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  • Mice  (17)
  • AIRCRAFT STABILITY AND CONTROL
  • American Association for the Advancement of Science (AAAS)  (17)
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  • 1
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    Compartmentalization of GABAergic inhibition by dendritic spines (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-05-11
    Description: gamma-aminobutyric acid-mediated (GABAergic) inhibition plays a critical role in shaping neuronal activity in the neocortex. Numerous experimental investigations have examined perisomatic inhibitory synapses, which control action potential output from pyramidal neurons. However, most inhibitory synapses in the neocortex are formed onto pyramidal cell dendrites, where theoretical studies suggest they may focally regulate cellular activity. The precision of GABAergic control over dendritic electrical and biochemical signaling is unknown. By using cell type-specific optical stimulation in combination with two-photon calcium (Ca(2+)) imaging, we show that somatostatin-expressing interneurons exert compartmentalized control over postsynaptic Ca(2+) signals within individual dendritic spines. This highly focal inhibitory action is mediated by a subset of GABAergic synapses that directly target spine heads. GABAergic inhibition thus participates in localized control of dendritic electrical and biochemical signaling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3752161/" 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/PMC3752161/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chiu, Chiayu Q -- Lur, Gyorgy -- Morse, Thomas M -- Carnevale, Nicholas T -- Ellis-Davies, Graham C R -- Higley, Michael J -- DC009977/DC/NIDCD NIH HHS/ -- GM053395/GM/NIGMS NIH HHS/ -- K01 MH097961/MH/NIMH NIH HHS/ -- MH099045/MH/NIMH NIH HHS/ -- NS011613/NS/NINDS NIH HHS/ -- NS069720/NS/NINDS NIH HHS/ -- R01 DC009977/DC/NIDCD NIH HHS/ -- R01 GM053395/GM/NIGMS NIH HHS/ -- R01 MH099045/MH/NIMH NIH HHS/ -- R01 NS011613/NS/NINDS NIH HHS/ -- R01 NS069720/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2013 May 10;340(6133):759-62. doi: 10.1126/science.1234274.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Yale 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/23661763" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Computer Simulation ; Dendritic Spines/*physiology ; Female ; Glutamic Acid/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Models, Neurological ; Neocortex/*physiology ; *Neural Inhibition ; Photic Stimulation ; Pyramidal Cells/*physiology ; Rhodopsin/metabolism ; Synapses/physiology ; gamma-Aminobutyric Acid/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Human chromosome 7: DNA sequence and biology (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-12
    Description: DNA sequence and annotation of the entire human chromosome 7, encompassing nearly 158 million nucleotides of DNA and 1917 gene structures, are presented. To generate a higher order description, additional structural features such as imprinted genes, fragile sites, and segmental duplications were integrated at the level of the DNA sequence with medical genetic data, including 440 chromosome rearrangement breakpoints associated with disease. This approach enabled the discovery of candidate genes for developmental diseases including autism.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2882961/" 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/PMC2882961/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scherer, Stephen W -- Cheung, Joseph -- MacDonald, Jeffrey R -- Osborne, Lucy R -- Nakabayashi, Kazuhiko -- Herbrick, Jo-Anne -- Carson, Andrew R -- Parker-Katiraee, Layla -- Skaug, Jennifer -- Khaja, Razi -- Zhang, Junjun -- Hudek, Alexander K -- Li, Martin -- Haddad, May -- Duggan, Gavin E -- Fernandez, Bridget A -- Kanematsu, Emiko -- Gentles, Simone -- Christopoulos, Constantine C -- Choufani, Sanaa -- Kwasnicka, Dorota -- Zheng, Xiangqun H -- Lai, Zhongwu -- Nusskern, Deborah -- Zhang, Qing -- Gu, Zhiping -- Lu, Fu -- Zeesman, Susan -- Nowaczyk, Malgorzata J -- Teshima, Ikuko -- Chitayat, David -- Shuman, Cheryl -- Weksberg, Rosanna -- Zackai, Elaine H -- Grebe, Theresa A -- Cox, Sarah R -- Kirkpatrick, Susan J -- Rahman, Nazneen -- Friedman, Jan M -- Heng, Henry H Q -- Pelicci, Pier Giuseppe -- Lo-Coco, Francesco -- Belloni, Elena -- Shaffer, Lisa G -- Pober, Barbara -- Morton, Cynthia C -- Gusella, James F -- Bruns, Gail A P -- Korf, Bruce R -- Quade, Bradley J -- Ligon, Azra H -- Ferguson, Heather -- Higgins, Anne W -- Leach, Natalia T -- Herrick, Steven R -- Lemyre, Emmanuelle -- Farra, Chantal G -- Kim, Hyung-Goo -- Summers, Anne M -- Gripp, Karen W -- Roberts, Wendy -- Szatmari, Peter -- Winsor, Elizabeth J T -- Grzeschik, Karl-Heinz -- Teebi, Ahmed -- Minassian, Berge A -- Kere, Juha -- Armengol, Lluis -- Pujana, Miguel Angel -- Estivill, Xavier -- Wilson, Michael D -- Koop, Ben F -- Tosi, Sabrina -- Moore, Gudrun E -- Boright, Andrew P -- Zlotorynski, Eitan -- Kerem, Batsheva -- Kroisel, Peter M -- Petek, Erwin -- Oscier, David G -- Mould, Sarah J -- Dohner, Hartmut -- Dohner, Konstanze -- Rommens, Johanna M -- Vincent, John B -- Venter, J Craig -- Li, Peter W -- Mural, Richard J -- Adams, Mark D -- Tsui, Lap-Chee -- 38103/Canadian Institutes of Health Research/Canada -- P01 GM061354/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 May 2;300(5620):767-72. Epub 2003 Apr 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Genomic Biology, The Hospital for Sick Children, Toronto, Ontario, Canada, M5G 1X8. steve@genet.sickkids.on.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12690205" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/genetics ; Chromosome Aberrations ; Chromosome Fragile Sites ; Chromosome Fragility ; Chromosome Mapping ; Chromosomes, Human, Pair 7/*genetics ; Computational Biology ; Congenital Abnormalities/genetics ; CpG Islands ; DNA, Complementary ; Databases, Genetic ; Euchromatin/genetics ; Expressed Sequence Tags ; Gene Duplication ; Genes, Overlapping ; Genetic Diseases, Inborn/genetics ; Genomic Imprinting ; Humans ; In Situ Hybridization, Fluorescence ; Limb Deformities, Congenital/genetics ; Mice ; Molecular Sequence Data ; Mutation ; Neoplasms/genetics ; Pseudogenes ; RNA/genetics ; Retroelements ; *Sequence Analysis, DNA ; Williams Syndrome/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Cleavage of proBDNF by tPA/plasmin is essential for long-term hippocampal plasticity (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-10-16
    Description: Long-term memory is thought to be mediated by protein synthesis-dependent, late-phase long-term potentiation (L-LTP). Two secretory proteins, tissue plasminogen activator (tPA) and brain-derived neurotrophic factor (BDNF), have been implicated in this process, but their relationship is unclear. Here we report that tPA, by activating the extracellular protease plasmin, converts the precursor proBDNF to the mature BDNF (mBDNF), and that such conversion is critical for L-LTP expression in mouse hippocampus. Moreover, application of mBDNF is sufficient to rescue L-LTP when protein synthesis is inhibited, which suggests that mBDNF is a key protein synthesis product for L-LTP expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pang, Petti T -- Teng, Henry K -- Zaitsev, Eugene -- Woo, Newton T -- Sakata, Kazuko -- Zhen, Shushuang -- Teng, Kenneth K -- Yung, Wing-Ho -- Hempstead, Barbara L -- Lu, Bai -- NS30658/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 Oct 15;306(5695):487-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section on Neural Development and Plasticity, Laboratory of Cellular and Synaptic Neurophysiology, National Institute of Child Health and Human Development (NICHD), Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15486301" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anisomycin/pharmacology ; Brain-Derived Neurotrophic Factor/*metabolism/pharmacology ; Electric Stimulation ; Excitatory Postsynaptic Potentials ; Fibrinolysin/*metabolism ; Hippocampus/*physiology ; In Vitro Techniques ; *Long-Term Potentiation ; Male ; Mice ; Mice, Knockout ; Precipitin Tests ; Protein Precursors/metabolism ; Protein Synthesis Inhibitors/pharmacology ; Synapses/*metabolism ; Synaptic Transmission ; Tissue Plasminogen Activator/*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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  • 4
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    Increased vascularization in mice overexpressing angiopoietin-1 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-17
    Description: The angiopoietins and members of the vascular endothelial growth factor (VEGF) family are the only growth factors thought to be largely specific for vascular endothelial cells. Targeted gene inactivation studies in mice have shown that VEGF is necessary for the early stages of vascular development and that angiopoietin-1 is required for the later stages of vascular remodeling. Here it is shown that transgenic overexpression of angiopoietin-1 in the skin of mice produces larger, more numerous, and more highly branched vessels. These results raise the possibility that angiopoietins can be used, alone or in combination with VEGF, to promote therapeutic angiogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suri, C -- McClain, J -- Thurston, G -- McDonald, D M -- Zhou, H -- Oldmixon, E H -- Sato, T N -- Yancopoulos, G D -- HL-24136/HL/NHLBI NIH HHS/ -- HL-59157/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1998 Oct 16;282(5388):468-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9774272" target="_blank"〉PubMed〈/a〉
    Keywords: Angiopoietin-1 ; Animals ; Capillaries/anatomy & histology/ultrastructure ; Endothelial Growth Factors/genetics/physiology ; Endothelium, Vascular/ultrastructure ; Gene Expression ; Keratinocytes/metabolism ; Lymphokines/genetics/physiology ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Mice, Transgenic ; *Neovascularization, Physiologic ; Skin/*blood supply/metabolism ; Transgenes ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors ; Venules/anatomy & histology/ultrastructure
    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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    Leakage-resistant blood vessels in mice transgenically overexpressing angiopoietin-1 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-05
    Description: Angiopoietin-1 (Ang1) and vascular endothelial growth factor (VEGF) are endothelial cell-specific growth factors. Direct comparison of transgenic mice overexpressing these factors in the skin revealed that the VEGF-induced blood vessels were leaky, whereas those induced by Ang1 were nonleaky. Moreover, vessels in Ang1-overexpressing mice were resistant to leaks caused by inflammatory agents. Coexpression of Ang1 and VEGF had an additive effect on angiogenesis but resulted in leakage-resistant vessels typical of Ang1. Ang1 therefore may be useful for reducing microvascular leakage in diseases in which the leakage results from chronic inflammation or elevated VEGF and, in combination with VEGF, for promoting growth of nonleaky vessels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thurston, G -- Suri, C -- Smith, K -- McClain, J -- Sato, T N -- Yancopoulos, G D -- McDonald, D M -- HL-24136/HL/NHLBI NIH HHS/ -- HL-59157/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 Dec 24;286(5449):2511-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Cardiovascular Research Institute, University of California, San Francisco, CA 94143-0452, USA. gavint@itsa.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10617467" target="_blank"〉PubMed〈/a〉
    Keywords: Angiopoietin-1 ; Animals ; Arterioles/anatomy & histology/physiology ; Binding Sites ; Capillaries/anatomy & histology/physiology ; *Capillary Permeability ; Ear ; Endothelial Growth Factors/genetics/*physiology ; Endothelium, Vascular/metabolism ; Inflammation/chemically induced ; Inflammation Mediators/pharmacology ; Lymphokines/genetics/*physiology ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Mice, Transgenic ; Microcirculation/anatomy & histology/*physiology ; Mustard Plant ; *Neovascularization, Physiologic ; Plant Extracts/pharmacology ; Plant Lectins ; Plant Oils ; Plants, Medicinal ; Platelet Activating Factor/pharmacology ; Ricin/metabolism ; Serotonin/pharmacology ; Skin/blood supply/metabolism ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors ; Venules/anatomy & histology/physiology
    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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    Identification of ubiquitin ligases required for skeletal muscle atrophy (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-10-27
    Description: Skeletal muscle adapts to decreases in activity and load by undergoing atrophy. To identify candidate molecular mediators of muscle atrophy, we performed transcript profiling. Although many genes were up-regulated in a single rat model of atrophy, only a small subset was universal in all atrophy models. Two of these genes encode ubiquitin ligases: Muscle RING Finger 1 (MuRF1), and a gene we designate Muscle Atrophy F-box (MAFbx), the latter being a member of the SCF family of E3 ubiquitin ligases. Overexpression of MAFbx in myotubes produced atrophy, whereas mice deficient in either MAFbx or MuRF1 were found to be resistant to atrophy. These proteins are potential drug targets for the treatment of muscle atrophy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bodine, S C -- Latres, E -- Baumhueter, S -- Lai, V K -- Nunez, L -- Clarke, B A -- Poueymirou, W T -- Panaro, F J -- Na, E -- Dharmarajan, K -- Pan, Z Q -- Valenzuela, D M -- DeChiara, T M -- Stitt, T N -- Yancopoulos, G D -- Glass, D J -- New York, N.Y. -- Science. 2001 Nov 23;294(5547):1704-8. Epub 2001 Oct 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY, 10591-6707, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11679633" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cloning, Molecular ; Creatine Kinase/genetics ; Creatine Kinase, MM Form ; *DNA-Binding Proteins ; Gene Deletion ; *Gene Expression Profiling ; Hindlimb Suspension ; Humans ; Immobilization ; Isoenzymes/genetics ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Muscle Denervation ; Muscle Proteins/genetics ; Muscle, Skeletal/growth & development/*metabolism/pathology/physiopathology ; Muscular Atrophy/*genetics/pathology/physiopathology ; MyoD Protein/genetics ; Myogenic Regulatory Factor 5 ; Myogenin/genetics ; Peptide Synthases/chemistry/deficiency/genetics/*metabolism ; Phenotype ; Protein Binding ; RNA, Messenger/analysis/genetics ; Rats ; Rats, Sprague-Dawley ; SKP Cullin F-Box Protein Ligases ; *Trans-Activators ; Up-Regulation
    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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    Sex determination in malaria parasites (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-30
    Description: A century ago, W. G. MacCallum identified distinct male and female forms in malaria parasites of both birds and humans. Since then, scientists have been puzzled by the high female-to-male ratios of parasites in Plasmodium infections and by the mechanism of sex determination. The sex ratio of malaria parasites was shown to become progressively more male as conditions that allow motility and subsequent fertilization by the male parasites become adverse. This resulted from an increased immune response against male gametes, which coincides with intense host erythropoietic activity. Natural and artificial induction of erythropoiesis in vertebrate hosts provoked a shift toward male parasite production. This change in parasite sex ratio led to reduced reproductive success in the parasite, which suggests that sex determination is adaptive and is regulated by the hematologic state of the host.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paul, R E -- Coulson, T N -- Raibaud, A -- Brey, P T -- New York, N.Y. -- Science. 2000 Jan 7;287(5450):128-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Biochimie et Biologie Moleculaire des Insectes, Institut Pasteur, 25 Rue du Dr. Roux, 75724 Paris Cedex 15, France. topotito@pasteur.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10615046" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/parasitology ; Animals ; Chickens ; Erythrocytes/parasitology ; *Erythropoiesis ; Erythropoietin/pharmacology ; Female ; Malaria/*blood/*parasitology ; Malaria, Avian/blood/parasitology ; Male ; Mice ; Plasmodium/growth & development/*physiology ; Plasmodium gallinaceum/growth & development/*physiology ; Recombinant Proteins/pharmacology ; Reproduction ; Reticulocytes/parasitology ; Sex Determination Processes ; Sex Ratio
    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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  • 8
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    Angiopoietin-2, a natural antagonist for Tie2 that disrupts in vivo angiogenesis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-04
    Description: Angiogenesis is thought to depend on a precise balance of positive and negative regulation. Angiopoietin-1 (Ang1) is an angiogenic factor that signals through the endothelial cell-specific Tie2 receptor tyrosine kinase. Like vascular endothelial growth factor, Ang1 is essential for normal vascular development in the mouse. An Ang1 relative, termed angiopoietin-2 (Ang2), was identified by homology screening and shown to be a naturally occurring antagonist for Ang1 and Tie2. Transgenic overexpression of Ang2 disrupts blood vessel formation in the mouse embryo. In adult mice and humans, Ang2 is expressed only at sites of vascular remodeling. Natural antagonists for vertebrate receptor tyrosine kinases are atypical; thus, the discovery of a negative regulator acting on Tie2 emphasizes the need for exquisite regulation of this angiogenic receptor system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maisonpierre, P C -- Suri, C -- Jones, P F -- Bartunkova, S -- Wiegand, S J -- Radziejewski, C -- Compton, D -- McClain, J -- Aldrich, T H -- Papadopoulos, N -- Daly, T J -- Davis, S -- Sato, T N -- Yancopoulos, G D -- New York, N.Y. -- Science. 1997 Jul 4;277(5322):55-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals Inc., 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9204896" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Angiopoietin-1 ; Angiopoietin-2 ; Animals ; Blood Vessels/embryology/*metabolism ; Cells, Cultured ; Cloning, Molecular ; Embryo, Mammalian/metabolism ; Endothelial Growth Factors/genetics/metabolism ; Endothelium, Vascular/*cytology/metabolism ; Female ; Humans ; Ligands ; Lymphokines/genetics/metabolism ; Membrane Glycoproteins/antagonists & inhibitors/metabolism ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; *Neovascularization, Physiologic ; Phosphorylation ; Proteins/chemistry/*metabolism ; Rats ; Rats, Sprague-Dawley ; Receptor Protein-Tyrosine Kinases/*antagonists & inhibitors/metabolism ; Receptor, TIE-2 ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
    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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    Genes for epilepsy mapped in the mouse (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-08-09
    Description: The neurological mutant mouse strain E1 is a model for complex partial seizures in humans. The inheritance of epileptic seizures with seven conventional chromosomal markers and over 60 endogenous proviral markers was studied by means of back-crosses of E1 with two seizure-resistant strains, DBA/2J and ABP/LeJ. The major gene responsible for this epileptic phenotype (El-1) was localized to a region distal with respect to the centromere on chromosome 9. At least one other gene, El-2, linked to proviral markers on chromosome 2, also influences the seizure phenotype. In addition, a potential modifier of seizures was detected in the DBA/2J background. The location of El-1 on distal chromosome 9 may allow identification of an epilepsy candidate gene in humans on the basis of conserved synteny with human chromosome 3.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rise, M L -- Frankel, W N -- Coffin, J M -- Seyfried, T N -- NS 23355/NS/NINDS NIH HHS/ -- R35CA44385/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Aug 9;253(5020):669-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Boston College, Chestnut Hill 02167.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1871601" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; Crosses, Genetic ; Epilepsy/*genetics ; Female ; Genetic Predisposition to Disease ; Male ; Mice ; Mice, Inbred Strains ; Mice, Neurologic Mutants/*genetics ; Recombination, Genetic ; Seizures/genetics ; Software
    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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  • 10
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    Recruitment of antigen-specific CD8+ T cells in response to infection is markedly efficient (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-09-05
    Description: The magnitude of antigen-specific CD8+ T cell responses is not fixed but correlates with the severity of infection. Although by definition T cell response size is the product of both the capacity to recruit naive T cells (clonal selection) and their subsequent proliferation (clonal expansion), it remains undefined how these two factors regulate antigen-specific T cell responses. We determined the relative contribution of recruitment and expansion by labeling naive T cells with unique genetic tags and transferring them into mice. Under disparate infection conditions with different pathogens and doses, recruitment of antigen-specific T cells was near constant and close to complete. Thus, naive T cell recruitment is highly efficient, and the magnitude of antigen-specific CD8+ T cell responses is primarily controlled by clonal expansion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van Heijst, Jeroen W J -- Gerlach, Carmen -- Swart, Erwin -- Sie, Daoud -- Nunes-Alves, Claudio -- Kerkhoven, Ron M -- Arens, Ramon -- Correia-Neves, Margarida -- Schepers, Koen -- Schumacher, Ton N M -- New York, N.Y. -- Science. 2009 Sep 4;325(5945):1265-9. doi: 10.1126/science.1175455.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19729659" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Ampicillin/therapeutic use ; Animals ; Anti-Bacterial Agents/therapeutic use ; Antigens/*immunology ; Antigens, Bacterial/immunology ; Antigens, Viral/immunology ; CD8-Positive T-Lymphocytes/*immunology ; Dendritic Cells/immunology ; Epitopes/immunology ; Genes, T-Cell Receptor alpha ; Genes, T-Cell Receptor beta ; Influenza A virus/immunology ; Listeriosis/drug therapy/*immunology ; *Lymphocyte Activation ; Lymphocyte Count ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Molecular Sequence Data ; Orthomyxoviridae Infections/immunology ; Ovalbumin/immunology ; Receptors, Antigen, T-Cell, alpha-beta/chemistry/immunology ; Spleen/immunology ; Vaccinia/immunology ; Virus Diseases/*immunology
    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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