred C57BL ; Models, Biological ; Polysaccharides, Bacterial/immunology/*metabolism ; Signal Transduction ; Specific Pathogen-Free Organisms ; Symbiosis ; T-Lymphocytes, Regulatory/immunology ; Th17 Cells/immunology ; Toll-Like Receptor 2/immunology/*metabolism
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    Aberrant overexpression of satellite repeats in pancreatic and other epithelial cancers (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-01-15
    Description: Satellite repeats in heterochromatin are transcribed into noncoding RNAs that have been linked to gene silencing and maintenance of chromosomal integrity. Using digital gene expression analysis, we showed that these transcripts are greatly overexpressed in mouse and human epithelial cancers. In 8 of 10 mouse pancreatic ductal adenocarcinomas (PDACs), pericentromeric satellites accounted for a mean 12% (range 1 to 50%) of all cellular transcripts, a mean 40-fold increase over that in normal tissue. In 15 of 15 human PDACs, alpha satellite transcripts were most abundant and HSATII transcripts were highly specific for cancer. Similar patterns were observed in cancers of the lung, kidney, ovary, colon, and prostate. Derepression of satellite transcripts correlated with overexpression of the long interspersed nuclear element 1 (LINE-1) retrotransposon and with aberrant expression of neuroendocrine-associated genes proximal to LINE-1 insertions. The overexpression of satellite transcripts in cancer may reflect global alterations in heterochromatin silencing and could potentially be useful as a biomarker for cancer detection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3701432/" 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/PMC3701432/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ting, David T -- Lipson, Doron -- Paul, Suchismita -- Brannigan, Brian W -- Akhavanfard, Sara -- Coffman, Erik J -- Contino, Gianmarco -- Deshpande, Vikram -- Iafrate, A John -- Letovsky, Stan -- Rivera, Miguel N -- Bardeesy, Nabeel -- Maheswaran, Shyamala -- Haber, Daniel A -- CA129933/CA/NCI NIH HHS/ -- L30 CA142210/CA/NCI NIH HHS/ -- P01 CA117969/CA/NCI NIH HHS/ -- R01 CA129933/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Feb 4;331(6017):593-6. doi: 10.1126/science.1200801. Epub 2011 Jan 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21233348" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinoma in Situ/genetics/pathology ; Carcinoma, Pancreatic Ductal/genetics/pathology ; Colonic Neoplasms/genetics/pathology ; DNA Methylation ; DNA, Neoplasm/genetics ; DNA, Satellite/*genetics ; Female ; Gene Expression ; Gene Expression Profiling ; Heterochromatin/chemistry/genetics ; Humans ; Long Interspersed Nucleotide Elements ; Lung Neoplasms/genetics/pathology ; Male ; Mice ; Mice, Nude ; Neoplasms/*genetics/pathology ; Neurosecretory Systems/metabolism ; Ovarian Neoplasms/genetics/pathology ; Pancreatic Neoplasms/*genetics/pathology ; Prostatic Neoplasms/genetics/pathology ; RNA, Neoplasm/*genetics/metabolism ; RNA, Untranslated/*genetics/metabolism ; Transcription, Genetic
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    Nectins establish a checkerboard-like cellular pattern in the auditory epithelium (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-07-30
    Description: In the auditory epithelium of the cochlea, the sensory hair cells and supporting cells are arranged in a checkerboard-like fashion, but the mechanism underlying this cellular patterning is unclear. We found that mouse hair cells and supporting cells express the immunoglobulin-like adhesion molecules nectin-1 and -3, respectively, and that their interaction mediates the heterotypic adhesion between these two cell types. Genetic removal of nectin-1 or -3 disrupted the checkerboard-like pattern, inducing aberrant attachment between hair cells. When cells expressing either nectin-1 or -3 were cocultured, they arranged themselves into a mosaic pattern. Thus, nectin-1 and -3 promote the formation of the checkerboard-like pattern of the auditory epithelia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Togashi, Hideru -- Kominami, Kanoko -- Waseda, Masazumi -- Komura, Hitomi -- Miyoshi, Jun -- Takeichi, Masatoshi -- Takai, Yoshimi -- New York, N.Y. -- Science. 2011 Aug 26;333(6046):1144-7. doi: 10.1126/science.1208467. Epub 2011 Jul 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular and Cellular Biology, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21798896" target="_blank"〉PubMed〈/a〉
    Keywords: Adherens Junctions/metabolism ; Animals ; *Cell Adhesion ; Cell Adhesion Molecules/genetics/*metabolism ; Cell Differentiation ; Cell Line ; Coculture Techniques ; HEK293 Cells ; Hair Cells, Auditory/*cytology/*metabolism ; Humans ; Mice ; Mice, Knockout ; Organ of Corti/*cytology/*metabolism ; Phenotype ; Protein Binding ; RNA, Messenger/genetics/metabolism
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    Mammalian genes are transcribed with widely different bursting kinetics (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-03-19
    Description: In prokaryotes and eukaryotes, most genes appear to be transcribed during short periods called transcriptional bursts, interspersed by silent intervals. We describe how such bursts generate gene-specific temporal patterns of messenger RNA (mRNA) synthesis in mammalian cells. To monitor transcription at high temporal resolution, we established various gene trap cell lines and transgenic cell lines expressing a short-lived luciferase protein from an unstable mRNA, and recorded bioluminescence in real time in single cells. Mathematical modeling identified gene-specific on- and off-switching rates in transcriptional activity and mean numbers of mRNAs produced during the bursts. Transcriptional kinetics were markedly altered by cis-regulatory DNA elements. Our analysis demonstrated that bursting kinetics are highly gene-specific, reflecting refractory periods during which genes stay inactive for a certain time before switching on again.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suter, David M -- Molina, Nacho -- Gatfield, David -- Schneider, Kim -- Schibler, Ueli -- Naef, Felix -- New York, N.Y. -- Science. 2011 Apr 22;332(6028):472-4. doi: 10.1126/science.1198817. Epub 2011 Mar 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Sciences III, University of Geneva, 30 Quai Ernest Ansermet, 1211 Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21415320" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Cells, Cultured ; Chromatin/physiology ; Circadian Rhythm/genetics ; Down-Regulation ; *Gene Expression ; Histones/metabolism ; Kinetics ; Luminescent Measurements ; Mice ; Models, Genetic ; NIH 3T3 Cells ; Promoter Regions, Genetic ; Protein Biosynthesis ; RNA, Messenger/genetics/metabolism ; Stochastic Processes ; *Transcription, Genetic ; Transcriptional Activation ; Transgenes ; Up-Regulation
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    The dynamic architecture of Hox gene clusters (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-10-15
    Description: The spatial and temporal control of Hox gene transcription is essential for patterning the vertebrate body axis. Although this process involves changes in histone posttranslational modifications, the existence of particular three-dimensional (3D) architectures remained to be assessed in vivo. Using high-resolution chromatin conformation capture methodology, we examined the spatial configuration of Hox clusters in embryonic mouse tissues where different Hox genes are active. When the cluster is transcriptionally inactive, Hox genes associate into a single 3D structure delimited from flanking regions. Once transcription starts, Hox clusters switch to a bimodal 3D organization where newly activated genes progressively cluster into a transcriptionally active compartment. This transition in spatial configurations coincides with the dynamics of chromatin marks, which label the progression of the gene clusters from a negative to a positive transcription status. This spatial compartmentalization may be key to process the colinear activation of these compact gene clusters.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Noordermeer, Daan -- Leleu, Marion -- Splinter, Erik -- Rougemont, Jacques -- De Laat, Wouter -- Duboule, Denis -- New York, N.Y. -- Science. 2011 Oct 14;334(6053):222-5. doi: 10.1126/science.1207194.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Research Centre Frontiers in Genetics, School of Life Sciences, Ecole Polytechnique Federale (EPFL), Lausanne, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21998387" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromatin/metabolism/ultrastructure ; Embryo, Mammalian/cytology/*metabolism ; Gene Expression Regulation, Developmental ; *Genes, Homeobox ; Histones/metabolism ; Mice ; Models, Genetic ; *Multigene Family ; Transcription, Genetic ; *Transcriptional Activation
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    Endocannabinoid hydrolysis generates brain prostaglandins that promote neuroinflammation (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-10-25
    Description: Phospholipase A(2)(PLA(2)) enzymes are considered the primary source of arachidonic acid for cyclooxygenase (COX)-mediated biosynthesis of prostaglandins. Here, we show that a distinct pathway exists in brain, where monoacylglycerol lipase (MAGL) hydrolyzes the endocannabinoid 2-arachidonoylglycerol to generate a major arachidonate precursor pool for neuroinflammatory prostaglandins. MAGL-disrupted animals show neuroprotection in a parkinsonian mouse model. These animals are spared the hemorrhaging caused by COX inhibitors in the gut, where prostaglandins are instead regulated by cytosolic PLA(2). These findings identify MAGL as a distinct metabolic node that couples endocannabinoid to prostaglandin signaling networks in the nervous system and suggest that inhibition of this enzyme may be a new and potentially safer way to suppress the proinflammatory cascades that underlie neurodegenerative disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249428/" 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/PMC3249428/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nomura, Daniel K -- Morrison, Bradley E -- Blankman, Jacqueline L -- Long, Jonathan Z -- Kinsey, Steven G -- Marcondes, Maria Cecilia G -- Ward, Anna M -- Hahn, Yun Kyung -- Lichtman, Aron H -- Conti, Bruno -- Cravatt, Benjamin F -- 5P01DA009789/DA/NIDA NIH HHS/ -- AG028040/AG/NIA NIH HHS/ -- DA017259/DA/NIDA NIH HHS/ -- DA026261/DA/NIDA NIH HHS/ -- F31 DA026261-03/DA/NIDA NIH HHS/ -- K99 DA030908/DA/NIDA NIH HHS/ -- K99 DA030908-01/DA/NIDA NIH HHS/ -- K99DA030908/DA/NIDA NIH HHS/ -- P01 DA009789/DA/NIDA NIH HHS/ -- P01 DA009789-14/DA/NIDA NIH HHS/ -- P01 DA017259/DA/NIDA NIH HHS/ -- P01 DA017259-08/DA/NIDA NIH HHS/ -- P01DA01725/DA/NIDA NIH HHS/ -- R00 DA030908/DA/NIDA NIH HHS/ -- R00 DA030908-02/DA/NIDA NIH HHS/ -- R00DA030908/DA/NIDA NIH HHS/ -- R01 AG028040/AG/NIA NIH HHS/ -- R01 AG028040-04/AG/NIA NIH HHS/ -- R03 DA027936/DA/NIDA NIH HHS/ -- R03 DA027936-02/DA/NIDA NIH HHS/ -- R03DA027936/DA/NIDA NIH HHS/ -- T32 DA007027/DA/NIDA NIH HHS/ -- T32 DA007027-33/DA/NIDA NIH HHS/ -- T32DA007027/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2011 Nov 11;334(6057):809-13. doi: 10.1126/science.1209200. Epub 2011 Oct 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Skaggs Institute for Chemical Biology and Department of Chemical Physiology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. dnomura@berkeley.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22021672" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arachidonic Acid/metabolism ; Arachidonic Acids/*metabolism ; Benzodioxoles/pharmacology ; Brain/drug effects/*metabolism/pathology ; Cannabinoid Receptor Modulators/*metabolism ; Cyclooxygenase 1/metabolism ; Cytokines/metabolism ; Eicosanoids/metabolism ; *Endocannabinoids ; Enzyme Inhibitors/pharmacology ; Glycerides/*metabolism ; Hydrolysis ; Inflammation/*metabolism/pathology ; Inflammation Mediators/pharmacology ; Lipopolysaccharides/pharmacology ; Liver/metabolism ; Lung/metabolism ; Metabolomics ; Mice ; Mice, Inbred C57BL ; Monoacylglycerol Lipases/antagonists & inhibitors/genetics/*metabolism ; Neuroprotective Agents/pharmacology ; Parkinsonian Disorders/metabolism/pathology ; Phospholipases A2/genetics/metabolism ; Piperidines/pharmacology ; Prostaglandins/biosynthesis/*metabolism ; Signal Transduction
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    AMP-activated protein kinase regulates neuronal polarization by interfering with PI 3-kinase localization (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-03-26
    Description: Axon-dendrite polarization is crucial for neural network wiring and information processing in the brain. Polarization begins with the transformation of a single neurite into an axon and its subsequent rapid extension, which requires coordination of cellular energy status to allow for transport of building materials to support axon growth. We found that activation of the energy-sensing adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) pathway suppressed axon initiation and neuronal polarization. Phosphorylation of the kinesin light chain of the Kif5 motor protein by AMPK disrupted the association of the motor with phosphatidylinositol 3-kinase (PI3K), preventing PI3K targeting to the axonal tip and inhibiting polarization and axon growth.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3325765/" 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/PMC3325765/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amato, Stephen -- Liu, Xiuxin -- Zheng, Bin -- Cantley, Lewis -- Rakic, Pasko -- Man, Heng-Ye -- GM41890/GM/NIGMS NIH HHS/ -- GM56203/GM/NIGMS NIH HHS/ -- K99CA133245/CA/NCI NIH HHS/ -- MH07907/MH/NIMH NIH HHS/ -- R00 CA133245/CA/NCI NIH HHS/ -- R01 GM056203/GM/NIGMS NIH HHS/ -- R01 NS014841/NS/NINDS NIH HHS/ -- R01 NS014841-32/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2011 Apr 8;332(6026):247-51. doi: 10.1126/science.1201678. Epub 2011 Mar 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Boston University, 5 Cummington Street, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21436401" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/*metabolism ; Aminoimidazole Carboxamide/analogs & derivatives/pharmacology ; Animals ; Axons/enzymology/*physiology/ultrastructure ; *Cell Polarity/drug effects ; Cells, Cultured ; Hippocampus/cytology/embryology ; Metformin/pharmacology ; Mice ; Microtubule-Associated Proteins/metabolism ; Neurons/cytology/drug effects/enzymology/*physiology ; Phosphatidylinositol 3-Kinase/*metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt/metabolism ; Rats ; Recombinant Fusion Proteins/metabolism ; Ribonucleotides/pharmacology ; Signal Transduction ; Tissue Culture Techniques
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    Retrovirology. More negative data for link between mouse virus and human disease (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-03-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- New York, N.Y. -- Science. 2011 Mar 11;331(6022):1253-4. doi: 10.1126/science.331.6022.1253.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21393520" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Tumor ; Fatigue Syndrome, Chronic/*virology ; Humans ; Male ; Mice ; Neoplasm Transplantation ; Prostatic Neoplasms/*virology ; *Recombination, Genetic ; Transplantation, Heterologous ; *Xenotropic murine leukemia virus-related virus/genetics/physiology
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  • 29
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    Ecology. Food and biodiversity (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-09-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Godfray, H Charles J -- New York, N.Y. -- Science. 2011 Sep 2;333(6047):1231-2. doi: 10.1126/science.1211815.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology and Oxford Martin School Institute of Biodiversity, University of Oxford, Oxford OX1 3PS, UK. charles.godfray@zoo.ox.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21885765" target="_blank"〉PubMed〈/a〉
    Keywords: *Agriculture ; Animals ; *Biodiversity ; Birds ; *Conservation of Natural Resources ; Crops, Agricultural/*growth & development ; *Ecosystem ; *Food ; Ghana ; India ; Population Density ; Trees
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    Molecular biology. Preference by exclusion (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Godley, Lucy A -- Mondragon, Alfonso -- New York, N.Y. -- Science. 2011 Feb 25;331(6020):1017-8. doi: 10.1126/science.1202090.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Hematology/Oncology, Department of Medicine, The University of Chicago, Chicago, IL 60637, USA. lgodley@medicine.bsd.uchicago.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21350155" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Catalytic Domain ; Crystallography, X-Ray ; Cysteine/chemistry ; DNA/*chemistry/metabolism ; DNA (Cytosine-5-)-Methyltransferase/*chemistry/*metabolism ; *DNA Methylation ; Dinucleoside Phosphates/chemistry/metabolism ; Humans ; Mice ; Models, Molecular ; Protein Structure, Tertiary ; Substrate Specificity
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    Different B cell populations mediate early and late memory during an endogenous immune response (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-02-12
    Description: Memory B cells formed in response to microbial antigens provide immunity to later infections; however, the inability to detect rare endogenous antigen-specific cells limits current understanding of this process. Using an antigen-based technique to enrich these cells, we found that immunization with a model protein generated B memory cells that expressed isotype-switched immunoglobulins (swIg) or retained IgM. The more numerous IgM(+) cells were longer lived than the swIg(+) cells. However, swIg(+) memory cells dominated the secondary response because of the capacity to become activated in the presence of neutralizing serum immunoglobulin. Thus, we propose that memory relies on swIg(+) cells until they disappear and serum immunoglobulin falls to a low level, in which case memory resides with durable IgM(+) reserves.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3993090/" 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/PMC3993090/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pape, Kathryn A -- Taylor, Justin J -- Maul, Robert W -- Gearhart, Patricia J -- Jenkins, Marc K -- F32 AI091033/AI/NIAID NIH HHS/ -- R01 AI036914/AI/NIAID NIH HHS/ -- R01 AI039614/AI/NIAID NIH HHS/ -- R37 AI027998/AI/NIAID NIH HHS/ -- T32 CA009138/CA/NCI NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2011 Mar 4;331(6021):1203-7. doi: 10.1126/science.1201730. Epub 2011 Feb 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21310965" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/immunology ; Antigens, CD38/analysis ; B-Lymphocyte Subsets/*immunology ; Cell Survival ; Female ; Germinal Center/cytology/immunology ; Immunization ; *Immunoglobulin Class Switching ; Immunoglobulin M/genetics/*immunology ; *Immunologic Memory ; Lymph Nodes/cytology/immunology ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred C57BL ; Mutation ; Phycocyanin/immunology ; Phycoerythrin/immunology ; Spleen/cytology/immunology
    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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    Proteoglycan-specific molecular switch for RPTPsigma clustering and neuronal extension (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-04-02
    Description: Heparan and chondroitin sulfate proteoglycans (HSPGs and CSPGs, respectively) regulate numerous cell surface signaling events, with typically opposite effects on cell function. CSPGs inhibit nerve regeneration through receptor protein tyrosine phosphatase sigma (RPTPsigma). Here we report that RPTPsigma acts bimodally in sensory neuron extension, mediating CSPG inhibition and HSPG growth promotion. Crystallographic analyses of a shared HSPG-CSPG binding site reveal a conformational plasticity that can accommodate diverse glycosaminoglycans with comparable affinities. Heparan sulfate and analogs induced RPTPsigma ectodomain oligomerization in solution, which was inhibited by chondroitin sulfate. RPTPsigma and HSPGs colocalize in puncta on sensory neurons in culture, whereas CSPGs occupy the extracellular matrix. These results lead to a model where proteoglycans can exert opposing effects on neuronal extension by competing to control the oligomerization of a common receptor.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3154093/" 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/PMC3154093/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coles, Charlotte H -- Shen, Yingjie -- Tenney, Alan P -- Siebold, Christian -- Sutton, Geoffrey C -- Lu, Weixian -- Gallagher, John T -- Jones, E Yvonne -- Flanagan, John G -- Aricescu, A Radu -- 090532/Wellcome Trust/United Kingdom -- 10976/Cancer Research UK/United Kingdom -- EY11559/EY/NEI NIH HHS/ -- G0700232/Medical Research Council/United Kingdom -- G0900084/Medical Research Council/United Kingdom -- HD29417/HD/NICHD NIH HHS/ -- R01 EY011559/EY/NEI NIH HHS/ -- R01 EY011559-19/EY/NEI NIH HHS/ -- R37 HD029417/HD/NICHD NIH HHS/ -- R37 HD029417-20/HD/NICHD NIH HHS/ -- Cancer Research UK/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2011 Apr 22;332(6028):484-8. doi: 10.1126/science.1200840. Epub 2011 Mar 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Structural Biology, 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/21454754" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Axons/*physiology ; Binding Sites ; Cell Membrane/metabolism ; Cells, Cultured ; Chondroitin Sulfate Proteoglycans/chemistry/*metabolism ; Chondroitin Sulfates/chemistry/metabolism ; Crystallography, X-Ray ; Extracellular Matrix ; Ganglia, Spinal ; Glypicans/metabolism ; Growth Cones/metabolism ; Heparan Sulfate Proteoglycans/chemistry/*metabolism ; Heparitin Sulfate/analogs & derivatives/chemistry/metabolism ; Humans ; Mice ; Models, Biological ; Models, Molecular ; Molecular Sequence Data ; Neurites/physiology ; Neurocan/metabolism ; Protein Conformation ; Protein Multimerization ; Protein Structure, Tertiary ; Receptor-Like Protein Tyrosine Phosphatases, Class 2/*chemistry/*metabolism ; Sensory Receptor Cells/*physiology
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    Exercise and genetic rescue of SCA1 via the transcriptional repressor Capicua (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-11-05
    Description: Spinocerebellar ataxia type 1 (SCA1) is a fatal neurodegenerative disease caused by expansion of a translated CAG repeat in Ataxin-1 (ATXN1). To determine the long-term effects of exercise, we implemented a mild exercise regimen in a mouse model of SCA1 and found a considerable improvement in survival accompanied by up-regulation of epidermal growth factor and consequential down-regulation of Capicua, which is an ATXN1 interactor. Offspring of Capicua mutant mice bred to SCA1 mice showed significant improvement of all disease phenotypes. Although polyglutamine-expanded Atxn1 caused some loss of Capicua function, further reduction of Capicua levels--either genetically or by exercise--mitigated the disease phenotypes by dampening the toxic gain of function. Thus, exercise might have long-term beneficial effects in other ataxias and neurodegenerative diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3232424/" 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/PMC3232424/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fryer, John D -- Yu, Peng -- Kang, Hyojin -- Mandel-Brehm, Caleigh -- Carter, Angela N -- Crespo-Barreto, Juan -- Gao, Yan -- Flora, Adriano -- Shaw, Chad -- Orr, Harry T -- Zoghbi, Huda Y -- 1F32NS055545/NS/NINDS NIH HHS/ -- HD24064/HD/NICHD NIH HHS/ -- NS022920/NS/NINDS NIH HHS/ -- NS045667/NS/NINDS NIH HHS/ -- NS27699/NS/NINDS NIH HHS/ -- NS27699-20S1/NS/NINDS NIH HHS/ -- P30 HD024064/HD/NICHD NIH HHS/ -- P30 HD024064-22/HD/NICHD NIH HHS/ -- P30 HD024064-23/HD/NICHD NIH HHS/ -- R01 NS027699/NS/NINDS NIH HHS/ -- R01 NS027699-20S1/NS/NINDS NIH HHS/ -- R01 NS027699-21/NS/NINDS NIH HHS/ -- R01 NS027699-22/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Nov 4;334(6056):690-3. doi: 10.1126/science.1212673.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22053053" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxin-1 ; Ataxins ; Cerebellum/metabolism ; Disease Models, Animal ; *Exercise Therapy ; Gene Knock-In Techniques ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Nerve Tissue Proteins/genetics ; Nuclear Proteins/genetics ; Repressor Proteins/genetics/*physiology ; Spinocerebellar Ataxias/genetics/*therapy
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    Cartilage acidic protein-1B (LOTUS), an endogenous Nogo receptor antagonist for axon tract formation (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-08-06
    Description: Neural circuitry formation depends on the molecular control of axonal projection during development. By screening with fluorophore-assisted light inactivation in the developing mouse brain, we identified cartilage acidic protein-1B as a key molecule for lateral olfactory tract (LOT) formation and named it LOT usher substance (LOTUS). We further identified Nogo receptor-1 (NgR1) as a LOTUS-binding protein. NgR1 is a receptor of myelin-derived axon growth inhibitors, such as Nogo, which prevent neural regeneration in the adult. LOTUS suppressed Nogo-NgR1 binding and Nogo-induced growth cone collapse. A defasciculated LOT was present in lotus-deficient mice but not in mice lacking both lotus- and ngr1. These findings suggest that endogenous antagonism of NgR1 by LOTUS is crucial for normal LOT formation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3244695/" 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/PMC3244695/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sato, Yasufumi -- Iketani, Masumi -- Kurihara, Yuji -- Yamaguchi, Megumi -- Yamashita, Naoya -- Nakamura, Fumio -- Arie, Yuko -- Kawasaki, Takahiko -- Hirata, Tatsumi -- Abe, Takaya -- Kiyonari, Hiroshi -- Strittmatter, Stephen M -- Goshima, Yoshio -- Takei, Kohtaro -- R37 NS033020/NS/NINDS NIH HHS/ -- R37 NS033020-19/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2011 Aug 5;333(6043):769-73. doi: 10.1126/science.1204144.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Pharmacology and Neurobiology, Yokohama City University Graduate School of Medicine, Yokohama 236-0004, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21817055" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Binding Sites ; Calcium-Binding Proteins/chemistry/genetics/*metabolism ; Cell Line ; Cells, Cultured ; GPI-Linked Proteins/genetics/metabolism ; Growth Cones/metabolism ; Humans ; Immunohistochemistry ; Ligands ; Mice ; Mice, Inbred ICR ; Myelin Proteins/genetics/*metabolism ; Olfactory Pathways/*cytology/*growth & development/metabolism ; Prosencephalon/embryology/metabolism ; Protein Binding ; Receptors, Cell Surface/genetics/*metabolism ; Signal Transduction
    Print ISSN: 0036-8075
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    Physiology. Synthetic physiology (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-06-28
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3553595/" 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/PMC3553595/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chow, Brian Y -- Boyden, Edward S -- R01 NS075421/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2011 Jun 24;332(6037):1508-9. doi: 10.1126/science.1208555.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21700858" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/analysis ; Gene Expression Regulation ; Genes, Reporter ; Genetic Engineering/*methods ; Glucagon-Like Peptide 1/genetics ; Insulin/blood ; *Light ; Light Signal Transduction ; Mice ; NFATC Transcription Factors/metabolism ; Rod Opsins/*genetics/metabolism ; Synthetic Biology/*methods
    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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    Medicine. The genetics of primary aldosteronism (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-02-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Funder, John W -- New York, N.Y. -- Science. 2011 Feb 11;331(6018):685-6. doi: 10.1126/science.1202887.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Prince Henry's Institute of Medical Research, Monash Medical Centre, Clayton, Victoria 3168, Australia. john.funder@princehenrys.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21310991" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Cortex Neoplasms/*genetics/physiopathology ; Adrenal Glands/pathology ; Adrenocortical Adenoma/*genetics/physiopathology ; Aldosterone/*metabolism ; Animals ; Disease Models, Animal ; Female ; G Protein-Coupled Inwardly-Rectifying Potassium Channels/*genetics/metabolism ; Humans ; Hyperaldosteronism/*genetics/physiopathology ; Hyperplasia ; Hypertension/physiopathology ; Male ; Mice ; Mutation
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    Three periods of regulatory innovation during vertebrate evolution (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-08-20
    Description: The gain, loss, and modification of gene regulatory elements may underlie a substantial proportion of phenotypic changes on animal lineages. To investigate the gain of regulatory elements throughout vertebrate evolution, we identified genome-wide sets of putative regulatory regions for five vertebrates, including humans. These putative regulatory regions are conserved nonexonic elements (CNEEs), which are evolutionarily conserved yet do not overlap any coding or noncoding mature transcript. We then inferred the branch on which each CNEE came under selective constraint. Our analysis identified three extended periods in the evolution of gene regulatory elements. Early vertebrate evolution was characterized by regulatory gains near transcription factors and developmental genes, but this trend was replaced by innovations near extracellular signaling genes, and then innovations near posttranslational protein modifiers.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3511857/" 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/PMC3511857/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lowe, Craig B -- Kellis, Manolis -- Siepel, Adam -- Raney, Brian J -- Clamp, Michele -- Salama, Sofie R -- Kingsley, David M -- Lindblad-Toh, Kerstin -- Haussler, David -- 1U01-HG004695/HG/NHGRI NIH HHS/ -- 5P41-HG002371/HG/NHGRI NIH HHS/ -- P41 HG002371/HG/NHGRI NIH HHS/ -- P50 HG002568/HG/NHGRI NIH HHS/ -- P50-HG02568/HG/NHGRI NIH HHS/ -- R01 HG004037/HG/NHGRI NIH HHS/ -- R01-HG004037/HG/NHGRI NIH HHS/ -- U01 HG004695/HG/NHGRI NIH HHS/ -- U54 HG003067/HG/NHGRI NIH HHS/ -- U54-HG003067/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Aug 19;333(6045):1019-24. doi: 10.1126/science.1202702.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Biomolecular Science and Engineering, University of California, Santa Cruz, CA 95064, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21852499" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Cattle ; *Conserved Sequence ; DNA, Intergenic/genetics ; *Evolution, Molecular ; Gene Expression Regulation ; Genes, Developmental ; Genome ; Humans ; Markov Chains ; Mice ; Oryzias/genetics ; Phylogeny ; Protein Processing, Post-Translational/genetics ; *Regulatory Elements, Transcriptional ; *Regulatory Sequences, Nucleic Acid ; Selection, Genetic ; Sequence Alignment ; Smegmamorpha/genetics ; Transcription Factors/genetics ; Vertebrates/*genetics
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    Isolation of single human hematopoietic stem cells capable of long-term multilineage engraftment (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-07-09
    Description: Lifelong blood cell production is dependent on rare hematopoietic stem cells (HSCs) to perpetually replenish mature cells via a series of lineage-restricted intermediates. Investigating the molecular state of HSCs is contingent on the ability to purify HSCs away from transiently engrafting cells. We demonstrated that human HSCs remain infrequent, using current purification strategies based on Thy1 (CD90) expression. By tracking the expression of several adhesion molecules in HSC-enriched subsets, we revealed CD49f as a specific HSC marker. Single CD49f(+) cells were highly efficient in generating long-term multilineage grafts, and the loss of CD49f expression identified transiently engrafting multipotent progenitors (MPPs). The demarcation of human HSCs and MPPs will enable the investigation of the molecular determinants of HSCs, with a goal of developing stem cell-based therapeutics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Notta, Faiyaz -- Doulatov, Sergei -- Laurenti, Elisa -- Poeppl, Armando -- Jurisica, Igor -- Dick, John E -- Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2011 Jul 8;333(6039):218-21. doi: 10.1126/science.1201219.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Stem Cell and Developmental Biology, Campbell Family Institute for Cancer Research/Ontario Cancer Institute, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21737740" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD34/analysis ; Antigens, Thy-1/analysis ; *Cell Lineage ; Cell Proliferation ; *Cell Separation ; Coculture Techniques ; Fetal Blood/cytology ; Flow Cytometry ; Gene Expression Profiling ; Hematopoiesis ; *Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/cytology/immunology/*physiology ; Humans ; Integrin alpha6/analysis ; Mice ; Mice, Inbred NOD ; Multipotent Stem Cells/cytology/immunology/*physiology ; Stromal Cells/cytology/physiology ; Transplantation, Heterologous
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    Medicine. Lipases in cachexia (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-07-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arner, Peter -- New York, N.Y. -- Science. 2011 Jul 8;333(6039):163-4. doi: 10.1126/science.1209418.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Karolinska Institutet at Karolinska University Hospital, Stockholm, Sweden. peter.arner@ki.se〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21737725" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/*enzymology ; Adipose Tissue/*enzymology/pathology ; Animals ; Cachexia/*enzymology/etiology/pathology/prevention & control ; Humans ; Lipase/deficiency/*metabolism ; *Lipolysis ; Lung Neoplasms/complications/enzymology/metabolism/pathology ; Melanoma, Experimental/complications/enzymology/metabolism/pathology ; Mice ; Models, Biological ; Muscle, Skeletal/metabolism/pathology ; Neoplasms/complications/*enzymology/metabolism/pathology ; Oxidation-Reduction ; Sterol Esterase/antagonists & inhibitors/deficiency/*metabolism ; Triglycerides/metabolism
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    GRK2-dependent S1PR1 desensitization is required for lymphocytes to overcome their attraction to blood (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-10-01
    Description: Lymphocytes egress from lymphoid organs in response to sphingosine-1-phosphate (S1P); minutes later they migrate from blood into tissue against the S1P gradient. The mechanisms facilitating cell movement against the gradient have not been defined. Here, we show that heterotrimeric guanine nucleotide-binding protein-coupled receptor kinase-2 (GRK2) functions in down-regulation of S1P receptor-1 (S1PR1) on blood-exposed lymphocytes. T and B cell movement from blood into lymph nodes is reduced in the absence of GRK2 but is restored in S1P-deficient mice. In the spleen, B cell movement between the blood-rich marginal zone and follicles is disrupted by GRK2 deficiency and by mutation of an S1PR1 desensitization motif. Moreover, delivery of systemic antigen into follicles is impaired. Thus, GRK2-dependent S1PR1 desensitization allows lymphocytes to escape circulatory fluids and migrate into lymphoid tissues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3267326/" 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/PMC3267326/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arnon, Tal I -- Xu, Ying -- Lo, Charles -- Pham, Trung -- An, Jinping -- Coughlin, Shaun -- Dorn, Gerald W -- Cyster, Jason G -- AI74847/AI/NIAID NIH HHS/ -- R01 AI074847/AI/NIAID NIH HHS/ -- R01 AI074847-05/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Sep 30;333(6051):1898-903. doi: 10.1126/science.1208248.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Microbiology and Immunology, University of California San Francisco, 513 Parnassus Avenue, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21960637" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Antibody Complex/immunology ; B-Lymphocytes/immunology/*physiology ; Blood ; Cell Movement ; Chemokines/physiology ; Chemotaxis, Leukocyte ; Down-Regulation ; G-Protein-Coupled Receptor Kinase 2/*metabolism ; Ligands ; Lymph Nodes/cytology ; Lysophospholipids/metabolism ; Mice ; Mice, Inbred C57BL ; Mutation ; Receptors, Lysosphingolipid/genetics/*metabolism ; Signal Transduction ; Sphingosine/analogs & derivatives/metabolism ; Spleen/cytology/immunology ; T-Lymphocytes/immunology/*physiology
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    Activation of visual pigments by light and heat (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-06-11
    Description: Vision begins with photoisomerization of visual pigments. Thermal energy can complement photon energy to drive photoisomerization, but it also triggers spontaneous pigment activation as noise that interferes with light detection. For half a century, the mechanism underlying this dark noise has remained controversial. We report here a quantitative relation between a pigment's photoactivation energy and its peak-absorption wavelength, lambda(max). Using this relation and assuming that pigment activations by light and heat go through the same ground-state isomerization energy barrier, we can predict the relative noise of diverse pigments with multi-vibrational-mode thermal statistics. The agreement between predictions and our measurements strongly suggests that pigment noise arises from canonical isomerization. The predicted high noise for pigments with lambda(max) in the infrared presumably explains why they apparently do not exist in nature.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4349410/" 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/PMC4349410/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luo, Dong-Gen -- Yue, Wendy W S -- Ala-Laurila, Petri -- Yau, King-Wai -- EY06837/EY/NEI NIH HHS/ -- R01 EY006837/EY/NEI NIH HHS/ -- R37 EY006837/EY/NEI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Jun 10;332(6035):1307-12. doi: 10.1126/science.1200172.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. dgluo@jhmi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21659602" target="_blank"〉PubMed〈/a〉
    Keywords: Ambystoma ; Animals ; Bufo marinus ; Goldfish ; Hot Temperature ; In Vitro Techniques ; Light ; *Light Signal Transduction ; Mice ; Mice, Inbred C57BL ; Photons ; Retinal Cone Photoreceptor Cells/physiology ; Retinal Pigments/chemistry/*physiology/radiation effects ; Rhodopsin/physiology
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    Induction of colonic regulatory T cells by indigenous Clostridium species (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-01-06
    Description: CD4(+) T regulatory cells (T(regs)), which express the Foxp3 transcription factor, play a critical role in the maintenance of immune homeostasis. Here, we show that in mice, T(regs) were most abundant in the colonic mucosa. The spore-forming component of indigenous intestinal microbiota, particularly clusters IV and XIVa of the genus Clostridium, promoted T(reg) cell accumulation. Colonization of mice by a defined mix of Clostridium strains provided an environment rich in transforming growth factor-beta and affected Foxp3(+) T(reg) number and function in the colon. Oral inoculation of Clostridium during the early life of conventionally reared mice resulted in resistance to colitis and systemic immunoglobulin E responses in adult mice, suggesting a new therapeutic approach to autoimmunity and allergy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3969237/" 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/PMC3969237/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Atarashi, Koji -- Tanoue, Takeshi -- Shima, Tatsuichiro -- Imaoka, Akemi -- Kuwahara, Tomomi -- Momose, Yoshika -- Cheng, Genhong -- Yamasaki, Sho -- Saito, Takashi -- Ohba, Yusuke -- Taniguchi, Tadatsugu -- Takeda, Kiyoshi -- Hori, Shohei -- Ivanov, Ivaylo I -- Umesaki, Yoshinori -- Itoh, Kikuji -- Honda, Kenya -- R00 DK085329/DK/NIDDK NIH HHS/ -- R01 AI052359/AI/NIAID NIH HHS/ -- R01 AI056154/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2011 Jan 21;331(6015):337-41. doi: 10.1126/science.1198469. Epub 2010 Dec 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Graduate School of Medicine, University of Tokyo, Tokyo 113-0033, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21205640" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/pharmacology ; Cecum/microbiology ; Cells, Cultured ; Clostridium/growth & development/*immunology ; Colitis/immunology/pathology/prevention & control ; Colon/*immunology/metabolism/*microbiology ; Feces/microbiology ; Forkhead Transcription Factors/metabolism ; Germ-Free Life ; Immunity, Innate ; Immunoglobulin E/biosynthesis ; Interleukin-10/immunology/metabolism ; Intestinal Mucosa/*immunology/metabolism ; Intestine, Small/immunology ; Metagenome ; Mice ; Mice, Inbred A ; Mice, Inbred BALB C ; Receptors, Pattern Recognition/physiology ; Specific Pathogen-Free Organisms ; T-Lymphocytes, Helper-Inducer/immunology ; T-Lymphocytes, Regulatory/*immunology/metabolism ; Transforming Growth Factor beta/metabolism
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    The antibacterial lectin RegIIIgamma promotes the spatial segregation of microbiota and host in the intestine (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-10-15
    Description: The mammalian intestine is home to ~100 trillion bacteria that perform important metabolic functions for their hosts. The proximity of vast numbers of bacteria to host intestinal tissues raises the question of how symbiotic host-bacterial relationships are maintained without eliciting potentially harmful immune responses. Here, we show that RegIIIgamma, a secreted antibacterial lectin, is essential for maintaining a ~50-micrometer zone that physically separates the microbiota from the small intestinal epithelial surface. Loss of host-bacterial segregation in RegIIIgamma(-/-) mice was coupled to increased bacterial colonization of the intestinal epithelial surface and enhanced activation of intestinal adaptive immune responses by the microbiota. Together, our findings reveal that RegIIIgamma is a fundamental immune mechanism that promotes host-bacterial mutualism by regulating the spatial relationships between microbiota and host.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321924/" 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/PMC3321924/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vaishnava, Shipra -- Yamamoto, Miwako -- Severson, Kari M -- Ruhn, Kelly A -- Yu, Xiaofei -- Koren, Omry -- Ley, Ruth -- Wakeland, Edward K -- Hooper, Lora V -- R01 DK070855/DK/NIDDK NIH HHS/ -- R01 DK070855-06/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Oct 14;334(6053):255-8. doi: 10.1126/science.1209791.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, The University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21998396" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity ; Animals ; Anti-Bacterial Agents/pharmacology ; Bacterial Load ; Gram-Negative Bacteria/immunology/*physiology ; Gram-Positive Bacteria/immunology/*physiology ; Homeostasis ; Immunoglobulin A/analysis ; Intestinal Mucosa/immunology/*microbiology ; Intestine, Small/immunology/*microbiology ; Lectins, C-Type/physiology ; *Metagenome ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Myeloid Differentiation Factor 88/genetics/metabolism ; Proteins/*metabolism ; Symbiosis ; T-Lymphocytes, Helper-Inducer/immunology
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    Protein tyrosine kinase Wee1B is essential for metaphase II exit in mouse oocytes (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-04-02
    Description: Waves of cyclin synthesis and degradation regulate the activity of Cdc2 protein kinase during the cell cycle. Cdc2 inactivation by Wee1B-mediated phosphorylation is necessary for arrest of the oocyte at G2-prophase, but it is unclear whether this regulation functions later during the metaphase-to-anaphase transition. We show that reactivation of a Wee1B pathway triggers the decrease in Cdc2 activity during egg activation. When Wee1B is down-regulated, oocytes fail to form a pronucleus in response to Ca(2+) signals. Calcium-calmodulin-dependent kinase II (CaMKII) activates Wee1B, and CaMKII-driven exit from metaphase II is inhibited by Wee1B down-regulation, demonstrating that exit from metaphase requires not only a proteolytic degradation of cyclin B but also the inhibitory phosphorylation of Cdc2 by Wee1B.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4104668/" 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/PMC4104668/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oh, Jeong Su -- Susor, Andrej -- Conti, Marco -- GM080527-05/GM/NIGMS NIH HHS/ -- HD052909/HD/NICHD NIH HHS/ -- R01 GM080527/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Apr 22;332(6028):462-5. doi: 10.1126/science.1199211. Epub 2011 Mar 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Reproductive Sciences, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, CA 94143-0556, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21454751" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CDC2 Protein Kinase/antagonists & inhibitors/metabolism ; Calcium/metabolism ; Calcium Signaling ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism ; Cell Cycle Proteins/genetics/*metabolism ; Cyclin B/genetics/metabolism ; Down-Regulation ; Female ; Gene Knockdown Techniques ; Maturation-Promoting Factor/metabolism ; *Meiosis ; *Metaphase ; Mice ; Mice, Inbred C57BL ; Oocytes/*physiology ; Phosphorylation ; Protein-Tyrosine Kinases/genetics/*metabolism ; RNA, Messenger/genetics/metabolism
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    Chronic fatigue syndrome. Studies point to possible contamination in XMRV findings (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-01-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2011 Jan 7;331(6013):17. doi: 10.1126/science.331.6013.17.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21212329" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Viral/biosynthesis ; Blood/virology ; Cells, Cultured ; DNA Contamination ; Fatigue Syndrome, Chronic/*virology ; Humans ; Mice ; Polymerase Chain Reaction ; Retroviridae Infections/*virology ; Sensitivity and Specificity ; Viremia ; Xenotropic murine leukemia virus-related virus/immunology/*isolation & ; purification/pathogenicity
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    Successful transmission of a retrovirus depends on the commensal microbiota (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-10-15
    Description: To establish chronic infections, viruses must develop strategies to evade the host's immune responses. Many retroviruses, including mouse mammary tumor virus (MMTV), are transmitted most efficiently through mucosal surfaces rich in microbiota. We found that MMTV, when ingested by newborn mice, stimulates a state of unresponsiveness toward viral antigens. This process required the intestinal microbiota, as antibiotic-treated mice or germ-free mice did not transmit infectious virus to their offspring. MMTV-bound bacterial lipopolysaccharide triggered Toll-like receptor 4 and subsequent interleukin-6 (IL-6)-dependent induction of the inhibitory cytokine IL-10. Thus, MMTV has evolved to rely on the interaction with the microbiota to induce an immune evasion pathway. Together, these findings reveal the fundamental importance of commensal microbiota in viral infections.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3519937/" 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/PMC3519937/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kane, Melissa -- Case, Laure K -- Kopaskie, Karyl -- Kozlova, Alena -- MacDearmid, Cameron -- Chervonsky, Alexander V -- Golovkina, Tatyana V -- AI082418/AI/NIAID NIH HHS/ -- AI090084/AI/NIAID NIH HHS/ -- CA100383/CA/NCI NIH HHS/ -- DK42086/DK/NIDDK NIH HHS/ -- P30 CA014599/CA/NCI NIH HHS/ -- R01 AI090084/AI/NIAID NIH HHS/ -- R01 CA134667/CA/NCI NIH HHS/ -- R56 AI090084/AI/NIAID NIH HHS/ -- T32 AI065382-01/AI/NIAID NIH HHS/ -- T32GM007183/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Oct 14;334(6053):245-9. doi: 10.1126/science.1210718.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, The University of Chicago, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21998394" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Anti-Bacterial Agents/pharmacology ; Antibodies, Viral/biosynthesis ; Antigens, Viral/immunology ; *Bacterial Physiological Phenomena ; Female ; Germ-Free Life ; *Immune Evasion ; Interleukin-10/genetics/metabolism ; Intestinal Mucosa/*virology ; Intestines/*microbiology ; Lipopolysaccharides/immunology/metabolism ; Mammary Tumor Virus, Mouse/*immunology/*pathogenicity ; *Metagenome ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Pregnancy ; Pregnancy Complications, Infectious/virology ; Retroviridae Infections/immunology/*transmission/virology ; Specific Pathogen-Free Organisms ; Toll-Like Receptor 4/immunology/metabolism ; Tumor Virus Infections/immunology/transmission/virology ; Virus Replication
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    Role for the membrane receptor guanylyl cyclase-C in attention deficiency and hyperactive behavior (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-08-13
    Description: Midbrain dopamine neurons regulate many important behavioral processes, and their dysfunctions are associated with several human neuropsychiatric disorders such as attention deficit hyperactivity disorder (ADHD) and schizophrenia. Here, we report that these neurons in mice selectively express guanylyl cyclase-C (GC-C), a membrane receptor previously thought to be expressed mainly in the intestine. GC-C activation potentiates the excitatory responses mediated by glutamate and acetylcholine receptors via the activity of guanosine 3',5'-monophosphate-dependent protein kinase (PKG). Mice in which GC-C has been knocked out exhibit hyperactivity and attention deficits. Moreover, their behavioral phenotypes are reversed by ADHD therapeutics and a PKG activator. These results indicate important behavioral and physiological functions for the GC-C/PKG signaling pathway within the brain and suggest new therapeutic targets for neuropsychiatric disorders related to the malfunctions of midbrain dopamine neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gong, Rong -- Ding, Cheng -- Hu, Ji -- Lu, Yao -- Liu, Fei -- Mann, Elizabeth -- Xu, Fuqiang -- Cohen, Mitchell B -- Luo, Minmin -- New York, N.Y. -- Science. 2011 Sep 16;333(6049):1642-6. doi: 10.1126/science.1207675. Epub 2011 Aug 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Program in Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21835979" target="_blank"〉PubMed〈/a〉
    Keywords: Amphetamine/administration & dosage ; Animals ; Attention ; Attention Deficit Disorder with Hyperactivity/genetics/*metabolism ; Behavior, Animal/drug effects ; Cyclic GMP/metabolism ; Cyclic GMP-Dependent Protein Kinases/*metabolism ; Disease Models, Animal ; Dopamine/metabolism ; Enzyme Activation ; Gastrointestinal Hormones/metabolism/pharmacology ; Glycine/analogs & derivatives/metabolism/pharmacology ; Impulsive Behavior ; Ligands ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Motor Activity/drug effects ; Natriuretic Peptides/metabolism/pharmacology ; Neurons/*metabolism ; Patch-Clamp Techniques ; Receptors, Glutamate/metabolism ; Receptors, Guanylate Cyclase-Coupled/genetics/*metabolism ; Receptors, Muscarinic/metabolism ; Receptors, Peptide/genetics/*metabolism ; Resorcinols/metabolism/pharmacology ; Signal Transduction ; Substantia Nigra/cytology/*metabolism ; Ventral Tegmental Area/cytology/*metabolism
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    Chemical and genetic engineering of selective ion channel-ligand interactions (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-09-03
    Description: Ionic flux mediates essential physiological and behavioral functions in defined cell populations. Cell type-specific activators of diverse ionic conductances are needed for probing these effects. We combined chemistry and protein engineering to enable the systematic creation of a toolbox of ligand-gated ion channels (LGICs) with orthogonal pharmacologic selectivity and divergent functional properties. The LGICs and their small-molecule effectors were able to activate a range of ionic conductances in genetically specified cell types. LGICs constructed for neuronal perturbation could be used to selectively manipulate neuron activity in mammalian brains in vivo. The diversity of ion channel tools accessible from this approach will be useful for examining the relationship between neuronal activity and animal behavior, as well as for cell biological and physiological applications requiring chemical control of ion conductance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3210548/" 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/PMC3210548/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Magnus, Christopher J -- Lee, Peter H -- Atasoy, Deniz -- Su, Helen H -- Looger, Loren L -- Sternson, Scott M -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Sep 2;333(6047):1292-6. doi: 10.1126/science.1206606.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Janelia Farm Research Campus, Howard Hughes Medical Institute, 19700 Helix Drive, Ashburn, VA 20147, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21885782" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzamides/chemistry/metabolism/pharmacology ; Bicyclo Compounds/chemistry/metabolism/pharmacology ; Brain/cytology/physiology ; Feeding Behavior ; Female ; HEK293 Cells ; Humans ; Ion Channel Gating ; Ligand-Gated Ion Channels/chemistry/*genetics/*metabolism ; Ligands ; Membrane Potentials ; Mice ; Mice, Inbred C57BL ; Mutagenesis ; Neurons/*physiology ; Patch-Clamp Techniques ; Protein Binding ; *Protein Engineering ; Protein Structure, Tertiary ; Quinuclidines/chemistry/metabolism/pharmacology ; Receptors, Glycine/genetics/metabolism ; Receptors, Nicotinic/chemistry/genetics/metabolism ; Receptors, Serotonin, 5-HT3/genetics/metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Small Molecule Libraries ; Stereoisomerism ; alpha7 Nicotinic Acetylcholine Receptor
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    A key enzyme in the biogenesis of lysosomes is a protease that regulates cholesterol metabolism (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-07-02
    Description: Mucolipidosis II is a severe lysosomal storage disorder caused by defects in the alpha and beta subunits of the hexameric N-acetylglucosamine-1-phosphotransferase complex essential for the formation of the mannose 6-phosphate targeting signal on lysosomal enzymes. Cleavage of the membrane-bound alpha/beta-subunit precursor by an unknown protease is required for catalytic activity. Here we found that the alpha/beta-subunit precursor is cleaved by the site-1 protease (S1P) that activates sterol regulatory element-binding proteins in response to cholesterol deprivation. S1P-deficient cells failed to activate the alpha/beta-subunit precursor and exhibited a mucolipidosis II-like phenotype. Thus, S1P functions in the biogenesis of lysosomes, and lipid-independent phenotypes of S1P deficiency may be caused by lysosomal dysfunction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marschner, Katrin -- Kollmann, Katrin -- Schweizer, Michaela -- Braulke, Thomas -- Pohl, Sandra -- New York, N.Y. -- Science. 2011 Jul 1;333(6038):87-90. doi: 10.1126/science.1205677.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Children's Hospital, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21719679" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CHO Cells ; Cell Line ; Cholesterol/*metabolism ; Chondrocytes/cytology ; Cricetinae ; Cricetulus ; Enzyme Precursors/chemistry/*metabolism ; HeLa Cells ; Humans ; Lipid Metabolism ; Lysosomes/enzymology/*metabolism/ultrastructure ; Mannosephosphates/metabolism ; Mice ; Morphogenesis ; Mucolipidoses/enzymology/genetics/metabolism/pathology ; N-Acetylgalactosamine-4-Sulfatase/metabolism ; Osteogenesis ; Proprotein Convertases/genetics/*metabolism ; Protein Subunits/chemistry/metabolism ; RNA, Small Interfering ; Serine Endopeptidases/genetics/*metabolism ; Transferases (Other Substituted Phosphate Groups)/chemistry/*metabolism
    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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    Distinct properties of the XY pseudoautosomal region crucial for male meiosis (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-02-19
    Description: Meiosis requires that each chromosome find its homologous partner and undergo at least one crossover. X-Y chromosome segregation hinges on efficient crossing-over in a very small region of homology, the pseudoautosomal region (PAR). We find that mouse PAR DNA occupies unusually long chromosome axes, potentially as shorter chromatin loops, predicted to promote double-strand break (DSB) formation. Most PARs show delayed appearance of RAD51/DMC1 foci, which mark DSB ends, and all PARs undergo delayed DSB-mediated homologous pairing. Analysis of Spo11beta isoform-specific transgenic mice revealed that late RAD51/DMC1 foci in the PAR are genetically distinct from both early PAR foci and global foci and that late PAR foci promote efficient X-Y pairing, recombination, and male fertility. Our findings uncover specific mechanisms that surmount the unique challenges of X-Y recombination.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3151169/" 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/PMC3151169/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kauppi, Liisa -- Barchi, Marco -- Baudat, Frederic -- Romanienko, Peter J -- Keeney, Scott -- Jasin, Maria -- R01 HD040916/HD/NICHD NIH HHS/ -- R01 HD040916-01/HD/NICHD NIH HHS/ -- R01 HD040916-10/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2011 Feb 18;331(6019):916-20. doi: 10.1126/science.1195774.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21330546" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Cycle Proteins/metabolism ; Chromatin/chemistry/metabolism ; *Chromosome Pairing ; Chromosome Segregation ; *Crossing Over, Genetic ; DNA Breaks, Double-Stranded ; Endodeoxyribonucleases/genetics/*metabolism ; Female ; In Situ Hybridization, Fluorescence ; Male ; *Meiosis ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Molecular Sequence Data ; Nuclear Proteins/metabolism ; Protein Isoforms ; Rad51 Recombinase/metabolism ; X Chromosome/*physiology ; Y Chromosome/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Conservation ecology. Embracing invasives (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-03-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vince, Gaia -- New York, N.Y. -- Science. 2011 Mar 18;331(6023):1383-4. doi: 10.1126/science.331.6023.1383.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21415332" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biodiversity ; *Conservation of Natural Resources ; *Ecosystem ; Ecuador ; Geography ; *Introduced Species ; Plants ; Trees
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Tissue engineering. Mending the youngest hearts (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-08-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2011 Aug 26;333(6046):1088-9. doi: 10.1126/science.333.6046.1088.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21868648" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Blood Vessel Prosthesis ; *Blood Vessel Prosthesis Implantation ; Blood Vessels/physiology ; Bone Marrow Cells/physiology ; Child, Preschool ; Clinical Trials as Topic ; Heart Defects, Congenital/*surgery ; Humans ; Mice ; Neovascularization, Physiologic ; Regeneration ; *Tissue Engineering ; Tissue Scaffolds
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    The leukemogenicity of AML1-ETO is dependent on site-specific lysine acetylation (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-07-19
    Description: The chromosomal translocations found in acute myelogenous leukemia (AML) generate oncogenic fusion transcription factors with aberrant transcriptional regulatory properties. Although therapeutic targeting of most leukemia fusion proteins remains elusive, the posttranslational modifications that control their function could be targetable. We found that AML1-ETO, the fusion protein generated by the t(8;21) translocation, is acetylated by the transcriptional coactivator p300 in leukemia cells isolated from t(8;21) AML patients, and that this acetylation is essential for its self-renewal-promoting effects in human cord blood CD34(+) cells and its leukemogenicity in mouse models. Inhibition of p300 abrogates the acetylation of AML1-ETO and impairs its ability to promote leukemic transformation. Thus, lysine acetyltransferases represent a potential therapeutic target in AML.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3251012/" 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/PMC3251012/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Lan -- Gural, Alexander -- Sun, Xiao-Jian -- Zhao, Xinyang -- Perna, Fabiana -- Huang, Gang -- Hatlen, Megan A -- Vu, Ly -- Liu, Fan -- Xu, Haiming -- Asai, Takashi -- Xu, Hao -- Deblasio, Tony -- Menendez, Silvia -- Voza, Francesca -- Jiang, Yanwen -- Cole, Philip A -- Zhang, Jinsong -- Melnick, Ari -- Roeder, Robert G -- Nimer, Stephen D -- GM62437/GM/NIGMS NIH HHS/ -- R01 GM062437/GM/NIGMS NIH HHS/ -- R01 GM062437-12/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Aug 5;333(6043):765-9. doi: 10.1126/science.1201662. Epub 2011 Jul 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Pharmacology and Chemistry Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21764752" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Cell Line ; Cell Line, Tumor ; *Cell Transformation, Neoplastic ; Core Binding Factor Alpha 2 Subunit/chemistry/*metabolism ; E1A-Associated p300 Protein/antagonists & inhibitors/*metabolism ; Fetal Blood/cytology ; Gene Expression Profiling ; Hematopoietic Stem Cells/*cytology/physiology ; Humans ; Leukemia, Myeloid, Acute/*metabolism/pathology ; Lysine/*metabolism ; Mice ; Mice, Inbred C57BL ; Mutant Proteins/metabolism ; Oncogene Proteins, Fusion/chemistry/*metabolism ; Preleukemia/metabolism/pathology ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Processing, Post-Translational ; Transcriptional Activation ; Tumor Cells, Cultured
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    Retrotransposons. Do jumping genes spawn diversity? (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-04-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2011 Apr 15;332(6027):300-1. doi: 10.1126/science.332.6027.300.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21493838" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/cytology/growth & development/*physiology ; Embryo, Mammalian/physiology ; Embryonic Stem Cells/physiology ; *Genetic Variation ; Genome, Human ; Humans ; *Interspersed Repetitive Sequences ; Long Interspersed Nucleotide Elements/*genetics ; Methyl-CpG-Binding Protein 2/genetics ; Mice ; *Neurogenesis ; Neurons/cytology/*physiology ; Rats ; Stem Cells/cytology/*physiology
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    SIRT6 promotes DNA repair under stress by activating PARP1 (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-06-18
    Description: Sirtuin 6 (SIRT6) is a mammalian homolog of the yeast Sir2 deacetylase. Mice deficient for SIRT6 exhibit genome instability. Here, we show that in mammalian cells subjected to oxidative stress SIRT6 is recruited to the sites of DNA double-strand breaks (DSBs) and stimulates DSB repair, through both nonhomologous end joining and homologous recombination. Our results indicate that SIRT6 physically associates with poly[adenosine diphosphate (ADP)-ribose] polymerase 1 (PARP1) and mono-ADP-ribosylates PARP1 on lysine residue 521, thereby stimulating PARP1 poly-ADP-ribosylase activity and enhancing DSB repair under oxidative stress.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mao, Zhiyong -- Hine, Christopher -- Tian, Xiao -- Van Meter, Michael -- Au, Matthew -- Vaidya, Amita -- Seluanov, Andrei -- Gorbunova, Vera -- F31 AG041603/AG/NIA NIH HHS/ -- R01 AG027237/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2011 Jun 17;332(6036):1443-6. doi: 10.1126/science.1202723.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Rochester, Rochester, NY 14627, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21680843" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; DNA/metabolism ; *DNA Breaks, Double-Stranded ; *DNA Repair ; Humans ; Mice ; Mice, Knockout ; *Oxidative Stress ; Paraquat/pharmacology ; Point Mutation ; Poly Adenosine Diphosphate Ribose/metabolism ; Poly(ADP-ribose) Polymerases/genetics/*metabolism ; Recombination, Genetic ; Signal Transduction ; Sirtuins/genetics/*metabolism ; Transfection
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    BRCA1 tumor suppression depends on BRCT phosphoprotein binding, but not its E3 ligase activity (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-10-29
    Description: Germline mutations of the breast cancer 1 (BRCA1) gene are a major cause of familial breast and ovarian cancer. The BRCA1 protein displays E3 ubiquitin ligase activity, and this enzymatic function is thought to be required for tumor suppression. To test this hypothesis, we generated mice that express an enzymatically defective Brca1. We found that this mutant Brca1 prevents tumor formation to the same degree as does wild-type Brca1 in three different genetically engineered mouse (GEM) models of cancer. In contrast, a mutation that ablates phosphoprotein recognition by the BRCA C terminus (BRCT) domains of BRCA1 elicits tumors in each of the three GEM models. Thus, BRCT phosphoprotein recognition, but not the E3 ligase activity, is required for BRCA1 tumor suppression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3904783/" 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/PMC3904783/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shakya, Reena -- Reid, Latarsha J -- Reczek, Colleen R -- Cole, Francesca -- Egli, Dieter -- Lin, Chyuan-Sheng -- deRooij, Dirk G -- Hirsch, Steffen -- Ravi, Kandasamy -- Hicks, James B -- Szabolcs, Matthias -- Jasin, Maria -- Baer, Richard -- Ludwig, Thomas -- F31-CA132626/CA/NCI NIH HHS/ -- F32-HD51392/HD/NICHD NIH HHS/ -- P01 CA097403/CA/NCI NIH HHS/ -- P01-CA97403/CA/NCI NIH HHS/ -- R01 CA137023/CA/NCI NIH HHS/ -- R01 HD040916/HD/NICHD NIH HHS/ -- R01 HD040916-10/HD/NICHD NIH HHS/ -- R01-CA137023/CA/NCI NIH HHS/ -- R01-HD40916/HD/NICHD NIH HHS/ -- T32-CA09503/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2011 Oct 28;334(6055):525-8. doi: 10.1126/science.1209909.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cancer Genetics, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22034435" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; BRCA1 Protein/chemistry/*metabolism ; Basic-Leucine Zipper Transcription Factors/genetics/metabolism ; Cells, Cultured ; Disease Models, Animal ; Embryonic Stem Cells/metabolism ; *Genes, BRCA1 ; Ligands ; Mammary Neoplasms, Experimental/*genetics/metabolism ; Mice ; Mutant Proteins/chemistry/genetics/metabolism ; Pancreatic Neoplasms/*genetics/metabolism ; Phosphoproteins/*metabolism ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Multimerization ; RING Finger Domains ; Tumor Suppressor Proteins/chemistry/metabolism ; Ubiquitin-Protein Ligases/chemistry/metabolism
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    Personalized medicine. Pushing the envelope in neuroblastoma therapy (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-09-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin-Frankel, Jennifer -- New York, N.Y. -- Science. 2011 Sep 16;333(6049):1569-71. doi: 10.1126/science.333.6049.1569.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21921174" target="_blank"〉PubMed〈/a〉
    Keywords: *Algorithms ; Animals ; Antineoplastic Agents/*therapeutic use ; Child ; Child, Preschool ; Clinical Trials as Topic ; Disease Models, Animal ; Gene Expression Profiling ; Humans ; Mice ; *Molecular Targeted Therapy ; Neuroblastoma/*drug therapy/*genetics ; *Precision Medicine
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    Clinical studies. Trying to reset the clock on type 1 diabetes (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-08-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin-Frankel, Jennifer -- New York, N.Y. -- Science. 2011 Aug 12;333(6044):819-21. doi: 10.1126/science.333.6044.819.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21835995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/administration & dosage/adverse effects/*therapeutic use ; Antigens, CD3/*immunology ; Clinical Trials as Topic ; Diabetes Mellitus, Type 1/*drug therapy/*immunology/pathology/prevention & ; control ; Humans ; Insulin-Secreting Cells/immunology/pathology ; Mice ; T-Lymphocytes/immunology
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    Make a bid for bird biodiversity (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-01-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kettle, Chris J -- New York, N.Y. -- Science. 2011 Jan 21;331(6015):282. doi: 10.1126/science.331.6015.282-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21252330" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biodiversity ; *Birds ; *Conservation of Natural Resources ; Endangered Species
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    An unorthodox approach to forest restoration (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-07-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kettle, Chris J -- Burslem, David F R P -- Ghazoul, Jaboury -- New York, N.Y. -- Science. 2011 Jul 1;333(6038):36; author reply 36-7. doi: 10.1126/science.333.6038.36-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21719660" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Specimen Banks ; *Conservation of Natural Resources ; *Ecosystem ; *Seeds/physiology ; *Trees ; Tropical Climate
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    Role for piRNAs and noncoding RNA in de novo DNA methylation of the imprinted mouse Rasgrf1 locus (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-05-14
    Description: Genomic imprinting causes parental origin-specific monoallelic gene expression through differential DNA methylation established in the parental germ line. However, the mechanisms underlying how specific sequences are selectively methylated are not fully understood. We have found that the components of the PIWI-interacting RNA (piRNA) pathway are required for de novo methylation of the differentially methylated region (DMR) of the imprinted mouse Rasgrf1 locus, but not other paternally imprinted loci. A retrotransposon sequence within a noncoding RNA spanning the DMR was targeted by piRNAs generated from a different locus. A direct repeat in the DMR, which is required for the methylation and imprinting of Rasgrf1, served as a promoter for this RNA. We propose a model in which piRNAs and a target RNA direct the sequence-specific methylation of Rasgrf1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3368507/" 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/PMC3368507/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Watanabe, Toshiaki -- Tomizawa, Shin-ichi -- Mitsuya, Kohzoh -- Totoki, Yasushi -- Yamamoto, Yasuhiro -- Kuramochi-Miyagawa, Satomi -- Iida, Naoko -- Hoki, Yuko -- Murphy, Patrick J -- Toyoda, Atsushi -- Gotoh, Kengo -- Hiura, Hitoshi -- Arima, Takahiro -- Fujiyama, Asao -- Sado, Takashi -- Shibata, Tatsuhiro -- Nakano, Toru -- Lin, Haifan -- Ichiyanagi, Kenji -- Soloway, Paul D -- Sasaki, Hiroyuki -- R01 CA098597/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2011 May 13;332(6031):848-52. doi: 10.1126/science.1203919.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Human Genetics and Department of Integrated Genetics, National Institute of Genetics, Research Organization of Information and Systems, Mishima, Shizuoka, 411-8540, Japan. toshwatatoshiakiwatanabe@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21566194" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Argonaute Proteins ; *DNA Methylation ; *Genomic Imprinting ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondrial Proteins/genetics/metabolism ; Models, Genetic ; Mutation ; Phospholipase D/genetics/metabolism ; Proteins/genetics/metabolism ; RNA, Small Interfering/*genetics/metabolism ; RNA, Untranslated/*genetics/metabolism ; Repetitive Sequences, Nucleic Acid ; Retroelements ; Spermatogonia/metabolism ; Testis/embryology/metabolism ; Transcription, Genetic ; ras-GRF1/*genetics
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    Microbiology. Girth and the gut (bacteria) (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-04-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2011 Apr 1;332(6025):32-3. doi: 10.1126/science.332.6025.32.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21454769" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/pharmacology ; Genes, Bacterial ; Humans ; Intestines/*microbiology ; Metagenome/drug effects ; Mice ; Obesity/*microbiology
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    Global DNA demethylation during mouse erythropoiesis in vivo (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-11-15
    Description: In the mammalian genome, 5'-CpG-3' dinucleotides are frequently methylated, correlating with transcriptional silencing. Genome-wide demethylation is thought to occur only twice during development, in primordial germ cells and in the pre-implantation embryo. These demethylation events are followed by de novo methylation, setting up a pattern inherited throughout development and modified only at tissue-specific loci. We studied DNA methylation in differentiating mouse erythroblasts in vivo by using genomic-scale reduced representation bisulfite sequencing (RRBS). Demethylation at the erythroid-specific beta-globin locus was coincident with global DNA demethylation at most genomic elements. Global demethylation was continuous throughout differentiation and required rapid DNA replication. Hence, DNA demethylation can occur globally during somatic cell differentiation, providing an experimental model for its study in development and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3230325/" 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/PMC3230325/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shearstone, Jeffrey R -- Pop, Ramona -- Bock, Christoph -- Boyle, Patrick -- Meissner, Alexander -- Socolovsky, Merav -- DK32520/DK/NIDDK NIH HHS/ -- R01 HL084168/HL/NHLBI NIH HHS/ -- R01 HL084168-02/HL/NHLBI NIH HHS/ -- R01 HL084168-03/HL/NHLBI NIH HHS/ -- R01 HL084168-04/HL/NHLBI NIH HHS/ -- R01 HL084168-04S1/HL/NHLBI NIH HHS/ -- R01 HL084168-05/HL/NHLBI NIH HHS/ -- T32-130807/PHS HHS/ -- New York, N.Y. -- Science. 2011 Nov 11;334(6057):799-802. doi: 10.1126/science.1207306.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22076376" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CpG Islands ; *DNA Methylation ; DNA Replication ; Dinucleoside Phosphates/metabolism ; Embryo, Mammalian ; Erythroblasts/*metabolism ; *Erythropoiesis ; Gene Expression Regulation, Developmental ; Genome ; Liver/embryology ; Locus Control Region ; Long Interspersed Nucleotide Elements ; Mice ; S Phase ; Sequence Analysis, DNA ; Transcription, Genetic ; beta-Globins/genetics
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    Human genome 10th anniversary. Digging deep into the microbiome (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2011 Feb 25;331(6020):1008-9. doi: 10.1126/science.331.6020.1008.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21350145" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteroides/*genetics/growth & development ; *Genes, Bacterial ; Genes, Essential ; Genes, rRNA ; Human Genome Project ; Humans ; Intestines/*microbiology ; *Metagenome ; Mice ; Mutagenesis, Insertional ; *Sequence Analysis, DNA
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    Function of rhodopsin in temperature discrimination in Drosophila (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-03-12
    Description: Many animals, including the fruit fly, are sensitive to small differences in ambient temperature. The ability of Drosophila larvae to choose their ideal temperature (18 degrees C) over other comfortable temperatures (19 degrees to 24 degrees C) depends on a thermosensory signaling pathway that includes a heterotrimeric guanine nucleotide-binding protein (G protein), a phospholipase C, and the transient receptor potential TRPA1 channel. We report that mutation of the gene (ninaE) encoding a classical G protein-coupled receptor (GPCR), Drosophila rhodopsin, eliminates thermotactic discrimination in the comfortable temperature range. This role for rhodopsin in thermotaxis toward 18 degrees C was light-independent. Introduction of mouse melanopsin restored normal thermotactic behavior in ninaE mutant larvae. We propose that rhodopsins represent a class of evolutionarily conserved GPCRs that are required for initiating thermosensory signaling cascades.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, Wei L -- Kwon, Young -- Adegbola, Abidemi A -- Luo, Junjie -- Chess, Andrew -- Montell, Craig -- GM085335/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Mar 11;331(6022):1333-6. doi: 10.1126/science.1198904.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, Center for Sensory Biology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21393546" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drosophila Proteins/genetics/metabolism/*physiology ; Drosophila melanogaster/genetics/*physiology ; Eye Proteins/genetics/*physiology ; Larva/genetics/physiology ; Light ; Mice ; Movement ; Mutation ; Photoreceptor Cells, Invertebrate/physiology ; Receptors, G-Protein-Coupled/genetics/physiology ; Rhodopsin/genetics/*physiology ; Rod Opsins/genetics/physiology ; *Signal Transduction ; TRPC Cation Channels/genetics/metabolism ; Temperature ; *Thermosensing
    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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    Nicotinic acetylcholine receptor beta2 subunits in the medial prefrontal cortex control attention (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-08-13
    Description: More than one-third of all people are estimated to experience mild to severe cognitive impairment as they age. Acetylcholine (ACh) levels in the brain diminish with aging, and nicotinic ACh receptor (nAChR) stimulation is known to enhance cognitive performance. The prefrontal cortex (PFC) is involved in a range of cognitive functions and is thought to mediate attentional focus. We found that mice carrying nAChR beta2-subunit deletions have impaired attention performance. Efficient lentiviral vector-mediated reexpression of functional beta2-subunit-containing nAChRs in PFC neurons of the prelimbic area (PrL) completely restored the attentional deficit but did not affect impulsive and motivational behavior. Our findings show that beta2-subunit expression in the PrL PFC is sufficient for endogenous nAChR-mediated cholinergic regulation of attentional performance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guillem, Karine -- Bloem, Bernard -- Poorthuis, Rogier B -- Loos, Maarten -- Smit, August B -- Maskos, Uwe -- Spijker, Sabine -- Mansvelder, Huibert D -- New York, N.Y. -- Science. 2011 Aug 12;333(6044):888-91. doi: 10.1126/science.1207079.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Integrative Neurophysiology, Center for Neurogenomics and Cognitive Research (CNCR), Neuroscience Campus Amsterdam, VU University, 1081 HV Amsterdam, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21836018" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/metabolism ; Animals ; *Attention ; Behavior, Animal ; *Cognition ; Gene Deletion ; Male ; Mice ; Mice, Knockout ; Motivation ; Neurons/*physiology ; Patch-Clamp Techniques ; Prefrontal Cortex/*physiology ; Reaction Time ; Receptors, Nicotinic/genetics/*metabolism ; Transduction, Genetic
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    Molecular biology. Translation goes global (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weiss, Robert B -- Atkins, John F -- New York, N.Y. -- Science. 2011 Dec 16;334(6062):1509-10. doi: 10.1126/science.1216974.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics, University of Utah, Salt Lake City, UT 84112, USA. bob.weiss@genetics.utah.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22174241" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gene Expression Profiling ; Gene Expression Regulation ; Humans ; Mice ; Open Reading Frames ; *Protein Biosynthesis ; *Proteome ; *RNA, Messenger/metabolism ; Ribosomes/metabolism
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    Adult neural function requires MeCP2 (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-06-04
    Description: Rett syndrome (RTT) is a postnatal neurological disorder caused by mutations in MECP2, encoding the epigenetic regulator methyl-CpG-binding protein 2 (MeCP2). The onset of RTT symptoms during early life together with findings suggesting neurodevelopmental abnormalities in RTT and mouse models of RTT raised the question of whether maintaining MeCP2 function exclusively during early life might protect against disease. We show by using an inducible model of RTT that deletion of Mecp2 in adult mice recapitulates the germline knock-out phenotype, underscoring the ongoing role of MeCP2 in adult neurological function. Moreover, unlike the effects of other epigenetic instructions programmed during early life, the effects of early MeCP2 function are lost soon after its deletion. These findings suggest that therapies for RTT must be maintained throughout life.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3150190/" 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/PMC3150190/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McGraw, Christopher M -- Samaco, Rodney C -- Zoghbi, Huda Y -- F31-NS073317/NS/NINDS NIH HHS/ -- HD024064/HD/NICHD NIH HHS/ -- NS057819/NS/NINDS NIH HHS/ -- P30 HD024064/HD/NICHD NIH HHS/ -- P30 HD024064-22/HD/NICHD NIH HHS/ -- R01 NS057819/NS/NINDS NIH HHS/ -- R01 NS057819-05/NS/NINDS NIH HHS/ -- T32-NS043124/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Jul 8;333(6039):186. doi: 10.1126/science.1206593. Epub 2011 Jun 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Developmental Biology, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21636743" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Animals ; Disease Models, Animal ; Gene Expression Regulation ; Learning ; Male ; Memory ; Methyl-CpG-Binding Protein 2/genetics/*physiology ; Mice ; Mice, Knockout ; *Nervous System Physiological Phenomena ; Rett Syndrome/genetics/*physiopathology
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    A family of IFN-gamma-inducible 65-kD GTPases protects against bacterial infection (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-05-10
    Description: Immune interferon gamma (IFN-gamma) is essential for mammalian host defense against intracellular pathogens. IFN-gamma induces nearly 2000 host genes, yet few have any assigned function. Here, we examined a complete mouse 65-kilodalton (kD) guanylate-binding protein (Gbp) gene family as part of a 43-member IFN-gamma-inducible guanosine triphosphatase (GTPase) superfamily in mouse and human genomes. Family-wide loss-of-function analysis found that at least four Gbps--Gbp1, Gbp6, Gbp7, and Gbp10--conferred cell-autonomous immunity to listerial or mycobacterial infection within macrophages and gene-deficient animals. These Gbps solicited host defense proteins, including the phagocyte oxidase, antimicrobial peptides, and autophagy effectors, to kill intracellular bacteria. Thus, specific 65-kD Gbps coordinate a potent oxidative and vesicular trafficking program to protect the host from infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Bae-Hoon -- Shenoy, Avinash R -- Kumar, Pradeep -- Das, Rituparna -- Tiwari, Sangeeta -- MacMicking, John D -- R01 AI068041-01A1/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2011 May 6;332(6030):717-21. doi: 10.1126/science.1201711.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Microbial Pathogenesis, Boyer Centre for Molecular Medicine, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21551061" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autophagy ; Cell Line ; GTP-Binding Proteins/chemistry/genetics/*metabolism ; Humans ; Immunity, Innate ; Interferon-gamma/*immunology ; Listeria monocytogenes/growth & development/immunology/pathogenicity ; Listeriosis/*immunology/metabolism/microbiology ; Lysosomes/metabolism ; Macrophages/*immunology/metabolism/*microbiology ; Mice ; Mycobacterium bovis/growth & development/immunology/pathogenicity ; NADPH Oxidase/metabolism ; Oxidation-Reduction ; Peptides/metabolism ; Phagocytosis ; Phagosomes/metabolism ; RNA Interference ; Tuberculosis/*immunology/metabolism/microbiology
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    A Burkholderia pseudomallei toxin inhibits helicase activity of translation factor eIF4A (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-11-15
    Description: The structure of BPSL1549, a protein of unknown function from Burkholderia pseudomallei, reveals a similarity to Escherichia coli cytotoxic necrotizing factor 1. We found that BPSL1549 acted as a potent cytotoxin against eukaryotic cells and was lethal when administered to mice. Expression levels of bpsl1549 correlate with conditions expected to promote or suppress pathogenicity. BPSL1549 promotes deamidation of glutamine-339 of the translation initiation factor eIF4A, abolishing its helicase activity and inhibiting translation. We propose to name BPSL1549 Burkholderia lethal factor 1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3364511/" 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/PMC3364511/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cruz-Migoni, Abimael -- Hautbergue, Guillaume M -- Artymiuk, Peter J -- Baker, Patrick J -- Bokori-Brown, Monika -- Chang, Chung-Te -- Dickman, Mark J -- Essex-Lopresti, Angela -- Harding, Sarah V -- Mahadi, Nor Muhammad -- Marshall, Laura E -- Mobbs, George W -- Mohamed, Rahmah -- Nathan, Sheila -- Ngugi, Sarah A -- Ong, Catherine -- Ooi, Wen Fong -- Partridge, Lynda J -- Phillips, Helen L -- Raih, M Firdaus -- Ruzheinikov, Sergei -- Sarkar-Tyson, Mitali -- Sedelnikova, Svetlana E -- Smither, Sophie J -- Tan, Patrick -- Titball, Richard W -- Wilson, Stuart A -- Rice, David W -- 085162/Wellcome Trust/United Kingdom -- BB/D011795/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/D524975/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/E025293/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- WT085162AIA/Wellcome Trust/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2011 Nov 11;334(6057):821-4. doi: 10.1126/science.1211915.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Biotechnology, Krebs Institute, University of Sheffield, Sheffield S10 2TN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22076380" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Bacterial Proteins/*chemistry/genetics/metabolism/*toxicity ; Bacterial Toxins/*chemistry/genetics/metabolism/*toxicity ; Burkholderia pseudomallei/*chemistry/*pathogenicity ; Catalytic Domain ; Cell Line ; Crystallography, X-Ray ; Cytotoxins/chemistry/genetics/metabolism/toxicity ; Escherichia coli Proteins/chemistry ; Eukaryotic Initiation Factor-4A/*antagonists & inhibitors/metabolism ; Glutamine/metabolism ; Humans ; Mice ; Mice, Inbred BALB C ; Models, Molecular ; Mutant Proteins/toxicity ; Peptide Chain Initiation, Translational/drug effects ; Protein Binding ; Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary
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    Cell biology. Autophagy's top chef (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-06-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cuervo, Ana Maria -- New York, N.Y. -- Science. 2011 Jun 17;332(6036):1392-3. doi: 10.1126/science.1208607.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental and Molecular Biology, Marion Bessin Liver Research Center and Institute for Aging Studies, Albert Einstein College of Medicine, Bronx, NY 10461, USA. ana-maria.cuervo@einstein.yu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21680833" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Animals ; *Autophagy ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/*metabolism ; Cell Nucleus/metabolism ; Cytosol/metabolism ; Humans ; Lysosomes/*metabolism ; Mice ; Mitogen-Activated Protein Kinase 1/metabolism ; Phagosomes/metabolism ; Phosphorylation ; *Transcription, Genetic
    Print ISSN: 0036-8075
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    Angiotensin II type 2 receptor signaling attenuates aortic aneurysm in mice through ERK antagonism (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-04-16
    Description: Angiotensin II (AngII) mediates progression of aortic aneurysm, but the relative contribution of its type 1 (AT1) and type 2 (AT2) receptors remains unknown. We show that loss of AT2 expression accelerates the aberrant growth and rupture of the aorta in a mouse model of Marfan syndrome (MFS). The selective AT1 receptor blocker (ARB) losartan abrogated aneurysm progression in the mice; full protection required intact AT2 signaling. The angiotensin-converting enzyme inhibitor (ACEi) enalapril, which limits signaling through both receptors, was less effective. Both drugs attenuated canonical transforming growth factor-beta (TGFbeta) signaling in the aorta, but losartan uniquely inhibited TGFbeta-mediated activation of extracellular signal-regulated kinase (ERK), by allowing continued signaling through AT2. These data highlight the protective nature of AT2 signaling and potentially inform the choice of therapies in MFS and related disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3097422/" 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/PMC3097422/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Habashi, Jennifer P -- Doyle, Jefferson J -- Holm, Tammy M -- Aziz, Hamza -- Schoenhoff, Florian -- Bedja, Djahida -- Chen, YiChun -- Modiri, Alexandra N -- Judge, Daniel P -- Dietz, Harry C -- P01 AR049698/AR/NIAMS NIH HHS/ -- P01 AR049698-07/AR/NIAMS NIH HHS/ -- R01 AR041135/AR/NIAMS NIH HHS/ -- R01 AR041135-17/AR/NIAMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Apr 15;332(6027):361-5. doi: 10.1126/science.1192152.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21493863" target="_blank"〉PubMed〈/a〉
    Keywords: Angiotensin II/metabolism ; Angiotensin II Type 1 Receptor Blockers/pharmacology/therapeutic use ; Angiotensin-Converting Enzyme Inhibitors/pharmacology/therapeutic use ; Animals ; Aorta ; Aortic Aneurysm/drug therapy/*metabolism/pathology/prevention & control ; Aortic Rupture/metabolism/pathology/prevention & control ; Disease Models, Animal ; Disease Progression ; Enalapril/pharmacology/therapeutic use ; Losartan/pharmacology/therapeutic use ; MAP Kinase Signaling System ; Marfan Syndrome/drug therapy/*metabolism/pathology ; Mice ; Mice, Knockout ; Mitogen-Activated Protein Kinase 1/*antagonists & inhibitors/metabolism ; Mitogen-Activated Protein Kinase 3/*antagonists & inhibitors/metabolism ; Receptor, Angiotensin, Type 2/genetics/*metabolism ; *Signal Transduction ; Transforming Growth Factor beta/metabolism
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    Hippo pathway inhibits Wnt signaling to restrain cardiomyocyte proliferation and heart size (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-04-23
    Description: Genetic regulation of mammalian heart size is poorly understood. Hippo signaling represents an organ-size control pathway in Drosophila, where it also inhibits cell proliferation and promotes apoptosis in imaginal discs. To determine whether Hippo signaling controls mammalian heart size, we inactivated Hippo pathway components in the developing mouse heart. Hippo-deficient embryos had overgrown hearts with elevated cardiomyocyte proliferation. Gene expression profiling and chromatin immunoprecipitation revealed that Hippo signaling negatively regulates a subset of Wnt target genes. Genetic interaction studies indicated that beta-catenin heterozygosity suppressed the Hippo cardiomyocyte overgrowth phenotype. Furthermore, the Hippo effector Yap interacts with beta-catenin on Sox2 and Snai2 genes. These data uncover a nuclear interaction between Hippo and Wnt signaling that restricts cardiomyocyte proliferation and controls heart size.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3133743/" 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/PMC3133743/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heallen, Todd -- Zhang, Min -- Wang, Jun -- Bonilla-Claudio, Margarita -- Klysik, Ela -- Johnson, Randy L -- Martin, James F -- R01 DE012324/DE/NIDCR NIH HHS/ -- R01 DE012324-12/DE/NIDCR NIH HHS/ -- R01 HD052785/HD/NICHD NIH HHS/ -- R01 HD052785-05/HD/NICHD NIH HHS/ -- R01 HD060579/HD/NICHD NIH HHS/ -- R01 HD060579-02/HD/NICHD NIH HHS/ -- R01 HL093484/HL/NHLBI NIH HHS/ -- R01 HL093484-01A1/HL/NHLBI NIH HHS/ -- R01HD052785/HD/NICHD NIH HHS/ -- R01HD060579/HD/NICHD NIH HHS/ -- T32 DE15355-04/DE/NIDCR NIH HHS/ -- New York, N.Y. -- Science. 2011 Apr 22;332(6028):458-61. doi: 10.1126/science.1199010.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Biosciences and Technology, Texas A&M System Health Science Center, 2121 West Holcombe Boulevard, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21512031" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Cardiomegaly/metabolism ; Cell Cycle Proteins/genetics/metabolism ; Cell Nucleus/metabolism ; Cell Proliferation ; Chromatin Immunoprecipitation ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Heart/*anatomy & histology/embryology ; Mice ; Mice, Transgenic ; Myocardium/cytology ; Myocytes, Cardiac/*cytology/*metabolism ; Organ Size ; Phosphoproteins/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; SOXB1 Transcription Factors/genetics/metabolism ; *Signal Transduction ; Transcription Factors/genetics/metabolism ; Wnt Proteins/*metabolism ; beta Catenin/genetics/metabolism
    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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    Imaging of Plasmodium liver stages to drive next-generation antimalarial drug discovery (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-11-19
    Description: Most malaria drug development focuses on parasite stages detected in red blood cells, even though, to achieve eradication, next-generation drugs active against both erythrocytic and exo-erythrocytic forms would be preferable. We applied a multifactorial approach to a set of 〉4000 commercially available compounds with previously demonstrated blood-stage activity (median inhibitory concentration 〈 1 micromolar) and identified chemical scaffolds with potent activity against both forms. From this screen, we identified an imidazolopiperazine scaffold series that was highly enriched among compounds active against Plasmodium liver stages. The orally bioavailable lead imidazolopiperazine confers complete causal prophylactic protection (15 milligrams/kilogram) in rodent models of malaria and shows potent in vivo blood-stage therapeutic activity. The open-source chemical tools resulting from our effort provide starting points for future drug discovery programs, as well as opportunities for researchers to investigate the biology of exo-erythrocytic forms.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3473092/" 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/PMC3473092/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meister, Stephan -- Plouffe, David M -- Kuhen, Kelli L -- Bonamy, Ghislain M C -- Wu, Tao -- Barnes, S Whitney -- Bopp, Selina E -- Borboa, Rachel -- Bright, A Taylor -- Che, Jianwei -- Cohen, Steve -- Dharia, Neekesh V -- Gagaring, Kerstin -- Gettayacamin, Montip -- Gordon, Perry -- Groessl, Todd -- Kato, Nobutaka -- Lee, Marcus C S -- McNamara, Case W -- Fidock, David A -- Nagle, Advait -- Nam, Tae-gyu -- Richmond, Wendy -- Roland, Jason -- Rottmann, Matthias -- Zhou, Bin -- Froissard, Patrick -- Glynne, Richard J -- Mazier, Dominique -- Sattabongkot, Jetsumon -- Schultz, Peter G -- Tuntland, Tove -- Walker, John R -- Zhou, Yingyao -- Chatterjee, Arnab -- Diagana, Thierry T -- Winzeler, Elizabeth A -- R01 AI079709/AI/NIAID NIH HHS/ -- R01 AI079709-04/AI/NIAID NIH HHS/ -- R01 AI090141/AI/NIAID NIH HHS/ -- R01 AI090141-02/AI/NIAID NIH HHS/ -- R01AI090141/AI/NIAID NIH HHS/ -- WT078285/Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2011 Dec 9;334(6061):1372-7. doi: 10.1126/science.1211936. Epub 2011 Nov 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, The Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22096101" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antimalarials/chemistry/pharmacokinetics/*pharmacology/therapeutic use ; Cell Line, Tumor ; *Drug Discovery ; Drug Evaluation, Preclinical ; Drug Resistance ; Erythrocytes/parasitology ; Humans ; Imidazoles/chemistry/pharmacokinetics/*pharmacology/therapeutic use ; Liver/*parasitology ; Malaria/*drug therapy/parasitology/prevention & control ; Mice ; Mice, Inbred BALB C ; Molecular Structure ; Piperazines/chemistry/pharmacokinetics/*pharmacology/therapeutic use ; Plasmodium/cytology/*drug effects/growth & development/physiology ; Plasmodium berghei/cytology/drug effects/growth & development/physiology ; Plasmodium falciparum/cytology/drug effects/growth & development/physiology ; Plasmodium yoelii/cytology/drug effects/growth & development/physiology ; Polymorphism, Single Nucleotide ; Protozoan Proteins/chemistry/genetics/metabolism ; Random Allocation ; Small Molecule Libraries ; Sporozoites/drug effects/growth & development
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    Correction of sickle cell disease in adult mice by interference with fetal hemoglobin silencing (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-10-15
    Description: Persistence of human fetal hemoglobin (HbF, alpha(2)gamma(2)) in adults lessens the severity of sickle cell disease (SCD) and the beta-thalassemias. Here, we show that the repressor BCL11A is required in vivo for silencing of gamma-globin expression in adult animals, yet dispensable for red cell production. BCL11A serves as a barrier to HbF reactivation by known HbF inducing agents. In a proof-of-principle test of BCL11A as a potential therapeutic target, we demonstrate that inactivation of BCL11A in SCD transgenic mice corrects the hematologic and pathologic defects associated with SCD through high-level pancellular HbF induction. Thus, interference with HbF silencing by manipulation of a single target protein is sufficient to reverse SCD.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3746545/" 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/PMC3746545/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, Jian -- Peng, Cong -- Sankaran, Vijay G -- Shao, Zhen -- Esrick, Erica B -- Chong, Bryan G -- Ippolito, Gregory C -- Fujiwara, Yuko -- Ebert, Benjamin L -- Tucker, Philip W -- Orkin, Stuart H -- K01 DK093543/DK/NIDDK NIH HHS/ -- T32 CA009172/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Nov 18;334(6058):993-6. doi: 10.1126/science.1211053. Epub 2011 Oct 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology/Oncology, Children's Hospital Boston and Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21998251" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Sickle Cell/blood/*genetics/pathology/*therapy ; Animals ; Carrier Proteins/genetics/*physiology ; DNA Methylation ; Embryo, Mammalian ; Epigenesis, Genetic ; Erythroid Cells/metabolism ; Fetal Hemoglobin/*genetics/metabolism ; *Gene Expression Regulation ; *Gene Silencing ; Histones/metabolism ; Humans ; Mice ; Mice, Knockout ; Mice, Transgenic ; Molecular Targeted Therapy ; Nuclear Proteins/genetics/*physiology ; gamma-Globins/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Trans-endocytosis of CD80 and CD86: a molecular basis for the cell-extrinsic function of CTLA-4 (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-04-09
    Description: Cytotoxic T lymphocyte antigen 4 (CTLA-4) is an essential negative regulator of T cell immune responses whose mechanism of action is the subject of debate. CTLA-4 shares two ligands (CD80 and CD86) with a stimulatory receptor, CD28. Here, we show that CTLA-4 can capture its ligands from opposing cells by a process of trans-endocytosis. After removal, these costimulatory ligands are degraded inside CTLA-4-expressing cells, resulting in impaired costimulation via CD28. Acquisition of CD86 from antigen-presenting cells is stimulated by T cell receptor engagement and observed in vitro and in vivo. These data reveal a mechanism of immune regulation in which CTLA-4 acts as an effector molecule to inhibit CD28 costimulation by the cell-extrinsic depletion of ligands, accounting for many of the known features of the CD28-CTLA-4 system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3198051/" 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/PMC3198051/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Qureshi, Omar S -- Zheng, Yong -- Nakamura, Kyoko -- Attridge, Kesley -- Manzotti, Claire -- Schmidt, Emily M -- Baker, Jennifer -- Jeffery, Louisa E -- Kaur, Satdip -- Briggs, Zoe -- Hou, Tie Z -- Futter, Clare E -- Anderson, Graham -- Walker, Lucy S K -- Sansom, David M -- 17851/Arthritis Research UK/United Kingdom -- BB/D011000/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/H013598/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0400931/Medical Research Council/United Kingdom -- G0401620/Medical Research Council/United Kingdom -- G0802382/Medical Research Council/United Kingdom -- G1000213/Medical Research Council/United Kingdom -- G9818340/Medical Research Council/United Kingdom -- Arthritis Research UK/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2011 Apr 29;332(6029):600-3. doi: 10.1126/science.1202947. Epub 2011 Apr 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Centre for Immune Regulation, School of Immunity and Infection, Institute of Biomedical Research, University of Birmingham Medical School, Birmingham B15 2TT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21474713" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/*immunology/metabolism ; Antigens, CD28/*immunology ; Antigens, CD80/*immunology/metabolism ; Antigens, CD86/*immunology/metabolism ; CHO Cells ; CTLA-4 Antigen ; Cricetinae ; Cricetulus ; Dendritic Cells/immunology ; *Endocytosis ; Humans ; Jurkat Cells ; Ligands ; Lymphocyte Activation ; Mice ; Mice, Transgenic ; Models, Biological ; Ovalbumin/immunology ; Receptors, Antigen, T-Cell/immunology ; Recombinant Fusion Proteins/metabolism ; T-Lymphocyte Subsets/*immunology/metabolism ; T-Lymphocytes, Regulatory/immunology/metabolism
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    Beyond predictions: biodiversity conservation in a changing climate (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-04-02
    Description: Climate change is predicted to become a major threat to biodiversity in the 21st century, but accurate predictions and effective solutions have proved difficult to formulate. Alarming predictions have come from a rather narrow methodological base, but a new, integrated science of climate-change biodiversity assessment is emerging, based on multiple sources and approaches. Drawing on evidence from paleoecological observations, recent phenological and microevolutionary responses, experiments, and computational models, we review the insights that different approaches bring to anticipating and managing the biodiversity consequences of climate change, including the extent of species' natural resilience. We introduce a framework that uses information from different sources to identify vulnerability and to support the design of conservation responses. Although much of the information reviewed is on species, our framework and conclusions are also applicable to ecosystems, habitats, ecological communities, and genetic diversity, whether terrestrial, marine, or fresh water.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dawson, Terence P -- Jackson, Stephen T -- House, Joanna I -- Prentice, Iain Colin -- Mace, Georgina M -- New York, N.Y. -- Science. 2011 Apr 1;332(6025):53-8. doi: 10.1126/science.1200303.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of the Environment, University of Dundee, Dundee DD1 4HN, Scotland, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21454781" target="_blank"〉PubMed〈/a〉
    Keywords: *Biodiversity ; *Climate Change ; *Conservation of Natural Resources
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    The C-terminal domain of RNA polymerase II is modified by site-specific methylation (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-04-02
    Description: The carboxy-terminal domain (CTD) of RNA polymerase II (RNAPII) in mammals undergoes extensive posttranslational modification, which is essential for transcriptional initiation and elongation. Here, we show that the CTD of RNAPII is methylated at a single arginine (R1810) by the coactivator-associated arginine methyltransferase 1 (CARM1). Although methylation at R1810 is present on the hyperphosphorylated form of RNAPII in vivo, Ser2 or Ser5 phosphorylation inhibits CARM1 activity toward this site in vitro, suggesting that methylation occurs before transcription initiation. Mutation of R1810 results in the misexpression of a variety of small nuclear RNAs and small nucleolar RNAs, an effect that is also observed in Carm1(-/-) mouse embryo fibroblasts. These results demonstrate that CTD methylation facilitates the expression of select RNAs, perhaps serving to discriminate the RNAPII-associated machinery recruited to distinct gene types.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3773223/" 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/PMC3773223/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sims, Robert J 3rd -- Rojas, Luis Alejandro -- Beck, David -- Bonasio, Roberto -- Schuller, Roland -- Drury, William J 3rd -- Eick, Dirk -- Reinberg, Danny -- F32 GM071166/GM/NIGMS NIH HHS/ -- GM-37120/GM/NIGMS NIH HHS/ -- GM-71166/GM/NIGMS NIH HHS/ -- R01 GM037120/GM/NIGMS NIH HHS/ -- R37 GM037120/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Apr 1;332(6025):99-103. doi: 10.1126/science.1202663.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute (HHMI), Department of Biochemistry, New York University School of Medicine, 522 First Avenue, Smilow 211, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21454787" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arginine/metabolism ; Cell Line ; HeLa Cells ; Humans ; Methylation ; Mice ; Mutation ; Protein Interaction Domains and Motifs ; Protein Structure, Tertiary ; Protein-Arginine N-Methyltransferases/metabolism ; RNA Polymerase II/genetics/*metabolism ; RNA, Small Nuclear/metabolism ; RNA, Small Nucleolar/metabolism ; Recombinant Proteins
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    Conservation. Economic importance of bats in agriculture (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-04-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boyles, Justin G -- Cryan, Paul M -- McCracken, Gary F -- Kunz, Thomas H -- New York, N.Y. -- Science. 2011 Apr 1;332(6025):41-2. doi: 10.1126/science.1201366.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology and Entomology, University of Pretoria, Pretoria 0002, South Africa. jgboyles@zoology.up.ac.za〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21454775" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture/*economics ; Animals ; Ascomycota ; Chiroptera/microbiology/*physiology ; *Conservation of Natural Resources ; Dermatomycoses/veterinary ; Ecosystem ; Energy-Generating Resources ; Population Dynamics ; Public Policy ; United States ; Wind
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    Npas4 regulates a transcriptional program in CA3 required for contextual memory formation (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-12-24
    Description: The rapid encoding of contextual memory requires the CA3 region of the hippocampus, but the necessary genetic pathways remain unclear. We found that the activity-dependent transcription factor Npas4 regulates a transcriptional program in CA3 that is required for contextual memory formation. Npas4 was specifically expressed in CA3 after contextual learning. Global knockout or selective deletion of Npas4 in CA3 both resulted in impaired contextual memory, and restoration of Npas4 in CA3 was sufficient to reverse the deficit in global knockout mice. By recruiting RNA polymerase II to promoters and enhancers of target genes, Npas4 regulates a learning-specific transcriptional program in CA3 that includes many well-known activity-regulated genes, which suggests that Npas4 is a master regulator of activity-regulated gene programs and is central to memory formation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4038289/" 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/PMC4038289/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramamoorthi, Kartik -- Fropf, Robin -- Belfort, Gabriel M -- Fitzmaurice, Helen L -- McKinney, Ross M -- Neve, Rachael L -- Otto, Tim -- Lin, Yingxi -- MH091220-01/MH/NIMH NIH HHS/ -- R01 MH091220/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2011 Dec 23;334(6063):1669-75. doi: 10.1126/science.1208049.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉McGovern Institute for Brain Research, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22194569" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/*genetics/*metabolism ; CA3 Region, Hippocampal/cytology/*physiology ; Conditioning (Psychology) ; Enhancer Elements, Genetic ; Fear ; Gene Deletion ; *Gene Expression Regulation ; Genes, Immediate-Early ; Learning ; *Memory ; Mice ; Mice, Knockout ; Neurons/physiology ; Promoter Regions, Genetic ; RNA Polymerase II/metabolism ; *Transcription, Genetic ; Transcriptional Activation
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    A synthetic optogenetic transcription device enhances blood-glucose homeostasis in mice (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-06-28
    Description: Synthetic biology has advanced the design of genetic devices that can be used to reprogram metabolic activities in mammalian cells. By functionally linking the signal transduction of melanopsin to the control circuit of the nuclear factor of activated T cells, we have designed a synthetic signaling cascade enabling light-inducible transgene expression in different cell lines grown in culture or bioreactors or implanted into mice. In animals harboring intraperitoneal hollow-fiber or subcutaneous implants containing light-inducible transgenic cells, the serum levels of the human glycoprotein secreted alkaline phosphatase could be remote-controlled with fiber optics or transdermally regulated through direct illumination. Light-controlled expression of the glucagon-like peptide 1 was able to attenuate glycemic excursions in type II diabetic mice. Synthetic light-pulse-transcription converters may have applications in therapeutics and protein expression technology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ye, Haifeng -- Daoud-El Baba, Marie -- Peng, Ren-Wang -- Fussenegger, Martin -- New York, N.Y. -- Science. 2011 Jun 24;332(6037):1565-8. doi: 10.1126/science.1203535.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biosystems Science and Engineering, Eidgenossische Technische Hochschule (ETH) Zurich, Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21700876" target="_blank"〉PubMed〈/a〉
    Keywords: Alkaline Phosphatase/genetics/metabolism ; Animals ; Bioreactors ; Blood Glucose/*metabolism ; Cell Line ; Cell Line, Tumor ; Diabetes Mellitus, Type 2/genetics/*metabolism ; GPI-Linked Proteins/genetics/metabolism ; *Gene Expression Regulation ; Genes, Reporter ; Genetic Engineering/*methods ; Glucagon-Like Peptide 1/genetics/metabolism ; Homeostasis ; Humans ; Insulin/blood ; Isoenzymes/genetics/metabolism ; *Light ; Light Signal Transduction ; Mice ; NFATC Transcription Factors/genetics/metabolism ; Optical Fibers ; Rod Opsins/genetics/metabolism ; Signal Transduction ; Synthetic Biology/*methods ; *Transcription, Genetic ; Transfection ; Transgenes
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    Partitioning regulatory mechanisms of within-host malaria dynamics using the effective propagation number (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-08-20
    Description: Immune clearance and resource limitation (via red blood cell depletion) shape the peaks and troughs of malaria parasitemia, which in turn affect disease severity and transmission. Quantitatively partitioning the relative roles of these effects through time is challenging. Using data from rodent malaria, we estimated the effective propagation number, which reflects the relative importance of contrasting within-host control mechanisms through time and is sensitive to the inoculating parasite dose. Our analysis showed that the capacity of innate responses to restrict initial parasite growth saturates with parasite dose and that experimentally enhanced innate immunity can affect parasite density indirectly via resource depletion. Such a statistical approach offers a tool to improve targeting of drugs or vaccines for human therapy by revealing the dynamics and interactions of within-host regulatory mechanisms.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3891600/" 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/PMC3891600/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Metcalf, C J E -- Graham, A L -- Huijben, S -- Barclay, V C -- Long, G H -- Grenfell, B T -- Read, A F -- Bjornstad, O N -- R01 GM089932/GM/NIGMS NIH HHS/ -- R01GM089932/GM/NIGMS NIH HHS/ -- R24 HD047879/HD/NICHD NIH HHS/ -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2011 Aug 19;333(6045):984-8. doi: 10.1126/science.1204588.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, Oxford University, Oxford OX1 3PS, UK. charlotte.metcalf@zoo.ox.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21852493" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity ; Animals ; Antibodies/immunology ; CD4-Positive T-Lymphocytes/immunology ; Erythrocyte Aging ; Erythrocyte Count ; Erythrocytes/*parasitology/physiology ; Host-Parasite Interactions ; Humans ; Immunity, Innate ; Interleukin-10/immunology/metabolism ; Malaria/blood/*immunology/*parasitology ; Mice ; Models, Biological ; Models, Statistical ; *Parasitemia/blood/immunology/parasitology ; Plasmodium chabaudi/immunology/*physiology ; Receptors, Interleukin-10/immunology ; Regression Analysis
    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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    Cell biology. Protease sets site-1 on lysosomes (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-07-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ye, Jin -- New York, N.Y. -- Science. 2011 Jul 1;333(6038):50-1. doi: 10.1126/science.1209417.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. jin.ye@utsouthwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21719668" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cholesterol/metabolism ; Chondrocytes/cytology ; Enzyme Precursors/chemistry/*metabolism ; Golgi Apparatus/metabolism ; Humans ; Lysosomes/enzymology/*metabolism ; Membrane Proteins/metabolism ; Metalloendopeptidases/metabolism ; Mice ; Proprotein Convertases/*metabolism ; Serine Endopeptidases/*metabolism ; Sterol Regulatory Element Binding Proteins/metabolism ; Transcription Factors/metabolism ; Transferases (Other Substituted Phosphate Groups)/chemistry/*metabolism
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  • 84
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    The molecular basis of acid insensitivity in the African naked mole-rat (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-12-17
    Description: Acid evokes pain by exciting nociceptors; the acid sensors are proton-gated ion channels that depolarize neurons. The naked mole-rat (Heterocephalus glaber) is exceptional in its acid insensitivity, but acid sensors (acid-sensing ion channels and the transient receptor potential vanilloid-1 ion channel) in naked mole-rat nociceptors are similar to those in other vertebrates. Acid inhibition of voltage-gated sodium currents is more profound in naked mole-rat nociceptors than in mouse nociceptors, however, which effectively prevents acid-induced action potential initiation. We describe a species-specific variant of the nociceptor sodium channel Na(V)1.7, which is potently blocked by protons and can account for acid insensitivity in this species. Thus, evolutionary pressure has selected for an Na(V)1.7 gene variant that tips the balance from proton-induced excitation to inhibition of action potential initiation to abolish acid nociception.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, Ewan St John -- Omerbasic, Damir -- Lechner, Stefan G -- Anirudhan, Gireesh -- Lapatsina, Liudmila -- Lewin, Gary R -- New York, N.Y. -- Science. 2011 Dec 16;334(6062):1557-60. doi: 10.1126/science.1213760.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Max-Delbruck Center for Molecular Medicine, Berlin-Buch, Germany. ewan.smith@mdc-berlin.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22174253" target="_blank"〉PubMed〈/a〉
    Keywords: Acid Sensing Ion Channels ; Acids/metabolism/*pharmacology ; Action Potentials ; Amino Acid Motifs ; Animals ; Ganglia, Spinal/cytology/physiology ; Mice ; Mole Rats/genetics/*physiology ; NAV1.7 Voltage-Gated Sodium Channel ; Nerve Tissue Proteins/metabolism ; Nociception/*physiology ; Rats ; Sodium Channels/genetics/*metabolism ; TRPV Cation Channels/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Transient regenerative potential of the neonatal mouse heart (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-02-26
    Description: Certain fish and amphibians retain a robust capacity for cardiac regeneration throughout life, but the same is not true of the adult mammalian heart. Whether the capacity for cardiac regeneration is absent in mammals or whether it exists and is switched off early after birth has been unclear. We found that the hearts of 1-day-old neonatal mice can regenerate after partial surgical resection, but this capacity is lost by 7 days of age. This regenerative response in 1-day-old mice was characterized by cardiomyocyte proliferation with minimal hypertrophy or fibrosis, thereby distinguishing it from repair processes. Genetic fate mapping indicated that the majority of cardiomyocytes within the regenerated tissue originated from preexisting cardiomyocytes. Echocardiography performed 2 months after surgery revealed that the regenerated ventricular apex had normal systolic function. Thus, for a brief period after birth, the mammalian heart appears to have the capacity to regenerate.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3099478/" 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/PMC3099478/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Porrello, Enzo R -- Mahmoud, Ahmed I -- Simpson, Emma -- Hill, Joseph A -- Richardson, James A -- Olson, Eric N -- Sadek, Hesham A -- HL100401-01/HL/NHLBI NIH HHS/ -- R01 HL077439/HL/NHLBI NIH HHS/ -- R01 HL077439-06/HL/NHLBI NIH HHS/ -- R01 HL077439-06W1/HL/NHLBI NIH HHS/ -- R01 HL077439-07/HL/NHLBI NIH HHS/ -- R01 HL077439-08/HL/NHLBI NIH HHS/ -- R01 HL093039/HL/NHLBI NIH HHS/ -- R01 HL093039-01A1/HL/NHLBI NIH HHS/ -- R01 HL093039-01A1W1/HL/NHLBI NIH HHS/ -- R01 HL093039-02/HL/NHLBI NIH HHS/ -- R01 HL093039-03/HL/NHLBI NIH HHS/ -- R01 HL115275/HL/NHLBI NIH HHS/ -- R37 HL053351/HL/NHLBI NIH HHS/ -- R37 HL053351-12/HL/NHLBI NIH HHS/ -- R37 HL053351-13/HL/NHLBI NIH HHS/ -- R37 HL053351-14/HL/NHLBI NIH HHS/ -- R37 HL053351-15/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2011 Feb 25;331(6020):1078-80. doi: 10.1126/science.1200708.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21350179" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Animals, Newborn ; Cardiomegaly ; Cell Lineage ; Cell Proliferation ; Echocardiography ; Fibrosis ; Heart/*physiology ; Heart Ventricles/surgery ; Mice ; Myocardial Contraction ; Myocardium/pathology ; Myocytes, Cardiac/*physiology ; *Regeneration ; Sarcomeres/ultrastructure ; Stroke Volume
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    Eosinophils sustain adipose alternatively activated macrophages associated with glucose homeostasis (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-03-26
    Description: Eosinophils are associated with helminth immunity and allergy, often in conjunction with alternatively activated macrophages (AAMs). Adipose tissue AAMs are necessary to maintain glucose homeostasis and are induced by the cytokine interleukin-4 (IL-4). Here, we show that eosinophils are the major IL-4-expressing cells in white adipose tissues of mice, and, in their absence, AAMs are greatly attenuated. Eosinophils migrate into adipose tissue by an integrin-dependent process and reconstitute AAMs through an IL-4- or IL-13-dependent process. Mice fed a high-fat diet develop increased body fat, impaired glucose tolerance, and insulin resistance in the absence of eosinophils, and helminth-induced adipose tissue eosinophilia enhances glucose tolerance. Our results suggest that eosinophils play an unexpected role in metabolic homeostasis through maintenance of adipose AAMs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3144160/" 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/PMC3144160/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Davina -- Molofsky, Ari B -- Liang, Hong-Erh -- Ricardo-Gonzalez, Roberto R -- Jouihan, Hani A -- Bando, Jennifer K -- Chawla, Ajay -- Locksley, Richard M -- 5F30DK083194-02/DK/NIDDK NIH HHS/ -- AI026918/AI/NIAID NIH HHS/ -- DK063720/DK/NIDDK NIH HHS/ -- DP1 OD006415/OD/NIH HHS/ -- F30 DK083194-03/DK/NIDDK NIH HHS/ -- R01 AI030663/AI/NIAID NIH HHS/ -- R01 DK076760/DK/NIDDK NIH HHS/ -- R01 DK081405/DK/NIDDK NIH HHS/ -- R01 HL076746/HL/NHLBI NIH HHS/ -- R37 AI026918/AI/NIAID NIH HHS/ -- R37 AI026918-24/AI/NIAID NIH HHS/ -- T32 AI007290/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Apr 8;332(6026):243-7. doi: 10.1126/science.1201475. Epub 2011 Mar 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143-0795, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21436399" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue ; Adipose Tissue, White/cytology/*immunology/*metabolism ; Animals ; Blood Glucose/*metabolism ; Cell Movement ; Dietary Fats/administration & dosage ; Eosinophilia/immunology ; Eosinophils/immunology/*physiology ; Glucose Intolerance ; Homeostasis ; Insulin/metabolism ; Insulin Resistance ; Interleukin-13/genetics/metabolism ; Interleukin-4/genetics/metabolism ; *Macrophage Activation ; Macrophages/*immunology/*metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Nippostrongylus ; Strongylida Infections/immunology/metabolism
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    Boosting CITES through research (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-02-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, Matthew J -- Williams, Richard J -- Purves, Drew W -- New York, N.Y. -- Science. 2011 Feb 18;331(6019):857; author reply 857-8. doi: 10.1126/science.331.6019.857-b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21330515" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Animals, Wild ; *Commerce ; *Conservation of Natural Resources ; *Endangered Species ; *International Cooperation ; Research
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    Cell biology. A hand to support the implantation window (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-02-19
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4775075/" 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/PMC4775075/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hewitt, Sylvia C -- Korach, Kenneth S -- ZIA ES070065-35/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2011 Feb 18;331(6019):863-4. doi: 10.1126/science.1202372.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Environmental Health Science, National Institutes of Health, Research Triangle Park, NC 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21330520" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/*genetics/*metabolism ; Cell Proliferation ; Embryo Implantation/*physiology ; Endometrium/cytology/*metabolism ; Epithelial Cells/cytology/physiology ; Estrogens/metabolism ; Female ; Fibroblast Growth Factors/*metabolism ; Gene Expression Profiling ; Mice ; Oligonucleotide Array Sequence Analysis ; Pregnancy ; Progesterone/*metabolism ; RNA, Messenger/genetics/metabolism ; *Signal Transduction ; Stromal Cells/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 89
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    Invasives: a major conservation threat (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-07-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lambertini, Marco -- Leape, Jim -- Marton-Lefevre, Julia -- Mittermeier, Russell A -- Rose, Mark -- Robinson, John G -- Stuart, Simon N -- Waldman, Bill -- Genovesi, Piero -- New York, N.Y. -- Science. 2011 Jul 22;333(6041):404-5. doi: 10.1126/science.333.6041.404-b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21778380" target="_blank"〉PubMed〈/a〉
    Keywords: Biodiversity ; *Conservation of Natural Resources ; *Ecosystem ; *Introduced Species
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    Development. A new focus on RNA in the lens (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-03-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duncan, Melinda K -- EY12221/EY/NEI NIH HHS/ -- EY15279/EY/NEI NIH HHS/ -- R01 EY012221/EY/NEI NIH HHS/ -- R01 EY015279/EY/NEI NIH HHS/ -- RR016472-10/RR/NCRR NIH HHS/ -- RR027273-01/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2011 Mar 25;331(6024):1523-4. doi: 10.1126/science.1204205.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, University of Delaware, Newark, DE 19716, USA. duncanm@udel.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21436425" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cataract/congenital/*genetics ; Cell Line ; Crystallins/genetics/metabolism ; Cytoplasmic Granules/metabolism ; Gene Expression ; *Gene Expression Regulation, Developmental ; Humans ; Lens, Crystalline/cytology/embryology/*metabolism ; Mice ; Mutation ; Protein Biosynthesis ; RNA, Messenger/*genetics/*metabolism ; Ribonucleoproteins/genetics/*metabolism
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    Phosphoproteomic analysis identifies Grb10 as an mTORC1 substrate that negatively regulates insulin signaling (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-06-11
    Description: The evolutionarily conserved serine-threonine kinase mammalian target of rapamycin (mTOR) plays a critical role in regulating many pathophysiological processes. Functional characterization of the mTOR signaling pathways, however, has been hampered by the paucity of known substrates. We used large-scale quantitative phosphoproteomics experiments to define the signaling networks downstream of mTORC1 and mTORC2. Characterization of one mTORC1 substrate, the growth factor receptor-bound protein 10 (Grb10), showed that mTORC1-mediated phosphorylation stabilized Grb10, leading to feedback inhibition of the phosphatidylinositol 3-kinase (PI3K) and extracellular signal-regulated, mitogen-activated protein kinase (ERK-MAPK) pathways. Grb10 expression is frequently down-regulated in various cancers, and loss of Grb10 and loss of the well-established tumor suppressor phosphatase PTEN appear to be mutually exclusive events, suggesting that Grb10 might be a tumor suppressor regulated by mTORC1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3195509/" 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/PMC3195509/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Yonghao -- Yoon, Sang-Oh -- Poulogiannis, George -- Yang, Qian -- Ma, Xiaoju Max -- Villen, Judit -- Kubica, Neil -- Hoffman, Gregory R -- Cantley, Lewis C -- Gygi, Steven P -- Blenis, John -- CA46595/CA/NCI NIH HHS/ -- GM051405/GM/NIGMS NIH HHS/ -- HG3456/HG/NHGRI NIH HHS/ -- R00 CA140789/CA/NCI NIH HHS/ -- R00 CA140789-04/CA/NCI NIH HHS/ -- R00CA140789/CA/NCI NIH HHS/ -- R01 GM041890/GM/NIGMS NIH HHS/ -- R01 GM051405/GM/NIGMS NIH HHS/ -- R01 GM051405-14/GM/NIGMS NIH HHS/ -- R01 GM056203/GM/NIGMS NIH HHS/ -- R01 HG003456/HG/NHGRI NIH HHS/ -- R01 HG003456-07/HG/NHGRI NIH HHS/ -- R37 CA046595/CA/NCI NIH HHS/ -- R37 CA046595-22/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2011 Jun 10;332(6035):1322-6. doi: 10.1126/science.1199484.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21659605" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibiotics, Antineoplastic/pharmacology ; Cell Line ; GRB10 Adaptor Protein/*metabolism ; Humans ; Insulin/*metabolism ; Mice ; Molecular Sequence Data ; Multiprotein Complexes ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphoproteins/metabolism ; Phosphorylation/drug effects ; Proteins/*metabolism ; Proteome/metabolism ; *Signal Transduction/drug effects ; Sirolimus/pharmacology ; TOR Serine-Threonine Kinases
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  • 92
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    Cell signaling. Getting to the heart of mechanotransduction (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-09-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hidalgo, Cecilia -- Donoso, Paulina -- New York, N.Y. -- Science. 2011 Sep 9;333(6048):1388-90. doi: 10.1126/science.1212183.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Physiology and Biophysics Program, Institute of Biomedical Sciences, and Center of Molecular Studies of the Cell, Faculty of Medicine, Universidad de Chile, Santiago, Chile. chidalgo@med.uchile.cl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21903799" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channels/metabolism ; Calcium Signaling ; Glutathione/metabolism ; *Mechanotransduction, Cellular ; Membrane Glycoproteins/metabolism ; Mice ; Muscular Dystrophy, Animal/physiopathology ; Myocardial Contraction ; Myocytes, Cardiac/*physiology ; NADPH Oxidase/metabolism ; Oxidation-Reduction ; Rats ; Reactive Oxygen Species/*metabolism ; Ryanodine Receptor Calcium Release Channel/metabolism
    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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    Neurodevelopmental disorders. New hope for a devastating neurological disorder (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-12-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2011 Dec 23;334(6063):1615. doi: 10.1126/science.334.6063.1615.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22194537" target="_blank"〉PubMed〈/a〉
    Keywords: Angelman Syndrome/*drug therapy/*genetics/therapy ; Animals ; Brain/cytology/drug effects ; Camptothecin/*analogs & derivatives/pharmacology ; Drug Evaluation, Preclinical ; Gene Expression Regulation ; Genetic Therapy ; Humans ; Mice ; Neurons/drug effects/physiology ; Topotecan/administration & dosage/*pharmacology/therapeutic use ; *Transcriptional Activation ; Ubiquitin-Protein Ligases/*genetics/metabolism
    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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  • 94
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    A molecular mechanism for circadian clock negative feedback (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-06-18
    Description: Circadian rhythms in mammals are generated by a feedback loop in which the three PERIOD (PER) proteins, acting in a large complex, inhibit the transcriptional activity of the CLOCK-BMAL1 dimer, which represses their own expression. Although fundamental, the mechanism of negative feedback in the mammalian clock, or any eukaryotic clock, is unknown. We analyzed protein constituents of PER complexes purified from mouse tissues and identified PSF (polypyrimidine tract-binding protein-associated splicing factor). Our analysis indicates that PSF within the PER complex recruits SIN3A, a scaffold for assembly of transcriptional inhibitory complexes and that the PER complex thereby rhythmically delivers histone deacetylases to the Per1 promoter, which repress Per1 transcription. These findings provide a function for the PER complex and a molecular mechanism for circadian clock negative feedback.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3859310/" 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/PMC3859310/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duong, Hao A -- Robles, Maria S -- Knutti, Darko -- Weitz, Charles J -- T32 NS007484/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2011 Jun 17;332(6036):1436-9. doi: 10.1126/science.1196766.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21680841" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/genetics/metabolism ; Animals ; CLOCK Proteins/genetics/metabolism ; *Circadian Clocks ; *Circadian Rhythm ; Cryptochromes/metabolism ; *Feedback, Physiological ; Histone Deacetylase 1/metabolism ; Histones/metabolism ; Liver/metabolism ; Lung/metabolism ; Mass Spectrometry ; Mice ; Period Circadian Proteins/*genetics/metabolism ; Promoter Regions, Genetic ; RNA-Binding Proteins/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Repressor Proteins/*metabolism ; Transcription, Genetic
    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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  • 95
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    Host proteasomal degradation generates amino acids essential for intracellular bacterial growth (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-11-19
    Description: Legionella pneumophila proliferates in environmental amoeba and human cells within the Legionella-containing vacuole (LCV). The exported AnkB F-box effector of L. pneumophila is anchored into the LCV membrane by host-mediated farnesylation. Here, we report that host proteasomal degradation of Lys(48)-linked polyubiquitinated proteins, assembled on the LCV by AnkB, generates amino acids required for intracellular bacterial proliferation. The severe defect of the ankB null mutant in proliferation within amoeba and human cells is rescued by supplementation of a mixture of amino acids or cysteine, serine, pyruvate, or citrate, similar to rescue by genetic complementation. Defect of the ankB mutant in intrapulmonary proliferation in mice is rescued upon injection of a mixture of amino acids or cysteine. Therefore, Legionella promotes eukaryotic proteasomal degradation to generate amino acids needed as carbon and energy sources for bacterial proliferation within evolutionarily distant hosts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Price, Christopher T D -- Al-Quadan, Tasneem -- Santic, Marina -- Rosenshine, Ilan -- Abu Kwaik, Yousef -- R01AI069321/AI/NIAID NIH HHS/ -- R01AI43965/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2011 Dec 16;334(6062):1553-7. doi: 10.1126/science.1212868. Epub 2011 Nov 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, College of Medicine, University of Louisville, KY 40202, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22096100" target="_blank"〉PubMed〈/a〉
    Keywords: Acanthamoeba/microbiology ; Amino Acids/*metabolism ; Animals ; Cell Proliferation ; F-Box Proteins/genetics/metabolism ; HEK293 Cells ; Humans ; Legionella pneumophila/*growth & development/*metabolism ; Legionnaires' Disease/metabolism/microbiology ; Lysine/metabolism ; Macrophages/metabolism/microbiology ; Mice ; Proteasome Endopeptidase Complex/*metabolism ; Ubiquitin/genetics/metabolism ; Ubiquitinated Proteins/metabolism ; Vacuoles/metabolism/microbiology
    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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  • 96
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    Structure of MyTH4-FERM domains in myosin VIIa tail bound to cargo (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-02-12
    Description: The unconventional myosin VIIa (MYO7A) is one of the five proteins that form a network of complexes involved in formation of stereocilia. Defects in these proteins cause syndromic deaf-blindness in humans [Usher syndrome I (USH1)]. Many disease-causing mutations occur in myosin tail homology 4-protein 4.1, ezrin, radixin, moesin (MyTH4-FERM) domains in the myosin tail that binds to another USH1 protein, Sans. We report the crystal structure of MYO7A MyTH4-FERM domains in complex with the central domain (CEN) of Sans at 2.8 angstrom resolution. The MyTH4 and FERM domains form an integral structural and functional supramodule binding to two highly conserved segments (CEN1 and 2) of Sans. The MyTH4-FERM/CEN complex structure provides mechanistic explanations for known deafness-causing mutations in MYO7A MyTH4-FERM. The structure will also facilitate mechanistic and functional studies of MyTH4-FERM domains in other myosins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Lin -- Pan, Lifeng -- Wei, Zhiyi -- Zhang, Mingjie -- New York, N.Y. -- Science. 2011 Feb 11;331(6018):757-60. doi: 10.1126/science.1198848.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Life Science, Molecular Neuroscience Center, State Key Laboratory of Molecular Neuroscience, Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21311020" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Crystallography, X-Ray ; Humans ; Mice ; Models, Molecular ; Molecular Sequence Data ; Mutation, Missense ; Myosins/*chemistry/metabolism ; Nerve Tissue Proteins/*chemistry/metabolism ; Protein Binding ; Protein Conformation ; Protein Structure, Tertiary ; Recombinant Fusion Proteins/chemistry/metabolism
    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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  • 97
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    Conservation: model management intensity (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-11-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hayashi, Kiyotada -- New York, N.Y. -- Science. 2011 Nov 4;334(6056):593-4; author reply 594-5. doi: 10.1126/science.334.6056.593-b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22053027" target="_blank"〉PubMed〈/a〉
    Keywords: *Agriculture ; Animals ; *Biodiversity ; *Conservation of Natural Resources ; Crops, Agricultural/*growth & development ; *Ecosystem ; *Food
    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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  • 98
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    Culture and biodiversity losses linked (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-01-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Tong -- Petriello, Michael Anthony -- New York, N.Y. -- Science. 2011 Jan 7;331(6013):30-1; author reply 31. doi: 10.1126/science.331.6013.30-b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21212339" target="_blank"〉PubMed〈/a〉
    Keywords: *Biodiversity ; *Conservation of Natural Resources ; *Culture ; Humans ; *Population Groups
    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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  • 99
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    Equilibrative nucleoside transporter 3 deficiency perturbs lysosome function and macrophage homeostasis (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-12-17
    Description: Lysosomal storage diseases (LSDs) are a group of heterogeneous disorders caused by defects in lysosomal enzymes or transporters, resulting in accumulation of undegraded macromolecules or metabolites. Macrophage numbers are expanded in several LSDs, leading to histiocytosis of unknown pathophysiology. Here, we found that mice lacking the equilibrative nucleoside transporter 3 (ENT3) developed a spontaneous and progressive macrophage-dominated histiocytosis. In the absence of ENT3, defective apoptotic cell clearance led to lysosomal nucleoside buildup, elevated intralysosomal pH, and altered macrophage function. The macrophage accumulation was partly due to increased macrophage colony-stimulating factor and receptor expression and signaling secondary to the lysosomal defects. These studies suggest a cellular and molecular basis for the development of histiocytosis in several human syndromes associated with ENT3 mutations and potentially other LSDs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsu, Chia-Lin -- Lin, Weiyu -- Seshasayee, Dhaya -- Chen, Yung-Hsiang -- Ding, Xiao -- Lin, Zhonghua -- Suto, Eric -- Huang, Zhiyu -- Lee, Wyne P -- Park, Hyunjoo -- Xu, Min -- Sun, Mei -- Rangell, Linda -- Lutman, Jeff L -- Ulufatu, Sheila -- Stefanich, Eric -- Chalouni, Cecile -- Sagolla, Meredith -- Diehl, Lauri -- Fielder, Paul -- Dean, Brian -- Balazs, Mercedesz -- Martin, Flavius -- New York, N.Y. -- Science. 2012 Jan 6;335(6064):89-92. doi: 10.1126/science.1213682. Epub 2011 Dec 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology, Genentech Inc., 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/22174130" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/metabolism ; Animals ; Apoptosis ; Cell Count ; Cell Proliferation ; Cells, Cultured ; Histiocytosis/*physiopathology ; *Homeostasis ; Humans ; Hydrogen-Ion Concentration ; Listeriosis/immunology/microbiology ; Lysosomal Storage Diseases/physiopathology ; Lysosomes/*physiology/ultrastructure ; Macrophage Colony-Stimulating Factor/metabolism ; Macrophages/immunology/*physiology/ultrastructure ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myelopoiesis ; Nucleoside Transport Proteins/genetics/*physiology ; Phagocytosis ; Receptor, Macrophage Colony-Stimulating Factor/metabolism ; Signal Transduction ; Thymocytes/immunology/physiology
    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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  • 100
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    Neuroscience. Ubiquitination inhibits neuronal exit (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-01-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Metin, Christine -- Luccardini, Camilla -- New York, N.Y. -- Science. 2010 Dec 24;330(6012):1754-5. doi: 10.1126/science.1200475.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut du Fer a Moulin, INSERM U839, 75005 Paris, France. christine.metin@inserm.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21205656" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Adhesion ; Cell Adhesion Molecules/metabolism ; Cell Movement ; Cerebellum/*cytology/embryology ; Immunoglobulins/metabolism ; Mice ; Morphogenesis ; Neurons/metabolism/*physiology ; Nuclear Proteins/*metabolism ; PDZ Domains ; Protein Binding ; Stem Cells/physiology ; Ubiquitin-Protein Ligases/*metabolism ; Ubiquitination
    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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