ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • General Chemistry  (3,792)
  • Mice  (1,035)
  • 2000-2004  (1,413)
  • 1920-1924
Collection
Keywords
Publisher
Years
Year
  • 101
    facet.materialart.
    Unknown
    Defining a link with asthma in mice congenitally deficient in eosinophils (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-09-18
    Description: Eosinophils are often dominant inflammatory cells present in the lungs of asthma patients. Nonetheless, the role of these leukocytes remains poorly understood. We have created a transgenic line of mice (PHIL) that are specifically devoid of eosinophils, but otherwise have a full complement of hematopoietically derived cells. Allergen challenge of PHIL mice demonstrated that eosinophils were required for pulmonary mucus accumulation and the airway hyperresponsiveness associated with asthma. The development of an eosinophil-less mouse now permits an unambiguous assessment of a number of human diseases that have been linked to this granulocyte, including allergic diseases, parasite infections, and tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, James J -- Dimina, Dawn -- Macias, MiMi P -- Ochkur, Sergei I -- McGarry, Michael P -- O'Neill, Katie R -- Protheroe, Cheryl -- Pero, Ralph -- Nguyen, Thanh -- Cormier, Stephania A -- Lenkiewicz, Elizabeth -- Colbert, Dana -- Rinaldi, Lisa -- Ackerman, Steven J -- Irvin, Charles G -- Lee, Nancy A -- AI025230/AI/NIAID NIH HHS/ -- AI033043/AI/NIAID NIH HHS/ -- AR08545/AR/NIAMS NIH HHS/ -- F32 AR008545/AR/NIAMS NIH HHS/ -- F32 AR008545-01/AR/NIAMS NIH HHS/ -- F32 AR008545-02/AR/NIAMS NIH HHS/ -- F32 AR008545-03/AR/NIAMS NIH HHS/ -- HL058723/HL/NHLBI NIH HHS/ -- HL065228/HL/NHLBI NIH HHS/ -- HL10105/HL/NHLBI NIH HHS/ -- HLEB67273/HL/NHLBI NIH HHS/ -- NCRR-COBRE P20RR1555/RR/NCRR NIH HHS/ -- P01-HL67004/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2004 Sep 17;305(5691):1773-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Pulmonary Medicine, Mayo Clinic Arizona, Scottsdale, AZ 85259, USA. jjlee@mayo.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15375267" target="_blank"〉PubMed〈/a〉
    Keywords: Allergens/immunology ; Animals ; Asthma/immunology/*pathology/*physiopathology ; Diphtheria Toxin/genetics ; Eosinophil Peroxidase ; Eosinophils/*physiology ; Gene Targeting ; Leukocyte Count ; Lung/immunology/*pathology/*physiopathology ; Mice ; Mice, Transgenic ; Models, Animal ; Mucus/secretion ; Ovalbumin/immunology ; Peptide Fragments/genetics ; Peroxidases/genetics ; Respiratory Hypersensitivity/immunology/pathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 102
    facet.materialart.
    Unknown
    Synthetic mammalian prions (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-03
    Description: Recombinant mouse prion protein (recMoPrP) produced in Escherichia coli was polymerized into amyloid fibrils that represent a subset of beta sheet-rich structures. Fibrils consisting of recMoPrP(89-230) were inoculated intracerebrally into transgenic (Tg) mice expressing MoPrP(89-231). The mice developed neurologic dysfunction between 380 and 660 days after inoculation. Brain extracts showed protease-resistant PrP by Western blotting; these extracts transmitted disease to wild-type FVB mice and Tg mice overexpressing PrP, with incubation times of 150 and 90 days, respectively. Neuropathological findings suggest that a novel prion strain was created. Our results provide compelling evidence that prions are infectious proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Legname, Giuseppe -- Baskakov, Ilia V -- Nguyen, Hoang-Oanh B -- Riesner, Detlev -- Cohen, Fred E -- DeArmond, Stephen J -- Prusiner, Stanley B -- AG02132/AG/NIA NIH HHS/ -- AG021601/AG/NIA NIH HHS/ -- AG10770/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2004 Jul 30;305(5684):673-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Neurodegenerative Diseases, University of California, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15286374" target="_blank"〉PubMed〈/a〉
    Keywords: Amyloid/chemistry/metabolism ; Animals ; Biopolymers ; Brain/metabolism/pathology ; Brain Chemistry ; Escherichia coli/genetics ; Female ; Glycosylation ; Male ; Mice ; Mice, Transgenic ; Plaque, Amyloid/pathology ; PrPSc Proteins/analysis/metabolism ; Prion Diseases/*etiology/pathology/transmission ; Prions/administration & dosage/biosynthesis/chemistry/*pathogenicity ; Protein Conformation ; Protein Folding ; Recombinant Proteins/administration & dosage/biosynthesis/chemistry ; Time Factors ; Tissue Extracts/administration & dosage ; Vacuoles/pathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 103
    facet.materialart.
    Unknown
    Protection from cardiac arrhythmia through ryanodine receptor-stabilizing protein calstabin2 (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-04-10
    Description: Ventricular arrhythmias can cause sudden cardiac death (SCD) in patients with normal hearts and in those with underlying disease such as heart failure. In animals with heart failure and in patients with inherited forms of exercise-induced SCD, depletion of the channel-stabilizing protein calstabin2 (FKBP12.6) from the ryanodine receptor-calcium release channel (RyR2) complex causes an intracellular Ca2+ leak that can trigger fatal cardiac arrhythmias. A derivative of 1,4-benzothiazepine (JTV519) increased the affinity of calstabin2 for RyR2, which stabilized the closed state of RyR2 and prevented the Ca2+ leak that triggers arrhythmias. Thus, enhancing the binding of calstabin2 to RyR2 may be a therapeutic strategy for common ventricular arrhythmias.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wehrens, Xander H T -- Lehnart, Stephan E -- Reiken, Steven R -- Deng, Shi-Xian -- Vest, John A -- Cervantes, Daniel -- Coromilas, James -- Landry, Donald W -- Marks, Andrew R -- New York, N.Y. -- Science. 2004 Apr 9;304(5668):292-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Cellular Biophysics, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15073377" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Arrhythmia Agents/*pharmacology/therapeutic use ; Calcium/metabolism ; Calcium-Transporting ATPases/metabolism ; Cell Line ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Death, Sudden, Cardiac/prevention & control ; Electric Stimulation ; Electrocardiography ; Heart/*drug effects/physiology ; Humans ; Isoproterenol/pharmacology ; Mice ; Myocardial Contraction ; Phosphorylation ; Physical Exertion ; Protein Binding ; Ryanodine Receptor Calcium Release Channel/*metabolism ; Sarcoplasmic Reticulum/metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases ; Tachycardia, Ventricular/metabolism/*prevention & control ; Tacrolimus Binding Proteins/deficiency/genetics/*metabolism ; Thiazepines/*pharmacology/therapeutic use
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 104
    facet.materialart.
    Unknown
    Gefitinib-sensitizing EGFR mutations in lung cancer activate anti-apoptotic pathways (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-07-31
    Description: Gefitinib (Iressa, Astra Zeneca Pharmaceuticals) is a tyrosine kinase inhibitor that targets the epidermal growth factor receptor (EGFR) and induces dramatic clinical responses in nonsmall cell lung cancers (NSCLCs) with activating mutations within the EGFR kinase domain. We report that these mutant EGFRs selectively activate Akt and signal transduction and activator of transcription (STAT) signaling pathways, which promote cell survival, but have no effect on extracellular signal-regulated kinase signaling, which induces proliferation. NSCLC cells expressing mutant EGFRs underwent extensive apoptosis after small interfering RNA-mediated knockdown of the mutant EGFR or treatment with pharmacological inhibitors of Akt and STAT signaling and were relatively resistant to apoptosis induced by conventional chemotherapeutic drugs. Thus, mutant EGFRs selectively transduce survival signals on which NSCLCs become dependent; inhibition of those signals by gefitinib may contribute to the drug's efficacy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sordella, Raffaella -- Bell, Daphne W -- Haber, Daniel A -- Settleman, Jeffrey -- P01 95281/PHS HHS/ -- New York, N.Y. -- Science. 2004 Aug 20;305(5687):1163-7. Epub 2004 Jul 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Molecular Therapeutics, Massachusetts General Hospital Cancer Center and Harvard Medical School, Building 149, 13th Street, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15284455" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/pharmacology ; *Apoptosis ; Carcinoma, Non-Small-Cell Lung/drug therapy/*genetics/pathology ; Catalytic Domain ; Cell Line ; Cell Line, Tumor ; Cell Survival ; DNA-Binding Proteins/antagonists & inhibitors/metabolism ; Enzyme Activation ; Humans ; Lung Neoplasms/drug therapy/*genetics/pathology ; Mice ; *Milk Proteins ; Mitogen-Activated Protein Kinases/metabolism ; Mutation ; Mutation, Missense ; Phosphorylation ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; Proto-Oncogene Proteins/antagonists & inhibitors/metabolism ; Proto-Oncogene Proteins c-akt ; Quinazolines/*pharmacology ; RNA, Small Interfering ; Receptor, Epidermal Growth Factor/*genetics/*metabolism ; STAT5 Transcription Factor ; Sequence Deletion ; Signal Transduction ; Trans-Activators/antagonists & inhibitors/metabolism ; Transfection ; Tyrosine/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 105
    facet.materialart.
    Unknown
    Rescue of dystrophic muscle through U7 snRNA-mediated exon skipping (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-06
    Description: Most mutations in the dystrophin gene create a frameshift or a stop in the mRNA and are associated with severe Duchenne muscular dystrophy. Exon skipping that naturally occurs at low frequency sometimes eliminates the mutation and leads to the production of a rescued protein. We have achieved persistent exon skipping that removes the mutated exon on the dystrophin messenger mRNA of the mdx mouse, by a single administration of an AAV vector expressing antisense sequences linked to a modified U7 small nuclear RNA. We report the sustained production of functional dystrophin at physiological levels in entire groups of muscles and the correction of the muscular dystrophy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goyenvalle, Aurelie -- Vulin, Adeline -- Fougerousse, Francoise -- Leturcq, France -- Kaplan, Jean-Claude -- Garcia, Luis -- Danos, Olivier -- New York, N.Y. -- Science. 2004 Dec 3;306(5702):1796-9. Epub 2004 Nov 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genethon & CNRS UMR 8115, 1, rue de l'Internationale, Evry, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15528407" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dependovirus/genetics ; Dystrophin/*genetics/metabolism ; *Exons ; *Genetic Therapy ; Genetic Vectors ; Introns ; Mice ; Mice, Inbred mdx ; Muscle Contraction ; Muscle Fibers, Skeletal/immunology/pathology ; Muscle, Skeletal/metabolism/pathology/physiology ; Muscular Dystrophy, Animal/genetics/pathology/physiopathology/*therapy ; Muscular Dystrophy, Duchenne/genetics/pathology/physiopathology/*therapy ; *Mutation ; Oligonucleotides, Antisense/*pharmacology ; RNA Splicing ; RNA, Messenger/genetics/metabolism ; RNA, Small Nuclear/genetics/*metabolism ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 106
    facet.materialart.
    Unknown
    Enhanced dendritic cell antigen capture via toll-like receptor-induced actin remodeling (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-25
    Description: Microbial products are sensed through Toll-like receptors (TLRs) and trigger a program of dendritic cell (DC) maturation that enables DCs to activate T cells. Although an accepted hallmark of this response is eventual down-regulation of DC endocytic capacity, we show that TLR ligands first acutely stimulate antigen macropinocytosis, leading to enhanced presentation on class I and class II major histocompatibility complex molecules. Simultaneously, actin-rich podosomes disappear, which suggests a coordinated redeployment of actin to fuel endocytosis. These reciprocal changes are transient and require p38 and extracellular signal-regulated kinase activation. Thus, the DC actin cytoskeleton can be rapidly mobilized in response to innate immune stimuli to enhance antigen capture and presentation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉West, Michele A -- Wallin, Robert P A -- Matthews, Stephen P -- Svensson, Henrik G -- Zaru, Rossana -- Ljunggren, Hans-Gustaf -- Prescott, Alan R -- Watts, Colin -- G0100536/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2004 Aug 20;305(5687):1153-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell Biology and Immunology, Wellcome Trust Biocentre, School of Life Sciences, University of Dundee, Dundee DD1 5EH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15326355" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*physiology ; Animals ; Antigen Presentation ; Antigens/*immunology ; Cell Membrane/physiology/ultrastructure ; Cells, Cultured ; Cytoskeleton/*physiology/ultrastructure ; Dendritic Cells/*immunology ; Down-Regulation ; Endocytosis ; Ligands ; Lipopolysaccharides/immunology ; Membrane Glycoproteins/*metabolism ; Mice ; Microscopy, Fluorescence ; Microscopy, Video ; Mitogen-Activated Protein Kinases/metabolism ; Pinocytosis ; Receptors, Cell Surface/*metabolism ; Signal Transduction ; Toll-Like Receptors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 107
    facet.materialart.
    Unknown
    MHC class I peptides as chemosensory signals in the vomeronasal organ (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-06
    Description: The mammalian vomeronasal organ detects social information about gender, status, and individuality. The molecular cues carrying this information remain largely unknown. Here, we show that small peptides that serve as ligands for major histocompatibility complex (MHC) class I molecules function also as sensory stimuli for a subset of vomeronasal sensory neurons located in the basal Gao- and V2R receptor-expressing zone of the vomeronasal epithelium. In behaving mice, the same peptides function as individuality signals underlying mate recognition in the context of pregnancy block. MHC peptides constitute a previously unknown family of chemosensory stimuli by which MHC genotypic diversity can influence social behavior.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leinders-Zufall, Trese -- Brennan, Peter -- Widmayer, Patricia -- S, Prashanth Chandramani -- Maul-Pavicic, Andrea -- Jager, Martina -- Li, Xiao-Hong -- Breer, Heinz -- Zufall, Frank -- Boehm, Thomas -- New York, N.Y. -- Science. 2004 Nov 5;306(5698):1033-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15528444" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Chemoreceptor Cells ; Female ; H-2 Antigens/metabolism ; Histocompatibility Antigens Class I/*metabolism ; Ligands ; Male ; Mice ; Mice, Inbred C57BL ; Olfactory Receptor Neurons/metabolism ; Peptides/*metabolism ; Receptors, Vasopressin/metabolism ; *Signal Transduction ; Smell/physiology ; Urine ; Vomeronasal Organ/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 108
    facet.materialart.
    Unknown
    Integrins regulate Rac targeting by internalization of membrane domains (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-07
    Description: Translocation of the small GTP-binding protein Rac1 to the cell plasma membrane is essential for activating downstream effectors and requires integrin-mediated adhesion of cells to extracellular matrix. We report that active Rac1 binds preferentially to low-density, cholesterol-rich membranes, and specificity is determined at least in part by membrane lipids. Cell detachment triggered internalization of plasma membrane cholesterol and lipid raft markers. Preventing internalization maintained Rac1 membrane targeting and effector activation in nonadherent cells. Regulation of lipid rafts by integrin signals may regulate the location of membrane domains such as lipid rafts and thereby control domain-specific signaling events in anchorage-dependent cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉del Pozo, Miguel A -- Alderson, Nazilla B -- Kiosses, William B -- Chiang, Hui-Hsien -- Anderson, Richard G W -- Schwartz, Martin A -- GM52016/GM/NIGMS NIH HHS/ -- HL 20948/HL/NHLBI NIH HHS/ -- R01 GM47214/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2004 Feb 6;303(5659):839-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. mdelpozo@scripps.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14764880" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD29/metabolism ; Binding Sites ; Cell Adhesion ; Cell Line ; Cell Membrane/*metabolism ; Cells, Cultured ; Cholera Toxin/metabolism ; Cholesterol/metabolism ; G(M1) Ganglioside/metabolism ; Glycosylphosphatidylinositols/metabolism ; Guanosine Triphosphate/metabolism ; Humans ; Integrins/*metabolism ; Liposomes/metabolism ; Membrane Microdomains/*metabolism ; Mice ; NIH 3T3 Cells ; Rats ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transfection ; rac1 GTP-Binding Protein/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 109
    facet.materialart.
    Unknown
    Cancer. Respect thy neighbor! (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Radisky, Derek C -- Bissell, Mina J -- New York, N.Y. -- Science. 2004 Feb 6;303(5659):775-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Life Sciences, Lawrence Berkeley National Laboratory, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14764858" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; *Cell Transformation, Neoplastic ; Epithelial Cells/*physiology ; Extracellular Matrix/physiology/ultrastructure ; Fibroblasts/*physiology ; Genetic Predisposition to Disease ; Humans ; Male ; Mice ; Models, Biological ; Neoplasms, Glandular and Epithelial/*etiology ; Prostatic Intraepithelial Neoplasia/etiology ; Receptors, Transforming Growth Factor beta/genetics/metabolism ; *Signal Transduction ; Stomach Neoplasms/etiology ; Stromal Cells/*physiology ; Transforming Growth Factor beta/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 110
    facet.materialart.
    Unknown
    Stress-dependent regulation of FOXO transcription factors by the SIRT1 deacetylase (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-21
    Description: The Sir2 deacetylase modulates organismal life-span in various species. However, the molecular mechanisms by which Sir2 increases longevity are largely unknown. We show that in mammalian cells, the Sir2 homolog SIRT1 appears to control the cellular response to stress by regulating the FOXO family of Forkhead transcription factors, a family of proteins that function as sensors of the insulin signaling pathway and as regulators of organismal longevity. SIRT1 and the FOXO transcription factor FOXO3 formed a complex in cells in response to oxidative stress, and SIRT1 deacetylated FOXO3 in vitro and within cells. SIRT1 had a dual effect on FOXO3 function: SIRT1 increased FOXO3's ability to induce cell cycle arrest and resistance to oxidative stress but inhibited FOXO3's ability to induce cell death. Thus, one way in which members of the Sir2 family of proteins may increase organismal longevity is by tipping FOXO-dependent responses away from apoptosis and toward stress resistance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brunet, Anne -- Sweeney, Lora B -- Sturgill, J Fitzhugh -- Chua, Katrin F -- Greer, Paul L -- Lin, Yingxi -- Tran, Hien -- Ross, Sarah E -- Mostoslavsky, Raul -- Cohen, Haim Y -- Hu, Linda S -- Cheng, Hwei-Ling -- Jedrychowski, Mark P -- Gygi, Steven P -- Sinclair, David A -- Alt, Frederick W -- Greenberg, Michael E -- NIHP30-HD18655/HD/NICHD NIH HHS/ -- P01 NS35138-17/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 Mar 26;303(5666):2011-5. Epub 2004 Feb 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, and Department of Neurobiology, Center for Blood Research (CBR) Institute for Biomedical Research, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14976264" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Apoptosis ; Cell Cycle ; Cell Line ; Cell Nucleus/metabolism ; Cells, Cultured ; Cerebellum/cytology ; Forkhead Transcription Factors ; Gene Expression Profiling ; Gene Expression Regulation ; Histone Deacetylases/genetics/*metabolism ; Humans ; Intracellular Signaling Peptides and Proteins ; Mice ; Mice, Knockout ; Neurons/cytology ; *Oxidative Stress ; Phosphorylation ; Proteins/genetics ; Recombinant Proteins/metabolism ; Sirtuin 1 ; Sirtuins/genetics/*metabolism ; Transcription Factors/genetics/*metabolism ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 111
    facet.materialart.
    Unknown
    NOBOX deficiency disrupts early folliculogenesis and oocyte-specific gene expression (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-25
    Description: Primordial ovarian follicles in mice form when somatic cells surround individual oocytes. We show that lack of Nobox, an oocyte-specific homeobox gene, accelerates postnatal oocyte loss and abolishes the transition from primordial to growing follicles in mice. Follicles are replaced by fibrous tissue in female mice lacking Nobox in a manner similar to nonsyndromic ovarian failure in women. Genes preferentially expressed in oocytes, including Oct4 and Gdf9, are down-regulated in Nobox-/- mice, whereas ubiquitous genes such as Bmp4, Kit, and Bax remain unaffected. Therefore, Nobox is critical for specifying an oocyte-restricted gene expression pattern essential for postnatal follicle development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rajkovic, Aleksandar -- Pangas, Stephanie A -- Ballow, Daniel -- Suzumori, Nobuhiro -- Matzuk, Martin M -- HD007165/HD/NICHD NIH HHS/ -- HD01426/HD/NICHD NIH HHS/ -- HD33438/HD/NICHD NIH HHS/ -- HD42500/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2004 Aug 20;305(5687):1157-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, TX 77030, USA. rajkovic@bcm.tmc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15326356" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Apoptosis ; Embryonic and Fetal Development/genetics ; Female ; Fertility ; Gene Deletion ; *Gene Expression Regulation, Developmental ; Gene Targeting ; *Genes, Homeobox ; Germ Cells/cytology/physiology ; Homeodomain Proteins/*genetics/*physiology ; Male ; Meiosis ; Mice ; Mice, Inbred C57BL ; Oocytes/*physiology ; Oogenesis ; Ovarian Follicle/*physiology ; Ovary/cytology/embryology/physiology ; Transcription Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 112
    facet.materialart.
    Unknown
    Neuroscience. Genetic control of cortical convolutions (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-03-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rakic, Pasko -- New York, N.Y. -- Science. 2004 Mar 26;303(5666):1983-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Yale University School of Medicine, New Haven, CT 06520, USA. pasko.rakic@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15044793" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Cell Division ; Cell Movement ; Cerebral Cortex/*abnormalities/embryology ; Cerebral Ventricles/cytology/embryology ; Female ; Frontal Lobe/*abnormalities/embryology ; Humans ; Intellectual Disability ; Male ; Mice ; Mutation ; Neurons/physiology ; Parietal Lobe/abnormalities/embryology ; Pedigree ; Receptors, G-Protein-Coupled/*genetics/*physiology ; Stem Cells/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 113
    facet.materialart.
    Unknown
    Developmental biology. Hox genes in the limb: a play in two acts (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-06-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deschamps, Jacqueline -- New York, N.Y. -- Science. 2004 Jun 11;304(5677):1610-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hubrecht Laboratory, Uppsalalaan 8, 3584CT Utrecht, Netherlands. jacqueli@niob.knaw.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15192209" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors ; *Body Patterning ; DNA-Binding Proteins/genetics/metabolism ; *Gene Expression Regulation, Developmental ; *Genes, Homeobox ; Hedgehog Proteins ; Kruppel-Like Transcription Factors ; Limb Buds/*embryology/metabolism ; Mice ; Morphogenesis ; *Nerve Tissue Proteins ; Trans-Activators/genetics/metabolism ; Transcription Factors/genetics/metabolism ; Zebrafish Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 114
    facet.materialart.
    Unknown
    Advanced cardiac morphogenesis does not require heart tube fusion (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-09-14
    Description: The bilateral cardiac mesoderm migrates from the lateral region of the embryo to the ventral midline, where it fuses to form the primitive heart tube. It is generally accepted that migration and fusion are essential for subsequent stages of cardiac morphogenesis. We present evidence that, in Foxp4 mutant embryonic mice, each bilateral heart-forming region is capable of developing into a highly differentiated four-chambered mammalian heart in the absence of midline fusion. These data demonstrate that left-right chamber specification, cardiac looping, septation, cardiac myocyte differentiation, and endocardial cushion formation are preprogrammed in the precardiac mesoderm and do not require midline positional identity or heart tube fusion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Shanru -- Zhou, Deying -- Lu, Min Min -- Morrisey, Edward E -- HL71589/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2004 Sep 10;305(5690):1619-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15361625" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Atrial Natriuretic Factor/metabolism ; Basic Helix-Loop-Helix Transcription Factors ; Body Patterning ; Cell Differentiation ; DNA-Binding Proteins/genetics/metabolism ; Endocardium/embryology ; Endoderm/cytology/metabolism ; Forkhead Transcription Factors ; Gene Targeting ; Heart/*embryology ; Heart Atria/embryology ; Heart Ventricles/embryology ; In Situ Hybridization ; Mesoderm/physiology ; Mice ; Morphogenesis ; Mutation ; Myocytes, Cardiac/*cytology ; Proto-Oncogene Proteins c-myc/metabolism ; Transcription Factors/metabolism ; Zebrafish Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 115
    facet.materialart.
    Unknown
    Modulation of Th1 activation and inflammation by the NF-kappaB repressor Foxj1 (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-14
    Description: Forkhead transcription factors play key roles in the regulation of immune responses. Here, we identify a role for one member of this family, Foxj1, in the regulation of T cell activation and autoreactivity. Foxj1 deficiency resulted in multiorgan systemic inflammation, exaggerated Th1 cytokine production, and T cell proliferation in autologous mixed lymphocyte reactions. Foxj1 suppressed NF-kappaB transcription activity in vitro, and Foxj1-deficient T cells possessed increased NF-kappaB activity in vivo, correlating with the ability of Foxj1 to regulate IkappaB proteins, particularly IkappaBbeta. Thus, Foxj1 likely modulates inflammatory reactions and prevents autoimmunity by antagonizing proinflammatory transcriptional activities. These results suggest a potentially general role for forkhead genes in the enforcement of lymphocyte quiescence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, Ling -- Spoor, Melanie S -- Gerth, Andrea J -- Brody, Steven L -- Peng, Stanford L -- AI01803/AI/NIAID NIH HHS/ -- AI057471/AI/NIAID NIH HHS/ -- DK52574/DK/NIDDK NIH HHS/ -- HL56244/HL/NHLBI NIH HHS/ -- HL63988/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2004 Feb 13;303(5660):1017-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Rheumatology, Department of Internal Medicine, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14963332" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; Autoimmunity ; Cell Division ; Cell Line ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Chimera ; Cytoplasm/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Forkhead Transcription Factors ; Gene Targeting ; Humans ; I-kappa B Proteins/genetics/metabolism ; *Inflammation ; Interferon-gamma/biosynthesis ; Interleukin-2/immunology ; Interleukins/biosynthesis ; *Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; NF-kappa B/antagonists & inhibitors/*metabolism ; NFATC Transcription Factors ; *Nuclear Proteins ; Th1 Cells/*immunology ; Th2 Cells/immunology ; Transcription Factors/genetics/*metabolism ; Transcriptional Activation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 116
    facet.materialart.
    Unknown
    Argonaute2 is the catalytic engine of mammalian RNAi (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-07-31
    Description: Gene silencing through RNA interference (RNAi) is carried out by RISC, the RNA-induced silencing complex. RISC contains two signature components, small interfering RNAs (siRNAs) and Argonaute family proteins. Here, we show that the multiple Argonaute proteins present in mammals are both biologically and biochemically distinct, with a single mammalian family member, Argonaute2, being responsible for messenger RNA cleavage activity. This protein is essential for mouse development, and cells lacking Argonaute2 are unable to mount an experimental response to siRNAs. Mutations within a cryptic ribonuclease H domain within Argonaute2, as identified by comparison with the structure of an archeal Argonaute protein, inactivate RISC. Thus, our evidence supports a model in which Argonaute contributes "Slicer" activity to RISC, providing the catalytic engine for RNAi.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Jidong -- Carmell, Michelle A -- Rivas, Fabiola V -- Marsden, Carolyn G -- Thomson, J Michael -- Song, Ji-Joon -- Hammond, Scott M -- Joshua-Tor, Leemor -- Hannon, Gregory J -- New York, N.Y. -- Science. 2004 Sep 3;305(5689):1437-41. Epub 2004 Jul 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, Watson School of Biological Sciences, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15284456" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Argonaute Proteins ; Catalysis ; Cell Line ; Cells, Cultured ; Central Nervous System/embryology ; Embryonic and Fetal Development ; Eukaryotic Initiation Factor-2 ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Humans ; In Situ Hybridization ; Mice ; MicroRNAs/metabolism ; Molecular Sequence Data ; Mutagenesis, Insertional ; Oligonucleotide Array Sequence Analysis ; Peptide Initiation Factors/chemistry/*metabolism ; Point Mutation ; *RNA Interference ; RNA, Double-Stranded ; RNA, Messenger/*metabolism ; RNA, Small Interfering/metabolism ; RNA-Induced Silencing Complex/chemistry/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 117
    facet.materialart.
    Unknown
    Innate antiviral responses by means of TLR7-mediated recognition of single-stranded RNA (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-21
    Description: Interferons (IFNs) are critical for protection from viral infection, but the pathways linking virus recognition to IFN induction remain poorly understood. Plasmacytoid dendritic cells produce vast amounts of IFN-alpha in response to the wild-type influenza virus. Here, we show that this requires endosomal recognition of influenza genomic RNA and signaling by means of Toll-like receptor 7 (TLR7) and MyD88. Single-stranded RNA (ssRNA) molecules of nonviral origin also induce TLR7-dependent production of inflammatory cytokines. These results identify ssRNA as a ligand for TLR7 and suggest that cells of the innate immune system sense endosomal ssRNA to detect infection by RNA viruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diebold, Sandra S -- Kaisho, Tsuneyasu -- Hemmi, Hiroaki -- Akira, Shizuo -- Reis e Sousa, Caetano -- New York, N.Y. -- Science. 2004 Mar 5;303(5663):1529-31. Epub 2004 Feb 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunobiology Laboratory, Cancer Research UK, London Research Institute, London WC2A 3PX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14976261" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Antigens, Differentiation/metabolism ; Cells, Cultured ; Cytokines/biosynthesis ; Dendritic Cells/*immunology ; Endocytosis ; Endosomes/immunology/virology ; Genome, Viral ; *Immunity, Innate ; Influenza A virus/genetics/*immunology ; Interferon-alpha/biosynthesis ; Ligands ; Membrane Glycoproteins/*metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Myeloid Differentiation Factor 88 ; Poly U/immunology ; Polyribonucleotides/immunology ; RNA/*immunology ; RNA, Viral/*immunology ; Receptors, Cell Surface/*metabolism ; Receptors, Immunologic/metabolism ; Signal Transduction ; Toll-Like Receptor 7
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 118
    facet.materialart.
    Unknown
    Neuroscience. Time is precious (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-04-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abeles, Moshe -- New York, N.Y. -- Science. 2004 Apr 23;304(5670):523-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gonda Brain Research Center, Bar Ilan University, Ramat-Gan, Israel, and Center for Neural Computation, the Hebrew University, Jerusalem, Israel. moshe.abeles@mail.biu.ac.il〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15105481" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Cats ; Cerebral Cortex/cytology/*physiology ; Mice ; Nerve Net/physiology ; Neurons/*physiology ; Synapses/physiology ; *Synaptic Transmission ; Time Factors ; 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
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 119
    facet.materialart.
    Unknown
    Genetics. The critical region in trisomy 21 (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-10-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, David L -- Gibbs, Richard A -- New York, N.Y. -- Science. 2004 Oct 22;306(5696):619-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Human Genetics and the Human Genome Sequencing Center, Baylor College of Medicine, Houston, TX 77030, USA. nelson@bcm.tmc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15499000" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Deletion ; Chromosomes, Human, Pair 21/*genetics ; Chromosomes, Mammalian/*genetics ; Craniofacial Abnormalities/genetics ; Crosses, Genetic ; *Disease Models, Animal ; Down Syndrome/*genetics/pathology ; Female ; Gene Duplication ; Humans ; Male ; Mice ; Recombination, Genetic ; Skull/abnormalities ; *Trisomy
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 120
    facet.materialart.
    Unknown
    Antigen bias in T cell cross-priming (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-05-29
    Description: Activated CD8+ T cells detect virally infected cells and tumor cells by recognition of major histocompatibility complex class I-bound peptides derived from degraded, endogenously produced proteins. In contrast, CD8+ T cell activation often occurs through interaction with specialized antigen-presenting cells displaying peptides acquired from an exogenous cellular source, a process termed cross-priming. Here, we observed a marked inefficiency in exogenous presentation of epitopes derived from signal sequences in mouse models. These data indicate that certain virus- and tumor-associated antigens may not be detected by CD8+ T cells because of impaired cross-priming. Such differences in the ability to cross-present antigens should form important considerations in vaccine design.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wolkers, Monika C -- Brouwenstijn, Nathalie -- Bakker, Arnold H -- Toebes, Mireille -- Schumacher, Ton N M -- New York, N.Y. -- Science. 2004 May 28;304(5675):1314-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunology, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15166378" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; Antigens, Viral/genetics/*immunology ; CD8-Positive T-Lymphocytes/*immunology ; Cell Line, Tumor ; *Cross-Priming ; Dendritic Cells/immunology ; Epitopes, T-Lymphocyte/*immunology ; Immune Tolerance ; Immunoglobulins/immunology/metabolism ; Influenza A virus/immunology ; Lymphocyte Activation ; Mice ; Papillomaviridae/immunology ; Protein Sorting Signals/genetics ; Recombinant Fusion Proteins/immunology ; T-Lymphocytes, Cytotoxic/immunology ; Transfection ; Vaccines/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 121
    facet.materialart.
    Unknown
    Biomedicine. Prion dormancy and disease (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carrell, Robin W -- New York, N.Y. -- Science. 2004 Dec 3;306(5702):1692-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cambridge Institute for Medical Research, University of Cambridge, Cambridge CB2 2XY, UK. rwc1000@cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15576598" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Appendix/chemistry ; Brain/pathology ; Carrier State ; Cattle ; Creutzfeldt-Jakob Syndrome/epidemiology/genetics/*metabolism/pathology ; Disease Outbreaks ; Encephalopathy, Bovine Spongiform/epidemiology/metabolism ; Genetic Predisposition to Disease ; Genotype ; Great Britain/epidemiology ; Humans ; Methionine ; Mice ; Mice, Transgenic ; Polymorphism, Genetic ; PrPC Proteins/analysis/chemistry/*genetics/pathogenicity ; Protein Conformation ; Valine
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 122
    facet.materialart.
    Unknown
    Neuroscience. Crossing the midline (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-06-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Woods, C Geoffrey -- New York, N.Y. -- Science. 2004 Jun 4;304(5676):1455-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Medicine Unit, School of Medicine, University of Leeds, LS9 7TF, UK. msjcgw@leeds.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15178787" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/metabolism/*physiology ; Cell Adhesion Molecules/metabolism ; Down-Regulation ; Gene Expression Profiling ; Gene Expression Regulation ; Glycoproteins/metabolism ; Humans ; Mice ; Morphogenesis ; Mutation ; Nerve Growth Factors/metabolism ; Nerve Tissue Proteins/metabolism ; Neural Pathways ; Ophthalmoplegia/*genetics/pathology/physiopathology ; Protein Structure, Tertiary ; Receptors, Cell Surface/metabolism ; Receptors, Immunologic/chemistry/*genetics/*metabolism ; Rhombencephalon/growth & development/metabolism/*pathology ; Scoliosis/*genetics/pathology/physiopathology ; Syndrome ; Tumor Suppressor Proteins/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 123
    facet.materialart.
    Unknown
    Requirement of JNK2 for scavenger receptor A-mediated foam cell formation in atherogenesis (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-30
    Description: In vitro studies suggest a role for c-Jun N-terminal kinases (JNKs) in proatherogenic cellular processes. We show that atherosclerosis-prone ApoE-/- mice simultaneously lacking JNK2 (ApoE-/- JNK2-/- mice), but not ApoE-/- JNK1-/- mice, developed less atherosclerosis than do ApoE-/- mice. Pharmacological inhibition of JNK activity efficiently reduced plaque formation. Macrophages lacking JNK2 displayed suppressed foam cell formation caused by defective uptake and degradation of modified lipoproteins and showed increased amounts of the modified lipoprotein-binding and -internalizing scavenger receptor A (SR-A), whose phosphorylation was markedly decreased. Macrophage-restricted deletion of JNK2 was sufficient to decrease atherogenesis. Thus, JNK2-dependent phosphorylation of SR-A promotes uptake of lipids in macrophages, thereby regulating foam cell formation, a critical step in atherogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ricci, Romeo -- Sumara, Grzegorz -- Sumara, Izabela -- Rozenberg, Izabela -- Kurrer, Michael -- Akhmedov, Alexander -- Hersberger, Martin -- Eriksson, Urs -- Eberli, Franz R -- Becher, Burkhard -- Boren, Jan -- Chen, Mian -- Cybulsky, Myron I -- Moore, Kathryn J -- Freeman, Mason W -- Wagner, Erwin F -- Matter, Christian M -- Luscher, Thomas F -- New York, N.Y. -- Science. 2004 Nov 26;306(5701):1558-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Research, Institute of Physiology, and Division of Cardiology, University Hospital Zurich, CH-8057 Zurich, Switzerland. romeo.ricci@cell.biol.ethz.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15567863" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD36/metabolism ; Aorta/chemistry/pathology ; Apolipoproteins E/genetics ; Arteriosclerosis/*metabolism/pathology ; Bone Marrow Transplantation ; Cells, Cultured ; Cholesterol/metabolism ; Cholesterol, Dietary/administration & dosage ; Diet, Atherogenic ; Endothelial Cells/physiology ; Foam Cells/*metabolism ; Lipoproteins, LDL/metabolism ; Macrophages/*metabolism ; Macrophages, Peritoneal/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitogen-Activated Protein Kinase 8/metabolism ; Mitogen-Activated Protein Kinase 9/genetics/*metabolism ; Muscle, Smooth, Vascular/cytology ; Myocytes, Smooth Muscle/physiology ; Phosphorylation ; Receptors, Immunologic/genetics/*metabolism ; Receptors, Scavenger ; Scavenger Receptors, Class A ; T-Lymphocytes/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 124
    facet.materialart.
    Unknown
    Neuroscience. Cellular interactions in the stem cell niche (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-05-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wurmser, Andrew E -- Palmer, Theo D -- Gage, Fred H -- New York, N.Y. -- Science. 2004 May 28;304(5675):1253-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, Salk Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15166350" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/cytology/physiology ; *Cell Communication ; Cell Differentiation ; Cell Division ; Cell Survival ; Cells, Cultured ; Coculture Techniques ; Embryo, Mammalian/cytology ; Endothelial Cells/cytology/*physiology ; Mice ; Neurons/cytology/*physiology ; Signal Transduction ; Stem Cells/cytology/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 125
    facet.materialart.
    Unknown
    Nutrient availability regulates SIRT1 through a forkhead-dependent pathway (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-18
    Description: Nutrient availability regulates life-span in a wide range of organisms. We demonstrate that in mammalian cells, acute nutrient withdrawal simultaneously augments expression of the SIRT1 deacetylase and activates the Forkhead transcription factor Foxo3a. Knockdown of Foxo3a expression inhibited the starvation-induced increase in SIRT1 expression. Stimulation of SIRT1 transcription by Foxo3a was mediated through two p53 binding sites present in the SIRT1 promoter, and a nutrient-sensitive physical interaction was observed between Foxo3a and p53. SIRT1 expression was not induced in starved p53-deficient mice. Thus, in mammalian cells, p53, Foxo3a, and SIRT1, three proteins separately implicated in aging, constitute a nutrient-sensing pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nemoto, Shino -- Fergusson, Maria M -- Finkel, Toren -- New York, N.Y. -- Science. 2004 Dec 17;306(5704):2105-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Branch, National Heart, Lung, and Blood Institute (NHLBI), Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15604409" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/metabolism ; Animals ; Binding Sites ; Culture Media ; Culture Media, Serum-Free ; DNA-Binding Proteins/*metabolism ; Forkhead Transcription Factors ; Gene Deletion ; Genes, p53 ; Glucose ; HeLa Cells ; Humans ; Mice ; Mice, Inbred C57BL ; Mutation ; PC12 Cells ; Promoter Regions, Genetic ; RNA, Small Interfering/pharmacology ; Rats ; Recombinant Fusion Proteins/metabolism ; Recombinant Proteins/metabolism ; Serum ; Sirtuin 1 ; Sirtuins/genetics/*metabolism ; *Starvation ; Transcription Factors/*metabolism ; Transcription, Genetic ; Tumor Suppressor Protein p53/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 126
    facet.materialart.
    Unknown
    Lack of a fusion requirement for development of bone marrow-derived epithelia (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-07-03
    Description: Analysis of developmental plasticity of bone marrow-derived cells (BMDCs) is complicated by the possibility of cell-cell fusion. Here we demonstrate that epithelial cells can develop from BMDCs without cell-cell fusion. We use the Cre/lox system together with beta-galactosidase and enhanced green fluorescent protein expression in transgenic mice to identify epithelial cells in the lung, liver, and skin that develop from BMDCs without cell fusion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harris, Robert G -- Herzog, Erica L -- Bruscia, Emanuela M -- Grove, Joanna E -- Van Arnam, John S -- Krause, Diane S -- DK61846/DK/NIDDK NIH HHS/ -- HL073742/HL/NHLBI NIH HHS/ -- HL63357/HL/NHLBI NIH HHS/ -- T32-HL07778/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2004 Jul 2;305(5680):90-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Laboratory Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15232107" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Cells/*physiology ; *Bone Marrow Transplantation ; Cell Differentiation ; *Cell Fusion ; Cobra Cardiotoxin Proteins/pharmacology ; Elapid Venoms/pharmacology ; Epithelial Cells/*cytology/metabolism ; Female ; Green Fluorescent Proteins ; Hepatocytes/cytology/metabolism ; Keratinocytes/cytology/metabolism ; Keratins/analysis ; Luminescent Proteins/metabolism ; Male ; Mice ; Mice, Transgenic ; Muscle Cells/cytology ; Radiation, Ionizing ; Recombinases/metabolism ; Recombination, Genetic ; Reverse Transcriptase Polymerase Chain Reaction ; Stem Cells/cytology/*physiology ; X Chromosome ; Y Chromosome ; beta-Galactosidase/biosynthesis/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 127
    facet.materialart.
    Unknown
    KIF1A alternately uses two loops to bind microtubules (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-03
    Description: The motor protein kinesin moves along microtubules, driven by adenosine triphosphate (ATP) hydrolysis. However, it remains unclear how kinesin converts the chemical energy into mechanical movement. We report crystal structures of monomeric kinesin KIF1A with three transition-state analogs: adenylyl imidodiphosphate (AMP-PNP), adenosine diphosphate (ADP)-vanadate, and ADP-AlFx (aluminofluoride complexes). These structures, together with known structures of the ADP-bound state and the adenylyl-(beta,gamma-methylene) diphosphate (AMP-PCP)-bound state, show that kinesin uses two microtubule-binding loops in an alternating manner to change its interaction with microtubules during the ATP hydrolysis cycle; loop L11 is extended in the AMP-PNP structure, whereas loop L12 is extended in the ADP structure. ADP-vanadate displays an intermediate structure in which a conformational change in two switch regions causes both loops to be raised from the microtubule, thus actively detaching kinesin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nitta, Ryo -- Kikkawa, Masahide -- Okada, Yasushi -- Hirokawa, Nobutaka -- New York, N.Y. -- Science. 2004 Jul 30;305(5684):678-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Anatomy, University of Tokyo, Graduate School of Medicine, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15286375" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Adenylyl Imidodiphosphate/metabolism ; Aluminum/metabolism ; Animals ; Binding Sites ; Crystallography, X-Ray ; Fluorides/metabolism ; Hydrogen Bonding ; Kinesin/*chemistry/*metabolism ; Mice ; Microtubules/*metabolism ; Models, Molecular ; Nerve Tissue Proteins/*chemistry/*metabolism ; Phosphates/metabolism ; Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Vanadates/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 128
    facet.materialart.
    Unknown
    CD8+ T cell cross-priming via transfer of proteasome substrates (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-05-29
    Description: "Cross-priming" describes the activation of naive CD8+ T cells by professional antigen-presenting cells that have acquired viral or tumor antigens from "donor" cells. Antigen transfer is believed to be mediated by donor cell-derived molecular chaperones bearing short peptide ligands generated by proteasome degradation of protein antigens. We show here that cross-priming is based on the transfer of proteasome substrates rather than peptides. These findings are potentially important for the rational design of vaccines that elicit CD8+ T cell responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Norbury, Christopher C -- Basta, Sameh -- Donohue, Keri B -- Tscharke, David C -- Princiotta, Michael F -- Berglund, Peter -- Gibbs, James -- Bennink, Jack R -- Yewdell, Jonathan W -- AI-056094-01/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2004 May 28;304(5675):1318-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda MD, 20892-0440, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15166379" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcysteine/*analogs & derivatives/pharmacology ; Animals ; *Antigen Presentation ; Antigens/*immunology/metabolism ; Antigens, Viral/immunology/metabolism ; CD8-Positive T-Lymphocytes/*immunology ; Cell Line ; *Cross-Priming ; Cysteine Endopeptidases/*metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Endoplasmic Reticulum/metabolism ; Humans ; Immunization ; Influenza A virus/immunology ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Molecular Chaperones/metabolism ; Multienzyme Complexes/*metabolism ; Ovalbumin/immunology/metabolism ; Peptide Fragments/immunology ; Proteasome Endopeptidase Complex ; Recombinant Fusion Proteins/immunology/metabolism ; Vaccines/immunology ; Vaccinia virus/genetics/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 129
    facet.materialart.
    Unknown
    Curcumin, a major constituent of turmeric, corrects cystic fibrosis defects (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-04-24
    Description: Cystic fibrosis is caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR). The most common mutation, DeltaF508, results in the production of a misfolded CFTR protein that is retained in the endoplasmic reticulum and targeted for degradation. Curcumin is a nontoxic Ca-adenosine triphosphatase pump inhibitor that can be administered to humans safely. Oral administration of curcumin to homozygous DeltaF508 CFTR mice in doses comparable, on a weight-per-weight basis, to those well tolerated by humans corrected these animals' characteristic nasal potential difference defect. These effects were not observed in mice homozygous for a complete knockout of the CFTR gene. Curcumin also induced the functional appearance of DeltaF508 CFTR protein in the plasma membranes of transfected baby hamster kidney cells. Thus, curcumin treatment may be able to correct defects associated with the homozygous expression of DeltaF508 CFTR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Egan, Marie E -- Pearson, Marilyn -- Weiner, Scott A -- Rajendran, Vanathy -- Rubin, Daniel -- Glockner-Pagel, Judith -- Canny, Susan -- Du, Kai -- Lukacs, Gergely L -- Caplan, Michael J -- DK17433/DK/NIDDK NIH HHS/ -- DK53428/DK/NIDDK NIH HHS/ -- GM42136/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2004 Apr 23;304(5670):600-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Yale University School of Medicine, 333 Cedar Street, Post Office Box 208026, New Haven, CT 06520-8026, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15105504" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Calnexin/metabolism ; Cell Line ; Cell Membrane/*metabolism ; Cricetinae ; Curcumin/administration & dosage/*pharmacology/therapeutic use ; Cystic Fibrosis/*drug therapy/genetics/physiopathology ; Cystic Fibrosis Transmembrane Conductance ; Regulator/chemistry/genetics/*metabolism ; Electrolytes/pharmacology ; Endoplasmic Reticulum/*metabolism ; Gene Targeting ; Glycosylation ; Humans ; Intestinal Mucosa/drug effects/physiology ; Intestinal Obstruction/prevention & control ; Isoproterenol/pharmacology ; Membrane Potentials/drug effects ; Mice ; Mice, Knockout ; Mutation ; Nasal Mucosa/*drug effects/physiology ; Polyethylene Glycols/pharmacology ; Protein Folding ; Rectum ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 130
    facet.materialart.
    Unknown
    CD8alphaalpha-mediated survival and differentiation of CD8 memory T cell precursors (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-04-24
    Description: Memory T cells are long-lived antigen-experienced T cells that are generally accepted to be direct descendants of proliferating primary effector cells. However, the factors that permit selective survival of these T cells are not well established. We show that homodimeric alpha chains of the CD8 molecule (CD8alphaalpha) are transiently induced on a selected subset of CD8alphabeta+ T cells upon antigenic stimulation. These CD8alphaalpha molecules promote the survival and differentiation of activated lymphocytes into memory CD8 T cells. Thus, memory precursors can be identified among primary effector cells and are selected for survival and differentiation by CD8alphaalpha.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Madakamutil, Loui T -- Christen, Urs -- Lena, Christopher J -- Wang-Zhu, Yiran -- Attinger, Antoine -- Sundarrajan, Monisha -- Ellmeier, Wilfried -- von Herrath, Matthias G -- Jensen, Peter -- Littman, Dan R -- Cheroutre, Hilde -- AI33614/AI/NIAID NIH HHS/ -- AI50263/AI/NIAID NIH HHS/ -- AI51973/AI/NIAID NIH HHS/ -- DK54451/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2004 Apr 23;304(5670):590-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉La Jolla Institute for Allergy and Immunology, 10355 Science Center Drive, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15105501" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; Antigens, CD8/*immunology ; Arenaviridae Infections/immunology ; CD8-Positive T-Lymphocytes/*immunology ; Cell Differentiation ; Cell Survival ; *Immunologic Memory ; Interferon-gamma/biosynthesis ; *Lymphocyte Activation ; Lymphocytic choriomeningitis virus/immunology ; Membrane Glycoproteins/immunology/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Receptors, Interleukin-7/immunology/metabolism ; T-Lymphocyte Subsets/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 131
    facet.materialart.
    Unknown
    Induction of protective IgA by intestinal dendritic cells carrying commensal bacteria (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-03-16
    Description: The enormous number of commensal bacteria in the lower intestine of vertebrates share abundant molecular patterns used for innate immune recognition of pathogenic bacteria. We show that, even though commensals are rapidly killed by macrophages, intestinal dendritic cells (DCs) can retain small numbers of live commensals for several days. This allows DCs to selectively induce IgA, which helps protect against mucosal penetration by commensals. The commensal-loaded DCs are restricted to the mucosal immune compartment by the mesenteric lymph nodes, which ensures that immune responses to commensal bacteria are induced locally, without potentially damaging systemic immune responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Macpherson, Andrew J -- Uhr, Therese -- New York, N.Y. -- Science. 2004 Mar 12;303(5664):1662-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Experimental Immunology, Universitatsspital, CH8091 Zurich, Switzerland. amacpher@pathol.unizh.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15016999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; B-Lymphocytes/immunology ; Bacteria/growth & development/*immunology/isolation & purification ; Dendritic Cells/*immunology/*microbiology ; Enterobacter cloacae/growth & development/immunology/isolation & purification ; Germ-Free Life ; Immunity, Innate ; *Immunity, Mucosal ; Immunoglobulin A/*biosynthesis/blood/immunology ; Intestinal Mucosa/*immunology/microbiology ; Intestines/*microbiology ; Leukocytes/immunology/microbiology ; Lymph Nodes/cytology/immunology/microbiology ; Macrophages/immunology/microbiology ; Mesentery ; Mice ; Mice, Inbred C57BL ; Peyer's Patches/cytology/immunology ; Phagocytosis ; Salmonella typhimurium/growth & development/immunology/isolation & purification ; Specific Pathogen-Free Organisms ; Spleen/cytology/microbiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 132
    facet.materialart.
    Unknown
    Microbiology. Pathogenic bacteria prefer heme (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-09-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rouault, Tracey A -- New York, N.Y. -- Science. 2004 Sep 10;305(5690):1577-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section on Human Iron Metabolism, Cell Biology and Metabolism Branch, the National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA. trou@helix.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15361615" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antimicrobial Cationic Peptides/metabolism ; Bloodletting ; Caenorhabditis elegans/microbiology ; Heme/*metabolism ; Hemoglobins/metabolism ; Hepcidins ; Humans ; Iron/blood/*metabolism ; Iron Isotopes ; Membrane Transport Proteins/genetics/metabolism ; Mice ; Staphylococcal Infections/microbiology ; Staphylococcus aureus/genetics/growth & development/*metabolism/*pathogenicity ; Transferrin/metabolism ; Virulence
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 133
    facet.materialart.
    Unknown
    Reactivation of the paternal X chromosome in early mouse embryos (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-01-31
    Description: It is generally accepted that paternally imprinted X inactivation occurs exclusively in extraembryonic lineages of mouse embryos, whereas cells of the embryo proper, derived from the inner cell mass (ICM), undergo only random X inactivation. Here we show that imprinted X inactivation, in fact, occurs in all cells of early embryos and that the paternal X is then selectively reactivated in cells allocated to the ICM. This contrasts with more differentiated cell types where X inactivation is highly stable and generally irreversible. Our observations illustrate that an important component of genome plasticity in early development is the capacity to reverse heritable gene silencing decisions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mak, Winifred -- Nesterova, Tatyana B -- de Napoles, Mariana -- Appanah, Ruth -- Yamanaka, Shinya -- Otte, Arie P -- Brockdorff, Neil -- New York, N.Y. -- Science. 2004 Jan 30;303(5658):666-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉X inactivation group, MRC Clinical Sciences Centre, ICSM, Hammersmith Hospital, London, W12 0NN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14752160" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Blastocyst/physiology ; Cell Cycle Proteins/genetics/metabolism ; Chromosomal Proteins, Non-Histone/genetics/metabolism ; Chromosomes, Mammalian/physiology ; *Dosage Compensation, Genetic ; Embryo, Mammalian/*physiology ; Embryonic and Fetal Development ; Female ; *Gene Expression Regulation, Developmental ; Genomic Imprinting ; Histones/metabolism ; Male ; Methylation ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Morula/physiology ; Polycomb Repressive Complex 2 ; Proteins/genetics/metabolism ; RNA, Long Noncoding ; RNA, Untranslated/genetics/metabolism ; Repressor Proteins/genetics/metabolism ; X Chromosome/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 134
    facet.materialart.
    Unknown
    Development. ES cells to the rescue (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-10-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chien, Kenneth R -- Moretti, Alessandra -- Laugwitz, Karl-Ludwig -- New York, N.Y. -- Science. 2004 Oct 8;306(5694):239-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Medicine, University of California San Diego, La Jolla, CA 92037, USA. kchien@ucsd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15472069" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; DNA-Binding Proteins/genetics ; Embryo Loss ; Embryo, Mammalian/*cytology ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Heart/*embryology ; Heart Defects, Congenital/embryology/*therapy ; Heart Diseases/therapy ; Humans ; Inhibitor of Differentiation Protein 1 ; Inhibitor of Differentiation Protein 2 ; Insulin-Like Growth Factor I/genetics/physiology ; Maternal-Fetal Exchange ; Mice ; Mice, Knockout ; Myocardium/cytology/metabolism ; Myocytes, Cardiac/cytology ; Oligonucleotide Array Sequence Analysis ; Pericardium/embryology/metabolism ; Pregnancy ; Proto-Oncogene Proteins/genetics/physiology ; Repressor Proteins/genetics ; *Stem Cell Transplantation ; Stem Cells/*physiology ; Transcription Factors/genetics ; Wnt Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 135
    facet.materialart.
    Unknown
    Regulation of an ATG7-beclin 1 program of autophagic cell death by caspase-8 (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-05-08
    Description: Caspases play a central role in apoptosis, a well-studied pathway of programmed cell death. Other programs of death potentially involving necrosis and autophagy may exist, but their relation to apoptosis and mechanisms of regulation remains unclear. We define a new molecular pathway in which activation of the receptor-interacting protein (a serine-threonine kinase) and Jun amino-terminal kinase induced cell death with the morphology of autophagy. Autophagic death required the genes ATG7 and beclin 1 and was induced by caspase-8 inhibition. Clinical therapies involving caspase inhibitors may arrest apoptosis but also have the unanticipated effect of promoting autophagic cell death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Li -- Alva, Ajjai -- Su, Helen -- Dutt, Parmesh -- Freundt, Eric -- Welsh, Sarah -- Baehrecke, Eric H -- Lenardo, Michael J -- GM59136/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2004 Jun 4;304(5676):1500-2. Epub 2004 May 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15131264" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Chloromethyl Ketones/pharmacology ; Animals ; Apoptosis Regulatory Proteins ; *Autophagy ; Caspase 8 ; *Caspase Inhibitors ; Caspases/genetics/*metabolism ; *Cell Death ; Cell Line ; Cells, Cultured ; Humans ; JNK Mitogen-Activated Protein Kinases ; MAP Kinase Kinase 7 ; MAP Kinase Signaling System ; Membrane Proteins ; Mice ; Mitogen-Activated Protein Kinase Kinases/genetics/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; Proteins/genetics/*metabolism ; RNA Interference ; Receptor-Interacting Protein Serine-Threonine Kinases
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 136
    facet.materialart.
    Unknown
    Increased nuclear NAD biosynthesis and SIRT1 activation prevent axonal degeneration (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-18
    Description: Axonal degeneration is an active program of self-destruction that is observed in many physiological and pathological settings. In Wallerian degeneration slow (wlds) mice, Wallerian degeneration in response to axonal injury is delayed because of a mutation that results in overexpression of a chimeric protein (Wlds) composed of the ubiquitin assembly protein Ufd2a and the nicotinamide adenine dinucleotide (NAD) biosynthetic enzyme Nmnat1. We demonstrate that increased Nmnat activity is responsible for the axon-sparing activity of the Wlds protein. Furthermore, we demonstrate that SIRT1, a mammalian ortholog of Sir2, is the downstream effector of increased Nmnat activity that leads to axonal protection. These findings suggest that novel therapeutic strategies directed at increasing the supply of NAD and/or Sir2 activation may be effective for treatment of diseases characterized by axonopathy and neurodegeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Araki, Toshiyuki -- Sasaki, Yo -- Milbrandt, Jeffrey -- AG05681/AG/NIA NIH HHS/ -- AG13730/AG/NIA NIH HHS/ -- NS40745/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 Aug 13;305(5686):1010-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15310905" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Axons/drug effects/*physiology ; Axotomy ; Benzamides/pharmacology ; Cell Line ; Cell Nucleus/metabolism ; Cell Survival ; Cells, Cultured ; Ganglia, Spinal/cytology ; Humans ; Lentivirus/genetics/physiology ; Mice ; Mutation ; NAD/*biosynthesis/pharmacology ; Naphthols/pharmacology ; Nerve Tissue Proteins/*metabolism ; Neuroprotective Agents/pharmacology ; Nicotinamide-Nucleotide Adenylyltransferase/*metabolism ; Poly(ADP-ribose) Polymerase Inhibitors ; Poly(ADP-ribose) Polymerases/metabolism ; RNA, Small Interfering ; Sirtuin 1 ; Sirtuins/antagonists & inhibitors/*metabolism ; Stilbenes/pharmacology ; Ubiquitin-Protein Ligases/genetics/metabolism ; Vincristine/pharmacology ; Wallerian Degeneration/metabolism/*physiopathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 137
    facet.materialart.
    Unknown
    Nicotine activation of alpha4* receptors: sufficient for reward, tolerance, and sensitization (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-06
    Description: The identity of nicotinic receptor subtypes sufficient to elicit both the acute and chronic effects of nicotine dependence is unknown. We engineered mutant mice with a4 nicotinic subunits containing a single point mutation, Leu9' --〉 Ala9' in the pore-forming M2 domain, rendering a4* receptors hypersensitive to nicotine. Selective activation of a4* nicotinic acetylcholine receptors with low doses of agonist recapitulates nicotine effects thought to be important in dependence, including reinforcement in response to acute nicotine administration, as well as tolerance and sensitization elicited by chronic nicotine administration. These data indicate that activation of a4* receptors is sufficient for nicotine-induced reward, tolerance, and sensitization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tapper, Andrew R -- McKinney, Sheri L -- Nashmi, Raad -- Schwarz, Johannes -- Deshpande, Purnima -- Labarca, Cesar -- Whiteaker, Paul -- Marks, Michael J -- Collins, Allan C -- Lester, Henry A -- DA-15663/DA/NIDA NIH HHS/ -- DA-3194/DA/NIDA NIH HHS/ -- MH-49716/MH/NIMH NIH HHS/ -- NS-11756/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 Nov 5;306(5698):1029-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15528443" target="_blank"〉PubMed〈/a〉
    Keywords: Alkaloids/metabolism ; Animals ; Azocines/metabolism ; Bicyclo Compounds, Heterocyclic/metabolism ; Brain/drug effects/metabolism ; Calcium/metabolism ; Cells, Cultured ; *Drug Tolerance ; Leucine ; Mice ; Mice, Inbred C57BL ; Motor Activity/drug effects ; Neurons/metabolism ; Nicotine/*pharmacology ; Point Mutation ; Pyridines/metabolism ; Quinolizines/metabolism ; Receptors, Nicotinic/genetics/*physiology ; *Reward ; Serine ; Tobacco Use Disorder/*metabolism ; Up-Regulation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 138
    facet.materialart.
    Unknown
    Lysosomal glycosphingolipid recognition by NKT cells (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-13
    Description: NKT cells represent a distinct lineage of T cells that coexpress a conserved alphabeta T cell receptor (TCR) and natural killer (NK) receptors. Although the TCR of NKT cells is characteristically autoreactive to CD1d, a lipid-presenting molecule, endogenous ligands for these cells have not been identified. We show that a lysosomal glycosphingolipid of previously unknown function, isoglobotrihexosylceramide (iGb3), is recognized both by mouse and human NKT cells. Impaired generation of lysosomal iGb3 in mice lacking beta-hexosaminidase b results in severe NKT cell deficiency, suggesting that this lipid also mediates development of NKT cells in the mouse. We suggest that expression of iGb3 in peripheral tissues may be involved in controlling NKT cell responses to infections and malignancy and in autoimmunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Dapeng -- Mattner, Jochen -- Cantu, Carlos 3rd -- Schrantz, Nicolas -- Yin, Ning -- Gao, Ying -- Sagiv, Yuval -- Hudspeth, Kelly -- Wu, Yun-Ping -- Yamashita, Tadashi -- Teneberg, Susann -- Wang, Dacheng -- Proia, Richard L -- Levery, Steven B -- Savage, Paul B -- Teyton, Luc -- Bendelac, Albert -- AI053725/AI/NIAID NIH HHS/ -- AI50847/AI/NIAID NIH HHS/ -- P20RR16459/RR/NCRR NIH HHS/ -- R01 AI38339/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2004 Dec 3;306(5702):1786-9. Epub 2004 Nov 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Chicago, Department of Pathology, Chicago, IL 60637, USA. dzhou@midway.uchicago.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15539565" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Antigens, CD1/immunology/metabolism ; Antigens, CD1d ; Autoimmunity ; Cell Line ; Cell Line, Tumor ; Cells, Cultured ; Dendritic Cells/immunology ; Galactosyltransferases/genetics/metabolism ; Globosides/chemistry/*immunology/metabolism ; Humans ; Hybridomas ; Infection/immunology ; Killer Cells, Natural/*immunology ; Ligands ; Lymphocyte Activation ; Lymphocyte Count ; Lysosomes/*metabolism ; Mice ; Mice, Inbred C57BL ; Neoplasms/immunology ; Plant Lectins/immunology ; Rats ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; Saposins/metabolism ; T-Lymphocyte Subsets/*immunology ; beta-N-Acetylhexosaminidases/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 139
    facet.materialart.
    Unknown
    Postnatal refinement of peripheral olfactory projections (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-06-05
    Description: Axonal projections from the olfactory epithelium to the olfactory bulb are organized into glomeruli according to the expressed odorant receptor. Using gene-targeted mice, we show that glomerular maturation proceeds along different time courses for two similar receptors and requires sensory input during distinct sensitive periods. During early development, some glomeruli are innervated by axons of neurons that do not express the same receptor. These heterogeneous glomeruli normally disappear with age, but they persist in adults deprived of sensory input by unilateral and permanent naris closure. Persistence may be due, in part, to prolonged survival of olfactory sensory neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zou, Dong-Jing -- Feinstein, Paul -- Rivers, Aimee L -- Mathews, Glennis A -- Kim, Ann -- Greer, Charles A -- Mombaerts, Peter -- Firestein, Stuart -- New York, N.Y. -- Science. 2004 Jun 25;304(5679):1976-9. Epub 2004 Jun 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Columbia University, New York, NY 10027, USA. dz98@columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15178749" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Axons/*physiology/ultrastructure ; Cell Death ; Cell Survival ; Dendrites/physiology/ultrastructure ; Gene Targeting ; Immunohistochemistry ; Mice ; Mice, Inbred C57BL ; Odors ; Olfactory Bulb/cytology/*growth & development ; *Olfactory Pathways ; Olfactory Receptor Neurons/cytology/*physiology ; Receptors, Odorant/genetics/*metabolism ; Sensory Deprivation ; Smell ; Synapses/ultrastructure
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 140
    facet.materialart.
    Unknown
    Cell biology. Tickling macrophages, a serious business (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-05-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zullig, Stephanie -- Hengartner, Michael O -- New York, N.Y. -- Science. 2004 May 21;304(5674):1123-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Biology, University of Zurich, CH-8057 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15155940" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, Surface ; *Apoptosis ; *Autoimmunity ; Germinal Center/cytology/metabolism ; Integrins/metabolism ; Lymph Nodes/metabolism ; Macrophage Activation ; Macrophages/immunology/*metabolism ; Membrane Glycoproteins/chemistry/*metabolism ; Mice ; *Milk Proteins ; Models, Biological ; Necrosis ; *Phagocytosis ; Phosphatidylserines/metabolism ; Protein Binding ; Receptors, Cell Surface/metabolism ; Spleen/cytology/immunology/metabolism ; Splenomegaly
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 141
    facet.materialart.
    Unknown
    Modulation of hematopoietic stem cell homing and engraftment by CD26 (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-18
    Description: Hematopoietic stem cell homing and engraftment are crucial to transplantation efficiency, and clinical engraftment is severely compromised when donor-cell numbers are limiting. The peptidase CD26 (DPPIV/dipeptidylpeptidase IV) removes dipeptides from the amino terminus of proteins. We present evidence that endogenous CD26 expression on donor cells negatively regulates homing and engraftment. By inhibition or deletion of CD26, it was possible to increase greatly the efficiency of transplantation. These results suggest that hematopoietic stem cell engraftment is not absolute, as previously suggested, and indicate that improvement of bone marrow transplant efficiency may be possible in the clinic.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Christopherson, Kent W 2nd -- Hangoc, Giao -- Mantel, Charlie R -- Broxmeyer, Hal E -- R01 DK53674/DK/NIDDK NIH HHS/ -- R01 HL56416/HL/NHLBI NIH HHS/ -- R01 HL67384/HL/NHLBI NIH HHS/ -- T32 DK07519/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2004 Aug 13;305(5686):1000-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology and the Walther Oncology Center, Indiana University School of Medicine, Indianapolis, IN 46202, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15310902" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle ; Cell Movement ; Cell Survival ; Chemokine CXCL12 ; Chemokines, CXC/pharmacology ; Chemotaxis/drug effects ; Dipeptidyl Peptidase 4/*physiology ; Female ; *Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*physiology ; Heterocyclic Compounds/pharmacology ; Mice ; Mice, Inbred C57BL ; Oligopeptides/pharmacology ; Receptors, CXCR4/antagonists & inhibitors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 142
    facet.materialart.
    Unknown
    Role of the kinase MST2 in suppression of apoptosis by the proto-oncogene product Raf-1 (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-25
    Description: The ablation of the protein kinase Raf-1 renders cells hypersensitive to apoptosis despite normal regulation of extracellular signal-regulated kinases, which suggests that apoptosis protection is mediated by a distinct pathway. We used proteomic analysis of Raf-1 signaling complexes to show that Raf-1 counteracts apoptosis by suppressing the activation of mammalian sterile 20-like kinase (MST2). Raf-1 prevents dimerization and phosphorylation of the activation loop of MST2 independently of its protein kinase activity. Depletion of MST2 from Raf-1-/- mouse or human cells abrogated sensitivity to apoptosis, whereas overexpression of MST2 induced apoptosis. Conversely, depletion of Raf-1 from Raf-1+/+ mouse or human cells led to MST2 activation and apoptosis. The concomitant depletion of both Raf-1 and MST2 prevented apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Neill, Eric -- Rushworth, Linda -- Baccarini, Manuela -- Kolch, Walter -- New York, N.Y. -- Science. 2004 Dec 24;306(5705):2267-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Beatson Institute for Cancer Research, Garscube Estate, Switchback Road, Glasgow G61 1BD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15618521" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/metabolism ; *Apoptosis ; COS Cells ; Cell Line, Tumor ; Dimerization ; Humans ; Mice ; Phosphorylation ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Proteomics ; Proto-Oncogene Proteins c-raf/genetics/*metabolism ; RNA, Small Interfering ; Signal Transduction ; Staurosporine/pharmacology ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 143
    facet.materialart.
    Unknown
    Specific GABAA circuits for visual cortical plasticity (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-03-16
    Description: Weak inhibition within visual cortex early in life prevents experience-dependent plasticity. Loss of responsiveness to an eye deprived of vision can be initiated prematurely by enhancing gamma-aminobutyric acid (GABA)-mediated transmission with benzodiazepines. Here, we use a mouse "knockin" mutation to alpha subunits that renders individual GABA type A (GABA(A)) receptors insensitive to diazepam to show that a particular inhibitory network controls expression of the critical period. Only alpha1-containing circuits were found to drive cortical plasticity, whereas alpha2-enriched connections separately regulated neuronal firing. This dissociation carries implications for models of brain development and the safe design of benzodiazepines for use in infants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fagiolini, Michela -- Fritschy, Jean-Marc -- Low, Karin -- Mohler, Hanns -- Rudolph, Uwe -- Hensch, Takao K -- New York, N.Y. -- Science. 2004 Mar 12;303(5664):1681-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Neuronal Circuit Development, RIKEN Brain Science Institute, 2-1 Hirosawa, Wako-shi, Saitama, 351-0198 Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15017002" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Diazepam/pharmacology ; Dominance, Ocular/*physiology ; Interneurons/*physiology ; Mice ; Mice, Inbred C57BL ; Models, Neurological ; Mutation ; Neural Inhibition ; *Neuronal Plasticity ; Neurons/*physiology ; Protein Subunits ; Pyridines/pharmacology ; Receptors, GABA-A/genetics/*physiology ; Synaptic Transmission ; Vision, Ocular ; Visual Cortex/growth & development/*physiology ; gamma-Aminobutyric Acid/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 144
    facet.materialart.
    Unknown
    Cancer. Gleevec, chapter two: new leukemia drug aims to overcome resistance (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Travis, John -- New York, N.Y. -- Science. 2004 Jul 16;305(5682):319-21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15256643" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/metabolism/pharmacology/therapeutic use ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Benzamides ; Dasatinib ; Drug Resistance, Neoplasm ; Enzyme Inhibitors/metabolism/pharmacology/therapeutic use ; Fusion Proteins, bcr-abl/*antagonists & inhibitors/genetics/metabolism ; Humans ; Imatinib Mesylate ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*drug therapy ; Mice ; Mutation ; Piperazines/*therapeutic use ; Pyrimidines/metabolism/pharmacology/*therapeutic use ; Thiazoles/metabolism/pharmacology/*therapeutic use
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 145
    facet.materialart.
    Unknown
    Endoplasmic reticulum stress links obesity, insulin action, and type 2 diabetes (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-10-16
    Description: Obesity contributes to the development of type 2 diabetes, but the underlying mechanisms are poorly understood. Using cell culture and mouse models, we show that obesity causes endoplasmic reticulum (ER) stress. This stress in turn leads to suppression of insulin receptor signaling through hyperactivation of c-Jun N-terminal kinase (JNK) and subsequent serine phosphorylation of insulin receptor substrate-1 (IRS-1). Mice deficient in X-box-binding protein-1 (XBP-1), a transcription factor that modulates the ER stress response, develop insulin resistance. These findings demonstrate that ER stress is a central feature of peripheral insulin resistance and type 2 diabetes at the molecular, cellular, and organismal levels. Pharmacologic manipulation of this pathway may offer novel opportunities for treating these common diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ozcan, Umut -- Cao, Qiong -- Yilmaz, Erkan -- Lee, Ann-Hwee -- Iwakoshi, Neal N -- Ozdelen, Esra -- Tuncman, Gurol -- Gorgun, Cem -- Glimcher, Laurie H -- Hotamisligil, Gokhan S -- AI32412/AI/NIAID NIH HHS/ -- DK52539/DK/NIDDK NIH HHS/ -- P05-CA100707/CA/NCI NIH HHS/ -- T32-DK07703/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2004 Oct 15;306(5695):457-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Complex Diseases, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15486293" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/metabolism ; Animals ; Cells, Cultured ; DNA-Binding Proteins/genetics/metabolism ; Diabetes Mellitus, Type 2/*metabolism ; Endoplasmic Reticulum/*metabolism ; Glucose/metabolism ; Homeostasis ; Insulin/*metabolism ; Insulin Receptor Substrate Proteins ; *Insulin Resistance ; Liver/metabolism ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Obese ; Mitogen-Activated Protein Kinase 8 ; Mitogen-Activated Protein Kinases/metabolism ; Muscle, Skeletal/metabolism ; Mutation ; Nuclear Proteins/genetics/metabolism ; Obesity/*metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/metabolism ; Rats ; Receptor, Insulin/metabolism ; Signal Transduction ; Transcription Factors ; Tunicamycin/pharmacology ; eIF-2 Kinase/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 146
    facet.materialart.
    Unknown
    Reconstitution of Ca2+-regulated membrane fusion by synaptotagmin and SNAREs (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-03-27
    Description: We investigated the effect of synaptotagmin I on membrane fusion mediated by neuronal SNARE proteins, SNAP-25, syntaxin, and synaptobrevin, which were reconstituted into vesicles. In the presence of Ca2+, the cytoplasmic domain of synaptotagmin I (syt) strongly stimulated membrane fusion when synaptobrevin densities were similar to those found in native synaptic vesicles. The Ca2+ dependence of syt-stimulated fusion was modulated by changes in lipid composition of the vesicles and by a truncation that mimics cleavage of SNAP-25 by botulinum neurotoxin A. Stimulation of fusion was abolished by disrupting the Ca2+-binding activity, or by severing the tandem C2 domains, of syt. Thus, syt and SNAREs are likely to represent the minimal protein complement for Ca2+-triggered exocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tucker, Ward C -- Weber, Thomas -- Chapman, Edwin R -- GM 56827/GM/NIGMS NIH HHS/ -- GM 66313/GM/NIGMS NIH HHS/ -- MH 61876/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2004 Apr 16;304(5669):435-8. Epub 2004 Mar 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Wisconsin, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15044754" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Calcium/*metabolism ; *Calcium-Binding Proteins ; Exocytosis ; Fluorescence Resonance Energy Transfer ; Lipid Bilayers ; Lipids/analysis ; Liposomes/chemistry/metabolism ; *Membrane Fusion ; Membrane Glycoproteins/chemistry/*metabolism ; Membrane Proteins/chemistry/*metabolism ; Mice ; Mutation ; Nerve Tissue Proteins/chemistry/*metabolism ; Protein Structure, Tertiary ; Qa-SNARE Proteins ; R-SNARE Proteins ; Rats ; Synaptic Vesicles/chemistry/metabolism ; Synaptosomal-Associated Protein 25 ; Synaptotagmin I ; Synaptotagmins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 147
    facet.materialart.
    Unknown
    Regulation of fasted blood glucose by resistin (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-21
    Description: The association between obesity and diabetes supports an endocrine role for the adipocyte in maintaining glucose homeostasis. Here we report that mice lacking the adipocyte hormone resistin exhibit low blood glucose levels after fasting, due to reduced hepatic glucose production. This is partly mediated by activation of adenosine monophosphate-activated protein kinase and decreased expression of gluconeogenic enzymes in the liver. The data thus support a physiological function for resistin in the maintenance of blood glucose during fasting. Remarkably, lack of resistin diminishes the increase in post-fast blood glucose normally associated with increased weight, suggesting a role for resistin in mediating hyperglycemia associated with obesity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Banerjee, Ronadip R -- Rangwala, Shamina M -- Shapiro, Jennifer S -- Rich, A Sophie -- Rhoades, Ben -- Qi, Yong -- Wang, Juan -- Rajala, Michael W -- Pocai, Alessandro -- Scherer, Phillipp E -- Steppan, Claire M -- Ahima, Rexford S -- Obici, Silvana -- Rossetti, Luciano -- Lazar, Mitchell A -- NIH T32-GM008216/GM/NIGMS NIH HHS/ -- P01 DK49210/DK/NIDDK NIH HHS/ -- P30 DK19525/DK/NIDDK NIH HHS/ -- P60 DK20541/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2004 Feb 20;303(5661):1195-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, and The Penn Diabetes Center, 611 CRB, 415 Curie Boulevard, Universityof 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/14976316" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases ; Adipocytes/metabolism ; Animals ; Blood Glucose/*metabolism ; Body Weight ; Diet ; Dietary Fats/administration & dosage ; *Fasting ; Gene Targeting ; Gluconeogenesis ; Glucose Tolerance Test ; Glucose-6-Phosphatase/metabolism ; Homeostasis ; Hormones, Ectopic/administration & dosage/blood/genetics/*physiology ; Insulin/blood ; Liver/metabolism ; Male ; Mice ; Multienzyme Complexes/metabolism ; Obesity/metabolism ; Phosphoenolpyruvate Carboxykinase (GTP)/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Recombinant Proteins/administration & dosage ; Resistin ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 148
    facet.materialart.
    Unknown
    Neuroscience. The mysteries of myelin unwrapped (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-05-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉ffrench-Constant, Charles -- Colognato, Holly -- Franklin, Robin J M -- New York, N.Y. -- Science. 2004 Apr 30;304(5671):688-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Cambridge, UK. cfc@mole.bio.cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15118149" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Axons/*physiology/*ultrastructure ; Genes, erbB-2 ; Laminin/physiology ; Mice ; Mice, Transgenic ; Myelin Sheath/*physiology/*ultrastructure ; Neural Conduction ; Neuregulin-1/chemistry/genetics/*physiology ; Neuregulins/chemistry/genetics/physiology ; Oligodendroglia/physiology ; Protein Isoforms/physiology ; Rats ; Receptor, ErbB-2/physiology ; Schwann Cells/physiology ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 149
    facet.materialart.
    Unknown
    Medicine. Caution urged on SARS vaccines (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, Eliot -- Enserink, Martin -- New York, N.Y. -- Science. 2004 Feb 13;303(5660):944-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14963300" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Canada ; China ; Clinical Trials as Topic ; *Disease Models, Animal ; Ferrets ; Humans ; Macaca fascicularis ; Mice ; SARS Virus/*immunology ; Severe Acute Respiratory Syndrome/*prevention & control ; United States ; United States Food and Drug Administration ; Vaccines, Inactivated ; Vaccines, Synthetic ; *Viral Vaccines/adverse effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 150
    facet.materialart.
    Unknown
    Immunology. UNGstoppable switching (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Unniraman, Shyam -- Fugmann, Sebastian D -- Schatz, David G -- New York, N.Y. -- Science. 2004 Aug 20;305(5687):1113-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA. shyam.unniraman@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15326342" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/enzymology/immunology/*physiology ; Cytidine Deaminase/metabolism ; DNA/metabolism ; DNA Glycosylases/antagonists & inhibitors/*metabolism ; DNA Repair ; DNA-(Apurinic or Apyrimidinic Site) Lyase/metabolism ; Genes, Immunoglobulin ; *Immunoglobulin Class Switching ; Mice ; Models, Genetic ; Models, Immunological ; Mutation ; Recombination, Genetic ; Somatic Hypermutation, Immunoglobulin ; Uracil-DNA Glycosidase
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 151
    facet.materialart.
    Unknown
    Neurobiology. Untangling Alzheimer's by paring plaques bolsters amyloid theory (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beckman, Mary -- New York, N.Y. -- Science. 2004 Aug 6;305(5685):762.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15297635" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/metabolism/pathology/*therapy ; Alzheimer Vaccines/therapeutic use ; Amyloid beta-Peptides/*immunology ; Animals ; Antibodies/therapeutic use ; Brain/pathology ; Brain Chemistry ; Clinical Trials as Topic ; Disease Models, Animal ; Humans ; *Immunotherapy ; Mice ; Mice, Transgenic ; Neurofibrillary Tangles/*pathology ; Plaque, Amyloid/*pathology ; tau Proteins/analysis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 152
    facet.materialart.
    Unknown
    A diarylquinoline drug active on the ATP synthase of Mycobacterium tuberculosis (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-14
    Description: The incidence of tuberculosis has been increasing substantially on a worldwide basis over the past decade, but no tuberculosis-specific drugs have been discovered in 40 years. We identified a diarylquinoline, R207910, that potently inhibits both drug-sensitive and drug-resistant Mycobacterium tuberculosis in vitro (minimum inhibitory concentration 0.06 mug/ml). In mice, R207910 exceeded the bactericidal activities of isoniazid and rifampin by at least 1 log unit. Substitution of drugs included in the World Health Organization's first-line tuberculosis treatment regimen (rifampin, isoniazid, and pyrazinamide) with R207910 accelerated bactericidal activity, leading to complete culture conversion after 2 months of treatment in some combinations. A single dose of R207910 inhibited mycobacterial growth for 1 week. Plasma levels associated with efficacy in mice were well tolerated in healthy human volunteers. Mutants selected in vitro suggest that the drug targets the proton pump of adenosine triphosphate (ATP) synthase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Andries, Koen -- Verhasselt, Peter -- Guillemont, Jerome -- Gohlmann, Hinrich W H -- Neefs, Jean-Marc -- Winkler, Hans -- Van Gestel, Jef -- Timmerman, Philip -- Zhu, Min -- Lee, Ennis -- Williams, Peter -- de Chaffoy, Didier -- Huitric, Emma -- Hoffner, Sven -- Cambau, Emmanuelle -- Truffot-Pernot, Chantal -- Lounis, Nacer -- Jarlier, Vincent -- New York, N.Y. -- Science. 2005 Jan 14;307(5707):223-7. Epub 2004 Dec 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Johnson & Johnson Pharmaceutical Research and Development, Turnhoutseweg 30, 2340 Beerse, Belgium. kandries@prdbe.jnj.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15591164" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antitubercular Agents/chemistry/pharmacokinetics/*pharmacology/therapeutic use ; Bacterial Proton-Translocating ATPases/*antagonists & ; inhibitors/chemistry/metabolism ; Diarylquinolines ; Dose-Response Relationship, Drug ; Drug Evaluation, Preclinical ; Drug Resistance, Bacterial ; Drug Therapy, Combination ; Enzyme Inhibitors/chemistry/pharmacology/therapeutic use ; Humans ; Male ; Mice ; Microbial Sensitivity Tests ; Molecular Sequence Data ; Mycobacterium smegmatis/drug effects/enzymology/growth & development ; Mycobacterium tuberculosis/*drug effects/enzymology/growth & development ; Point Mutation ; Protein Subunits/antagonists & inhibitors/chemistry ; Quinolines/chemistry/pharmacokinetics/*pharmacology/*therapeutic use ; Tuberculosis/*drug therapy/microbiology ; Tuberculosis, Multidrug-Resistant/drug therapy/microbiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 153
    facet.materialart.
    Unknown
    Uracil DNA glycosylase activity is dispensable for immunoglobulin class switch (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-25
    Description: Activation-induced cytidine deaminase (AID) is required for the DNA cleavage step in immunoglobulin class switch recombination (CSR). AID is proposed to deaminate cytosine to generate uracil (U) in either mRNA or DNA. In the second instance, DNA cleavage depends on uracil DNA glycosylase (UNG) for removal of U. Using phosphorylated histone gamma-H2AX focus formation as a marker of DNA cleavage, we found that the UNG inhibitor Ugi did not inhibit DNA cleavage in immunoglobulin heavy chain (IgH) locus during CSR, even though Ugi blocked UNG binding to DNA and strongly inhibited CSR. Strikingly, UNG mutants that had lost the capability of removing U rescued CSR in UNG-/- B cells. These results indicate that UNG is involved in the repair step of CSR yet by an unknown mechanism. The dispensability of U removal in the DNA cleavage step of CSR requires a reconsideration of the model of DNA deamination by AID.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Begum, Nasim A -- Kinoshita, Kazuo -- Kakazu, Naoki -- Muramatsu, Masamichi -- Nagaoka, Hitoshi -- Shinkura, Reiko -- Biniszkiewicz, Detlev -- Boyer, Laurie A -- Jaenisch, Rudolf -- Honjo, Tasuku -- New York, N.Y. -- Science. 2004 Aug 20;305(5687):1160-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Chemistry and Molecular Biology, Graduate School of Medicine, Kyoto University, Yoshida Sakyo-ku, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15326357" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/enzymology/immunology/*physiology ; Cell Line, Tumor ; Cytidine Deaminase/metabolism ; DNA/*metabolism ; DNA Glycosylases/antagonists & inhibitors/genetics/*metabolism ; DNA Repair ; *Genes, Immunoglobulin ; *Immunoglobulin Class Switching ; Immunoglobulin Heavy Chains/genetics ; Immunoglobulin Switch Region ; Mice ; Mutation ; Precipitin Tests ; Recombination, Genetic ; Transfection ; Uracil/metabolism ; Uracil-DNA Glycosidase ; Viral Proteins/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 154
    facet.materialart.
    Unknown
    Disulfide-dependent multimeric assembly of resistin family hormones (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-05-25
    Description: Resistin, founding member of the resistin-like molecule (RELM) hormone family, is secreted selectively from adipocytes and induces liver-specific antagonism of insulin action, thus providing a potential molecular link between obesity and diabetes. Crystal structures of resistin and RELMbeta reveal an unusual multimeric structure. Each protomer comprises a carboxy-terminal disulfide-rich beta-sandwich "head" domain and an amino-terminal alpha-helical "tail" segment. The alpha-helical segments associate to form three-stranded coiled coils, and surface-exposed interchain disulfide linkages mediate the formation of tail-to-tail hexamers. Analysis of serum samples shows that resistin circulates in two distinct assembly states, likely corresponding to hexamers and trimers. Infusion of a resistin mutant, lacking the intertrimer disulfide bonds, in pancreatic-insulin clamp studies reveals substantially more potent effects on hepatic insulin sensitivity than those observed with wild-type resistin. This result suggests that processing of the intertrimer disulfide bonds may reflect an obligatory step toward activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Patel, Saurabh D -- Rajala, Michael W -- Rossetti, Luciano -- Scherer, Philipp E -- Shapiro, Lawrence -- New York, N.Y. -- Science. 2004 May 21;304(5674):1154-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biophysics, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15155948" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/metabolism ; Adiponectin ; Amino Acid Sequence ; Animals ; Cell Line ; Crystallization ; Crystallography, X-Ray ; Culture Media, Conditioned ; Disulfides/*chemistry ; Glucose/metabolism ; Hormones, Ectopic/*chemistry/genetics/*metabolism/pharmacology ; Humans ; Insulin/administration & dosage/blood ; Insulin Resistance ; *Intercellular Signaling Peptides and Proteins ; Liver/metabolism ; Mice ; Molecular Sequence Data ; Molecular Weight ; Mutation ; Protein Folding ; Protein Structure, Quaternary ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Proteins/chemistry/metabolism ; Resistin
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 155
    facet.materialart.
    Unknown
    Immunology. Keeping the gut microflora at bay (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-03-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kraehenbuhl, Jean-Pierre -- Corbett, Max -- New York, N.Y. -- Science. 2004 Mar 12;303(5664):1624-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Swiss Institute for Experimental Cancer Research, CH1066 Epalinges, Switzerland. jean-pierre.kraehenbuhl@isrec.unil.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15016988" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; B-Lymphocytes/immunology ; Bacteria/growth & development/*immunology ; Dendritic Cells/*immunology/microbiology ; Digestive System/*microbiology ; Humans ; Immunity, Innate ; *Immunity, Mucosal ; Immunoglobulin A/biosynthesis/immunology ; Intestinal Mucosa/*immunology/*microbiology ; Lymph Nodes/*immunology/microbiology ; Mesentery ; Mice ; Spleen/immunology/microbiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 156
    facet.materialart.
    Unknown
    Neuroscience. Locating a new step in pain's pathway (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-05-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, Jean -- New York, N.Y. -- Science. 2004 May 7;304(5672):811.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15131280" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dinoprostone/*metabolism ; Glycine/metabolism ; Inflammation/physiopathology ; Mice ; Mice, Knockout ; Neurons/*metabolism ; Pain/*physiopathology ; Receptors, Glycine/genetics/*metabolism ; Signal Transduction ; Spinal Cord/cytology/*metabolism ; Synaptic Transmission
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 157
    facet.materialart.
    Unknown
    Requirement of Rac1 and Rac2 expression by mature dendritic cells for T cell priming (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-25
    Description: Upon maturation, dendritic cells (DCs) acquire the unique ability to activate naive T cells. We used time-lapse video microscopy and two-photon imaging of intact lymph nodes to show that after establishing initial contact between their dendrites and naive T lymphocytes, mature DCs migrate toward the contacted lymphocytes. Subsequently, the DCs tightly entrap the T cells within a complex net of membrane extensions. The Rho family guanosine triphosphatases Rac1 and Rac2 but not Rho itself control the formation of dendrites in mature DCs, their polarized short-range migration toward T cells, and T cell priming.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benvenuti, Federica -- Hugues, Stephanie -- Walmsley, Marita -- Ruf, Sandra -- Fetler, Luc -- Popoff, Michel -- Tybulewicz, Victor L J -- Amigorena, Sebastian -- New York, N.Y. -- Science. 2004 Aug 20;305(5687):1150-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite INSERM 365, Institut Curie, 26 rue d'Ulm, 75005 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15326354" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD4-Positive T-Lymphocytes/*immunology/physiology ; Cell Communication ; Cell Polarity ; Cell Surface Extensions/physiology/ultrastructure ; Cytoskeleton/physiology ; Dendritic Cells/immunology/*physiology/ultrastructure ; *Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Microscopy, Video ; rac GTP-Binding Proteins/antagonists & inhibitors/genetics/*metabolism ; rac1 GTP-Binding Protein/antagonists & inhibitors/genetics/*metabolism ; rho GTP-Binding Proteins/antagonists & inhibitors/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 158
    facet.materialart.
    Unknown
    The involvement of the anterior cingulate cortex in remote contextual fear memory (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-05-08
    Description: Although the molecular, cellular, and systems mechanisms required for initial memory processing have been intensively investigated, those underlying permanent memory storage remain elusive. We present neuroanatomical, pharmacological, and genetic results demonstrating that the anterior cingulate cortex plays a critical role in remote memory for contextual fear conditioning. Imaging of activity-dependent genes shows that the anterior cingulate is activated by remote memory and that this activation is impaired by a null alpha-CaMKII mutation that blocks remote memory. Accordingly, reversible inactivation of this structure in normal mice disrupts remote memory without affecting recent memory.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frankland, Paul W -- Bontempi, Bruno -- Talton, Lynn E -- Kaczmarek, Leszek -- Silva, Alcino J -- New York, N.Y. -- Science. 2004 May 7;304(5672):881-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Neurobiology, Psychiatry, Psychology and Brain Research Institute, UCLA, 695 Charles Young Drive South, Los Angeles, CA 90095-1761, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15131309" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/genetics/metabolism ; Cerebral Cortex/*physiology ; Conditioning (Psychology) ; Cues ; *Fear ; Gene Expression ; Gene Expression Profiling ; Genes, fos ; Gyrus Cinguli/*physiology ; Hippocampus/physiology ; Memory/drug effects/*physiology ; Mental Recall/physiology ; Mice ; Mice, Inbred C57BL ; Neuronal Plasticity ; Neurons/physiology ; Proto-Oncogene Proteins c-fos/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 159
    facet.materialart.
    Unknown
    Molecular biology. HNFs--linking the liver and pancreatic islets in diabetes (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kulkarni, Rohit N -- Kahn, C Ronald -- New York, N.Y. -- Science. 2004 Feb 27;303(5662):1311-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Molecular Physiology, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA. rohit.kulkarni@joslin.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14988544" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; DNA-Binding Proteins/metabolism ; Diabetes Mellitus, Type 2/*genetics/metabolism ; *Gene Expression Regulation ; Hepatocyte Nuclear Factor 1 ; Hepatocyte Nuclear Factor 1-alpha ; Hepatocyte Nuclear Factor 1-beta ; Hepatocyte Nuclear Factor 3-beta ; Hepatocyte Nuclear Factor 4 ; Hepatocyte Nuclear Factor 6 ; Hepatocytes/*metabolism ; Homeodomain Proteins/genetics/metabolism ; Humans ; Insulin/metabolism ; Insulin Resistance ; Islets of Langerhans/*metabolism ; Mice ; Mutation ; Nuclear Proteins/metabolism ; Oligonucleotide Array Sequence Analysis ; Phosphoproteins/genetics/metabolism ; Polymorphism, Single Nucleotide ; Promoter Regions, Genetic ; Signal Transduction ; Trans-Activators/genetics/metabolism ; Transcription Factors/genetics/*metabolism ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 160
    facet.materialart.
    Unknown
    Natural killer cell signaling pathways (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-30
    Description: Natural killer (NK) cells are lymphocytes of the innate immune system that are involved in the early defenses against foreign cells, as well as autologous cells undergoing various forms of stress, such as microbial infection or tumor transformation. NK cell activation is controlled by a dynamic balance between complementary and antagonistic pathways that are initiated upon interaction with potential target cells. NK cells express an array of activating cell surface receptors that can trigger cytolytic programs, as well as cytokine or chemokine secretion. Some of these activating cell surface receptors initiate protein tyrosine kinase (PTK)-dependent pathways through noncovalent associations with transmembrane signaling adaptors that harbor intracytoplasmic ITAMs (immunoreceptor tyrosine-based activation motifs). Additional cell surface receptors that are not directly coupled to ITAMs also participate in NK cell activation. These include NKG2D, which is noncovalently associated to the DAP10 transmembrane signaling adaptor, as well as integrins and cytokine receptors. NK cells also express cell surface inhibitory receptors that antagonize activating pathways through protein tyrosine phosphatases (PTPs). These inhibitory cell surface receptors are characterized by intracytoplasmic ITIMs (immunoreceptor tyrosine-based inhibition motifs). The tyrosine-phosphorylation status of several signaling components that are substrates for both PTKs and PTPs is thus key to the propagation of the NK cell effector pathways. Understanding the integration of these multiple signals is central to the understanding and manipulation of NK cell effector signaling pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vivier, Eric -- Nunes, Jacques A -- Vely, Frederic -- New York, N.Y. -- Science. 2004 Nov 26;306(5701):1517-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre d'Immunologie de Marseille-Luminy, INSERM-CNRS-Univ. Mediterranee, Campus de Luminy, Case 906, 13288 Marseille cedex 09, France. vivier@ciml.univ-mrs.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15567854" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; Amino Acid Motifs ; Animals ; Antibody-Dependent Cell Cytotoxicity ; Cytokines/metabolism ; Humans ; Killer Cells, Natural/immunology/*physiology ; Lymphocyte Activation ; Membrane Proteins/metabolism ; Mice ; Models, Immunological ; NK Cell Lectin-Like Receptor Subfamily K ; Phosphoproteins/metabolism ; Phosphorylation ; Protein Tyrosine Phosphatases/metabolism ; Protein-Tyrosine Kinases/metabolism ; Receptors, Immunologic/chemistry/metabolism/physiology ; Receptors, Natural Killer Cell ; *Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 161
    facet.materialart.
    Unknown
    Characterization of a common susceptibility locus for asthma-related traits (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-04-10
    Description: Susceptibility to asthma depends on variation at an unknown number of genetic loci. To identify susceptibility genes on chromosome 7p, we adopted a hierarchical genotyping design, leading to the identification of a 133-kilobase risk-conferring segment containing two genes. One of these coded for an orphan G protein-coupled receptor named GPRA (G protein-coupled receptor for asthma susceptibility), which showed distinct distribution of protein isoforms between bronchial biopsies from healthy and asthmatic individuals. In three cohorts from Finland and Canada, single nucleotide polymorphism-tagged haplotypes associated with high serum immunoglobulin E or asthma. The murine ortholog of GPRA was up-regulated in a mouse model of ovalbumin-induced inflammation. Together, these data implicate GPRA in the pathogenesis of atopy and asthma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Laitinen, Tarja -- Polvi, Anne -- Rydman, Pia -- Vendelin, Johanna -- Pulkkinen, Ville -- Salmikangas, Paula -- Makela, Siru -- Rehn, Marko -- Pirskanen, Asta -- Rautanen, Anna -- Zucchelli, Marco -- Gullsten, Harriet -- Leino, Marina -- Alenius, Harri -- Petays, Tuula -- Haahtela, Tari -- Laitinen, Annika -- Laprise, Catherine -- Hudson, Thomas J -- Laitinen, Lauri A -- Kere, Juha -- New York, N.Y. -- Science. 2004 Apr 9;304(5668):300-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉GeneOS Limited, 00251 Helsinki, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15073379" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Alternative Splicing ; Animals ; Asthma/*genetics/metabolism ; Bronchi/chemistry/cytology ; Chromosomes, Human, Pair 7/*genetics ; Epithelial Cells/chemistry ; Female ; Finland ; Gene Expression ; Genes ; Genetic Linkage ; *Genetic Predisposition to Disease ; Genetic Variation ; Genotype ; *Haplotypes ; Humans ; Hypersensitivity/genetics/metabolism ; Immunoglobulin E/blood ; Inflammation/genetics ; Lung/metabolism ; Male ; Mice ; Myocytes, Smooth Muscle/chemistry ; Polymorphism, Single Nucleotide ; Quebec ; Receptors, G-Protein-Coupled/analysis/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 162
    facet.materialart.
    Unknown
    Neuroscience. Zif and the survival of memory (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-05-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Izquierdo, Ivan -- Cammarota, Martin -- New York, N.Y. -- Science. 2004 May 7;304(5672):829-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centro de Memoria, Departamento de Bioquimica, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos 2600-Anexo, 90035-003 Porto Alegre, RS, Brazil. izquier@terra.com.br〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15131293" target="_blank"〉PubMed〈/a〉
    Keywords: Amnesia/physiopathology ; Amygdala/physiology ; Animals ; Brain/*physiology ; Brain-Derived Neurotrophic Factor/genetics/physiology ; Conditioning (Psychology) ; Cues ; Extinction, Psychological ; *Fear ; Gyrus Cinguli/physiology ; Hippocampus/physiology ; Memory/*physiology ; Mental Recall/*physiology ; Mice ; Neurons/physiology ; Oligonucleotides, Antisense/pharmacology ; Proto-Oncogene Proteins c-fos/metabolism ; Repression, Psychology ; Time Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 163
    facet.materialart.
    Unknown
    Involvement of mammalian Mus81 in genome integrity and tumor suppression (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-06-19
    Description: Mus81-Eme1 endonuclease has been implicated in the rescue of stalled replication forks and the resolution of meiotic recombination intermediates in yeast. We used gene targeting to study the physiological requirements of Mus81 in mammals. Mus81-/- mice are viable and fertile, which indicates that mammalian Mus81 is not essential for recombination processes associated with meiosis. Mus81-deficient mice and cells were hypersensitive to the DNA cross-linking agent mitomycin C but not to gamma-irradiation. Remarkably, both homozygous Mus81-/- and heterozygous Mus81+/- mice exhibited a similar susceptibility to spontaneous chromosomal damage and a profound and equivalent predisposition to lymphomas and other cancers. These studies demonstrate a critical role for the proper biallelic expression of the mammalian Mus81 in the maintenance of genomic integrity and tumor suppression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McPherson, John Peter -- Lemmers, Benedicte -- Chahwan, Richard -- Pamidi, Ashwin -- Migon, Eva -- Matysiak-Zablocki, Elzbieta -- Moynahan, Mary Ellen -- Essers, Jeroen -- Hanada, Katsuhiro -- Poonepalli, Anuradha -- Sanchez-Sweatman, Otto -- Khokha, Rama -- Kanaar, Roland -- Jasin, Maria -- Hande, M Prakash -- Hakem, Razqallah -- New York, N.Y. -- Science. 2004 Jun 18;304(5678):1822-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ontario Cancer Institute, 620 University Avenue, Suite 706, Toronto, Ontario, Canada M5G 2C1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15205536" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Chromosome Aberrations ; DNA Damage ; DNA-Binding Proteins/*genetics/*physiology ; Embryo, Mammalian/cytology ; Embryonic and Fetal Development ; *Endonucleases ; Gamma Rays ; Gene Targeting ; Genetic Predisposition to Disease ; *Genome ; *Genomic Instability ; Heterozygote ; Lymphoma/etiology/genetics/pathology ; Meiosis ; Mice ; Mitomycin/pharmacology ; Neoplasms/etiology/*genetics ; Recombination, Genetic ; Saccharomyces cerevisiae Proteins ; Sister Chromatid Exchange ; Stem Cells ; T-Lymphocytes/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 164
    facet.materialart.
    Unknown
    Mighty mice: inspiration for rogue athletes? (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2004 Jul 30;305(5684):633.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15286359" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Clinical Trials as Topic ; *Doping in Sports ; Genetic Therapy ; Humans ; Insulin-Like Growth Factor I/biosynthesis/*genetics/*pharmacology/therapeutic use ; Mice ; Muscle, Skeletal/drug effects/*growth & development/metabolism ; *Sports
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 165
    facet.materialart.
    Unknown
    NO parkin in Parkinson's disease (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-06-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lancaster, Jack R Jr -- New York, N.Y. -- Science. 2004 Jun 25;304(5679):1905; author reply 1905.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15218128" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; MPTP Poisoning/metabolism ; Mice ; Nitric Oxide/*metabolism ; Nitric Oxide Donors/pharmacology ; Parkinson Disease/*metabolism ; S-Nitrosoglutathione/pharmacology ; Ubiquitin-Protein Ligases/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 166
    facet.materialart.
    Unknown
    Overriding imatinib resistance with a novel ABL kinase inhibitor (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-07-17
    Description: Resistance to the ABL kinase inhibitor imatinib (STI571 or Gleevec) in chronic myeloid leukemia (CML) occurs through selection for tumor cells harboring BCR-ABL kinase domain point mutations that interfere with drug binding. Crystallographic studies predict that most imatinib-resistant mutants should remain sensitive to inhibitors that bind ABL with less stringent conformational requirements. BMS-354825 is an orally bioavailable ABL kinase inhibitor with two-log increased potency relative to imatinib that retains activity against 14 of 15 imatinib-resistant BCR-ABL mutants. BMS-354825 prolongs survival of mice with BCR-ABL-driven disease and inhibits proliferation of BCR-ABL-positive bone marrow progenitor cells from patients with imatinib-sensitive and imatinib-resistant CML. These data illustrate how molecular insight into kinase inhibitor resistance can guide the design of second-generation targeted therapies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shah, Neil P -- Tran, Chris -- Lee, Francis Y -- Chen, Ping -- Norris, Derek -- Sawyers, Charles L -- New York, N.Y. -- Science. 2004 Jul 16;305(5682):399-401.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology and Oncology, Department of Medicine, The David Geffen School of Medicine, University of California, Los Angeles, CA, 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15256671" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; Antineoplastic Agents/metabolism/*pharmacology/therapeutic use ; Benzamides ; Binding Sites ; Cell Division/drug effects ; Cell Line ; Clinical Trials, Phase I as Topic ; Dasatinib ; Drug Resistance, Neoplasm ; Enzyme Inhibitors/metabolism/pharmacology/therapeutic use ; Fusion Proteins, bcr-abl/*antagonists & inhibitors/chemistry/genetics/metabolism ; Hematopoietic Stem Cells/drug effects ; Humans ; Imatinib Mesylate ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*drug therapy ; Mice ; Mice, SCID ; Mutation ; Piperazines/*pharmacology/therapeutic use ; Protein Conformation ; Pyrimidines/metabolism/*pharmacology/therapeutic use ; Thiazoles/metabolism/*pharmacology/therapeutic use ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 167
    facet.materialart.
    Unknown
    Neuroscience. Calcium and CREST for healthy dendrites (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-01-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jefferis, Gregory S X E -- Komiyama, Takaki -- Luo, Liqun -- New York, N.Y. -- Science. 2004 Jan 9;303(5655):179-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences and Neurosciences Program, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14715999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; CREB-Binding Protein ; Calcium/*metabolism ; Calcium Signaling ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Nucleus/metabolism ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein/metabolism ; DNA-Binding Proteins/metabolism ; Dendrites/*physiology/ultrastructure ; Mice ; Neurons/physiology/ultrastructure ; Nuclear Proteins/metabolism ; Rats ; Recombinant Fusion Proteins/metabolism ; Trans-Activators/chemistry/genetics/*metabolism ; Transcription Factors/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
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 168
    facet.materialart.
    Unknown
    TRPM4 regulates calcium oscillations after T cell activation (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-20
    Description: TRPM4 has recently been described as a calcium-activated nonselective (CAN) cation channel that mediates membrane depolarization. However, the functional importance of TRPM4 in the context of calcium (Ca2+) signaling and its effect on cellular responses are not known. Here, the molecular inhibition of endogenous TRPM4 in T cells was shown to suppress TRPM4 currents, with a profound influence on receptor-mediated Ca2+ mobilization. Agonist-mediated oscillations in intracellular Ca2+ concentration ([Ca2+]i), which are driven by store-operated Ca2+ influx, were transformed into a sustained elevation in [Ca2+]i. This increase in Ca2+ influx enhanced interleukin-2 production. Thus, TRPM4-mediated depolarization modulates Ca2+ oscillations, with downstream effects on cytokine production in T lymphocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Launay, Pierre -- Cheng, Henrique -- Srivatsan, Subhashini -- Penner, Reinhold -- Fleig, Andrea -- Kinet, Jean-Pierre -- R01-AI46734/AI/NIAID NIH HHS/ -- R01-AI50200/AI/NIAID NIH HHS/ -- R01-GM63954/GM/NIGMS NIH HHS/ -- R01-GM65360/GM/NIGMS NIH HHS/ -- R01-NS40927/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 Nov 19;306(5700):1374-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15550671" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blotting, Western ; Calcium/*metabolism ; Calcium Channels/immunology/*metabolism ; *Calcium Signaling ; Cation Transport Proteins/immunology/*metabolism ; Cell Line ; Cell Line, Tumor ; Humans ; Immunoprecipitation ; Interleukin-2/metabolism ; Jurkat Cells ; *Lymphocyte Activation ; Membrane Potentials ; Mice ; Patch-Clamp Techniques ; Phytohemagglutinins/pharmacology ; RNA Interference ; Sodium/metabolism ; T-Lymphocytes/immunology/*metabolism ; TRPM Cation Channels
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 169
    facet.materialart.
    Unknown
    Basic and clinical immunology meeting. Genes crisscross disease lines (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin, Jennifer -- New York, N.Y. -- Science. 2004 Aug 6;305(5685):773.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15297646" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmune Diseases/*genetics ; Gene Expression Profiling ; *Genes ; Haplotypes ; Humans ; *Immune System ; Mice ; Neoplasms/genetics ; *RNA Interference
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 170
    facet.materialart.
    Unknown
    Research on aging. Gene links calorie deprivation and long life in rodents (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-06-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin, Jennifer -- New York, N.Y. -- Science. 2004 Jun 18;304(5678):1731.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15205503" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/*physiology ; Animals ; *Apoptosis ; *Caloric Restriction ; Cell Differentiation ; Diet ; Gene Expression Regulation ; Histone Deacetylases/genetics/*metabolism ; Humans ; Insulin/metabolism ; Longevity ; Mice ; Rats ; Receptors, Cytoplasmic and Nuclear/metabolism ; Sirtuin 1 ; Sirtuins/genetics/*metabolism ; Somatomedins/metabolism ; Transcription Factors/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 171
    facet.materialart.
    Unknown
    Reproductive biology. Textbook rewrite? Adult mammals may produce eggs after all (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-03-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin, Jennifer -- New York, N.Y. -- Science. 2004 Mar 12;303(5664):1593.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15016968" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/adverse effects/therapeutic use ; Cell Death ; Cell Division ; Female ; Fertility/drug effects ; Germ Cells/*physiology ; Humans ; Mice ; Oocytes/*physiology ; *Oogenesis ; Ovarian Follicle/cytology ; Ovary/*cytology/physiology/transplantation ; Stem Cells/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 172
    facet.materialart.
    Unknown
    Immunology. Unexpectedly, ancient molecule tied to asthma (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-06-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin, Jennifer -- New York, N.Y. -- Science. 2004 Jun 11;304(5677):1577.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15192186" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Asthma/*enzymology/immunology ; Chitinase/antagonists & inhibitors/*metabolism ; Gaucher Disease/enzymology ; Humans ; Interleukin-13/*metabolism ; Lung/*enzymology ; Mice ; Th2 Cells/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 173
    facet.materialart.
    Unknown
    Genetic dissection of complex traits with chromosome substitution strains of mice (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-03-20
    Description: Chromosome substitution strains (CSSs) have been proposed as a simple and powerful way to identify quantitative trait loci (QTLs) affecting developmental, physiological, and behavioral processes. Here, we report the construction of a complete CSS panel for a vertebrate species. The CSS panel consists of 22 mouse strains, each of which carries a single chromosome substituted from a donor strain (A/J) onto a common host background (C57BL/6J). A survey of 53 traits revealed evidence for 150 QTLs affecting serum levels of sterols and amino acids, diet-induced obesity, and anxiety. These results demonstrate that CSSs greatly facilitate the detection and identification of genes that control the wide diversity of naturally occurring phenotypic variation in the A/J and C57BL/6J inbred strains.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Singer, Jonathan B -- Hill, Annie E -- Burrage, Lindsay C -- Olszens, Keith R -- Song, Junghan -- Justice, Monica -- O'Brien, William E -- Conti, David V -- Witte, John S -- Lander, Eric S -- Nadeau, Joseph H -- GM07250/GM/NIGMS NIH HHS/ -- HD07518/HD/NICHD NIH HHS/ -- RR12305/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2004 Apr 16;304(5669):445-8. Epub 2004 Mar 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15031436" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/blood ; Animals ; Anxiety/genetics ; *Chromosome Mapping ; Chromosomes, Mammalian/*genetics ; Crosses, Genetic ; Diet ; Female ; Genetic Predisposition to Disease ; Genetic Variation ; Male ; Mice ; Mice, Inbred A ; Mice, Inbred C57BL ; Microsatellite Repeats ; Obesity/genetics/physiopathology ; Phenotype ; *Quantitative Trait Loci ; *Quantitative Trait, Heritable ; Sterols/blood ; Weight Gain
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 174
    facet.materialart.
    Unknown
    Activation of apoptosis in vivo by a hydrocarbon-stapled BH3 helix (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-09-09
    Description: BCL-2 family proteins constitute a critical control point for the regulation of apoptosis. Protein interaction between BCL-2 members is a prominent mechanism of control and is mediated through the amphipathic alpha-helical BH3 segment, an essential death domain. We used a chemical strategy, termed hydrocarbon stapling, to generate BH3 peptides with improved pharmacologic properties. The stapled peptides, called "stabilized alpha-helix of BCL-2 domains" (SAHBs), proved to be helical, protease-resistant, and cell-permeable molecules that bound with increased affinity to multidomain BCL-2 member pockets. A SAHB of the BH3 domain from the BID protein specifically activated the apoptotic pathway to kill leukemia cells. In addition, SAHB effectively inhibited the growth of human leukemia xenografts in vivo. Hydrocarbon stapling of native peptides may provide a useful strategy for experimental and therapeutic modulation of protein-protein interactions in many signaling pathways.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1360987/" 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/PMC1360987/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walensky, Loren D -- Kung, Andrew L -- Escher, Iris -- Malia, Thomas J -- Barbuto, Scott -- Wright, Renee D -- Wagner, Gerhard -- Verdine, Gregory L -- Korsmeyer, Stanley J -- K08 HL074049/HL/NHLBI NIH HHS/ -- K08HL074049/HL/NHLBI NIH HHS/ -- R37CA50239/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2004 Sep 3;305(5689):1466-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Pediatric Hematology/Oncology and Children's Hospital Boston, Massachusetts, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15353804" target="_blank"〉PubMed〈/a〉
    Keywords: *Alkenes ; Animals ; *Apoptosis ; BH3 Interacting Domain Death Agonist Protein ; Bridged Compounds/chemical synthesis/chemistry/metabolism/*pharmacology ; Carrier Proteins/chemistry ; Cell Division/drug effects ; Cell Line, Tumor ; Cell Membrane/metabolism ; Cytochromes c/metabolism ; Dose-Response Relationship, Drug ; Endosomes/metabolism ; Humans ; Jurkat Cells ; Leukemia, Experimental/*drug therapy/pathology ; Leukemic Infiltration ; Mice ; Mice, SCID ; Mitochondria, Liver/drug effects/metabolism ; *Molecular Mimicry ; Neoplasm Transplantation ; Peptide Fragments/*chemistry ; Peptides/chemical synthesis/chemistry/metabolism/*pharmacology ; Protein Binding ; Protein Engineering ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Proto-Oncogene Proteins/*chemistry ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Transplantation, Heterologous
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 175
    facet.materialart.
    Unknown
    Rapid rewiring of arcuate nucleus feeding circuits by leptin (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-04-06
    Description: The fat-derived hormone leptin regulates energy balance in part by modulating the activity of neuropeptide Y and proopiomelanocortin neurons in the hypothalamic arcuate nucleus. To study the intrinsic activity of these neurons and their responses to leptin, we generated mice that express distinct green fluorescent proteins in these two neuronal types. Leptin-deficient (ob/ob) mice differed from wild-type mice in the numbers of excitatory and inhibitory synapses and postsynaptic currents onto neuropeptide Y and proopiomelanocortin neurons. When leptin was delivered systemically to ob/ob mice, the synaptic density rapidly normalized, an effect detectable within 6 hours, several hours before leptin's effect on food intake. These data suggest that leptin-mediated plasticity in the ob/ob hypothalamus may underlie some of the hormone's behavioral effects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pinto, Shirly -- Roseberry, Aaron G -- Liu, Hongyan -- Diano, Sabrina -- Shanabrough, Marya -- Cai, Xiaoli -- Friedman, Jeffrey M -- Horvath, Tamas L -- DK060711/DK/NIDDK NIH HHS/ -- F32DK61176/DK/NIDDK NIH HHS/ -- F32NS046921/NS/NINDS NIH HHS/ -- R01 DK041096/DK/NIDDK NIH HHS/ -- R01 DK061619/DK/NIDDK NIH HHS/ -- RR014451/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2004 Apr 2;304(5667):110-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Genetics, Rockefeller University, 1230 York Avenue, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15064421" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arcuate Nucleus of Hypothalamus/cytology/*physiology ; Body Weight/drug effects ; Eating ; Evoked Potentials ; Excitatory Postsynaptic Potentials ; *Feeding Behavior/drug effects ; Ghrelin ; Glutamic Acid/analysis ; Green Fluorescent Proteins ; In Vitro Techniques ; Leptin/genetics/pharmacology/*physiology ; Luminescent Proteins/analysis ; Mice ; Mice, Obese ; Mice, Transgenic ; Neuronal Plasticity/*physiology ; Neurons/drug effects/*physiology ; Neuropeptide Y/genetics/physiology ; Patch-Clamp Techniques ; Peptide Hormones/pharmacology ; Pro-Opiomelanocortin/genetics/physiology ; Recombinant Fusion Proteins/analysis ; Synapses/chemistry/ultrastructure ; Tetrodotoxin/pharmacology ; Transgenes ; gamma-Aminobutyric Acid/analysis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 176
    facet.materialart.
    Unknown
    Mammalian tissue oxygen levels modulate iron-regulatory protein activities in vivo (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-18
    Description: The iron-regulatory proteins (IRPs) posttranscriptionally regulate expression of transferrin receptor, ferritin, and other iron metabolism proteins. Although both IRPs can regulate expression of the same target genes, IRP2-/- mice significantly misregulate iron metabolism and develop neurodegeneration, whereas IRP1-/- mice are spared. We found that IRP2-/- cells misregulated iron metabolism when cultured in 3 to 6% oxygen, which is comparable to physiological tissue concentrations, but not in 21% oxygen, a concentration that activated IRP1 and allowed it to substitute for IRP2. Thus, IRP2 dominates regulation of mammalian iron homeostasis because it alone registers iron concentrations and modulates its RNA-binding activity at physiological oxygen tensions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyron-Holtz, Esther G -- Ghosh, Manik C -- Rouault, Tracey A -- New York, N.Y. -- Science. 2004 Dec 17;306(5704):2087-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15604406" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Ferritins/biosynthesis/metabolism ; Gene Expression Regulation ; Homeostasis ; Iron/*metabolism ; Iron Regulatory Protein 1/genetics/*metabolism ; Iron Regulatory Protein 2/genetics/*metabolism ; Lymphocytes/*metabolism ; Macrophages/*metabolism ; Mice ; Oxidants/metabolism ; Oxygen/*physiology ; RNA/metabolism ; Receptors, Transferrin/biosynthesis/metabolism ; Response Elements ; Spleen/cytology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 177
    facet.materialart.
    Unknown
    Abnormal cytokinesis in cells deficient in the breast cancer susceptibility protein BRCA2 (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-09-18
    Description: Germ-line mutations inactivating BRCA2 predispose to cancer. BRCA2-deficient cells exhibit alterations in chromosome number (aneuploidy), as well as structurally aberrant chromosomes. Here, we show that BRCA2 deficiency impairs the completion of cell division by cytokinesis. BRCA2 inactivation in murine embryo fibroblasts (MEFs) and HeLa cells by targeted gene disruption or RNA interference delays and prevents cell cleavage. Impeded cell separation is accompanied by abnormalities in myosin II organization during the late stages in cytokinesis. BRCA2 may have a role in regulating these events, as it localizes to the cytokinetic midbody. Our findings thus link cytokinetic abnormalities to a hereditary cancer syndrome characterized by chromosomal instability and may help to explain why BRCA2-deficient tumors are frequently aneuploid.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Daniels, Matthew J -- Wang, Yunmei -- Lee, Miyoung -- Venkitaraman, Ashok R -- New York, N.Y. -- Science. 2004 Oct 29;306(5697):876-9. Epub 2004 Sep 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Cambridge, Cancer Research UK, Department of Oncology and the Medical Research Council (MRC) Cancer Cell Unit, Hutchison/MRC Research Centre, Hills Road, Cambridge CB2 2XZ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15375219" target="_blank"〉PubMed〈/a〉
    Keywords: Anaphase ; Aneuploidy ; Animals ; BRCA2 Protein/*physiology ; *Cell Division ; Cell Line, Tumor ; Cell Nucleus/physiology ; Cells, Cultured ; Embryo, Mammalian ; Gene Targeting ; Genes, BRCA2 ; HeLa Cells ; Humans ; Mice ; Mitosis ; Myosin Type II/metabolism ; RNA, Small Interfering
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 178
    facet.materialart.
    Unknown
    Impaired degradation of mutant alpha-synuclein by chaperone-mediated autophagy (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-31
    Description: Aberrant alpha-synuclein degradation is implicated in Parkinson's disease pathogenesis because the protein accumulates in the Lewy inclusion bodies associated with the disease. Little is known, however, about the pathways by which wild-type alpha-synuclein is normally degraded. We found that wild-type alpha-synuclein was selectively translocated into lysosomes for degradation by the chaperone-mediated autophagy pathway. The pathogenic A53T and A30P alpha-synuclein mutants bound to the receptor for this pathway on the lysosomal membrane, but appeared to act as uptake blockers, inhibiting both their own degradation and that of other substrates. These findings may underlie the toxic gain-of-function by the mutants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cuervo, Ana Maria -- Stefanis, Leonidas -- Fredenburg, Ross -- Lansbury, Peter T -- Sulzer, David -- AG021904/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2004 Aug 27;305(5688):1292-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Structural Biology, Marion Bessin Liver Research Center, Albert Einstein College of Medicine, Bronx, NY 10461, USA. amcuervo@aecom.yu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15333840" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Antigens, CD/metabolism ; *Autophagy ; Cells, Cultured ; Glyceraldehyde-3-Phosphate Dehydrogenases/metabolism/pharmacology ; Half-Life ; Intracellular Membranes/metabolism ; Lysosome-Associated Membrane Glycoproteins ; Lysosomes/*metabolism ; Male ; Mice ; Molecular Chaperones/*metabolism ; Mutation ; Nerve Tissue Proteins/chemistry/genetics/*metabolism ; Neurons/metabolism ; PC12 Cells ; Protein Binding ; Protein Transport ; Rats ; Rats, Wistar ; Synucleins ; alpha-Synuclein
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 179
    facet.materialart.
    Unknown
    Reduction of particulate air pollution lowers the risk of heritable mutations in mice (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-05-15
    Description: Urban and industrial air pollution can cause elevated heritable mutation rates in birds and rodents. The relative importance of airborne particulate matter versus gas-phase substances in causing these genetic effects under ambient conditions has been unclear. Here we show that high-efficiency particulate-air (HEPA) filtration of ambient air significantly reduced heritable mutation rates at repetitive DNA loci in laboratory mice housed outdoors near a major highway and two integrated steel mills. These findings implicate exposure to airborne particulate matter as a principal factor contributing to elevated mutation rates in sentinel mice and add to accumulating evidence that air pollution may pose genetic risks to humans and wildlife.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Somers, Christopher M -- McCarry, Brian E -- Malek, Farideh -- Quinn, James S -- New York, N.Y. -- Science. 2004 May 14;304(5673):1008-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, McMaster University, 1280 Main Street West, Hamilton, Ontario L8S 4K1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15143280" target="_blank"〉PubMed〈/a〉
    Keywords: Air Pollutants/*toxicity ; Air Pollution/*adverse effects ; Animals ; Fathers ; Female ; Filtration/instrumentation ; *Germ-Line Mutation ; Industry ; Male ; Meiosis ; Mice ; Mutagens/*toxicity ; Ontario ; Particle Size ; Polycyclic Hydrocarbons, Aromatic/analysis/toxicity ; Spermatogenesis ; Spermatogonia/drug effects/physiology ; Steel ; Tandem Repeat Sequences
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 180
    facet.materialart.
    Unknown
    Gene therapy insertional mutagenesis insights (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-01-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dave, Utpal P -- Jenkins, Nancy A -- Copeland, Neal G -- New York, N.Y. -- Science. 2004 Jan 16;303(5656):333.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mouse Cancer Genetics Program, National Cancer Institute, Center for Cancer Research, Frederick, MD 21702, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14726584" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; DNA-Binding Proteins/*genetics ; Gene Expression ; *Genetic Therapy/adverse effects ; Genetic Vectors ; Humans ; LIM Domain Proteins ; Leukemia, T-Cell/etiology/*genetics ; Metalloproteins/*genetics ; Mice ; *Mutagenesis, Insertional ; Proto-Oncogene Proteins ; Receptors, Interleukin-2/*genetics ; Retroviridae/*genetics ; Severe Combined Immunodeficiency/genetics/therapy ; Virus Integration
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 181
    facet.materialart.
    Unknown
    Development. Making sense of the sensory lineage (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bronner-Fraser, Marianne -- New York, N.Y. -- Science. 2004 Feb 13;303(5660):966-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉California Institute of Technology, Pasadena, CA 91125, USA. mbronner@caltech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14963317" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Lineage ; Cell Movement ; Cell Nucleus/metabolism ; Central Nervous System/embryology ; Cytoskeletal Proteins/*metabolism ; Mice ; Models, Neurological ; Multipotent Stem Cells/*physiology ; Neural Crest/*cytology/embryology/physiology ; Neurons, Afferent/*cytology/physiology ; Proto-Oncogene Proteins/*metabolism ; Signal Transduction ; Time Factors ; Trans-Activators/*metabolism ; Transcription Factors/metabolism ; Wnt Proteins ; *Zebrafish Proteins ; beta Catenin
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 182
    facet.materialart.
    Unknown
    Immunology. Policing the immune system (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-10-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, Ingrid -- New York, N.Y. -- Science. 2004 Oct 22;306(5696):596-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15498987" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD3/immunology ; Autoimmune Diseases/immunology ; Cell Line, Tumor ; DNA-Binding Proteins/genetics ; Diabetes Mellitus, Type 1/immunology/therapy ; Forkhead Transcription Factors ; Humans ; Hypersensitivity/immunology ; Immune Tolerance ; Immunotherapy ; Mice ; Neoplasms/immunology/therapy ; T-Lymphocytes/immunology/*physiology ; Transplantation Immunology ; Virus Diseases/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 183
    facet.materialart.
    Unknown
    Immunology. The Robin Hood of antigen presentation (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-01-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉De Libero, Gennaro -- New York, N.Y. -- Science. 2004 Jan 23;303(5657):485-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Research, University Hospital Basel, Basel CH-4031, Switzerland. gennaro.delibero@unibas.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14739449" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; Antigen-Presenting Cells/immunology/metabolism ; Antigens, Bacterial/immunology ; Antigens, CD1/chemistry/immunology/metabolism ; Carrier Proteins/*metabolism ; Cell Membrane/immunology/metabolism ; Endosomes/immunology/metabolism ; Glycolipids/immunology/metabolism ; Glycoproteins/chemistry/deficiency/*metabolism ; Hydrophobic and Hydrophilic Interactions ; Killer Cells, Natural/immunology ; Lipids/*immunology ; Lipoproteins/immunology/metabolism ; Lymphocyte Activation ; Mice ; Mycobacterium/*immunology ; Oxazoles/*immunology/metabolism ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 184
    facet.materialart.
    Unknown
    Medicine. Targeting apoptotic pathways in cancer cells (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-09-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Denicourt, Catherine -- Dowdy, Steven F -- New York, N.Y. -- Science. 2004 Sep 3;305(5689):1411-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Cellular and Molecular Medicine, University of California San Diego School of Medicine, La Jolla, CA 92093-0686, USA. sdowdy@ucsd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15353788" target="_blank"〉PubMed〈/a〉
    Keywords: Alkynes/chemical synthesis/chemistry/metabolism/*pharmacology ; Amino Acid Substitution ; Animals ; *Apoptosis ; Bridged Compounds/chemical synthesis/chemistry/metabolism/*pharmacology ; Carrier Proteins/metabolism ; Cell Membrane/metabolism ; Diynes ; Endocytosis ; Glioblastoma/drug therapy ; Humans ; Inhibitor of Apoptosis Proteins ; Intracellular Signaling Peptides and Proteins ; Leukemia, Experimental/drug therapy ; Leukemic Infiltration/drug therapy ; Ligands ; Mice ; Mitochondria/metabolism ; Mitochondrial Proteins/metabolism ; *Molecular Mimicry ; Peptide Fragments/chemistry ; Peptide Library ; Peptides/chemical synthesis/chemistry/metabolism/*pharmacology ; Protein Binding ; Protein Engineering ; Protein Interaction Mapping ; Protein Structure, Secondary ; Proteins/antagonists & inhibitors/chemistry/metabolism ; Proto-Oncogene Proteins/chemistry ; Tetrazoles/chemical synthesis/chemistry/metabolism/*pharmacology ; 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
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 185
    facet.materialart.
    Unknown
    A network of control mediated by regulator of calcium/calmodulin-dependent signaling (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-10-23
    Description: Calmodulin (CaM) is a major effector for the intracellular actions of Ca2+ in nearly all cell types. We identified a CaM-binding protein, designated regulator of calmodulin signaling (RCS). G protein-coupled receptor (GPCR)-dependent activation of protein kinase A (PKA) led to phosphorylation of RCS at Ser55 and increased its binding to CaM. Phospho-RCS acted as a competitive inhibitor of CaM-dependent enzymes, including protein phosphatase 2B (PP2B, also called calcineurin). Increasing RCS phosphorylation blocked GPCR- and PP2B-mediated suppression of L-type Ca2+ currents in striatal neurons. Conversely, genetic deletion of RCS significantly increased this modulation. Through a molecular mechanism that amplifies GPCR- and PKA-mediated signaling and attenuates GPCR- and PP2B-mediated signaling, RCS synergistically increases the phosphorylation of key proteins whose phosphorylation is regulated by PKA and PP2B.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rakhilin, S V -- Olson, P A -- Nishi, A -- Starkova, N N -- Fienberg, A A -- Nairn, A C -- Surmeier, D J -- Greengard, P -- DA10044/DA/NIDA NIH HHS/ -- DA12958/DA/NIDA NIH HHS/ -- MH40899/MH/NIMH NIH HHS/ -- NS34696/NS/NINDS NIH HHS/ -- P01 DA010044/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2004 Oct 22;306(5696):698-701.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15499021" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcineurin/metabolism ; Calcineurin Inhibitors ; Calcium/*metabolism ; Calcium Channels, L-Type/metabolism ; Calcium Signaling ; Calmodulin/*metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Dopamine and cAMP-Regulated Phosphoprotein 32 ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neostriatum/cytology/metabolism ; Nerve Tissue Proteins/metabolism ; Neurons/metabolism ; Phosphoproteins/*metabolism ; Phosphorylation ; Receptor, Muscarinic M1/metabolism ; Receptors, Dopamine D1/metabolism ; *Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 186
    facet.materialart.
    Unknown
    Cell biology. Integrins, rafts, Rac, and Rho (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guan, Jun-Lin -- New York, N.Y. -- Science. 2004 Feb 6;303(5659):773-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Medicine, Cornell University, Ithaca, NY 14853, USA. jg19@cornell.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14764856" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/metabolism ; Cell Adhesion ; Cell Membrane/*metabolism ; Cell Movement ; Cholesterol/metabolism ; Focal Adhesion Kinase 1 ; Focal Adhesion Protein-Tyrosine Kinases ; G(M1) Ganglioside/metabolism ; Glycosylphosphatidylinositols/metabolism ; Integrins/*metabolism ; Lipid Metabolism ; Liposomes/metabolism ; Membrane Microdomains/*metabolism ; Mice ; Microtubules/metabolism ; Models, Biological ; Protein-Serine-Threonine Kinases/metabolism ; Protein-Tyrosine Kinases/metabolism ; *Signal Transduction ; p21-Activated Kinases ; rac GTP-Binding Proteins/*metabolism ; rho GTP-Binding Proteins/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 187
    facet.materialart.
    Unknown
    Comment on "Uracil DNA glycosylase activity is dispensable for immunoglobulin class switch" (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stivers, James T -- GM56834-09/GM/NIGMS NIH HHS/ -- R01 GM056834/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2004 Dec 17;306(5704):2042; author reply 2042.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Johns Hopkins Medical School, 725 North Wolfe Street, Baltimore, MD 21205, USA. jstivers@jhmi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15604391" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/enzymology/immunology/*physiology ; Catalysis ; DNA/*metabolism ; DNA Damage ; DNA Glycosylases/*metabolism ; DNA Repair ; Humans ; *Immunoglobulin Class Switching ; Mice ; Mutation ; Recombination, Genetic ; Uracil/metabolism ; Uracil-DNA Glycosidase ; Viral Proteins/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 188
    facet.materialart.
    Unknown
    Foxg1 suppresses early cortical cell fate (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-01-06
    Description: During mammalian cerebral corticogenesis, progenitor cells become progressively restricted in the types of neurons they can produce. The molecular mechanism that determines earlier versus later born neuron fate is unknown. We demonstrate here that the generation of the earliest born neurons, the Cajal-Retzius cells, is suppressed by the telencephalic transcription factor Foxg1. In Foxg1 null mutants, we observed an excess of Cajal-Retzius neuron production in the cortex. By conditionally inactivating Foxg1 in cortical progenitors that normally produce deep-layer cortical neurons, we demonstrate that Foxg1 is constitutively required to suppress Cajal-Retzius cell fate. Hence, the competence to generate the earliest born neurons during later cortical development is actively suppressed but not lost.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanashima, Carina -- Li, Suzanne C -- Shen, Lijian -- Lai, Eseng -- Fishell, Gord -- EY11124/EY/NEI NIH HHS/ -- HD29584/HD/NICHD NIH HHS/ -- NS32993/NS/NINDS NIH HHS/ -- NS39007/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 Jan 2;303(5654):56-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Genetics Program and the Department of Cell Biology, The Skirball Institute of Biomolecular Medicine, New York University Medical Center, 540 First Avenue, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14704420" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Adhesion Molecules, Neuronal/metabolism ; Cell Differentiation ; Cell Lineage ; Cerebral Cortex/*cytology/embryology ; Crosses, Genetic ; DNA-Binding Proteins/*genetics/*metabolism ; Doxycycline/pharmacology ; Extracellular Matrix Proteins/metabolism ; Female ; Forkhead Transcription Factors ; Gene Expression Regulation, Developmental ; Male ; Mice ; Mice, Transgenic ; Mutation ; Nerve Tissue Proteins/*genetics/*metabolism ; Neurons/*cytology/*physiology ; Serine Endopeptidases ; Stem Cells/cytology/*physiology ; Telencephalon/embryology/metabolism ; Time Factors ; Transcription Factors/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 189
    facet.materialart.
    Unknown
    Autoimmune disease and impaired uptake of apoptotic cells in MFG-E8-deficient mice (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-05-25
    Description: Apoptotic cells expose phosphatidylserine and are swiftly engulfed by macrophages. Milk fat globule epidermal growth factor (EGF) factor 8 (MFG-E8) is a protein that binds to apoptotic cells by recognizing phosphatidylserine and that enhances the engulfment of apoptotic cells by macrophages. We report that tingible body macrophages in the germinal centers of the spleen and lymph nodes strongly express MFG-E8. Many apoptotic lymphocytes were found on the MFG-E8-/- tingible body macrophages, but they were not efficiently engulfed. The MFG-E8-/- mice developed splenomegaly, with the formation of numerous germinal centers, and suffered from glomerulonephritis as a result of autoantibody production. These data demonstrate that MFG-E8 has a critical role in removing apoptotic B cells in the germinal centers and that its failure can lead to autoimmune diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanayama, Rikinari -- Tanaka, Masato -- Miyasaka, Kay -- Aozasa, Katsuyuki -- Koike, Masato -- Uchiyama, Yasuo -- Nagata, Shigekazu -- New York, N.Y. -- Science. 2004 May 21;304(5674):1147-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Osaka University Medical School, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15155946" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Antinuclear/blood ; Antigens, CD/analysis ; Antigens, Differentiation, Myelomonocytic/analysis ; *Antigens, Surface ; *Apoptosis ; Autoantibodies/biosynthesis/blood ; Autoimmune Diseases/*immunology ; B-Lymphocytes/immunology ; Blotting, Northern ; Female ; Gene Targeting ; Germinal Center/cytology/immunology/metabolism ; Glomerulonephritis/*immunology ; In Situ Nick-End Labeling ; Macrophage Activation ; Macrophages/immunology/*metabolism/ultrastructure ; Macrophages, Peritoneal/immunology/metabolism ; Membrane Glycoproteins/genetics/*metabolism ; Mice ; *Milk Proteins ; *Phagocytosis ; Phosphatidylserines/metabolism ; Protein Binding ; Spleen/cytology/metabolism/pathology ; Splenomegaly/pathology ; T-Lymphocytes/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 190
    facet.materialart.
    Unknown
    De novo crypt formation and juvenile polyposis on BMP inhibition in mouse intestine (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-03-16
    Description: Little is known about the signaling mechanisms that determine the highly regular patterning of the intestinal epithelium into crypts and villi. With the use of mouse models, we show that bone morphogenetic protein (BMP)-4 expression occurs exclusively in the intravillus mesenchyme. Villus epithelial cells respond to the BMP signal. Inhibition of BMP signaling by transgenic expression of noggin results in the formation of numerous ectopic crypt units perpendicular to the crypt-villus axis. These changes phenocopy the intestinal histopathology of patients with the cancer predisposition syndrome juvenile polyposis (JP), including the frequent occurrence of intraepithelial neoplasia. Many JP cases are known to harbor mutations in BMP pathway genes. These data indicate that intestinal BMP signaling represses de novo crypt formation and polyp growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haramis, Anna-Pavlina G -- Begthel, Harry -- van den Born, Maaike -- van Es, Johan -- Jonkheer, Suzanne -- Offerhaus, G Johan A -- Clevers, Hans -- New York, N.Y. -- Science. 2004 Mar 12;303(5664):1684-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hubrecht Laboratory, Netherlands Institute for Developmental Biology, Uppsalalaan 8, 3584 CT Utrecht, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15017003" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoma/pathology ; Animals ; Bone Morphogenetic Protein 4 ; Bone Morphogenetic Proteins/antagonists & inhibitors/genetics/*metabolism ; Carrier Proteins ; Cell Differentiation ; Cytoskeletal Proteins/metabolism ; Intestinal Mucosa/embryology/*growth & development/metabolism ; Intestinal Neoplasms/pathology ; Intestinal Polyposis/metabolism/*pathology ; Intestine, Small/embryology/*growth & development/metabolism ; Mesoderm/metabolism ; Mice ; Mice, Transgenic ; Proteins/genetics/metabolism ; *Signal Transduction ; Trans-Activators/metabolism ; Xenopus ; Xenopus Proteins ; beta Catenin
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 191
    facet.materialart.
    Unknown
    Hepcidin regulates cellular iron efflux by binding to ferroportin and inducing its internalization (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-10-30
    Description: Hepcidin is a peptide hormone secreted by the liver in response to iron loading and inflammation. Decreased hepcidin leads to tissue iron overload, whereas hepcidin overproduction leads to hypoferremia and the anemia of inflammation. Ferroportin is an iron exporter present on the surface of absorptive enterocytes, macrophages, hepatocytes, and placental cells. Here we report that hepcidin bound to ferroportin in tissue culture cells. After binding, ferroportin was internalized and degraded, leading to decreased export of cellular iron. The posttranslational regulation of ferroportin by hepcidin may thus complete a homeostatic loop: Iron regulates the secretion of hepcidin, which in turn controls the concentration of ferroportin on the cell surface.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nemeth, Elizabeta -- Tuttle, Marie S -- Powelson, Julie -- Vaughn, Michael B -- Donovan, Adriana -- Ward, Diane McVey -- Ganz, Tomas -- Kaplan, Jerry -- DK065029/DK/NIDDK NIH HHS/ -- DK30534/DK/NIDDK NIH HHS/ -- HL26922/HL/NHLBI NIH HHS/ -- T35HL007744/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2004 Dec 17;306(5704):2090-3. Epub 2004 Oct 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15514116" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antimicrobial Cationic Peptides/chemical ; synthesis/genetics/*metabolism/pharmacology ; Biological Transport ; Cation Transport Proteins/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Cytosol/metabolism ; Ferritins/metabolism ; HeLa Cells ; Hepcidins ; Homeostasis ; Humans ; Iron/*metabolism ; Iron Regulatory Protein 2/metabolism ; Lysosomes/metabolism ; Mice ; Protein Binding ; RNA, Messenger/genetics/metabolism ; Receptor, Epidermal Growth Factor/metabolism ; Recombinant Fusion Proteins/metabolism ; Transfection ; Transferrin/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 192
    facet.materialart.
    Unknown
    Dendrite development regulated by CREST, a calcium-regulated transcriptional activator (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-01-13
    Description: The lasting effects of neuronal activity on brain development involve calcium-dependent gene expression. Using a strategy called transactivator trap, we cloned a calcium-responsive transactivator called CREST (for calcium-responsive transactivator). CREST is a SYT-related nuclear protein that interacts with adenosine 3',5'-monophosphate (cAMP) response element-binding protein (CREB)-binding protein (CBP) and is expressed in the developing brain. Mice that have a targeted disruption of the crest gene are viable but display defects in cortical and hippocampal dendrite development. Cortical neurons from crest mutant mice are compromised in calcium-dependent dendritic growth. Thus, calcium activation of CREST-mediated transcription helps regulate neuronal morphogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aizawa, Hiroyuki -- Hu, Shu-Ching -- Bobb, Kathryn -- Balakrishnan, Karthik -- Ince, Gulayse -- Gurevich, Inga -- Cowan, Mitra -- Ghosh, Anirvan -- MH60598/MH/NIMH NIH HHS/ -- NS39993/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 Jan 9;303(5655):197-202.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14716005" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blotting, Northern ; Brain/cytology/embryology/growth & development/metabolism ; CREB-Binding Protein ; Calcium/*metabolism ; Calcium Channels/metabolism ; Cell Line ; Cells, Cultured ; Cerebral Cortex/cytology/embryology/metabolism ; Cloning, Molecular ; Dendrites/*physiology/ultrastructure ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Gene Library ; Gene Targeting ; Humans ; In Situ Hybridization ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Mutation ; Nervous System/embryology/growth & development/metabolism ; Neurons/*physiology/ultrastructure ; Nuclear Proteins/metabolism ; Protein Structure, Tertiary ; Rats ; Recombinant Fusion Proteins/metabolism ; Trans-Activators/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
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 193
    facet.materialart.
    Unknown
    COX-2-derived prostacyclin confers atheroprotection on female mice (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-20
    Description: Female gender affords relative protection from cardiovascular disease until the menopause. We report that estrogen acts on estrogen receptor subtype alpha to up-regulate the production of atheroprotective prostacyclin, PGI2, by activation of cyclooxygenase 2 (COX-2). This mechanism restrained both oxidant stress and platelet activation that contribute to atherogenesis in female mice. Deletion of the PGI2 receptor removed the atheroprotective effect of estrogen in ovariectomized female mice. This suggests that chronic treatment of patients with selective inhibitors of COX-2 could undermine protection from cardiovascular disease in premenopausal females.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Egan, Karine M -- Lawson, John A -- Fries, Susanne -- Koller, Beverley -- Rader, Daniel J -- Smyth, Emer M -- Fitzgerald, Garret A -- HL62250/HL/NHLBI NIH HHS/ -- HL70128/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2004 Dec 10;306(5703):1954-7. Epub 2004 Nov 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Translational Medicine and Therapeutics, University of Pennsylvania, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15550624" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antioxidants/metabolism ; Arteriosclerosis/metabolism/pathology/*prevention & control ; Cardiovascular Diseases/chemically induced ; Cells, Cultured ; Cyclooxygenase 2 ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase Inhibitors/adverse effects/pharmacology ; Epoprostenol/biosynthesis/metabolism/*physiology ; Estradiol/pharmacology ; Estrogen Receptor alpha/metabolism ; Female ; Hydrogen Peroxide/pharmacology ; Isoenzymes/*metabolism ; Lactones/adverse effects/pharmacology ; Lipid Peroxidation ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle, Smooth, Vascular/drug effects/metabolism ; Myocytes, Smooth Muscle/cytology/drug effects/metabolism ; Ovariectomy ; Oxidative Stress ; Platelet Activation ; Prostaglandin-Endoperoxide Synthases/*metabolism ; Receptors, Epoprostenol/genetics/physiology ; Receptors, LDL/genetics/physiology ; Sex Characteristics ; Sulfones/adverse effects/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 194
    facet.materialart.
    Unknown
    Niemann-Pick C1 Like 1 protein is critical for intestinal cholesterol absorption (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-21
    Description: Dietary cholesterol consumption and intestinal cholesterol absorption contribute to plasma cholesterol levels, a risk factor for coronary heart disease. The molecular mechanism of sterol uptake from the lumen of the small intestine is poorly defined. We show that Niemann-Pick C1 Like 1(NPC1L1) protein plays a critical role in the absorption of intestinal cholesterol. NPC1L1 expression is enriched in the small intestine and is in the brush border membrane of enterocytes. Although otherwise phenotypically normal, NPC1L1-deficient mice exhibit a substantial reduction in absorbed cholesterol, which is unaffected by dietary supplementation of bile acids. Ezetimibe, a drug that inhibits cholesterol absorption, had no effect in NPC1L1 knockout mice, suggesting that NPC1L1 resides in an ezetimibe-sensitive pathway responsible for intestinal cholesterol absorption.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Altmann, Scott W -- Davis, Harry R Jr -- Zhu, Li-Ji -- Yao, Xiaorui -- Hoos, Lizbeth M -- Tetzloff, Glen -- Iyer, Sai Prasad N -- Maguire, Maureen -- Golovko, Andrei -- Zeng, Ming -- Wang, Luquan -- Murgolo, Nicholas -- Graziano, Michael P -- New York, N.Y. -- Science. 2004 Feb 20;303(5661):1201-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiovascular/Endocrine Research, Schering-Plough Research Institute, 2015 Galloping Hill Road, Kenilworth, NJ, 07033-0539, USA. scott.altmann@spcorp.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14976318" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Anticholesteremic Agents/pharmacology ; Azetidines/pharmacology ; Cholesterol/*metabolism ; Cholesterol, Dietary/*metabolism ; Cholic Acid/administration & dosage/pharmacology ; Computational Biology ; Enterocytes/*metabolism ; Ezetimibe ; Female ; Gene Expression Profiling ; Humans ; *Intestinal Absorption/drug effects ; Intestine, Small/metabolism ; Jejunum/metabolism ; Liver/metabolism ; Male ; Membrane Proteins/chemistry/genetics/*metabolism ; Membrane Transport Proteins/chemistry/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; Oligonucleotide Array Sequence Analysis ; Proteins/chemistry/genetics/*metabolism ; Rats ; Rats, Sprague-Dawley
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 195
    facet.materialart.
    Unknown
    Neuroscience. The fat-brain axis enters a new dimension (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-04-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elmquist, Joel K -- Flier, Jeffrey S -- New York, N.Y. -- Science. 2004 Apr 2;304(5667):63-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15064411" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arcuate Nucleus of Hypothalamus/growth & development/*physiology ; Axons/*physiology ; Body Weight ; Eating ; Excitatory Postsynaptic Potentials ; Feeding Behavior ; Ghrelin ; Homeostasis ; Hypothalamus/growth & development/*physiology ; Leptin/*physiology ; Mice ; Mice, Obese ; Neurites/physiology ; Neuronal Plasticity/*physiology ; Neurons/*physiology ; Neuropeptide Y/physiology ; Neurotransmitter Agents/metabolism ; Paraventricular Hypothalamic Nucleus/cytology/growth & development/physiology ; Peptide Hormones/physiology ; Pro-Opiomelanocortin/physiology ; Receptors, Cell Surface/metabolism ; Receptors, Leptin ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 196
    facet.materialart.
    Unknown
    A toll-like receptor that prevents infection by uropathogenic bacteria (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-03-06
    Description: Toll-like receptors (TLRs) recognize molecular patterns displayed by microorganisms, and their subsequent activation leads to the transcription of appropriate host-defense genes. Here we report the cloning and characterization of a member of the mammalian TLR family, TLR11, that displays a distinct pattern of expression in macrophages and liver, kidney, and bladder epithelial cells. Cells expressing TLR11 fail to respond to known TLR ligands but instead respond specifically to uropathogenic bacteria. Mice lacking TLR11 are highly susceptible to infection of the kidneys by uropathogenic bacteria, indicating a potentially important role for TLR11 in preventing infection of internal organs of the urogenital system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Dekai -- Zhang, Guolong -- Hayden, Matthew S -- Greenblatt, Matthew B -- Bussey, Crystal -- Flavell, Richard A -- Ghosh, Sankar -- GM07205/GM/NIGMS NIH HHS/ -- R01-AI59440/AI/NIAID NIH HHS/ -- R37-AI33443/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2004 Mar 5;303(5663):1522-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology and Department of Molecular Biophysics and Biochemistry, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15001781" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Cloning, Molecular ; Codon, Terminator ; Colony Count, Microbial ; Disease Susceptibility ; Epithelial Cells/metabolism ; Escherichia coli/growth & development/immunology/*pathogenicity ; Escherichia coli Infections/*immunology/microbiology ; Gene Expression Profiling ; Humans ; Immunity, Innate ; Kidney/immunology/*metabolism/microbiology ; Ligands ; Liver/metabolism ; Macrophages/metabolism ; Mice ; Mice, Knockout ; Molecular Sequence Data ; NF-kappa B/metabolism ; Polymorphism, Genetic ; Receptors, Cell Surface/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Toll-Like Receptors ; Transfection ; Tumor Necrosis Factor-alpha/metabolism ; Urinary Bladder/immunology/*metabolism/microbiology ; Urinary Tract Infections/*immunology/microbiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 197
    facet.materialart.
    Unknown
    Actin polymerization-driven molecular movement of mDia1 in living cells (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-03-27
    Description: mDia1, a Rho effector, belongs to the Formin family of proteins, which shares the conserved tandem FH1-FH2 unit structure. Formins including mDia1 accelerate actin nucleation while interacting with actin filament fast-growing ends. Here our single-molecule imaging revealed fast directional movement of mDia1 FH1-FH2 for tens of microns in living cells. The movement of mDia1 FH1-FH2 was blocked by actin-perturbing drugs, and the speed of mDia1 FH1-FH2 movement appeared to correlate with actin elongation rates. In vitro, mDia1 FH1-FH2 associated persistently with the growing actin barbed end. mDia1 probably moves processively along the growing end of actin filaments in cells, and Formins may be a molecular motility machinery that is independent from motor proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Higashida, Chiharu -- Miyoshi, Takushi -- Fujita, Akiko -- Oceguera-Yanez, Fabian -- Monypenny, James -- Andou, Yoshikazu -- Narumiya, Shuh -- Watanabe, Naoki -- New York, N.Y. -- Science. 2004 Mar 26;303(5666):2007-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Kyoto University Faculty of Medicine, Yoshida Konoe-cho, Sakyo-ku, Kyoto, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15044801" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/drug effects/*physiology/ultrastructure ; Actins/*metabolism ; Animals ; Bicyclo Compounds, Heterocyclic/metabolism/pharmacology ; Biopolymers ; Carrier Proteins/chemistry/metabolism/*physiology ; Cytochalasin D/metabolism/pharmacology ; *Depsipeptides ; Mice ; Microtubules/drug effects/physiology ; Movement ; Mutation ; Myosins/physiology ; Peptides, Cyclic/pharmacology ; Recombinant Fusion Proteins/chemistry/metabolism ; Thiazoles/metabolism/pharmacology ; Thiazolidines ; Xenopus ; rhoA GTP-Binding Protein/metabolism/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 198
    facet.materialart.
    Unknown
    Early-life blockade of the 5-HT transporter alters emotional behavior in adult mice (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-10-30
    Description: Reduced serotonin transporter (5-HTT) expression is associated with abnormal affective and anxiety-like symptoms in humans and rodents, but the mechanism of this effect is unknown. Transient inhibition of 5-HTT during early development with fluoxetine, a commonly used serotonin selective reuptake inhibitor, produced abnormal emotional behaviors in adult mice. This effect mimicked the behavioral phenotype of mice genetically deficient in 5-HTT expression. These findings indicate a critical role of serotonin in the maturation of brain systems that modulate emotional function in the adult and suggest a developmental mechanism to explain how low-expressing 5-HTT promoter alleles increase vulnerability to psychiatric disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ansorge, Mark S -- Zhou, Mingming -- Lira, Alena -- Hen, Rene -- Gingrich, Jay A -- New York, N.Y. -- Science. 2004 Oct 29;306(5697):879-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sackler Institute for Developmental Psychobiology, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15514160" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; *Anxiety/chemically induced ; Avoidance Learning/drug effects ; Behavior, Animal/drug effects ; Brain/drug effects/growth & development ; Central Nervous System/drug effects/growth & development ; *Emotions/drug effects ; Feeding Behavior/drug effects ; Fluoxetine/adverse effects/*toxicity ; Humans ; Membrane Glycoproteins/antagonists & inhibitors/genetics/*physiology ; Membrane Transport Modulators ; Membrane Transport Proteins/antagonists & inhibitors/genetics/*physiology ; Mice ; Motor Activity/drug effects ; Nerve Tissue Proteins/antagonists & inhibitors/genetics/*physiology ; Polymorphism, Genetic ; Random Allocation ; Serotonin Plasma Membrane Transport Proteins ; Serotonin Uptake Inhibitors/adverse effects/*toxicity ; Stress, Physiological
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 199
    facet.materialart.
    Unknown
    Tryptophan hydroxylase-2 controls brain serotonin synthesis (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-07-13
    Description: Dysregulation of brain serotonin contributes to many psychiatric disorders. Tryptophan hydroxylase-2 (Tph2), rather than Tph1, is preferentially expressed in the brain. We report a functional (C1473G) single-nucleotide polymorphism in mouse Tph2 that results in the substitution of Pro447 with Arg447 and leads to decreased serotonin levels in PC12 cells. Moreover, in BALB/cJ and DBA/2 mice that are homozygous for the 1473G allele, brain serotonin tissue content and synthesis are reduced in comparison to C57Bl/6 and 129X1/SvJ mice that are homozygous for the 1473C allele. Our data provide direct evidence for a fundamental role of Tph2 in brain serotonin synthesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Xiaodong -- Beaulieu, Jean-Martin -- Sotnikova, Tatyana D -- Gainetdinov, Raul R -- Caron, Marc G -- MH60451/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2004 Jul 9;305(5681):217.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute Laboratory, Department of Cell Biology, and Center for Models of Human Disease, Institute for Genome Sciences and Policy, Box 3287, 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/15247473" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Animals ; Brain/*metabolism ; Brain Stem/metabolism ; Corpus Striatum/metabolism ; Frontal Lobe/metabolism ; Humans ; Mice ; Mice, Inbred Strains ; Molecular Sequence Data ; PC12 Cells ; Polymorphism, Single Nucleotide ; Rats ; Reverse Transcriptase Polymerase Chain Reaction ; Serotonin/*biosynthesis ; Transfection ; Tryptophan Hydroxylase/chemistry/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 200
    facet.materialart.
    Unknown
    Comment on "Cerebellar LTD and learning-dependent timing of conditioned eyelid responses" (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-04-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Christian, Kimberly M -- Poulos, Andrew M -- Lavond, David G -- Thompson, Richard F -- AG14751/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2004 Apr 9;304(5668):211; author reply 211.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience Program, University of Southern California, 3641 Watt Way, Los Angeles, CA 90089-2520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15073358" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Blinking ; Cerebellum/*physiology ; *Conditioning, Eyelid ; *Learning ; *Long-Term Synaptic Depression ; Mice ; Mutation ; Purkinje Cells/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...