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  • Rats  (681)
  • Cells, Cultured  (408)
  • American Association for the Advancement of Science (AAAS)  (989)
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  • 1995-1999  (503)
  • 1990-1994  (486)
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  • American Association for the Advancement of Science (AAAS)  (989)
  • American Meteorological Society
  • PANGAEA
  • Springer  (23)
  • Wiley-Blackwell  (1)
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  • 1
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    Structural basis for a Ca2+-sensing function of the metabotropic glutamate receptors (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-28
    Description: The metabotropic glutamate receptors (mGluRs) are widely distributed in the brain and play important roles in synaptic plasticity. Here it is shown that some types of mGluRs are activated not only by glutamate but also by extracellular Ca2+ (Ca2+o). A single amino acid residue was found to determine the sensitivity of mGluRs to Ca2+o. One of the receptors, mGluR1alpha, but not its point mutant with reduced sensitivity to Ca2+o, caused morphological changes when transfected into mammalian cells. Thus, the sensing of Ca2+o by mGluRs may be important in cells under physiological condition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kubo, Y -- Miyashita, T -- Murata, Y -- New York, N.Y. -- Science. 1998 Mar 13;279(5357):1722-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurophysiology, Tokyo Metropolitan Institute for Neuroscience, Musashidai 2-6, Fuchu, Tokyo 183-8526, Japan. ykubo@tmin.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9497291" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/ultrastructure ; Amino Acid Sequence ; Animals ; Binding Sites ; Brain/metabolism ; CHO Cells ; Calcium/*metabolism/pharmacology ; Cell Size ; Cricetinae ; Cyclic AMP/metabolism ; G Protein-Coupled Inwardly-Rectifying Potassium Channels ; Glutamic Acid/metabolism/pharmacology ; Molecular Sequence Data ; Oocytes ; Point Mutation ; Potassium Channels/metabolism ; *Potassium Channels, Inwardly Rectifying ; Rats ; Receptors, Metabotropic Glutamate/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Second Messenger Systems ; Transfection ; Xenopus laevis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Induction of lens differentiation by activation of a bZIP transcription factor, L-Maf (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-04-29
    Description: After the vertebrate lens is induced from head ectoderm, lens-specific genes are expressed. Transcriptional regulation of the lens-specific alphaA-crystallin gene is controlled by an enhancer element, alphaCE2. A gene encoding an alphaCE2-binding protein, L-maf(lens-specific maf), was isolated. L-maf expression is initiated in the lens placode and is restricted to lens cells. The gene product L-Maf regulates the expression of multiple genes expressed in the lens, and ectopic expression of this transcription factor converts chick embryonic ectodermal cells and cultured cells into lens fibers. Thus, vertebrate lens induction and differentiation can be triggered by the activation of L-Maf.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ogino, H -- Yasuda, K -- New York, N.Y. -- Science. 1998 Apr 3;280(5360):115-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate School of Biological Sciences, Nara Institute of Science and Technology, 8916-5 Takayama, Ikoma 630-0101, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9525857" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Basic-Leucine Zipper Transcription Factors ; Cell Differentiation ; Cells, Cultured ; Chick Embryo ; Crystallins/genetics ; DNA, Complementary ; DNA-Binding Proteins/chemistry/genetics ; Ectoderm ; Enhancer Elements, Genetic ; Eye Proteins/genetics ; G-Box Binding Factors ; *Gene Expression Regulation, Developmental ; Genes, Reporter ; Intermediate Filament Proteins/genetics ; Lens, Crystalline/*cytology/*embryology/metabolism ; Maf Transcription Factors ; Molecular Sequence Data ; Promoter Regions, Genetic ; Recombinant Fusion Proteins/metabolism ; Transcription Factors/chemistry/genetics/*metabolism ; *Transcription, Genetic ; Transcriptional Activation ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Role of phosphorylation in regulation of the assembly of endocytic coat complexes (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-07
    Description: Clathrin-mediated endocytosis involves cycles of assembly and disassembly of clathrin coat components and their accessory proteins. Dephosphorylation of rat brain extract was shown to promote the assembly of dynamin 1, synaptojanin 1, and amphiphysin into complexes that also included clathrin and AP-2. Phosphorylation of dynamin 1 and synaptojanin 1 inhibited their binding to amphiphysin, whereas phosphorylation of amphiphysin inhibited its binding to AP-2 and clathrin. Thus, phosphorylation regulates the association and dissociation cycle of the clathrin-based endocytic machinery, and calcium-dependent dephosphorylation of endocytic proteins could prepare nerve terminals for a burst of endocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slepnev, V I -- Ochoa, G C -- Butler, M H -- Grabs, D -- De Camilli, P -- CA46128/CA/NCI NIH HHS/ -- NS36251/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1998 Aug 7;281(5378):821-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Cell Biology, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9694653" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Protein Complex alpha Subunits ; Adaptor Protein Complex beta Subunits ; Adaptor Proteins, Vesicular Transport ; Adenosine Triphosphate/metabolism ; Animals ; Binding Sites ; Carbazoles/pharmacology ; Chromatography, Affinity ; Clathrin/*metabolism ; Cyclosporine/pharmacology ; Dimerization ; Dynamin I ; Dynamins ; *Endocytosis ; Enzyme Inhibitors/pharmacology ; GTP Phosphohydrolases/*metabolism ; Indole Alkaloids ; Membrane Proteins/*metabolism ; Nerve Tissue Proteins/*metabolism ; Phosphoric Monoester Hydrolases/*metabolism ; Rats ; Recombinant Fusion Proteins/metabolism ; src Homology Domains
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Bid for better beef gives Japan a leg up on cattle (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Normile, D -- New York, N.Y. -- Science. 1998 Dec 11;282(5396):1975-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9874644" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Husbandry/*methods ; Animals ; Blastocyst ; Cattle/embryology/*genetics ; Cell Differentiation ; Cells, Cultured ; *Cloning, Organism ; Embryo Transfer/veterinary ; Fallopian Tubes/cytology ; Female ; Japan ; *Nuclear Transfer Techniques ; Oocytes ; Ovarian Follicle/cytology ; Pregnancy
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Cholinergic switching within neocortical inhibitory networks (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-14
    Description: Differential actions of acetylcholine on the excitability of two subtypes of interneurons in layer V of the rat visual cortex were examined. Acetylcholine excited low-threshold spike (LTS) cells through nicotinic receptors, whereas it elicited hyperpolarization in fast spiking (FS) cells through muscarinic receptors. Axons of LTS cells were mainly distributed vertically to upper layers, and those of FS cells were primarily confined to layer V. Thus, cortical cholinergic activation may reduce some forms of intralaminar inhibition, promote intracolumnar inhibition, and change the direction of information flow within cortical circuits.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xiang, Z -- Huguenard, J R -- Prince, D A -- NS 06477/NS/NINDS NIH HHS/ -- NS 07280/NS/NINDS NIH HHS/ -- NS 12151/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Aug 14;281(5379):985-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Stanford University Medical Center, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9703513" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/*physiology ; Animals ; Hexamethonium/pharmacology ; In Vitro Techniques ; Interneurons/physiology ; Membrane Potentials ; Muscarinic Antagonists/pharmacology ; Nerve Net/*physiology ; *Neural Inhibition ; Nicotinic Antagonists/pharmacology ; Patch-Clamp Techniques ; Rats ; Rats, Sprague-Dawley ; Receptors, Nicotinic/physiology ; Scopolamine Hydrobromide/pharmacology ; Visual Cortex/cytology/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Molecular basis of T cell inactivation by CTLA-4 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-18
    Description: CTLA-4, a negative regulator of T cell function, was found to associate with the T cell receptor (TCR) complex zeta chain in primary T cells. The association of TCRzeta with CTLA-4, reconstituted in 293 transfectants, was enhanced by p56(lck)-induced tyrosine phosphorylation. Coexpression of the CTLA-4-associated tyrosine phosphatase, SHP-2, resulted in dephosphorylation of TCRzeta bound to CTLA-4 and abolished the p56(lck)-inducible TCRzeta-CTLA-4 interaction. Thus, CTLA-4 inhibits TCR signal transduction by binding to TCRzeta and inhibiting tyrosine phosphorylation after T cell activation. These findings have broad implications for the negative regulation of T cell function and T cell tolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, K M -- Chuang, E -- Griffin, M -- Khattri, R -- Hong, D K -- Zhang, W -- Straus, D -- Samelson, L E -- Thompson, C B -- Bluestone, J A -- P01 AI35294-6/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1998 Dec 18;282(5397):2263-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ben May Institute for Cancer Research, and Committee on Immunology, University of Chicago, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9856951" target="_blank"〉PubMed〈/a〉
    Keywords: Abatacept ; Animals ; Antigens, CD ; Antigens, Differentiation/*metabolism ; CTLA-4 Antigen ; Cell Line ; Cells, Cultured ; Humans ; *Immunoconjugates ; Intracellular Signaling Peptides and Proteins ; *Lymphocyte Activation ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck)/genetics/metabolism ; Membrane Proteins/*metabolism ; Mice ; Mice, Inbred BALB C ; Models, Immunological ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein Tyrosine Phosphatase, Non-Receptor Type 11 ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 ; Protein Tyrosine Phosphatases/genetics/metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Recombinant Fusion Proteins/metabolism ; SH2 Domain-Containing Protein Tyrosine Phosphatases ; *Signal Transduction ; T-Lymphocytes/*immunology ; Transfection ; src Homology Domains
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    FADD: essential for embryo development and signaling from some, but not all, inducers of apoptosis (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-04-16
    Description: FADD (also known as Mort-1) is a signal transducer downstream of cell death receptor CD95 (also called Fas). CD95, tumor necrosis factor receptor type 1 (TNFR-1), and death receptor 3 (DR3) did not induce apoptosis in FADD-deficient embryonic fibroblasts, whereas DR4, oncogenes E1A and c-myc, and chemotherapeutic agent adriamycin did. Mice with a deletion in the FADD gene did not survive beyond day 11.5 of embryogenesis; these mice showed signs of cardiac failure and abdominal hemorrhage. Chimeric embryos showing a high contribution of FADD null mutant cells to the heart reproduce the phenotype of FADD-deficient mutants. Thus, not only death receptors, but also receptors that couple to developmental programs, may use FADD for signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yeh, W C -- de la Pompa, J L -- McCurrach, M E -- Shu, H B -- Elia, A J -- Shahinian, A -- Ng, M -- Wakeham, A -- Khoo, W -- Mitchell, K -- El-Deiry, W S -- Lowe, S W -- Goeddel, D V -- Mak, T W -- CA13106/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Mar 20;279(5358):1954-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Amgen Institute, University of Toronto, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9506948" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD95/genetics/physiology ; *Apoptosis ; Carrier Proteins/genetics/*physiology ; Cell Transformation, Neoplastic ; Cells, Cultured ; Doxorubicin/pharmacology ; *Embryonic and Fetal Development ; Endothelium, Vascular/embryology ; Fas-Associated Death Domain Protein ; Female ; Gene Expression ; Gene Targeting ; Heart/*embryology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation ; Oncogenes ; Receptors, Tumor Necrosis Factor/genetics/physiology ; Signal Transduction ; Tumor Necrosis Factor-alpha/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Cloned transgenic calves produced from nonquiescent fetal fibroblasts (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-20
    Description: An efficient system for genetic modification and large-scale cloning of cattle is of importance for agriculture, biotechnology, and human medicine. Here, actively dividing fetal fibroblasts were genetically modified with a marker gene, a clonal line was selected, and the cells were fused to enucleated mature oocytes. Out of 28 embryos transferred to 11 recipient cows, three healthy, identical, transgenic calves were generated. Furthermore, the life-span of near senescent fibroblasts could be extended by nuclear transfer, as indicated by population doublings in fibroblast lines derived from a 40-day-old fetal clone. With the ability to extend the life-span of these primary cultured cells, this system would be useful for inducing complex genetic modifications in cattle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cibelli, J B -- Stice, S L -- Golueke, P J -- Kane, J J -- Jerry, J -- Blackwell, C -- Ponce de Leon, F A -- Robl, J M -- New York, N.Y. -- Science. 1998 May 22;280(5367):1256-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Veterinary and Animal Sciences, University of Massachusetts, Amherst, MA 01003, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9596577" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Animals, Genetically Modified ; Blastocyst ; Cattle/embryology/*genetics ; Cell Aging ; Cell Division ; Cell Nucleus/genetics ; Cells, Cultured ; Clone Cells ; *Cloning, Organism ; Embryo Transfer ; Female ; Fetus/cytology ; Fibroblasts/*cytology ; G1 Phase ; Male ; Nuclear Transfer Techniques ; Oocytes/cytology ; Transfection ; Transgenes
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Protein kinase B kinases that mediate phosphatidylinositol 3,4,5-trisphosphate-dependent activation of protein kinase B (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-21
    Description: Protein kinase B (PKB) is activated in response to phosphoinositide 3-kinases and their lipid products phosphatidylinositol 3,4, 5-trisphosphate [PtdIns(3,4,5)P3] and PtdIns(3,4)P2 in the signaling pathways used by a wide variety of growth factors, antigens, and inflammatory stimuli. PKB is a direct target of these lipids, but this regulation is complex. The lipids can bind to the pleckstrin homologous domain of PKB, causing its translocation to the membrane, and also enable upstream, Thr308-directed kinases to phosphorylate and activate PKB. Four isoforms of these PKB kinases were purified from sheep brain. They bound PtdIns(3,4,5)P3 and associated with lipid vesicles containing it. These kinases contain an NH2-terminal catalytic domain and a COOH-terminal pleckstrin homologous domain, and their heterologous expression augments receptor activation of PKB, which suggests they are the primary signal transducers that enable PtdIns(3,4,5)P3 or PtdIns- (3,4)P2 to activate PKB and hence to control signaling pathways regulating cell survival, glucose uptake, and glycogen metabolism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stephens, L -- Anderson, K -- Stokoe, D -- Erdjument-Bromage, H -- Painter, G F -- Holmes, A B -- Gaffney, P R -- Reese, C B -- McCormick, F -- Tempst, P -- Coadwell, J -- Hawkins, P T -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1998 Jan 30;279(5351):710-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Inositide Laboratory, The Babraham Institute, Babraham, Cambridge CB2 4AT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9445477" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Phosphoinositide-Dependent Protein Kinases ; Alternative Splicing ; Amino Acid Sequence ; Animals ; Cell Line ; Cell Membrane/enzymology ; Cloning, Molecular ; DNA, Complementary ; Drosophila ; Drosophila Proteins ; Enzyme Activation ; Humans ; Liposomes/metabolism ; Molecular Sequence Data ; Open Reading Frames ; Phosphatidylinositol Phosphates/*metabolism ; Phosphorylation ; Platelet-Derived Growth Factor/pharmacology ; Protein-Serine-Threonine Kinases/chemistry/genetics/isolation & ; purification/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-akt ; Rats ; Recombinant Proteins/metabolism ; Sheep ; *Signal Transduction
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Transition from moderate to excessive drug intake: change in hedonic set point (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-09
    Description: Differential access to cocaine self-administration produced two patterns of drug intake in rats. With 1 hour of access per session, drug intake remained low and stable. In contrast, with 6 hours of access, drug intake gradually escalated over days. After escalation, drug consumption was characterized by an increased early drug loading and an upward shift in the cocaine dose-response function, suggesting an increase in hedonic set point. After 1 month of abstinence, escalation of cocaine intake was reinstated to a higher level than before. These findings may provide an animal model for studying the development of excessive drug intake and the basis of addiction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ahmed, S H -- Koob, G F -- DA04398/DA/NIDA NIH HHS/ -- DA08467/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1998 Oct 9;282(5387):298-300.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Psychopharmacology, Department of Neuropharmacology, CVN-7, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. aserge@sage.scripps.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9765157" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Addictive ; Cocaine/*administration & dosage ; Cocaine-Related Disorders/*etiology ; Dose-Response Relationship, Drug ; Drug Tolerance ; Male ; Rats ; Rats, Wistar ; Reinforcement (Psychology) ; Time Factors
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  • 11
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    Target-specific expression of presynaptic mossy fiber plasticity (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-21
    Description: Mossy fiber synaptic transmission at hippocampal CA3 pyramidal cells and interneurons was compared in rat brain slices to determine whether mossy terminals are functionally equivalent. Tetanic stimulation of mossy fibers induced long-term potentiation in pyramidal neurons but was either without effect or it induced depression at synapses onto interneurons. Unlike transmission onto pyramidal neurons, transmission onto interneurons was not potentiated after adenosine 3',5'-monophosphate (cAMP) activation. Furthermore, metabotropic glutamate receptor depression of transmission onto interneurons did not involve cAMP-dependent pathways. Thus, synaptic terminals arising from a common afferent pathway do not function as a single compartment but are specialized, depending on their postsynaptic target.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maccaferri, G -- Toth, K -- McBain, C J -- New York, N.Y. -- Science. 1998 Feb 27;279(5355):1368-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Neurophysiology, Room 5A72, Building 49, National Institute of Child Health and Human Development, 9000 Rockville Pike, Bethesda MD 20892-4495, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9478900" target="_blank"〉PubMed〈/a〉
    Keywords: Afferent Pathways ; Animals ; Colforsin/pharmacology ; Cyclic AMP/metabolism ; Cycloleucine/analogs & derivatives/pharmacology ; Cyclopropanes/pharmacology ; Electric Stimulation ; Excitatory Postsynaptic Potentials/drug effects ; Glycine/analogs & derivatives/pharmacology ; Hippocampus/cytology/*physiology ; In Vitro Techniques ; Interneurons/drug effects/*physiology ; *Long-Term Potentiation ; Mossy Fibers, Hippocampal/*physiology ; Pyramidal Cells/drug effects/*physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, Metabotropic Glutamate/agonists/physiology ; Synaptic Transmission/drug effects
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
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    An essential role for ectodomain shedding in mammalian development (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-13
    Description: The ectodomains of numerous proteins are released from cells by proteolysis to yield soluble intercellular regulators. The responsible protease, tumor necrosis factor-alpha converting enzyme (TACE), has been identified only in the case when tumor necrosis factor-alpha (TNFalpha) is released. Analyses of cells lacking this metalloproteinase-disintegrin revealed an expanded role for TACE in the processing of other cell surface proteins, including a TNF receptor, the L-selectin adhesion molecule, and transforming growth factor-alpha (TGFalpha). The phenotype of mice lacking TACE suggests an essential role for soluble TGFalpha in normal development and emphasizes the importance of protein ectodomain shedding in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peschon, J J -- Slack, J L -- Reddy, P -- Stocking, K L -- Sunnarborg, S W -- Lee, D C -- Russell, W E -- Castner, B J -- Johnson, R S -- Fitzner, J N -- Boyce, R W -- Nelson, N -- Kozlosky, C J -- Wolfson, M F -- Rauch, C T -- Cerretti, D P -- Paxton, R J -- March, C J -- Black, R A -- CA43793/CA/NCI NIH HHS/ -- DK53804/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1998 Nov 13;282(5392):1281-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunex Corporation, Seattle, WA 98101, USA. peschon@immunex.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9812885" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins ; Amino Acid Sequence ; Animals ; Catalytic Domain ; Cell Membrane/*metabolism ; Cells, Cultured ; Crosses, Genetic ; *Embryonic and Fetal Development ; L-Selectin/metabolism ; Ligands ; Membrane Proteins/*metabolism ; Metalloendopeptidases/chemistry/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; Phenotype ; Protein Processing, Post-Translational ; Receptors, Tumor Necrosis Factor/metabolism ; Transforming Growth Factor alpha/metabolism ; Tumor Necrosis Factor-alpha/*metabolism
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  • 13
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    Src activation in the induction of long-term potentiation in CA1 hippocampal neurons (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-21
    Description: Long-term potentiation (LTP) is an activity-dependent strengthening of synaptic efficacy that is considered to be a model of learning and memory. Protein tyrosine phosphorylation is necessary to induce LTP. Here, induction of LTP in CA1 pyramidal cells of rats was prevented by blocking the tyrosine kinase Src, and Src activity was increased by stimulation producing LTP. Directly activating Src in the postsynaptic neuron enhanced excitatory synaptic responses, occluding LTP. Src-induced enhancement of alpha-amino-3-hydroxy-5-methylisoxazolepropionic acid (AMPA) receptor-mediated synaptic responses required raised intracellular Ca2+ and N-methyl-D-aspartate (NMDA) receptors. Thus, Src activation is necessary and sufficient for inducing LTP and may function by up-regulating NMDA receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lu, Y M -- Roder, J C -- Davidow, J -- Salter, M W -- New York, N.Y. -- Science. 1998 Feb 27;279(5355):1363-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute, Mount Sinai Hospital, and Department of Molecular and Medical Genetics, University of Toronto, M5S 1A8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9478899" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium/metabolism ; Electric Stimulation ; Enzyme Activation ; Excitatory Postsynaptic Potentials/drug effects ; Hippocampus/cytology/enzymology/*physiology ; In Vitro Techniques ; *Long-Term Potentiation ; Molecular Sequence Data ; Oligopeptides/pharmacology ; Patch-Clamp Techniques ; Peptide Fragments/pharmacology ; Proto-Oncogene Proteins pp60(c-src)/pharmacology ; Pyramidal Cells/enzymology/*physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/physiology ; Receptors, N-Methyl-D-Aspartate/physiology ; Recombinant Proteins/pharmacology ; Up-Regulation ; src-Family Kinases/*metabolism
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  • 14
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    Neurons and silicon get intimate (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, R F -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):578-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10328734" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Electric Stimulation ; Electrodes ; Electrodes, Implanted ; *Electronics ; Electrophysiology ; Humans ; Nerve Net/*physiology ; Nervous System Diseases/*therapy ; Neurons/*physiology ; Rats ; Silicon ; *Transistors, Electronic
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  • 15
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    Stem cells. Rat spinal cord function partially restored (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1826-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610569" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/cytology ; Cell Differentiation ; Cell Survival ; Embryo, Mammalian ; Mice ; Neurons/cytology ; Oligodendroglia/cytology ; Rats ; Spinal Cord/cytology/*physiology ; Spinal Cord Injuries/*therapy ; *Stem Cell Transplantation ; Stem Cells/cytology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    Key brain receptor gets an unusual regulator (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1999 Nov 12;286(5443):1265-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610528" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*enzymology ; Brain/*enzymology ; Cloning, Molecular ; Glutamic Acid/metabolism ; Neurons/metabolism ; Racemases and Epimerases/*genetics/metabolism ; Rats ; Receptors, N-Methyl-D-Aspartate/metabolism ; Serine/*biosynthesis/metabolism ; Stereoisomerism ; Synapses/metabolism
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  • 17
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    Filling in the blanks of the GABAB receptor (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):14-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9917254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/metabolism ; Cells, Cultured ; Dimerization ; Drug Design ; Humans ; Neurons/*metabolism ; Potassium Channels/metabolism ; Rats ; Receptors, GABA-B/*chemistry/*metabolism ; Signal Transduction ; gamma-Aminobutyric Acid/metabolism
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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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    Rapid spine delivery and redistribution of AMPA receptors after synaptic NMDA receptor activation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-12
    Description: To monitor changes in alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptor distribution in living neurons, the AMPA receptor subunit GluR1 was tagged with green fluorescent protein (GFP). This protein (GluR1-GFP) was functional and was transiently expressed in hippocampal CA1 neurons. In dendrites visualized with two-photon laser scanning microscopy or electron microscopy, most of the GluR1-GFP was intracellular, mimicking endogenous GluR1 distribution. Tetanic synaptic stimulation induced a rapid delivery of tagged receptors into dendritic spines as well as clusters in dendrites. These postsynaptic trafficking events required synaptic N-methyl-D-aspartate (NMDA) receptor activation and may contribute to the enhanced AMPA receptor-mediatedtransmission observed during long-term potentiation and activity-dependent synaptic maturation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shi, S H -- Hayashi, Y -- Petralia, R S -- Zaman, S H -- Wenthold, R J -- Svoboda, K -- Malinow, R -- New York, N.Y. -- Science. 1999 Jun 11;284(5421):1811-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10364548" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Dendrites/*metabolism/ultrastructure ; Electric Stimulation ; Hippocampus/cytology/physiology ; Humans ; Long-Term Potentiation ; *Neuronal Plasticity ; Neurons/*physiology ; Organ Culture Techniques ; Rats ; Receptor Aggregation ; Receptors, AMPA/*metabolism ; Receptors, N-Methyl-D-Aspartate/*physiology ; Recombinant Fusion Proteins/metabolism ; Synapses/metabolism/*physiology ; Synaptic Transmission ; Tetany
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  • 19
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    Calmodulin dependence of presynaptic metabotropic glutamate receptor signaling (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-05
    Description: Glutamatergic neurotransmission is controlled by presynaptic metabotropic glutamate receptors (mGluRs). A subdomain in the intracellular carboxyl-terminal tail of group III mGluRs binds calmodulin and heterotrimeric guanosine triphosphate-binding protein (G protein) betagamma subunits in a mutually exclusive manner. Mutations interfering with calmodulin binding and calmodulin antagonists inhibit G protein-mediated modulation of ionic currents by mGluR 7. Calmodulin antagonists also prevent inhibition of excitatory neurotransmission via presynaptic mGluRs. These results reveal a novel mechanism of presynaptic modulation in which Ca(2+)-calmodulin is required to release G protein betagamma subunits from the C-tail of group III mGluRs in order to mediate glutamatergic autoinhibition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Connor, V -- El Far, O -- Bofill-Cardona, E -- Nanoff, C -- Freissmuth, M -- Karschin, A -- Airas, J M -- Betz, H -- Boehm, S -- New York, N.Y. -- Science. 1999 Nov 5;286(5442):1180-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurochemistry, Max Planck Institute for Brain Research, Deutschordenstrasse 46, 60528 Frankfurt, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10550060" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium/metabolism ; Calmodulin/antagonists & inhibitors/*metabolism ; Cells, Cultured ; Dimerization ; G Protein-Coupled Inwardly-Rectifying Potassium Channels ; GTP-Binding Proteins/*metabolism ; Glutamic Acid/*metabolism ; Hippocampus/cytology/metabolism ; Humans ; Mice ; Molecular Sequence Data ; Neurons/metabolism ; Potassium Channels/metabolism ; *Potassium Channels, Inwardly Rectifying ; Presynaptic Terminals/metabolism ; Propionates/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Metabotropic Glutamate/antagonists & inhibitors/*metabolism ; Recombinant Fusion Proteins/metabolism ; Sesterterpenes ; Signal Transduction ; Swine ; *Synaptic Transmission ; Terpenes/pharmacology
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  • 20
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    A role for DNA-PK in retroviral DNA integration (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-24
    Description: Retroviral DNA integration is catalyzed by the viral protein integrase. Here, it is shown that DNA-dependent protein kinase (DNA-PK), a host cell protein, also participates in the reaction. DNA-PK-deficient murine scid cells infected with three different retroviruses showed a substantial reduction in retroviral DNA integration and died by apoptosis. Scid cell killing was not observed after infection with an integrase-defective virus, suggesting that abortive integration is the trigger for death in these DNA repair-deficient cells. These results suggest that the initial events in retroviral integration are detected as DNA damage by the host cell and that completion of the integration process requires the DNA-PK-mediated repair pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Daniel, R -- Katz, R A -- Skalka, A M -- AI40721/AI/NIAID NIH HHS/ -- AI40835/AI/NIAID NIH HHS/ -- CA71515/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):644-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cancer Research, Fox Chase Cancer Center, 7701 Burholme Avenue, Philadelphia, PA 19111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10213687" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; CHO Cells ; Cell Survival ; Cells, Cultured ; Cricetinae ; DNA Damage ; *DNA Repair ; DNA, Viral/*genetics/metabolism ; DNA-Activated Protein Kinase ; *DNA-Binding Proteins ; Genetic Vectors ; HIV-1/genetics ; Integrases/genetics/metabolism ; Mice ; Mutation ; Protein-Serine-Threonine Kinases/*metabolism ; Retroviridae/*genetics/physiology ; *Virus Integration ; Virus Replication
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  • 21
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    CD3- and CD28-dependent induction of PDE7 required for T cell activation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-05
    Description: Costimulation of both the CD3 and CD28 receptors is essential for T cell activation. Induction of adenosine 3',5'-monophosphate (cAMP)-specific phosphodiesterase-7 (PDE7) was found to be a consequence of such costimulation. Increased PDE7 in T cells correlated with decreased cAMP, increased interleukin-2 expression, and increased proliferation. Selectively reducing PDE7 expression with a PDE7 antisense oligonucleotide inhibited T cell proliferation; inhibition was reversed by blocking the cAMP signaling pathways that operate through cAMP-dependent protein kinase (PKA). Thus, PDE7 induction and consequent suppression of PKA activity is required for T cell activation, and inhibition of PDE7 could be an approach to treating T cell-dependent disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, L -- Yee, C -- Beavo, J A -- DK21723/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1999 Feb 5;283(5403):848-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Molecular and Cellular Biology Program, Box 357280, University of Washington School of Medicine, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9933169" target="_blank"〉PubMed〈/a〉
    Keywords: 3',5'-Cyclic-AMP Phosphodiesterases/*biosynthesis/genetics/metabolism ; Antibodies ; Antigens, CD28/immunology/*physiology ; Antigens, CD3/immunology/*physiology ; CD4-Positive T-Lymphocytes/enzymology/immunology ; Cells, Cultured ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Cyclic Nucleotide Phosphodiesterases, Type 7 ; Enzyme Induction ; Humans ; Interleukin-2/biosynthesis ; Isoenzymes/*biosynthesis/genetics/metabolism ; *Lymphocyte Activation ; Oligonucleotides, Antisense/pharmacology ; RNA, Messenger/genetics/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; T-Lymphocytes/*enzymology/*immunology/metabolism ; Tumor Cells, Cultured
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  • 22
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    AP-2 recruitment to synaptotagmin stimulated by tyrosine-based endocytic motifs (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-24
    Description: Clathrin-mediated endocytosis is initiated by the recruitment of the clathrin adaptor protein AP-2 to the plasma membrane where the membrane protein synaptotagmin is thought to act as a docking site. AP-2 also interacts with endocytic motifs present in other cargo proteins. Peptides with a tyrosine-based endocytic motif stimulated binding of AP-2 to synaptotagmin and enhanced AP-2 recruitment to the plasma membrane of neuronal and non-neuronal cells. This suggests a mechanism by which nucleation of clathrin-coated pits is stimulated by the loading of cargo proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haucke, V -- De Camilli, P -- CA46128/CA/NCI NIH HHS/ -- NS36252/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Aug 20;285(5431):1268-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Howard Hughes Medical Institute, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10455054" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Protein Complex alpha Subunits ; Adaptor Proteins, Vesicular Transport ; Animals ; Binding Sites ; CHO Cells ; *Calcium-Binding Proteins ; Cattle ; Cell Membrane/metabolism ; Clathrin/*metabolism ; Coated Pits, Cell-Membrane/*metabolism ; Cricetinae ; *Endocytosis ; Membrane Glycoproteins/chemistry/*metabolism ; Membrane Proteins/*metabolism ; Nerve Tissue Proteins/chemistry/*metabolism ; Neurons/metabolism ; Oligopeptides/chemistry/metabolism/*pharmacology ; Phospholipase D/metabolism ; Protein Binding ; Rats ; Recombinant Fusion Proteins/metabolism ; Synaptic Membranes/*metabolism ; Synaptotagmins ; Tyrosine/chemistry
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  • 23
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    Linear differentiation of cytotoxic effectors into memory T lymphocytes (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-12
    Description: A central question in immunology is the origin of long-lived T cell memory that confers protection against recurrent infection. The differentiation of naive T cell receptor transgenic CD8+ cells into effector cytotoxic T lymphocytes (CTLs) and memory CD8+ cells was studied. Memory CD8+ cells that were generated after strong antigenic stimulation were the progeny of cytotoxic effectors and retained antigen-specific cytolytic activity 10 weeks after adoptive transfer to antigen-free recipient mice. Thus, potential vaccines based on CTL memory will require the differentiation of naive cells into post-effector memory T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Opferman, J T -- Ober, B T -- Ashton-Rickardt, P G -- 5T32 AI07090/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Mar 12;283(5408):1745-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Committee on Immunology, Department of Pathology, Committee on Developmental Biology, The University of Chicago, Gwen Knapp Center for Lupus and Immunology Research, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10073942" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Apoptosis ; CD8-Positive T-Lymphocytes/*cytology/*immunology ; Cell Differentiation ; Cell Division ; Cell Lineage ; Cells, Cultured ; Cytotoxicity, Immunologic ; Dose-Response Relationship, Immunologic ; H-Y Antigen/immunology ; *Immunologic Memory ; Lymphocyte Activation ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Transgenic ; Perforin ; Pore Forming Cytotoxic Proteins ; T-Lymphocyte Subsets/cytology/*immunology ; T-Lymphocytes, Cytotoxic/cytology/*immunology
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  • 24
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    The nature of the principal type 1 interferon-producing cells in human blood (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-12
    Description: Interferons (IFNs) are the most important cytokines in antiviral immune responses. "Natural IFN-producing cells" (IPCs) in human blood express CD4 and major histocompatibility complex class II proteins, but have not been isolated and further characterized because of their rarity, rapid apoptosis, and lack of lineage markers. Purified IPCs are here shown to be the CD4(+)CD11c- type 2 dendritic cell precursors (pDC2s), which produce 200 to 1000 times more IFN than other blood cells after microbial challenge. pDC2s are thus an effector cell type of the immune system, critical for antiviral and antitumor immune responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Siegal, F P -- Kadowaki, N -- Shodell, M -- Fitzgerald-Bocarsly, P A -- Shah, K -- Ho, S -- Antonenko, S -- Liu, Y J -- New York, N.Y. -- Science. 1999 Jun 11;284(5421):1835-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Saint Vincents Hospital and Medical Center, New York, NY 10011, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10364556" target="_blank"〉PubMed〈/a〉
    Keywords: CD40 Ligand ; Cell Lineage ; Cell Separation ; Cells, Cultured ; Dendritic Cells/cytology/*immunology/ultrastructure ; Humans ; Interferon Type I/*biosynthesis ; Interferon-alpha/*biosynthesis/genetics ; Interferon-beta/biosynthesis/genetics ; Interleukin-3/pharmacology ; Leukocytes, Mononuclear/immunology ; Membrane Glycoproteins/pharmacology ; Organelles/ultrastructure ; RNA, Messenger/genetics/metabolism ; Simplexvirus/immunology ; Stem Cells/cytology/immunology
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  • 25
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    Techsigting. Neural regeneration. Some nerve! (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sikorski, R -- Peters, R -- New York, N.Y. -- Science. 1999 Apr 16;284(5413):453.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10232993" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cell Separation ; Chick Embryo ; Neural Crest/*cytology/embryology ; Neuroglia/*cytology ; Neurons/*cytology ; Rats ; Regeneration ; Sciatic Nerve/*cytology/embryology ; Stem Cells/*cytology
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  • 26
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    Role of DNA 5-methylcytosine transferase in cell transformation by fos (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-15
    Description: The Fos and Jun oncoproteins form dimeric complexes that stimulate transcription of genes containing activator protein-1 regulatory elements. We found, by representational difference analysis, that expression of DNA 5-methylcytosine transferase (dnmt1) in fos-transformed cells is three times the expression in normal fibroblasts and that fos-transformed cells contain about 20 percent more 5-methylcytosine than normal fibroblasts. Transfection of the gene encoding Dnmt1 induced morphological transformation, whereas inhibition of dnmt1 expression or activity resulted in reversion of fos transformation. Inhibition of histone deacetylase, which associates with methylated DNA, also caused reversion. These results suggest that fos may transform cells through alterations in DNA methylation and in histone deacetylation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bakin, A V -- Curran, T -- P30 CA21765/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 15;283(5400):387-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9888853" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine ; Acetylation ; Animals ; Cell Size ; *Cell Transformation, Neoplastic ; Cytosine/analogs & derivatives/metabolism ; DNA (Cytosine-5-)-Methyltransferase/genetics/*metabolism ; DNA Methylation ; Enzyme Inhibitors/pharmacology ; Gene Expression Regulation, Neoplastic ; *Genes, fos ; Histone Deacetylase Inhibitors ; Histones/metabolism ; Hydroxamic Acids/pharmacology ; Proto-Oncogene Proteins c-fos/*metabolism ; Rats ; Transcription, Genetic ; Transfection
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Pigment epithelium-derived factor: a potent inhibitor of angiogenesis (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-10
    Description: In the absence of disease, the vasculature of the mammalian eye is quiescent, in part because of the action of angiogenic inhibitors that prevent vessels from invading the cornea and vitreous. Here, an inhibitor responsible for the avascularity of these ocular compartments is identified as pigment epithelium-derived factor (PEDF), a protein previously shown to have neurotrophic activity. The amount of inhibitory PEDF produced by retinal cells was positively correlated with oxygen concentrations, suggesting that its loss plays a permissive role in ischemia-driven retinal neovascularization. These results suggest that PEDF may be of therapeutic use, especially in retinopathies where pathological neovascularization compromises vision and leads to blindness.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dawson, D W -- Volpert, O V -- Gillis, P -- Crawford, S E -- Xu, H -- Benedict, W -- Bouck, N P -- New York, N.Y. -- Science. 1999 Jul 9;285(5425):245-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology-Immunology, Department of Pathology, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Medical School, Chicago, IL 60611, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10398599" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Antibodies/immunology ; Cattle ; Cells, Cultured ; Chemotaxis/drug effects ; Culture Media, Conditioned ; Endothelial Growth Factors/metabolism ; Endothelium, Vascular/cytology/drug effects/physiology ; Eye/blood supply ; *Eye Proteins ; Humans ; Lymphokines/metabolism ; Mice ; Neovascularization, Pathologic/*drug therapy/metabolism/pathology ; Neovascularization, Physiologic/*drug effects ; *Nerve Growth Factors ; Oxygen/physiology ; Proteins/genetics/immunology/*pharmacology/*physiology ; RNA, Messenger/genetics/metabolism ; Rats ; Retina/*metabolism/pathology ; Retinal Neovascularization/*drug therapy ; Retinal Vessels/growth & development ; Serpins/genetics/immunology/*pharmacology/*physiology ; Tumor Cells, Cultured ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Defective thymocyte maturation in p44 MAP kinase (Erk 1) knockout mice (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-13
    Description: The p42 and p44 mitogen-activated protein kinases (MAPKs), also called Erk2 and Erk1, respectively, have been implicated in proliferation as well as in differentiation programs. The specific role of the p44 MAPK isoform in the whole animal was evaluated by generation of p44 MAPK-deficient mice by homologous recombination in embryonic stem cells. The p44 MAPK-/- mice were viable, fertile, and of normal size. Thus, p44 MAPK is apparently dispensable and p42 MAPK (Erk2) may compensate for its loss. However, in p44 MAPK-/- mice, thymocyte maturation beyond the CD4+CD8+ stage was reduced by half, with a similar diminution in the thymocyte subpopulation expressing high levels of T cell receptor (CD3high). In p44 MAPK-/- thymocytes, proliferation in response to activation with a monoclonal antibody to the T cell receptor in the presence of phorbol myristate acetate was severely reduced even though activation of p42 MAPK was more sustained in these cells. The p44 MAPK apparently has a specific role in thymocyte development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pages, G -- Guerin, S -- Grall, D -- Bonino, F -- Smith, A -- Anjuere, F -- Auberger, P -- Pouyssegur, J -- New York, N.Y. -- Science. 1999 Nov 12;286(5443):1374-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Signaling, Developmental Biology and Cancer Research, CNRS UMR 6543, Centre A. Lacassagne, 33 Avenue de Valombrose, 06189 Nice, France. gpages@unice.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10558995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Antigens, CD/analysis ; Antigens, CD3/immunology ; Cell Differentiation ; Cell Division ; Cells, Cultured ; DNA/biosynthesis ; Enzyme Activation ; Gene Targeting ; Isoenzymes/genetics/metabolism ; Mice ; Mice, Knockout ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3 ; Mitogen-Activated Protein Kinases/deficiency/genetics/*metabolism ; Phosphorylation ; Polymorphism, Restriction Fragment Length ; Receptors, Antigen, T-Cell, alpha-beta/analysis/physiology ; T-Lymphocyte Subsets/*cytology/enzymology/immunology ; Tetradecanoylphorbol Acetate/pharmacology ; Thymus Gland/*cytology
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    Focal adhesion motility revealed in stationary fibroblasts (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-05
    Description: Focal adhesions (FAs) are clustered integrins and associated proteins that mediate cell adhesion and signaling. A green fluorescent protein-beta1 integrin chimera was used to label FAs in living cells. In stationary cells, FAs were highly motile, moving linearly for several plaque lengths toward the cell center. FA motility was independent of cell density and resulted from contraction of associated actin fibers. In migrating cells, FAs were stationary and only moved in the tail. FA motility in stationary cells suggests that cell movement may be regulated by a clutch-like mechanism by which the affinity of integrins to substrate may be altered in response to migratory cues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smilenov, L B -- Mikhailov, A -- Pelham, R J -- Marcantonio, E E -- Gundersen, G G -- GM42026/GM/NIGMS NIH HHS/ -- GM44585/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 5;286(5442):1172-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10550057" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Actins/physiology ; Animals ; Antigens, CD29/*metabolism ; *Cell Adhesion ; Cell Count ; Cell Line ; *Cell Movement ; Fibroblasts/*cytology/metabolism ; Fluorescence ; Green Fluorescent Proteins ; Luminescent Proteins ; Mice ; Microscopy, Interference ; Rats ; Recombinant Fusion Proteins/metabolism
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    Abnormal morphogenesis but intact IKK activation in mice lacking the IKKalpha subunit of IkappaB kinase (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-09
    Description: The oligomeric IkappaB kinase (IKK) is composed of three polypeptides: IKKalpha and IKKbeta, the catalytic subunits, and IKKgamma, a regulatory subunit. IKKalpha and IKKbeta are similar in structure and thought to have similar function-phosphorylation of the IkappaB inhibitors in response to proinflammatory stimuli. Such phosphorylation leads to degradation of IkappaB and activation of nuclear factor kappaB transcription factors. The physiological function of these protein kinases was explored by analysis of IKKalpha-deficient mice. IKKalpha was not required for activation of IKK and degradation of IkappaB by proinflammatory stimuli. Instead, loss of IKKalpha interfered with multiple morphogenetic events, including limb and skeletal patterning and proliferation and differentiation of epidermal keratinocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, Y -- Baud, V -- Delhase, M -- Zhang, P -- Deerinck, T -- Ellisman, M -- Johnson, R -- Karin, M -- R01 AI43477/AI/NIAID NIH HHS/ -- R37 ES04151/ES/NIEHS NIH HHS/ -- RR04050/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):316-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Cancer Center, University of California San Diego, La Jolla, CA 92093-0636, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10195896" target="_blank"〉PubMed〈/a〉
    Keywords: Abnormalities, Multiple/enzymology/genetics ; Animals ; Apoptosis ; Body Patterning ; Bone and Bones/abnormalities/embryology ; Cell Differentiation ; Cell Nucleus/metabolism ; Cells, Cultured ; DNA-Binding Proteins/metabolism ; Dimerization ; *Embryonic and Fetal Development ; Enzyme Activation ; Epidermis/cytology/embryology ; Female ; Gene Targeting ; I-kappa B Kinase ; I-kappa B Proteins ; Keratinocytes ; Limb Deformities, Congenital/enzymology ; Male ; Mice ; *Morphogenesis ; Mutation ; Phosphorylation ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Skin/embryology ; Skin Abnormalities/enzymology
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    NMDA receptor-mediated K+ efflux and neuronal apoptosis (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-09
    Description: Neuronal death induced by activating N-methyl-D-aspartate (NMDA) receptors has been linked to Ca2+ and Na+ influx through associated channels. Whole-cell recording from cultured mouse cortical neurons revealed a NMDA-evoked outward current, INMDA-K, carried by K+ efflux at membrane potentials positive to -86 millivolts. Cortical neurons exposed to NMDA in medium containing reduced Na+ and Ca2+ (as found in ischemic brain tissue) lost substantial intracellular K+ and underwent apoptosis. Both K+ loss and apoptosis were attenuated by increasing extracellular K+, even when voltage-gated Ca2+ channels were blocked. Thus NMDA receptor-mediated K+ efflux may contribute to neuronal apoptosis after brain ischemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, S P -- Yeh, C -- Strasser, U -- Tian, M -- Choi, D W -- NS 30337/NS/NINDS NIH HHS/ -- NS 32636/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):336-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for the Study of Nervous System Injury and Department of Neurology, 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/10195902" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Calcium/metabolism/pharmacology ; Calcium Channels/metabolism ; Cells, Cultured ; Cerebral Cortex/*cytology/metabolism ; Culture Techniques ; Glutamic Acid/metabolism ; Ion Channel Gating ; Ion Transport ; Membrane Potentials ; Mice ; N-Methylaspartate/pharmacology ; Neocortex/cytology/embryology/metabolism ; Neurons/*cytology/metabolism ; Patch-Clamp Techniques ; Potassium/*metabolism ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Sodium/metabolism/pharmacology
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    Blockade of NMDA receptors and apoptotic neurodegeneration in the developing brain (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-05
    Description: Programmed cell death (apoptosis) occurs during normal development of the central nervous system. However, the mechanisms that determine which neurons will succumb to apoptosis are poorly understood. Blockade of N-methyl-D-aspartate (NMDA) glutamate receptors for only a few hours during late fetal or early neonatal life triggered widespread apoptotic neurodegeneration in the developing rat brain, suggesting that the excitatory neurotransmitter glutamate, acting at NMDA receptors, controls neuronal survival. These findings may have relevance to human neurodevelopmental disorders involving prenatal (drug-abusing mothers) or postnatal (pediatric anesthesia) exposure to drugs that block NMDA receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ikonomidou, C -- Bosch, F -- Miksa, M -- Bittigau, P -- Vockler, J -- Dikranian, K -- Tenkova, T I -- Stefovska, V -- Turski, L -- Olney, J W -- AG 11355/AG/NIA NIH HHS/ -- DA 05072/DA/NIDA NIH HHS/ -- MH 38894/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):70-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatric Neurology, Charite-Virchow Clinics, Humboldt University, Augustenburger Platz 1, 13353 Berlin, Germany. hrissanthi.ikonomidou@charite.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9872743" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Brain/*cytology/drug effects/embryology/growth & development ; Calcium Channel Blockers/pharmacology ; Dizocilpine Maleate/pharmacology ; Dopamine Antagonists/pharmacology ; Dose-Response Relationship, Drug ; Excitatory Amino Acid Antagonists/pharmacology ; Fetus ; Haloperidol/pharmacology ; Immunohistochemistry ; In Situ Nick-End Labeling ; Microscopy, Electron ; Muscarinic Antagonists/pharmacology ; *Nerve Degeneration ; Neurons/*cytology/drug effects/metabolism ; Quinoxalines/pharmacology ; Rats ; Receptors, N-Methyl-D-Aspartate/*antagonists & inhibitors/metabolism ; Scopolamine Hydrobromide/pharmacology
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    Requirement for type 2 NO synthase for IL-12 signaling in innate immunity (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-13
    Description: Interleukin-12 (IL-12) and type 2 NO synthase (NOS2) are crucial for defense against bacterial and parasitic pathogens, but their relationship in innate immunity is unknown. In the absence of NOS2 activity, IL-12 was unable to prevent spreading of Leishmania parasites, did not stimulate natural killer (NK) cells for cytotoxicity or interferon-gamma (IFN-gamma) release, and failed to activate Tyk2 kinase and to tyrosine phosphorylate Stat4 (the central signal transducer of IL-12) in NK cells. Activation of Tyk2 in NK cells by IFN-alpha/beta also required NOS2. Thus, NOS2-derived NO is a prerequisite for cytokine signaling and function in innate immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diefenbach, A -- Schindler, H -- Rollinghoff, M -- Yokoyama, W M -- Bogdan, C -- New York, N.Y. -- Science. 1999 May 7;284(5416):951-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Klinische Mikrobiologie, Immunologie und Hygiene, Universitat Erlangen, Wasserturmstrasse 3, D-91054 Erlangen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10320373" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Cyclic GMP/metabolism ; Cytotoxicity, Immunologic ; DNA-Binding Proteins/metabolism ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Immunity, Innate ; Interferon-gamma/biosynthesis/genetics ; Interferons/pharmacology ; Interleukin-12/pharmacology/*physiology ; Janus Kinase 2 ; Killer Cells, Natural/*immunology/metabolism ; *Leishmania major ; Leishmaniasis, Cutaneous/*immunology/metabolism ; Lysine/analogs & derivatives/pharmacology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Nitric Oxide/metabolism ; Nitric Oxide Synthase/antagonists & inhibitors/*metabolism ; Nitric Oxide Synthase Type II ; Phosphorylation ; Protein-Tyrosine Kinases/metabolism ; Proteins/metabolism ; *Proto-Oncogene Proteins ; STAT4 Transcription Factor ; *Signal Transduction ; TYK2 Kinase ; Trans-Activators/metabolism ; Up-Regulation
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    Building neural representations of habits (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-27
    Description: Memories for habits and skills ("implicit or procedural memory") and memories for facts ("explicit or episodic memory") are built up in different brain systems and are vulnerable to different neurodegenerative disorders in humans. So that the striatum-based mechanisms underlying habit formation could be studied, chronic recordings from ensembles of striatal neurons were made with multiple tetrodes as rats learned a T-maze procedural task. Large and widely distributed changes in the neuronal activity patterns occurred in the sensorimotor striatum during behavioral acquisition, culminating in task-related activity emphasizing the beginning and end of the automatized procedure. The new ensemble patterns remained stable during weeks of subsequent performance of the same task. These results suggest that the encoding of action in the sensorimotor striatum undergoes dynamic reorganization as habit learning proceeds.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jog, M S -- Kubota, Y -- Connolly, C I -- Hillegaart, V -- Graybiel, A M -- R03 MH57878/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1745-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉London Health Sciences Center, London, Ontario N6A 5A5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10576743" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Behavior, Animal ; Brain Mapping ; Corpus Striatum/*physiology ; Electrodes, Implanted ; Evoked Potentials ; *Habits ; Locomotion ; *Maze Learning ; Memory/physiology ; Motor Activity ; Neurons/physiology ; Rats ; Reaction Time
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    Cell survival promoted by the Ras-MAPK signaling pathway by transcription-dependent and -independent mechanisms (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-11-13
    Description: A mechanism by which the Ras-mitogen-activated protein kinase (MAPK) signaling pathway mediates growth factor-dependent cell survival was characterized. The MAPK-activated kinases, the Rsks, catalyzed the phosphorylation of the pro-apoptotic protein BAD at serine 112 both in vitro and in vivo. The Rsk-induced phosphorylation of BAD at serine 112 suppressed BAD-mediated apoptosis in neurons. Rsks also are known to phosphorylate the transcription factor CREB (cAMP response element-binding protein) at serine 133. Activated CREB promoted cell survival, and inhibition of CREB phosphorylation at serine 133 triggered apoptosis. These findings suggest that the MAPK signaling pathway promotes cell survival by a dual mechanism comprising the posttranslational modification and inactivation of a component of the cell death machinery and the increased transcription of pro-survival genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonni, A -- Brunet, A -- West, A E -- Datta, S R -- Takasu, M A -- Greenberg, M E -- NIHP30-HD18655/HD/NICHD NIH HHS/ -- P01 HD 24926/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 12;286(5443):1358-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, and Department of Neurobiology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10558990" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Brain-Derived Neurotrophic Factor/pharmacology ; Carrier Proteins/genetics/metabolism ; *Cell Survival ; Cells, Cultured ; Cerebellum/cytology ; Cyclic AMP Response Element-Binding Protein/metabolism ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Flavonoids/pharmacology ; Insulin-Like Growth Factor I/pharmacology ; MAP Kinase Kinase 1 ; *MAP Kinase Signaling System ; Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors/metabolism ; Mitogen-Activated Protein Kinases/antagonists & inhibitors/metabolism ; Mutation ; Neurons/*cytology/metabolism ; Phosphorylation ; Phosphoserine/metabolism ; *Protein-Serine-Threonine Kinases ; Rats ; Rats, Long-Evans ; Recombinant Fusion Proteins/metabolism ; Ribosomal Protein S6 Kinases/genetics/*metabolism ; *Transcription, Genetic ; Transfection ; bcl-Associated Death Protein ; ras Proteins/metabolism
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  • 36
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    Gating of BDNF-induced synaptic potentiation by cAMP (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-18
    Description: Neurotrophins have been implicated in activity-dependent synaptic plasticity, but the underlying intracellular mechanisms remain largely unknown. Synaptic potentiation induced by brain-derived neurotrophic factor (BDNF), but not neurotrophin 3, was prevented by blockers of adenosine 3',5'-monophosphate (cAMP) signaling. Activators of cAMP signaling alone were ineffective in modifying synaptic efficacy but greatly enhanced the potentiation effect of BDNF. Blocking cAMP signaling abolished the facilitation of BDNF-induced potentiation by presynaptic activity. Thus synaptic actions of BDNF are gated by cAMP. Activity and other coincident signals that modulate cAMP concentrations may specify the action of secreted neurotrophins on developing nerve terminals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boulanger, L -- Poo, M M -- NS 37831/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jun 18;284(5422):1982-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California at San Diego, La Jolla, CA 92093-0357, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10373115" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain-Derived Neurotrophic Factor/*pharmacology ; *Carbazoles ; Cells, Cultured ; Cyclic AMP/analogs & derivatives/pharmacology/*physiology ; Cycloleucine/analogs & derivatives/pharmacology ; *Excitatory Postsynaptic Potentials/drug effects ; Indoles/pharmacology ; Nerve Growth Factors/pharmacology ; Neuronal Plasticity ; Neurons/cytology/physiology ; Neurotrophin 3 ; Okadaic Acid/pharmacology ; Patch-Clamp Techniques ; Pyrroles/pharmacology ; Signal Transduction ; Synapses/drug effects/*physiology ; *Synaptic Transmission/drug effects ; Thionucleotides/pharmacology ; Xenopus
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    Cancer research. A new way to combat therapy side effects (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferber, D -- New York, N.Y. -- Science. 1999 Sep 10;285(5434):1651, 1653.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10523177" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/*adverse effects ; Apoptosis/*drug effects ; Benzothiazoles ; Cell Division/drug effects/radiation effects ; Cells, Cultured ; Drug Evaluation, Preclinical ; Gamma Rays/*adverse effects ; Humans ; Mice ; Neoplasms/drug therapy/radiotherapy/*therapy ; Radiation Dosage ; Radiation Tolerance/*drug effects ; Thiazoles/*pharmacology ; Toluene/*analogs & derivatives/pharmacology ; Tumor Suppressor Protein p53/*antagonists & inhibitors/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Dissecting dendrite dynamics (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, S J -- New York, N.Y. -- Science. 1999 Mar 19;283(5409):1860-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305, USA. sjsmith@leland.stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10206891" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; Action Potentials ; Animals ; Dendrites/*physiology/ultrastructure ; Excitatory Amino Acid Antagonists/pharmacology ; Glutamic Acid/metabolism ; Hippocampus/cytology ; Microscopy, Fluorescence ; Neurons/physiology/ultrastructure ; Pseudopodia/*physiology/ultrastructure ; Rats ; Receptors, N-Methyl-D-Aspartate/*physiology ; Synapses/*physiology/ultrastructure ; Synaptic Membranes/physiology
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    The role of local actin instability in axon formation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-19
    Description: The role of localized instability of the actin network in specifying axonal fate was examined with the use of rat hippocampal neurons in culture. During normal neuronal development, actin dynamics and instability polarized to a single growth cone before axon formation. Consistently, global application of actin-depolymerizing drugs and of the Rho-signaling inactivator toxin B to nonpolarized cells produced neurons with multiple axons. Moreover, disruption of the actin network in one individual growth cone induced its neurite to become the axon. Thus, local instability of the actin network restricted to a single growth cone is a physiological signal specifying neuronal polarization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bradke, F -- Dotti, C G -- New York, N.Y. -- Science. 1999 Mar 19;283(5409):1931-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉European Molecular Biology Laboratory, Cell Biology Programme, Meyerhofstrasse 1, 69012 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10082468" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism/*physiology ; Animals ; Axons/*physiology/ultrastructure ; *Bacterial Proteins ; Bacterial Toxins/pharmacology ; Bicyclo Compounds, Heterocyclic/pharmacology ; Cell Polarity ; Cells, Cultured ; Cytochalasin D/pharmacology ; GTP Phosphohydrolases/antagonists & inhibitors/metabolism ; Growth Cones/drug effects/*physiology/ultrastructure ; Hippocampus ; Microtubules/physiology/ultrastructure ; Neurites/*physiology/ultrastructure ; Phenotype ; Pseudopodia/drug effects/ultrastructure ; Rats ; Signal Transduction ; Thiazoles/pharmacology ; Thiazolidines
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  • 40
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    Apaf-1 and caspase-9 in p53-dependent apoptosis and tumor inhibition (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-02
    Description: The ability of p53 to promote apoptosis in response to mitogenic oncogenes appears to be critical for its tumor suppressor function. Caspase-9 and its cofactor Apaf-1 were found to be essential downstream components of p53 in Myc-induced apoptosis. Like p53 null cells, mouse embryo fibroblast cells deficient in Apaf-1 and caspase-9, and expressing c-Myc, were resistant to apoptotic stimuli that mimic conditions in developing tumors. Inactivation of Apaf-1 or caspase-9 substituted for p53 loss in promoting the oncogenic transformation of Myc-expressing cells. These results imply a role for Apaf-1 and caspase-9 in controlling tumor development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Soengas, M S -- Alarcon, R M -- Yoshida, H -- Giaccia, A J -- Hakem, R -- Mak, T W -- Lowe, S W -- CA13106/CA/NCI NIH HHS/ -- CA64489/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 2;284(5411):156-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10102818" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptotic Protease-Activating Factor 1 ; Caspase 9 ; Caspases/genetics/*physiology ; Cell Division ; Cell Transformation, Neoplastic ; Cells, Cultured ; Cytochrome c Group/metabolism ; Genes, myc ; *Genes, p53 ; Genes, ras ; Mice ; Mice, Nude ; Mitochondria/metabolism ; Mutation ; Neoplasms, Experimental/genetics/metabolism/*pathology ; Proteins/genetics/*physiology ; Tumor Suppressor Protein p53/metabolism
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  • 41
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    Precisely localized LTD in the neocortex revealed by infrared-guided laser stimulation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-03
    Description: In a direct approach to elucidate the origin of long-term depression (LTD), glutamate was applied onto dendrites of neurons in rat neocortical slices. An infrared-guided laser stimulation was used to release glutamate from caged glutamate in the focal spot of an ultraviolet laser. A burst of light flashes caused an LTD-like depression of glutamate receptor responses, which was highly confined to the region of "tetanic" stimulation (〈10 micrometers). A similar depression of glutamate receptor responses was observed during LTD of synaptic transmission. A spatially highly specific postsynaptic mechanism can account for the LTD induced by glutamate release.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dodt, H -- Eder, M -- Frick, A -- Zieglgansberger, W -- New York, N.Y. -- Science. 1999 Oct 1;286(5437):110-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institute of Psychiatry, Kraepelinstrasse 2, 80804 Munich, Germany. dodt@mpipsykl.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10506556" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dizocilpine Maleate/pharmacology ; Electric Stimulation ; Excitatory Amino Acid Antagonists/pharmacology ; Excitatory Postsynaptic Potentials ; Glutamates/pharmacology ; Glutamic Acid/metabolism ; In Vitro Techniques ; Infrared Rays ; Lasers ; Microscopy, Video ; Neocortex/cytology/*physiology ; *Neuronal Plasticity ; Patch-Clamp Techniques ; Photolysis ; Pyramidal Cells/*physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, Glutamate/*metabolism ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/metabolism ; Synapses/*physiology ; *Synaptic Transmission
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  • 42
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    Putting stem cells to work (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Solter, D -- Gearhart, J -- New York, N.Y. -- Science. 1999 Mar 5;283(5407):1468-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Max Planck Institute of Immunology, Freiburg, Germany. solter@immunbio.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10206877" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bioethics ; Blastocyst/*cytology ; *Cell Differentiation ; Cell Line ; Cells, Cultured ; Cloning, Organism ; Cytoplasm/physiology ; Embryo, Mammalian/cytology ; Humans ; Mice ; Nuclear Transfer Techniques ; Stem Cells/*cytology
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  • 43
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    Requirement for diverse, low-abundance peptides in positive selection of T cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-05
    Description: Whether a single major histocompatibility complex (MHC)-bound peptide can drive the positive selection of large numbers of T cells has been a controversial issue. A diverse population of self peptides was shown to be essential for the in vivo development of CD4 T cells. Mice in which all but 5 percent of MHC class II molecules were bound by a single peptide had wild-type numbers of CD4 T cells. However, when the diversity within this 5 percent was lost, CD4 T cell development was impaired. Blocking the major peptide-MHC complex in thymus organ culture had no effect on T cell development, indicating that positive selection occurred on the diverse peptides present at low levels. This requirement for peptide diversity indicates that the interaction between self peptides and T cell receptors during positive selection is highly specific.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barton, G M -- Rudensky, A Y -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):67-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular and Cellular Biology Program of the University of Washington and Fred Hutchinson Cancer Research Center, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9872742" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; CD4-Positive T-Lymphocytes/cytology/*immunology/metabolism ; CD8-Positive T-Lymphocytes/cytology/immunology/metabolism ; Cells, Cultured ; Histocompatibility Antigens Class II/*immunology/metabolism ; Lymphocyte Activation ; Lymphocyte Culture Test, Mixed ; Mice ; Mice, Knockout ; Mice, Transgenic ; Peptides/*immunology/metabolism ; Receptors, Antigen, T-Cell/*immunology ; Recombinant Fusion Proteins/metabolism ; Spleen/immunology ; Thymus Gland/immunology
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  • 44
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    Biological action of leptin as an angiogenic factor (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-11
    Description: Leptin is a hormone that regulates food intake, and its receptor (OB-Rb) is expressed primarily in the hypothalamus. Here, it is shown that OB-Rb is also expressed in human vasculature and in primary cultures of human endothelial cells. In vitro and in vivo assays revealed that leptin has angiogenic activity. In vivo, leptin induced neovascularization in corneas from normal rats but not in corneas from fa/fa Zucker rats, which lack functional leptin receptors. These observations indicate that the vascular endothelium is a target for leptin and suggest a physiological mechanism whereby leptin-induced angiogenesis may facilitate increased energy expenditure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sierra-Honigmann, M R -- Nath, A K -- Murakami, C -- Garcia-Cardena, G -- Papapetropoulos, A -- Sessa, W C -- Madge, L A -- Schechner, J S -- Schwabb, M B -- Polverini, P J -- Flores-Riveros, J R -- New York, N.Y. -- Science. 1998 Sep 11;281(5383):1683-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, CT 06536, USA. rocio_sierra-honigmann@qm.yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9733517" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/metabolism ; Amino Acid Sequence ; Animals ; Carrier Proteins/analysis/*physiology ; Cells, Cultured ; Corneal Neovascularization ; DNA-Binding Proteins/metabolism ; Endothelial Growth Factors/pharmacology ; Endothelium, Vascular/chemistry/cytology/*physiology ; Energy Metabolism ; Humans ; Leptin ; Lipid Metabolism ; Lymphokines/pharmacology ; Molecular Sequence Data ; *Neovascularization, Physiologic ; Phosphorylation ; Proteins/pharmacology/*physiology ; Rats ; Rats, Zucker ; *Receptors, Cell Surface ; Receptors, Leptin ; STAT3 Transcription Factor ; Trans-Activators/metabolism ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
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  • 45
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    Gene therapy. Treating with HIV (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sikorski, R -- Peters, R -- New York, N.Y. -- Science. 1998 Nov 20;282(5393):1438.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9867652" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/virology ; Genetic Therapy/*methods ; *Genetic Vectors ; HIV/*genetics/physiology ; Neurons/virology ; Rats ; Retina/virology
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  • 46
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    Regulation of cocaine reward by CREB (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-18
    Description: Cocaine regulates the transcription factor CREB (adenosine 3', 5'-monophosphate response element binding protein) in rat nucleus accumbens, a brain region that is important for addiction. Overexpression of CREB in this region decreases the rewarding effects of cocaine and makes low doses of the drug aversive. Conversely, overexpression of a dominant-negative mutant CREB increases the rewarding effects of cocaine. Altered transcription of dynorphin likely contributes to these effects: Its expression is increased by overexpression of CREB and decreased by overexpression of mutant CREB. Moreover, blockade of kappa opioid receptors (on which dynorphin acts) antagonizes the negative effect of CREB on cocaine reward. These results identify an intracellular cascade-culminating in gene expression-through which exposure to cocaine modifies subsequent responsiveness to the drug.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carlezon, W A Jr -- Thome, J -- Olson, V G -- Lane-Ladd, S B -- Brodkin, E S -- Hiroi, N -- Duman, R S -- Neve, R L -- Nestler, E J -- New York, N.Y. -- Science. 1998 Dec 18;282(5397):2272-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Psychiatry, Center for Genes and Behavior, Yale University School of Medicine and Connecticut Mental Health Center, New Haven, CT 06508, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9856954" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cocaine/administration & dosage/*pharmacology ; Conditioning (Psychology) ; Cyclic AMP Response Element-Binding Protein/genetics/*metabolism ; Dose-Response Relationship, Drug ; Dynorphins/genetics/metabolism ; Gene Expression ; Gene Expression Regulation ; Gene Transfer Techniques ; Genetic Vectors ; Naltrexone/analogs & derivatives/pharmacology ; Narcotic Antagonists/pharmacology ; Neurons/metabolism ; Nucleus Accumbens/*metabolism ; Point Mutation ; RNA, Messenger/genetics/metabolism ; Rats ; Receptors, Opioid, kappa/antagonists & inhibitors/metabolism ; *Reward ; Simplexvirus/genetics
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    Research drought looms afer Neurolab mission (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-05-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lawler, A -- New York, N.Y. -- Science. 1998 Apr 24;280(5363):515-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9575093" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Nervous System Physiological Phenomena ; Rats ; *Research ; Space Flight ; *Spacecraft ; United States ; United States National Aeronautics and Space Administration ; *Weightlessness
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  • 48
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    Control of alternative splicing of potassium channels by stress hormones (1998)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1998-05-09
    Description: Many molecular mechanisms for neural adaptation to stress remain unknown. Expression of alternative splice variants of Slo, a gene encoding calcium- and voltage-activated potassium channels, was measured in rat adrenal chromaffin tissue from normal and hypophysectomized animals. Hypophysectomy triggered an abrupt decrease in the proportion of Slo transcripts containing a "STREX" exon. The decrease was prevented by adrenocorticotropic hormone injections. In Xenopus oocytes, STREX variants produced channels with functional properties associated with enhanced repetitive firing. Thus, the hormonal stress axis is likely to control the excitable properties of epinephrine-secreting cells by regulating alternative splicing of Slo messenger RNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xie, J -- McCobb, D P -- New York, N.Y. -- Science. 1998 Apr 17;280(5362):443-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Neurobiology and Behavior, Cornell University, Ithaca, NY 14853, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9545224" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Medulla/*metabolism ; Adrenocorticotropic Hormone/metabolism/*pharmacology ; *Alternative Splicing ; Amino Acid Sequence ; Animals ; Chromaffin Cells/*metabolism ; Corticosterone/blood/*metabolism ; Dexamethasone/pharmacology ; Epinephrine/secretion ; Exons ; Female ; Hypophysectomy ; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits ; Large-Conductance Calcium-Activated Potassium Channels ; Male ; Molecular Sequence Data ; Oocytes ; Phenylethanolamine N-Methyltransferase/genetics ; Polymerase Chain Reaction ; Potassium Channels/*genetics ; *Potassium Channels, Calcium-Activated ; RNA, Messenger/genetics/metabolism ; Rats ; Rats, Sprague-Dawley ; Xenopus
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  • 49
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    Conversion of neuronal growth cone responses from repulsion to attraction by cyclic nucleotides (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-04
    Description: Nerve growth is regulated by attractive and repulsive factors in the nervous system. Microscopic gradients of Collapsin-1/Semaphorin III/D (Sema III) and myelin-associated glycoprotein trigger repulsive turning responses by growth cones of cultured Xenopus spinal neurons; the repulsion can be converted to attraction by pharmacological activation of the guanosine 3',5'-monophosphate (cGMP) and adenosine 3',5'-monophosphate signaling pathways, respectively. Sema III also causes the collapse of cultured rat sensory growth cones, which can be inhibited by activation of the cGMP pathway. Thus cyclic nucleotides can regulate growth cone behaviors and may be targets for designing treatments to alleviate the inhibition of nerve regeneration by repulsive factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Song, H -- Ming, G -- He, Z -- Lehmann, M -- McKerracher, L -- Tessier-Lavigne, M -- Poo, M -- NS22764/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1998 Sep 4;281(5382):1515-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California at San Diego, La Jolla, CA 92093-0357, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9727979" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Calcium/physiology ; Cells, Cultured ; Cyclic AMP/analogs & derivatives/pharmacology/*physiology ; Cyclic GMP/analogs & derivatives/pharmacology/*physiology ; Ganglia, Spinal/cytology ; Glycoproteins/*physiology ; Myelin-Associated Glycoprotein/physiology ; Nerve Growth Factors/*physiology ; Nerve Tissue Proteins/physiology ; Neurites/*physiology ; Neurons/cytology/*physiology ; Neuropilin-1 ; Rats ; Recombinant Proteins ; Semaphorin-3A ; Spinal Cord/cytology ; Thionucleotides/pharmacology ; Xenopus
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    Functional expression of a mammalian odorant receptor (1998)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1998-01-31
    Description: Candidate mammalian odorant receptors were first cloned some 6 years ago. The physiological function of these receptors in initiating transduction in olfactory receptor neurons remains to be established. Here, a recombinant adenovirus was used to drive expression of a particular receptor gene in an increased number of sensory neurons in the rat olfactory epithelium. Electrophysiological recording showed that increased expression of a single gene led to greater sensitivity to a small subset of odorants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhao, H -- Ivic, L -- Otaki, J M -- Hashimoto, M -- Mikoshiba, K -- Firestein, S -- New York, N.Y. -- Science. 1998 Jan 9;279(5348):237-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Interdepartmental Neuroscience Program, Yale University, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9422698" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics/physiology ; Aldehydes/metabolism/*pharmacology ; Animals ; Electrophysiology ; Female ; Gene Expression ; Genetic Vectors ; Green Fluorescent Proteins ; Luminescent Proteins/analysis/genetics ; Male ; *Odors ; Olfactory Receptor Neurons/*physiology/virology ; Patch-Clamp Techniques ; Rats ; Rats, Sprague-Dawley ; Receptors, Odorant/genetics/metabolism/*physiology ; Recombinant Proteins
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    Ligand binding. Molecular barbells (1998)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1998-12-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peters, R -- Sikorski, R -- New York, N.Y. -- Science. 1998 Nov 20;282(5393):1439.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9867653" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Cattle ; Cyclic GMP/chemistry/*metabolism ; Cyclic GMP-Dependent Protein Kinase Type I ; Cyclic GMP-Dependent Protein Kinases/chemistry/*metabolism ; Dimerization ; Ion Channel Gating ; Ion Channels/chemistry/*metabolism ; Ligands ; Polyethylene Glycols ; Rats ; Retinal Rod Photoreceptor Cells/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Prevention of cardiac hypertrophy in mice by calcineurin inhibition (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-11
    Description: Hypertrophic cardiomyopathy (HCM) is an inherited form of heart disease that affects 1 in 500 individuals. Here it is shown that calcineurin, a calcium-regulated phosphatase, plays a critical role in the pathogenesis of HCM. Administration of the calcineurin inhibitors cyclosporin and FK506 prevented disease in mice that were genetically predisposed to develop HCM as a result of aberrant expression of tropomodulin, myosin light chain-2, or fetal beta-tropomyosin in the heart. Cyclosporin had a similar effect in a rat model of pressure-overload hypertrophy. These results suggest that calcineurin inhibitors merit investigation as potential therapeutics for certain forms of human heart disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sussman, M A -- Lim, H W -- Gude, N -- Taigen, T -- Olson, E N -- Robbins, J -- Colbert, M C -- Gualberto, A -- Wieczorek, D F -- Molkentin, J D -- HL58224-01/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1998 Sep 11;281(5383):1690-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Cardiovascular Biology, Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9733519" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcineurin/metabolism ; *Calcineurin Inhibitors ; Calcium/metabolism ; *Cardiac Myosins ; Cardiomegaly/metabolism/pathology/*prevention & control ; Cardiomyopathy, Dilated/pathology/*prevention & control ; Cardiomyopathy, Hypertrophic/genetics/metabolism/pathology/*prevention & control ; Carrier Proteins/genetics ; Cyclosporine/*pharmacology ; Female ; Mice ; Mice, Transgenic ; *Microfilament Proteins ; Models, Cardiovascular ; Myocardium/*metabolism/pathology ; Myosin Light Chains/genetics/metabolism ; Rats ; Signal Transduction ; Tacrolimus/*pharmacology ; Tropomodulin ; Tropomyosin/genetics
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    Regulation of nerve growth mediated by inositol 1,4,5-trisphosphate receptors in growth cones (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-30
    Description: The inositol 1,4,5-trisphosphate (IP3) receptor (IP3R) acts as a Ca2+ release channel on internal Ca2+ stores. Type 1 IP3R (IP3R1) is enriched in growth cones of neurons in chick dorsal root ganglia. Depletion of internal Ca2+ stores and inhibition of IP3 signaling with drugs inhibited neurite extension. Microinjection of heparin, a competitive IP3R blocker, induced neurite retraction. Acute localized loss of function of IP3R1 in the growth cone induced by chromophore-assisted laser inactivation resulted in growth arrest and neurite retraction. IP3-induced Ca2+ release in growth cones appears to have a crucial role in control of nerve growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takei, K -- Shin, R M -- Inoue, T -- Kato, K -- Mikoshiba, K -- New York, N.Y. -- Science. 1998 Nov 27;282(5394):1705-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Calciosignal Net Project, Exploratory Research for Advanced Technology (ERATO), Japan Science and Technology Corporation (JST), Bunkyo-Ku, Tokyo 113-0021, Japan. kohtaro@ims.u-tokyo.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9831561" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Calcium Channels/*metabolism ; Calcium Signaling ; Cells, Cultured ; Cerebellum/metabolism ; Chick Embryo ; Ganglia, Spinal/cytology ; Growth Cones/*metabolism ; Heparin/pharmacology ; Inositol 1,4,5-Trisphosphate/*metabolism ; Inositol 1,4,5-Trisphosphate Receptors ; Lasers ; Lithium Chloride/pharmacology ; Mice ; Microscopy, Video ; Microsomes/metabolism ; Microtubules/metabolism ; Neurites/drug effects/*physiology ; Pseudopodia/drug effects/physiology ; Receptors, Cytoplasmic and Nuclear/*metabolism ; Signal Transduction ; Thapsigargin/pharmacology
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    Transmission of chronic nociception by spinal neurons expressing the substance P receptor (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-24
    Description: Substance P receptor (SPR)-expressing spinal neurons were ablated with the selective cytotoxin substance P-saporin. Loss of these neurons resulted in a reduction of thermal hyperalgesia and mechanical allodynia associated with persistent neuropathic and inflammatory pain states. This loss appeared to be permanent. Responses to mildly painful stimuli and morphine analgesia were unaffected by this treatment. These results identify a target for treating persistent pain and suggest that the small population of SPR-expressing neurons in the dorsal horn of the spinal cord plays a pivotal role in the generation and maintenance of chronic neuropathic and inflammatory pain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nichols, M L -- Allen, B J -- Rogers, S D -- Ghilardi, J R -- Honore, P -- Luger, N M -- Finke, M P -- Li, J -- Lappi, D A -- Simone, D A -- Mantyh, P W -- 23970/PHS HHS/ -- 31223/PHS HHS/ -- DEO 7288/DE/NIDCR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1558-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Preventive Sciences, University of Minnesota, Minneapolis, MN 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10567262" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dose-Response Relationship, Drug ; Ganglia, Spinal/drug effects/physiology ; *Immunotoxins ; Inflammation/physiopathology ; Ligation ; *N-Glycosyl Hydrolases ; Neuralgia/drug therapy/physiopathology ; Pain/*drug therapy/*physiopathology ; Plant Proteins/administration & dosage/*pharmacology ; Posterior Horn Cells/drug effects/*physiology ; Rats ; Receptors, Neurokinin-1/*metabolism ; Ribosome Inactivating Proteins, Type 1 ; Spinal Nerves ; Substance P/administration & dosage/*pharmacology ; Time Factors
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    First components found for new kidney filter (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1999 Oct 8;286(5438):225-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577188" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Cells, Cultured ; Chromosomes, Human, Pair 19/genetics ; Cytoskeletal Proteins ; Humans ; Intercellular Junctions/metabolism/ultrastructure ; Kidney Glomerulus/blood supply/chemistry/*metabolism/*ultrastructure ; Membrane Proteins ; Mice ; Mice, Knockout ; Microscopy, Electron ; Mutation ; Nephrotic Syndrome/congenital/genetics/pathology ; Proteins/chemistry/genetics/*metabolism
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    Contact-dependent inhibition of cortical neurite growth mediated by notch signaling (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-26
    Description: The exuberant growth of neurites during development becomes markedly reduced as cortical neurons mature. In vitro studies of neurons from mouse cerebral cortex revealed that contact-mediated Notch signaling regulates the capacity of neurons to extend and elaborate neurites. Up-regulation of Notch activity was concomitant with an increase in the number of interneuronal contacts and cessation of neurite growth. In neurons with low Notch activity, which readily extend neurites, up-regulation of Notch activity either inhibited extension or caused retraction of neurites. Conversely, in more mature neurons that had ceased their growth after establishing numerous connections and displayed high Notch activity, inhibition of Notch signaling promoted neurite extension. Thus, the formation of neuronal contacts results in activation of Notch receptors, leading to restriction of neuronal growth and a subsequent arrest in maturity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sestan, N -- Artavanis-Tsakonas, S -- Rakic, P -- NS14841/NS/NINDS NIH HHS/ -- NS26084/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):741-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Neurobiology, 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/10531053" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Communication ; Cell Count ; Cell Differentiation ; Cell Movement ; Cell Nucleus/metabolism ; Cell Size ; Cells, Cultured ; Cerebral Cortex/*cytology/embryology ; Contact Inhibition ; Humans ; Ligands ; Membrane Proteins/*metabolism ; Mice ; Mitosis ; Neurites/chemistry/*physiology ; Neurons/*cytology/metabolism ; Protein Structure, Tertiary ; Receptor, Notch1 ; Receptor, Notch2 ; Receptors, Cell Surface/*metabolism ; Signal Transduction ; *Transcription Factors ; Transcriptional Activation ; Up-Regulation
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    Dynamic control of CaMKII translocation and localization in hippocampal neurons by NMDA receptor stimulation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-02
    Description: Calcium-calmodulin-dependent protein kinase II (CaMKII) is thought to increase synaptic strength by phosphorylating postsynaptic density (PSD) ion channels and signaling proteins. It is shown that N-methyl-D-aspartate (NMDA) receptor stimulation reversibly translocates green fluorescent protein-tagged CaMKII from an F-actin-bound to a PSD-bound state. The translocation time was controlled by the ratio of expressed beta-CaMKII to alpha-CaMKII isoforms. Although F-actin dissociation into the cytosol required autophosphorylation of or calcium-calmodulin binding to beta-CaMKII, PSD translocation required binding of calcium-calmodulin to either the alpha- or beta-CaMKII subunits. Autophosphorylation of CaMKII indirectly prolongs its PSD localization by increasing the calmodulin-binding affinity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, K -- Meyer, T -- GM-48113/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 2;284(5411):162-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Department of Pharmacology and Cancer Biology, Box 3709, 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/10102820" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Calcium/pharmacology ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cells, Cultured ; Cytosol/metabolism ; Dendrites/*enzymology ; Electric Stimulation ; Glutamic Acid/pharmacology ; Green Fluorescent Proteins ; Hippocampus/cytology/*enzymology ; Isoenzymes/metabolism ; Luminescent Proteins ; Microscopy, Fluorescence ; Nerve Tissue Proteins/analysis ; Neurons/*enzymology ; Phosphorylation ; Rats ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Synapses/*enzymology ; Tumor Cells, Cultured
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    Stem cells as potential nerve therapy (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steghaus-Kovac, S -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):650-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10454911" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bioethics ; Diffuse Cerebral Sclerosis of Schilder/*therapy ; Embryo, Mammalian/cytology ; Financing, Government ; Germany ; Humans ; Mice ; Myelin Sheath/*physiology ; Oligodendroglia/*cytology/physiology/transplantation ; Rats ; Research Support as Topic ; Spinal Cord ; Stem Cells/*cytology/physiology
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    Perforin gene defects in familial hemophagocytic lymphohistiocytosis (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-03
    Description: Familial hemophagocytic lymphohistiocytosis (FHL) is a rare, rapidly fatal, autosomal recessive immune disorder characterized by uncontrolled activation of T cells and macrophages and overproduction of inflammatory cytokines. Linkage analyses indicate that FHL is genetically heterogeneous and linked to 9q21.3-22, 10q21-22, or another as yet undefined locus. Sequencing of the coding regions of the perforin gene of eight unrelated 10q21-22-linked FHL patients revealed homozygous nonsense mutations in four patients and missense mutations in the other four patients. Cultured lymphocytes from patients had defective cytotoxic activity, and immunostaining revealed little or no perforin in the granules. Thus, defects in perforin are responsible for 10q21-22-linked FHL. Perforin-based effector systems are, therefore, involved not only in the lysis of abnormal cells but also in the down-regulation of cellular immune activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stepp, S E -- Dufourcq-Lagelouse, R -- Le Deist, F -- Bhawan, S -- Certain, S -- Mathew, P A -- Henter, J I -- Bennett, M -- Fischer, A -- de Saint Basile, G -- Kumar, V -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1957-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and the Graduate Program in Immunology, University of Texas Southwestern Medical School, Dallas, TX 75235, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10583959" target="_blank"〉PubMed〈/a〉
    Keywords: Antigen-Presenting Cells/immunology ; Cell Death ; Cell Line ; Cells, Cultured ; Chromosome Mapping ; Chromosomes, Human, Pair 10/*genetics ; Codon, Terminator ; Cytoplasmic Granules/chemistry ; Cytotoxicity, Immunologic ; Frameshift Mutation ; Genetic Linkage ; Granzymes ; Heterozygote ; Histiocytosis, Non-Langerhans-Cell/*genetics/immunology ; Humans ; Lymphocyte Activation ; Membrane Glycoproteins/analysis/*genetics/physiology ; Mutation, Missense ; Perforin ; Point Mutation ; Pore Forming Cytotoxic Proteins ; Serine Endopeptidases/analysis ; T-Lymphocytes, Cytotoxic/chemistry/immunology
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    PEG antibodies (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peters, R -- Sikorsky, R -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):434.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577206" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites, Antibody ; Biological Availability ; Half-Life ; Immunoglobulin Fab Fragments/*immunology/*metabolism ; Male ; Polyethylene Glycols/*metabolism ; Rats ; Rats, Wistar
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    Introducing proteins into the body's cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strauss, E -- New York, N.Y. -- Science. 1999 Sep 3;285(5433):1466-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10498525" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/*metabolism ; Cells, Cultured ; Drug Carriers ; *Drug Delivery Systems ; Gene Products, tat/chemistry/*metabolism ; Humans ; Mice ; Protein Denaturation ; Protein Folding ; Recombinant Fusion Proteins/administration & dosage/chemistry/*metabolism ; beta-Galactosidase/administration & dosage/chemistry/*metabolism
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    Specific lipopolysaccharide found in cystic fibrosis airway Pseudomonas aeruginosa (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-24
    Description: Cystic fibrosis (CF) patients develop chronic airway infections with Pseudomonas aeruginosa (PA). Pseudomonas aeruginosa synthesized lipopolysaccharide (LPS) with a variety of penta- and hexa-acylated lipid A structures under different environmental conditions. CF patient PA synthesized LPS with specific lipid A structures indicating unique recognition of the CF airway environment. CF-specific lipid A forms containing palmitate and aminoarabinose were associated with resistance to cationic antimicrobial peptides and increased inflammatory responses, indicating that they are likely to be involved in airway disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ernst, R K -- Yi, E C -- Guo, L -- Lim, K B -- Burns, J L -- Hackett, M -- Miller, S I -- R21 R13400/PHS HHS/ -- R55 HL 48888/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1561-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10567263" target="_blank"〉PubMed〈/a〉
    Keywords: Acylation ; Arabinose/analogs & derivatives/analysis/metabolism ; Bacterial Proteins/genetics/physiology ; Cells, Cultured ; Cystic Fibrosis/complications/*microbiology ; Drug Resistance, Microbial ; Humans ; Infant ; Interleukin-8/biosynthesis ; Lipid A/*biosynthesis/*chemistry ; Lipopolysaccharides/chemistry/immunology ; Magnesium/pharmacology ; Mutation ; Palmitates/analysis/metabolism ; Peptides/pharmacology ; Polymyxins/pharmacology ; Pseudomonas Infections/*microbiology ; Pseudomonas aeruginosa/drug effects/genetics/*metabolism/pathogenicity ; Respiratory System/*microbiology ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; Virulence
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    Regulation of myosin phosphatase by a specific interaction with cGMP- dependent protein kinase Ialpha (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-24
    Description: Contraction and relaxation of smooth muscle are regulated by myosin light-chain kinase and myosin phosphatase through phosphorylation and dephosphorylation of myosin light chains. Cyclic guanosine monophosphate (cGMP)-dependent protein kinase Ialpha (cGKIalpha) mediates physiologic relaxation of vascular smooth muscle in response to nitric oxide and cGMP. It is shown here that cGKIalpha is targeted to the smooth muscle cell contractile apparatus by a leucine zipper interaction with the myosin-binding subunit (MBS) of myosin phosphatase. Uncoupling of the cGKIalpha-MBS interaction prevents cGMP-dependent dephosphorylation of myosin light chain, demonstrating that this interaction is essential to the regulation of vascular smooth muscle cell tone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Surks, H K -- Mochizuki, N -- Kasai, Y -- Georgescu, S P -- Tang, K M -- Ito, M -- Lincoln, T M -- Mendelsohn, M E -- HL09330/HL/NHLBI NIH HHS/ -- HL55309/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1583-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Cardiology Research Institute and Cardiology Division, Department of Medicine, Tufts University School of Medicine and New England Medical Center, Boston, MA 02111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10567269" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Substitution ; Animals ; Cells, Cultured ; Cyclic GMP-Dependent Protein Kinase Type I ; Cyclic GMP-Dependent Protein Kinases/chemistry/genetics/*metabolism ; Histones/metabolism ; Humans ; Isoenzymes/chemistry/metabolism ; Leucine Zippers ; Muscle Contraction ; Muscle Relaxation ; Muscle, Smooth, Vascular/*enzymology/physiology ; Mutagenesis, Site-Directed ; Myosin Light Chains/*metabolism ; Myosin-Light-Chain Phosphatase ; Phosphoprotein Phosphatases/chemistry/*metabolism ; Phosphorylation ; Precipitin Tests ; Rats ; Recombinant Fusion Proteins/metabolism ; Substrate Specificity ; Transfection ; Two-Hybrid System Techniques
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    Microglial activation resulting from CD40-CD40L interaction after beta-amyloid stimulation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-22
    Description: Alzheimer's disease (AD) has a substantial inflammatory component, and activated microglia may play a central role in neuronal degeneration. CD40 expression was increased on cultured microglia treated with freshly solublized amyloid-beta (Abeta, 500 nanomolar) and on microglia from a transgenic murine model of AD (Tg APPsw). Increased tumor necrosis factor alpha production and induction of neuronal injury occurred when Abeta-stimulated microglia were treated with CD40 ligand (CD40L). Microglia from Tg APPsw mice deficient for CD40L demonstrated reduction in activation, suggesting that the CD40-CD40L interaction is necessary for Abeta-induced microglial activation. Finally, abnormal tau phosphorylation was reduced in Tg APPsw animals deficient for CD40L, suggesting that the CD40-CD40L interaction is an early event in AD pathogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tan, J -- Town, T -- Paris, D -- Mori, T -- Suo, Z -- Crawford, F -- Mattson, M P -- Flavell, R A -- Mullan, M -- New York, N.Y. -- Science. 1999 Dec 17;286(5448):2352-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Roskamp Institute, University of South Florida, 3515 East Fletcher Avenue, Tampa, FL 33613, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10600748" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/metabolism ; Amyloid beta-Peptides/*metabolism/pharmacology ; Animals ; Antigens, CD40/biosynthesis/*metabolism ; CD40 Ligand ; Cell Death ; Cells, Cultured ; Interferon-gamma/pharmacology ; Interleukins/pharmacology ; Ligands ; Membrane Glycoproteins/*metabolism/pharmacology ; Mice ; Mice, Transgenic ; Microglia/cytology/immunology/*metabolism ; Neurons/cytology ; Peptide Fragments/pharmacology ; Phosphorylation ; Signal Transduction ; Tumor Necrosis Factor-alpha/biosynthesis/pharmacology ; tau Proteins/metabolism
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    Potential target found for antimetastasis drugs (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finkel, E -- New York, N.Y. -- Science. 1999 Jul 2;285(5424):33-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10428697" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/therapeutic use ; Clinical Trials as Topic ; Cloning, Molecular ; *Glucuronidase ; Glycoside Hydrolases/*antagonists & inhibitors/*genetics/isolation & ; purification/metabolism ; Humans ; Mice ; Neoplasm Metastasis/*prevention & control ; Rats ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Mapping smells in the brain (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1999 Jul 23;285(5427):508.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10447477" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Mapping ; Diagnostic Imaging ; Light ; Mice ; *Odors ; Olfactory Bulb/*physiology ; Olfactory Receptor Neurons/physiology ; Rats ; Receptors, Odorant/*physiology ; Smell/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Two-metal-Ion catalysis in adenylyl cyclase (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: Adenylyl cyclase (AC) converts adenosine triphosphate (ATP) to cyclic adenosine monophosphate, a ubiquitous second messenger that regulates many cellular functions. Recent structural studies have revealed much about the structure and function of mammalian AC but have not fully defined its active site or catalytic mechanism. Four crystal structures were determined of the catalytic domains of AC in complex with two different ATP analogs and various divalent metal ions. These structures provide a model for the enzyme-substrate complex and conclusively demonstrate that two metal ions bind in the active site. The similarity of the active site of AC to those of DNA polymerases suggests that the enzymes catalyze phosphoryl transfer by the same two-metal-ion mechanism and likely have evolved from a common ancestor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tesmer, J J -- Sunahara, R K -- Johnson, R A -- Gosselin, G -- Gilman, A G -- Sprang, S R -- DK38828/DK/NIDDK NIH HHS/ -- DK46371/DK/NIDDK NIH HHS/ -- GM34497/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):756-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biochemistry, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235-9050, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10427002" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Adenylyl Cyclase Inhibitors ; Adenylyl Cyclases/chemistry/genetics/*metabolism ; Animals ; Aspartic Acid/metabolism ; Binding Sites ; Catalysis ; Crystallography, X-Ray ; Deoxyadenine Nucleotides/metabolism/pharmacology ; Dideoxynucleotides ; Dimerization ; Enzyme Inhibitors/metabolism ; Hydrogen Bonding ; Ligands ; Magnesium/*metabolism ; Manganese/*metabolism ; Models, Molecular ; Mutation ; Protein Conformation ; Protein Folding ; Rats ; Thionucleotides/metabolism/pharmacology ; Zinc/*metabolism
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    Proapoptotic Bcl-2 relative Bim required for certain apoptotic responses, leukocyte homeostasis, and to preclude autoimmunity (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-27
    Description: Apoptosis can be triggered by members of the Bcl-2 protein family, such as Bim, that share only the BH3 domain with this family. Gene targeting in mice revealed important physiological roles for Bim. Lymphoid and myeloid cells accumulated, T cell development was perturbed, and most older mice accumulated plasma cells and succumbed to autoimmune kidney disease. Lymphocytes were refractory to apoptotic stimuli such as cytokine deprivation, calcium ion flux, and microtubule perturbation but not to others. Thus, Bim is required for hematopoietic homeostasis and as a barrier to autoimmunity. Moreover, particular death stimuli appear to activate apoptosis through distinct BH3-only proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bouillet, P -- Metcalf, D -- Huang, D C -- Tarlinton, D M -- Kay, T W -- Kontgen, F -- Adams, J M -- Strasser, A -- CA43540/CA/NCI NIH HHS/ -- CA80188/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1735-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria 3050, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10576740" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins ; Autoimmune Diseases/etiology ; *Autoimmunity ; B-Lymphocytes/physiology ; Carrier Proteins/*physiology ; Cells, Cultured ; Crosses, Genetic ; Female ; Gene Targeting ; Glomerulonephritis/etiology ; Hematopoietic Stem Cells/physiology ; Homeostasis ; Leukocyte Count ; Leukocytes/*physiology ; Male ; *Membrane Proteins ; Mice ; Mice, Transgenic ; *Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-bcl-2/physiology ; Signal Transduction ; T-Lymphocyte Subsets/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Vessel cooption, regression, and growth in tumors mediated by angiopoietins and VEGF (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-18
    Description: In contrast with the prevailing view that most tumors and metastases begin as avascular masses, evidence is presented here that a subset of tumors instead initially grows by coopting existing host vessels. This coopted host vasculature does not immediately undergo angiogenesis to support the tumor but instead regresses, leading to a secondarily avascular tumor and massive tumor cell loss. Ultimately, however, the remaining tumor is rescued by robust angiogenesis at the tumor margin. The expression patterns of the angiogenic antagonist angiopoietin-2 and of pro-angiogenic vascular endothelial growth factor (VEGF) suggest that these proteins may be critical regulators of this balance between vascular regression and growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holash, J -- Maisonpierre, P C -- Compton, D -- Boland, P -- Alexander, C R -- Zagzag, D -- Yancopoulos, G D -- Wiegand, S J -- New York, N.Y. -- Science. 1999 Jun 18;284(5422):1994-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10373119" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/blood supply/pathology ; Angiopoietin-1 ; Angiopoietin-2 ; Animals ; Apoptosis ; Blood Vessels/pathology ; Endothelial Growth Factors/genetics/*physiology ; Endothelium, Vascular/pathology/physiology ; Glioblastoma/blood supply/pathology ; Glioma/blood supply/pathology ; In Situ Hybridization ; Lymphokines/genetics/*physiology ; Male ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Mice, Inbred C57BL ; Muscle, Smooth, Vascular/pathology/physiology ; Neoplasm Transplantation ; Neoplasms, Experimental/*blood supply/*pathology ; *Neovascularization, Pathologic ; Proteins/genetics/*physiology ; Rats ; Rats, Sprague-Dawley ; Up-Regulation ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
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    New clues to how neurons strengthen their connections (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1999 Jun 11;284(5421):1755-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10391789" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/cytology/physiology ; Cells, Cultured ; Dendrites/physiology/ultrastructure ; Glutamic Acid/*physiology ; Long-Term Potentiation/*physiology ; Mice ; Neurons/physiology ; Rats ; Receptors, AMPA/*physiology ; Receptors, N-Methyl-D-Aspartate/*physiology ; Synapses/*physiology
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    Odor response properties of rat olfactory receptor neurons (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-26
    Description: Molecular biology studies of olfaction have identified a multigene family of molecular receptors that are likely to be involved in odor transduction mechanisms. However, because previous functional data on peripheral coding were mainly collected from inferior vertebrates, it has been difficult to document the degree of specificity of odor interaction mechanisms. As a matter of fact, studies of the functional expression of olfactory receptors have not demonstrated the low or high specificity of olfactory receptors. In this study, the selectivity of olfactory receptor neurons was investigated in the rat at the cellular level under physiological conditions by unitary extracellular recordings. Individual olfactory receptor neurons were broadly responsive to qualitatively distinct odor compounds. We conclude that peripheral coding is based on activated arrays of olfactory receptor cells with overlapping tuning profiles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duchamp-Viret, P -- Chaput, M A -- Duchamp, A -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2171-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Neurosciences et Systemes Sensoriels, CNRS, UMR, Universite Claude Bernard, 43 boulevard du 11 novembre 1918, 69622 Villeurbanne cedex, France. pduchamp@olfac.univ-lyon1.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10381881" target="_blank"〉PubMed〈/a〉
    Keywords: Acetophenones ; Action Potentials ; Animals ; Anisoles ; Benzaldehydes ; Camphor ; Cyclohexenes ; *Odors ; Olfactory Receptor Neurons/*physiology ; Pentanols ; Rats ; Rats, Wistar ; Receptors, Odorant/genetics/*physiology ; Terpenes
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    KDR receptor: a key marker defining hematopoietic stem cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-08
    Description: Studies on pluripotent hematopoietic stem cells (HSCs) have been hindered by lack of a positive marker, comparable to the CD34 marker of hematopoietic progenitor cells (HPCs). In human postnatal hematopoietic tissues, 0.1 to 0.5% of CD34(+) cells expressed vascular endothelial growth factor receptor 2 (VEGFR2, also known as KDR). Pluripotent HSCs were restricted to the CD34+KDR+ cell fraction. Conversely, lineage-committed HPCs were in the CD34+KDR- subset. On the basis of limiting dilution analysis, the HSC frequency in the CD34+KDR+ fraction was 20 percent in bone marrow (BM) by mouse xenograft assay and 25 to 42 percent in BM, peripheral blood, and cord blood by 12-week long-term culture (LTC) assay. The latter values rose to 53 to 63 percent in LTC supplemented with VEGF and to greater than 95 percent for the cell subfraction resistant to growth factor starvation. Thus, KDR is a positive functional marker defining stem cells and distinguishing them from progenitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ziegler, B L -- Valtieri, M -- Porada, G A -- De Maria, R -- Muller, R -- Masella, B -- Gabbianelli, M -- Casella, I -- Pelosi, E -- Bock, T -- Zanjani, E D -- Peschle, C -- New York, N.Y. -- Science. 1999 Sep 3;285(5433):1553-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Hematology and Oncology, University of Tubingen, Otfried-Muller-Strasse 10, D-72076 Tubingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10477517" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD34/*analysis ; Bone Marrow Cells/cytology ; Cell Lineage ; Cell Separation ; Cells, Cultured ; Endothelial Growth Factors/pharmacology ; Female ; Fetal Blood/cytology ; Fetus ; Flow Cytometry ; *Hematopoiesis ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/chemistry/*cytology/drug effects/physiology ; Humans ; Lymphokines/pharmacology ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Phenotype ; Pregnancy ; Receptor Protein-Tyrosine Kinases/*analysis/physiology ; Receptors, Growth Factor/*analysis/physiology ; Receptors, Vascular Endothelial Growth Factor ; Sheep ; Transplantation, Heterologous ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
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    Reciprocal control of T helper cell and dendritic cell differentiation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-19
    Description: It is not known whether subsets of dendritic cells provide different cytokine microenvironments that determine the differentiation of either type-1 T helper (TH1) or TH2 cells. Human monocyte (pDC1)-derived dendritic cells (DC1) were found to induce TH1 differentiation, whereas dendritic cells (DC2) derived from CD4+CD3-CD11c- plasmacytoid cells (pDC2) induced TH2 differentiation by use of a mechanism unaffected by interleukin-4 (IL-4) or IL-12. The TH2 cytokine IL-4 enhanced DC1 maturation and killed pDC2, an effect potentiated by IL-10 but blocked by CD40 ligand and interferon-gamma. Thus, a negative feedback loop from the mature T helper cells may selectively inhibit prolonged TH1 or TH2 responses by regulating survival of the appropriate dendritic cell subset.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rissoan, M C -- Soumelis, V -- Kadowaki, N -- Grouard, G -- Briere, F -- de Waal Malefyt, R -- Liu, Y J -- New York, N.Y. -- Science. 1999 Feb 19;283(5405):1183-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Schering-Plough, Laboratory for Immunological Research, 27 chemin des Peupliers, Boite Postale 11, 69571, Dardilly, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10024247" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD40 ; Apoptosis ; CD40 Ligand ; Cell Differentiation ; Cell Lineage ; Cell Survival ; Cells, Cultured ; Coculture Techniques ; Dendritic Cells/*cytology/immunology ; Feedback ; Humans ; Interferon-gamma/biosynthesis/pharmacology ; Interleukin-12/biosynthesis/pharmacology/physiology ; Interleukin-4/biosynthesis/pharmacology/*physiology ; Interleukins/biosynthesis/pharmacology ; Lymphocyte Activation ; Membrane Glycoproteins/pharmacology ; Stem Cells/cytology ; Th1 Cells/*cytology/immunology ; Th2 Cells/*cytology/immunology
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    Dual function of the selenoprotein PHGPx during sperm maturation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-28
    Description: The selenoprotein phospholipid hydroperoxide glutathione peroxidase (PHGPx) changes its physical characteristics and biological functions during sperm maturation. PHGPx exists as a soluble peroxidase in spermatids but persists in mature spermatozoa as an enzymatically inactive, oxidatively cross-linked, insoluble protein. In the midpiece of mature spermatozoa, PHGPx protein represents at least 50 percent of the capsule material that embeds the helix of mitochondria. The role of PHGPx as a structural protein may explain the mechanical instability of the mitochondrial midpiece that is observed in selenium deficiency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ursini, F -- Heim, S -- Kiess, M -- Maiorino, M -- Roveri, A -- Wissing, J -- Flohe, L -- New York, N.Y. -- Science. 1999 Aug 27;285(5432):1393-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dipartmento di Chimica Biologica, Universita di Padova, Viale G. Colombo 3, I-35121 Padova, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10464096" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electrophoresis, Gel, Two-Dimensional ; Electrophoresis, Polyacrylamide Gel ; Glutathione Peroxidase/chemistry/isolation & purification/*physiology ; Infertility, Male/metabolism ; Male ; Mitochondria/chemistry/enzymology ; Oxidation-Reduction ; Proteins/chemistry/isolation & purification/*physiology ; Rats ; Rats, Wistar ; Selenium/deficiency/*physiology ; Selenoproteins ; Solubility ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; Spermatids/chemistry/enzymology ; *Spermatogenesis ; Spermatozoa/chemistry/enzymology/*physiology
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    UDP-GlcNAc 2-epimerase: a regulator of cell surface sialylation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: Modification of cell surface molecules with sialic acid is crucial for their function in many biological processes, including cell adhesion and signal transduction. Uridine diphosphate-N-acetylglucosamine 2-epimerase (UDP-GlcNAc 2-epimerase) is an enzyme that catalyzes an early, rate-limiting step in the sialic acid biosynthetic pathway. UDP-GlcNAc 2-epimerase was found to be a major determinant of cell surface sialylation in human hematopoietic cell lines and a critical regulator of the function of specific cell surface adhesion molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keppler, O T -- Hinderlich, S -- Langner, J -- Schwartz-Albiez, R -- Reutter, W -- Pawlita, M -- New York, N.Y. -- Science. 1999 May 21;284(5418):1372-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Applied Tumor Virology Program, Tumor Immunology Program, Deutsches Krebsforschungszentrum, Im Neuenheimer Feld 280, D-69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/metabolism ; Antigens, CD14/biosynthesis ; Antigens, CD15/biosynthesis ; Antigens, Differentiation, B-Lymphocyte/metabolism ; Carbohydrate Epimerases/genetics/metabolism ; Cell Adhesion Molecules/metabolism ; Cell Membrane/*metabolism ; Culture Media ; *Escherichia coli Proteins ; Glycoconjugates/*metabolism ; HL-60 Cells ; Histocompatibility Antigens Class I/biosynthesis ; Humans ; Lectins/metabolism ; Oligosaccharides/biosynthesis ; Rats ; Sialic Acid Binding Ig-like Lectin 2 ; Sialic Acids/*biosynthesis ; Transcription, Genetic ; Transfection ; Tumor Cells, Cultured
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    A nonpeptidyl mimic of superoxide dismutase with therapeutic activity in rats (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-09
    Description: Many human diseases are associated with the overproduction of oxygen free radicals that inflict cell damage. A manganese(II) complex with a bis(cyclohexylpyridine)-substituted macrocyclic ligand (M40403) was designed to be a functional mimic of the superoxide dismutase (SOD) enzymes that normally remove these radicals. M40403 had high catalytic SOD activity and was chemically and biologically stable in vivo. Injection of M40403 into rat models of inflammation and ischemia-reperfusion injury protected the animals against tissue damage. Such mimics may result in better clinical therapies for diseases mediated by superoxide radicals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Salvemini, D -- Wang, Z Q -- Zweier, J L -- Samouilov, A -- Macarthur, H -- Misko, T P -- Currie, M G -- Cuzzocrea, S -- Sikorski, J A -- Riley, D P -- New York, N.Y. -- Science. 1999 Oct 8;286(5438):304-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MetaPhore Pharmaceuticals, 1910 Innerbelt Business Center Drive, St. Louis, MO 63114, USA. dsalvemini@metaphore.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10514375" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Inflammatory Agents, Non-Steroidal/chemical ; synthesis/chemistry/metabolism/*therapeutic use ; Cytoprotection ; Dinoprostone/metabolism ; Dose-Response Relationship, Drug ; Drug Design ; Drug Stability ; Inflammation/*drug therapy ; Interleukin-1/metabolism ; L-Lactate Dehydrogenase/metabolism ; Male ; Manganese ; Molecular Mimicry ; Neutrophils/drug effects ; Organometallic Compounds/chemical synthesis/chemistry/metabolism/*toxicity ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury/*drug therapy ; Splanchnic Circulation ; *Superoxide Dismutase/metabolism ; Superoxides/*metabolism ; Time Factors ; Tumor Necrosis Factor-alpha/metabolism
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    Cholesterol-lowering drugs may boost bones (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, G -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1825-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610568" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anticholesteremic Agents/*pharmacology ; Bone Density/*drug effects ; Bone Morphogenetic Protein 2 ; Bone Morphogenetic Proteins/biosynthesis ; Clinical Trials as Topic ; Female ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/*pharmacology ; Lovastatin/*pharmacology ; Mice ; Osteogenesis/*drug effects ; Osteoporosis/drug therapy ; Rats ; Simvastatin/pharmacology ; *Transforming Growth Factor beta
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    Harnessing the power of stem cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, G -- New York, N.Y. -- Science. 1999 Mar 5;283(5407):1432-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10206866" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Cell Lineage ; Cells, Cultured ; Embryo, Mammalian/cytology ; Endoderm/cytology ; Hematopoietic Stem Cells/cytology ; Humans ; Mesoderm/cytology ; Neurons/cytology ; Stem Cells/*cytology/physiology
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 79
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    Modulation of respiratory frequency by peptidergic input to rhythmogenic neurons in the preBotzinger complex (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-24
    Description: Neurokinin-1 receptor (NK1R) and mu-opioid receptor (muOR) agonists affected respiratory rhythm when injected directly into the preBotzinger Complex (preBotC), the hypothesized site for respiratory rhythmogenesis in mammals. These effects were mediated by actions on preBotC rhythmogenic neurons. The distribution of NK1R+ neurons anatomically defined the preBotC. Type 1 neurons in the preBotC, which have rhythmogenic properties, expressed both NK1Rs and muORs, whereas type 2 neurons expressed only NK1Rs. These findings suggest that the preBotC is a definable anatomic structure with unique physiological function and that a subpopulation of neurons expressing both NK1Rs and muORs generate respiratory rhythm and modulate respiratory frequency.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2811082/" 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/PMC2811082/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gray, P A -- Rekling, J C -- Bocchiaro, C M -- Feldman, J L -- HL37941/HL/NHLBI NIH HHS/ -- HL40959/HL/NHLBI NIH HHS/ -- R01 HL040959/HL/NHLBI NIH HHS/ -- R01 HL040959-12/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1566-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, University of California Los Angeles, Box 951763, Los Angeles, CA 90095-1763, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10567264" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-/pharmacology ; Female ; In Vitro Techniques ; Medulla Oblongata/cytology/drug effects/*physiology ; Mice ; Mice, Inbred BALB C ; Neurons/chemistry/drug effects/*physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, GABA-B/analysis/physiology ; Receptors, Neurokinin-1/agonists/analysis/*physiology ; Receptors, Opioid, mu/agonists/analysis/*physiology ; Respiratory Mechanics/drug effects/*physiology ; Substance P/pharmacology ; 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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  • 80
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    Light-independent role of CRY1 and CRY2 in the mammalian circadian clock (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-26
    Description: Cryptochrome (CRY), a photoreceptor for the circadian clock in Drosophila, binds to the clock component TIM in a light-dependent fashion and blocks its function. In mammals, genetic evidence suggests a role for CRYs within the clock, distinct from hypothetical photoreceptor functions. Mammalian CRY1 and CRY2 are here shown to act as light-independent inhibitors of CLOCK-BMAL1, the activator driving Per1 transcription. CRY1 or CRY2 (or both) showed light-independent interactions with CLOCK and BMAL1, as well as with PER1, PER2, and TIM. Thus, mammalian CRYs act as light-independent components of the circadian clock and probably regulate Per1 transcriptional cycling by contacting both the activator and its feedback inhibitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Griffin, E A Jr -- Staknis, D -- Weitz, C J -- MH-59943/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):768-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston, MA 02115 USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10531061" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; ARNTL Transcription Factors ; Animals ; Basic Helix-Loop-Helix Transcription Factors ; *Biological Clocks ; CLOCK Proteins ; Cell Cycle Proteins ; Cells, Cultured ; *Circadian Rhythm ; Cryptochromes ; Dimerization ; *Drosophila Proteins ; *Eye Proteins ; Flavoproteins/metabolism/*physiology ; *Gene Expression Regulation ; Genes, Reporter ; Helix-Loop-Helix Motifs ; Humans ; Intracellular Signaling Peptides and Proteins ; *Light ; Mice ; Nuclear Proteins/antagonists & inhibitors/*genetics/metabolism ; Period Circadian Proteins ; *Photoreceptor Cells, Invertebrate ; Receptors, G-Protein-Coupled ; Trans-Activators/antagonists & inhibitors/metabolism ; Transcription Factors/antagonists & inhibitors/metabolism ; Transcriptional Activation ; Transfection
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 81
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    Functional human corneal equivalents constructed from cell lines (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-11
    Description: Human corneal equivalents comprising the three main layers of the cornea (epithelium, stroma, and endothelium) were constructed. Each cellular layer was fabricated from immortalized human corneal cells that were screened for use on the basis of morphological, biochemical, and electrophysiological similarity to their natural counterparts. The resulting corneal equivalents mimicked human corneas in key physical and physiological functions, including morphology, biochemical marker expression, transparency, ion and fluid transport, and gene expression. Morphological and functional equivalents to human corneas that can be produced in vitro have immediate applications in toxicity and drug efficacy testing, and form the basis for future development of implantable tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Griffith, M -- Osborne, R -- Munger, R -- Xiong, X -- Doillon, C J -- Laycock, N L -- Hakim, M -- Song, Y -- Watsky, M A -- New York, N.Y. -- Science. 1999 Dec 10;286(5447):2169-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Ottawa Eye Institute and Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa Hospital-General Campus, Ottawa, Ontario K1H 8L6, Canada. mgriffith@ogh.on.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10591651" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Testing Alternatives ; *Biomedical Engineering ; Cell Line ; Cells, Cultured ; Chondroitin Sulfates ; Collagen ; *Cornea/cytology/growth & development/physiology ; Corneal Opacity/chemically induced ; Corneal Stroma/cytology/growth & development/physiology ; Corneal Transplantation ; Cross-Linking Reagents ; *Culture Techniques ; Electrophysiology ; Endothelium, Corneal/cytology/growth & development ; Epithelium, Corneal/cytology/growth & development ; Gene Expression ; Glutaral ; Humans ; Ion Channels ; Ouabain/pharmacology ; Patch-Clamp Techniques ; Sodium Dodecyl Sulfate/pharmacology
    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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  • 82
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    Activity-induced potentiation of developing neuromuscular synapses (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-11
    Description: Electrical activity plays a critical role in shaping the structure and function of synaptic connections in the nervous system. In Xenopus nerve-muscle cultures, a brief burst of action potentials in the presynaptic neuron induced a persistent potentiation of neuromuscular synapses that exhibit immature synaptic functions. Induction of potentiation required an elevation of postsynaptic Ca2+ and expression of potentiation appeared to involve an increased probability of transmitter secretion from the presynaptic nerve terminal. Thus, activity-dependent persistent synaptic enhancement may reflect properties characteristic of immature synaptic connections, and bursting activity in developing spinal neurons may promote functional maturation of the neuromuscular synapse.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wan, J -- Poo, M -- NS22764/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Sep 10;285(5434):1725-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, 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/10481007" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Animals ; Bungarotoxins/pharmacology ; Calcineurin/physiology ; Calcineurin Inhibitors ; Calcium/metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors/metabolism ; Cells, Cultured ; Chelating Agents/pharmacology ; Egtazic Acid/analogs & derivatives/pharmacology ; Electric Stimulation ; *Excitatory Postsynaptic Potentials/drug effects ; Long-Term Potentiation ; Motor Neurons/*physiology ; Neuromuscular Junction/drug effects/*physiology ; *Neuronal Plasticity/drug effects ; Patch-Clamp Techniques ; Receptors, Cholinergic/physiology ; Spinal Cord ; *Synaptic Transmission ; Xenopus
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  • 83
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    CD1d-restricted immunoglobulin G formation to GPI-anchored antigens mediated by NKT cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-08
    Description: Immunoglobulin G (IgG) responses require major histocompatibility complex (MHC)-restricted recognition of peptide fragments by conventional CD4(+) helper T cells. Immunoglobulin G responses to glycosylphosphatidylinositol (GPI)- anchored protein antigens, however, were found to be regulated in part through CD1d-restricted recognition of the GPI moiety by thymus-dependent, interleukin-4-producing CD4(+), natural killer cell antigen 1.1 [(NK1.1)+] helper T cells. The CD1-NKT cell pathway regulated immunogobulin G responses to the GPI-anchored surface antigens of Plasmodium and Trypanosoma and may be a general mechanism for rapid, MHC-unrestricted antibody responses to diverse pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schofield, L -- McConville, M J -- Hansen, D -- Campbell, A S -- Fraser-Reid, B -- Grusby, M J -- Tachado, S D -- AI-40171/AI/NIAID NIH HHS/ -- GM 41071/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 8;283(5399):225-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, Post Office, Royal Melbourne Hospital, Victoria 3050, Australia. schofield@wehi.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9880256" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Antigen-Presenting Cells/immunology ; Antigens/analysis ; Antigens, CD1/*immunology ; Antigens, Ly ; Antigens, Protozoan/*immunology ; Antigens, Surface ; Cells, Cultured ; Glycosylphosphatidylinositols/*immunology ; Immunoglobulin G/*biosynthesis ; Interleukin-4/biosynthesis ; Lectins, C-Type ; Leishmania mexicana/immunology ; Major Histocompatibility Complex ; Mice ; Mice, Inbred Strains ; NK Cell Lectin-Like Receptor Subfamily B ; Plasmodium/immunology ; Proteins/analysis ; Protozoan Proteins/immunology ; T-Lymphocyte Subsets/*immunology ; T-Lymphocytes, Helper-Inducer/*immunology ; Trypanosoma brucei brucei/immunology ; Variant Surface Glycoproteins, Trypanosoma/immunology
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  • 84
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    HMG-1 as a late mediator of endotoxin lethality in mice (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-10
    Description: Endotoxin, a constituent of Gram-negative bacteria, stimulates macrophages to release large quantities of tumor necrosis factor (TNF) and interleukin-1 (IL-1), which can precipitate tissue injury and lethal shock (endotoxemia). Antagonists of TNF and IL-1 have shown limited efficacy in clinical trials, possibly because these cytokines are early mediators in pathogenesis. Here a potential late mediator of lethality is identified and characterized in a mouse model. High mobility group-1 (HMG-1) protein was found to be released by cultured macrophages more than 8 hours after stimulation with endotoxin, TNF, or IL-1. Mice showed increased serum levels of HMG-1 from 8 to 32 hours after endotoxin exposure. Delayed administration of antibodies to HMG-1 attenuated endotoxin lethality in mice, and administration of HMG-1 itself was lethal. Septic patients who succumbed to infection had increased serum HMG-1 levels, suggesting that this protein warrants investigation as a therapeutic target.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, H -- Bloom, O -- Zhang, M -- Vishnubhakat, J M -- Ombrellino, M -- Che, J -- Frazier, A -- Yang, H -- Ivanova, S -- Borovikova, L -- Manogue, K R -- Faist, E -- Abraham, E -- Andersson, J -- Andersson, U -- Molina, P E -- Abumrad, N N -- Sama, A -- Tracey, K J -- New York, N.Y. -- Science. 1999 Jul 9;285(5425):248-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Emergency Medicine and Department of Surgery, North Shore University Hospital-New York University School of Medicine, Manhasset, NY 11030, USA. hwang@picower.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10398600" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteremia/*blood ; Carrier Proteins/genetics/immunology/*metabolism/toxicity ; Cell Line ; Cells, Cultured ; Endotoxemia/*blood ; Endotoxins/blood/*toxicity ; HMGB1 Protein ; High Mobility Group Proteins/genetics/immunology/*metabolism/toxicity ; Humans ; Immune Sera/immunology ; Immunization, Passive ; Interferon-gamma/pharmacology ; Interleukin-1/pharmacology ; Lethal Dose 50 ; Leukocytes, Mononuclear/metabolism ; Lipopolysaccharides/toxicity ; Macrophages/*metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; RNA, Messenger/genetics/metabolism ; Time Factors ; Tumor Necrosis Factor-alpha/pharmacology
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  • 85
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    Ca2+-induced apoptosis through calcineurin dephosphorylation of BAD (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-09
    Description: The Ca2+-activated protein phosphatase calcineurin induces apoptosis, but the mechanism is unknown. Calcineurin was found to dephosphorylate BAD, a pro-apoptotic member of the Bcl-2 family, thus enhancing BAD heterodimerization with Bcl-xL and promoting apoptosis. The Ca2+-induced dephosphorylation of BAD correlated with its dissociation from 14-3-3 in the cytosol and translocation to mitochondria where Bcl-xL resides. In hippocampal neurons, L-glutamate, an inducer of Ca2+ influx and calcineurin activation, triggered mitochondrial targeting of BAD and apoptosis, which were both suppressible by coexpression of a dominant-inhibitory mutant of calcineurin or pharmacological inhibitors of this phosphatase. Thus, a Ca2+-inducible mechanism for apoptosis induction operates by regulating BAD phosphorylation and localization in cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, H G -- Pathan, N -- Ethell, I M -- Krajewski, S -- Yamaguchi, Y -- Shibasaki, F -- McKeon, F -- Bobo, T -- Franke, T F -- Reed, J C -- AG-1593/AG/NIA NIH HHS/ -- CA-69381/CA/NCI NIH HHS/ -- HD25938/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):339-43.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Burnham Institute, 10901 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/10195903" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins ; Animals ; *Apoptosis ; Calcineurin/genetics/*metabolism ; Calcineurin Inhibitors ; Calcium/*metabolism/pharmacology ; Carrier Proteins/chemistry/*metabolism ; Cell Line ; Cells, Cultured ; Dimerization ; Enzyme Inhibitors/pharmacology ; Glutamic Acid/pharmacology ; Hippocampus/cytology ; Humans ; Mitochondria/metabolism ; Neurons/cytology/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/metabolism ; Proteins/metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Rats ; Recombinant Fusion Proteins/metabolism ; Transfection ; *Tyrosine 3-Monooxygenase ; bcl-Associated Death Protein ; bcl-X Protein
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  • 86
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    Stimulation of bone formation in vitro and in rodents by statins (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-03
    Description: Osteoporosis and other diseases of bone loss are a major public health problem. Here it is shown that the statins, drugs widely used for lowering serum cholesterol, also enhance new bone formation in vitro and in rodents. This effect was associated with increased expression of the bone morphogenetic protein-2 (BMP-2) gene in bone cells. Lovastatin and simvastatin increased bone formation when injected subcutaneously over the calvaria of mice and increased cancellous bone volume when orally administered to rats. Thus, in appropriate doses, statins may have therapeutic applications for the treatment of osteoporosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mundy, G -- Garrett, R -- Harris, S -- Chan, J -- Chen, D -- Rossini, G -- Boyce, B -- Zhao, M -- Gutierrez, G -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1946-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉OsteoScreen, 2040 Babcock Road, San Antonio, TX 78229, USA. mundy@uthscsa.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10583956" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Density/*drug effects ; Bone Morphogenetic Protein 2 ; Bone Morphogenetic Proteins/biosynthesis/genetics/pharmacology ; Cell Line ; Female ; Fibroblast Growth Factor 1 ; Fibroblast Growth Factor 2/pharmacology ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology ; Lovastatin/*pharmacology ; Male ; Mice ; Mice, Inbred ICR ; Organ Culture Techniques ; Osteoblasts/*drug effects/metabolism ; Osteoclasts/drug effects ; Osteogenesis/*drug effects ; Osteoporosis/drug therapy ; Ovariectomy ; Promoter Regions, Genetic/drug effects ; Rats ; Recombinant Proteins/pharmacology ; Simvastatin/*pharmacology ; Skull ; Transfection ; *Transforming Growth Factor beta
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  • 87
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    A role for the proteasome in the light response of the timeless clock protein (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-11
    Description: The cyclic expression of the period (PER) and timeless (TIM) proteins is critical for the molecular circadian feedback loop in Drosophila. The entrainment by light of the circadian clock is mediated by a reduction in TIM levels. To elucidate the mechanism of this process, the sensitivity of TIM regulation by light was tested in an in vitro assay with inhibitors of candidate proteolytic pathways. The data suggested that TIM is degraded through a ubiquitin-proteasome mechanism. In addition, in cultures from third-instar larvae, TIM degradation was blocked specifically by inhibitors of proteasome activity. Degradation appeared to be preceded by tyrosine phosphorylation. Finally, TIM was ubiquitinated in response to light in cultured cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Naidoo, N -- Song, W -- Hunter-Ensor, M -- Sehgal, A -- New York, N.Y. -- Science. 1999 Sep 10;285(5434):1737-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Neuroscience, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10481010" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcysteine/analogs & derivatives/pharmacology ; Animals ; *Biological Clocks ; Cells, Cultured ; *Circadian Rhythm ; Cysteine Endopeptidases/*physiology ; Cysteine Proteinase Inhibitors/pharmacology ; Darkness ; Drosophila ; *Drosophila Proteins ; Feedback ; Insect Proteins/*metabolism ; Leucine/analogs & derivatives/pharmacology ; Leupeptins/pharmacology ; *Light ; Multienzyme Complexes/*physiology ; Neurons/*metabolism ; Phosphorylation ; Phosphotyrosine/metabolism ; Protease Inhibitors/pharmacology ; Proteasome Endopeptidase Complex ; Ubiquitins/metabolism
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  • 88
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    Role of heteromer formation in GABAB receptor function (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-05
    Description: Recently, GBR1, a seven-transmembrane domain protein with high affinity for gamma-aminobutyric acid (GABA)B receptor antagonists, was identified. Here, a GBR1-related protein, GBR2, was shown to be coexpressed with GBR1 in many brain regions and to interact with it through a short domain in the carboxyl-terminal cytoplasmic tail. Heterologously expressed GBR2 mediated inhibition of adenylyl cyclase; however, inwardly rectifying potassium channels were activated by GABAB receptor agonists only upon coexpression with GBR1 and GBR2. Thus, the interaction of these receptors appears to be crucial for important physiological effects of GABA and provides a mechanism in receptor signaling pathways that involve a heterotrimeric GTP-binding protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuner, R -- Kohr, G -- Grunewald, S -- Eisenhardt, G -- Bach, A -- Kornau, H C -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):74-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉BASF-LYNX Bioscience AG, Department of Neuroscience, Im Neuenheimer Feld 515, D-69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9872744" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclase Inhibitors ; Amino Acid Sequence ; Animals ; Brain/*metabolism ; Cell Line ; Cyclic AMP/metabolism ; Dimerization ; G Protein-Coupled Inwardly-Rectifying Potassium Channels ; GABA-B Receptor Agonists ; Humans ; In Situ Hybridization ; Molecular Sequence Data ; Neurons/metabolism ; Potassium/metabolism ; Potassium Channels/metabolism ; *Potassium Channels, Inwardly Rectifying ; RNA, Messenger/genetics/metabolism ; Rats ; Receptors, GABA/*chemistry/*metabolism ; Receptors, GABA-B/*chemistry/*metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Sequence Alignment
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  • 89
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    Synergistic signaling in fetal brain by STAT3-Smad1 complex bridged by p300 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-16
    Description: The cytokines LIF (leukemia inhibitory factor) and BMP2 (bone morphogenetic protein-2) signal through different receptors and transcription factors, namely STATs (signal transducers and activators of transcription) and Smads. LIF and BMP2 were found to act in synergy on primary fetal neural progenitor cells to induce astrocytes. The transcriptional coactivator p300 interacts physically with STAT3 at its amino terminus in a cytokine stimulation-independent manner, and with Smad1 at its carboxyl terminus in a cytokine stimulation-dependent manner. The formation of a complex between STAT3 and Smad1, bridged by p300, is involved in the cooperative signaling of LIF and BMP2 and the subsequent induction of astrocytes from neural progenitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakashima, K -- Yanagisawa, M -- Arakawa, H -- Kimura, N -- Hisatsune, T -- Kawabata, M -- Miyazono, K -- Taga, T -- New York, N.Y. -- Science. 1999 Apr 16;284(5413):479-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Cell Biology, Cell Fate Modulation Research Unit, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 101-0062, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10205054" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/cytology ; Bone Morphogenetic Protein 2 ; Bone Morphogenetic Protein Receptors ; Bone Morphogenetic Proteins/metabolism/pharmacology ; COS Cells ; Cell Differentiation ; Cell Nucleus/metabolism ; Cells, Cultured ; Cytokines/*pharmacology ; DNA-Binding Proteins/*metabolism ; E1A-Associated p300 Protein ; Glial Fibrillary Acidic Protein/genetics ; Growth Inhibitors/metabolism/pharmacology ; *Interleukin-6 ; Leukemia Inhibitory Factor ; Leukemia Inhibitory Factor Receptor alpha Subunit ; Lymphokines/metabolism/pharmacology ; Mice ; Nuclear Proteins/*metabolism ; Promoter Regions, Genetic ; Receptors, Cell Surface/metabolism ; Receptors, Cytokine/metabolism ; *Receptors, Growth Factor ; Receptors, OSM-LIF ; STAT3 Transcription Factor ; Sequence Deletion ; *Signal Transduction ; Smad Proteins ; Smad1 Protein ; Stem Cells/cytology/metabolism ; Telencephalon/embryology/metabolism ; Trans-Activators/*metabolism ; *Transcriptional Activation ; *Transforming Growth Factor beta
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    Probing alcoholism's 'dark side' (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, R F -- New York, N.Y. -- Science. 1999 Sep 3;285(5433):1473.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10498528" target="_blank"〉PubMed〈/a〉
    Keywords: Alcoholism/cerebrospinal fluid/*metabolism ; Animals ; Brain/*metabolism ; Corticotropin-Releasing Hormone/cerebrospinal fluid/*metabolism ; Dopamine/metabolism ; Humans ; Rats ; Substance Withdrawal Syndrome/metabolism/prevention & control
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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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    Meeting. American Chemical Society. Raising a glass to health and nanotubes (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, R F -- New York, N.Y. -- Science. 1999 Sep 24;285(5436):2053, 2055.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10523196" target="_blank"〉PubMed〈/a〉
    Keywords: Acetaldehyde/*metabolism ; Animals ; Carbon ; Electronics ; Ethanol/metabolism ; Glucose/chemistry/metabolism ; Glycosylation End Products, Advanced/*metabolism ; Hemoglobin A, Glycosylated/chemistry ; Humans ; Rats
    Print ISSN: 0036-8075
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  • 92
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    Long-term depression in hippocampal interneurons: joint requirement for pre- and postsynaptic events (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-28
    Description: Long-term depression (LTD) is a well-known form of synaptic plasticity of principal neurons in the mammalian brain. Whether such changes occur in interneurons is still controversial. CA3 hippocampal interneurons expressing Ca2+-permeable AMPA receptors exhibited LTD after tetanic stimulation of CA3 excitatory inputs. LTD was independent of NMDA receptors and required both Ca2+ influx through postsynaptic AMPA receptors and activation of presynaptic mGluR7-like receptors. These results point to the capability of interneurons to undergo plastic changes of synaptic strength through joint activation of pre- and postsynaptic glutamate receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Laezza, F -- Doherty, J J -- Dingledine, R -- New York, N.Y. -- Science. 1999 Aug 27;285(5432):1411-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience Graduate Program, Department of Pharmacology, Emory University School of Medicine, Atlanta, GA 30322, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10464102" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Egtazic Acid/analogs & derivatives/pharmacology ; Electric Stimulation ; Hippocampus/cytology/*physiology ; In Vitro Techniques ; Interneurons/*physiology ; Male ; *Neuronal Plasticity ; Patch-Clamp Techniques ; Pyramidal Cells/physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/drug effects/*metabolism ; Receptors, Metabotropic Glutamate/drug effects/*metabolism ; Synapses/*physiology ; Synaptic Transmission ; Tetany
    Print ISSN: 0036-8075
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  • 93
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    Modulation of brain reward circuitry by leptin (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-30
    Description: Leptin, a hormone secreted by fat cells, suppresses food intake and promotes weight loss. To assess the action of this hormone on brain reward circuitry, changes in the rewarding effect of lateral hypothalamic stimulation were measured after leptin administration. At five stimulation sites near the fornix, the effectiveness of the rewarding electrical stimulation was enhanced by chronic food restriction and attenuated by intracerebroventricular infusion of leptin. In contrast, the rewarding effect of stimulating neighboring sites was insensitive to chronic food restriction and was enhanced by leptin in three of four cases. These opposing effects of leptin may mirror complementary changes in the rewarding effects of feeding and of competing behaviors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fulton, S -- Woodside, B -- Shizgal, P -- New York, N.Y. -- Science. 2000 Jan 7;287(5450):125-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Studies in Behavioural Neurobiology, Concordia University, Montreal, QC, H3G 1M8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10615045" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electric Stimulation ; Energy Metabolism ; Feeding Behavior ; Food Deprivation/*physiology ; Hypothalamic Area, Lateral/drug effects/*physiology ; Injections, Intraventricular ; Leptin/administration & dosage/*pharmacology ; Male ; Neurons/physiology ; Neuropeptides/physiology ; Rats ; Rats, Long-Evans ; Recombinant Proteins/administration & dosage/pharmacology ; *Reward ; Self Stimulation/physiology ; Time Factors
    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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  • 94
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    Heartthrobs (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanck, D -- New York, N.Y. -- Science. 1998 Feb 13;279(5353):1004.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Chicago, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9490476" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channels/*metabolism ; Ion Channel Gating ; Muscle, Skeletal/metabolism ; Myocardial Contraction/*physiology ; Myocardium/*metabolism ; Rats ; Ryanodine Receptor Calcium Release Channel/metabolism ; Sarcolemma/metabolism ; Sarcoplasmic Reticulum/metabolism ; Sodium Channels/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 95
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    Regulation of NMDA receptors by an associated phosphatase-kinase signaling complex (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-03
    Description: Regulation of N-methyl-D-aspartate (NMDA) receptor activity by kinases and phosphatases contributes to the modulation of synaptic transmission. Targeting of these enzymes near the substrate is proposed to enhance phosphorylation-dependent modulation. Yotiao, an NMDA receptor-associated protein, bound the type I protein phosphatase (PP1) and the adenosine 3',5'-monophosphate (cAMP)-dependent protein kinase (PKA) holoenzyme. Anchored PP1 was active, limiting channel activity, whereas PKA activation overcame constitutive PP1 activity and conferred rapid enhancement of NMDA receptor currents. Hence, yotiao is a scaffold protein that physically attaches PP1 and PKA to NMDA receptors to regulate channel activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Westphal, R S -- Tavalin, S J -- Lin, J W -- Alto, N M -- Fraser, I D -- Langeberg, L K -- Sheng, M -- Scott, J D -- F32 NS010202/NS/NINDS NIH HHS/ -- GM 48231/GM/NIGMS NIH HHS/ -- NS10202/NS/NINDS NIH HHS/ -- NS10543/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Jul 2;285(5424):93-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Vollum Institute, Oregon Health Sciences University, 3181 S.W. Sam Jackson Road, Portland, OR 97201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10390370" target="_blank"〉PubMed〈/a〉
    Keywords: A Kinase Anchor Proteins ; *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; Binding Sites ; Carrier Proteins/*metabolism ; Cell Line ; Cyclic AMP/analogs & derivatives/pharmacology ; Cyclic AMP-Dependent Protein Kinases/*metabolism ; Cytoskeletal Proteins/*metabolism ; Enzyme Inhibitors/pharmacology ; Holoenzymes/metabolism ; Humans ; Molecular Sequence Data ; Okadaic Acid/pharmacology ; Patch-Clamp Techniques ; Peptide Fragments/pharmacology ; Phosphoprotein Phosphatases/*metabolism ; Phosphorylation ; Rats ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Thionucleotides/pharmacology ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 96
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    Anti-inflammatory properties of cytochrome P450 epoxygenase-derived eicosanoids (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-24
    Description: The epoxyeicosatrienoic acids (EETs) are products of cytochrome P450 epoxygenases that have vasodilatory properties similar to that of endothelium-derived hyperpolarizing factor. The cytochrome P450 isoform CYP2J2 was cloned and identified as a potential source of EETs in human endothelial cells. Physiological concentrations of EETs or overexpression of CYP2J2 decreased cytokine-induced endothelial cell adhesion molecule expression, and EETs prevented leukocyte adhesion to the vascular wall by a mechanism involving inhibition of transcription factor NF-kappaB and IkappaB kinase. The inhibitory effects of EETs were independent of their membrane-hyperpolarizing effects, suggesting that these molecules play an important nonvasodilatory role in vascular inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2720027/" 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/PMC2720027/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Node, K -- Huo, Y -- Ruan, X -- Yang, B -- Spiecker, M -- Ley, K -- Zeldin, D C -- Liao, J K -- HL-52233/HL/NHLBI NIH HHS/ -- HL-58108/HL/NHLBI NIH HHS/ -- P01 HL048743/HL/NHLBI NIH HHS/ -- P01 HL048743-080008/HL/NHLBI NIH HHS/ -- P01 HL048743-090008/HL/NHLBI NIH HHS/ -- R01 HL052233/HL/NHLBI NIH HHS/ -- R01 HL052233-05/HL/NHLBI NIH HHS/ -- R01 HL052233-06/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 Aug 20;285(5431):1276-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vascular Medicine and Atherosclerosis Unit, Cardiovascular Division, Brigham and Women's Hospital and Harvard Medical School, 221 Longwood Avenue, LMRC-322, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10455056" target="_blank"〉PubMed〈/a〉
    Keywords: 8,11,14-Eicosatrienoic Acid/analogs & derivatives/*metabolism/*pharmacology ; Animals ; *Anti-Inflammatory Agents, Non-Steroidal/metabolism/pharmacology ; Carotid Arteries/cytology ; Cattle ; Cell Adhesion/drug effects ; Cell Adhesion Molecules/biosynthesis ; Cells, Cultured ; Coronary Vessels/enzymology ; Cytochrome P-450 Enzyme System/genetics/*metabolism ; DNA-Binding Proteins/metabolism ; Endothelium, Vascular/enzymology/*metabolism ; Humans ; Hydroxyeicosatetraenoic Acids/pharmacology ; I-kappa B Kinase ; *I-kappa B Proteins ; Mice ; Mice, Inbred C57BL ; NF-kappa B/antagonists & inhibitors/metabolism ; Oxygenases/genetics/*metabolism ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; Tumor Necrosis Factor-alpha/antagonists & inhibitors/pharmacology ; Vascular Cell Adhesion Molecule-1/biosynthesis/genetics
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    American Chemical Society. Chemists mix it up in California (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, R F -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):243-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10232968" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biocompatible Materials ; *Biomedical Engineering ; Brain/*drug effects/metabolism ; Caffeine/administration & dosage/adverse effects/*pharmacology ; Catalysis ; Genetic Engineering ; Genetic Therapy/*methods ; Humans ; Polycarboxylate Cement/chemical synthesis ; Polymers/chemical synthesis ; Rats ; Substance-Related Disorders/*etiology
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  • 98
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    Enhanced cortical dopamine output and antipsychotic-like effects of raclopride by alpha2 adrenoceptor blockade (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-03
    Description: Clozapine exerts superior clinical efficacy and markedly enhances cortical dopamine output compared with classical antipsychotic drugs. Here the alpha2 adrenoceptor antagonist idazoxan was administered to rats alone or in combination with the D2/3 dopamine receptor antagonist raclopride. Dopamine efflux in the medial prefrontal cortex and conditioned avoidance responding were analyzed. Idazoxan selectively potentiated the cortical output of dopamine and augmented the suppression of conditioned avoidance responding induced by raclopride. These results challenge basic assumptions underlying the dopamine hypothesis of schizophrenia and provide insight into clozapine's mode of action.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hertel, P -- Fagerquist, M V -- Svensson, T H -- New York, N.Y. -- Science. 1999 Oct 1;286(5437):105-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Pharmacology, Section of Neuropsychopharmacology, Karolinska Institute, S-171 77 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10506554" target="_blank"〉PubMed〈/a〉
    Keywords: *Adrenergic alpha-2 Receptor Antagonists ; Adrenergic alpha-Antagonists/pharmacology ; Animals ; Antipsychotic Agents/*pharmacology ; Avoidance Learning/drug effects ; Catalepsy/chemically induced ; Conditioning (Psychology) ; Corpus Striatum/drug effects/metabolism ; Dopamine/*metabolism ; Dopamine Antagonists/*pharmacology ; Dose-Response Relationship, Drug ; Drug Synergism ; Idazoxan/*pharmacology ; Nucleus Accumbens/drug effects/metabolism ; Prefrontal Cortex/*drug effects/metabolism ; Raclopride ; Rats ; Receptors, Adrenergic, alpha-2/metabolism ; Salicylamides/*pharmacology ; Schizophrenia/drug therapy/metabolism
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  • 99
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    Neuronal activity-dependent cell survival mediated by transcription factor MEF2 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-26
    Description: During mammalian development, electrical activity promotes the calcium-dependent survival of neurons that have made appropriate synaptic connections. However, the mechanisms by which calcium mediates neuronal survival during development are not well characterized. A transcription-dependent mechanism was identified by which calcium influx into neurons promoted cell survival. The transcription factor MEF2 was selectively expressed in newly generated postmitotic neurons and was required for the survival of these neurons. Calcium influx into cerebellar granule neurons led to activation of p38 mitogen-activated protein kinase-dependent phosphorylation and activation of MEF2. Once activated, MEF2 regulated neuronal survival by stimulating MEF2-dependent gene transcription. These findings demonstrate that MEF2 is a calcium-regulated transcription factor and define a function for MEF2 during nervous system development that is distinct from previously well-characterized functions of MEF2 during muscle differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mao, Z -- Bonni, A -- Xia, F -- Nadal-Vicens, M -- Greenberg, M E -- 5T32NS07112/NS/NINDS NIH HHS/ -- NS28829/NS/NINDS NIH HHS/ -- P30-HD18655/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):785-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Department of Neurology, Children's Hospital and Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10531066" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Calcium/metabolism ; Calcium Channels, L-Type/metabolism ; Cell Differentiation ; Cell Survival ; Cells, Cultured ; Cerebellum/cytology/metabolism ; Cerebral Cortex/cytology/embryology/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Dimerization ; Immunohistochemistry ; MEF2 Transcription Factors ; Mitogen-Activated Protein Kinases/metabolism ; Mitosis ; Mutation ; Myogenic Regulatory Factors ; Neurons/*cytology/*metabolism ; Phosphorylation ; Rats ; Signal Transduction ; Transcription Factors/genetics/*metabolism ; *Transcription, Genetic ; Transfection ; p38 Mitogen-Activated Protein Kinases
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  • 100
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    Preliminary data touch off genetic food fight (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, M -- New York, N.Y. -- Science. 1999 Feb 19;283(5405):1094-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10075564" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biotechnology ; Crops, Agricultural/*adverse effects ; Digestive System/pathology ; Food Technology ; Great Britain ; *Growth ; *Immunity ; Infection/pathology ; Lectins/genetics ; Plant Lectins ; Plants, Genetically Modified/*adverse effects ; Rats ; Solanum tuberosum/adverse effects/*genetics
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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