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  • Mice  (201)
  • Male  (169)
  • Research Support as Topic
  • American Association for the Advancement of Science (AAAS)  (365)
  • American Association of Petroleum Geologists (AAPG)
  • Nature Publishing Group (NPG)
  • 2000-2004  (365)
  • 2003  (365)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (365)
  • American Association of Petroleum Geologists (AAPG)
  • Nature Publishing Group (NPG)
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  • 2000-2004  (365)
Year
  • 1
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    Disrupted timing of discontinuous but not continuous movements by cerebellar lesions (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-31
    Description: Patients with cerebellar damage are known to exhibit deficits in the temporal control of movements. We report that these deficits are restricted to discontinuous movements. Cerebellar patients exhibited no deficit in temporal variability when producing continuous, rhythmic movements. We hypothesize that the temporal properties of continuous movements are emergent and reflect the operation of other control parameters not associated with the cerebellum. In contrast, discontinuous movements require an explicit representation of the temporal goal, a function of the cerebellum. The requirement for explicit temporal representation provides a parsimonious account of cerebellar involvement in a range of tasks.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Spencer, Rebecca M C -- Zelaznik, Howard N -- Diedrichsen, Jorn -- Ivry, Richard B -- NS17778/NS/NINDS NIH HHS/ -- NS30256/NS/NINDS NIH HHS/ -- NS40813/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 May 30;300(5624):1437-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University of California, Berkeley, 3210 Tolman Hall #1650, Berkeley, CA 94720, USA. rspencer@socrates.berkeley.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12775842" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Aged, 80 and over ; Cerebellar Diseases/*physiopathology ; Cerebellum/physiology/*physiopathology ; Female ; Humans ; Male ; Middle Aged ; *Motor Activity ; Movement ; *Psychomotor Performance ; Spinocerebellar Degenerations/*physiopathology ; Time 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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  • 2
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    Obesity drug pipeline not so fat (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gura, Trisha -- New York, N.Y. -- Science. 2003 Feb 7;299(5608):849-52.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12574616" target="_blank"〉PubMed〈/a〉
    Keywords: Agouti-Related Protein ; Animals ; Anti-Obesity Agents/adverse effects/pharmacology/*therapeutic use ; Appetite/drug effects ; Arcuate Nucleus of Hypothalamus/metabolism ; Ciliary Neurotrophic Factor/therapeutic use ; Clinical Trials as Topic ; Cyclobutanes/adverse effects/therapeutic use ; Energy Intake ; Ghrelin ; Humans ; Hunger/drug effects ; Intercellular Signaling Peptides and Proteins ; Lactones/adverse effects/therapeutic use ; Leptin/metabolism/therapeutic use ; Mice ; Nerve Tissue Proteins/adverse effects/therapeutic use ; Neurons/metabolism ; Neuropeptide Y/metabolism/pharmacology ; Obesity/*drug therapy/metabolism ; Peptide Fragments ; Peptide Hormones/metabolism/pharmacology ; Peptide YY/metabolism/pharmacology ; Phentermine/adverse effects/therapeutic use ; Proteins/metabolism ; Receptors, Corticotropin/metabolism ; Receptors, Melanocortin ; Weight Loss ; alpha-MSH/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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  • 3
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    Retrograde viral delivery of IGF-1 prolongs survival in a mouse ALS model (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-09
    Description: Amyotrophic lateral sclerosis (ALS) is a progressive, lethal neuromuscular disease that is associated with the degeneration of spinal and brainstem motor neurons, leading to atrophy of limb, axial, and respiratory muscles. The cause of ALS is unknown, and there is no effective therapy. Neurotrophic factors are candidates for therapeutic evaluation in ALS. Although chronic delivery of molecules to the central nervous system has proven difficult, we recently discovered that adeno-associated virus can be retrogradely transported efficiently from muscle to motor neurons of the spinal cord. We report that insulin-like growth factor 1 prolongs life and delays disease progression, even when delivered at the time of overt disease symptoms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaspar, Brian K -- Llado, Jeronia -- Sherkat, Nushin -- Rothstein, Jeffrey D -- Gage, Fred H -- AG12992/AG/NIA NIH HHS/ -- AG21876/AG/NIA NIH HHS/ -- NS33958/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Aug 8;301(5634):839-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12907804" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/pathology/physiopathology/*therapy ; Animals ; Apoptosis ; Base Sequence ; Caspase 9 ; Caspases/metabolism ; Cell Count ; Dependovirus/*genetics ; Disease Models, Animal ; Disease Progression ; Gene Transfer Techniques ; *Genetic Therapy ; *Genetic Vectors/administration & dosage ; Glial Cell Line-Derived Neurotrophic Factor ; Green Fluorescent Proteins ; Insulin-Like Growth Factor I/*genetics ; Luminescent Proteins/genetics ; Male ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Motor Neurons/pathology/virology ; Muscle, Skeletal/virology ; Nerve Growth Factors/genetics ; *Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Random Allocation ; Spinal Cord/chemistry/pathology/virology ; Superoxide Dismutase/genetics/metabolism ; Ubiquitin/analysis
    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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    Evolutionary discrimination of mammalian conserved non-genic sequences (CNGs) (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-04
    Description: Analysis of the human and mouse genomes identified an abundance of conserved non-genic sequences (CNGs). The significance and evolutionary depth of their conservation remain unanswered. We have quantified levels and patterns of conservation of 191 CNGs of human chromosome 21 in 14 mammalian species. We found that CNGs are significantly more conserved than protein-coding genes and noncoding RNAS (ncRNAs) within the mammalian class from primates to monotremes to marsupials. The pattern of substitutions in CNGs differed from that seen in protein-coding and ncRNA genes and resembled that of protein-binding regions. About 0.3% to 1% of the human genome corresponds to a previously unknown class of extremely constrained CNGs shared among mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dermitzakis, Emmanouil T -- Reymond, Alexandre -- Scamuffa, Nathalie -- Ucla, Catherine -- Kirkness, Ewen -- Rossier, Colette -- Antonarakis, Stylianos E -- New York, N.Y. -- Science. 2003 Nov 7;302(5647):1033-5. Epub 2003 Oct 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Medical Genetics and National Center of Competence in Research (NCCR) Frontiers in Genetics, University of Geneva Medical School and University Hospitals, 1211 Geneva, Switzerland. Emmanouil.Dermitzakis@medecine.unige.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14526086" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Chromosomes, Human, Pair 21/*genetics ; Chromosomes, Mammalian/*genetics ; *Conserved Sequence ; DNA, Intergenic/*genetics ; Discriminant Analysis ; *Evolution, Molecular ; Female ; Genetic Code ; Genome ; Humans ; Male ; Mammals/*genetics ; Molecular Sequence Data ; Polymerase Chain Reaction ; Proteins/genetics ; RNA, Untranslated/genetics ; Selection, Genetic ; Sequence Alignment ; Species Specificity ; Time ; 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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  • 5
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    Mutations in dynein link motor neuron degeneration to defects in retrograde transport (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-06
    Description: Degenerative disorders of motor neurons include a range of progressive fatal diseases such as amyotrophic lateral sclerosis (ALS), spinal-bulbar muscular atrophy (SBMA), and spinal muscular atrophy (SMA). Although the causative genetic alterations are known for some cases, the molecular basis of many SMA and SBMA-like syndromes and most ALS cases is unknown. Here we show that missense point mutations in the cytoplasmic dynein heavy chain result in progressive motor neuron degeneration in heterozygous mice, and in homozygotes this is accompanied by the formation of Lewy-like inclusion bodies, thus resembling key features of human pathology. These mutations exclusively perturb neuron-specific functions of dynein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hafezparast, Majid -- Klocke, Rainer -- Ruhrberg, Christiana -- Marquardt, Andreas -- Ahmad-Annuar, Azlina -- Bowen, Samantha -- Lalli, Giovanna -- Witherden, Abi S -- Hummerich, Holger -- Nicholson, Sharon -- Morgan, P Jeffrey -- Oozageer, Ravi -- Priestley, John V -- Averill, Sharon -- King, Von R -- Ball, Simon -- Peters, Jo -- Toda, Takashi -- Yamamoto, Ayumu -- Hiraoka, Yasushi -- Augustin, Martin -- Korthaus, Dirk -- Wattler, Sigrid -- Wabnitz, Philipp -- Dickneite, Carmen -- Lampel, Stefan -- Boehme, Florian -- Peraus, Gisela -- Popp, Andreas -- Rudelius, Martina -- Schlegel, Juergen -- Fuchs, Helmut -- Hrabe de Angelis, Martin -- Schiavo, Giampietro -- Shima, David T -- Russ, Andreas P -- Stumm, Gabriele -- Martin, Joanne E -- Fisher, Elizabeth M C -- New York, N.Y. -- Science. 2003 May 2;300(5620):808-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurodegenerative Disease, Institute of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730604" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anterior Horn Cells/pathology ; Apoptosis ; *Axonal Transport ; Cell Differentiation ; Cell Movement ; Central Nervous System/embryology ; Chromosome Mapping ; Dimerization ; Dyneins/chemistry/*genetics/*physiology ; Female ; Ganglia, Spinal/pathology ; Golgi Apparatus/metabolism/ultrastructure ; Heterozygote ; Homozygote ; Lewy Bodies/pathology ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Motor Neuron Disease/*genetics/pathology/physiopathology ; Motor Neurons/*physiology/ultrastructure ; Mutation ; Mutation, Missense ; *Nerve Degeneration ; Peptide Fragments/metabolism ; Phenotype ; Point Mutation ; Spinal Nerves/growth & development ; Tetanus Toxin/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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    Environmental Protection Agency. Access to proposals triggers sharp debate (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Renner, Rebecca -- New York, N.Y. -- Science. 2003 Mar 7;299(5612):1501.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12624242" target="_blank"〉PubMed〈/a〉
    Keywords: *Access to Information ; Government Agencies ; *Intellectual Property ; National Institutes of Health (U.S.) ; Privacy ; Research Support as Topic ; United States ; *United States Environmental Protection Agency
    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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    Comment on "Tumor response to radiotherapy regulated by endothelial cell apoptosis" (II) (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, Martin -- Bristow, Robert -- Glazer, Peter -- Hill, Richard -- McBride, William -- McKenna, Gillies -- Muschel, Ruth -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1894; author reply 1894.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Radiation Oncology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671275" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Disease Models, Animal ; Endothelium, Vascular/*pathology/radiation effects ; Melanoma, Experimental/blood supply/immunology/pathology/*radiotherapy ; Mice ; Radiation Tolerance ; Sphingomyelin Phosphodiesterase/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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  • 8
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    Lateralized cognitive processes and lateralized task control in the human brain (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-19
    Description: The principles underlying human hemispheric specialization are poorly understood. We used functional magnetic resonance imaging of letter and visuospatial decision tasks with identical word stimuli to address two unresolved problems. First, hemispheric specialization depended on the nature of the task rather than on the nature of the stimulus. Second, analysis of frontal candidate regions for cognitive control showed increased coupling between left anterior cingulate cortex (ACC) and left inferior frontal gyrus during letter decisions, whereas right ACC showed enhanced coupling with right parietal areas during visuospatial decisions. Cognitive control is thus localized in the same hemisphere as task execution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stephan, Klaas E -- Marshall, John C -- Friston, Karl J -- Rowe, James B -- Ritzl, Afra -- Zilles, Karl -- Fink, Gereon R -- 077029/Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2003 Jul 18;301(5631):384-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Medicine (IME), Research Centre Julich, 52425 Julich, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12869765" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Brain/*physiology ; Brain Mapping ; *Cognition ; Functional Laterality ; Gyrus Cinguli/physiology ; Humans ; *Language ; Magnetic Resonance Imaging ; Male ; Parietal Lobe/physiology ; Prefrontal Cortex/physiology ; Space Perception ; Visual 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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  • 9
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    Altered patterns of sleep and behavioral adaptability in NPAS2-deficient mice (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-05
    Description: Animal behavior is synchronized to the 24-hour light:dark (LD) cycle by regulatory programs that produce circadian fluctuations in gene expression throughout the body. In mammals, the transcription factor CLOCK controls circadian oscillation in the suprachiasmatic nucleus of the brain; its paralog, neuronal PAS domain protein 2 (NPAS2), performs a similar function in other forebrain sites. To investigate the role of NPAS2 in behavioral manifestations of circadian rhythm, we studied locomotor activity, sleep patterns, and adaptability to both light- and restricted food-driven entrainment in NPAS2-deficient mice. Our results indicate that NPAS2 plays a substantive role in maintaining circadian behaviors in normal LD and feeding conditions and that NPAS2 is critical for adaptability to food restriction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dudley, Carol A -- Erbel-Sieler, Claudia -- Estill, Sandi Jo -- Reick, Martin -- Franken, Paul -- Pitts, SiNae -- McKnight, Steven L -- 37919/PHS HHS/ -- 4R37 MH59388/MH/NIMH NIH HHS/ -- 5T3DK07328/DK/NIDDK NIH HHS/ -- HL 64148/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2003 Jul 18;301(5631):379-83. Epub 2003 Jul 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9152, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12843397" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; Animals ; Basic Helix-Loop-Helix Transcription Factors ; Behavior, Animal ; Biological Clocks/*physiology ; Body Weight ; CLOCK Proteins ; Circadian Rhythm/*physiology ; Crosses, Genetic ; Darkness ; Eating ; Electroencephalography ; Electromyography ; Female ; Food ; Gene Targeting ; Light ; Male ; Mice ; Mice, Inbred C57BL ; *Motor Activity ; Nerve Tissue Proteins/genetics/*physiology ; Prosencephalon/physiology ; *Sleep ; Suprachiasmatic Nucleus/physiology ; Trans-Activators/genetics/physiology ; Transcription Factors/genetics/*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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  • 10
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    Aging and genome maintenance: lessons from the mouse? (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-01
    Description: Recent progress in the science of aging is driven largely by the use of model systems, ranging from yeast and nematodes to mice. These models have revealed conservation in genetic pathways that balance energy production and its damaging by-products with pathways that preserve somatic maintenance. Maintaining genome integrity has emerged as a major factor in longevity and cell viability. Here we discuss the use of mouse models with defects in genome maintenance for understanding the molecular basis of aging in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hasty, Paul -- Campisi, Judith -- Hoeijmakers, Jan -- van Steeg, Harry -- Vijg, Jan -- AG17242/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2003 Feb 28;299(5611):1355-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Medicine, University of Texas Health Science Center, San Antonio, TX 78245, USA. hastye@uthscsa.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12610296" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging/genetics ; Aging, Premature/*genetics ; Animals ; Apoptosis ; Cell Aging ; *DNA Damage ; DNA Helicases/genetics/metabolism ; *DNA Repair/genetics ; Exodeoxyribonucleases ; *Genome ; Genome, Human ; Humans ; Longevity/genetics ; Mice ; Mutation ; Reactive Oxygen Species/metabolism ; RecQ Helicases ; Syndrome ; Telomere/physiology ; 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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  • 11
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    Polyubiquitination of p53 by a ubiquitin ligase activity of p300 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-12
    Description: Rapid turnover of the tumor suppressor protein p53 requires the MDM2 ubiquitin ligase, and both interact with p300-CREB-binding protein transcriptional coactivator proteins. p53 is stabilized by the binding of p300 to the oncoprotein E1A, suggesting that p300 regulates p53 degradation. Purified p300 exhibited intrinsic ubiquitin ligase activity that was inhibited by E1A. In vitro, p300 with MDM2 catalyzed p53 polyubiquitination, whereas MDM2 catalyzed p53 monoubiquitination. E1A expression caused a decrease in polyubiquitinated but not monoubiquitinated p53 in cells. Thus, generation of the polyubiquitinated forms of p53 that are targeted for proteasome degradation requires the intrinsic ubiquitin ligase activities of MDM2 and p300.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grossman, Steven R -- Deato, Maria E -- Brignone, Chrystelle -- Chan, Ho Man -- Kung, Andrew L -- Tagami, Hideaki -- Nakatani, Yoshihiro -- Livingston, David M -- CA15751/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Apr 11;300(5617):342-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12690203" target="_blank"〉PubMed〈/a〉
    Keywords: Adenovirus E1A Proteins/metabolism ; Animals ; Catalysis ; Cells, Cultured ; E1A-Associated p300 Protein ; Embryo, Mammalian ; Fibroblasts/metabolism ; Humans ; Ligases/antagonists & inhibitors/metabolism ; Mice ; Nuclear Proteins/antagonists & inhibitors/*metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-mdm2 ; Recombinant Fusion Proteins/metabolism ; Recombinant Proteins/metabolism ; Trans-Activators/antagonists & inhibitors/*metabolism ; Transfection ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/*metabolism ; Ubiquitin-Protein Ligases ; Ubiquitins/*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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  • 12
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    Ecology. New count of old whales adds up to big debate (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lubick, Naomi -- New York, N.Y. -- Science. 2003 Jul 25;301(5632):451.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12881542" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atlantic Ocean ; Conservation of Natural Resources ; DNA, Mitochondrial/genetics ; *Ecosystem ; Female ; Genetic Variation ; Genetics, Population ; Male ; Mutation ; Population Density ; Population Dynamics ; Time Factors ; *Whales/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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  • 13
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    Reversing the inactivation of peroxiredoxins caused by cysteine sulfinic acid formation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-26
    Description: The active-site cysteine of peroxiredoxins is selectively oxidized to cysteine sulfinic acid during catalysis, which leads to inactivation of peroxidase activity. This oxidation was thought to be irreversible. However, by metabolic labeling of mammalian cells with 35S, we show that the sulfinic form of peroxiredoxin I, produced during the exposure of cells to H2O2, is rapidly reduced to the catalytically active thiol form. The mammalian cells' ability to reduce protein sulfinic acid might serve as a mechanism to repair oxidatively damaged proteins or represent a new type of cyclic modification by which the function of various proteins is regulated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Woo, Hyun Ae -- Chae, Ho Zoon -- Hwang, Sung Chul -- Yang, Kap-Seok -- Kang, Sang Won -- Kim, Kanghwa -- Rhee, Sue Goo -- New York, N.Y. -- Science. 2003 Apr 25;300(5619):653-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cell Signaling Research and Division of Molecular Life Sciences, Ewha Womans University, Seoul 120-750, Korea.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12714748" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Catalysis ; Cell Line ; Cycloheximide/pharmacology ; Cysteine/*analogs & derivatives/*metabolism ; Dimerization ; HeLa Cells ; Humans ; Hydrogen Peroxide/*metabolism ; Methionine/metabolism ; Mice ; Neurotransmitter Agents ; Oxidation-Reduction ; Peroxidases/chemistry/*metabolism ; Peroxiredoxins ; Protein Synthesis Inhibitors/pharmacology ; Spectrometry, Mass, Electrospray Ionization ; Sulfhydryl Compounds/metabolism ; Sulfinic Acids/metabolism ; Tumor Cells, Cultured
    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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  • 14
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    Chromosomal instability and tumors promoted by DNA hypomethylation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eden, Amir -- Gaudet, Francois -- Waghmare, Alpana -- Jaenisch, Rudolf -- CA87869/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Apr 18;300(5618):455.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Nine Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12702868" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes, Mammalian/*genetics/physiology ; DNA (Cytosine-5-)-Methyltransferase/genetics/metabolism ; *DNA Methylation ; Fibroblasts/metabolism ; Genes, Neurofibromatosis 1 ; Genes, p53 ; Humans ; *Loss of Heterozygosity ; Mice ; Mutation ; Neoplasms/genetics ; Recombination, Genetic ; Sarcoma/*genetics ; Soft Tissue Neoplasms/*genetics
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  • 15
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    Whales before whaling in the North Atlantic (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-26
    Description: It is well known that hunting dramatically reduced all baleen whale populations, yet reliable estimates of former whale abundances are elusive. Based on coalescent models for mitochondrial DNA sequence variation, the genetic diversity of North Atlantic whales suggests population sizes of approximately 240,000 humpback, 360,000 fin, and 265,000 minke whales. Estimates for fin and humpback whales are far greater than those previously calculated for prewhaling populations and 6 to 20 times higher than present-day population estimates. Such discrepancies suggest the need for a quantitative reevaluation of historical whale populations and a fundamental revision in our conception of the natural state of the oceans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roman, Joe -- Palumbi, Stephen R -- New York, N.Y. -- Science. 2003 Jul 25;301(5632):508-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Organismic and Evolutionary Biology, Harvard University, 16 Divinity Avenue, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12881568" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atlantic Ocean ; Base Sequence ; Conservation of Natural Resources ; DNA, Mitochondrial/genetics ; *Ecosystem ; Female ; Genetic Variation ; Genetics, Population ; Male ; Molecular Sequence Data ; Population Density ; Population Dynamics ; Time Factors ; *Whales/classification/genetics
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    A heterozygote advantage (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hedrick, Philip W -- New York, N.Y. -- Science. 2003 Oct 3;302(5642):57.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14526061" target="_blank"〉PubMed〈/a〉
    Keywords: Ethnic Groups/*genetics ; Female ; Genetic Variation ; Genotype ; Haplotypes ; *Heterozygote ; Humans ; Kuru/*genetics ; Male ; Middle Aged ; Papua New Guinea ; PrPC Proteins/*genetics ; *Selection, Genetic
    Print ISSN: 0036-8075
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  • 17
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    Infectious disease. An avian flu jumps to people (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wuethrich, Bernice -- New York, N.Y. -- Science. 2003 Mar 7;299(5612):1504.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12624244" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Birds/virology ; Chickens/virology ; Child ; China/epidemiology ; Hong Kong/epidemiology ; Humans ; Influenza A virus/genetics/immunology/*pathogenicity ; Influenza Vaccines ; Influenza in Birds/epidemiology/*virology ; Influenza, Human/*virology ; Male ; Virulence ; World Health Organization
    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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  • 18
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    Biomedicine. Ataxin-1 regulators in the spotlight (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heintz, Nathaniel -- New York, N.Y. -- Science. 2003 Jul 4;301(5629):59-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Rockefeller University, New York, NY 10021, USA. heintz@rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12843383" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins ; Amino Acid Substitution ; Animals ; Ataxin-1 ; Ataxins ; Cell Nucleus/metabolism ; Disease Progression ; Mice ; Mice, Transgenic ; Mutation ; Nerve Tissue Proteins/*chemistry/genetics/*metabolism ; Nuclear Proteins/*chemistry/genetics/*metabolism ; Peptides ; Phosphorylation ; *Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-akt ; Purkinje Cells/metabolism/ultrastructure ; Signal Transduction ; Spinocerebellar Ataxias/etiology/genetics/pathology/*physiopathology ; *Trinucleotide Repeat Expansion ; Tyrosine 3-Monooxygenase/*metabolism
    Print ISSN: 0036-8075
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  • 19
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    Insulin staining of ES cell progeny from insulin uptake (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rajagopal, Jayaraj -- Anderson, William J -- Kume, Shoen -- Martinez, Olga I -- Melton, Douglas A -- New York, N.Y. -- Science. 2003 Jan 17;299(5605):363.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Howard Hughes Medical Institute, Harvard University, 7 Divinity Avenue, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12532008" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/immunology ; Apoptosis ; Cell Differentiation ; Cell Line ; Embryo, Mammalian/*cytology ; Humans ; Insulin/*analysis/genetics/immunology/*metabolism ; Islets of Langerhans/*cytology/metabolism ; Mice ; Microscopy, Confocal ; RNA, Messenger/genetics/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Stem Cells/*cytology/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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  • 20
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    Demography of dietary restriction and death in Drosophila (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-23
    Description: Dietary restriction (DR) increases life-span in organisms from yeast to mammals, presumably by slowing the accumulation of aging-related damage. Here we show that in Drosophila, DR extends life-span entirely by reducing the short-term risk of death. Two days after the application of DR at any age for the first time, previously fully fed flies are no more likely to die than flies of the same age that have been subjected to long-term DR. DR of mammals may also reduce short-term risk of death, and hence DR instigated at any age could generate a full reversal of mortality.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mair, William -- Goymer, Patrick -- Pletcher, Scott D -- Partridge, Linda -- New York, N.Y. -- Science. 2003 Sep 19;301(5640):1731-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University College London, Darwin Building, Gower Street, London WC1E 6BT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14500985" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Animals ; *Caloric Restriction ; Demography ; *Diet ; Drosophila/*physiology ; Female ; *Longevity ; Male ; Mortality ; Reproduction ; Risk ; Temperature ; Time Factors
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  • 21
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    Scanning human gene deserts for long-range enhancers (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nobrega, Marcelo A -- Ovcharenko, Ivan -- Afzal, Veena -- Rubin, Edward M -- HL66728/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 17;302(5644):413.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉U.S. Department of Energy Joint Genome Institute, Walnut Creek, CA 94598, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14563999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anura/genetics ; Base Sequence ; Conserved Sequence ; *DNA, Intergenic ; *Drosophila Proteins ; *Enhancer Elements, Genetic ; Evolution, Molecular ; Gene Expression Regulation ; Genes, Reporter ; Humans ; Introns ; Mice ; Mice, Transgenic ; Nuclear Proteins/*genetics ; Synteny ; Takifugu/genetics ; Tetraodontiformes/genetics ; Xenopus/genetics ; Zebrafish/genetics
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 22
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    Immunology. Hide and seek in the peptidome (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yewdell, Jonathan W -- New York, N.Y. -- Science. 2003 Sep 5;301(5638):1334-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892-0440, USA. jyewdell@nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12958347" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; CD8-Positive T-Lymphocytes/immunology ; Codon ; Cysteine Endopeptidases/metabolism ; Epstein-Barr Virus Nuclear Antigens/chemistry/*genetics/*immunology/metabolism ; Herpesvirus 4, Human/physiology ; Histocompatibility Antigens Class I/*immunology ; Humans ; Mice ; Mice, Transgenic ; Multienzyme Complexes/metabolism ; Peptides/genetics/*immunology/*metabolism ; Proteasome Endopeptidase Complex ; *Protein Biosynthesis ; Reading Frames ; Ribosomes/metabolism ; Self Tolerance ; Virus Latency
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 23
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    Requirement of hippocampal neurogenesis for the behavioral effects of antidepressants (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-09
    Description: Various chronic antidepressant treatments increase adult hippocampal neurogenesis, but the functional importance of this phenomenon remains unclear. Here, using genetic and radiological methods, we show that disrupting antidepressant-induced neurogenesis blocks behavioral responses to antidepressants. Serotonin 1A receptor null mice were insensitive to the neurogenic and behavioral effects of fluoxetine, a serotonin selective reuptake inhibitor. X-irradiation of a restricted region of mouse brain containing the hippocampus prevented the neurogenic and behavioral effects of two classes of antidepressants. These findings suggest that the behavioral effects of chronic antidepressants may be mediated by the stimulation of neurogenesis in the hippocampus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Santarelli, Luca -- Saxe, Michael -- Gross, Cornelius -- Surget, Alexandre -- Battaglia, Fortunato -- Dulawa, Stephanie -- Weisstaub, Noelia -- Lee, James -- Duman, Ronald -- Arancio, Ottavio -- Belzung, Catherine -- Hen, Rene -- New York, N.Y. -- Science. 2003 Aug 8;301(5634):805-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurobiology and Behavior, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12907793" target="_blank"〉PubMed〈/a〉
    Keywords: 8-Hydroxy-2-(di-n-propylamino)tetralin/pharmacology ; Animals ; Antidepressive Agents/*pharmacology ; Antidepressive Agents, Second-Generation/pharmacology ; Antidepressive Agents, Tricyclic/pharmacology ; Behavior, Animal/*drug effects ; Cell Division/drug effects/radiation effects ; Conditioning (Psychology) ; Dentate Gyrus/cytology/drug effects/physiology ; Fear ; Feeding Behavior/drug effects ; Fluoxetine/*pharmacology ; Grooming/drug effects ; Hippocampus/cytology/drug effects/*physiology/radiation effects ; Long-Term Potentiation/radiation effects ; Male ; Mice ; Mice, Knockout ; Neurons/drug effects/*physiology ; Receptors, Serotonin/genetics/metabolism ; Receptors, Serotonin, 5-HT1 ; Stress, Physiological/drug therapy/physiopathology ; Synaptic Transmission/radiation effects
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  • 24
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    Infectious diseases. Searching for a SARS agenda (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-06-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, Martin -- New York, N.Y. -- Science. 2003 Jun 6;300(5625):1487-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12791953" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biomedical Research ; Communicable Diseases, Emerging/diagnosis/prevention & control/transmission ; Disease Outbreaks ; Disease Reservoirs ; Humans ; National Institutes of Health (U.S.) ; Research Support as Topic ; SARS Virus/immunology ; *Severe Acute Respiratory Syndrome/diagnosis/epidemiology/prevention & ; control/transmission ; United States ; Viral Vaccines/economics
    Print ISSN: 0036-8075
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  • 25
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    DNA: a programmable force sensor (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-19
    Description: Direct quantification of biomolecular interaction by single-molecule force spectroscopy has evolved into a powerful tool for materials and life sciences. We introduce an approach in which the unbinding forces required to break intermolecular bonds are measured in a differential format by comparison with a known reference bond (here, a short DNA duplex). In addition to a marked increase in sensitivity and force resolution, which enabled us to resolve single-base pair mismatches, this concept allows for highly specific parallel assays. This option was exploited to overcome cross-reactions of antibodies in a protein biochip application.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Albrecht, Christian -- Blank, Kerstin -- Lalic-Multhaler, Mio -- Hirler, Siegfried -- Mai, Thao -- Gilbert, Ilka -- Schiffmann, Susanne -- Bayer, Tom -- Clausen-Schaumann, Hauke -- Gaub, Hermann E -- New York, N.Y. -- Science. 2003 Jul 18;301(5631):367-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nanotype GmbH, Lochhamer Schlag 12, 82166 Grafelfing, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12869761" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies ; *Base Pair Mismatch ; *Biosensing Techniques ; Carbocyanines ; Cross Reactions ; *DNA/chemistry/genetics/metabolism ; Dimethylpolysiloxanes ; Fluorescence ; Fluorescent Dyes ; Glass ; Humans ; Immunoassay ; Interleukin-5/analysis/immunology ; Mice ; Microscopy, Atomic Force ; Nucleic Acid Conformation ; Nucleic Acid Hybridization ; Oligodeoxyribonucleotides/chemistry/metabolism ; *Oligonucleotide Array Sequence Analysis ; *Protein Array Analysis ; Protein Binding ; Silicones ; Temperature ; Thermodynamics
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  • 26
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    Low potential for climatic stress adaptation in a rainforest Drosophila species (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-05
    Description: The ability of sensitive rainforest species to evolve in response to climate change is largely unknown. We show that the Australian tropical rainforest fly Drosophila birchii exhibits clinal variation in desiccation resistance, but the most resistant population lacks the ability to evolve further resistance even after intense selection for over 30 generations. Parent-offspring comparisons indicate low heritable variation for this trait but high levels of genetic variation for morphology. D. birchii also exhibits abundant genetic variation at microsatellite loci. The low potential for resistance evolution highlights the importance of assessing evolutionary potential in targeted ecological traits and species from threatened habitats.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffmann, A A -- Hallas, R J -- Dean, J A -- Schiffer, M -- New York, N.Y. -- Science. 2003 Jul 4;301(5629):100-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Environmental Stress and Adaptation Research, La Trobe University, Bundoora, Victoria 3086, Australia. A.Hoffmann@latrobe.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12843394" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; Animals ; Australia ; *Biological Evolution ; *Climate ; Crosses, Genetic ; Dehydration ; Drosophila/*genetics/*physiology ; Ecosystem ; Environment ; Female ; *Genetic Variation ; Geography ; Inbreeding ; Male ; Microsatellite Repeats ; Selection, Genetic ; Trees
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  • 27
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    Epidermal viral immunity induced by CD8alpha+ dendritic cells but not by Langerhans cells (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-27
    Description: The classical paradigm for dendritic cell function derives from the study of Langerhans cells, which predominate within skin epidermis. After an encounter with foreign agents, Langerhans cells are thought to migrate to draining lymph nodes, where they initiate T cell priming. Contrary to this, we show here that infection of murine epidermis by herpes simplex virus did not result in the priming of virus-specific cytotoxic T lymphocytes by Langerhans cells. Rather, the priming response required a distinct CD8alpha+ dendritic cell subset. Thus, the traditional view of Langerhans cells in epidermal immunity needs to be revisited to accommodate a requirement for other dendritic cells in this response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allan, Rhys S -- Smith, Chris M -- Belz, Gabrielle T -- van Lint, Allison L -- Wakim, Linda M -- Heath, William R -- Carbone, Francis R -- New York, N.Y. -- Science. 2003 Sep 26;301(5641):1925-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, The University of Melbourne, Melbourne, Victoria 3010, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14512632" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Antigens, CD/analysis ; Antigens, CD8/*analysis ; Antigens, Viral/immunology ; Cell Separation ; Chimera ; Cytotoxicity, Immunologic ; Dendritic Cells/*immunology ; Epidermis/*immunology ; H-2 Antigens/analysis/immunology ; Herpes Simplex/*immunology ; Herpesvirus 1, Human/*immunology ; Histocompatibility Antigens Class II/analysis ; Langerhans Cells/*immunology ; Lectins, C-Type/analysis ; Lymph Nodes/immunology ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Mice, Transgenic ; Receptors, Cell Surface/analysis ; T-Lymphocytes, Cytotoxic/*immunology ; Viral Envelope Proteins/immunology
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  • 28
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    Optical imaging of a tactile illusion in area 3b of the primary somatosensory cortex (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-23
    Description: In the tactile funneling illusion, the simultaneous presentation of brief stimuli at multiple points on the skin produces a single focal sensation at the center of the stimulus pattern even when no physical stimulus occurs at that site. Consistent with the funneling percept, we show with optical imaging in area 3b of the primary somatosensory cortex (SI) that simultaneous stimulation of two fingertips produces a single focal cortical activation between the single fingertip activation regions. Thus, in contrast to traditional views of the body map, topographic representation in the SI reflects the perceived rather than the physical location of peripheral stimulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Li M -- Friedman, Robert M -- Roe, Anna W -- New York, N.Y. -- Science. 2003 Oct 31;302(5646):881-5. Epub 2003 Sep 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14500850" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Brain Mapping ; Diagnostic Imaging ; Electrophysiology ; Female ; Fingers ; Humans ; Illusions/*physiology ; Male ; Perception/*physiology ; Physical Stimulation ; Saimiri ; Somatosensory Cortex/*physiology ; Touch/*physiology
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    SARS. Researcher told to stay home after China trip (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, Martin -- New York, N.Y. -- Science. 2003 May 23;300(5623):1216.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12764163" target="_blank"〉PubMed〈/a〉
    Keywords: China ; Humans ; Male ; Middle Aged ; New York City ; *Quarantine ; *Research Personnel ; Severe Acute Respiratory Syndrome/*prevention & control ; *Travel
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Defective CD8 T cell memory following acute infection without CD4 T cell help (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-12
    Description: The CD8+ cytotoxic T cell response to pathogens is thought to be CD4+ helper T cell independent because infectious agents provide their own inflammatory signals. Mice that lack CD4+ T cells mount a primary CD8 response to Listeria monocytogenes equal to that of wild-type mice and rapidly clear the infection. However, protective memory to a challenge is gradually lost in the former animals. Memory CD8+ T cells from normal mice can respond rapidly, but memory CD8+ T cells that are generated without CD4 help are defective in their ability to respond to secondary encounters with antigen. The results highlight a previously undescribed role for CD4 help in promoting protective CD8 memory development.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2778341/" 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/PMC2778341/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, Joseph C -- Bevan, Michael J -- AI 19335/AI/NIAID NIH HHS/ -- R01 AI019335/AI/NIAID NIH HHS/ -- R01 AI019335-19/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2003 Apr 11;300(5617):339-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and the Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12690202" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; CD8-Positive T-Lymphocytes/*immunology/transplantation ; Cytotoxicity, Immunologic ; Genes, MHC Class II ; Immunization ; *Immunologic Memory ; Interferon-gamma/biosynthesis ; Listeria monocytogenes/genetics/immunology ; Listeriosis/*immunology ; Mice ; Mice, Inbred C57BL ; Ovalbumin/biosynthesis/genetics/immunology ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes, Helper-Inducer/*immunology
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    Derepression of BDNF transcription involves calcium-dependent phosphorylation of MeCP2 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-01
    Description: Mutations in MeCP2, which encodes a protein that has been proposed to function as a global transcriptional repressor, are the cause of Rett syndrome (RT T), an X-linked progressive neurological disorder. Although the selective inactivation of MeCP2 in neurons is sufficient to confer a Rett-like phenotype in mice, the specific functions of MeCP2 in postmitotic neurons are not known. We find that MeCP2 binds selectively to BDNF promoter III and functions to repress expression of the BDNF gene. Membrane depolarization triggers the calcium-dependent phosphorylation and release of MeCP2 from BDNF promoter III, thereby facilitating transcription. These studies indicate that MeCP2 plays a key role in the control of neuronal activity-dependent gene regulation and suggest that the deregulation of this process may underlie the pathology of RT T.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Wen G -- Chang, Qiang -- Lin, Yingxi -- Meissner, Alexander -- West, Anne E -- Griffith, Eric C -- Jaenisch, Rudolf -- Greenberg, Michael E -- HD 18655/HD/NICHD NIH HHS/ -- NS28829/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 31;302(5646):885-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14593183" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain-Derived Neurotrophic Factor/*genetics ; Calcium/*metabolism ; Cell Membrane/physiology ; Cells, Cultured ; *Chromosomal Proteins, Non-Histone ; Cloning, Molecular ; CpG Islands ; DNA Methylation ; DNA-Binding Proteins/*metabolism ; Electrophoretic Mobility Shift Assay ; *Gene Expression Regulation ; Gene Silencing ; Histones/metabolism ; Methyl-CpG-Binding Protein 2 ; Methylation ; Mice ; Mice, Knockout ; Neurons/metabolism/physiology ; Phosphorylation ; Potassium Chloride/pharmacology ; Precipitin Tests ; Promoter Regions, Genetic ; Rats ; *Repressor Proteins ; Rett Syndrome/genetics ; *Transcription, Genetic
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    Diverse psychotomimetics act through a common signaling pathway (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-25
    Description: Three distinct classes of drugs: dopaminergic agonists (such as D-amphetamine), serotonergic agonists (such as LSD), and glutamatergic antagonists (such as PCP) all induce psychotomimetic states in experimental animals that closely resemble schizophrenia symptoms in humans. Here we implicate a common signaling pathway in mediating these effects. In this pathway, dopamine- and an adenosine 3',5'-monophosphate (cAMP)-regulated phospho-protein of 32 kilodaltons (DARPP-32) is phosphorylated or dephosphorylated at three sites, in a pattern predicted to cause a synergistic inhibition of protein phosphatase-1 and concomitant regulation of its downstream effector proteins glycogen synthesis kinase-3 (GSK-3), cAMP response element-binding protein (CREB), and c-Fos. In mice with a genetic deletion of DARPP-32 or with point mutations in phosphorylation sites of DARPP-32, the effects of D-amphetamine, LSD, and PCP on two behavioral parameters-sensorimotor gating and repetitive movements-were strongly attenuated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Svenningsson, Per -- Tzavara, Eleni T -- Carruthers, Robert -- Rachleff, Ilan -- Wattler, Sigrid -- Nehls, Michael -- McKinzie, David L -- Fienberg, Allen A -- Nomikos, George G -- Greengard, Paul -- DA10044/DA/NIDA NIH HHS/ -- MH40899/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2003 Nov 21;302(5649):1412-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14631045" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine/pharmacology ; Animals ; Brain/drug effects/*metabolism ; Central Nervous System Agents/*pharmacology ; Corpus Striatum/drug effects/metabolism ; Cyclic AMP Response Element-Binding Protein/metabolism ; Dextroamphetamine/pharmacology ; Dopamine/metabolism ; Dopamine and cAMP-Regulated Phosphoprotein 32 ; Frontal Lobe/drug effects/metabolism ; Genes, fos ; Glycogen Synthase Kinase 3/metabolism ; Lysergic Acid Diethylamide/pharmacology ; Male ; Mice ; Mice, Knockout ; Motor Activity/drug effects ; Nerve Tissue Proteins/metabolism ; Phencyclidine/pharmacology ; Phosphoprotein Phosphatases/antagonists & inhibitors ; Phosphoproteins/*metabolism ; Phosphorylation ; Protein Phosphatase 1 ; RNA, Messenger/genetics/metabolism ; Receptors, Dopamine D1/genetics/metabolism ; Reflex, Startle/drug effects ; *Signal Transduction ; Synaptic Transmission
    Print ISSN: 0036-8075
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    Ecology and evolution. Darwin's hummingbirds (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Altshuler, Douglas L -- Clark, Christopher James -- New York, N.Y. -- Science. 2003 Apr 25;300(5619):588-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, California Institute of Technology, Pasadena, CA 91104, USA. doug@caltech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12714728" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Beak/*anatomy & histology ; *Biological Evolution ; Birds/*anatomy & histology/physiology ; Body Constitution ; Dominica ; Ecosystem ; Feeding Behavior ; Female ; Flowers/*anatomy & histology ; Heliconiaceae/*anatomy & histology ; Male ; Pigmentation ; Saint Lucia ; *Sex Characteristics
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    The dog genome: survey sequencing and comparative analysis (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-27
    Description: A survey of the dog genome sequence (6.22 million sequence reads; 1.5x coverage) demonstrates the power of sample sequencing for comparative analysis of mammalian genomes and the generation of species-specific resources. More than 650 million base pairs (〉25%) of dog sequence align uniquely to the human genome, including fragments of putative orthologs for 18,473 of 24,567 annotated human genes. Mutation rates, conserved synteny, repeat content, and phylogeny can be compared among human, mouse, and dog. A variety of polymorphic elements are identified that will be valuable for mapping the genetic basis of diseases and traits in the dog.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kirkness, Ewen F -- Bafna, Vineet -- Halpern, Aaron L -- Levy, Samuel -- Remington, Karin -- Rusch, Douglas B -- Delcher, Arthur L -- Pop, Mihai -- Wang, Wei -- Fraser, Claire M -- Venter, J Craig -- New York, N.Y. -- Science. 2003 Sep 26;301(5641):1898-903.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Institute for Genomic Research, Rockville, MD 20850, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14512627" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes, Mammalian/genetics ; Computational Biology ; Conserved Sequence ; Contig Mapping ; DNA, Intergenic ; Dogs/*genetics ; Genetic Variation ; *Genome ; Genome, Human ; Genomics ; Humans ; Long Interspersed Nucleotide Elements ; Male ; Mice/genetics ; Molecular Sequence Data ; Mutation ; Phylogeny ; Physical Chromosome Mapping ; Polymorphism, Single Nucleotide ; RNA, Messenger/genetics ; Repetitive Sequences, Nucleic Acid ; Sequence Alignment ; *Sequence Analysis, DNA ; Short Interspersed Nucleotide Elements ; Synteny
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    Single molecule profiling of alternative pre-mRNA splicing (2003)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2003-08-09
    Description: Alternative pre-messenger RNA splicing is an important mechanism for generating protein diversity and may explain in part how mammalian complexity arises from a surprisingly small complement of genes. Here, we describe "digital polony exon profiling,"a single molecule-based technology for studying complex alternative pre-messenger RNA splicing. This technology allows researchers to monitor the combinatorial diversity of exon inclusion in individual transcripts. A minisequencing strategy provides single nucleotide resolution, and the digital nature of the technology allows quantitation of individual splicing variants. Digital polony exon profiling can be used to investigate the physiological and pathological roles of alternately spliced messenger RNAs, as well as the mechanisms by which these messenger RNAs are produced.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, Jun -- Shendure, Jay -- Mitra, Robi D -- Church, George M -- 5U54GM62119/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Aug 8;301(5634):836-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12907803" target="_blank"〉PubMed〈/a〉
    Keywords: Acrylamide ; *Alternative Splicing ; Animals ; Antigens, CD44/genetics ; Brain/metabolism ; Cell Line ; Cell Line, Transformed ; Cyclic AMP Response Element-Binding Protein ; *Exons ; Humans ; Mice ; Microtubule-Associated Proteins/genetics ; Nerve Tissue Proteins/genetics ; Polymerase Chain Reaction/*methods ; Polymorphism, Single Nucleotide ; Protein Isoforms ; RNA Precursors/*genetics/metabolism ; RNA-Binding Proteins ; SMN Complex Proteins
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    Disruption of transforming growth factor-beta signaling in ELF beta-spectrin-deficient mice (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-25
    Description: Disruption of the adaptor protein ELF, a beta-spectrin, leads to disruption of transforming growth factor-beta (TGF-beta) signaling by Smad proteins in mice. Elf-/- mice exhibit a phenotype similar to smad2+/-/smad3+/- mutant mice of midgestational death due to gastrointestinal, liver, neural, and heart defects. We show that TGF-beta triggers phosphorylation and association of ELF with Smad3 and Smad4, followed by nuclear translocation. ELF deficiency results in mislocalization of Smad3 and Smad4 and loss of the TGF-beta-dependent transcriptional response, which could be rescued by overexpression of the COOH-terminal region of ELF. This study reveals an unexpected molecular link between a major dynamic scaffolding protein and a key signaling pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tang, Yi -- Katuri, Varalakshmi -- Dillner, Allan -- Mishra, Bibhuti -- Deng, Chu-Xia -- Mishra, Lopa -- R01 DK56111/DK/NIDDK NIH HHS/ -- R01 DK58637/DK/NIDDK NIH HHS/ -- R03 DK53861/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2003 Jan 24;299(5606):574-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Developmental Biology, Department of Medicine, Georgetown University, Washington, DC 20007, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12543979" target="_blank"〉PubMed〈/a〉
    Keywords: Abnormalities, Multiple ; Animals ; Carrier Proteins/metabolism ; Cell Membrane/metabolism ; Cell Nucleus/metabolism ; Contractile Proteins/metabolism ; DNA-Binding Proteins/metabolism ; Embryonic and Fetal Development ; Filamins ; Gene Targeting ; Genes, fos ; Liver/abnormalities/embryology/*metabolism ; Mice ; Mice, Knockout ; Microfilament Proteins/metabolism ; Microscopy, Confocal ; Mutation ; Phenotype ; Phosphorylation ; Platelet-Derived Growth Factor/pharmacology ; *Signal Transduction ; Smad2 Protein ; Smad3 Protein ; Smad4 Protein ; Spectrin/genetics/*metabolism ; Trans-Activators/metabolism ; Transcriptional Activation ; Transforming Growth Factor beta/*metabolism/pharmacology ; Tumor Cells, Cultured
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    Genetics. Where do male genes live? (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schlotterer, Christian -- New York, N.Y. -- Science. 2003 Jan 31;299(5607):670-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Tierzucht und Genetik, Veterinarmedizinische Universitat Wien, 1210 Wien, Austria. christian.schloetterer@vu-wien.ac.at〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12560539" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anopheles/genetics ; Chromosome Mapping ; Chromosomes/*genetics ; Drosophila melanogaster/*genetics ; Evolution, Molecular ; Female ; *Gene Expression ; Gene Expression Profiling ; *Genes, Insect ; Genes, Recessive ; Genetic Linkage ; Male ; Models, Genetic ; Oligonucleotide Array Sequence Analysis ; Retroelements ; Sex Characteristics ; X Chromosome/*genetics ; Y Chromosome/genetics
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    STAT1-dependent innate immunity to a Norwalk-like virus (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-08
    Description: Norwalk-like caliciviruses (Noroviruses) cause over 90% of nonbacterial epidemic gastroenteritis worldwide, but the pathogenesis of norovirus infection is poorly understood because these viruses do not grow in cultured cells and there is no small animal model. Here, we report a previously unknown murine norovirus. Analysis of Murine Norovirus 1 infection revealed that signal transducer and activator of transcription 1-dependent innate immunity, but not T and B cell-dependent adaptive immunity, is essential for norovirus resistance. The identification of host molecules essential for murine norovirus resistance may provide targets for prevention or control of an important human disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karst, Stephanie M -- Wobus, Christiane E -- Lay, Margarita -- Davidson, John -- Virgin, Herbert W 4th -- R01 AI49286/AI/NIAID NIH HHS/ -- T32-CA09547/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Mar 7;299(5612):1575-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12624267" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology ; Brain/virology ; Caliciviridae Infections/*immunology ; DNA-Binding Proteins/genetics/*physiology ; Genes, RAG-1 ; Genome, Viral ; Homeodomain Proteins/physiology ; *Immunity, Innate ; Immunocompromised Host ; Intestines/virology ; Liver/virology ; Membrane Proteins ; Mice ; Mutation ; Norovirus/classification/*immunology/*isolation & purification/pathogenicity ; Phylogeny ; RNA, Viral/analysis ; Receptor, Interferon alpha-beta ; Receptors, Interferon/genetics/physiology ; STAT1 Transcription Factor ; Spleen/virology ; T-Lymphocytes/immunology ; Trans-Activators/genetics/*physiology ; Virulence
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    Hox10 and Hox11 genes are required to globally pattern the mammalian skeleton (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-19
    Description: Mice in which all members of the Hox10 or Hox11 paralogous group are disrupted provide evidence that these Hox genes are involved in global patterning of the axial and appendicular skeleton. In the absence of Hox10 function, no lumbar vertebrae are formed. Instead, ribs project from all posterior vertebrae, extending caudally from the last thoracic vertebrae to beyond the sacral region. In the absence of Hox11 function, sacral vertebrae are not formed and instead these vertebrae assume a lumbar identity. The redundancy among these paralogous family members is so great that this global aspect of Hox patterning is not apparent in mice that are mutant for five of the six paralogous alleles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wellik, Deneen M -- Capecchi, Mario R -- New York, N.Y. -- Science. 2003 Jul 18;301(5631):363-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and University of Utah, Salt Lake City, UT 84112, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12869760" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; *Body Patterning ; Bone and Bones/*embryology ; Female ; Forelimb/embryology ; Gene Expression Regulation, Developmental ; *Genes, Homeobox ; Hindlimb/embryology ; Homeodomain Proteins/*genetics/physiology ; Male ; Mice ; Mice, Mutant Strains ; Mutation ; Oncogene Proteins/*genetics/physiology ; Phenotype ; Spine/*embryology
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    Cell biology. Apoptosis--the calcium connection (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Demaurex, Nicolas -- Distelhorst, Clark -- New York, N.Y. -- Science. 2003 Apr 4;300(5616):65-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Geneva Medical Center, Geneva, Switzerland. nicolas.demaurex@medecine.unige.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12677047" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; BH3 Interacting Domain Death Agonist Protein ; Calcium/*metabolism ; Calcium Channels/metabolism ; *Calcium Signaling ; Calcium-Transporting ATPases/metabolism ; Carrier Proteins/metabolism ; Endoplasmic Reticulum/*metabolism ; Inositol 1,4,5-Trisphosphate Receptors ; Membrane Proteins/metabolism ; Mice ; Mice, Knockout ; Mitochondria/*metabolism ; Models, Biological ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Receptors, Cytoplasmic and Nuclear/metabolism ; Ryanodine Receptor Calcium Release Channel/metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases ; bcl-2 Homologous Antagonist-Killer Protein ; bcl-2-Associated X Protein
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    Requirement of Cks2 for the first metaphase/anaphase transition of mammalian meiosis (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-26
    Description: We generated mice lacking Cks2, one of two mammalian homologs of the yeast Cdk1-binding proteins, Suc1 and Cks1, and found them to be viable but sterile in both sexes. Sterility is due to failure of both male and female germ cells to progress past the first meiotic metaphase. The chromosomal events up through the end of prophase I are normal in both CKS2-/- males and females, suggesting that the phenotype is due directly to failure to enter anaphase and not a consequence of a checkpoint-mediated metaphase I arrest.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Spruck, Charles H -- de Miguel, Maria P -- Smith, Adrian P L -- Ryan, Aimee -- Stein, Paula -- Schultz, Richard M -- Lincoln, A Jeannine -- Donovan, Peter J -- Reed, Steven I -- CA74224/CA/NCI NIH HHS/ -- HD22681/HD/NICHD NIH HHS/ -- HD38252/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2003 Apr 25;300(5619):647-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, MB-7, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12714746" target="_blank"〉PubMed〈/a〉
    Keywords: *Anaphase ; Animals ; Apoptosis ; *CDC2-CDC28 Kinases ; CDC28 Protein Kinase, S cerevisiae/genetics/*physiology ; Chromosome Segregation ; Cyclin A/metabolism ; Cyclin B/metabolism ; Epididymis/cytology/physiology ; Female ; Gene Targeting ; In Situ Hybridization ; Infertility, Female/physiopathology ; Infertility, Male/physiopathology ; Male ; *Meiosis ; *Metaphase ; Mice ; Mutation ; Oocytes/*physiology ; Ovary/cytology/physiology ; RNA, Messenger/genetics/metabolism ; Recombination, Genetic ; Spermatocytes/*physiology ; Spermatogenesis ; Testis/cytology/physiology
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    Eating disorders and obesity (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reslewic, Susan -- New York, N.Y. -- Science. 2003 May 16;300(5622):1091.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12750498" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; Humans ; Male ; Nutrition Policy ; Obesity/*psychology ; United States
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Asymmetrical allocation of NMDA receptor epsilon2 subunits in hippocampal circuitry (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-10
    Description: Despite its implications for higher order functions of the brain, little is currently known about the molecular basis of left-right asymmetry of the brain. Here we report that synaptic distribution of N-methyl-D-aspartate (NMDA) receptor GluRepsilon2 (NR2B) subunits in the adult mouse hippocampus is asymmetrical between the left and right and between the apical and basal dendrites of single neurons. These asymmetrical allocations of epsilon2 subunits differentiate the properties of NMDA receptors and synaptic plasticity between the left and right hippocampus. These results provide a molecular basis for the structural and functional asymmetry of the mature brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kawakami, Ryosuke -- Shinohara, Yoshiaki -- Kato, Yuichiro -- Sugiyama, Hiroyuki -- Shigemoto, Ryuichi -- Ito, Isao -- New York, N.Y. -- Science. 2003 May 9;300(5621):990-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Graduate School of Medical Science, Kyushu University, Fukuoka 812-8582, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12738868" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bicuculline/pharmacology ; Dendrites/metabolism/physiology ; Denervation ; Electric Stimulation ; Excitatory Amino Acid Antagonists/pharmacology ; Excitatory Postsynaptic Potentials ; *Functional Laterality ; Hippocampus/*metabolism/physiology ; In Vitro Techniques ; Long-Term Potentiation ; Mice ; Mice, Inbred C57BL ; Neuronal Plasticity ; Patch-Clamp Techniques ; Perforant Pathway/physiology ; Phenols/pharmacology ; Piperidines/pharmacology ; Pyramidal Cells/*metabolism/physiology ; Quinoxalines/pharmacology ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/*metabolism ; Synapses/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Inflammatory blockade restores adult hippocampal neurogenesis (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-15
    Description: Cranial radiation therapy causes a progressive decline in cognitive function that is linked to impaired neurogenesis. Chronic inflammation accompanies radiation injury, suggesting that inflammatory processes may contribute to neural stem cell dysfunction. Here, we show that neuroinflammation alone inhibits neurogenesis and that inflammatory blockade with indomethacin, a common nonsteroidal anti-inflammatory drug, restores neurogenesis after endotoxin-induced inflammation and augments neurogenesis after cranial irradiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Monje, Michelle L -- Toda, Hiroki -- Palmer, Theo D -- F30 NS04696701/NS/NINDS NIH HHS/ -- MH20016-05/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2003 Dec 5;302(5651):1760-5. Epub 2003 Nov 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stanford University, Department of Neurosurgery, MSLS P309, Mail Code 5487, 1201 Welch Road, Stanford, CA 94305-5487, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14615545" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology ; Antigens, CD/metabolism ; Apoptosis ; Cell Differentiation ; Cells, Cultured ; Coculture Techniques ; Culture Media, Conditioned ; Cytokine Receptor gp130 ; Cytokines/physiology ; Dentate Gyrus/cytology/drug effects/physiology/radiation effects ; Female ; Gamma Rays ; Hippocampus/cytology/drug effects/*physiology/radiation effects ; In Situ Nick-End Labeling ; Indomethacin/*pharmacology ; Inflammation/drug therapy/*physiopathology ; Interleukin-6/pharmacology/physiology ; Lipopolysaccharides/pharmacology ; Membrane Glycoproteins/metabolism ; Mice ; Microglia/*physiology ; Mitotic Index ; Neurons/drug effects/*physiology/radiation effects ; Rats ; Rats, Inbred F344 ; Receptors, Interleukin-6/metabolism ; Recombinant Proteins/pharmacology ; Signal Transduction ; Stem Cells/physiology
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    Eukaryotic intron loss (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mourier, Tobias -- Jeffares, Daniel C -- New York, N.Y. -- Science. 2003 May 30;300(5624):1393.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Evolutionary Biology, Zoological Institute, University of Copenhagen, Universitetsparken 15, DK-2100 Copenhagen O, Denmark. tmourier@zi.ku.dk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12775832" target="_blank"〉PubMed〈/a〉
    Keywords: Angiosperms/genetics ; Animals ; Caenorhabditis elegans/genetics ; DNA, Complementary/genetics ; Eukaryota/genetics ; *Eukaryotic Cells ; Fungi/genetics ; Humans ; Insects/genetics ; Interspersed Repetitive Sequences ; *Introns ; Mice ; Plasmodium/genetics ; RNA-Directed DNA Polymerase/metabolism ; Rats ; *Recombination, Genetic ; Takifugu/genetics ; Templates, Genetic
    Print ISSN: 0036-8075
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    TRB3: a tribbles homolog that inhibits Akt/PKB activation by insulin in liver (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-06-07
    Description: Insulin resistance is a major hallmark in the development of type II diabetes, which is characterized by the failure of insulin to promote glucose uptake in muscle and to suppress glucose production in liver. The serine-threonine kinase Akt (PKB) is a principal target of insulin signaling that inhibits hepatic glucose output when glucose is available from food. Here we show that TRB3, a mammalian homolog of Drosophila tribbles, functions as a negative modulator of Akt. TRB3 expression is induced in liver under fasting conditions, and TRB3 disrupts insulin signaling by binding directly to Akt and blocking activation of the kinase. Amounts of TRB3 RNA and protein were increased in livers of db/db diabetic mice compared with those in wild-type mice. Hepatic overexpression of TRB3 in amounts comparable to those in db/db mice promoted hyperglycemia and glucose intolerance. Our results suggest that, by interfering with Akt activation, TRB3 contributes to insulin resistance in individuals with susceptibility to type II diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Du, Keyong -- Herzig, Stephan -- Kulkarni, Rohit N -- Montminy, Marc -- New York, N.Y. -- Science. 2003 Jun 6;300(5625):1574-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Peptide Biology Laboratories, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037-1002, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12791994" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics/physiology ; Amino Acid Substitution ; Animals ; Blood Glucose/metabolism ; Cell Cycle Proteins/genetics/*metabolism ; Cell Line ; Diabetes Mellitus/genetics/metabolism ; Enzyme Activation ; Fasting ; Genetic Vectors ; Glucose/metabolism ; Glucose Intolerance ; Glycogen Synthase Kinase 3/metabolism ; Humans ; Insulin/blood/*metabolism ; Insulin Resistance ; Insulin-Like Growth Factor I/pharmacology ; Liver/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Phosphorylation ; Polymerase Chain Reaction ; Protein-Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-akt ; RNA Interference ; Rats ; Repressor Proteins ; Signal Transduction ; Transfection ; Transgenes ; Tumor Cells, Cultured ; Two-Hybrid System Techniques
    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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    Reelin promotes peripheral synapse elimination and maturation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-02
    Description: Reelin is an extracellular protein that is crucial for layer formation in the embryonic brain. Here, we demonstrate that Reelin functions postnatally to regulate the development of the neuromuscular junction. Reelin is required for motor end-plate maturation and proper nerve-muscle connectivity, and it directly promotes synapse elimination. Unlike layer formation, neuromuscular junction development requires a function of Reelin that is not mediated by Disabled1 or very-low-density lipoprotein receptors and apolipoprotein E receptor 2 receptors but by a distinct mechanism involving its protease activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Quattrocchi, Carlo C -- Huang, Cheng -- Niu, Sanyong -- Sheldon, Michael -- Benhayon, David -- Cartwright, Joiner Jr -- Mosier, Dennis R -- Keller, Flavio -- D'Arcangelo, Gabriella -- New York, N.Y. -- Science. 2003 Aug 1;301(5633):649-53.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Cain Foundation Laboratories, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12893944" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Axons/metabolism ; Cell Adhesion Molecules, Neuronal/genetics/metabolism/pharmacology/*physiology ; Culture Media, Conditioned ; Diaphragm/innervation ; Extracellular Matrix Proteins/genetics/metabolism/pharmacology/*physiology ; LDL-Receptor Related Proteins ; Mice ; Mice, Neurologic Mutants ; Microscopy, Confocal ; Microscopy, Electron ; Motor Endplate/ultrastructure ; Motor Neurons/metabolism ; Muscle, Skeletal/innervation ; Mutation ; Nerve Tissue Proteins/genetics/metabolism ; Neuromuscular Junction/*growth & ; development/metabolism/*physiology/ultrastructure ; Receptors, LDL/genetics/metabolism ; Receptors, Lipoprotein/genetics/metabolism ; Schwann Cells/metabolism ; Serine Endopeptidases ; Serine Proteinase Inhibitors/pharmacology ; Sulfones/pharmacology ; Synapses/*physiology/ultrastructure
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    Single neurons in the monkey hippocampus and learning of new associations (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-06-07
    Description: The medial temporal lobe is crucial for the ability to learn and retain new declarative memories. This form of memory includes the ability to quickly establish novel associations between unrelated items. To better understand the patterns of neural activity during associative memory formation, we recorded the activity of hippocampal neurons of macaque monkeys as they learned new associations. Hippocampal neurons signaled learning by changing their stimulus-selective response properties. This change in the pattern of selective neural activity occurred before, at the same time as, or after learning, which suggests that these neurons are involved in the initial formation of new associative memories.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wirth, Sylvia -- Yanike, Marianna -- Frank, Loren M -- Smith, Anne C -- Brown, Emery N -- Suzuki, Wendy A -- New York, N.Y. -- Science. 2003 Jun 6;300(5625):1578-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neural Science, New York University, New York, NY 10003, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12791995" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Analysis of Variance ; Animals ; Association Learning/*physiology ; Electrophysiology ; Hippocampus/cytology/*physiology ; Macaca mulatta ; Magnetic Resonance Imaging ; Male ; Memory/*physiology ; Neurons/*physiology
    Print ISSN: 0036-8075
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    Brazilian science at a crossroads (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Castro Moreira, Ildeu -- New York, N.Y. -- Science. 2003 Jul 11;301(5630):141.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12855773" target="_blank"〉PubMed〈/a〉
    Keywords: Brazil ; Educational Status ; Humans ; Research ; Research Support as Topic ; *Science/education ; Technology
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    A muscleblind knockout model for myotonic dystrophy (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-13
    Description: The neuromuscular disease myotonic dystrophy (DM) is caused by microsatellite repeat expansions at two different genomic loci. Mutant DM transcripts are retained in the nucleus together with the muscleblind (Mbnl) proteins, and these abnormal RNAs somehow interfere with pre-mRNA splicing regulation. Here, we show that disruption of the mouse Mbnl1 gene leads to muscle, eye, and RNA splicing abnormalities that are characteristic of DM disease. Our results support the hypothesis that manifestations of DM can result from sequestration of specific RNA binding proteins by a repetitive element expansion in a mutant RNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kanadia, Rahul N -- Johnstone, Karen A -- Mankodi, Ami -- Lungu, Codrin -- Thornton, Charles A -- Esson, Douglas -- Timmers, Adrian M -- Hauswirth, William W -- Swanson, Maurice S -- AR46799/AR/NIAMS NIH HHS/ -- AR46806/AR/NIAMS NIH HHS/ -- AR48143/AR/NIAMS NIH HHS/ -- R01 AR046799/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1978-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, Powell Gene Therapy Center, Gainesville, FL 32610, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671308" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Animals ; CELF1 Protein ; Cataract/etiology/pathology ; Cell Nucleus/metabolism ; Chloride Channels/genetics/metabolism ; DNA-Binding Proteins ; Disease Models, Animal ; Electromyography ; Exons ; Gene Targeting ; Introns ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle Fibers, Skeletal/pathology ; Muscle Relaxation ; Muscle, Skeletal/pathology/physiopathology ; Myocardium/metabolism ; Myotonic Dystrophy/*genetics/pathology/*physiopathology ; Protein Isoforms ; RNA Splicing ; RNA-Binding Proteins/*genetics/metabolism/*physiology ; Reverse Transcriptase Polymerase Chain Reaction ; Trinucleotide Repeat Expansion ; Troponin T/genetics/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Modification of ocular defects in mouse developmental glaucoma models by tyrosinase (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-08
    Description: Mutations in the cytochrome P450 family 1, subfamily B, polypeptide 1 (CYP1B1) gene are a common cause of human primary congenital glaucoma (PCG). Here we show that Cyp1b1-/- mice have ocular drainage structure abnormalities resembling those reported in human PCG patients. Using Cyp1b1-/- mice, we identified the tyrosinase gene (Tyr) as a modifier of the drainage structure phenotype, with Tyr deficiency increasing the magnitude of dysgenesis. The severe dysgenesis in eyes lacking both CYP1B1 and TYR was alleviated by administration of the tyrosinase product dihydroxyphenylalanine (l-dopa). Tyr also modified the drainage structure dysgenesis in mice with a mutant Foxc1 gene, which is also involved in PCG. These experiments raise the possibility that a tyrosinase/l-dopa pathway modifies human PCG, which could open new therapeutic avenues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Libby, Richard T -- Smith, Richard S -- Savinova, Olga V -- Zabaleta, Adriana -- Martin, Janice E -- Gonzalez, Frank J -- John, Simon W M -- CA34196/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Mar 7;299(5612):1578-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Jackson Laboratory, Bar Harbor, ME 04609, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12624268" target="_blank"〉PubMed〈/a〉
    Keywords: Albinism, Ocular/genetics/pathology ; Animals ; Anterior Eye Segment/*abnormalities ; Aryl Hydrocarbon Hydroxylases/deficiency/genetics ; Cornea/abnormalities ; Cytochrome P-450 CYP1B1 ; *DNA-Binding Proteins ; Disease Models, Animal ; Female ; Forkhead Transcription Factors ; Glaucoma/*congenital/enzymology/*genetics/pathology ; Intraocular Pressure ; Iris/abnormalities ; Levodopa/administration & dosage/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Monophenol Monooxygenase/deficiency/*genetics/metabolism ; Mutation ; Phenotype ; Pregnancy ; Trabecular Meshwork/abnormalities ; Transcription Factors/genetics
    Print ISSN: 0036-8075
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    Stability of retrieved memory: inverse correlation with trace dominance (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-23
    Description: In memory consolidation, the memory trace stabilizes and becomes resistant to certain amnesic agents. The textbook account is that for any memorized item, consolidation starts and ends just once. However, evidence has accumulated that upon activation in retrieval, the trace may reconsolidate. Whereas some authors reported transient renewed susceptibility of retrieved memories to consolidation blockers, others could not detect it. Here, we report that in both conditioned taste aversion in the rat and fear conditioning in the medaka fish, the stability of retrieved memory is inversely correlated with the control of behavior by that memory. This result may explain some conflicting findings on reconsolidation of activated memories.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eisenberg, Mark -- Kobilo, Tali -- Berman, Diego E -- Dudai, Yadin -- New York, N.Y. -- Science. 2003 Aug 22;301(5636):1102-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Weizmann Institute of Science, Rehovot 76100, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12934010" target="_blank"〉PubMed〈/a〉
    Keywords: Aminobenzoates/pharmacology ; Analysis of Variance ; Animals ; Anisomycin/administration & dosage/pharmacology ; Avoidance Learning ; Cerebral Cortex/drug effects ; Conditioning (Psychology) ; Cues ; Electroshock ; *Extinction, Psychological/drug effects ; Fear ; Male ; *Memory ; *Mental Recall ; Oryzias ; Rats ; Rats, Wistar ; Taste ; meta-Aminobenzoates
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    Biomedical research. Looks can be deceptive (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Casassus, Barbara -- New York, N.Y. -- Science. 2003 Jul 4;301(5629):35.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12843371" target="_blank"〉PubMed〈/a〉
    Keywords: Academies and Institutes/*economics ; Biomedical Research/*economics ; *Budgets ; Financing, Government ; France ; *Government Agencies ; Research Support as Topic
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    Does rejection hurt? An FMRI study of social exclusion (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-11
    Description: A neuroimaging study examined the neural correlates of social exclusion and tested the hypothesis that the brain bases of social pain are similar to those of physical pain. Participants were scanned while playing a virtual ball-tossing game in which they were ultimately excluded. Paralleling results from physical pain studies, the anterior cingulate cortex (ACC) was more active during exclusion than during inclusion and correlated positively with self-reported distress. Right ventral prefrontal cortex (RVPFC) was active during exclusion and correlated negatively with self-reported distress. ACC changes mediated the RVPFC-distress correlation, suggesting that RVPFC regulates the distress of social exclusion by disrupting ACC activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eisenberger, Naomi I -- Lieberman, Matthew D -- Williams, Kipling D -- R21MH66709-01/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 10;302(5643):290-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, Franz Hall, University of California, Los Angeles, Los Angeles, CA 90095-1563, USA. neisenbe@ucla.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14551436" target="_blank"〉PubMed〈/a〉
    Keywords: Brain Mapping ; *Emotions ; Female ; Gyrus Cinguli/*physiology ; Humans ; Magnetic Resonance Imaging ; Male ; Pain/*physiopathology ; Prefrontal Cortex/*physiology ; *Rejection (Psychology) ; *Social Isolation
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    Questions of methodology (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Neiburger, E J -- New York, N.Y. -- Science. 2003 Jan 31;299(5607):660-1; author reply 660-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12561822" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal ; *Body Temperature Regulation ; *Hair/anatomy & histology ; Hair Color ; Lions/*anatomy & histology/*physiology ; Male ; *Research Design ; Sexual Behavior, Animal ; Thermography
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    Regulation of NF-kappaB-dependent lymphocyte activation and development by paracaspase (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-25
    Description: Paracaspase (MALT1), a member of an evolutionarily conserved superfamily of caspase-like proteins, has been shown to bind and colocalize with the protein Bcl10 in vitro and, because of this association, has been suggested to be involved in the CARMA1-Bcl10 pathway of antigen-induced nuclear factor kappaB (NF-kappaB) activation. We demonstrate that primary T and B lymphocytes from paracaspase-deficient mice are defective in antigen-receptor-induced NF-kappaB activation, cytokine production, and proliferation. Paracaspase acts downstream of Bcl10 to induce NF-kappaB activation and is required for the normal development of B cells, indicating that paracaspase provides the missing link between Bcl10 and activation of the IkappaB kinase complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ruefli-Brasse, Astrid A -- French, Dorothy M -- Dixit, Vishva M -- New York, N.Y. -- Science. 2003 Nov 28;302(5650):1581-4. Epub 2003 Oct 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Oncology Department, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14576442" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Animals ; Antibody Formation ; Antigens, CD/analysis ; B-Lymphocyte Subsets/immunology/physiology ; B-Lymphocytes/*immunology/metabolism/physiology ; Caspases ; Cell Differentiation ; Cell Division ; Cell Survival ; Cells, Cultured ; Cytokines/metabolism ; Gene Deletion ; Gene Targeting ; Guanylate Kinase ; I-kappa B Kinase ; *Lymphocyte Activation ; Lymphoma, B-Cell, Marginal Zone/chemistry/*metabolism ; Mice ; Mice, Inbred C57BL ; NF-kappa B/*metabolism ; Neoplasm Proteins/chemistry/*metabolism ; Nucleoside-Phosphate Kinase/metabolism ; Phosphorylation ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/metabolism ; Receptors, Antigen, B-Cell/metabolism ; Receptors, Antigen, T-Cell/metabolism ; Signal Transduction ; T-Lymphocyte Subsets/immunology/physiology ; T-Lymphocytes/*immunology/metabolism/physiology ; Transfection
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    Role of adaptor TRIF in the MyD88-independent toll-like receptor signaling pathway (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-12
    Description: Stimulation of Toll-like receptors (TLRs) triggers activation of a common MyD88-dependent signaling pathway as well as a MyD88-independent pathway that is unique to TLR3 and TLR4 signaling pathways leading to interferon (IFN)-beta production. Here we disrupted the gene encoding a Toll/IL-1 receptor (TIR) domain-containing adaptor, TRIF. TRIF-deficient mice were defective in both TLR3- and TLR4-mediated expression of IFN-beta and activation of IRF-3. Furthermore, inflammatory cytokine production in response to the TLR4 ligand, but not to other TLR ligands, was severely impaired in TRIF-deficient macrophages. Mice deficient in both MyD88 and TRIF showed complete loss of nuclear factor kappa B activation in response to TLR4 stimulation. These findings demonstrate that TRIF is essential for TLR3- and TLR4-mediated signaling pathways facilitating mammalian antiviral host defense.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamamoto, Masahiro -- Sato, Shintaro -- Hemmi, Hiroaki -- Hoshino, Katsuaki -- Kaisho, Tsuneyasu -- Sanjo, Hideki -- Takeuchi, Osamu -- Sugiyama, Masanaka -- Okabe, Masaru -- Takeda, Kiyoshi -- Akira, Shizuo -- New York, N.Y. -- Science. 2003 Aug 1;301(5633):640-3. Epub 2003 Jul 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamada-oka, Suita Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12855817" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Adaptor Proteins, Vesicular Transport/genetics/*physiology ; Animals ; Antigens, Differentiation/*physiology ; Cells, Cultured ; Cytokines/biosynthesis ; DNA-Binding Proteins/metabolism ; Dimerization ; Embryo, Mammalian ; Fibroblasts/metabolism ; Gene Expression Regulation ; Gene Targeting ; Interferon Regulatory Factor-3 ; Interferon-beta/genetics/*metabolism ; JNK Mitogen-Activated Protein Kinases ; Ligands ; Lipopolysaccharides/immunology/pharmacology ; Macrophages, Peritoneal/immunology/metabolism ; Membrane Glycoproteins/*metabolism ; Mice ; Mice, Inbred C57BL ; Mitogen-Activated Protein Kinases/metabolism ; Myeloid Differentiation Factor 88 ; NF-kappa B/metabolism ; Poly I-C/pharmacology ; Receptors, Cell Surface/*metabolism ; Receptors, Immunologic/*physiology ; *Signal Transduction ; Toll-Like Receptor 3 ; Toll-Like Receptor 4 ; Toll-Like Receptors ; Transcription Factors/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Development. Longing for ligand: hedgehog, patched, and cell death (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guerrero, Isabel -- Ruiz i Altaba, Ariel -- New York, N.Y. -- Science. 2003 Aug 8;301(5634):774-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centro de Biologia Molecular "Severo Ochoa," CSIC-UAM, Universidad Autonoma de Madrid, Madrid E-28049, Spain. iguerrero@cbm.uam.es〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12907783" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Caspase 3 ; Caspases/metabolism ; Central Nervous System/cytology/*embryology ; Chick Embryo ; Drosophila/growth & development/metabolism ; Drosophila Proteins/metabolism ; Hedgehog Proteins ; Humans ; Intracellular Signaling Peptides and Proteins ; Ligands ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Mutation ; Neoplasms/etiology ; Protein Binding ; Protein Structure, Tertiary ; Receptors, Cell Surface ; Signal Transduction ; Trans-Activators/*metabolism ; Wings, Animal/growth & development
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Neuroscience. Snooty exchanges are key to mouse society (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2003 Feb 21;299(5610):1163.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12595661" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Animal ; Cues ; Female ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred CBA ; Neurons/*physiology ; Neurons, Afferent/*physiology ; Olfactory Bulb/cytology/*physiology ; Olfactory Pathways ; Olfactory Receptor Neurons/physiology ; Pheromones/*physiology ; Receptors, Odorant/physiology ; Sex Characteristics ; Smell ; Species Specificity ; Vomeronasal Organ/cytology/*physiology
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    Cell therapy of alpha-sarcoglycan null dystrophic mice through intra-arterial delivery of mesoangioblasts (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-12
    Description: Preclinical or clinical trials for muscular dystrophies have met with modest success, mainly because of inefficient delivery of viral vectors or donor cells to dystrophic muscles. We report here that intra-arterial delivery of wild-type mesoangioblasts, a class of vessel-associated stem cells, corrects morphologically and functionally the dystrophic phenotype of virtually all downstream muscles in adult immunocompetent alpha-sarcoglycan (alpha-SG) null mice, a model organism for limb-girdle muscular dystrophy. When mesoangioblasts isolated from juvenile dystrophic mice and transduced with a lentiviral vector expressing alpha-SG were injected into the femoral artery of dystrophic mice, they reconstituted skeletal muscle in a manner similar to that seen in wild-type cells. The success of this protocol was mainly due to widespread distribution of donor stem cells through the capillary network, a distinct advantage of this strategy over previous approaches.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sampaolesi, Maurilio -- Torrente, Yvan -- Innocenzi, Anna -- Tonlorenzi, Rossana -- D'Antona, Giuseppe -- Pellegrino, M Antonietta -- Barresi, Rita -- Bresolin, Nereo -- De Angelis, M Gabriella Cusella -- Campbell, Kevin P -- Bottinelli, Roberto -- Cossu, Giulio -- 1322/Telethon/Italy -- 463/BI/Telethon/Italy -- New York, N.Y. -- Science. 2003 Jul 25;301(5632):487-92. Epub 2003 Jul 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cell Research Institute, H. S. Raffaele, Via Olgettina 58, 20132 Milan, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12855815" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Vessels/cytology/embryology ; Cell Differentiation ; Cell Line ; Cell Movement ; Cytoskeletal Proteins/*genetics/*metabolism ; Dystrophin/metabolism ; Endothelium, Vascular/physiology ; Female ; Femoral Artery ; Genetic Vectors ; Lentivirus/genetics ; Locomotion ; Male ; Membrane Glycoproteins/*genetics/*metabolism ; Mesoderm/cytology ; Mice ; Mice, Knockout ; Mice, Transgenic ; Muscle Contraction ; Muscle Fibers, Skeletal/cytology/physiology ; Muscle, Skeletal/cytology/metabolism/pathology/*physiology ; Muscular Dystrophy, Animal/metabolism/pathology/*therapy ; Regeneration ; Sarcoglycans ; *Stem Cell Transplantation ; Stem Cells/*physiology ; Transfection
    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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    Infectious diseases. Singapore lab faulted in SARS case (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, Martin -- New York, N.Y. -- Science. 2003 Sep 26;301(5641):1824.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14512588" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Containment of Biohazards/*standards ; Humans ; Laboratories/*standards ; Laboratory Infection/*transmission ; Male ; Severe Acute Respiratory Syndrome/*transmission ; Singapore
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    Abnormal coronary function in mice deficient in alpha1H T-type Ca2+ channels (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-25
    Description: Calcium ion (Ca2+) influx through voltage-gated Ca2+ channels is important for the regulation of vascular tone. Activation of L-type Ca2+ channels initiates muscle contraction; however, the role of T-type Ca2+ channels (T-channels) is not clear. We show that mice deficient in the alpha1H T-type Ca2+ channel (alpha(1)3.2-null) have constitutively constricted coronary arterioles and focal myocardial fibrosis. Coronary arteries isolated from alpha(1)3.2-null arteries showed normal contractile responses, but reduced relaxation in response to acetylcholine and nitroprusside. Furthermore, acute blockade of T-channels with Ni2+ prevented relaxation of wild-type coronary arteries. Thus, Ca2+ influx through alpha1H T-type Ca2+ channels is essential for normal relaxation of coronary arteries.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Chien-Chang -- Lamping, Kathryn G -- Nuno, Daniel W -- Barresi, Rita -- Prouty, Sally J -- Lavoie, Julie L -- Cribbs, Leanne L -- England, Sarah K -- Sigmund, Curt D -- Weiss, Robert M -- Williamson, Roger A -- Hill, Joseph A -- Campbell, Kevin P -- New York, N.Y. -- Science. 2003 Nov 21;302(5649):1416-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Iowa, Iowa City, IA 52242, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14631046" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/pharmacology ; Animals ; Arteries/drug effects/*physiology ; Calcium/*metabolism ; Calcium Channels, T-Type/genetics/*physiology ; Coronary Vessels/drug effects/pathology/*physiology ; Echocardiography ; Electrocardiography ; Endothelium, Vascular/drug effects/physiology ; Female ; Fibrosis ; Ganglia, Spinal/cytology ; Gene Targeting ; Heart/physiology ; Heart Rate ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle, Smooth, Vascular/physiology ; Myocardium/pathology ; Neurons/metabolism ; Nickel/pharmacology ; Nitric Oxide/physiology ; Nitric Oxide Donors/pharmacology ; Nitroprusside/pharmacology ; Patch-Clamp Techniques ; Vasoconstriction/drug effects ; *Vasodilation/drug effects
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Dishevelled 2 recruits beta-arrestin 2 to mediate Wnt5A-stimulated endocytosis of Frizzled 4 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-06
    Description: Wnt proteins, regulators of development in many organisms, bind to seven transmembrane-spanning (7TMS) receptors called frizzleds, thereby recruiting the cytoplasmic molecule dishevelled (Dvl) to the plasma membrane.Frizzled-mediated endocytosis of Wg (a Drosophila Wnt protein) and lysosomal degradation may regulate the formation of morphogen gradients. Endocytosis of Frizzled 4 (Fz4) in human embryonic kidney 293 cells was dependent on added Wnt5A protein and was accomplished by the multifunctional adaptor protein beta-arrestin 2 (betaarr2), which was recruited to Fz4 by binding to phosphorylated Dvl2. These findings provide a previously unrecognized mechanism for receptor recruitment of beta-arrestin and demonstrate that Dvl plays an important role in the endocytosis of frizzled, as well as in promoting signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Wei -- ten Berge, Derk -- Brown, Jeff -- Ahn, Seungkirl -- Hu, Liaoyuan A -- Miller, William E -- Caron, Marc G -- Barak, Larry S -- Nusse, Roel -- Lefkowitz, Robert J -- HL 16037/HL/NHLBI NIH HHS/ -- HL 61365/HL/NHLBI NIH HHS/ -- NS 19576/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Sep 5;301(5638):1391-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Departments of Medicine and Biochemistry, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12958364" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Arrestins/genetics/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Clathrin/metabolism ; Cytoplasm/metabolism ; *Endocytosis ; Frizzled Receptors ; Humans ; Mice ; Phosphoproteins/metabolism ; Phosphorylation ; Protein Kinase C/antagonists & inhibitors/metabolism ; Proteins/genetics/*metabolism ; Proto-Oncogene Proteins/*metabolism/pharmacology ; RNA, Small Interfering ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Wnt Proteins
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    Human chromosome 7: DNA sequence and biology (2003)
    American Association for the Advancement of Science (AAAS)
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    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
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    Thalamic control of visceral nociception mediated by T-type Ca2+ channels (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-04
    Description: Sensations from viscera, like fullness, easily become painful if the stimulus persists. Mice lacking alpha1G T-type Ca2+ channels show hyperalgesia to visceral pain. Thalamic infusion of a T-type blocker induced similar hyperalgesia in wild-type mice. In response to visceral pain, the ventroposterolateral thalamic neurons evokeda surge of single spikes, which then slowly decayed as T type-dependent burst spikes gradually increased. In alpha1G-deficient neurons, the single-spike response persisted without burst spikes. These results indicate that T-type Ca2+ channels underlie an antinociceptive mechanism operating in the thalamus andsupport the idea that burst firing plays a critical role in sensory gating in the thalamus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Daesoo -- Park, Donghyun -- Choi, Soonwook -- Lee, Sukchan -- Sun, Minjeong -- Kim, Chanki -- Shin, Hee-Sup -- New York, N.Y. -- Science. 2003 Oct 3;302(5642):117-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Creative Research Initiative Center for Calcium and Learning, Korea Institutes of Science and Technology, Seoul 136-791, Korea.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14526084" target="_blank"〉PubMed〈/a〉
    Keywords: Abdominal Pain/physiopathology ; Acetic Acid/pharmacology ; Action Potentials ; Analysis of Variance ; Animals ; Calcium Channel Blockers/pharmacology ; Calcium Channels, T-Type/genetics/*physiology ; Female ; Magnesium Sulfate/pharmacology ; Male ; Mibefradil/pharmacology ; Mice ; Mice, Inbred C57BL ; Mutation ; Neurons/physiology ; Pain/*physiopathology ; Pain Measurement ; Ventral Thalamic Nuclei/*physiology ; Viscera
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    Global health. Bill Gates plans a hit list, with NIH's help (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, Martin -- New York, N.Y. -- Science. 2003 Jan 31;299(5607):641.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12560522" target="_blank"〉PubMed〈/a〉
    Keywords: *Developing Countries ; *Foundations ; *Global Health ; National Institutes of Health (U.S.) ; Research Support as Topic ; United States
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    VDAC2 inhibits BAK activation and mitochondrial apoptosis (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-26
    Description: The multidomain proapoptotic molecules BAK or BAX are required to initiate the mitochondrial pathway of apoptosis. How cells maintain the potentially lethal proapoptotic effector BAK in a monomeric inactive conformation at mitochondria is unknown. In viable cells, we found BAK complexed with mitochondrial outer-membrane protein VDAC2, a VDAC isoform present in low abundance that interacts specifically with the inactive conformer of BAK. Cells deficient in VDAC2, but not cells lacking the more abundant VDAC1, exhibited enhanced BAK oligomerization and were more susceptible to apoptotic death. Conversely, overexpression of VDAC2 selectively prevented BAK activation and inhibited the mitochondrial apoptotic pathway. Death signals activate "BH3-only" molecules such as tBID, BIM, or BAD, which displace VDAC2 from BAK, enabling homo-oligomerization of BAK and apoptosis. Thus, VDAC2, an isoform restricted to mammals, regulates the activity of BAK and provides a connection between mitochondrial physiology and the core apoptotic pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheng, Emily H Y -- Sheiko, Tatiana V -- Fisher, Jill K -- Craigen, William J -- Korsmeyer, Stanley J -- NS42319/NS/NINDS NIH HHS/ -- R37CA50239/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Jul 25;301(5632):513-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, 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/12881569" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; BH3 Interacting Domain Death Agonist Protein ; Biopolymers ; Carrier Proteins/metabolism/pharmacology ; Cell Line ; Cells, Cultured ; Etoposide/pharmacology ; Humans ; Intracellular Membranes/metabolism ; Jurkat Cells ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Mitochondria/*metabolism ; Mitochondria, Liver/metabolism ; Porins/genetics/isolation & purification/*metabolism ; Protein Binding ; Protein Conformation ; Protein Structure, Tertiary ; Proto-Oncogene Proteins/metabolism ; *Proto-Oncogene Proteins c-bcl-2 ; Recombinant Proteins/pharmacology ; Staurosporine/pharmacology ; Voltage-Dependent Anion Channel 1 ; Voltage-Dependent Anion Channel 2 ; Voltage-Dependent Anion Channels ; bcl-2 Homologous Antagonist-Killer Protein ; bcl-2-Associated X Protein
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The chemistry of sexual deception in an orchid-wasp pollination system (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-18
    Description: The "sexually deceptive" orchid Chiloglottis trapeziformis attracts males of its pollinator species, the thynnine wasp Neozeleboria cryptoides, by emitting a unique volatile compound, 2-ethyl-5-propylcyclohexan-1,3-dione, which is also produced by female wasps as a male-attracting sex pheromone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schiestl, Florian P -- Peakall, Rod -- Mant, Jim G -- Ibarra, Fernando -- Schulz, Claudia -- Franke, Stephan -- Francke, Wittko -- New York, N.Y. -- Science. 2003 Oct 17;302(5644):437-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Botany and Zoology, The Australian National University, Canberra ACT 0200, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14564006" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cyclohexanones/chemistry/isolation & purification/*metabolism ; Female ; Flowers/metabolism ; Gas Chromatography-Mass Spectrometry ; Male ; Molecular Structure ; Odors ; Orchidaceae/*metabolism ; *Pollen ; Sex Attractants/chemistry/isolation & purification/*metabolism ; Sexual Behavior, Animal ; Spectroscopy, Fourier Transform Infrared ; Wasps/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Medicine. The need for a global HIV vaccine enterprise (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-06-28
    Description: A new collaborative model of research is needed to increase resources, to prioritize the R (ii) to increase the pace, reduce the overlap, and more systematically explore the elements of and delivery systems for vaccines; (iii) to use common standards for the prompt comparative testing of vaccine candidates; (iv) to expand resources for manufacturing vaccine candidates to speed their use in human trials; and (v) to increase the capacity for international clinical trials and to focus this effort toward quickly measuring the effectiveness of vaccine protection as prototype vaccine candidates are identified.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Klausner, Richard D -- Fauci, Anthony S -- Corey, Lawrence -- Nabel, Gary J -- Gayle, Helene -- Berkley, Seth -- Haynes, Barton F -- Baltimore, David -- Collins, Chris -- Douglas, R Gordon -- Esparza, Jose -- Francis, Donald P -- Ganguly, N K -- Gerberding, Julie Louise -- Johnston, Margaret I -- Kazatchkine, Michel D -- McMichael, Andrew J -- Makgoba, Malegapuru W -- Pantaleo, Giuseppe -- Piot, Peter -- Shao, Yiming -- Tramont, Edmund -- Varmus, Harold -- Wasserheit, Judith N -- New York, N.Y. -- Science. 2003 Jun 27;300(5628):2036-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bill and Melinda Gates Foundation, Seattle, WA 98102, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12829768" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines/administration & dosage/economics/immunology ; Academies and Institutes/economics/organization & administration ; Biotechnology/economics ; Clinical Trials as Topic/standards ; Drug Design ; Drug Evaluation, Preclinical/standards ; Drug Industry/economics ; Financial Support ; *Global Health ; HIV Infections/*prevention & control ; HIV-1/*immunology ; Humans ; Intellectual Property ; International Cooperation ; Multicenter Studies as Topic ; Private Sector ; *Public Policy ; Public Sector ; Research Support as Topic ; Vaccination
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    SCNM1, a putative RNA splicing factor that modifies disease severity in mice (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-16
    Description: The severity of many inherited disorders is influenced by genetic background. We describe a modifier interaction in C57BL/6Jmice that converts a chronic movement disorder into a lethal neurological disease. The primary mutation (medJ) changes a splice donor site of the sodium channel gene Scn8a (Nav1.6). The modifier mutation is characteristic of strain C57BL/6Jand introduces a nonsense codon into sodium channel modifier 1 (SCNM1), a zinc finger protein and a putative splice factor. An internally deleted SCNM1 protein is also predicted as a result of exon skipping associated with disruption of a consensus exonic splicing enhancer. The effect of the modifier mutation is to reduce the abundance of correctly spliced sodium channel transcripts below the threshold for survival. Our finding that genetic variation in a putative RNA splicing factor influences disease susceptibility in mice raises the possibility that a similar mechanism modifies the severity of human inherited disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buchner, David A -- Trudeau, Michelle -- Meisler, Miriam H -- GM24872/GM/NIGMS NIH HHS/ -- T32 DC00011/DC/NIDCD NIH HHS/ -- T32 GM07544/GM/NIGMS NIH HHS/ -- T32 HG00040/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2003 Aug 15;301(5635):967-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics, University of Michigan School of Medicine, Ann Arbor, MI 48109-0618, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12920299" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Animals ; Carrier Proteins/chemistry/*genetics/metabolism ; Chromosome Mapping ; Codon, Nonsense ; Codon, Terminator ; Genetic Predisposition to Disease ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Mice, Neurologic Mutants ; Mice, Transgenic ; Molecular Sequence Data ; Movement Disorders/genetics/metabolism ; Mutation ; NAV1.6 Voltage-Gated Sodium Channel ; *Nerve Tissue Proteins ; Nervous System Diseases/*genetics/metabolism ; Phenotype ; Phylogeny ; *RNA Splicing ; RNA, Messenger/genetics/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Sodium Channels/*genetics/metabolism ; Zinc Fingers
    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. Consent from donors for embryo and stem cell research (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-16
    Description: As research with human embryos and embryonic stem cells proceeds, the authors of this Policy Forum argue that all donors of biological materials should give informed consent, including oocyte and sperm donors. Informed consent is particularly important because of the diverse opinions and strong emotions that surround such research. Some gamete donors who are willing to help women and couples bear children may object to the use of their genetic materials for certain types of research.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lo, Bernard -- Chou, Vicki -- Cedars, Marcelle I -- Gates, Elena -- Taylor, Robert N -- Wagner, Richard M -- Wolf, Leslie -- Yamamoto, Keith R -- New York, N.Y. -- Science. 2003 Aug 15;301(5635):921.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Medical Ethics, School of Medicine at the University of California, San Francisco, CA 94143, USA. bernie@medicine.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12920284" target="_blank"〉PubMed〈/a〉
    Keywords: *Embryo Research ; Embryo, Mammalian/*cytology ; Female ; Humans ; *Informed Consent ; Male ; Oocytes ; Reproductive Techniques, Assisted ; Spermatozoa ; *Stem Cells ; *Tissue Donors
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    Erythrocyte G protein-coupled receptor signaling in malarial infection (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-23
    Description: Erythrocytic mechanisms involved in malarial infection are poorly understood. We have found that signaling via the erythrocyte beta2-adrenergic receptor and heterotrimeric guanine nucleotide-binding protein (Galphas) regulated the entry of the human malaria parasite Plasmodium falciparum. Agonists that stimulate cyclic adenosine 3',5'-monophosphate production led to an increase in malarial infection that could be blocked by specific receptor antagonists. Moreover, peptides designed to inhibit Galphas protein function reduced parasitemia in P. falciparum cultures in vitro, and beta-antagonists reduced parasitemia of P. berghei infections in an in vivo mouse model. Thus, signaling via the erythrocyte beta2-adrenergic receptor and Galphas may regulate malarial infection across parasite species.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harrison, Travis -- Samuel, Benjamin U -- Akompong, Thomas -- Hamm, Heidi -- Mohandas, Narla -- Lomasney, Jon W -- Haldar, Kasturi -- AI39071/AI/NIAID NIH HHS/ -- DK32094/DK/NIDDK NIH HHS/ -- EY06062/EY/NEI NIH HHS/ -- EY10291/EY/NEI NIH HHS/ -- HL03961/HL/NHLBI NIH HHS/ -- HL55591/HL/NHLBI NIH HHS/ -- HL69630/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2003 Sep 19;301(5640):1734-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Feinberg School of Medicine, Northwestern University, 303 Chicago Avenue, Chicago, IL 60611, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14500986" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic beta-2 Receptor Agonists ; Adrenergic beta-2 Receptor Antagonists ; Adrenergic beta-Agonists/pharmacology ; Adrenergic beta-Antagonists/pharmacology ; Alprenolol/pharmacology ; Animals ; Catecholamines/metabolism ; Cyclic AMP/metabolism ; Erythrocyte Membrane/metabolism ; Erythrocytes/metabolism/*parasitology ; GTP-Binding Protein alpha Subunits, Gs/chemistry/*metabolism ; Humans ; Malaria/metabolism/*parasitology ; Membrane Microdomains/metabolism ; Mice ; Parasitemia ; Peptide Fragments/pharmacology ; Plasmodium berghei/*physiology ; Plasmodium falciparum/growth & development/*physiology ; Propranolol/pharmacology ; Purinergic P1 Receptor Agonists ; Purinergic P1 Receptor Antagonists ; Receptors, Adrenergic, beta-2/*metabolism ; Receptors, Purinergic P1/metabolism ; Signal Transduction ; Stereoisomerism ; Vacuoles/parasitology
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    Antiretroviral drugs for tuberculosis control in the era of HIV/AIDS (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-16
    Description: Human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) has dramatically increased the incidence of tuberculosis (TB) in subSaharan Africa, where up to 60% of TB patients are coinfected with HIV and each year 200,000 TB deaths are attributable to HIV coinfection. Now HIV threatens control of TB in Asia, Eastern Europe, and Latin America. Antiretroviral (ARV) drugs can prevent TB by preserving immunity, but cohort analysis shows that early therapy, plus high levels of coverage and compliance, will be needed to avert a significant fraction of TB cases. However, ARV drugs could enhance the treatment of TB, and TB programs provide an important entry point for the treatment of HIV/AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, Brian G -- Dye, Christopher -- New York, N.Y. -- Science. 2003 Sep 12;301(5639):1535-7. Epub 2003 Aug 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Communicable Diseases, World Health Organization, 1211 Geneva 27, Switzerland. williamsbg@who.int〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12920302" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*complications/drug ; therapy/immunology/mortality ; Africa South of the Sahara/epidemiology ; Anti-HIV Agents/*therapeutic use ; Antitubercular Agents/therapeutic use ; CD4 Lymphocyte Count ; Cohort Studies ; Developing Countries ; Drug Therapy, Combination ; Female ; HIV Infections/*complications/drug therapy/immunology/mortality ; Hiv-1 ; Hiv-2 ; Humans ; Incidence ; Male ; Survival Rate ; Tuberculosis/complications/drug therapy/epidemiology/*prevention & control
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    Europe, science, and unity (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kennedy, Donald -- New York, N.Y. -- Science. 2003 Aug 29;301(5637):1157.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12947165" target="_blank"〉PubMed〈/a〉
    Keywords: Europe ; European Union ; International Cooperation ; *Public Policy ; *Research ; Research Support as Topic ; *Science ; United States
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    Biomedicine. Love, honor, and protect (your liver) (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davidson, Alan J -- Zon, Leonard I -- New York, N.Y. -- Science. 2003 Feb 7;299(5608):835-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Division of Hematology/Oncology, Children's Hospital, Howard Hughes Medical Institute, Boston, MA 02115, USA. zon@hhmi.tchlab.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12574609" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbon Tetrachloride/toxicity ; Cell Communication ; Cell Division ; Coculture Techniques ; Drug-Induced Liver Injury ; Endothelial Growth Factors/metabolism/*physiology ; Endothelium, Vascular/*cytology/physiology ; Hepatocyte Growth Factor/physiology/secretion ; Hepatocytes/*physiology ; Interleukin-6/physiology/secretion ; Liver/blood supply/*cytology/pathology/*physiology ; Liver Diseases/metabolism/pathology/prevention & control ; *Liver Regeneration ; Mice ; Necrosis ; Signal Transduction ; Up-Regulation ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factor Receptor-1/*metabolism ; Vascular Endothelial Growth Factor Receptor-2/metabolism
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    Kin discrimination and the benefit of helping in cooperatively breeding vertebrates (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-25
    Description: In many cooperatively breeding vertebrates, a dominant breeding pair is assisted in offspring care by nonbreeding helpers. A leading explanation for this altruistic behavior is Hamilton's idea that helpers gain indirect fitness benefits by rearing relatives (kin selection). Many studies have shown that helpers typically provide care for relatives, but relatively few have shown that helpers provide closer kin with preferential care (kin discrimination), fueling the suggestion that kin selection only poorly accounts for the evolution of cooperative breeding in vertebrates. We used meta-analysis to show that (i) individuals consistently discriminate between kin, and (ii) stronger discrimination occurs in species where the benefits of helping are greater. These results suggest a general role for kin selection and that the relative importance of kin selection varies across species, as predicted by Hamilton's rule.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Griffin, Ashleigh S -- West, Stuart A -- New York, N.Y. -- Science. 2003 Oct 24;302(5645):634-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Cell, Animal and Population Biology, University of Edinburgh, King's Buildings, West Mains Road, Edinburgh EH9 3JT, UK. a.griffin@ed.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14576431" target="_blank"〉PubMed〈/a〉
    Keywords: Altruism ; Animals ; *Behavior, Animal ; Birds/*physiology ; Breeding ; *Cooperative Behavior ; Family ; Female ; *Helping Behavior ; Male ; Mammals/*physiology ; Probability ; Sexual Behavior, Animal ; Social Behavior ; Species Specificity
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    Gene therapy. Seeking the cause of induced leukemias in X-SCID trial (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2003 Jan 24;299(5606):495.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12543948" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Advisory Committees ; Cell Division ; *Clinical Trials as Topic ; DNA-Binding Proteins/genetics/physiology ; France ; Genetic Diseases, X-Linked/therapy ; Genetic Therapy/*adverse effects ; Genetic Vectors ; Humans ; Interleukin Receptor Common gamma Subunit ; LIM Domain Proteins ; Leukemia/*etiology/genetics ; Male ; Metalloproteins/genetics/physiology ; Proto-Oncogene Proteins ; Receptors, Interleukin-7/genetics ; Retroviridae/genetics ; Risk Factors ; Severe Combined Immunodeficiency/*therapy ; T-Lymphocyte Subsets/physiology ; United States ; United States Food and Drug Administration
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    Neuroscience. ORs rule the roost in the olfactory system (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewcock, Joseph W -- Reed, Randall R -- New York, N.Y. -- Science. 2003 Dec 19;302(5653):2078-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular Biology and Genetics, 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/14684811" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Alleles ; Animals ; Cell Nucleus/metabolism ; Chromosomes, Artificial, Yeast ; Feedback, Physiological ; *Gene Expression Regulation ; Genes, Reporter ; Mice ; Mice, Transgenic ; Multigene Family ; Odors ; Olfactory Receptor Neurons/*metabolism ; Promoter Regions, Genetic ; Pseudogenes ; Receptors, Odorant/*genetics/*metabolism ; Signal Transduction ; Transgenes
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    Science and government. Disclosure in regulatory science (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Michaels, David -- Wagner, Wendy -- New York, N.Y. -- Science. 2003 Dec 19;302(5653):2073.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Environmental and Occupational Health, George Washington University School of Public Health and Health Services, Washington, DC, 20052, USA. eohdmm@gwumc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14684806" target="_blank"〉PubMed〈/a〉
    Keywords: Confidentiality ; *Conflict of Interest ; *Disclosure ; *Government Regulation ; *Private Sector ; Public Policy ; Research/*standards ; Research Support as Topic ; United States ; *United States Government Agencies
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    LRP: role in vascular wall integrity and protection from atherosclerosis (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-12
    Description: Vascular smooth muscle cell (SMC) proliferation and migration are important events in the development of atherosclerosis. The low-density lipoprotein receptor-related protein (LRP1) mediates suppression of SMC migration induced by platelet-derived growth factor (PDGF). Here we show that LRP1 forms a complex with the PDGF receptor (PDGFR). Inactivation of LRP1 in vascular SMCs of mice causes PDGFR overexpression and abnormal activation of PDGFR signaling, resulting in disruption of the elastic layer, SMC proliferation, aneurysm formation, and marked susceptibility to cholesterol-induced atherosclerosis. The development of these abnormalities was reduced by treatment with Gleevec, an inhibitor of PDGF signaling. Thus, LRP1 has a pivotal role in protecting vascular wall integrity and preventing atherosclerosis by controlling PDGFR activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boucher, Philippe -- Gotthardt, Michael -- Li, Wei-Ping -- Anderson, Richard G W -- Herz, Joachim -- GM 52016/GM/NIGMS NIH HHS/ -- HL20948/HL/NHLBI NIH HHS/ -- HL63762/HL/NHLBI NIH HHS/ -- NS43408/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Apr 11;300(5617):329-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9046, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12690199" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta/cytology/metabolism/*pathology ; Arteriosclerosis/*pathology/physiopathology/*prevention & control ; Benzamides ; Cattle ; Cell Division ; Cell Line ; Cholesterol, Dietary/administration & dosage ; Diet, Atherogenic ; Elastin/analysis ; Enzyme Inhibitors/pharmacology ; Imatinib Mesylate ; Ligands ; Low Density Lipoprotein Receptor-Related ; Protein-1/genetics/metabolism/*physiology ; Mesenteric Arteries/cytology/pathology ; Mice ; Mice, Knockout ; Mice, Transgenic ; Muscle, Smooth, Vascular/cytology/*metabolism/pathology ; Myocytes, Smooth Muscle/*metabolism/physiology ; Phosphorylation ; Piperazines/pharmacology ; Platelet-Derived Growth Factor/metabolism/pharmacology ; Proto-Oncogene Proteins c-sis ; Pyrimidines/pharmacology ; Receptor, Platelet-Derived Growth Factor beta/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Mono- versus polyubiquitination: differential control of p53 fate by Mdm2 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-13
    Description: Although Mdm2-mediated ubiquitination is essential for both degradation and nuclear export of p53, the molecular basis for the differential effects of Mdm2 remains unknown. Here we show that low levels of Mdm2 activity induce monoubiquitination and nuclear export of p53, whereas high levels promote p53's polyubiquitination and nuclear degradation. A p53-ubiquitin fusion protein that mimics monoubiquitinated p53 was found to accumulate in the cytoplasm in an Mdm2-independent manner, indicating that monoubiquitination is critical for p53 trafficking. These results clarify the nature of ubiquitination-mediated p53 regulation and suggest that distinct mechanisms regulate p53 function in accordance with the levels of Mdm2 activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Muyang -- Brooks, Christopher L -- Wu-Baer, Foon -- Chen, Delin -- Baer, Richard -- Gu, Wei -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1972-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cancer Genetics and Department of Pathology, College of Physicians & Surgeons, Columbia University, 1150 St. Nicholas Avenue, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671306" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Animals ; Cell Line, Tumor ; Cell Nucleus/*metabolism ; Cells, Cultured ; Cytoplasm/metabolism ; Humans ; Mice ; Mice, Knockout ; Mutation ; *Nuclear Proteins ; Protein Transport ; Proto-Oncogene Proteins/genetics/*metabolism ; Proto-Oncogene Proteins c-mdm2 ; Recombinant Fusion Proteins/metabolism ; Transfection ; Tumor Suppressor Protein p53/genetics/*metabolism ; Ubiquitin/genetics/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Phosphatidylserine receptor is required for clearance of apoptotic cells (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-04
    Description: Cells undergoing apoptosis during development are removed by phagocytes, but the underlying mechanisms of this process are not fully understood. Phagocytes lacking the phosphatidylserine receptor (PSR) were defective in removing apoptotic cells. Consequently, in PSR-deficient mice, dead cells accumulated in the lung and brain, causing abnormal development and leading to neonatal lethality. A fraction of PSR knockout mice manifested a hyperplasic brain phenotype resembling that of mice deficient in the cell death-associated genes encoding Apaf-1, caspase-3, and caspase-9, which suggests that phagocytes may also be involved in promoting apoptosis. These data demonstrate a critical role for PSR in early stages of mammalian organogenesis and suggest that this receptor may be involved in respiratory distress syndromes and congenital brain malformations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Ming O -- Sarkisian, Matthew R -- Mehal, Wajahat Z -- Rakic, Pasko -- Flavell, Richard A -- New York, N.Y. -- Science. 2003 Nov 28;302(5650):1560-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14645847" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Brain/abnormalities/cytology/*embryology ; Cell Division ; Cell Nucleus/ultrastructure ; Epithelial Cells/physiology/ultrastructure ; Eye/embryology ; Eye Abnormalities/etiology ; Hematopoietic Stem Cell Transplantation ; In Situ Nick-End Labeling ; Inflammation ; Lung/cytology/*embryology/physiology ; Macrophages/*physiology ; Mesoderm/ultrastructure ; Mice ; Mice, Knockout ; Necrosis ; Neurons/cytology ; Phagocytosis ; Phenotype ; Phosphatidylserines/metabolism ; Pulmonary Surfactants/metabolism ; Receptors, Cell Surface/genetics/*metabolism ; Respiratory Insufficiency/etiology ; Reverse Transcriptase Polymerase Chain Reaction
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    Allosteric activators of glucokinase: potential role in diabetes therapy (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-19
    Description: Glucokinase (GK) plays a key role in whole-body glucose homeostasis by catalyzing the phosphorylation of glucose in cells that express this enzyme, such as pancreatic beta cells and hepatocytes. We describe a class of antidiabetic agents that act as nonessential, mixed-type GK activators (GKAs) that increase the glucose affinity and maximum velocity (Vmax) of GK. GKAs augment both hepatic glucose metabolism and glucose-induced insulin secretion from isolated rodent pancreatic islets, consistent with the expression and function of GK in both cell types. In several rodent models of type 2 diabetes mellitus, GKAs lowered blood glucose levels, improved the results of glucose tolerance tests, and increased hepatic glucose uptake. These findings may lead to the development of new drug therapies for diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grimsby, Joseph -- Sarabu, Ramakanth -- Corbett, Wendy L -- Haynes, Nancy-Ellen -- Bizzarro, Fred T -- Coffey, John W -- Guertin, Kevin R -- Hilliard, Darryl W -- Kester, Robert F -- Mahaney, Paige E -- Marcus, Linda -- Qi, Lida -- Spence, Cheryl L -- Tengi, John -- Magnuson, Mark A -- Chu, Chang An -- Dvorozniak, Mark T -- Matschinsky, Franz M -- Grippo, Joseph F -- New York, N.Y. -- Science. 2003 Jul 18;301(5631):370-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Metabolic Diseases, Hoffmann-La Roche Inc., Nutley, NJ 07110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12869762" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Allosteric Regulation ; Animals ; Blood Glucose/metabolism ; *Carrier Proteins ; Diabetes Mellitus, Type 2/*drug therapy/metabolism ; Dose-Response Relationship, Drug ; Drug Evaluation, Preclinical ; Enzyme Activation ; Enzyme Activators/chemistry/pharmacology ; Glucokinase/*metabolism ; Glucose/*metabolism ; Glucose Tolerance Test ; Homeostasis ; Humans ; Hypoglycemic Agents/chemistry/pharmacology ; Insulin/blood/*secretion ; Islets of Langerhans/*drug effects/secretion ; Keto Acids/metabolism ; Liver/*drug effects/metabolism ; Liver Glycogen/biosynthesis ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Proteins/metabolism/pharmacology ; Rats ; Rats, Wistar ; Recombinant Proteins/metabolism ; Stereoisomerism ; Thiazoles/chemistry/*pharmacology
    Print ISSN: 0036-8075
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    Reprogramming control of an allosteric signaling switch through modular recombination (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-27
    Description: Many eukaryotic signaling proteins are composed of simple modular binding domains, yet they can display sophisticated behaviors such as allosteric gating and multi-input signal integration, properties essential for complex cellular circuits. To understand how such behavior can emerge from combinations of simple domains, we engineered variants of the actin regulatory protein N-WASP (neuronal Wiskott-Aldrich syndrome protein) in which the "output" domain of N-WASP was recombined with heterologous autoinhibitory "input" domains. Synthetic switch proteins were created with diverse gating behaviors in response to nonphysiological inputs. Thus, this type of modular framework can facilitate the evolution or engineering of cellular signaling circuits.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dueber, John E -- Yeh, Brian J -- Chak, Kayam -- Lim, Wendell A -- New York, N.Y. -- Science. 2003 Sep 26;301(5641):1904-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Biological Sciences, University of California, San Francisco, CA 94143-2240, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14512628" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Allosteric Regulation ; Amino Acid Motifs ; Animals ; Combinatorial Chemistry Techniques ; Evolution, Molecular ; Ligands ; Male ; Nerve Tissue Proteins/*chemistry/genetics/*metabolism ; Oocytes/metabolism ; Peptide Library ; Protein Engineering ; Protein Structure, Tertiary ; Recombinant Fusion Proteins/chemistry/metabolism ; Recombination, Genetic ; *Signal Transduction ; Wiskott-Aldrich Syndrome Protein, Neuronal ; Xenopus ; cdc42 GTP-Binding Protein/metabolism ; src Homology Domains
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    Stem cells: still here, still waiting (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kennedy, Donald -- New York, N.Y. -- Science. 2003 May 9;300(5621):865.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12738815" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Cell Culture Techniques ; *Cell Line ; Cloning, Organism ; *Embryo Research ; Embryo, Mammalian/*cytology ; Humans ; Mice ; Politics ; Public Policy ; *Stem Cells ; United States
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    Spongiform degeneration in mahoganoid mutant mice (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-01
    Description: mahoganoid is a mouse coat-color mutation whose pigmentary phenotype and genetic interactions resemble those of Attractin (Atrn). Atrn mutations also cause spongiform neurodegeneration. Here, we show that a null mutation for mahoganoid causes a similar age-dependent neuropathology that includes many features of prion diseases but without accumulation of protease-resistant prion protein. The gene mutated in mahoganoid encodes a RING-containing protein with E3 ubiquitin ligase activity in vitro. Similarities in phenotype, expression, and genetic interactions suggest that mahoganoid and Atrn genes are part of a conserved pathway for regulated protein turnover whose function is essential for neuronal viability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, Lin -- Lu, Xin-Yun -- Jolly, Aaron F -- Eldridge, Adam G -- Watson, Stanley J -- Jackson, Peter K -- Barsh, Gregory S -- Gunn, Teresa M -- New York, N.Y. -- Science. 2003 Jan 31;299(5607):710-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Department of Genetics, Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12560552" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Animals ; Blotting, Northern ; Brain/metabolism/*pathology ; Carrier Proteins/chemistry/*genetics/*metabolism ; Crosses, Genetic ; Female ; Gene Expression ; Ligases/metabolism ; Male ; Membrane Proteins/genetics ; Mice ; Mice, Inbred C3H ; Mice, Mutant Strains ; Mice, Transgenic ; Models, Biological ; Molecular Sequence Data ; *Mutation ; Neurodegenerative Diseases/*genetics/metabolism/*pathology ; Neurons/metabolism/pathology ; Pigmentation ; Prions/metabolism ; RNA, Messenger/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Transgenes ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases ; Vacuoles/ultrastructure
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    Origin and migration of the Alpine Iceman (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-01
    Description: The Alpine Iceman provides a unique window into the Neolithic-Copper Age of Europe. We compared the radiogenic (strontium and lead) and stable (oxygen and carbon) isotope composition of the Iceman's teeth and bones, as well as 40Ar/39Ar mica ages from his intestine, to local geology and hydrology, and we inferred his habitat and range from childhood to adult life. The Iceman's origin can be restricted to a few valleys within approximately 60 kilometers south(east) of the discovery site. His migration during adulthood is indicated by contrasting isotopic compositions of enamel, bones, and intestinal content. This demonstrates that the Alpine valleys of central Europe were permanently inhabited during the terminal Neolithic.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muller, Wolfgang -- Fricke, Henry -- Halliday, Alex N -- McCulloch, Malcolm T -- Wartho, Jo-Anne -- New York, N.Y. -- Science. 2003 Oct 31;302(5646):862-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research School of Earth Sciences, Australian National University, Canberra, ACT 0200, Australia. wolfgang.mueller@anu.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14593178" target="_blank"〉PubMed〈/a〉
    Keywords: Aluminum Silicates ; Argon/analysis ; Austria ; Bone and Bones/chemistry ; Carbon Isotopes/analysis ; Dental Enamel/chemistry ; Drinking ; *Emigration and Immigration ; *Environment ; Femur/chemistry ; Gastrointestinal Contents/chemistry ; Geological Phenomena ; Geology ; Humans ; Ice ; Isotopes/*analysis ; Italy ; Lead/analysis ; Male ; *Mummies ; Oxygen Isotopes/analysis ; *Paleontology ; Soil/analysis ; Strontium Isotopes/analysis ; Water
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Untangling desmosomal knots with electron tomography (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-04
    Description: Cell adhesion by adherens junctions and desmosomes relies on interactions between cadherin molecules. However, the molecular interfaces that define molecular specificity and that mediate adhesion remain controversial. We used electron tomography of plastic sections from neonatal mouse skin to visualize the organization of desmosomes in situ. The resulting three-dimensional maps reveal individual cadherin molecules forming discrete groups and interacting through their tips. Fitting of an x-ray crystal structure for C-cadherin to these maps is consistent with a flexible intermolecular interface mediated by an exchange of amino-terminal tryptophans. This flexibility suggests a novel mechanism for generating both cis and trans interactions and for propagating these adhesive interactions along the junction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, Wanzhong -- Cowin, Pamela -- Stokes, David L -- R01 GM47429/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 3;302(5642):109-13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skirball Institute of Biomolecular Medicine, New York University School of Medicine, 540 First Avenue, New York, NY 10016, USA..〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14526082" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Cadherins/*chemistry/*ultrastructure ; Cell Adhesion ; Crystallography, X-Ray ; Cytoskeletal Proteins/chemistry/ultrastructure ; Desmoplakins ; Desmosomes/*chemistry/*ultrastructure ; Dimerization ; Epidermis/chemistry/ultrastructure ; Freeze Substitution ; Hydrophobic and Hydrophilic Interactions ; *Image Processing, Computer-Assisted ; Mice ; Microscopy, Electron/methods ; Protein Binding ; Protein Conformation ; Protein Structure, Tertiary ; *Tomography ; Tryptophan/chemistry ; Xenopus Proteins
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    Diminished pupillary light reflex at high irradiances in melanopsin-knockout mice (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-11
    Description: In the mammalian retina, a small subset of retinal ganglion cells (RGCs) are intrinsically photosensitive, express the opsin-like protein melanopsin, and project to brain nuclei involved in non-image-forming visual functions such as pupillary light reflex and circadian photoentrainment. We report that in mice with the melanopsin gene ablated, RGCs retrograde-labeled from the suprachiasmatic nuclei were no longer intrinsically photosensitive, although their number, morphology, and projections were unchanged. These animals showed a pupillary light reflex indistinguishable from that of the wild type at low irradiances, but at high irradiances the reflex was incomplete, a pattern that suggests that the melanopsin-associated system and the classical rod/cone system are complementary in function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lucas, R J -- Hattar, S -- Takao, M -- Berson, D M -- Foster, R G -- Yau, K-W -- R01 EY006837/EY/NEI NIH HHS/ -- R01 EY006837-16A1/EY/NEI NIH HHS/ -- R01 EY014596/EY/NEI NIH HHS/ -- R01 EY014596-01/EY/NEI NIH HHS/ -- R37 EY006837/EY/NEI NIH HHS/ -- R37 EY006837-13/EY/NEI NIH HHS/ -- R37 EY006837-14/EY/NEI NIH HHS/ -- R37 EY006837-15/EY/NEI NIH HHS/ -- R37 EY006837-15S1/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2003 Jan 10;299(5604):245-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Integrative and Molecular Neuroscience, Division of Neuroscience and Psychological Medicine, Faculty of Medicine, Imperial College London, Charing Cross Campus, St. Dunstans Road, London W6 8RF, UK. r.j.lucas@ic.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12522249" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Ocular ; Animals ; Carbachol/pharmacology ; Circadian Rhythm ; Darkness ; *Light ; Light Signal Transduction ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Olivary Nucleus/cytology/physiology ; Phenotype ; Photoreceptor Cells, Vertebrate/physiology ; Pupil/drug effects/*physiology ; *Reflex, Pupillary ; Retinal Degeneration/genetics/physiopathology ; Retinal Ganglion Cells/*physiology ; Rod Opsins/*genetics/*physiology ; Suprachiasmatic Nucleus/physiology
    Print ISSN: 0036-8075
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    Genetics. Modifying the message (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nadeau, Joseph H -- New York, N.Y. -- Science. 2003 Aug 15;301(5635):927-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Case Western Reserve University, Cleveland, OH 44106, USA. jhn4@cwru.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12920288" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/*genetics/physiology ; Cloning, Molecular ; Codon, Terminator ; Exons ; Gene Expression Regulation ; Humans ; Ion Transport ; Mice ; Mice, Inbred C57BL ; Mice, Neurologic Mutants ; Mutation ; NAV1.6 Voltage-Gated Sodium Channel ; *Nerve Tissue Proteins ; Nervous System Diseases/*genetics/metabolism ; Phenotype ; RNA Precursors/genetics/metabolism ; *RNA Splicing ; RNA, Messenger/genetics/metabolism ; Sodium/metabolism ; Sodium Channels/*genetics/metabolism ; Transcription, Genetic ; Zinc Fingers
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    Transcription-coupled events associating with immunoglobulin switch region chromatin (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-20
    Description: Class switch recombination (CSR) at the antibody immunoglobulin locus is regulated by germline transcription (GLT)-coupled modifications in the accessibility of the switch region, where CSR takes place. Here we show that histone acetylation of switch regions is linked to CSR but that histone acetylation cannot alone promote CSR or GLT. Activation-induced cytidine deaminase (AID) specifically associates with the CSR target chromatin in a GLT-coupled manner, which may occur potentially by means of physical interaction between AID and the transcription machinery. These data indicate an important role of GLT in the regulation of chromatin accessibility, strongly suggesting that the target of AID is chromatin DNA. Our results give insights on the role of AID and the regulatory mechanism of CSR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nambu, Yukiko -- Sugai, Manabu -- Gonda, Hiroyuki -- Lee, Chung-Gi -- Katakai, Tomoya -- Agata, Yasutoshi -- Yokota, Yoshifumi -- Shimizu, Akira -- New York, N.Y. -- Science. 2003 Dec 19;302(5653):2137-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Molecular Biology and Genetics, Kyoto University, 53 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14684824" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; B-Lymphocytes/*immunology ; Cells, Cultured ; Chromatin/*metabolism ; Cytidine Deaminase/*metabolism ; DNA/metabolism ; Histone Deacetylase Inhibitors ; Histones/metabolism ; Hydroxamic Acids/pharmacology ; *Immunoglobulin Class Switching ; Immunoglobulin E/biosynthesis ; Immunoglobulin G/biosynthesis ; *Immunoglobulin Switch Region ; Interleukin-4/immunology ; Lipopolysaccharides/immunology ; Lymphocyte Activation ; Mice ; Precipitin Tests ; RNA/metabolism ; RNA Polymerase II/metabolism ; Recombination, Genetic ; *Transcription, Genetic ; Transforming Growth Factor beta/immunology ; Transforming Growth Factor beta1
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    Breakthrough of the year. Scorecard 2002 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 2003 Dec 19;302(5653):2041.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14684789" target="_blank"〉PubMed〈/a〉
    Keywords: Astronomical Phenomena ; Astronomy ; Climate ; Elementary Particles ; Forecasting ; Genomics ; Research Support as Topic ; Science/*trends
    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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  • 93
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    Biomedicine. Nota bene: weathering the big chill (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, Orla -- New York, N.Y. -- Science. 2003 Jan 24;299(5606):530.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12543964" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Platelets/metabolism/*physiology ; Blood Preservation ; *Cold Temperature ; Humans ; Kupffer Cells/physiology ; Macrophage-1 Antigen/*metabolism ; Mice ; Phagocytosis ; Platelet Glycoprotein GPIb-IX Complex/*metabolism ; *Platelet Transfusion ; Refrigeration
    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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    Generation of viable cholesterol-free mice (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wechsler, A -- Brafman, A -- Shafir, M -- Heverin, M -- Gottlieb, H -- Damari, G -- Gozlan-Kelner, S -- Spivak, I -- Moshkin, O -- Fridman, E -- Becker, Y -- Skaliter, R -- Einat, P -- Faerman, A -- Bjorkhem, I -- Feinstein, E -- New York, N.Y. -- Science. 2003 Dec 19;302(5653):2087.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Quark Biotech, Inc., 10265 Carnegie Avenue, Cleveland, OH 44106, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14684813" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue ; Animals ; Bile Acids and Salts/biosynthesis ; Cholesterol/blood/*deficiency/metabolism/*physiology ; Desmosterol/*metabolism ; Female ; Gene Targeting ; Growth ; Humans ; Infertility ; Liver/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Models, Animal ; Nerve Tissue Proteins/*genetics/metabolism ; Oxidoreductases Acting on CH-CH Group Donors/*genetics/metabolism ; Phenotype ; Sex Characteristics ; Testis/pathology
    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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    Synchronization of cellular clocks in the suprachiasmatic nucleus (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-25
    Description: Individual cellular clocks in the suprachiasmatic nucleus (SCN), the circadian center, are integrated into a stable and robust pacemaker with a period length of about 24 hours. We used real-time analysis of gene expression to show synchronized rhythms of clock gene transcription across hundreds of neurons within the mammalian SCN in organotypic slice culture. Differentially phased neuronal clocks are topographically arranged across the SCN. A protein synthesis inhibitor set all cell clocks to the same initial phase and, after withdrawal, intrinsic interactions among cell clocks reestablished the stable program of gene expression across the assemblage. Na+-dependent action potentials contributed to establishing cellular synchrony and maintaining spontaneous oscillation across the SCN.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamaguchi, Shun -- Isejima, Hiromi -- Matsuo, Takuya -- Okura, Ryusuke -- Yagita, Kazuhiro -- Kobayashi, Masaki -- Okamura, Hitoshi -- New York, N.Y. -- Science. 2003 Nov 21;302(5649):1408-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Brain Science, Department of Brain Sciences, 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/14631044" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Action Potentials/drug effects ; Animals ; Basic Helix-Loop-Helix Transcription Factors ; Biological Clocks/*physiology ; CLOCK Proteins ; Cell Cycle Proteins ; Circadian Rhythm/*physiology ; Cycloheximide/pharmacology ; Gene Expression ; Glyceraldehyde-3-Phosphate Dehydrogenases/genetics/metabolism ; Luminescence ; Mice ; Mice, Knockout ; Mice, Transgenic ; Neurons/*physiology ; Nuclear Proteins/genetics/metabolism ; Organ Culture Techniques ; Period Circadian Proteins ; Promoter Regions, Genetic ; Protein Synthesis Inhibitors/pharmacology ; Signal Transduction ; Sodium/metabolism ; Suppression, Genetic ; Suprachiasmatic Nucleus/cytology/*physiology ; Tetrodotoxin/pharmacology ; Trans-Activators/metabolism ; Transcription Factors/metabolism ; Transcription, Genetic
    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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  • 96
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    Hematopoietic cell regulation by Rac1 and Rac2 guanosine triphosphatases (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-18
    Description: The Rho guanosine triphosphatases (GTPases) Rac1 and Rac2 are critical signaling regulators in mammalian cells. The deletion of both Rac1 and Rac2 murine alleles leads to a massive egress of hematopoietic stem/progenitor cells (HSC/Ps) into the blood from the marrow, whereas Rac1-/- but not Rac2-/- HSC/Ps fail to engraft in the bone marrow of irradiated recipient mice. In contrast, Rac2, but not Rac1, regulates superoxide production and directed migration in neutrophils, and in each cell type, the two GTPases play distinct roles in actin organization, cell survival, and proliferation. Thus, Rac1 and Rac2 regulate unique aspects of hematopoietic development and function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gu, Yi -- Filippi, Marie-Dominique -- Cancelas, Jose A -- Siefring, Jamie E -- Williams, Emily P -- Jasti, Aparna C -- Harris, Chad E -- Lee, Andrew W -- Prabhakar, Rethinasamy -- Atkinson, Simon J -- Kwiatkowski, David J -- Williams, David A -- DK62757/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 17;302(5644):445-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Experimental Hematology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14564009" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Apoptosis ; Bone Marrow Transplantation ; Cell Adhesion ; Cell Cycle ; Cell Movement ; Cell Size ; Colony-Forming Units Assay ; Cyclin D1/metabolism ; Fibronectins/metabolism ; Hematopoiesis ; Hematopoietic Stem Cell Mobilization ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*physiology ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Mitogen-Activated Protein Kinases/metabolism ; Neutrophils/*physiology ; *Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Recombination, Genetic ; Signal Transduction ; Stem Cell Factor/pharmacology ; Superoxides/metabolism ; rac GTP-Binding Proteins/genetics/*metabolism ; rac1 GTP-Binding Protein/genetics/*metabolism
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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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    Spying on the brain, one neuron at a time (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2003 Apr 4;300(5616):78-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12677054" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Cerebral Cortex/cytology/*physiology ; Dendrites/*physiology/ultrastructure ; Humans ; Lasers ; Learning ; Mice ; Microscopy, Fluorescence, Multiphoton/methods ; *Neuronal Plasticity ; Neurons/physiology ; Synapses/*physiology ; Vibrissae/physiology ; Visual Cortex/cytology/*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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  • 98
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    Anterior-posterior guidance of commissural axons by Wnt-frizzled signaling (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-13
    Description: Commissural neurons in the mammalian dorsal spinal cord send axons ventrally toward the floor plate, where they cross the midline and turn anteriorly toward the brain; a gradient of chemoattractant(s) inside the spinal cord controls this turning. In rodents, several Wnt proteins stimulate the extension of commissural axons after midline crossing (postcrossing). We found that Wnt4 messenger RNA is expressed in a decreasing anterior-to-posterior gradient in the floor plate, and that a directed source of Wnt4 protein attracted postcrossing commissural axons. Commissural axons in mice lacking the Wnt receptor Frizzled3 displayed anterior-posterior guidance defects after midline crossing. Thus, Wnt-Frizzled signaling guides commissural axons along the anterior-posterior axis of the spinal cord.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lyuksyutova, Anna I -- Lu, Chin-Chun -- Milanesio, Nancy -- King, Leslie A -- Guo, Nini -- Wang, Yanshu -- Nathans, Jeremy -- Tessier-Lavigne, Marc -- Zou, Yimin -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1984-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Pharmacology and Physiology, University of Chicago, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671310" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology/ultrastructure ; Brain/embryology/metabolism ; COS Cells ; Central Nervous System/cytology/*embryology/metabolism ; Cues ; Culture Techniques ; Diffusion ; Frizzled Receptors ; Gene Expression Profiling ; Growth Cones/physiology/ultrastructure ; In Situ Hybridization ; *Membrane Proteins ; Mice ; Mice, Knockout ; Neurons/*physiology ; Proteins/pharmacology ; Proto-Oncogene Proteins/*metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, G-Protein-Coupled/genetics/*metabolism ; *Signal Transduction ; Spinal Cord/*cytology/embryology/metabolism ; Transfection ; Wnt Proteins ; Wnt4 Protein
    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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  • 99
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    Influence of life stress on depression: moderation by a polymorphism in the 5-HTT gene (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-19
    Description: In a prospective-longitudinal study of a representative birth cohort, we tested why stressful experiences lead to depression in some people but not in others. A functional polymorphism in the promoter region of the serotonin transporter (5-HT T) gene was found to moderate the influence of stressful life events on depression. Individuals with one or two copies of the short allele of the 5-HT T promoter polymorphism exhibited more depressive symptoms, diagnosable depression, and suicidality in relation to stressful life events than individuals homozygous for the long allele. This epidemiological study thus provides evidence of a gene-by-environment interaction, in which an individual's response to environmental insults is moderated by his or her genetic makeup.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caspi, Avshalom -- Sugden, Karen -- Moffitt, Terrie E -- Taylor, Alan -- Craig, Ian W -- Harrington, HonaLee -- McClay, Joseph -- Mill, Jonathan -- Martin, Judy -- Braithwaite, Antony -- Poulton, Richie -- MH45070/MH/NIMH NIH HHS/ -- MH49414/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2003 Jul 18;301(5631):386-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Social, Genetic, and Developmental Psychiatry Research Centre, Institute of Psychiatry, King's College London, PO80 De Crespigny Park, London, SE5 8AF, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12869766" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; *Alleles ; Carrier Proteins/*genetics ; Child ; Child Abuse ; Depression/etiology/*genetics ; Depressive Disorder/etiology/*genetics ; Disease Susceptibility ; Female ; Genetic Predisposition to Disease ; Heterozygote ; Homozygote ; Humans ; Longitudinal Studies ; Male ; Membrane Glycoproteins/*genetics ; *Membrane Transport Proteins ; Monoamine Oxidase/genetics ; *Nerve Tissue Proteins ; *Polymorphism, Genetic ; Probability ; Promoter Regions, Genetic ; Serotonin Plasma Membrane Transport Proteins ; Stress, Psychological/*genetics ; Suicide, Attempted
    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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    Melanin, nutrition, and the lion's mane (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hill, Geoffrey E -- McGraw, Kevin J -- New York, N.Y. -- Science. 2003 Jan 31;299(5607):660; author reply 660.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12561820" target="_blank"〉PubMed〈/a〉
    Keywords: *Animal Nutritional Physiological Phenomena ; Animals ; Diet ; Female ; *Hair Color ; Lions/*anatomy & histology/*physiology ; Male ; Melanins/analysis ; Testosterone/*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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