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  • Mice  (181)
  • Earth model, also for more shallow analyses !
  • 2000-2004  (193)
  • 1980-1984
  • 1925-1929
  • 2000  (193)
  • 1
    Electronic Resource
    Electronic Resource
    Neutralizing antibody provided protection against enterovirus type 71 lethal challenge in neonatal mice (2000)
    Springer
    Journal of biomedical science 7 (2000), S. 523-528 
    Details
    ISSN: 1423-0127
    Keywords: Enterovirus type 71 ; Experimental infection ; Mice ; Neutralizing antibody ; Vaccine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Experimental infection with enterovirus type 71 (EV71) induced death in neonatal mice in an age- and dose-dependent manner. The mortality rate was 100% following intraperitoneal inoculation 1-day-old ICR mice and this gradually decreased as the age at the time of inoculation increased (60% in 3-day-old mice and no deaths occurred in mice older than 6 days of age). A lethal dose greater than 108 PFU was necessary. Lethargy, failure to gain weight, rear limb tremors and paralysis were observed in the infected mice before death. EV71 was isolated from various tissues of the dead mice. Using a reverse transcription polymerase chain reaction technique with a specific primer pair, a 332-bp product was detected in the tissues that produced a culture positive for EV71. Protection against EV71 challenge in neonatal mice was demonstrated following passive transfer of serum from actively immunized adult mice 1 day after inoculation with the virus. Pups from hyperimmune dams were resistant to EV71 challenge. Additionally, maternal immunization with a formalin-inactivated whole-virus vaccine prolonged the survival of pups after EV71 lethal challenge.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02253368
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Co-housing in a stable hierarchical group is not aversive for dominant and subordinate individuals (2000)
    Springer
    Neuroscience and behavioral physiology 30 (2000), S. 195-200 
    Details
    ISSN: 1573-899X
    Keywords: Mice ; dominance ; subordinacy ; stress ; aggression ; locomotor activity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The behavior of individaals and their responses to external stimuli are controlled by the microsocial environment, which for most mammals is associated with dominant-subordinate relationships. Physiological and behavioral differences between dominant and subordinate individuals may be ‘primary’ (genetically determined) or ‘secondary’ (due to position in the group's hierarchical structure). A series of experiments was conducted to investigate the physiological (pain response threshold), immunological (thymus, spleen weights, primary immune response), and behavioral (motor activity, behavior in a shuttle box test) characteristics of dominant and subordinate individuals in groups of three laboratory mice formed on the basis of linear hierarchy. Assessment of the effects of group conditions was made using a conditioned reflex location preference test. The results showed: 1) there are no statistically significant differences in physiological and behavioral (except for motor activity) parameters between dominant and subordinate mice; 2) co-housing of dominant and subordinate individuals in groups with stable hierarchical relationships was not aversive for them.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02463158
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  • 3
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    That "Dahm" layer - Comments on renaming the D" (2000)
    In:  Eos, Trans., Am. Geophys. Un., Jena, Physica-Verlag, vol. 81, no. 19, pp. 210, pp. 2096, (ISSN: 1340-4202)
    Details
    Publication Date: 2000
    Keywords: Earth model, also for more shallow analyses ! ; Seismology ; Velocity depth profile ; double-prime
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    BIBLIOGRAPHY SEISMOLOGY
  • 4
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    The COSY Project: verification of global seismic modeling algorithms (2000)
    In:  Phys. Earth Plan. Int., Stuttgart, Schweizerbart'sche Verlagsbuchhandlung, vol. 119, no. 1-2, pp. 3-23, pp. 2271, (ISSN 0016-8548, ISBN 3-510-50045-8)
    Details
    Publication Date: 2000
    Keywords: Seismology ; Review article ; Project report/description ; Synthetic seismograms ; Clevede ; PEPI ; Earth model, also for more shallow analyses !
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    BIBLIOGRAPHY SEISMOLOGY
  • 5
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    That "Dahm" layer - Comments on renaming the D" (2000)
    In:  Eos, Trans., Am. Geophys. Un., Berlin, Ges. f. Geowissenschaften e.V., vol. 81, no. 19, pp. 210, pp. L02309, (ISSN 0343-5164)
    Details
    Publication Date: 2000
    Keywords: Earth model, also for more shallow analyses ! ; Seismology ; Velocity depth profile ; double-prime
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    BIBLIOGRAPHY SEISMOLOGY
  • 6
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    Rheological structure and dynamical response of the Deep seismic sounding (espec. cont. crust) profile BALTIC in the SE Fennoscandian Shield (2000)
    In:  Tectonophysics, Tokyo, Conseil de l'Europe, vol. 320, no. 3-4, pp. 175-194, pp. L01306, (ISSN: 1340-4202)
    Details
    Publication Date: 2000
    Keywords: Dynamic ; Tectonics ; Reflection seismics ; Refraction seismics ; EUROPROBE (Geol. and Geophys. in eastern Europe) ; Rheology ; Earth model, also for more shallow analyses ! ; Velocity depth profile ; Inelastic
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    BIBLIOGRAPHY SEISMOLOGY
  • 7
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    That "Dahm" layer - Reply (2000)
    In:  Eos, Trans., Am. Geophys. Un., Warszawa, Conseil de l'Europe, vol. 81, no. 19, pp. 210, pp. L19608, (ISBN: 0-12-018847-3)
    Details
    Publication Date: 2000
    Keywords: Earth model, also for more shallow analyses ! ; Seismology ; Velocity depth profile ; double-prime
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    BIBLIOGRAPHY SEISMOLOGY
  • 8
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    An Eocene magmatic belt across central Tibet: mantle subduction triggered by the Indian collision? (2000)
    In:  Terra Nova, Oslo, Wiley, vol. 12, no. 3, pp. 102-108, pp. B08303, (ISSN: 1340-4202)
    Details
    Publication Date: 2000
    Keywords: Plate tectonics ; China ; Geol. aspects ; Volcanology ; Subduction zone ; Earth model, also for more shallow analyses ! ; Schaerer ; Scharer
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    BIBLIOGRAPHY SEISMOLOGY
  • 9
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    Gravitational stability of spherical self-gravitating relaxation models (2000)
    In:  Geophys. J. Int., Veldhoven, Kluwer, vol. 142, no. 2, pp. 351-360, pp. 2502, (ISSN: 1340-4202)
    Details
    Publication Date: 2000
    Keywords: Modelling ; Gravimetry, Gravitation ; Inelastic ; Rheology ; Earth model, also for more shallow analyses ! ; isostasy ; GJI
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    BIBLIOGRAPHY SEISMOLOGY
  • 10
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    Electrical conductivity and crustal structure beneath the central Hellenides around the Gulf of Corinth (Greece) and their relationship with the seismotectonics (2000)
    In:  Geophys. J. Int., Darmstadt, Wissenschaftliche Buchgesellschaft, vol. 142, no. 3, pp. 948-969, pp. B09404, (ISSN: 1340-4202)
    Details
    Publication Date: 2000
    Keywords: Earth model, also for more shallow analyses ! ; CRUST ; Anisotropy ; Electromagnetic methods/phenomena ; magneto-tellurics ; GJI
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    BIBLIOGRAPHY SEISMOLOGY
  • 11
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    Complete synthetic seismograms for 3-D heterogeneous Earth models computed using modified DSM operators and their applicability to inversion for Earth structure (2000)
    In:  Phys. Earth Plan. Int., Washington, D.C., AGU, vol. 119, no. 1-2, pp. 25-36, pp. 8011, (ISSN: 1340-4202)
    Details
    Publication Date: 2000
    Keywords: Modelling ; Synthetic seismograms ; Three dimensional ; Inhomogeneity ; PEPI ; Earth model, also for more shallow analyses ! ; Seismology
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    BIBLIOGRAPHY SEISMOLOGY
  • 12
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    Crustal versus asthenospheric relaxation and post-seismic deformation for shallow normal faulting earthquakes: the Umbria-Marche (central Italy) case (2000)
    In:  Geophys. J. Int., Tokyo, Lawrence Livermore National Laboratory, vol. 141, no. 3, pp. F7-F11, pp. L18610, (ISSN: 1340-4202)
    Details
    Publication Date: 2000
    Keywords: Crustal deformation (cf. Earthquake precursor: deformation or strain) ; Inelastic ; Rheology ; Earthquake ; Earth model, also for more shallow analyses ! ; Modelling
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    BIBLIOGRAPHY SEISMOLOGY
  • 13
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    Moho depth variation in southern California from teleseismic receiver functions (2000)
    In:  J. Geophys. Res., Kunming, China, 3-4, vol. 105, no. B2, pp. 2969-2980, pp. B05308, (ISSN: 1340-4202)
    Details
    Publication Date: 2000
    Keywords: Seismology ; Modelling ; Velocity depth profile ; Teleseismic events ; Earth model, also for more shallow analyses ! ; Plate tectonics ; Tectonics ; 7205 ; Seismology ; Continental ; crust ; (1242) ; 7260 ; Theory ; and ; modeling ; 8105 ; Tectonophysics ; Continental ; margins ; JGR ; sedimentary ; basins ; 8150 ; Plate ; boundary--general ; (3040)
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  • 14
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    Topography of the transition zone seismic discontinuities (2000)
    In:  Rev. Geophys., Luxembourg, Conseil de l'Europe, vol. 38, no. 1, pp. 141-158, pp. 1484, (ISSN 0343-5164)
    Details
    Publication Date: 2000
    Keywords: Earth model, also for more shallow analyses ! ; Seismology ; 410 ; 660 ; earth mantle ; Subduction zone ; Waves ; Wave propagation ; 3630 ; Mineralogy ; petrology ; rock ; chemistry ; Experimental ; mineralogy ; and ; petrology ; 3939 ; Mineral ; physics ; Physical ; thermodynamics ; 7203 ; Seismology ; Body ; wave ; propagation ; 8124 ; Tectonophysics ; Earth's ; interior--composition ; and ; state ; (old ; 8105)
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  • 15
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    Perspectives: neurobiology. The CRYs fo flies and mice (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hardin, P E -- Glossop, N R -- New York, N.Y. -- Science. 1999 Dec 24;286(5449):2460-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Houston, Houston, TX 77204, USA. phardin@uh.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10636810" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Animals ; Basic Helix-Loop-Helix Transcription Factors ; Biological Clocks/*physiology ; CLOCK Proteins ; Cell Cycle Proteins ; Circadian Rhythm/*physiology ; Cryptochromes ; Darkness ; Drosophila ; *Drosophila Proteins ; *Eye Proteins ; Feedback ; Flavoproteins/genetics/*physiology ; Gene Expression Regulation ; Light ; Mice ; Mice, Knockout ; Nuclear Proteins/*genetics/metabolism ; Period Circadian Proteins ; *Photoreceptor Cells, Invertebrate ; Promoter Regions, Genetic ; Receptors, G-Protein-Coupled ; Repressor Proteins/genetics/physiology ; Suprachiasmatic Nucleus/metabolism ; Trans-Activators/physiology ; Transcription Factors/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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  • 16
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    Photic induction of mPer1 and mPer2 in cry-deficient mice lacking a biological clock (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-05
    Description: Mice lacking mCry1 and mCry2 are behaviorally arrhythmic. As shown here, cyclic expression of the clock genes mPer1 and mPer2 (mammalian Period genes 1 and 2) in the suprachiasmatic nucleus and peripheral tissues is abolished and mPer1 and mPer2 mRNA levels are constitutively high. These findings indicate that the biological clock is eliminated in the absence of both mCRY1 and mCRY2 (mammalian cryptochromes 1 and 2) and support the idea that mammalian CRY proteins act in the negative limb of the circadian feedback loop. The mCry double-mutant mice retain the ability to have mPer1 and mPer2 expression induced by a brief light stimulus known to phase-shift the biological clock in wild-type animals. Thus, mCRY1 and mCRY2 are dispensable for light-induced phase shifting of the biological clock.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okamura, H -- Miyake, S -- Sumi, Y -- Yamaguchi, S -- Yasui, A -- Muijtjens, M -- Hoeijmakers, J H -- van der Horst, G T -- New York, N.Y. -- Science. 1999 Dec 24;286(5449):2531-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Brain Science, Kobe University School of Medicine, Kobe 650-0017, Japan. okamurah@kobe-u.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10617474" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks/*physiology ; Cell Cycle Proteins ; Circadian Rhythm/*physiology ; Cryptochromes ; *Drosophila Proteins ; *Eye Proteins ; Feedback ; Flavoproteins/genetics/*physiology ; Gene Expression Regulation ; In Situ Hybridization ; *Light ; Liver/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mutation ; Nuclear Proteins/*genetics ; Period Circadian Proteins ; *Photoreceptor Cells, Invertebrate ; Polymerase Chain Reaction ; RNA, Messenger/genetics/metabolism ; Receptors, G-Protein-Coupled ; Retina/metabolism ; Suprachiasmatic Nucleus/metabolism ; Transcription 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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  • 17
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    Leakage-resistant blood vessels in mice transgenically overexpressing angiopoietin-1 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-05
    Description: Angiopoietin-1 (Ang1) and vascular endothelial growth factor (VEGF) are endothelial cell-specific growth factors. Direct comparison of transgenic mice overexpressing these factors in the skin revealed that the VEGF-induced blood vessels were leaky, whereas those induced by Ang1 were nonleaky. Moreover, vessels in Ang1-overexpressing mice were resistant to leaks caused by inflammatory agents. Coexpression of Ang1 and VEGF had an additive effect on angiogenesis but resulted in leakage-resistant vessels typical of Ang1. Ang1 therefore may be useful for reducing microvascular leakage in diseases in which the leakage results from chronic inflammation or elevated VEGF and, in combination with VEGF, for promoting growth of nonleaky vessels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thurston, G -- Suri, C -- Smith, K -- McClain, J -- Sato, T N -- Yancopoulos, G D -- McDonald, D M -- HL-24136/HL/NHLBI NIH HHS/ -- HL-59157/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 Dec 24;286(5449):2511-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Cardiovascular Research Institute, University of California, San Francisco, CA 94143-0452, USA. gavint@itsa.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10617467" target="_blank"〉PubMed〈/a〉
    Keywords: Angiopoietin-1 ; Animals ; Arterioles/anatomy & histology/physiology ; Binding Sites ; Capillaries/anatomy & histology/physiology ; *Capillary Permeability ; Ear ; Endothelial Growth Factors/genetics/*physiology ; Endothelium, Vascular/metabolism ; Inflammation/chemically induced ; Inflammation Mediators/pharmacology ; Lymphokines/genetics/*physiology ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Mice, Transgenic ; Microcirculation/anatomy & histology/*physiology ; Mustard Plant ; *Neovascularization, Physiologic ; Plant Extracts/pharmacology ; Plant Lectins ; Plant Oils ; Plants, Medicinal ; Platelet Activating Factor/pharmacology ; Ricin/metabolism ; Serotonin/pharmacology ; Skin/blood supply/metabolism ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors ; Venules/anatomy & histology/physiology
    Print ISSN: 0036-8075
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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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    Role of the mouse ank gene in control of tissue calcification and arthritis (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-07-15
    Description: Mutation at the mouse progressive ankylosis (ank) locus causes a generalized, progressive form of arthritis accompanied by mineral deposition, formation of bony outgrowths, and joint destruction. Here, we show that the ank locus encodes a multipass transmembrane protein (ANK) that is expressed in joints and other tissues and controls pyrophosphate levels in cultured cells. A highly conserved gene is present in humans and other vertebrates. These results identify ANK-mediated control of pyrophosphate levels as a possible mechanism regulating tissue calcification and susceptibility to arthritis in higher animals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ho, A M -- Johnson, M D -- Kingsley, D M -- 5T32GM07365/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Jul 14;289(5477):265-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology and Howard Hughes Medical Institute, Beckman Center B300, Stanford University School of Medicine, Stanford, CA 94305-5327, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10894769" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis/*genetics/metabolism/pathology ; Base Sequence ; Biological Transport ; COS Cells ; Calcinosis/*genetics ; Chromosome Mapping ; Cloning, Molecular ; Dna ; Diphosphates/*metabolism ; Durapatite/metabolism ; Gene Expression ; Genetic Complementation Test ; Humans ; Membrane Proteins/*genetics/metabolism/*physiology ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Mutation ; Phenotype ; Phosphate Transport Proteins ; Physical Chromosome Mapping ; Sequence Homology, Nucleic Acid ; Tissue Distribution
    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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  • 19
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    Regulation of area identity in the mammalian neocortex by Emx2 and Pax6 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-04-15
    Description: The contribution of extrinsic and genetic mechanisms in determining areas of the mammalian neocortex has been a contested issue. This study analyzes the roles of the regulatory genes Emx2 and Pax6, which are expressed in opposing gradients in the neocortical ventricular zone, in specifying areas. Changes in the patterning of molecular markers and area-specific connections between the cortex and thalamus suggest that arealization of the neocortex is disproportionately altered in Emx2 and Pax6 mutant mice in opposing manners predicted from their countergradients of expression: rostral areas expand and caudal areas contract in Emx2 mutants, whereas the opposite effect is seen in Pax6 mutants. These findings suggest that Emx2 and Pax6 cooperate to regulate arealization of the neocortex and to confer area identity to cortical cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bishop, K M -- Goudreau, G -- O'Leary, D D -- NS31558/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2000 Apr 14;288(5464):344-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurobiology Laboratory, The Salk Institute for Biological Studies, 10010 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/10764649" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Mapping ; Cadherins/biosynthesis/genetics ; DNA-Binding Proteins/*genetics/physiology ; Eye Proteins ; *Gene Expression ; Gene Expression Regulation, Developmental ; *Genes, Homeobox ; *Genes, Regulator ; Homeodomain Proteins/*genetics/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Mice, Mutant Strains ; Morphogenesis ; Neocortex/*embryology/metabolism ; Neural Pathways ; Occipital Lobe/embryology/metabolism ; Paired Box Transcription Factors ; Repressor Proteins ; Somatosensory Cortex/embryology/metabolism ; Thalamus/embryology ; Transcription Factors ; Visual Cortex/embryology/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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  • 20
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    Effects of environment on compensatory mutations to ameliorate costs of antibiotic resistance (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-26
    Description: Most types of antibiotic resistance impose a biological cost on bacterial fitness. These costs can be compensated, usually without loss of resistance, by second-site mutations during the evolution of the resistant bacteria in an experimental host or in a laboratory medium. Different fitness-compensating mutations were selected depending on whether the bacteria evolved through serial passage in mice or in a laboratory medium. This difference in mutation spectra was caused by either a growth condition-specific formation or selection of the compensated mutants. These results suggest that bacterial evolution to reduce the costs of antibiotic resistance can take different trajectories within and outside a host.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bjorkman, J -- Nagaev, I -- Berg, O G -- Hughes, D -- Andersson, D I -- New York, N.Y. -- Science. 2000 Feb 25;287(5457):1479-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bacteriology, Swedish Institute for Infectious Disease Control, S-171 82 Solna, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10688795" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Animals ; Anti-Bacterial Agents/*pharmacology ; *Antiporters ; Carrier Proteins/genetics ; Culture Media ; Drug Resistance, Microbial/*genetics ; Escherichia coli Proteins ; Evolution, Molecular ; Female ; Fusidic Acid/pharmacology ; Membrane Proteins/genetics ; Mice ; Mice, Inbred BALB C ; *Mutation ; Peptide Elongation Factor G/genetics ; Ribosomal Proteins/genetics ; Salmonella typhimurium/*drug effects/*genetics/growth & development/metabolism ; Selection, Genetic ; Serial Passage ; Streptomycin/pharmacology ; Suppression, 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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  • 21
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    Prostaglandin D2 as a mediator of allergic asthma (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-17
    Description: Allergic asthma is caused by the aberrant expansion in the lung of T helper cells that produce type 2 (TH2) cytokines and is characterized by infiltration of eosinophils and bronchial hyperreactivity. This disease is often triggered by mast cells activated by immunoglobulin E (IgE)-mediated allergic challenge. Activated mast cells release various chemical mediators, including prostaglandin D2 (PGD2), whose role in allergic asthma has now been investigated by the generation of mice deficient in the PGD receptor (DP). Sensitization and aerosol challenge of the homozygous mutant (DP-/-) mice with ovalbumin (OVA) induced increases in the serum concentration of IgE similar to those in wild-type mice subjected to this model of asthma. However, the concentrations of TH2 cytokines and the extent of lymphocyte accumulation in the lung of OVA-challenged DP-/- mice were greatly reduced compared with those in wild-type animals. Moreover, DP-/- mice showed only marginal infiltration of eosinophils and failed to develop airway hyperreactivity. Thus, PGD2 functions as a mast cell-derived mediator to trigger asthmatic responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsuoka, T -- Hirata, M -- Tanaka, H -- Takahashi, Y -- Murata, T -- Kabashima, K -- Sugimoto, Y -- Kobayashi, T -- Ushikubi, F -- Aze, Y -- Eguchi, N -- Urade, Y -- Yoshida, N -- Kimura, K -- Mizoguchi, A -- Honda, Y -- Nagai, H -- Narumiya, S -- New York, N.Y. -- Science. 2000 Mar 17;287(5460):2013-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Kyoto University Faculty of Medicine, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10720327" target="_blank"〉PubMed〈/a〉
    Keywords: Allergens/immunology ; Animals ; Asthma/immunology/metabolism/pathology/*physiopathology ; Bronchial Hyperreactivity ; Bronchoalveolar Lavage Fluid/cytology/immunology ; Crosses, Genetic ; Female ; Gene Targeting ; Humans ; Immunoglobulin E/blood ; Interferon-gamma/metabolism ; Interleukins/metabolism ; Lung/immunology/metabolism/pathology ; Lymphocytes/immunology ; Male ; Mast Cells/metabolism ; Mice ; Mice, Inbred C57BL ; Mucus/secretion ; Ovalbumin/immunology ; Prostaglandin D2/metabolism/*physiology ; *Receptors, Immunologic ; Receptors, Prostaglandin/genetics/metabolism/*physiology ; Respiratory Mucosa/secretion
    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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    Localized Rac activation dynamics visualized in living cells (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-10-13
    Description: Signaling proteins are thought to be tightly regulated spatially and temporally in order to generate specific and localized effects. For Rac and other small guanosine triphosphatases, binding to guanosine triphosphate leads to interaction with downstream targets and regulates subcellular localization. A method called FLAIR (fluorescence activation indicator for Rho proteins) was developed to quantify the spatio-temporal dynamics of the Rac1 nucleotide state in living cells. FLAIR revealed precise spatial control of growth factor-induced Rac activation, in membrane ruffles and in a gradient of activation at the leading edge of motile cells. FLAIR exemplifies a generally applicable approach for examining spatio-temporal control of protein activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kraynov, V S -- Chamberlain, C -- Bokoch, G M -- Schwartz, M A -- Slabaugh, S -- Hahn, K M -- AG15430/AG/NIA NIH HHS/ -- GM39434/GM/NIGMS NIH HHS/ -- R01 GM-57464/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 2000 Oct 13;290(5490):333-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, The Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11030651" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Actins/metabolism ; Animals ; Biosensing Techniques ; Blood ; Cell Membrane/*enzymology/physiology/ultrastructure ; *Cell Movement ; Cell Nucleus/*enzymology ; Cell Polarity ; Enzyme Activation ; Fluorescence ; Guanosine Triphosphate/*metabolism ; Mice ; Nuclear Envelope/enzymology ; Platelet-Derived Growth Factor/pharmacology ; Recombinant Fusion Proteins/metabolism ; Spectrometry, Fluorescence ; rac1 GTP-Binding Protein/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Selective inhibition of NF-kappaB activation by a peptide that blocks the interaction of NEMO with the IkappaB kinase complex (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-01
    Description: Activation of the transcription factor nuclear factor (NF)-kappaB by proinflammatory stimuli leads to increased expression of genes involved in inflammation. Activation of NF-kappaB requires the activity of an inhibitor of kappaB (IkappaB)-kinase (IKK) complex containing two kinases (IKKalpha and IKKbeta) and the regulatory protein NEMO (NF-kappaB essential modifier). An amino-terminal alpha-helical region of NEMO associated with a carboxyl-terminal segment of IKKalpha and IKKbeta that we term the NEMO-binding domain (NBD). A cell-permeable NBD peptide blocked association of NEMO with the IKK complex and inhibited cytokine-induced NF-kappaB activation and NF-kappaB-dependent gene expression. The peptide also ameliorated inflammatory responses in two experimental mouse models of acute inflammation. The NBD provides a target for the development of drugs that would block proinflammatory activation of the IKK complex without inhibiting basal NF-kappaB activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉May, M J -- D'Acquisto, F -- Madge, L A -- Glockner, J -- Pober, J S -- Ghosh, S -- AI 33443/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2000 Sep 1;289(5484):1550-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology and Department of Molecular Biophysics and Biochemistry, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10968790" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/chemistry/pharmacology ; COS Cells ; Cells, Cultured ; E-Selectin/biosynthesis/genetics ; Endothelium, Vascular/metabolism ; Gene Expression Regulation ; HeLa Cells ; Humans ; I-kappa B Kinase ; Inflammation/drug therapy ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; NF-kappa B/*metabolism ; Peptides/chemistry/*pharmacology ; Point Mutation ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism
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    A role for histone acetylation in the developmental regulation of VDJ recombination (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-22
    Description: VDJ recombination is developmentally regulated in vivo by enhancer-dependent changes in the accessibility of chromosomal recombination signal sequences to the recombinase, but the molecular nature of these changes is unknown. Here histone H3 acetylation was measured along versions of a transgenic VDJ recombination reporter and the endogenous T cell receptor alpha/delta locus. Enhancer activity was shown to impart long-range, developmentally regulated changes in H3 acetylation, and H3 acetylation status was tightly linked to VDJ recombination. H3 hyperacetylation is proposed as a molecular mechanism coupling enhancer activity to accessibility for VDJ recombination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McMurry, M T -- Krangel, M S -- GM 41052/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Jan 21;287(5452):495-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Post Office Box 3010, 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/10642553" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Chromatin/metabolism ; DNA Nucleotidyltransferases/metabolism ; DNA-Binding Proteins/metabolism ; Enhancer Elements, Genetic ; *Gene Rearrangement, T-Lymphocyte ; *Genes, T-Cell Receptor alpha ; Genes, T-Cell Receptor beta ; *Genes, T-Cell Receptor delta ; Histones/*metabolism ; Homeodomain Proteins/metabolism ; Humans ; Mice ; Mice, Transgenic ; Nuclear Proteins ; Protein Sorting Signals ; *Recombination, Genetic ; T-Lymphocytes/*metabolism ; Transgenes ; VDJ Recombinases
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    Functional requirement for class I MHC in CNS development and plasticity (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-16
    Description: Class I major histocompatibility complex (class I MHC) molecules, known to be important for immune responses to antigen, are expressed also by neurons that undergo activity-dependent, long-term structural and synaptic modifications. Here, we show that in mice genetically deficient for cell surface class I MHC or for a class I MHC receptor component, CD3zeta, refinement of connections between retina and central targets during development is incomplete. In the hippocampus of adult mutants, N-methyl-D-aspartate receptor-dependent long-term potentiation (LTP) is enhanced, and long-term depression (LTD) is absent. Specific class I MHC messenger RNAs are expressed by distinct mosaics of neurons, reflecting a potential for diverse neuronal functions. These results demonstrate an important role for these molecules in the activity-dependent remodeling and plasticity of connections in the developing and mature mammalian central nervous system (CNS).〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2175035/" 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/PMC2175035/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huh, G S -- Boulanger, L M -- Du, H -- Riquelme, P A -- Brotz, T M -- Shatz, C J -- 1F32EY07016/EY/NEI NIH HHS/ -- EY06912/EY/NEI NIH HHS/ -- F32 EY007016/EY/NEI NIH HHS/ -- F32 EY007016-02/EY/NEI NIH HHS/ -- F32 EY007016-03/EY/NEI NIH HHS/ -- MH48108/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 15;290(5499):2155-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA. gshuh@alum.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11118151" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD3/genetics/*physiology ; Brain/growth & development/*physiology ; Excitatory Postsynaptic Potentials ; Gene Expression Profiling ; Genes, MHC Class I ; Geniculate Bodies/physiology ; Hippocampus/growth & development/physiology ; Histocompatibility Antigens Class I/genetics/*physiology ; In Situ Hybridization ; Long-Term Potentiation ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Mutant Strains ; Neural Pathways ; *Neuronal Plasticity ; Neurons/*physiology ; Receptors, GABA-A/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Retina/growth & development/physiology ; Retinal Ganglion Cells/physiology ; Signal Transduction ; Synapses/*physiology ; Synaptic Transmission ; Visual Pathways
    Print ISSN: 0036-8075
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    Property claims. A deluge of patents creates legal hassles for research (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-04-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 2000 Apr 14;288(5464):255-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10777404" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biotechnology ; Drug Industry ; Europe ; Genome ; Mice ; *Mice, Knockout/genetics ; *Mice, Transgenic/genetics ; National Institutes of Health (U.S.) ; *Patents as Topic ; *Research/legislation & jurisprudence ; Sequence Analysis, DNA ; Technology Transfer ; United States ; Universities
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    Epitopes involved in antibody-mediated protection from Ebola virus (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-04
    Description: To determine the ability of antibodies to provide protection from Ebola viruses, monoclonal antibodies (mAbs) to the Ebola glycoprotein were generated and evaluated for efficacy. We identified several protective mAbs directed toward five unique epitopes on Ebola glycoprotein. One of the epitopes is conserved among all Ebola viruses that are known to be pathogenic for humans. Some protective mAbs were also effective therapeutically when administered to mice 2 days after exposure to lethal Ebola virus. The identification of protective mAbs has important implications for developing vaccines and therapies for Ebola virus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, J A -- Hevey, M -- Bakken, R -- Guest, S -- Bray, M -- Schmaljohn, A L -- Hart, M K -- New York, N.Y. -- Science. 2000 Mar 3;287(5458):1664-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Virology Division, U.S. Army Medical Research Institute of Infectious Diseases, 1425 Porter Street, Fort Detrick, Frederick, MD 21702-5011, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10698744" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/*immunology ; Antibodies, Viral/*immunology ; Antibody Affinity ; Antigens, Viral/immunology ; Binding, Competitive ; Complement System Proteins/immunology ; Ebolavirus/*immunology/physiology ; Epitopes/immunology ; Female ; Hemorrhagic Fever, Ebola/*prevention & control/therapy ; Humans ; Immunoglobulin G/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Neutralization Tests ; Specific Pathogen-Free Organisms ; Viral Envelope Proteins/*immunology ; Viral Plaque Assay
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    Crystal structure of a gammadelta T cell receptor ligand T22: a truncated MHC-like fold (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-15
    Description: Murine T10 and T22 are highly related nonclassical major histocompatibility complex (MHC) class Ib proteins that bind to certain gammadelta T cell receptors (TCRs) in the absence of other components. The crystal structure of T22b at 3.1 angstroms reveals similarities to MHC class I molecules, but one side of the normal peptide-binding groove is severely truncated, which allows direct access to the beta-sheet floor. Potential gammadelta TCR-binding sites can be inferred from functional mapping of T10 and T22 point mutants and allelic variants. Thus, T22 represents an unusual variant of the MHC-like fold and indicates that gammadelta and alphabeta TCRs interact differently with their respective MHC ligands.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wingren, C -- Crowley, M P -- Degano, M -- Chien, Y -- Wilson, I A -- AI33431/AI/NIAID NIH HHS/ -- CA58896/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2000 Jan 14;287(5451):310-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and the Skaggs Institute for Chemical Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10634787" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Substitution ; Animals ; Binding Sites ; Crystallography, X-Ray ; Glycosylation ; Histocompatibility Antigens Class I/*chemistry ; Hydrogen Bonding ; Ligands ; Mice ; Models, Molecular ; Point Mutation ; Protein Conformation ; Protein Folding ; Protein Structure, Quaternary ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Proteins/*chemistry/immunology/metabolism ; Receptors, Antigen, T-Cell, gamma-delta/immunology/*metabolism ; Surface Properties ; beta 2-Microglobulin/chemistry
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    Treatment of murine colitis by Lactococcus lactis secreting interleukin-10 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-08-26
    Description: The cytokine interleukin-10 (IL-10) has shown promise in clinical trials for treatment of inflammatory bowel disease (IBD). Using two mouse models, we show that the therapeutic dose of IL-10 can be reduced by localized delivery of a bacterium genetically engineered to secrete the cytokine. Intragastric administration of IL-10-secreting Lactococcus lactis caused a 50% reduction in colitis in mice treated with dextran sulfate sodium and prevented the onset of colitis in IL-10(-/-) mice. This approach may lead to better methods for cost-effective and long-term management of IBD in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steidler, L -- Hans, W -- Schotte, L -- Neirynck, S -- Obermeier, F -- Falk, W -- Fiers, W -- Remaut, E -- New York, N.Y. -- Science. 2000 Aug 25;289(5483):1352-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Ghent University and Flanders Interuniversity Institute for Biotechnology, K. L. Ledeganckstraat 35, 9000 Gent, Belgium. lothar.steidler@dmb.rug.ac.be〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10958782" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport ; Colitis/immunology/pathology/prevention & control/therapy ; Colon/immunology/metabolism/microbiology/pathology ; Dextran Sulfate ; Inflammatory Bowel Diseases/immunology/pathology/prevention & control/*therapy ; Interleukin-10/*administration & dosage/*biosynthesis/genetics/metabolism ; Intestinal Mucosa/metabolism/pathology ; Lactococcus lactis/*genetics/immunology/*metabolism ; Mice ; Probiotics/*therapeutic use ; Recombinant Proteins/administration & dosage/biosynthesis/metabolism
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    Involvement of cellular caveolae in bacterial entry into mast cells (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-08-05
    Description: Caveolae are subcellular structures implicated in the import and transcytosis of macromolecules and in transmembrane signaling. To date, evidence for the existence of caveolae in hematopoietic cells has been ambiguous. Caveolae were detected in the microvilli and intracellular vesicles of cultured mouse bone marrow-derived mast cells (BMMCs). CD48, a receptor for FimH-expressing (type 1 fimbriated) Escherichia coli, was specifically localized to plasmalemmal caveolae in BMMCs. The involvement of caveolae in bacterial entry into BMMCs was indicated because caveolae-disrupting and -usurping agents specifically blocked E. coli entry, and markers of caveolae were actively recruited to sites of bacterial entry. The formation of bacteria-encapsulating caveolar chambers in BMMCs represents a distinct mechanism of microbial entry into phagocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shin, J S -- Gao, Z -- Abraham, S N -- AI 35678/AI/NIAID NIH HHS/ -- CA 14236/CA/NCI NIH HHS/ -- DK 50814/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2000 Aug 4;289(5480):785-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Pathology and Microbiology, 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/10926542" target="_blank"〉PubMed〈/a〉
    Keywords: Adhesins, Bacterial/*metabolism ; *Adhesins, Escherichia coli ; Animals ; Antigens, CD/analysis/*metabolism ; Bacterial Adhesion ; Caveolin 1 ; *Caveolins ; Cell Fractionation ; Cell Membrane/chemistry/*metabolism/microbiology/ultrastructure ; Cholera Toxin/pharmacology ; Cyclodextrins/pharmacology ; *Endocytosis ; Escherichia coli/*metabolism/pathogenicity ; *Fimbriae Proteins ; Glycosylphosphatidylinositols/analysis ; Mast Cells/*metabolism/*microbiology/ultrastructure ; Membrane Proteins/analysis ; Mice ; Microscopy, Confocal ; Microscopy, Fluorescence ; Microscopy, Immunoelectron
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    Intellectual property. NIH cuts deal on use of OncoMouse (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 2000 Jan 28;287(5453):567.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10691532" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Mice ; *Mice, Transgenic ; *National Institutes of Health (U.S.) ; *Neoplasms, Experimental ; *Patents as Topic ; Research Support as Topic ; United States
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    Lipid research. Possible new way to lower cholesterol (2000)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2000-09-19
    Description: Clinicians may soon be able to mount a multipronged attack against cholesterol, the artery-clogging lipid whose buildup in the body is a major contributor to heart attacks and other cardiovascular diseases. In work reported on page 1524, a team has pinpointed a biological master switch in mice that controls three pathways that work together to both rid the body of excess cholesterol and prevent its absorption from the intestine. The work suggests a new mechanism for reducing cholesterol, for example, with drugs that turn up the activity of the master switch, a protein known as the retinoid X receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferber, D -- New York, N.Y. -- Science. 2000 Sep 1;289(5484):1446-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10991725" target="_blank"〉PubMed〈/a〉
    Keywords: ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters/*metabolism ; Animals ; Bile Acids and Salts ; Biological Transport/drug effects ; Cholesterol/*metabolism ; Cholesterol, Dietary/administration & dosage ; DNA-Binding Proteins/metabolism ; Glycoproteins/*metabolism ; Humans ; Intestinal Absorption/drug effects ; Intestines/drug effects/*metabolism ; Liver/metabolism ; Macrophages/metabolism ; Mice ; Orphan Nuclear Receptors ; *Receptors, Cytoplasmic and Nuclear ; Receptors, Retinoic Acid/*metabolism ; Receptors, Thyroid Hormone/metabolism ; Retinoid X Receptors ; Transcription Factors/*metabolism
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    Immunology. A touch of antibody class (2000)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2000-06-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stavnezer, J -- New York, N.Y. -- Science. 2000 May 12;288(5468):984-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, 55 Lake Avenue N., Worcester, MA 01655, USA. Janet.Stavnezer@umassmed.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10841719" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology ; Cytokines/immunology ; DNA/genetics/*metabolism ; Genes, Immunoglobulin ; *Immunoglobulin Class Switching ; Immunoglobulin Heavy Chains/genetics ; *Immunoglobulin Switch Region ; Mice ; Mice, Transgenic ; Models, Genetic ; *Nucleic Acid Hybridization ; RNA/genetics/*metabolism ; RNA Splicing ; Recombination, Genetic ; Ribonuclease H/genetics/metabolism ; Templates, Genetic ; Transcription, Genetic
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    Regulation of cell fate decision of undifferentiated spermatogonia by GDNF (2000)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2000-02-26
    Description: The molecular control of self-renewal and differentiation of stem cells has remained enigmatic. Transgenic loss-of-function and overexpression models now show that the dosage of glial cell line-derived neurotrophic factor (GDNF), produced by Sertoli cells, regulates cell fate decisions of undifferentiated spermatogonial cells that include the stem cells for spermatogenesis. Gene-targeted mice with one GDNF-null allele show depletion of stem cell reserves, whereas mice overexpressing GDNF show accumulation of undifferentiated spermatogonia. They are unable to respond properly to differentiation signals and undergo apoptosis upon retinoic acid treatment. Nonmetastatic testicular tumors are regularly formed in older GDNF-overexpressing mice. Thus, GDNF contributes to paracrine regulation of spermatogonial self-renewal and differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meng, X -- Lindahl, M -- Hyvonen, M E -- Parvinen, M -- de Rooij, D G -- Hess, M W -- Raatikainen-Ahokas, A -- Sainio, K -- Rauvala, H -- Lakso, M -- Pichel, J G -- Westphal, H -- Saarma, M -- Sariola, H -- New York, N.Y. -- Science. 2000 Feb 25;287(5457):1489-93.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Programs of Developmental Biology, Molecular Neurobiology, Electron Microscopy Unit, Institute of Biotechnology, Viikki Biocenter, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10688798" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/drug effects ; Cell Cycle ; Cell Differentiation/drug effects ; Cobalt/metabolism ; *Drosophila Proteins ; Female ; Gene Expression ; Gene Targeting ; Glial Cell Line-Derived Neurotrophic Factor ; Glial Cell Line-Derived Neurotrophic Factor Receptors ; Male ; Mice ; Mice, Transgenic ; Mitosis ; *Nerve Growth Factors ; Nerve Tissue Proteins/genetics/*physiology ; Proto-Oncogene Proteins/genetics/metabolism ; Proto-Oncogene Proteins c-ret ; Receptor Protein-Tyrosine Kinases/genetics/metabolism ; Sertoli Cells/cytology/physiology ; *Spermatogenesis ; Spermatogonia/*cytology/drug effects ; Stem Cells/*cytology ; Testicular Neoplasms/pathology ; Testis/anatomy & histology ; Vitamin A/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Two-amino acid molecular switch in an epithelial morphogen that regulates binding to two distinct receptors (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-10-20
    Description: Ectodysplasin, a member of the tumor necrosis factor family, is encoded by the anhidrotic ectodermal dysplasia (EDA) gene. Mutations in EDA give rise to a clinical syndrome characterized by loss of hair, sweat glands, and teeth. EDA-A1 and EDA-A2 are two isoforms of ectodysplasin that differ only by an insertion of two amino acids. This insertion functions to determine receptor binding specificity, such that EDA-A1 binds only the receptor EDAR, whereas EDA-A2 binds only the related, but distinct, X-linked ectodysplasin-A2 receptor (XEDAR). In situ binding and organ culture studies indicate that EDA-A1 and EDA-A2 are differentially expressed and play a role in epidermal morphogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yan, M -- Wang, L C -- Hymowitz, S G -- Schilbach, S -- Lee, J -- Goddard, A -- de Vos, A M -- Gao, W Q -- Dixit, V M -- New York, N.Y. -- Science. 2000 Oct 20;290(5491):523-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Oncology, 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/11039935" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Binding Sites ; Cell Line ; DNA-Binding Proteins/metabolism ; Ectodermal Dysplasia/genetics ; Ectodysplasins ; Epidermis/embryology/*metabolism ; Humans ; *I-kappa B Proteins ; In Situ Hybridization ; Ligands ; Membrane Proteins/*chemistry/*metabolism ; Mice ; Models, Molecular ; Molecular Sequence Data ; Morphogenesis ; NF-kappa B/metabolism ; Phosphorylation ; Point Mutation ; Protein Conformation ; Proteins/metabolism ; Receptors, Cell Surface/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; TNF Receptor-Associated Factor 6 ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Induction and maintenance of the neuronal cholinergic phenotype in the central nervous system by BMP-9 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-07-15
    Description: Bone morphogenetic proteins (BMPs) have multiple functions in the developing nervous system. A member of this family, BMP-9, was found to be highly expressed in the embryonic mouse septum and spinal cord, indicating a possible role in regulating the cholinergic phenotype. In cultured neurons, BMP-9 directly induced the expression of the cholinergic gene locus encoding choline acetyltransferase and the vesicular acetylcholine transporter and up-regulated acetylcholine synthesis. The effect was reversed upon withdrawal of BMP-9. Intracerebroventricular injection of BMP-9 increased acetylcholine levels in vivo. Although certain other BMPs also up-regulated the cholinergic phenotype in vitro, they were less effective than BMP-9. These data indicate that BMP-9 is a differentiating factor for cholinergic central nervous system neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lopez-Coviella, I -- Berse, B -- Krauss, R -- Thies, R S -- Blusztajn, J K -- P01 AG09525/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2000 Jul 14;289(5477):313-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry and Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA 02118, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10894782" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/biosynthesis ; Animals ; Bone Morphogenetic Proteins/*physiology ; Carrier Proteins/genetics ; Cells, Cultured ; Central Nervous System ; Choline O-Acetyltransferase/genetics ; Embryo, Mammalian/metabolism ; Fibroblast Growth Factor 2/physiology ; Gene Expression Regulation, Developmental ; Gene Expression Regulation, Enzymologic ; Growth Differentiation Factor 2 ; *Membrane Transport Proteins ; Mice ; Neurons/metabolism ; Phenotype ; RNA, Messenger/metabolism ; Septum of Brain/embryology/metabolism ; Spinal Cord/embryology/metabolism ; Up-Regulation ; Vesicular Acetylcholine Transport Proteins ; *Vesicular Transport Proteins
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    Transgenic mouse model of stunned myocardium (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-22
    Description: Stunned myocardium is a syndrome of reversible contractile failure that frequently complicates coronary artery disease. Cardiac excitation is uncoupled from contraction at the level of the myofilaments. Selective proteolysis of the thin filament protein troponin I has been correlated with stunned myocardium. Here, transgenic mice expressing the major degradation product of troponin I (TnI1-193) in the heart were found to develop ventricular dilatation, diminished contractility, and reduced myofilament calcium responsiveness, recapitulating the phenotype of stunned myocardium. Proteolysis of troponin I also occurs in ischemic human cardiac muscle. Thus, troponin I proteolysis underlies the pathogenesis of a common acquired form of heart failure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphy, A M -- Kogler, H -- Georgakopoulos, D -- McDonough, J L -- Kass, D A -- Van Eyk, J E -- Marban, E -- HL 44065/HL/NHLBI NIH HHS/ -- HL 63038/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2000 Jan 21;287(5452):488-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Johns Hopkins University School of Medicine, Ross Building 1144, 720 Rutland Avenue, Baltimore, MD 21205, USA. murphy@jhmi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10642551" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/metabolism ; Adrenergic beta-Agonists/pharmacology ; Animals ; Calcium/metabolism ; Cardiomegaly/pathology ; Dilatation, Pathologic ; *Disease Models, Animal ; Heart Rate ; Heart Ventricles/pathology ; Humans ; Isoproterenol/pharmacology ; Mice ; Mice, Inbred C57BL ; *Mice, Transgenic ; Myocardial Contraction ; Myocardial Stunning/*metabolism/pathology/physiopathology ; Myocardium/*metabolism/pathology ; Myofibrils/metabolism ; Troponin I/genetics/*metabolism ; Ventricular Function, Left
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    Perspectives: drug delivery. Regulating export of ER cargo (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aridor, M -- Balch, W E -- New York, N.Y. -- Science. 2000 Feb 4;287(5454):816-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Biology, Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10691557" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport ; Cell Line ; Drug Delivery Systems ; Endoplasmic Reticulum/*metabolism/secretion ; Golgi Apparatus/metabolism ; Growth Hormone/chemistry/metabolism/secretion ; Immunophilins/chemistry/metabolism ; Insulin/chemistry/metabolism/secretion ; Ligands ; Mice ; Models, Biological ; Protein Conformation ; Protein Engineering ; Protein Folding ; Recombinant Fusion Proteins/*chemistry/*metabolism/secretion ; Tacrolimus Binding Proteins
    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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    Role of the enteric nervous system in the fluid and electrolyte secretion of rotavirus diarrhea (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-22
    Description: The mechanism underlying the intestinal fluid loss in rotavirus diarrhea, which often afflicts children in developing countries, is not known. One hypothesis is that the rotavirus evokes intestinal fluid and electrolyte secretion by activation of the nervous system in the intestinal wall, the enteric nervous system (ENS). Four different drugs that inhibit ENS functions were used to obtain experimental evidence for this hypothesis in mice in vitro and in vivo. The involvement of the ENS in rotavirus diarrhea indicates potential sites of action for drugs in the treatment of the disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lundgren, O -- Peregrin, A T -- Persson, K -- Kordasti, S -- Uhnoo, I -- Svensson, L -- New York, N.Y. -- Science. 2000 Jan 21;287(5452):491-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Goteborg University, Box 432, S-405 30 Goteborg, Sweden. ove.lundgren@fysiologi.gu.se〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10642552" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Body Water/*secretion ; Diarrhea/drug therapy/*physiopathology ; Electrolytes/*metabolism ; Enteric Nervous System/drug effects/*physiopathology ; Hexamethonium/pharmacology ; In Vitro Techniques ; Intestinal Mucosa/drug effects/*secretion ; Intestine, Small/innervation ; Lidocaine/pharmacology ; Mecamylamine/pharmacology ; Mice ; Mice, Inbred BALB C ; Nicotinic Antagonists/pharmacology ; Patch-Clamp Techniques ; Rotavirus Infections/drug therapy/*physiopathology ; Synaptic Transmission/drug effects ; Tetrodotoxin/pharmacology ; Theophylline/pharmacology
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    Regulation of antigen-specific CD8+ T cell homeostasis by perforin and interferon-gamma (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-11-18
    Description: T cell memory depends on factors that regulate expansion and death of these cells after antigenic stimulation. Mice deficient in perforin and interferon-gamma (IFN-gamma) exhibited increased expansion, altered immunodominance, and decreased death of antigen-specific CD8+ T cells after infection with an attenuated strain of Listeria monocytogenes, which was cleared from these mice. Expansion of CD8+ T cells was controlled by perforin, whereas IFN-gamma regulated immunodominance and the death phase. Thus, perforin and IFN-gamma regulate distinct elements of CD8+ T cell homeostasis independently of their role as antimicrobial effector molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Badovinac, V P -- Tvinnereim, A R -- Harty, J T -- AI36864/AI/NIAID NIH HHS/ -- AI42767/AI/NIAID NIH HHS/ -- T32AI07511/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 2000 Nov 17;290(5495):1354-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Interdisciplinary Graduate Program in Immunology, 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/11082062" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; Antigens, Bacterial/immunology ; Apoptosis ; CD8-Positive T-Lymphocytes/cytology/*immunology ; Homeostasis ; Immunodominant Epitopes/*immunology ; *Immunologic Memory ; Interferon-gamma/*physiology ; Listeria monocytogenes/immunology ; Listeriosis/*immunology ; Lymphocytic Choriomeningitis/immunology ; Membrane Glycoproteins/*physiology ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Perforin ; Pore Forming Cytotoxic Proteins
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    Inhibition of experimental liver cirrhosis in mice by telomerase gene delivery (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-26
    Description: Accelerated telomere loss has been proposed to be a factor leading to end-stage organ failure in chronic diseases of high cellular turnover such as liver cirrhosis. To test this hypothesis directly, telomerase-deficient mice, null for the essential telomerase RNA (mTR) gene, were subjected to genetic, surgical, and chemical ablation of the liver. Telomere dysfunction was associated with defects in liver regeneration and accelerated the development of liver cirrhosis in response to chronic liver injury. Adenoviral delivery of mTR into the livers of mTR(-/-) mice with short dysfunctional telomeres restored telomerase activity and telomere function, alleviated cirrhotic pathology, and improved liver function. These studies indicate that telomere dysfunction contributes to chronic diseases of continual cellular loss-replacement and encourage the evaluation of "telomerase therapy" for such diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rudolph, K L -- Chang, S -- Millard, M -- Schreiber-Agus, N -- DePinho, R A -- K08 AG001019/AG/NIA NIH HHS/ -- R01HD28317/HD/NICHD NIH HHS/ -- R01HD34880/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2000 Feb 18;287(5456):1253-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Adult Oncology, Medicine and Genetics, Dana-Farber Cancer Institute, 44 Binney Street (M413), and Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10678830" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Animals ; Apoptosis ; Carbon Tetrachloride/toxicity ; Gene Transfer Techniques ; *Genetic Therapy ; Genetic Vectors ; Hepatectomy ; Liver/enzymology/*pathology ; Liver Cirrhosis, Experimental/enzymology/pathology/physiopathology/*therapy ; *Liver Regeneration ; Mice ; Mice, Knockout ; Mice, Transgenic ; Mitosis ; Spleen/enzymology ; Telomerase/*genetics/metabolism ; Telomere/physiology/ultrastructure ; Transforming Growth Factor beta/metabolism
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    CD95/CD95 ligand interactions on epithelial cells in host defense to Pseudomonas aeruginosa (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-10-20
    Description: Pseudomonas aeruginosa causes severe infections, particularly of the lung, that are life threatening. Here, we show that P. aeruginosa infection induces apoptosis of lung epithelial cells by activation of the endogenous CD95/CD95 ligand system. Deficiency of CD95 or CD95 ligand on epithelial cells prevented apoptosis of lung epithelial cells in vivo as well as in vitro. The importance of CD95/CD95 ligand-mediated lung epithelial cell apoptosis was demonstrated by the rapid development of sepsis in CD95- or CD95 ligand-deficient mice, but not in normal mice, after P. aeruginosa infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grassme, H -- Kirschnek, S -- Riethmueller, J -- Riehle, A -- von Kurthy, G -- Lang, F -- Weller, M -- Gulbins, E -- New York, N.Y. -- Science. 2000 Oct 20;290(5491):527-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Tuebingen, Gmelinstrasse 5, 72076 Tuebingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11039936" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/genetics/*metabolism ; *Apoptosis ; Bone Marrow Transplantation ; Cell Line ; Epithelial Cells/*immunology/microbiology/pathology ; Fas Ligand Protein ; Humans ; In Situ Nick-End Labeling ; Lung/*immunology/microbiology/pathology ; Lung Diseases/*immunology/microbiology/pathology ; Membrane Glycoproteins/genetics/*metabolism ; Mice ; Mice, Inbred C3H ; Pseudomonas Infections/*immunology/microbiology/pathology ; Pseudomonas aeruginosa/immunology/*pathogenicity ; Sepsis/microbiology ; Spleen/microbiology
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    Spongiform disease. Experts downplay new vCJD fears (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balter, M -- New York, N.Y. -- Science. 2000 Sep 8;289(5485):1663-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11001722" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Animals, Domestic ; Carrier State/*veterinary ; Cattle ; Creutzfeldt-Jakob Syndrome/epidemiology/prevention & control/*transmission ; Cricetinae ; Encephalopathy, Bovine Spongiform/epidemiology/prevention & control/*transmission ; Great Britain/epidemiology ; Humans ; Mice ; Prion Diseases/*transmission ; Species Specificity
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    Biomedicine. Protein loss in cancer cachexia (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-10-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tisdale, M J -- New York, N.Y. -- Science. 2000 Sep 29;289(5488):2293-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pharmaceutical Sciences Research Institute, Aston University, Birmingham B4 7ET, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11041796" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Proteins/metabolism ; Cachexia/drug therapy/etiology/*metabolism/pathology ; Cell Differentiation ; Cysteine Endopeptidases/genetics/metabolism ; Cytokines/pharmacology ; Homeostasis ; Humans ; Interferon-gamma/pharmacology ; Mice ; Multienzyme Complexes/genetics/metabolism ; Muscle Proteins/*metabolism ; Muscle, Skeletal/cytology/*metabolism/pathology ; MyoD Protein/genetics/metabolism ; Myosins/genetics/metabolism ; NF-kappa B/*metabolism ; Neoplasms/*complications ; Promoter Regions, Genetic ; Proteasome Endopeptidase Complex ; Proteoglycans ; Transcription, Genetic ; Tumor Necrosis Factor-alpha/pharmacology ; Ubiquitins/metabolism
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    A primitive T cell-independent mechanism of intestinal mucosal IgA responses to commensal bacteria (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-06-24
    Description: The immunoglobulin A (IgA) is produced to defend mucosal surfaces from environmental organisms, but host defenses against the very heavy load of intestinal commensal microorganisms are poorly understood. The IgA against intestinal commensal bacterial antigens was analyzed; it was not simply "natural antibody" but was specifically induced and responded to antigenic changes within an established gut flora. In contrast to IgA responses against exotoxins, a significant proportion of this specific anti-commensal IgA induction was through a pathway that was independent of T cell help and of follicular lymphoid tissue organization, which may reflect an evolutionarily primitive form of specific immune defense.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Macpherson, A J -- Gatto, D -- Sainsbury, E -- Harriman, G R -- Hengartner, H -- Zinkernagel, R M -- New York, N.Y. -- Science. 2000 Jun 23;288(5474):2222-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Experimental Immunology, Universitatsspital, Schmelzbergstrasse 12, CH8091, Zurich, Switzerland. amacpher@pathol.unizh.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10864873" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Specificity ; Antigens, Bacterial/immunology ; B-Lymphocytes/*immunology ; Bacterial Proteins/immunology ; Enterobacter cloacae/*immunology ; Escherichia coli/*immunology ; Genes, T-Cell Receptor ; Germ-Free Life ; *Immunity, Mucosal ; Immunoglobulin A, Secretory/*biosynthesis/immunology ; Intestinal Mucosa/*immunology/microbiology ; Lipopolysaccharides/immunology ; Mice ; Mice, Inbred C57BL ; Peritoneum/cytology ; Plasma Cells/immunology ; Porins/immunology ; Specific Pathogen-Free Organisms ; T-Lymphocytes/*immunology
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    Genetics. Was Lamarck just a little bit right? (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balter, M -- New York, N.Y. -- Science. 2000 Apr 7;288(5463):38.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10766632" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; *DNA Methylation ; France ; *Gene Expression Regulation ; Gene Silencing ; Hair Color/genetics ; History, 18th Century ; History, 19th Century ; Mice ; *Mutation ; Plants/genetics
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    Requirement of JNK for stress-induced activation of the cytochrome c-mediated death pathway (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-05-08
    Description: The c-Jun NH2-terminal kinase (JNK) is activated when cells are exposed to ultraviolet (UV) radiation. However, the functional consequence of JNK activation in UV-irradiated cells has not been established. It is shown here that JNK is required for UV-induced apoptosis in primary murine embryonic fibroblasts. Fibroblasts with simultaneous targeted disruptions of all the functional Jnk genes were protected against UV-stimulated apoptosis. The absence of JNK caused a defect in the mitochondrial death signaling pathway, including the failure to release cytochrome c. These data indicate that mitochondria are influenced by proapoptotic signal transduction through the JNK pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tournier, C -- Hess, P -- Yang, D D -- Xu, J -- Turner, T K -- Nimnual, A -- Bar-Sagi, D -- Jones, S N -- Flavell, R A -- Davis, R J -- New York, N.Y. -- Science. 2000 May 5;288(5467):870-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Program in Molecular Medicine, Department of Biochemistry & Molecular Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10797012" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptotic Protease-Activating Factor 1 ; Caspase 3 ; Caspase 9 ; Caspases/metabolism ; Cell Count ; Cell Division ; Cells, Cultured ; Cytochrome c Group/*metabolism ; DNA Fragmentation ; Enzyme Activation ; Fibroblasts ; Gene Targeting ; JNK Mitogen-Activated Protein Kinases ; MAP Kinase Signaling System ; Methyl Methanesulfonate/pharmacology ; Mice ; Mitochondria/metabolism ; Mitogen-Activated Protein Kinases/genetics/*metabolism ; NF-kappa B/metabolism ; *Protein-Serine-Threonine Kinases ; Proteins/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Tumor Suppressor Protein p53/metabolism ; Ultraviolet Rays
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Structural mechanism for STI-571 inhibition of abelson tyrosine kinase (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-16
    Description: The inadvertent activation of the Abelson tyrosine kinase (Abl) causes chronic myelogenous leukemia (CML). A small-molecule inhibitor of Abl (STI-571) is effective in the treatment of CML. We report the crystal structure of the catalytic domain of Abl, complexed to a variant of STI-571. Critical to the binding of STI-571 is the adoption by the kinase of an inactive conformation, in which a centrally located "activation loop" is not phosphorylated. The conformation of this loop is distinct from that in active protein kinases, as well as in the inactive form of the closely related Src kinases. These results suggest that compounds that exploit the distinctive inactivation mechanisms of individual protein kinases can achieve both high affinity and high specificity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schindler, T -- Bornmann, W -- Pellicena, P -- Miller, W T -- Clarkson, B -- Kuriyan, J -- GM29362/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Sep 15;289(5486):1938-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratories of Molecular Biophysics and Howard Hughes Medical Institute, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10988075" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/chemistry/*pharmacology ; Benzamides ; Catalytic Domain ; Crystallography, X-Ray ; Enzyme Activation ; Enzyme Inhibitors/chemistry/*pharmacology ; Humans ; Imatinib Mesylate ; Mice ; Models, Molecular ; Phosphorylation ; *Piperazines ; Protein Conformation ; Proto-Oncogene Proteins c-abl/*antagonists & inhibitors/chemistry/metabolism ; Pyrimidines/chemistry/*pharmacology ; Recombinant Fusion Proteins ; Structure-Activity Relationship
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A structural framework for deciphering the link between I-Ag7 and autoimmune diabetes (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-04-25
    Description: Susceptibility to murine and human insulin-dependent diabetes mellitus correlates strongly with major histocompatibility complex (MHC) class II I-A or HLA-DQ alleles that lack an aspartic acid at position beta57. I-Ag7 lacks this aspartate and is the only class II allele expressed by the nonobese diabetic mouse. The crystal structure of I-Ag7 was determined at 2.6 angstrom resolution as a complex with a high-affinity peptide from the autoantigen glutamic acid decarboxylase (GAD) 65. I-Ag7 has a substantially wider peptide-binding groove around beta57, which accounts for distinct peptide preferences compared with other MHC class II alleles. Loss of Asp(beta57) leads to an oxyanion hole in I-Ag7 that can be filled by peptide carboxyl residues or, perhaps, through interaction with the T cell receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Corper, A L -- Stratmann, T -- Apostolopoulos, V -- Scott, C A -- Garcia, K C -- Kang, A S -- Wilson, I A -- Teyton, L -- CA58896/CA/NCI NIH HHS/ -- DK55037/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2000 Apr 21;288(5465):505-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Skaggs Institute for Chemical Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10775108" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Aspartic Acid/chemistry ; Crystallography, X-Ray ; Diabetes Mellitus, Type 1/*immunology ; Drosophila melanogaster ; *Genes, MHC Class II ; Glutamate Decarboxylase/metabolism ; Histocompatibility Antigens Class II/*chemistry/genetics/metabolism ; Humans ; Hydrogen Bonding ; Mice ; Mice, Inbred NOD ; Models, Molecular ; Molecular Sequence Data ; Peptide Library ; Protein Binding ; Protein Conformation ; Protein Structure, Secondary ; Receptors, Antigen, T-Cell/metabolism ; Recombinant Proteins/chemistry/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Development of CD8alpha-positive dendritic cells from a common myeloid progenitor (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-16
    Description: Dendritic cells (DCs) are critical in both initiating adaptive immune responses and maintaining tolerance to self antigens. These apparently contradictory roles have been suggested to depend on different subsets of DCs that arise from either myeloid or lymphoid hematopoietic origins, respectively. Although DC expression of CD8alpha is attributed to a lymphoid origin, here we show that both CD8alpha+ and CD8alpha- DCs can arise from clonogenic common myeloid progenitors in both thymus and spleen. Thus, expression of CD8alpha is not indicative of a lymphoid origin, and phenotypic and functional differences among DC subsets are likely to reflect maturation status rather than ontogeny.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Traver, D -- Akashi, K -- Manz, M -- Merad, M -- Miyamoto, T -- Engleman, E G -- Weissman, I L -- 5T32 AI-07290/AI/NIAID NIH HHS/ -- CA42551/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 15;290(5499):2152-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11118150" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/analysis ; Antigens, CD8/*analysis ; B-Lymphocytes/cytology/immunology ; Cell Lineage ; Dendritic Cells/*cytology/*immunology ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/cytology ; Immunophenotyping ; Mice ; Mice, Inbred C57BL ; Myeloid Progenitor Cells/*cytology/transplantation ; Spleen/*cytology/immunology ; T-Lymphocytes/cytology/immunology ; Thymus Gland/*cytology/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Obesity. Enzyme blocker prompts mice to shed weight (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-08-05
    Description: A multidisciplinary team may have discovered an important new weapon in the battle of the bulge. On page 2379 of this issue, the team reports that a molecule that is needed for fat synthesis in the body may play a key role in appetite signaling in the brain. Moreover, the investigators produced a synthetic inhibitor of this molecule that spurred a dramatic drop in appetite and weight in mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gura, T -- New York, N.Y. -- Science. 2000 Jun 30;288(5475):2299-300.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10917820" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Appetite/drug effects ; Appetite Depressants/*pharmacology ; Brain/metabolism ; Enzyme Inhibitors/*pharmacology ; Fasting ; Fatty Acid Synthases/*antagonists & inhibitors ; Humans ; Liver/drug effects/metabolism ; Malonyl Coenzyme A/metabolism ; Mice ; Neuropeptide Y/genetics/metabolism ; Obesity/*drug therapy ; RNA, Messenger/genetics/metabolism ; Weight Loss/*drug effects
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    Circadian rhythms. Two feedback loops run mammalian clock (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-06-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 2000 May 12;288(5468):943-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10841707" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Animals ; Basic Helix-Loop-Helix Transcription Factors ; Biological Clocks/genetics/*physiology ; CLOCK Proteins ; Cell Cycle Proteins ; Cell Nucleus/metabolism ; Circadian Rhythm/genetics/*physiology ; Cryptochromes ; Drosophila/metabolism ; *Drosophila Proteins ; *Eye Proteins ; Feedback ; Flavoproteins/genetics/*metabolism ; *Gene Expression Regulation ; Mice ; Mutation ; Nuclear Proteins/genetics/*metabolism ; Period Circadian Proteins ; *Photoreceptor Cells, Invertebrate ; Receptors, G-Protein-Coupled ; Trans-Activators/genetics/metabolism ; Transcription Factors/genetics/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 53
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    Transport of peptide-MHC class II complexes in developing dendritic cells (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-04-25
    Description: Major histocompatibility complex class II (MHC II) molecules capture peptides within the endocytic pathway to generate T cell receptor (TCR) ligands. Immature dendritic cells (DCs) sequester intact antigens in lysosomes, processing and converting antigens into peptide-MHC II complexes upon induction of DC maturation. The complexes then accumulate in distinctive, nonlysosomal MHC II+ vesicles that appear to migrate to the cell surface. Although the vesicles exclude soluble lysosomal contents and antigen-processing machinery, many contain MHC I and B7 costimulatory molecules. After arrival at the cell surface, the MHC and costimulatory molecules remain clustered. Thus, transport of peptide-MHC II complexes by DCs not only accomplishes transfer from late endocytic compartments to the plasma membrane, but does so in a manner that selectively concentrates TCR ligands and costimulatory molecules for T cell contact.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Turley, S J -- Inaba, K -- Garrett, W S -- Ebersold, M -- Unternaehrer, J -- Steinman, R M -- Mellman, I -- AI-13013/AI/NIAID NIH HHS/ -- AI-34098/AI/NIAID NIH HHS/ -- AI-39672/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2000 Apr 21;288(5465):522-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Section of Immunobiology, Ludwig Institute for Cancer Research, Yale University School of Medicine, 333 Cedar Street, Post Office Box 208002, New Haven, CT 06520-8002, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10775112" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; *Antigen Presentation ; Antigens, CD/immunology/metabolism ; Antigens, CD86 ; B-Lymphocytes/immunology/metabolism ; Bicyclo Compounds, Heterocyclic/pharmacology ; Biological Transport ; Cell Membrane/immunology/metabolism ; Cells, Cultured ; Dendritic Cells/*immunology/*metabolism ; Endocytosis ; Endosomes/immunology/metabolism ; Histocompatibility Antigens Class I/immunology/metabolism ; Histocompatibility Antigens Class II/immunology/*metabolism ; Kinetics ; Ligands ; Lipopolysaccharides/immunology ; Lysosomes/immunology/metabolism ; Membrane Glycoproteins/immunology/metabolism ; Mice ; Mice, Inbred C3H ; Muramidase/immunology/*metabolism ; Peptide Fragments/immunology/*metabolism ; Receptors, Antigen, T-Cell/metabolism ; Thiazoles/pharmacology ; Thiazolidines
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Angiogenesis research. Cancer drugs found to work in new way (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-04-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 2000 Apr 14;288(5464):245.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10777399" target="_blank"〉PubMed〈/a〉
    Keywords: Angiogenesis Inhibitors/*administration & dosage/therapeutic use/toxicity ; Animals ; Antineoplastic Combined Chemotherapy Protocols/*administration & ; dosage/therapeutic use/toxicity ; Clinical Trials as Topic ; Cyclohexanes ; Humans ; Mice ; Neoplasms/*drug therapy/pathology ; Neoplasms, Experimental/drug therapy/pathology ; Neovascularization, Pathologic/*drug therapy/pathology ; Sesquiterpenes/administration & dosage/therapeutic use
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    Family of bitter taste receptors found (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-04-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 2000 Mar 24;287(5461):2133-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10744529" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Chemoreceptor Cells/*physiology ; Humans ; Mice ; Multigene Family ; Receptors, Cell Surface/genetics/*physiology ; *Taste ; Taste Buds/*physiology ; Transducin/biosynthesis
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    NF-kappaB-induced loss of MyoD messenger RNA: possible role in muscle decay and cachexia (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-29
    Description: MyoD regulates skeletal muscle differentiation (SMD) and is essential for repair of damaged tissue. The transcription factor nuclear factor kappa B (NF-kappaB) is activated by the cytokine tumor necrosis factor (TNF), a mediator of skeletal muscle wasting in cachexia. Here, the role of NF-kappaB in cytokine-induced muscle degeneration was explored. In differentiating C2C12 myocytes, TNF-induced activation of NF-kappaB inhibited SMD by suppressing MyoD mRNA at the posttranscriptional level. In contrast, in differentiated myotubes, TNF plus interferon-gamma (IFN-gamma) signaling was required for NF-kappaB-dependent down-regulation of MyoD and dysfunction of skeletal myofibers. MyoD mRNA was also down-regulated by TNF and IFN-gamma expression in mouse muscle in vivo. These data elucidate a possible mechanism that may underlie the skeletal muscle decay in cachexia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guttridge, D C -- Mayo, M W -- Madrid, L V -- Wang, C Y -- Baldwin, A S Jr -- AI35098/AI/NIAID NIH HHS/ -- CA72771/CA/NCI NIH HHS/ -- K01 CA78595/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2000 Sep 29;289(5488):2363-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lineberger Comprehensive Cancer Center, Curriculum in Genetics and Molecular Biology, Department of Biology, University of North Carolina, Chapel Hill, Mason Farm Road, Campus Box 7295, Chapel Hill, NC, 27599-7295, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11009425" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CHO Cells ; Cachexia/*etiology/metabolism/pathology ; Cell Differentiation ; Cell Line ; Cricetinae ; DNA-Binding Proteins/genetics/metabolism ; Down-Regulation ; *I-kappa B Proteins ; Interferon-gamma/pharmacology ; Interleukins/pharmacology ; Mice ; Mice, Inbred Strains ; Mice, Nude ; Muscle, Skeletal/*cytology/*metabolism/pathology ; MyoD Protein/*genetics/metabolism ; NF-kappa B/genetics/*metabolism ; RNA, Messenger/genetics/metabolism ; Transcription Factor RelA ; Transcription, Genetic ; Transfection ; Tumor Necrosis Factor-alpha/*pharmacology
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    Allosteric effects of Pit-1 DNA sites on long-term repression in cell type specification (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-11-10
    Description: Reciprocal gene activation and restriction during cell type differentiation from a common lineage is a hallmark of mammalian organogenesis. A key question, then, is whether a critical transcriptional activator of cell type-specific gene targets can also restrict expression of the same genes in other cell types. Here, we show that whereas the pituitary-specific POU domain factor Pit-1 activates growth hormone gene expression in one cell type, the somatotrope, it restricts its expression from a second cell type, the lactotrope. This distinction depends on a two-base pair spacing in accommodation of the bipartite POU domains on a conserved growth hormone promoter site. The allosteric effect on Pit-1, in combination with other DNA binding factors, results in the recruitment of a corepressor complex, including nuclear receptor corepressor N-CoR, which, unexpectedly, is required for active long-term repression of the growth hormone gene in lactotropes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scully, K M -- Jacobson, E M -- Jepsen, K -- Lunyak, V -- Viadiu, H -- Carriere, C -- Rose, D W -- Hooshmand, F -- Aggarwal, A K -- Rosenfeld, M G -- R01 DK18477/DK/NIDDK NIH HHS/ -- R01 DK54802/DK/NIDDK NIH HHS/ -- R01 GM49327/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Nov 10;290(5494):1127-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Endocrinology and Metabolism, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11073444" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Regulation ; Animals ; Base Sequence ; Binding Sites ; Cell Line ; Conserved Sequence ; Crystallization ; DNA/*metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Female ; *Gene Expression Regulation ; Genes, Reporter ; Growth Hormone/*genetics ; Male ; Mice ; Mice, Transgenic ; Models, Molecular ; Molecular Sequence Data ; Nuclear Proteins/genetics/metabolism ; Nuclear Receptor Co-Repressor 1 ; Pituitary Gland/cytology/*metabolism ; Prolactin/*genetics ; Promoter Regions, Genetic ; Protein Conformation ; Protein Structure, Tertiary ; Rats ; Repressor Proteins/chemistry/genetics/*metabolism ; Transcription Factor Pit-1 ; Transcription Factors/chemistry/genetics/*metabolism ; Transcriptional Activation
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    Requirement for DARPP-32 in progesterone-facilitated sexual receptivity in female rats and mice (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-11
    Description: DARPP-32, a dopamine- and adenosine 3',5'-monophosphate (cAMP)-regulated phosphoprotein (32 kilodaltons in size), is an obligate intermediate in progesterone (P)-facilitated sexual receptivity in female rats and mice. The facilitative effect of P on sexual receptivity in female rats was blocked by antisense oligonucleotides to DARPP-32. Homozygous mice carrying a null mutation for the DARPP-32 gene exhibited minimal levels of P-facilitated sexual receptivity when compared to their wild-type littermates. P significantly increased hypothalamic cAMP levels and cAMP-dependent protein kinase activity. These increases were not inhibited by a D1 subclass dopamine receptor antagonist. P also enhanced phosphorylation of DARPP-32 on threonine 34 in the hypothalamus of mice. DARPP-32 activation is thus an obligatory step in progestin receptor regulation of sexual receptivity in rats and mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mani, S K -- Fienberg, A A -- O'Callaghan, J P -- Snyder, G L -- Allen, P B -- Dash, P K -- Moore, A N -- Mitchell, A J -- Bibb, J -- Greengard, P -- O'Malley, B W -- MH49662/MH/NIMH NIH HHS/ -- MH57442/MH/NIMH NIH HHS/ -- NS 35457/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 2000 Feb 11;287(5455):1053-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA. smani@bcm.tmc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10669419" target="_blank"〉PubMed〈/a〉
    Keywords: 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine/pharmacology ; Animals ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Dopamine/pharmacology ; Dopamine Agonists/pharmacology ; Dopamine and cAMP-Regulated Phosphoprotein 32 ; Female ; Hypothalamus/metabolism ; Injections, Intraventricular ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; *Nerve Tissue Proteins ; Oligonucleotides, Antisense/pharmacology ; Phosphoproteins/genetics/*metabolism ; Phosphorylation ; Posture ; Progesterone/*pharmacology ; Proteins/genetics/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Progesterone/metabolism ; Serotonin/pharmacology ; Sexual Behavior, Animal/*drug effects ; Signal Transduction
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    Perspectives: signal transduction. Signals to move cells (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dekker, L V -- Segal, A W -- New York, N.Y. -- Science. 2000 Feb 11;287(5455):982-3, 985.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Molecular Medicine, University College London, London, UK. rmhalvd@ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10691572" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/metabolism ; Chemotaxis/*physiology ; Chemotaxis, Leukocyte/*physiology ; Enzyme Activation ; GTP Phosphohydrolases/metabolism ; Heterotrimeric GTP-Binding Proteins/metabolism ; Isoenzymes/metabolism ; Leukocytes/physiology ; Macrophages/physiology ; Mice ; Mice, Knockout ; Phosphatidylinositol 3-Kinases/*metabolism ; Phosphatidylinositol Phosphates/metabolism ; *Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Receptors, Formyl Peptide ; Receptors, Immunologic/metabolism ; Receptors, Interleukin/metabolism ; Receptors, Interleukin-8A ; Receptors, Peptide/metabolism ; *Signal Transduction ; rac GTP-Binding Proteins/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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    Enhanced morphine analgesia in mice lacking beta-arrestin 2 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-05
    Description: The ability of morphine to alleviate pain is mediated through a heterotrimeric guanine nucleotide binding protein (G protein)-coupled heptahelical receptor (GPCR), the mu opioid receptor (muOR). The efficiency of GPCR signaling is tightly regulated and ultimately limited by the coordinated phosphorylation of the receptors by specific GPCR kinases and the subsequent interaction of the phosphorylated receptors with beta-arrestin 1 and beta-arrestin 2. Functional deletion of the beta-arrestin 2 gene in mice resulted in remarkable potentiation and prolongation of the analgesic effect of morphine, suggesting that muOR desensitization was impaired. These results provide evidence in vivo for the physiological importance of beta-arrestin 2 in regulating the function of a specific GPCR, the muOR. Moreover, they suggest that inhibition of beta-arrestin 2 function might lead to enhanced analgesic effectiveness of morphine and provide potential new avenues for the study and treatment of pain, narcotic tolerance, and dependence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bohn, L M -- Lefkowitz, R J -- Gainetdinov, R R -- Peppel, K -- Caron, M G -- Lin, F T -- F32 DA006023/DA/NIDA NIH HHS/ -- HL16037/HL/NHLBI NIH HHS/ -- NS 19576/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Dec 24;286(5449):2495-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute Laboratories, Departments of Cell Biology and Medicine, 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/10617462" target="_blank"〉PubMed〈/a〉
    Keywords: Analgesia ; Analgesics, Opioid/administration & dosage/metabolism/*pharmacology ; Animals ; Arrestins/genetics/*physiology ; Binding Sites ; Body Temperature/drug effects ; Brain/metabolism ; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-/pharmacology ; GTP-Binding Proteins/metabolism ; Guanosine 5'-O-(3-Thiotriphosphate)/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Morphine/administration & dosage/metabolism/*pharmacology ; Naloxone/metabolism/pharmacology ; Narcotic Antagonists/metabolism/pharmacology ; Pain Measurement ; Pain Threshold ; Phosphorylation ; Receptors, Opioid, mu/*metabolism ; Signal Transduction
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    Bracing p53 for the war on cancer (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1999 Dec 24;286(5449):2431.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10636794" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/chemistry/*pharmacology/therapeutic use ; Cell Division/drug effects ; DNA/metabolism ; Genes, p53 ; Humans ; Mice ; Mutation ; Neoplasms, Experimental/drug therapy/pathology ; *Protein Folding ; Pyrimidines/chemistry/*pharmacology ; Tumor Suppressor Protein p53/*chemistry/genetics/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Breakthrough of the year. Capturing the promise of youth (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, G -- New York, N.Y. -- Science. 1999 Dec 17;286(5448):2238-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10636772" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Bioethics ; *Biomedical Research ; Cell Culture Techniques ; Cell Differentiation ; Cell Line ; *Embryo Research ; Embryo, Mammalian/*cytology ; Humans ; Internationality ; Mice ; Public Policy ; *Stem Cells/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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    Molecular biology. Tackling biology with no holds barred, at 800 miles per hour (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-08-05
    Description: Peter Schultz launched his academic career by exploring what made living organisms such powerful synthetic chemists. His work led him to conclude that the key to nature's success was its strategy of generating millions of possible chemical solutions to a problem and then screening for the ones that worked best. Now Schultz is applying this approach to working out the functions of the thousands of unknown genes being turned out by the world's genome projects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, R F -- New York, N.Y. -- Science. 2000 Jul 14;289(5477):233.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10917843" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Catalytic/chemistry ; *Bacteria/chemistry/genetics ; Biology ; Chemistry/*trends ; Chemistry, Pharmaceutical ; Combinatorial Chemistry Techniques ; Mice
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    Hot pepper receptor could help manage pain (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-04-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, G -- New York, N.Y. -- Science. 2000 Apr 14;288(5464):241-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10777396" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Capsaicin/metabolism/*pharmacology ; *Hot Temperature ; Mice ; Mice, Knockout ; Neurons, Afferent/physiology ; Nociceptors/*physiology ; Pain/drug therapy/*physiopathology ; Receptors, Drug/*physiology ; TRPV Cation Channels
    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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    Prevention of acute liver failure in rats with reversibly immortalized human hepatocytes (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-26
    Description: Because of a critical shortage in suitable organs, many patients with terminal liver disease die each year before liver transplantation can be performed. Transplantation of isolated hepatocytes has been proposed for the temporary metabolic support of patients awaiting liver transplantation or spontaneous reversion of their liver disease. A major limitation of this form of therapy is the present inability to isolate an adequate number of transplantable hepatocytes. A highly differentiated cell line, NKNT-3, was generated by retroviral transfer in normal primary adult human hepatocytes of an immortalizing gene that can be subsequently and completely excised by Cre/Lox site-specific recombination. When transplanted into the spleen of rats under transient immunosuppression, reversibly immortalized NKNT-3 cells provided life-saving metabolic support during acute liver failure induced by 90% hepatectomy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kobayashi, N -- Fujiwara, T -- Westerman, K A -- Inoue, Y -- Sakaguchi, M -- Noguchi, H -- Miyazaki, M -- Cai, J -- Tanaka, N -- Fox, I J -- Leboulch, P -- DK48794/DK/NIDDK NIH HHS/ -- HL55435/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2000 Feb 18;287(5456):1258-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉First Department of Surgery and Department of Cell Biology, Okayama University Medical School, 2-5-1 Shikata-cho, Okayama 700-8558, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10678831" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Antigens, Polyomavirus Transforming/genetics ; Cell Culture Techniques/*methods ; Cell Differentiation ; Cell Line ; *Cell Transplantation ; Gene Expression ; Genetic Vectors ; Hepatectomy ; Humans ; Integrases/metabolism ; Liver/*cytology/metabolism/pathology ; Liver Failure, Acute/metabolism/pathology/*prevention & control/therapy ; Liver Regeneration ; Mice ; Mice, SCID ; Rats ; Retroviridae/genetics ; Spleen/cytology ; Transfection ; *Viral Proteins
    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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    Can old cells learn new tricks? (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, G -- New York, N.Y. -- Science. 2000 Feb 25;287(5457):1418-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10722390" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animal Experimentation ; Animals ; Bioethics ; *Biomedical Research ; Bone Marrow Cells/cytology/physiology ; Cell Differentiation ; Cell Separation ; Cell Transplantation ; Cells, Cultured ; Child ; *Embryo Research ; Embryo, Mammalian/*cytology ; Federal Government ; Humans ; Mice ; Middle Aged ; Stem Cells/*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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    From marrow to brain: expression of neuronal phenotypes in adult mice (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-02
    Description: After intravascular delivery of genetically marked adult mouse bone marrow into lethally irradiated normal adult hosts, donor-derived cells expressing neuronal proteins (neuronal phenotypes) developed in the central nervous system. Flow cytometry revealed a population of donor-derived cells in the brain with characteristics distinct from bone marrow. Confocal microscopy of individual cells showed that hundreds of marrow-derived cells in brain sections expressed gene products typical of neurons (NeuN, 200-kilodalton neurofilament, and class III beta-tubulin) and were able to activate the transcription factor cAMP response element-binding protein (CREB). The generation of neuronal phenotypes in the adult brain 1 to 6 months after an adult bone marrow transplant demonstrates a remarkable plasticity of adult tissues with potential clinical applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brazelton, T R -- Rossi, F M -- Keshet, G I -- Blau, H M -- AG09521/AG/NIA NIH HHS/ -- CA59717/CA/NCI NIH HHS/ -- HD18179/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 1;290(5497):1775-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Pharmacology, CCSR 4215, 269 Campus Drive, Stanford University, Stanford, CA 94305-5175, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11099418" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers/analysis ; Bone Marrow Cells/*cytology ; *Bone Marrow Transplantation ; Brain/*cytology ; Cell Differentiation ; Cell Size ; Cyclic AMP Response Element-Binding Protein/metabolism ; Flow Cytometry ; Gene Expression ; Green Fluorescent Proteins ; Luminescent Proteins/analysis ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microscopy, Confocal ; Nerve Tissue Proteins/analysis/genetics ; Neurons/chemistry/*cytology/metabolism ; Olfactory Bulb/cytology ; Phenotype ; Phosphorylation
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    How rotavirus causes diarrhea (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 2000 Jan 21;287(5452):409, 411.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10671159" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Water/secretion ; Diarrhea/*physiopathology ; Enteric Nervous System/drug effects/*physiopathology ; Intestinal Mucosa/drug effects/secretion ; Intestine, Small/innervation ; Lidocaine/pharmacology ; Mice ; Rotavirus Infections/*physiopathology ; Synaptic Transmission/drug effects
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The genetic program of hematopoietic stem cells (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-06-02
    Description: Blood cell production originates from a rare population of multipotent, self-renewing stem cells. A genome-wide gene expression analysis was performed in order to define regulatory pathways in stem cells as well as their global genetic program. Subtracted complementary DNA libraries from highly purified murine fetal liver stem cells were analyzed with bioinformatic and array hybridization strategies. A large percentage of the several thousand gene products that have been characterized correspond to previously undescribed molecules with properties suggestive of regulatory functions. The complete data, available in a biological process-oriented database, represent the molecular phenotype of the hematopoietic stem cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Phillips, R L -- Ernst, R E -- Brunk, B -- Ivanova, N -- Mahan, M A -- Deanehan, J K -- Moore, K A -- Overton, G C -- Lemischka, I R -- R01-DK42989/DK/NIDDK NIH HHS/ -- R01-RR04026/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2000 Jun 2;288(5471):1635-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10834841" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Computational Biology ; Databases, Factual ; Expressed Sequence Tags ; *Gene Expression Profiling ; Gene Library ; *Genes ; Hematopoietic Stem Cells/chemistry/cytology/*physiology ; Liver/cytology/embryology ; Membrane Proteins/chemistry/genetics/physiology ; Mice ; Molecular Sequence Data ; Polymerase Chain Reaction ; Proteins/chemistry/*genetics/*physiology ; Signal Transduction ; Transcription Factors/chemistry/genetics/physiology
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    Immunology. Lymphocyte survival--ignorance is BLys (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-08-29
    Description: As if the TNF receptor and ligand superfamily was not big enough, two new receptors and their ligands have now been added to it. As Laabi and Strasser explain in their Perspective, the receptors BCMA and TACI and their ligands BAFF/BLys and APRIL, respectively, are important for B lymphocyte survival, proliferation, and differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Laabi, Y -- Strasser, A -- New York, N.Y. -- Science. 2000 Aug 11;289(5481):883-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, Post Office Royal Victoria, Australia. laabi@wehi.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10960320" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; B-Cell Activating Factor ; B-Cell Maturation Antigen ; B-Lymphocytes/*cytology/*immunology/metabolism ; CD40 Ligand ; Cell Differentiation ; Cell Division ; Cell Survival ; Cytokines/metabolism ; Humans ; Ligands ; Lymphocyte Activation ; Membrane Glycoproteins/metabolism ; Membrane Proteins/*metabolism ; Mice ; NF-kappa B/metabolism ; Neoplasms/etiology/pathology ; Receptors, Antigen, B-Cell/metabolism ; Receptors, Tumor Necrosis Factor/*metabolism ; Signal Transduction ; Transcription Factors/metabolism ; Transmembrane Activator and CAML Interactor Protein ; Tumor Necrosis Factor Ligand Superfamily Member 13 ; Tumor Necrosis Factor-alpha/*metabolism
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    Toxicity of ALS-linked SOD1 mutants (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-05-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williamson, T L -- Corson, L B -- Huang, L -- Burlingame, A -- Liu, J -- Bruijn, L I -- Cleveland, D W -- New York, N.Y. -- Science. 2000 Apr 21;288(5465):399.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Institute for Cancer Research, University of California at San Diego, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10798964" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/*enzymology/genetics/pathology ; Animals ; Apoptosis ; Cells, Cultured ; Copper/metabolism ; Humans ; Mice ; Motor Neurons/metabolism/*pathology ; Mutation ; Neurofilament Proteins/metabolism ; Nitrates/metabolism ; Superoxide Dismutase/*genetics/*metabolism ; Yeasts/cytology/metabolism ; Zinc/*metabolism/toxicity
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Response of Schwann cells to action potentials in development (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-24
    Description: Sensory axons become functional late in development when Schwann cells (SC) stop proliferating and differentiate into distinct phenotypes. We report that impulse activity in premyelinated axons can inhibit proliferation and differentiation of SCs. This neuron-glial signaling is mediated by adenosine triphosphate acting through P2 receptors on SCs and intracellular signaling pathways involving Ca2+, Ca2+/calmodulin kinase, mitogen-activated protein kinase, cyclic adenosine 3',5'-monophosphate response element binding protein, and expression of c-fos and Krox-24. Adenosine triphosphate arrests maturation of SCs in an immature morphological stage and prevents expression of O4, myelin basic protein, and the formation of myelin. Through this mechanism, functional activity in the developing nervous system could delay terminal differentiation of SCs until exposure to appropriate axon-derived signals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stevens, B -- Fields, R D -- New York, N.Y. -- Science. 2000 Mar 24;287(5461):2267-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Developmental Neurobiology, National Institutes of Health, National Institute of Child Health and Human Development, Building 49, Room 5A38, 49 Convent Drive, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10731149" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Adenosine Triphosphate/metabolism ; Animals ; Axons/*physiology ; Calcium/metabolism ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Differentiation ; Cell Division ; Cells, Cultured ; Coculture Techniques ; Cyclic AMP Response Element-Binding Protein/metabolism ; DNA-Binding Proteins/genetics/metabolism ; Early Growth Response Protein 1 ; Electric Stimulation ; Ganglia, Spinal/physiology ; Gene Expression Regulation, Developmental ; Genes, fos ; *Immediate-Early Proteins ; Mice ; Microscopy, Confocal ; Myelin Sheath/metabolism ; Neurons, Afferent/*physiology ; Phosphorylation ; Proto-Oncogene Proteins c-fos/metabolism ; Receptors, Purinergic P2/metabolism ; Schwann Cells/*cytology/*physiology ; Signal Transduction ; Transcription Factors/genetics/metabolism
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    Alzheimer's congress. Further progress on a beta-amyloid vaccine (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-08-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Helmuth, L -- New York, N.Y. -- Science. 2000 Jul 21;289(5478):375.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10939941" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*drug therapy/immunology/pathology/psychology ; Amyloid beta-Peptides/administration & dosage/*immunology ; Animals ; Antibodies/analysis ; Autoimmunity ; Clinical Trials, Phase I as Topic ; Humans ; *Maze Learning ; *Memory, Short-Term ; Mice ; Plaque, Amyloid/pathology ; Vaccination ; Vaccines/*therapeutic use
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    NMDA receptor-dependent synaptic reinforcement as a crucial process for memory consolidation (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-11-10
    Description: The hippocampal CA1 region is crucial for converting new memories into long-term memories, a process believed to continue for week(s) after initial learning. By developing an inducible, reversible, and CA1-specific knockout technique, we could switch N-methyl-D-aspartate (NMDA) receptor function off or on in CA1 during the consolidation period. Our data indicate that memory consolidation depends on the reactivation of the NMDA receptor, possibly to reinforce site-specific synaptic modifications to consolidate memory traces. Such a synaptic reinforcement process may also serve as a cellular means by which the new memory is transferred from the hippocampus to the cortex for permanent storage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shimizu, E -- Tang, Y P -- Rampon, C -- Tsien, J Z -- New York, N.Y. -- Science. 2000 Nov 10;290(5494):1170-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Princeton University, Princeton, NJ 08544-1014, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11073458" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conditioning (Psychology) ; Doxycycline/pharmacology ; Excitatory Postsynaptic Potentials ; Fear ; Green Fluorescent Proteins ; Hippocampus/*physiology ; Long-Term Potentiation ; Luminescent Proteins/biosynthesis ; Maze Learning ; Memory/*physiology ; Mice ; Mice, Knockout ; Mice, Transgenic ; Receptors, AMPA/physiology ; Receptors, N-Methyl-D-Aspartate/genetics/*physiology ; Retention (Psychology) ; Synapses/*physiology ; Synaptic Transmission ; Time Factors
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The glucocorticoid receptor: rapid exchange with regulatory sites in living cells (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-26
    Description: Steroid receptors bind to site-specific response elements in chromatin and modulate gene expression in a hormone-dependent fashion. With the use of a tandem array of mouse mammary tumor virus reporter elements and a form of glucocorticoid receptor labeled with green fluorescent protein, targeting of the receptor to response elements in live mouse cells was observed. Photobleaching experiments provide direct evidence that the hormone-occupied receptor undergoes rapid exchange between chromatin and the nucleoplasmic compartment. Thus, the interaction of regulatory proteins with target sites in chromatin is a more dynamic process than previously believed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McNally, J G -- Muller, W G -- Walker, D -- Wolford, R -- Hager, G L -- New York, N.Y. -- Science. 2000 Feb 18;287(5456):1262-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Receptor Biology and Gene Expression, Building 41, Room B602, National Cancer Institute, Bethesda, MD 20892-5055, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10678832" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Cell Line, Transformed ; Cell Nucleus/metabolism ; Chromatin/*metabolism ; Dexamethasone/metabolism/*pharmacology ; Green Fluorescent Proteins ; In Situ Hybridization, Fluorescence ; Ligands ; Luminescent Proteins ; Mammary Tumor Virus, Mouse/genetics ; Mice ; Microscopy, Confocal ; Microscopy, Fluorescence ; Nucleosomes/metabolism ; Receptors, Glucocorticoid/*metabolism ; *Response Elements ; *Terminal Repeat Sequences
    Print ISSN: 0036-8075
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    Inflammation dampened by gelatinase A cleavage of monocyte chemoattractant protein-3 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-08-19
    Description: Tissue degradation by the matrix metalloproteinase gelatinase A is pivotal to inflammation and metastases. Recognizing the catalytic importance of substrate-binding exosites outside the catalytic domain, we screened for extracellular substrates using the gelatinase A hemopexin domain as bait in the yeast two-hybrid system. Monocyte chemoattractant protein-3 (MCP-3) was identified as a physiological substrate of gelatinase A. Cleaved MCP-3 binds to CC-chemokine receptors-1, -2, and -3, but no longer induces calcium fluxes or promotes chemotaxis, and instead acts as a general chemokine antagonist that dampens inflammation. This suggests that matrix metalloproteinases are both effectors and regulators of the inflammatory response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McQuibban, G A -- Gong, J H -- Tam, E M -- McCulloch, C A -- Clark-Lewis, I -- Overall, C M -- New York, N.Y. -- Science. 2000 Aug 18;289(5482):1202-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Biomedical Research Centre, University of British Columbia, Vancouver, BC V6T 1Z3, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10947989" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Catalytic Domain ; Cell Line ; Chemokine CCL7 ; Chemokines/antagonists & inhibitors/metabolism ; Chemotaxis, Leukocyte ; Collagen/metabolism ; *Cytokines ; Enzyme Activation ; Gene Library ; Hemopexin/chemistry/metabolism ; Humans ; Inflammation/*metabolism/pathology ; Mass Spectrometry ; Matrix Metalloproteinase 2/chemistry/*metabolism ; Mice ; Monocyte Chemoattractant Proteins/*metabolism ; Protein Binding ; Protein Structure, Tertiary ; Receptors, Chemokine/antagonists & inhibitors/metabolism ; Recombinant Proteins/metabolism ; Tissue Inhibitor of Metalloproteinase-2/metabolism ; Two-Hybrid System Techniques
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    A critical role for murine complement regulator crry in fetomaternal tolerance (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-22
    Description: Complement is a component of natural immunity. Its regulation is needed to protect tissues from inflammation, but mice with a disrupted gene for the complement regulator decay accelerating factor were normal. Mice that were deficient in another murine complement regulator, Crry, were generated to investigate its role in vivo. Survival of Crry-/- embryos was compromised because of complement deposition and concomitant placenta inflammation. Complement activation at the fetomaternal interface caused the fetal loss because breeding to C3-/- mice rescued Crry-/- mice from lethality. Thus, the regulation of complement is critical in fetal control of maternal processes that mediate tissue damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, C -- Mao, D -- Holers, V M -- Palanca, B -- Cheng, A M -- Molina, H -- R01 AI40576-01/AI/NIAID NIH HHS/ -- R01 AI44912-01/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2000 Jan 21;287(5452):498-501.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, 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/10642554" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Complement Activation ; Complement C3/analysis/immunology ; Embryo, Mammalian/*immunology/metabolism ; *Embryonic and Fetal Development ; Female ; Gene Targeting ; *Immune Tolerance ; Mice ; Neutrophil Infiltration ; Pregnancy ; Receptors, Complement/genetics/*physiology ; Trophoblasts/immunology/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Impaired nociception and pain sensation in mice lacking the capsaicin receptor (2000)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2000-04-15
    Description: The capsaicin (vanilloid) receptor VR1 is a cation channel expressed by primary sensory neurons of the "pain" pathway. Heterologously expressed VR1 can be activated by vanilloid compounds, protons, or heat (〉43 degrees C), but whether this channel contributes to chemical or thermal sensitivity in vivo is not known. Here, we demonstrate that sensory neurons from mice lacking VR1 are severely deficient in their responses to each of these noxious stimuli. VR1-/- mice showed normal responses to noxious mechanical stimuli but exhibited no vanilloid-evoked pain behavior, were impaired in the detection of painful heat, and showed little thermal hypersensitivity in the setting of inflammation. Thus, VR1 is essential for selective modalities of pain sensation and for tissue injury-induced thermal hyperalgesia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caterina, M J -- Leffler, A -- Malmberg, A B -- Martin, W J -- Trafton, J -- Petersen-Zeitz, K R -- Koltzenburg, M -- Basbaum, A I -- Julius, D -- NS07265/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2000 Apr 14;288(5464):306-13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94143-0450, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10764638" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Temperature/drug effects ; Calcium/metabolism ; Capsaicin/metabolism/*pharmacology ; Cells, Cultured ; Diterpenes/pharmacology ; Ganglia, Spinal/cytology ; Gene Targeting ; Hot Temperature ; Hydrogen-Ion Concentration ; Inflammation/physiopathology ; Mice ; Mice, Knockout ; Nerve Fibers/physiology ; Neurons/physiology ; Neurons, Afferent/*physiology ; Nociceptors/*physiology ; Pain/*physiopathology ; Pain Threshold ; Receptors, Drug/*physiology ; Spinal Cord/cytology/physiology ; TRPV Cation Channels
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    Turning blood into brain: cells bearing neuronal antigens generated in vivo from bone marrow (2000)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2000-12-02
    Description: Bone marrow stem cells give rise to a variety of hematopoietic lineages and repopulate the blood throughout adult life. We show that, in a strain of mice incapable of developing cells of the myeloid and lymphoid lineages, transplanted adult bone marrow cells migrated into the brain and differentiated into cells that expressed neuron-specific antigens. These findings raise the possibility that bone marrow-derived cells may provide an alternative source of neurons in patients with neurodegenerative diseases or central nervous system injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mezey, E -- Chandross, K J -- Harta, G -- Maki, R A -- McKercher, S R -- AI30656/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 1;290(5497):1779-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basic Neuroscience Program, Laboratory of Developmental Neurogenetics, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA. mezey@codon.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11099419" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/analysis ; Biomarkers/analysis ; Bone Marrow Cells/*cytology/physiology ; *Bone Marrow Transplantation ; Brain/*cytology ; Cell Differentiation ; Cell Movement ; Female ; Immunoenzyme Techniques ; Intermediate Filament Proteins/analysis ; Male ; Mice ; Mice, Knockout ; Microscopy, Confocal ; Nerve Tissue Proteins/analysis/immunology ; Nestin ; Neurons/chemistry/*cytology/immunology ; Phosphopyruvate Hydratase/analysis ; *Stem Cell Transplantation ; Stem Cells/chemistry/*cytology ; Y Chromosome
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    Perspectives: microbiology. Mice are not furry petri dishes (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bull, J -- Levin, B -- New York, N.Y. -- Science. 2000 Feb 25;287(5457):1409-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Integrative Biology, University of Texas, Austin 78712, USA. bull@bull.biosci.utexas.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10722389" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Animals ; Anti-Bacterial Agents/*pharmacology ; Culture Media ; Drug Resistance, Microbial/*genetics ; Evolution, Molecular ; Fusidic Acid/pharmacology ; Genes, Bacterial ; Mice ; *Mutation ; Salmonella/*drug effects/*genetics/growth & development ; Selection, Genetic ; Streptomycin/pharmacology
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    Fas preassociation required for apoptosis signaling and dominant inhibition by pathogenic mutations (2000)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2000-07-06
    Description: Heterozygous mutations encoding abnormal forms of the death receptor Fas dominantly interfere with Fas-induced lymphocyte apoptosis in human autoimmune lymphoproliferative syndrome. This effect, rather than depending on ligand-induced receptor oligomerization, was found to stem from ligand- independent interaction of wild-type and mutant Fas receptors through a specific region in the extracellular domain. Preassociated Fas complexes were found in living cells by means of fluorescence resonance energy transfer between variants of green fluorescent protein. These results show that formation of preassociated receptor complexes is necessary for Fas signaling and dominant interference in human disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Siegel, R M -- Frederiksen, J K -- Zacharias, D A -- Chan, F K -- Johnson, M -- Lynch, D -- Tsien, R Y -- Lenardo, M J -- NS27177/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2000 Jun 30;288(5475):2354-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10875918" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/*chemistry/genetics/*metabolism ; *Apoptosis ; Autoimmune Diseases/physiopathology ; Cell Line ; Cell Membrane/metabolism ; Cross-Linking Reagents ; Fas Ligand Protein ; Humans ; Ligands ; Lymphocytes/cytology ; Lymphoproliferative Disorders/physiopathology ; Macromolecular Substances ; Membrane Glycoproteins/*metabolism ; Mice ; Mutation ; Point Mutation ; Recombinant Fusion Proteins/chemistry/metabolism ; *Signal Transduction ; Succinimides ; Tumor Cells, Cultured
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    Abolition and reversal of strain differences in behavioral responses to drugs of abuse after a brief experience (2000)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2000-07-21
    Description: Inbred strains of mice are largely used to identify the genetic basis of normal and pathological behaviors. This report demonstrates that a moderate period of food shortage, an ecologically common experience, can reverse or abolish strain differences in behavioral responses to the abused psychostimulant amphetamine. The period of food shortage occurred when the animals were mature and was terminated before the administration of amphetamine. Strain differences in behavior appear highly dependent on environmental experiences. Consequently, to identify biological determinants of behavior, an integrated approach considering the interaction between environmental and genetic factors needs to be used.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cabib, S -- Orsini, C -- Le Moal, M -- Piazza, P V -- New York, N.Y. -- Science. 2000 Jul 21;289(5478):463-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dipartimento di Psicologia, Universita "La Sapienza" via dei Marsi 78, Roma I-00185, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10903209" target="_blank"〉PubMed〈/a〉
    Keywords: Amphetamine/*pharmacology ; Animals ; Behavior, Animal/*drug effects ; Central Nervous System Stimulants/*pharmacology ; Conditioning (Psychology)/drug effects ; *Food Deprivation ; Genes ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Motor Activity/drug effects ; Phenotype ; Species Specificity ; Substance-Related Disorders/*etiology ; Weight Loss
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    Failure to regulate TNF-induced NF-kappaB and cell death responses in A20-deficient mice (2000)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2000-09-29
    Description: A20 is a cytoplasmic zinc finger protein that inhibits nuclear factor kappaB (NF-kappaB) activity and tumor necrosis factor (TNF)-mediated programmed cell death (PCD). TNF dramatically increases A20 messenger RNA expression in all tissues. Mice deficient for A20 develop severe inflammation and cachexia, are hypersensitive to both lipopolysaccharide and TNF, and die prematurely. A20-deficient cells fail to terminate TNF-induced NF-kappaB responses. These cells are also more susceptible than control cells to undergo TNF-mediated PCD. Thus, A20 is critical for limiting inflammation by terminating TNF-induced NF-kappaB responses in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3582399/" 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/PMC3582399/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, E G -- Boone, D L -- Chai, S -- Libby, S L -- Chien, M -- Lodolce, J P -- Ma, A -- 5T32GM07183/GM/NIGMS NIH HHS/ -- R01 DK052751/DK/NIDDK NIH HHS/ -- T32GM07839/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Sep 29;289(5488):2350-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, The University of Chicago, 5841 South Maryland Avenue, MC 6084, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11009421" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Cachexia/pathology/physiopathology ; Cells, Cultured ; Cysteine Endopeptidases ; DNA/metabolism ; DNA-Binding Proteins/genetics/metabolism ; Fibroblasts/metabolism ; Gene Targeting ; *I-kappa B Proteins ; Inflammation/pathology/*physiopathology ; Interleukin-1/pharmacology ; Intestines/pathology ; Intracellular Signaling Peptides and Proteins ; Kidney/pathology ; Lipopolysaccharides/immunology ; Liver/pathology ; Mice ; NF-kappa B/*metabolism ; Nuclear Proteins ; Phosphorylation ; Proteins/genetics/*physiology ; Skin/pathology ; T-Lymphocytes/cytology/metabolism ; Tumor Necrosis Factor-alpha/*pharmacology ; Zinc Fingers
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    Ubiquitin protein ligase activity of IAPs and their degradation in proteasomes in response to apoptotic stimuli (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-05-08
    Description: To determine why proteasome inhibitors prevent thymocyte death, we examined whether proteasomes degrade anti-apoptotic molecules in cells induced to undergo apoptosis. The c-IAP1 and XIAP inhibitors of apoptosis were selectively lost in glucocorticoid- or etoposide-treated thymocytes in a proteasome-dependent manner before death. IAPs catalyzed their own ubiquitination in vitro, an activity requiring the RING domain. Overexpressed wild-type c-IAP1, but not a RING domain mutant, was spontaneously ubiquitinated and degraded, and stably expressed XIAP lacking the RING domain was relatively resistant to apoptosis-induced degradation and, correspondingly, more effective at preventing apoptosis than wild-type XIAP. Autoubiquitination and degradation of IAPs may be a key event in the apoptotic program.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Y -- Fang, S -- Jensen, J P -- Weissman, A M -- Ashwell, J D -- New York, N.Y. -- Science. 2000 May 5;288(5467):874-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immune Cell Biology, Division of Basic Sciences, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10797013" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Cells, Cultured ; Cysteine Endopeptidases/*metabolism ; Dexamethasone/pharmacology ; Etoposide/pharmacology ; Hybridomas ; Inhibitor of Apoptosis Proteins ; Ligases/*metabolism ; Mice ; Mice, Inbred C57BL ; Multienzyme Complexes/*metabolism ; Proteasome Endopeptidase Complex ; Protein Structure, Tertiary ; Proteins/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; T-Lymphocytes/cytology/drug effects/*metabolism ; Thymus Gland/cytology ; Transfection ; Ubiquitin-Protein Ligases ; Ubiquitins/metabolism ; X-Linked Inhibitor of Apoptosis Protein
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    Response to RAG-mediated VDJ cleavage by NBS1 and gamma-H2AX (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-09
    Description: Genetic disorders affecting cellular responses to DNA damage are characterized by high rates of translocations involving antigen receptor loci and increased susceptibility to lymphoid malignancies. We report that the Nijmegen breakage syndrome protein (NBS1) and histone gamma-H2AX, which associate with irradiation-induced DNA double-strand breaks (DSBs), are also found at sites of VDJ (variable, diversity, joining) recombination-induced DSBs. In developing thymocytes, NBS1 and gamma-H2AX form nuclear foci that colocalize with the T cell receptor alpha locus in response to recombination activating gene (RAG) protein-mediated VDJ cleavage. Our results suggest that surveillance of T cell receptor recombination intermediates by NBS1 and gamma-H2AX may be important for preventing oncogenic translocations.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4721589/" 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/PMC4721589/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, H T -- Bhandoola, A -- Difilippantonio, M J -- Zhu, J -- Brown, M J -- Tai, X -- Rogakou, E P -- Brotz, T M -- Bonner, W M -- Ried, T -- Nussenzweig, A -- Z99 CA999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 8;290(5498):1962-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11110662" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Nucleus/metabolism ; DNA Damage ; DNA-Binding Proteins/metabolism ; Fluorescent Antibody Technique ; *Gene Rearrangement, alpha-Chain T-Cell Antigen Receptor ; *Genes, T-Cell Receptor alpha ; Histones/*metabolism ; Homeodomain Proteins/metabolism ; Mice ; Mice, Transgenic ; Microscopy, Confocal ; Molecular Sequence Data ; Nuclear Proteins/*metabolism ; Phosphorylation ; *Recombination, Genetic ; T-Lymphocytes/*metabolism
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    Similar requirements of a plant symbiont and a mammalian pathogen for prolonged intracellular survival (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-31
    Description: Brucella abortus, a mammalian pathogen, and Rhizobium meliloti, a phylogenetically related plant symbiont, establish chronic infections in their respective hosts. Here a highly conserved B. abortus homolog of the R. meliloti bacA gene, which encodes a putative cytoplasmic membrane transport protein required for symbiosis, was identified. An isogenic B. abortus bacA mutant exhibited decreased survival in macrophages and greatly accelerated clearance from experimentally infected mice compared to the virulent parental strain. Thus, the bacA gene product is critical for the maintenance of two very diverse host-bacterial relationships.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉LeVier, K -- Phillips, R W -- Grippe, V K -- Roop, R M 2nd -- Walker, G C -- GM31030/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Mar 31;287(5462):2492-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10741969" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Bacterial/immunology ; Bacterial Proteins/genetics/*physiology ; Brucella abortus/genetics/*pathogenicity/physiology ; Brucellosis/immunology/*microbiology ; Cells, Cultured ; Female ; Hypersensitivity, Delayed ; Liver/microbiology ; Macrophages/immunology/*microbiology ; Medicago sativa/microbiology ; Membrane Proteins/genetics/*physiology ; *Membrane Transport Proteins ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Mutagenesis, Insertional ; Sinorhizobium meliloti/genetics/*physiology ; Spleen/microbiology ; Symbiosis ; Virulence
    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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  • 87
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    Impaired prion replication in spleens of mice lacking functional follicular dendritic cells (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-05-20
    Description: In scrapie-infected mice, prions are found associated with splenic but not circulating B and T lymphocytes and in the stroma, which contains follicular dendritic cells (FDCs). Formation and maintenance of mature FDCs require the presence of B cells expressing membrane-bound lymphotoxin-alpha/beta. Treatment of mice with soluble lymphotoxin-beta receptor results in the disappearance of mature FDCs from the spleen. We show that this treatment abolishes splenic prion accumulation and retards neuroinvasion after intraperitoneal scrapie inoculation. These data provide evidence that FDCs are the principal sites for prion replication in the spleen.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Montrasio, F -- Frigg, R -- Glatzel, M -- Klein, M A -- Mackay, F -- Aguzzi, A -- Weissmann, C -- New York, N.Y. -- Science. 2000 May 19;288(5469):1257-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neuropathology, Department of Pathology, University of Zurich, Schmelzbergstrasse 12, CH-8091 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10818004" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/genetics/immunology ; Dendritic Cells, Follicular/metabolism/*pathology/*virology ; Immunoglobulins/genetics ; Lymphotoxin beta Receptor ; Lymphotoxin-alpha/antagonists & inhibitors/genetics/immunology ; Mice ; Mice, Inbred C57BL ; Mice, SCID ; PrPSc Proteins/administration & dosage/*biosynthesis ; Receptors, Tumor Necrosis Factor/antagonists & inhibitors/genetics/immunology ; Recombinant Fusion Proteins/administration & dosage ; Scrapie/immunology/metabolism ; Signal Transduction/genetics/immunology ; Spleen/immunology/metabolism/*pathology/*virology ; Virus Replication/genetics/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 88
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    Hematopoietic stem cell quiescence maintained by p21cip1/waf1 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-10
    Description: Relative quiescence is a defining characteristic of hematopoietic stem cells, while their progeny have dramatic proliferative ability and inexorably move toward terminal differentiation. The quiescence of stem cells has been conjectured to be of critical biologic importance in protecting the stem cell compartment, which we directly assessed using mice engineered to be deficient in the G1 checkpoint regulator, cyclin-dependent kinase inhibitor, p21cip1/waf1 (p21). In the absence of p21, hematopoietic stem cell proliferation and absolute number were increased under normal homeostatic conditions. Exposing the animals to cell cycle-specific myelotoxic injury resulted in premature death due to hematopoietic cell depletion. Further, self-renewal of primitive cells was impaired in serially transplanted bone marrow from p21-/- mice, leading to hematopoietic failure. Therefore, p21 is the molecular switch governing the entry of stem cells into the cell cycle, and in its absence, increased cell cycling leads to stem cell exhaustion. Under conditions of stress, restricted cell cycling is crucial to prevent premature stem cell depletion and hematopoietic death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheng, T -- Rodrigues, N -- Shen, H -- Yang, Y -- Dombkowski, D -- Sykes, M -- Scadden, D T -- AI07387/AI/NIAID NIH HHS/ -- DK50234/DK/NIDDK NIH HHS/ -- HL44851/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 2000 Mar 10;287(5459):1804-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Hematology, AIDS Research Center, Massachusetts General Hospital Cancer Center, Transplantation Biology Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10710306" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antimetabolites/pharmacology ; Blood Cell Count ; Bone Marrow Transplantation ; Cell Count ; *Cell Cycle ; Cell Death ; Cell Differentiation ; Cell Division ; Coculture Techniques ; Colony-Forming Units Assay ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/genetics/*physiology ; Female ; Fluorouracil/pharmacology ; *Hematopoiesis ; Hematopoietic Stem Cells/*cytology/drug effects/physiology ; Homeostasis ; Male ; Mice ; Mice, Inbred Strains
    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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  • 89
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    Role of the guanosine triphosphatase Rac2 in T helper 1 cell differentiation (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-06-24
    Description: T helper 1 (TH1) cells mediate cellular immunity, whereas TH2 cells potentiate antiparasite and humoral immunity. We used a complementary DNA subtraction method, representational display analysis, to show that the small guanosine triphosphatase Rac2 is expressed selectively in murine TH1 cells. Rac induces the interferon-gamma (IFN-gamma) promoter through cooperative activation of the nuclear factor kappa B and p38 mitogen-activated protein kinase pathways. Tetracycline-regulated transgenic mice expressing constitutively active Rac2 in T cells exhibited enhanced IFN-gamma production. Dominant-negative Rac inhibited IFN-gamma production in murine T cells. Moreover, T cells from Rac2-/- mice showed decreased IFN-gamma production under TH1 conditions in vitro. Thus, Rac2 activates TH1-specific signaling and IFN-gamma gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, B -- Yu, H -- Zheng, W -- Voll, R -- Na, S -- Roberts, A W -- Williams, D A -- Davis, R J -- Ghosh, S -- Flavell, R A -- New York, N.Y. -- Science. 2000 Jun 23;288(5474):2219-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology and Howard Hughes Medical Institute, Yale University School of Medicine, 310 Cedar Street, New Haven, CT 06520-8011, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10864872" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cells, Cultured ; Cytokines/biosynthesis/genetics ; Gene Expression Regulation ; Humans ; Interferon-gamma/biosynthesis/*genetics ; JNK Mitogen-Activated Protein Kinases ; Jurkat Cells ; Lymphocyte Activation ; Mice ; Mice, Transgenic ; Mitogen-Activated Protein Kinases/metabolism ; NF-kappa B/metabolism ; Promoter Regions, Genetic ; Signal Transduction ; Th1 Cells/cytology/*immunology/*metabolism ; Transfection ; p38 Mitogen-Activated Protein Kinases ; rac GTP-Binding Proteins/genetics/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 90
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    Biomedicine. New insights into type 2 diabetes (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-08-06
    Description: Researchers studying type 2 diabetes are optimistic that they are closing in on the elusive causes of the world's most prevalent metabolic disorder--although no one is willing to bet the bank on it. Using both biochemical and genetic approaches, diabetes researchers have identified multiple intracellular signaling pathways that appear to lie at the heart of this condition, which affects some 250 million people worldwide and is the leading cause of blindness, kidney failure, and amputation among adults. And in the process, they have thrown out much of the dogma of the past 10 years.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alper, J -- New York, N.Y. -- Science. 2000 Jul 7;289(5476):37-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10928926" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/metabolism ; Animals ; Diabetes Mellitus, Type 2/*metabolism ; Glucose/metabolism ; Humans ; Insulin/*metabolism ; Insulin Receptor Substrate Proteins ; Insulin Resistance ; Intracellular Signaling Peptides and Proteins ; Islets of Langerhans/metabolism ; Liver/metabolism ; Mice ; Mice, Knockout ; Muscles/metabolism ; Phosphoproteins/genetics/*metabolism ; Receptor, Insulin/metabolism ; Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 91
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    Impaired cued and contextual memory in NPAS2-deficient mice (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-06-24
    Description: Neuronal PAS domain protein 2 (NPAS2) is a basic helix-loop-helix (bHLH) PAS domain transcription factor expressed in multiple regions of the vertebrate brain. Targeted insertion of a beta-galactosidase reporter gene (lacZ) resulted in the production of an NPAS2-lacZ fusion protein and an altered form of NPAS2 lacking the bHLH domain. The neuroanatomical expression pattern of NPAS2-lacZ was temporally and spatially coincident with formation of the mature frontal association/limbic forebrain pathway. NPAS2-deficient mice were subjected to a series of behavioral tests and were found to exhibit deficits in the long-term memory arm of the cued and contextual fear task. Thus, NPAS2 may serve a dedicated regulatory role in the acquisition of specific types of memory.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garcia, J A -- Zhang, D -- Estill, S J -- Michnoff, C -- Rutter, J -- Reick, M -- Scott, K -- Diaz-Arrastia, R -- McKnight, S L -- AG12297/AG/NIA NIH HHS/ -- AG16450/AG/NIA NIH HHS/ -- NS01763/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 2000 Jun 23;288(5474):2226-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10864874" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avoidance Learning ; Basic Helix-Loop-Helix Transcription Factors ; Behavior, Animal ; Brain/metabolism/*physiology ; Conditioning (Psychology) ; Cues ; Fear ; Gene Targeting ; Helix-Loop-Helix Motifs ; Learning/*physiology ; Limbic System/metabolism/physiology ; Male ; Memory/*physiology ; Mice ; Nerve Tissue Proteins/chemistry/genetics/*physiology ; Prosencephalon/metabolism/physiology ; Recombinant Fusion Proteins/chemistry/metabolism ; Touch ; Transcription Factors/chemistry/genetics/*physiology ; Transcriptional Activation ; Transfection ; beta-Galactosidase/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 92
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    Development. p73--guilt by association? (2000)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2000-08-05
    Description: It has been assumed that the new members of the p53 protein family, p63 and p73, would have the same job as p53, namely, forcing cells to die if they or their DNA is damaged. Now, as Morrison and Kinoshita explain in their Perspective, one particular form of p73 has been found to be a survival factor rather than a death factor for sympathetic neurons during development (Pozniak et al.).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morrison, R S -- Kinoshita, Y -- New York, N.Y. -- Science. 2000 Jul 14;289(5477):257-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurological Surgery, University of Washington School of Medicine, Box 356470, Seattle, WA 98195-6470, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10917851" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; DNA-Binding Proteins/genetics/*physiology ; Genes, Tumor Suppressor ; Mice ; Neurons/*physiology ; Nuclear Proteins/genetics/*physiology ; Sympathetic Nervous System/cytology/*growth & development/physiology ; Tumor Suppressor Protein p53/genetics/physiology ; Tumor Suppressor Proteins
    Print ISSN: 0036-8075
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  • 93
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    Requirement for RORgamma in thymocyte survival and lymphoid organ development (2000)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2000-07-06
    Description: Most developing thymocytes undergo apoptosis because they cannot interact productively with molecules encoded by the major histocompatibility complex. Here, we show that mice lacking the orphan nuclear hormone receptor RORgamma lose thymic expression of the anti-apoptotic factor Bcl-xL. RORgamma thus regulates the survival of CD4+8+ thymocytes and may control the temporal window during which thymocytes can undergo positive selection. RORgamma was also required for development of lymph nodes and Peyer's patches, but not splenic follicles. In its absence, there was loss of a population of CD3-CD4+CD45+ cells that normally express RORgamma and that are likely early progenitors of lymphoid organs. Hence, RORgamma has critical functions in T cell repertoire selection and lymphoid organogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, Z -- Unutmaz, D -- Zou, Y R -- Sunshine, M J -- Pierani, A -- Brenner-Morton, S -- Mebius, R E -- Littman, D R -- New York, N.Y. -- Science. 2000 Jun 30;288(5475):2369-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine and Howard Hughes Medical Institute, New York University School of Medicine, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10875923" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; *CDC2-CDC28 Kinases ; Cell Count ; Cell Cycle ; Cell Survival ; Crosses, Genetic ; Cyclin-Dependent Kinase 2 ; Cyclin-Dependent Kinases/metabolism ; DNA-Binding Proteins/genetics/metabolism ; Female ; Gene Targeting ; Inhibitor of Differentiation Protein 2 ; Lymphoid Tissue/cytology/embryology/*growth & development ; Male ; Mice ; Mice, Inbred C57BL ; Nuclear Receptor Subfamily 1, Group F, Member 3 ; Protein-Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins c-bcl-2/genetics/metabolism ; Receptors, Cytoplasmic and Nuclear/genetics/*physiology ; *Receptors, Retinoic Acid ; *Receptors, Thyroid Hormone ; *Repressor Proteins ; T-Lymphocyte Subsets/*cytology ; Thymus Gland/*cytology ; *Transcription Factors ; bcl-X Protein
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  • 94
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    Roles of PLC-beta2 and -beta3 and PI3Kgamma in chemoattractant-mediated signal transduction (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-11
    Description: The roles of phosphoinositide 3-kinase (PI3K) and phospholipase C (PLC) in chemoattractant-elicited responses were studied in mice lacking these key enzymes. PI3Kgamma was required for chemoattractant-induced production of phosphatidylinositol 3,4,5-trisphosphate [PtdIns (3,4,5)P3] and has an important role in chemoattractant-induced superoxide production and chemotaxis in mouse neutrophils and in production of T cell-independent antigen-specific antibodies composed of the immunoglobulin lambda light chain (TI-IglambdaL). The study of the mice lacking PLC-beta2 and -beta3 revealed that the PLC pathways have an important role in chemoattractant-mediated production of superoxide and regulation of protein kinases, but not chemotaxis. The PLC pathways also appear to inhibit the chemotactic activity induced by certain chemoattractants and to suppress TI-IglambdaL production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Z -- Jiang, H -- Xie, W -- Zhang, Z -- Smrcka, A V -- Wu, D -- New York, N.Y. -- Science. 2000 Feb 11;287(5455):1046-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Rochester, Rochester, NY 14642, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10669417" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology ; Chemokine CCL4 ; Chemotactic Factors/*pharmacology ; Chemotaxis, Leukocyte/*physiology ; Immunoglobulin lambda-Chains/biosynthesis ; Isoenzymes/*metabolism ; Macrophage Inflammatory Proteins/pharmacology ; Mice ; N-Formylmethionine Leucyl-Phenylalanine/pharmacology ; Neutrophil Infiltration ; Neutrophils/metabolism/*physiology ; Peritonitis/immunology ; Phosphatidylinositol 3-Kinases/*metabolism ; Phosphatidylinositol Phosphates/metabolism ; Phospholipase C beta ; Phosphorylation ; *Signal Transduction ; Skin Ulcer/pathology ; Superoxides/metabolism ; Type C Phospholipases/*metabolism
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  • 95
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    Generalized potential of adult neural stem cells (2000)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2000-06-02
    Description: The differentiation potential of stem cells in tissues of the adult has been thought to be limited to cell lineages present in the organ from which they were derived, but there is evidence that some stem cells may have a broader differentiation repertoire. We show here that neural stem cells from the adult mouse brain can contribute to the formation of chimeric chick and mouse embryos and give rise to cells of all germ layers. This demonstrates that an adult neural stem cell has a very broad developmental capacity and may potentially be used to generate a variety of cell types for transplantation in different diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clarke, D L -- Johansson, C B -- Wilbertz, J -- Veress, B -- Nilsson, E -- Karlstrom, H -- Lendahl, U -- Frisen, J -- New York, N.Y. -- Science. 2000 Jun 2;288(5471):1660-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Molecular Biology, Medical Nobel Institute, Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10834848" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/cytology/physiology ; Brain/*cytology ; Cell Aggregation ; *Cell Differentiation ; Cell Lineage ; Cells, Cultured ; Chick Embryo ; Coculture Techniques ; Ectoderm/cytology ; Embryonic and Fetal Development ; Endoderm/cytology ; Liver/cytology/embryology ; Mesoderm/cytology ; Mice ; Microinjections ; Morula/cytology/physiology ; Muscles/cytology/embryology ; Stem Cell Transplantation ; Stem Cells/*cytology/physiology ; Transplantation Chimera
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  • 96
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    Signal transduction through prion protein (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-16
    Description: The cellular prion protein PrPc is a glycosylphosphatidylinositol-anchored cell-surface protein whose biological function is unclear. We used the murine 1C11 neuronal differentiation model to search for PrPc-dependent signal transduction through antibody-mediated cross-linking. A caveolin-1-dependent coupling of PrPc to the tyrosine kinase Fyn was observed. Clathrin might also contribute to this coupling. The ability of the 1C11 cell line to trigger PrPc-dependent Fyn activation was restricted to its fully differentiated serotonergic or noradrenergic progenies. Moreover, the signaling activity of PrPc occurred mainly at neurites. Thus, PrPc may be a signal transduction protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mouillet-Richard, S -- Ermonval, M -- Chebassier, C -- Laplanche, J L -- Lehmann, S -- Launay, J M -- Kellermann, O -- New York, N.Y. -- Science. 2000 Sep 15;289(5486):1925-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Differenciation Cellulaire, CNRS-Institut Pasteur, 75724 Paris Cedex 15, France. srichard@pasteur.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10988071" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caveolin 1 ; *Caveolins ; Cell Compartmentation ; Cell Differentiation ; Enzyme Activation ; Membrane Proteins/metabolism ; Mice ; Neurons/cytology/metabolism ; PrPC Proteins/*metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-fyn ; *Signal Transduction
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  • 97
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    Subgroup of reproductive functions of progesterone mediated by progesterone receptor-B isoform (2000)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2000-09-08
    Description: Progesterone regulates reproductive function through two intracellular receptors, progesterone receptor-A (PR-A) and progesterone receptor-B (PR-B), that arise from a single gene and function as transcriptional regulators of progesterone-responsive genes. Although in vitro studies show that PR isoforms can display different transcriptional regulatory activities, their physiological significance is unknown. By selective ablation of PR-A in mice, we show that the PR-B isoform modulates a subset of reproductive functions of progesterone by regulation of a subset of progesterone-responsive target genes. Thus, PR-A and PR-B are functionally distinct mediators of progesterone action in vivo and should provide suitable targets for generation of tissue-selective progestins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mulac-Jericevic, B -- Mullinax, R A -- DeMayo, F J -- Lydon, J P -- Conneely, O M -- HD32007/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2000 Sep 8;289(5485):1751-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10976068" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division/drug effects ; Crosses, Genetic ; *Embryo Implantation ; Epithelial Cells/cytology/drug effects ; Epithelium/drug effects/metabolism ; Estradiol/pharmacology ; Female ; Gene Expression Regulation ; Male ; Mammary Glands, Animal/cytology/drug effects ; Mice ; Mice, Knockout ; Ovariectomy ; Ovulation ; Progesterone/pharmacology/*physiology ; Protein Isoforms ; Receptors, Progesterone/genetics/*physiology ; *Reproduction ; Uterus/cytology/drug effects/metabolism/*physiology
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  • 98
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    Cell biology. Bacterial spelunkers (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-08-19
    Description: Bacteria that are engulfed by phagocytic cells of the immune system are usually destroyed once inside the host cell but not always. Why is it that sometimes engulfed bacteria survive and thrive quite happily inside the host cell? As Mulvey and Hultgren explain in their Perspective, the answer may lie in small indentations in the host cell plasma membrane called caveolae that direct certain signal transduction pathways inside the host cell (Shin et al.). If bacteria adhere to regions of the host cell surface that is rich in caveolae, they are better able to survive once inside the cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mulvey, M A -- Hultgren, S J -- New York, N.Y. -- Science. 2000 Aug 4;289(5480):732-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110-1093, USA. mulvey@borcim.wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10950716" target="_blank"〉PubMed〈/a〉
    Keywords: Adhesins, Bacterial/metabolism ; *Adhesins, Escherichia coli ; Animals ; Antigens, CD/metabolism ; Bacterial Adhesion ; Caveolin 1 ; *Caveolins ; Cell Membrane/chemistry/*metabolism/microbiology/ultrastructure ; *Endocytosis ; Escherichia coli/*metabolism/pathogenicity ; *Fimbriae Proteins ; Glycosylphosphatidylinositols/metabolism ; Macrophages/microbiology ; Mast Cells/metabolism/*microbiology/ultrastructure ; Membrane Proteins/analysis ; Mice ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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    Posttranslational N-myristoylation of BID as a molecular switch for targeting mitochondria and apoptosis (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-02
    Description: Many apoptotic molecules relocate subcellularly in cells undergoing apoptosis. The pro-apoptotic protein BID underwent posttranslational (rather than classic cotranslational) N-myristoylation when cleavage by caspase 8 caused exposure of a glycine residue. N-myristoylation enabled the targeting of a complex of p7 and myristoylated p15 fragments of BID to artificial membranes bearing the lipid composition of mitochondria, as well as to intact mitochondria. This post-proteolytic N-myristoylation serves as an activating switch, enhancing BID-induced release of cytochrome c and cell death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zha, J -- Weiler, S -- Oh, K J -- Wei, M C -- Korsmeyer, S J -- CA50239-13/CA/NCI NIH HHS/ -- K01 CA82231/CA/NCI NIH HHS/ -- T32 CA72320-01A1/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 1;290(5497):1761-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Dana-Farber Cancer Institute, Departments of Pathology and Medicine, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11099414" target="_blank"〉PubMed〈/a〉
    Keywords: Acyltransferases/genetics/metabolism ; Animals ; *Apoptosis ; BH3 Interacting Domain Death Agonist Protein ; Carrier Proteins/chemistry/*metabolism ; Caspase 8 ; Caspase 9 ; Caspases/metabolism ; Cytochrome c Group/metabolism ; Humans ; Intracellular Membranes/*metabolism ; Jurkat Cells ; Liposomes/metabolism ; Mice ; Mitochondria/*metabolism ; Myristic Acid/*metabolism ; Peptide Fragments/metabolism ; Protein Conformation ; Protein Processing, Post-Translational ; Protein Structure, Tertiary ; Protein Transport ; Recombinant Fusion Proteins/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 100
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    Cross talk between interferon-gamma and -alpha/beta signaling components in caveolar membrane domains (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-07-06
    Description: Definition of cellular responses to cytokines often involves cross-communication through their respective receptors. Here, signaling by interferon-gamma (IFN-gamma) is shown to depend on the IFN-alpha/beta receptor components. Although these IFNs transmit signals through distinct receptor complexes, the IFN-alpha/beta receptor component, IFNAR1, facilitates efficient assembly of IFN-gamma-activated transcription factors. This cross talk is contingent on a constitutive subthreshold IFN-alpha/beta signaling and the association between the two nonligand-binding receptor components, IFNAR1 and IFNGR2, in the caveolar membrane domains. This aspect of signaling cross talk by IFNs may apply to other cytokines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takaoka, A -- Mitani, Y -- Suemori, H -- Sato, M -- Yokochi, T -- Noguchi, S -- Tanaka, N -- Taniguchi, T -- New York, N.Y. -- Science. 2000 Jun 30;288(5475):2357-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Graduate School of Medicine and Faculty of Medicine, University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo 113-0033, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10875919" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/*metabolism ; Cells, Cultured ; Cytopathogenic Effect, Viral ; DNA-Binding Proteins/metabolism ; Dimerization ; Encephalomyocarditis virus/drug effects/physiology ; Interferon Type I/*metabolism ; Interferon-alpha/genetics/metabolism/pharmacology ; Interferon-beta/genetics/metabolism/pharmacology ; Interferon-gamma/*metabolism/pharmacology ; Janus Kinase 1 ; Janus Kinase 2 ; Membrane Proteins ; Mice ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein-Tyrosine Kinases/metabolism ; *Proto-Oncogene Proteins ; *Receptor Cross-Talk ; Receptor, Interferon alpha-beta ; Receptors, Interferon/genetics/*metabolism ; Recombinant Proteins ; STAT1 Transcription Factor ; *Signal Transduction ; Trans-Activators/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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