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
  • Aerodynamics  (189)
  • Mice  (189)
  • 1995-1999  (378)
  • 1999  (378)
  • 101
    facet.materialart.
    Unknown
    Transduction of human CD34+ cells that mediate long-term engraftment of NOD/SCID mice by HIV vectors (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-29
    Description: Efficient gene transfer into human hematopoietic stem cells (HSCs) is an important goal in the study of the hematopoietic system as well as for gene therapy of hematopoietic disorders. A lentiviral vector based on the human immunodeficiency virus (HIV) was able to transduce human CD34+ cells capable of stable, long-term reconstitution of nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice. High-efficiency transduction occurred in the absence of cytokine stimulation and resulted in transgene expression in multiple lineages of human hematopoietic cells for up to 22 weeks after transplantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyoshi, H -- Smith, K A -- Mosier, D E -- Verma, I M -- Torbett, B E -- CA44360/CA/NCI NIH HHS/ -- DK49886/DK/NIDDK NIH HHS/ -- HL53670/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 29;283(5402):682-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9924027" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD34/*analysis ; Bone Marrow Cells/cytology ; Cell Division ; Cell Survival ; Colony-Forming Units Assay ; Gene Expression ; *Gene Transfer Techniques ; *Genetic Vectors ; Green Fluorescent Proteins ; HIV/*genetics ; Hematopoiesis ; *Hematopoietic Stem Cell Transplantation ; *Hematopoietic Stem Cells/cytology/immunology ; Humans ; Leukemia Virus, Murine/genetics ; Luminescent Proteins/genetics ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Promoter Regions, Genetic ; Transfection ; Transgenes
    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
    Viral clearance without destruction of infected cells during acute HBV infection (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-30
    Description: Viral clearance during hepatitis B virus (HBV) infection has been thought to reflect the destruction of infected hepatocytes by CD8(+) T lymphocytes. However, in this study, HBV DNA was shown to largely disappear from the liver and the blood of acutely infected chimpanzees long before the peak of T cell infiltration and most of the liver disease. These results demonstrate that noncytopathic antiviral mechanisms contribute to viral clearance during acute viral hepatitis by purging HBV replicative intermediates from the cytoplasm and covalently closed circular viral DNA from the nucleus of infected cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guidotti, L G -- Rochford, R -- Chung, J -- Shapiro, M -- Purcell, R -- Chisari, F V -- R01 AI20001/AI/NIAID NIH HHS/ -- R01 AI40696/AI/NIAID NIH HHS/ -- R37 CA40489/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 30;284(5415):825-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10221919" target="_blank"〉PubMed〈/a〉
    Keywords: Acute Disease ; Animals ; Cytotoxicity, Immunologic ; DNA, Circular/analysis ; DNA, Viral/analysis/blood ; Hepatitis B/*immunology/pathology/virology ; Hepatitis B Antibodies/blood ; Hepatitis B Core Antigens/analysis ; Hepatitis B virus/genetics/*immunology/isolation & purification/physiology ; Killer Cells, Natural/immunology ; Liver/immunology/pathology/*virology ; Mice ; Mice, Transgenic ; Pan troglodytes ; T-Lymphocytes/immunology ; Time Factors ; Virus Replication
    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
    HIV vaccines. Magic of the occult? (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Montefiori, D -- Moore, J P -- New York, N.Y. -- Science. 1999 Jan 15;283(5400):336-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for AIDS Research, Department of Surgery, Duke University Medical Center, Durham, NC 27710, USA. monte005@mc.duke.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9925493" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/*immunology ; Animals ; COS Cells ; Cell Fusion ; Coculture Techniques ; Epitopes/immunology ; HIV Antibodies/biosynthesis/*immunology ; HIV Antigens/*immunology ; HIV Envelope Protein gp120/immunology ; HIV Envelope Protein gp41/immunology ; HIV-1/*immunology/physiology ; Mice ; Neutralization Tests ; Transfection ; Tumor Cells, Cultured
    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
    Mouse models of tumor development in neurofibromatosis type 1 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-11
    Description: Neurofibromatosis type 1 (NF1) is a prevalent familial cancer syndrome resulting from germ line mutations in the NF1 tumor suppressor gene. Hallmark features of the disease are the development of benign peripheral nerve sheath tumors (neurofibromas), which can progress to malignancy. Unlike humans, mice that are heterozygous for a mutation in Nf1 do not develop neurofibromas. However, as described here, chimeric mice composed in part of Nf1-/- cells do, which demonstrates that loss of the wild-type Nf1 allele is rate-limiting in tumor formation. In addition, mice that carry linked germ line mutations in Nf1 and p53 develop malignant peripheral nerve sheath tumors (MPNSTs), which supports a cooperative and causal role for p53 mutations in MPNST development. These two mouse models provide the means to address fundamental aspects of disease development and to test therapeutic strategies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cichowski, K -- Shih, T S -- Schmitt, E -- Santiago, S -- Reilly, K -- McLaughlin, M E -- Bronson, R T -- Jacks, T -- New York, N.Y. -- Science. 1999 Dec 10;286(5447):2172-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology and Center for Cancer Research and Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10591652" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chimera ; *Disease Models, Animal ; Female ; *Genes, Neurofibromatosis 1 ; Genes, p53 ; Germ-Line Mutation ; Humans ; Loss of Heterozygosity ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation ; Nerve Sheath Neoplasms/*genetics/*pathology ; Nerve Tissue Proteins/analysis/physiology ; Neurofibromatosis 1/*genetics/*pathology ; Neurofibromin 1 ; Proteins/analysis/physiology ; S100 Proteins/analysis ; Schwann Cells/chemistry/ultrastructure ; Stem Cells
    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
    GAD, a single autoantigen for diabetes (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉von Boehmer, H -- Sarukhan, A -- New York, N.Y. -- Science. 1999 May 14;284(5417):1135, 1137.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM U373, Faculte Necker, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10366347" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoantigens/genetics/*immunology/physiology ; DNA, Antisense ; Diabetes Mellitus, Type 1/enzymology/*immunology/therapy ; Glutamate Decarboxylase/genetics/*immunology/physiology ; Humans ; Islets of Langerhans/*enzymology/immunology ; Lymphocyte Activation ; Mice ; Mice, Inbred NOD ; Mice, Transgenic ; Self Tolerance ; T-Lymphocytes/immunology ; Transgenes
    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
    Modulation of respiratory frequency by peptidergic input to rhythmogenic neurons in the preBotzinger complex (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-24
    Description: Neurokinin-1 receptor (NK1R) and mu-opioid receptor (muOR) agonists affected respiratory rhythm when injected directly into the preBotzinger Complex (preBotC), the hypothesized site for respiratory rhythmogenesis in mammals. These effects were mediated by actions on preBotC rhythmogenic neurons. The distribution of NK1R+ neurons anatomically defined the preBotC. Type 1 neurons in the preBotC, which have rhythmogenic properties, expressed both NK1Rs and muORs, whereas type 2 neurons expressed only NK1Rs. These findings suggest that the preBotC is a definable anatomic structure with unique physiological function and that a subpopulation of neurons expressing both NK1Rs and muORs generate respiratory rhythm and modulate respiratory frequency.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2811082/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2811082/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gray, P A -- Rekling, J C -- Bocchiaro, C M -- Feldman, J L -- HL37941/HL/NHLBI NIH HHS/ -- HL40959/HL/NHLBI NIH HHS/ -- R01 HL040959/HL/NHLBI NIH HHS/ -- R01 HL040959-12/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1566-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, University of California Los Angeles, Box 951763, Los Angeles, CA 90095-1763, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10567264" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-/pharmacology ; Female ; In Vitro Techniques ; Medulla Oblongata/cytology/drug effects/*physiology ; Mice ; Mice, Inbred BALB C ; Neurons/chemistry/drug effects/*physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, GABA-B/analysis/physiology ; Receptors, Neurokinin-1/agonists/analysis/*physiology ; Receptors, Opioid, mu/agonists/analysis/*physiology ; Respiratory Mechanics/drug effects/*physiology ; Substance P/pharmacology ; Synaptic Transmission/drug effects
    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
    Requirement for Tec kinases Rlk and Itk in T cell receptor signaling and immunity (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-24
    Description: T cell receptor (TCR) signaling requires activation of Zap-70 and Src family tyrosine kinases, but requirements for other tyrosine kinases are less clear. Combined deletion in mice of two Tec kinases, Rlk and Itk, caused marked defects in TCR responses including proliferation, cytokine production, and apoptosis in vitro and adaptive immune responses to Toxoplasma gondii in vivo. Molecular events immediately downstream from the TCR were intact in rlk-/-itk-/- cells, but intermediate events including inositol trisphosphate production, calcium mobilization, and mitogen-activated protein kinase activation were impaired, establishing Tec kinases as critical regulators of TCR signaling required for phospholipase C-gamma activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schaeffer, E M -- Debnath, J -- Yap, G -- McVicar, D -- Liao, X C -- Littman, D R -- Sher, A -- Varmus, H E -- Lenardo, M J -- Schwartzberg, P L -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):638-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Human Genome Research Institute, National Cancer Institute, National Institute for Allergy and Infectious Diseases, NIH, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10213685" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; CD4-CD8 Ratio ; Calcium Signaling ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Diglycerides/metabolism ; Gene Targeting ; Inositol Phosphates/metabolism ; Interferon-gamma/biosynthesis ; Interleukin-2/biosynthesis/pharmacology ; Isoenzymes/metabolism ; Killer Cells, Natural/immunology ; Lymphocyte Activation ; Mice ; Mutation ; Phospholipase C gamma ; Phosphorylation ; Protein-Tyrosine Kinases/genetics/*metabolism ; Receptors, Antigen, T-Cell/*metabolism ; *Signal Transduction ; T-Lymphocytes/*enzymology/*immunology ; Toxoplasmosis, Animal/immunology ; Type C Phospholipases/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
    Light-independent role of CRY1 and CRY2 in the mammalian circadian clock (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-26
    Description: Cryptochrome (CRY), a photoreceptor for the circadian clock in Drosophila, binds to the clock component TIM in a light-dependent fashion and blocks its function. In mammals, genetic evidence suggests a role for CRYs within the clock, distinct from hypothetical photoreceptor functions. Mammalian CRY1 and CRY2 are here shown to act as light-independent inhibitors of CLOCK-BMAL1, the activator driving Per1 transcription. CRY1 or CRY2 (or both) showed light-independent interactions with CLOCK and BMAL1, as well as with PER1, PER2, and TIM. Thus, mammalian CRYs act as light-independent components of the circadian clock and probably regulate Per1 transcriptional cycling by contacting both the activator and its feedback inhibitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Griffin, E A Jr -- Staknis, D -- Weitz, C J -- MH-59943/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):768-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston, MA 02115 USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10531061" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; ARNTL Transcription Factors ; Animals ; Basic Helix-Loop-Helix Transcription Factors ; *Biological Clocks ; CLOCK Proteins ; Cell Cycle Proteins ; Cells, Cultured ; *Circadian Rhythm ; Cryptochromes ; Dimerization ; *Drosophila Proteins ; *Eye Proteins ; Flavoproteins/metabolism/*physiology ; *Gene Expression Regulation ; Genes, Reporter ; Helix-Loop-Helix Motifs ; Humans ; Intracellular Signaling Peptides and Proteins ; *Light ; Mice ; Nuclear Proteins/antagonists & inhibitors/*genetics/metabolism ; Period Circadian Proteins ; *Photoreceptor Cells, Invertebrate ; Receptors, G-Protein-Coupled ; Trans-Activators/antagonists & inhibitors/metabolism ; Transcription Factors/antagonists & inhibitors/metabolism ; Transcriptional Activation ; Transfection
    Print ISSN: 0036-8075
    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
    Mitochondrial diseases in man and mouse (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-05
    Description: Over the past 10 years, mitochondrial defects have been implicated in a wide variety of degenerative diseases, aging, and cancer. Studies on patients with these diseases have revealed much about the complexities of mitochondrial genetics, which involves an interplay between mutations in the mitochondrial and nuclear genomes. However, the pathophysiology of mitochondrial diseases has remained perplexing. The essential role of mitochondrial oxidative phosphorylation in cellular energy production, the generation of reactive oxygen species, and the initiation of apoptosis has suggested a number of novel mechanisms for mitochondrial pathology. The importance and interrelationship of these functions are now being studied in mouse models of mitochondrial disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wallace, D C -- AG13154/AG/NIA NIH HHS/ -- HL45572/HL/NHLBI NIH HHS/ -- NS21328/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Mar 5;283(5407):1482-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Molecular Medicine, Emory University, 1462 Clifton Road, Suite 420, Atlanta, GA 30322, USA. dwallace@gmm.gen.emory.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10066162" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/genetics ; Animals ; DNA, Mitochondrial/*genetics ; Humans ; Metabolic Diseases/*genetics/metabolism ; Mice ; Mitochondria/*genetics/metabolism ; Mitochondrial Myopathies/*genetics/metabolism ; Mutation ; Neoplasms/genetics/metabolism ; Oxidative Phosphorylation
    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
    CD1d-restricted immunoglobulin G formation to GPI-anchored antigens mediated by NKT cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-08
    Description: Immunoglobulin G (IgG) responses require major histocompatibility complex (MHC)-restricted recognition of peptide fragments by conventional CD4(+) helper T cells. Immunoglobulin G responses to glycosylphosphatidylinositol (GPI)- anchored protein antigens, however, were found to be regulated in part through CD1d-restricted recognition of the GPI moiety by thymus-dependent, interleukin-4-producing CD4(+), natural killer cell antigen 1.1 [(NK1.1)+] helper T cells. The CD1-NKT cell pathway regulated immunogobulin G responses to the GPI-anchored surface antigens of Plasmodium and Trypanosoma and may be a general mechanism for rapid, MHC-unrestricted antibody responses to diverse pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schofield, L -- McConville, M J -- Hansen, D -- Campbell, A S -- Fraser-Reid, B -- Grusby, M J -- Tachado, S D -- AI-40171/AI/NIAID NIH HHS/ -- GM 41071/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 8;283(5399):225-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, Post Office, Royal Melbourne Hospital, Victoria 3050, Australia. schofield@wehi.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9880256" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Antigen-Presenting Cells/immunology ; Antigens/analysis ; Antigens, CD1/*immunology ; Antigens, Ly ; Antigens, Protozoan/*immunology ; Antigens, Surface ; Cells, Cultured ; Glycosylphosphatidylinositols/*immunology ; Immunoglobulin G/*biosynthesis ; Interleukin-4/biosynthesis ; Lectins, C-Type ; Leishmania mexicana/immunology ; Major Histocompatibility Complex ; Mice ; Mice, Inbred Strains ; NK Cell Lectin-Like Receptor Subfamily B ; Plasmodium/immunology ; Proteins/analysis ; Protozoan Proteins/immunology ; T-Lymphocyte Subsets/*immunology ; T-Lymphocytes, Helper-Inducer/*immunology ; Trypanosoma brucei brucei/immunology ; Variant Surface Glycoproteins, Trypanosoma/immunology
    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
    HMG-1 as a late mediator of endotoxin lethality in mice (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-10
    Description: Endotoxin, a constituent of Gram-negative bacteria, stimulates macrophages to release large quantities of tumor necrosis factor (TNF) and interleukin-1 (IL-1), which can precipitate tissue injury and lethal shock (endotoxemia). Antagonists of TNF and IL-1 have shown limited efficacy in clinical trials, possibly because these cytokines are early mediators in pathogenesis. Here a potential late mediator of lethality is identified and characterized in a mouse model. High mobility group-1 (HMG-1) protein was found to be released by cultured macrophages more than 8 hours after stimulation with endotoxin, TNF, or IL-1. Mice showed increased serum levels of HMG-1 from 8 to 32 hours after endotoxin exposure. Delayed administration of antibodies to HMG-1 attenuated endotoxin lethality in mice, and administration of HMG-1 itself was lethal. Septic patients who succumbed to infection had increased serum HMG-1 levels, suggesting that this protein warrants investigation as a therapeutic target.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, H -- Bloom, O -- Zhang, M -- Vishnubhakat, J M -- Ombrellino, M -- Che, J -- Frazier, A -- Yang, H -- Ivanova, S -- Borovikova, L -- Manogue, K R -- Faist, E -- Abraham, E -- Andersson, J -- Andersson, U -- Molina, P E -- Abumrad, N N -- Sama, A -- Tracey, K J -- New York, N.Y. -- Science. 1999 Jul 9;285(5425):248-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Emergency Medicine and Department of Surgery, North Shore University Hospital-New York University School of Medicine, Manhasset, NY 11030, USA. hwang@picower.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10398600" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteremia/*blood ; Carrier Proteins/genetics/immunology/*metabolism/toxicity ; Cell Line ; Cells, Cultured ; Endotoxemia/*blood ; Endotoxins/blood/*toxicity ; HMGB1 Protein ; High Mobility Group Proteins/genetics/immunology/*metabolism/toxicity ; Humans ; Immune Sera/immunology ; Immunization, Passive ; Interferon-gamma/pharmacology ; Interleukin-1/pharmacology ; Lethal Dose 50 ; Leukocytes, Mononuclear/metabolism ; Lipopolysaccharides/toxicity ; Macrophages/*metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; RNA, Messenger/genetics/metabolism ; Time Factors ; Tumor Necrosis Factor-alpha/pharmacology
    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
    Gene defect linked to Rett syndrome (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gura, T -- New York, N.Y. -- Science. 1999 Oct 1;286(5437):27.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10532886" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chromosomal Proteins, Non-Histone ; Chromosome Mapping ; DNA-Binding Proteins/*genetics ; Female ; *Gene Expression Regulation ; Humans ; Male ; Methyl-CpG-Binding Protein 2 ; Mice ; Mice, Knockout ; Mutation ; Repressor Proteins/*genetics ; Rett Syndrome/*genetics ; X Chromosome/*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
  • 113
    facet.materialart.
    Unknown
    A chemical inhibitor of p53 that protects mice from the side effects of cancer therapy (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-11
    Description: Chemotherapy and radiation therapy for cancer often have severe side effects that limit their efficacy. Because these effects are in part determined by p53-mediated apoptosis, temporary suppression of p53 has been suggested as a therapeutic strategy to prevent damage of normal tissues during treatment of p53-deficient tumors. To test this possibility, a small molecule was isolated for its ability to reversibly block p53-dependent transcriptional activation and apoptosis. This compound, pifithrin-alpha, protected mice from the lethal genotoxic stress associated with anticancer treatment without promoting the formation of tumors. Thus, inhibitors of p53 may be useful drugs for reducing the side effects of cancer therapy and other types of stress associated with p53 induction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Komarov, P G -- Komarova, E A -- Kondratov, R V -- Christov-Tselkov, K -- Coon, J S -- Chernov, M V -- Gudkov, A V -- CA60730/CA/NCI NIH HHS/ -- CA75179/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Sep 10;285(5434):1733-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Illinois at Chicago, Chicago, IL 60607, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10481009" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/*adverse effects/pharmacology ; Apoptosis/*drug effects ; Benzothiazoles ; Cell Division/drug effects ; Cell Line ; Cell Nucleus/drug effects/metabolism ; Cytoplasm/drug effects/metabolism ; DNA/biosynthesis ; DNA Damage ; G2 Phase/drug effects ; Gamma Rays/*adverse effects ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Nude ; Neoplasms/drug therapy/radiotherapy/*therapy ; Radiation Tolerance/*drug effects ; Thiazoles/*pharmacology ; Time Factors ; Toluene/*analogs & derivatives/pharmacology ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/*antagonists & inhibitors/physiology ; Ultraviolet Rays/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
  • 114
    facet.materialart.
    Unknown
    In vivo protein transduction: delivery of a biologically active protein into the mouse (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-08
    Description: Delivery of therapeutic proteins into tissues and across the blood-brain barrier is severely limited by the size and biochemical properties of the proteins. Here it is shown that intraperitoneal injection of the 120-kilodalton beta-galactosidase protein, fused to the protein transduction domain from the human immunodeficiency virus TAT protein, results in delivery of the biologically active fusion protein to all tissues in mice, including the brain. These results open new possibilities for direct delivery of proteins into patients in the context of protein therapy, as well as for epigenetic experimentation with model organisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwarze, S R -- Ho, A -- Vocero-Akbani, A -- Dowdy, S F -- New York, N.Y. -- Science. 1999 Sep 3;285(5433):1569-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10477521" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood-Brain Barrier ; Brain/metabolism ; Cell Membrane/metabolism ; Drug Carriers ; *Drug Delivery Systems ; Fluorescein-5-isothiocyanate ; Gene Products, tat/administration & dosage/*metabolism ; Humans ; Injections, Intraperitoneal ; Jurkat Cells ; Lipid Bilayers ; Mice ; Mice, Inbred C57BL ; Microscopy, Confocal ; Microscopy, Fluorescence ; Muscle, Skeletal/metabolism ; Recombinant Fusion Proteins/administration & dosage/*metabolism ; Spleen/metabolism ; Tissue Distribution ; Tumor Cells, Cultured ; beta-Galactosidase/administration & dosage/*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
  • 115
    facet.materialart.
    Unknown
    Stimulation of bone formation in vitro and in rodents by statins (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-03
    Description: Osteoporosis and other diseases of bone loss are a major public health problem. Here it is shown that the statins, drugs widely used for lowering serum cholesterol, also enhance new bone formation in vitro and in rodents. This effect was associated with increased expression of the bone morphogenetic protein-2 (BMP-2) gene in bone cells. Lovastatin and simvastatin increased bone formation when injected subcutaneously over the calvaria of mice and increased cancellous bone volume when orally administered to rats. Thus, in appropriate doses, statins may have therapeutic applications for the treatment of osteoporosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mundy, G -- Garrett, R -- Harris, S -- Chan, J -- Chen, D -- Rossini, G -- Boyce, B -- Zhao, M -- Gutierrez, G -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1946-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉OsteoScreen, 2040 Babcock Road, San Antonio, TX 78229, USA. mundy@uthscsa.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10583956" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Density/*drug effects ; Bone Morphogenetic Protein 2 ; Bone Morphogenetic Proteins/biosynthesis/genetics/pharmacology ; Cell Line ; Female ; Fibroblast Growth Factor 1 ; Fibroblast Growth Factor 2/pharmacology ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology ; Lovastatin/*pharmacology ; Male ; Mice ; Mice, Inbred ICR ; Organ Culture Techniques ; Osteoblasts/*drug effects/metabolism ; Osteoclasts/drug effects ; Osteogenesis/*drug effects ; Osteoporosis/drug therapy ; Ovariectomy ; Promoter Regions, Genetic/drug effects ; Rats ; Recombinant Proteins/pharmacology ; Simvastatin/*pharmacology ; Skull ; Transfection ; *Transforming Growth Factor beta
    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
    Persistence of memory CD8 T cells in MHC class I-deficient mice (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-13
    Description: An understanding of how T cell memory is maintained is crucial for the rational design of vaccines. Memory T cells were shown to persist indefinitely in major histocompatibility complex (MHC) class I-deficient mice and retained the ability to make rapid cytokine responses upon reencounter with antigen. In addition, memory CD8 T cells, unlike naive cells, divided without MHC-T cell receptor interactions. This "homeostatic" proliferation is likely to be important in maintaining memory T cell numbers in the periphery. Thus, after naive CD8 T cells differentiate into memory cells, they evolve an MHC class I-independent "life-style" and do not require further stimulation with specific or cross-reactive antigen for their maintenance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murali-Krishna, K -- Lau, L L -- Sambhara, S -- Lemonnier, F -- Altman, J -- Ahmed, R -- AI30048/AI/NIAID NIH HHS/ -- NS21496/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 12;286(5443):1377-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Emory Vaccine Center and Department of Microbiology and Immunology, Emory University, Atlanta, GA 30322, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10558996" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Antigens, CD44/analysis ; Antigens, Viral/immunology ; CD8-Positive T-Lymphocytes/cytology/*immunology ; Cell Division ; Epitopes/immunology ; Histocompatibility Antigens Class I/*immunology ; Homeostasis ; *Immunologic Memory ; Interferon-gamma/biosynthesis ; Lymphocytic Choriomeningitis/immunology ; Lymphocytic choriomeningitis virus/*immunology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Radiation Chimera ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocyte Subsets/cytology/*immunology ; beta 2-Microglobulin/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
  • 117
    facet.materialart.
    Unknown
    Seeking ligands for lonely orphan receptors (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gustafsson, J A -- New York, N.Y. -- Science. 1999 May 21;284(5418):1285-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Nutrition, Karolinska Institutet, NOVUM Huddinge Hospital, Huddinge, Sweden. jan-ake.gustafsson@mednut.ki.se〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10383308" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bile Acids and Salts/biosynthesis ; Chenodeoxycholic Acid/*metabolism ; Cholesterol/*metabolism ; Cholesterol 7-alpha-Hydroxylase/biosynthesis/*genetics ; Cholic Acid/metabolism ; Cytochrome P-450 Enzyme System/metabolism ; DNA-Binding Proteins/*metabolism ; Fatty Acids/metabolism ; Gene Expression Regulation, Enzymologic ; Homeostasis ; Humans ; Ligands ; Liver/metabolism ; Mice ; Orphan Nuclear Receptors ; Receptors, Cytoplasmic and Nuclear/*metabolism ; Steroid Hydroxylases/metabolism ; Transcription Factors/*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
  • 118
    facet.materialart.
    Unknown
    New lead found to a possible "insulin pill" (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gura, T -- New York, N.Y. -- Science. 1999 May 7;284(5416):886.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10357667" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ascomycota/*metabolism ; CHO Cells ; Cricetinae ; Diabetes Mellitus, Type 2/*drug therapy ; Drug Evaluation, Preclinical ; Hypoglycemic Agents/chemistry/isolation & purification/metabolism/*therapeutic ; use ; Indoles/chemistry/isolation & purification/metabolism/*therapeutic use ; Insulin/metabolism/pharmacology ; Mice ; Mice, Mutant Strains ; Receptor, Insulin/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
  • 119
    facet.materialart.
    Unknown
    Chlamydia protein linked to heart disease (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gura, T -- New York, N.Y. -- Science. 1999 Feb 26;283(5406):1238-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10084921" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmune Diseases/immunology/microbiology ; Bacterial Proteins/*immunology ; Chlamydia/*immunology/metabolism ; Chlamydia Infections/complications/immunology ; Heart/microbiology ; Humans ; Mice ; *Molecular Mimicry ; Myocarditis/immunology/*microbiology ; Myocardium/*immunology ; Myosins/*immunology ; Peptides/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
  • 120
    facet.materialart.
    Unknown
    Rapid and reversible effects of activity on acetylcholine receptor density at the neuromuscular junction in vivo (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-16
    Description: Quantitative fluorescence imaging was used to study the regulation of acetylcholine receptor (AChR) number and density at neuromuscular junctions in living adult mice. At fully functional synapses, AChRs have a half-life of about 14 days. However, 2 hours after neurotransmission was blocked, the half-life of the AChRs was now less than a day; the rate was 25 times faster than before. Most of the lost receptors were not quickly replaced. Direct muscle stimulation or restoration of synaptic transmission inhibited this process. AChRs that were removed from nonfunctional synapses resided for hours in the perijunctional membrane before being locally internalized. Dispersed AChRs could also reaggregate at the junction once neurotransmission was restored. The rapid and reversible alterations in AChR density at the neuromuscular junction in vivo parallel changes thought to occur in the central nervous system at synapses undergoing potentiation and depression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akaaboune, M -- Culican, S M -- Turney, S G -- Lichtman, J W -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):503-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, MO 63110, USA. mohammed@nmj.wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10521340" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bungarotoxins/pharmacology ; Cell Membrane/metabolism ; Curare/pharmacology ; Diffusion ; Electric Stimulation ; Fluorescent Dyes ; Half-Life ; Mice ; *Muscle Contraction ; Muscle Denervation ; Neuromuscular Blockade ; Neuromuscular Blocking Agents/pharmacology ; Neuromuscular Junction/*physiology ; Receptor Aggregation ; Receptors, Cholinergic/*metabolism ; Rhodamines/pharmacology ; *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
  • 121
    facet.materialart.
    Unknown
    Perspectives: neurobiology. PrP's double causes trouble (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weissmann, C -- Aguzzi, A -- New York, N.Y. -- Science. 1999 Oct 29;286(5441):914-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Prion Unit/Neurogenetics, Imperial College School of Medicine at St. Mary's, London W2 1PG, UK. c.weissmann@ic.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577243" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; GPI-Linked Proteins ; Humans ; Mice ; Mice, Knockout ; Open Reading Frames ; Phenotype ; Prion Diseases/*genetics ; Prions/*genetics ; Tissue Distribution
    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
    Synergistic signaling in fetal brain by STAT3-Smad1 complex bridged by p300 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-16
    Description: The cytokines LIF (leukemia inhibitory factor) and BMP2 (bone morphogenetic protein-2) signal through different receptors and transcription factors, namely STATs (signal transducers and activators of transcription) and Smads. LIF and BMP2 were found to act in synergy on primary fetal neural progenitor cells to induce astrocytes. The transcriptional coactivator p300 interacts physically with STAT3 at its amino terminus in a cytokine stimulation-independent manner, and with Smad1 at its carboxyl terminus in a cytokine stimulation-dependent manner. The formation of a complex between STAT3 and Smad1, bridged by p300, is involved in the cooperative signaling of LIF and BMP2 and the subsequent induction of astrocytes from neural progenitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakashima, K -- Yanagisawa, M -- Arakawa, H -- Kimura, N -- Hisatsune, T -- Kawabata, M -- Miyazono, K -- Taga, T -- New York, N.Y. -- Science. 1999 Apr 16;284(5413):479-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Cell Biology, Cell Fate Modulation Research Unit, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 101-0062, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10205054" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/cytology ; Bone Morphogenetic Protein 2 ; Bone Morphogenetic Protein Receptors ; Bone Morphogenetic Proteins/metabolism/pharmacology ; COS Cells ; Cell Differentiation ; Cell Nucleus/metabolism ; Cells, Cultured ; Cytokines/*pharmacology ; DNA-Binding Proteins/*metabolism ; E1A-Associated p300 Protein ; Glial Fibrillary Acidic Protein/genetics ; Growth Inhibitors/metabolism/pharmacology ; *Interleukin-6 ; Leukemia Inhibitory Factor ; Leukemia Inhibitory Factor Receptor alpha Subunit ; Lymphokines/metabolism/pharmacology ; Mice ; Nuclear Proteins/*metabolism ; Promoter Regions, Genetic ; Receptors, Cell Surface/metabolism ; Receptors, Cytokine/metabolism ; *Receptors, Growth Factor ; Receptors, OSM-LIF ; STAT3 Transcription Factor ; Sequence Deletion ; *Signal Transduction ; Smad Proteins ; Smad1 Protein ; Stem Cells/cytology/metabolism ; Telencephalon/embryology/metabolism ; Trans-Activators/*metabolism ; *Transcriptional Activation ; *Transforming Growth Factor beta
    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
    Genetic mechanisms of age regulation of human blood coagulation factor IX (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: Blood coagulation capacity increases with age in healthy individuals. Through extensive longitudinal analyses of human factor IX gene expression in transgenic mice, two essential age-regulatory elements, AE5' and AE3', have been identified. These elements are required and together are sufficient for normal age regulation of factor IX expression. AE5', a PEA-3 related element present in the 5' upstream region of the gene encoding factor IX, is responsible for age-stable expression of the gene. AE3', in the middle of the 3' untranslated region, is responsible for age-associated elevation in messenger RNA levels. In a concerted manner, AE5' and AE3' recapitulate natural patterns of the advancing age-associated increase in factor IX gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kurachi, S -- Deyashiki, Y -- Takeshita, J -- Kurachi, K -- AG13283/AG/NIA NIH HHS/ -- HL38644/HL/NHLBI NIH HHS/ -- HL53713/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):739-43.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics, University of Michigan Medical School, Ann Arbor, MI 48109-0618, USA. kkurachi@umich.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426997" target="_blank"〉PubMed〈/a〉
    Keywords: *3' Untranslated Regions ; Aging/blood/*genetics ; Animals ; Consensus Sequence ; DNA Footprinting ; Dinucleotide Repeats ; Factor IX/*genetics/metabolism ; Female ; *Gene Expression Regulation ; Genetic Vectors ; Humans ; Male ; Mice ; Mice, Transgenic ; RNA, Messenger/genetics/metabolism ; *Regulatory Sequences, Nucleic Acid ; Transcription Factors/genetics/metabolism ; Transcription, Genetic ; Tumor Cells, Cultured
    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
    Behind the headlines of endostatin's ups and downs (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1999 Feb 26;283(5406):1250-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10084928" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/pharmacology/*therapeutic use ; Clinical Trials as Topic ; Collagen/pharmacology/*therapeutic use ; Endostatins ; Humans ; Mice ; Neoplasms, Experimental/blood supply/*drug therapy/pathology ; Neovascularization, Pathologic/*drug therapy ; Newspapers as Topic ; Peptide Fragments/pharmacology/*therapeutic use ; Recombinant Proteins/pharmacology/therapeutic use ; Reproducibility of Results
    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
    STAT5 interaction with the T cell receptor complex and stimulation of T cell proliferation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-08
    Description: The role of STAT (signal transducer and activator of transcription) proteins in T cell receptor (TCR) signaling was analyzed. STAT5 became immediately and transiently phosphorylated on tyrosine 694 in response to TCR stimulation. Expression of the protein tyrosine kinase Lck, a key signaling protein in the TCR complex, activated DNA binding of transfected STAT5A and STAT5B to specific STAT inducible elements. The role of Lck in STAT5 activation was confirmed in a Lck-deficient T cell line in which the activation of STAT5 by TCR stimulation was abolished. Expression of Lck induced specific interaction of STAT5 with the subunits of the TCR, indicating that STAT5 may be directly involved in TCR signaling. Stimulation of T cell clones and primary T cell lines also induced the association of STAT5 with the TCR complex. Inhibition of STAT5 function by expression of a dominant negative mutant STAT5 reduced antigen-stimulated proliferation of T cells. Thus, TCR stimulation appears to directly activate STAT5, which may participate in the regulation of gene transcription and T cell proliferation during immunological responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Welte, T -- Leitenberg, D -- Dittel, B N -- al-Ramadi, B K -- Xie, B -- Chin, Y E -- Janeway, C A Jr -- Bothwell, A L -- Bottomly, K -- Fu, X Y -- AI34522/AI/NIAID NIH HHS/ -- GM46367/GM/NIGMS NIH HHS/ -- GM55590/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Jan 8;283(5399):222-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, 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/9880255" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies ; Antigen-Presenting Cells/immunology ; Antigens/immunology ; Cell Division ; Cell Line ; DNA-Binding Proteins/genetics/*metabolism ; Interferon-gamma/pharmacology ; Interleukin-2/pharmacology ; *Lymphocyte Activation ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck)/genetics/metabolism ; Membrane Proteins/genetics/immunology/metabolism ; Mice ; Mice, Transgenic ; *Milk Proteins ; Phosphorylation ; Phosphotyrosine/metabolism ; Receptors, Antigen, T-Cell/genetics/immunology/*metabolism ; STAT5 Transcription Factor ; Signal Transduction ; T-Lymphocytes, Helper-Inducer/cytology/*immunology/metabolism ; Th2 Cells/immunology/metabolism ; Trans-Activators/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
  • 126
    facet.materialart.
    Unknown
    Memory T cells don't need practice (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hagmann, M -- New York, N.Y. -- Science. 1999 Nov 12;286(5443):1267-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610529" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Antigen Presentation ; CD8-Positive T-Lymphocytes/*immunology/transplantation ; Cell Division ; Histocompatibility Antigens Class I/immunology/metabolism ; Histocompatibility Antigens Class II/immunology ; *Immunologic Memory ; Lymphocyte Activation ; Mice ; Mice, Transgenic ; T-Lymphocyte Subsets/cytology/*immunology ; T-Lymphocytes, Helper-Inducer/*immunology/transplantation
    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
    Fusion-competent vaccines: broad neutralization of primary isolates of HIV (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-15
    Description: Current recombinant human immunodeficiency virus (HIV) gp120 protein vaccine candidates are unable to elicit antibodies capable of neutralizing infectivity of primary isolates from patients. Here, "fusion-competent" HIV vaccine immunogens were generated that capture the transient envelope-CD4-coreceptor structures that arise during HIV binding and fusion. In a transgenic mouse immunization model, these formaldehyde-fixed whole-cell vaccines elicited antibodies capable of neutralizing infectivity of 23 of 24 primary HIV isolates from diverse geographic locations and genetic clades A to E. Development of these fusion-dependent immunogens may lead to a broadly effective HIV vaccine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉LaCasse, R A -- Follis, K E -- Trahey, M -- Scarborough, J D -- Littman, D R -- Nunberg, J H -- AI33856/AI/NIAID NIH HHS/ -- AI41165/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 15;283(5400):357-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Montana Biotechnology Center and Division of Biological Sciences, University of Montana, Missoula, MT 59812, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9888845" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/*immunology ; Animals ; Antigens, CD4/metabolism ; Cell Fusion ; Coculture Techniques ; Epitopes/immunology ; Gene Products, env/chemistry/*immunology/metabolism ; Giant Cells ; HIV Antibodies/biosynthesis/*immunology ; HIV Antigens/chemistry/*immunology ; HIV Envelope Protein gp120/chemistry/immunology/metabolism ; HIV Envelope Protein gp41/chemistry/immunology/metabolism ; HIV Infections/virology ; HIV-1/*immunology/isolation & purification/physiology ; Humans ; Mice ; Mice, Transgenic ; Neutralization Tests ; Protein Conformation ; Receptors, CCR5/metabolism ; Tumor Cells, Cultured
    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
    DNA topoisomerase IIbeta and neural development (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-30
    Description: DNA topoisomerase IIbeta is shown to have an unsuspected and critical role in neural development. Neurogenesis was normal in IIbeta mutant mice, but motor axons failed to contact skeletal muscles, and sensory axons failed to enter the spinal cord. Despite an absence of innervation, clusters of acetylcholine receptors were concentrated in the central region of skeletal muscles, thereby revealing patterning mechanisms that are autonomous to skeletal muscle. The defects in motor axon growth in IIbeta mutant mice resulted in a breathing impairment and death of the pups shortly after birth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, X -- Li, W -- Prescott, E D -- Burden, S J -- Wang, J C -- NS10537/NS/NINDS NIH HHS/ -- NS27963/NS/NINDS NIH HHS/ -- NS36193/NS/NINDS NIH HHS/ -- R01 NS036193/NS/NINDS NIH HHS/ -- R01 NS036193-02/NS/NINDS NIH HHS/ -- R01 NS041311/NS/NINDS NIH HHS/ -- R01 NS041311-03/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 2000 Jan 7;287(5450):131-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skirball Institute of Molecular Medicine, New York University Medical School, 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/10615047" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology/ultrastructure ; Cell Lineage ; Cues ; DNA Repair ; DNA Topoisomerases, Type II/genetics/*metabolism ; DNA-Binding Proteins ; Diaphragm/chemistry/embryology/innervation ; Embryonic and Fetal Development ; Gene Targeting ; Intercostal Muscles/innervation ; Mice ; Mice, Knockout ; Motor Neurons/physiology/ultrastructure ; Muscle, Skeletal/embryology/*innervation ; Neuromuscular Junction/*embryology/growth & development ; Neurons, Afferent/physiology/ultrastructure ; Presynaptic Terminals/ultrastructure ; Receptors, Cholinergic/analysis ; Skin/innervation ; Spinal Cord/embryology/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
  • 129
    facet.materialart.
    Unknown
    An adhesin of the yeast pathogen Candida glabrata mediating adherence to human epithelial cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-27
    Description: Candida glabrata is an important fungal pathogen of humans that is responsible for about 15 percent of mucosal and systemic candidiasis. Candida glabrata adhered avidly to human epithelial cells in culture. By means of a genetic approach and a strategy allowing parallel screening of mutants, it was possible to clone a lectin from a Candida species. Deletion of this adhesin reduced adherence of C. glabrata to human epithelial cells by 95 percent. The adhesin, encoded by the EPA1 gene, is likely a glucan-cross-linked cell-wall protein and binds to host-cell carbohydrate, specifically recognizing asialo-lactosyl-containing carbohydrates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cormack, B P -- Ghori, N -- Falkow, S -- New York, N.Y. -- Science. 1999 Jul 23;285(5427):578-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Stanford University School of Medicine, Fairchild D039, 299 Campus Drive, Stanford, CA 94305-5124, USA. bcormack@jhmi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10417386" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium/metabolism ; Candida/*genetics/*pathogenicity/physiology ; Candidiasis, Vulvovaginal/microbiology ; Carbohydrates/pharmacology ; Cell Adhesion ; Cloning, Molecular ; Epithelial Cells/*microbiology ; Female ; *Fungal Proteins ; Genes, Fungal ; Humans ; Lectins/chemistry/*genetics/metabolism ; Ligands ; Mice ; Mice, Inbred DBA ; Molecular Sequence Data ; Mutagenesis, Insertional ; Mutation ; Plasmids ; Polymerase Chain Reaction ; Transformation, Genetic ; Tumor Cells, Cultured ; Virulence/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
  • 130
    facet.materialart.
    Unknown
    Anti-inflammatory properties of cytochrome P450 epoxygenase-derived eicosanoids (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-24
    Description: The epoxyeicosatrienoic acids (EETs) are products of cytochrome P450 epoxygenases that have vasodilatory properties similar to that of endothelium-derived hyperpolarizing factor. The cytochrome P450 isoform CYP2J2 was cloned and identified as a potential source of EETs in human endothelial cells. Physiological concentrations of EETs or overexpression of CYP2J2 decreased cytokine-induced endothelial cell adhesion molecule expression, and EETs prevented leukocyte adhesion to the vascular wall by a mechanism involving inhibition of transcription factor NF-kappaB and IkappaB kinase. The inhibitory effects of EETs were independent of their membrane-hyperpolarizing effects, suggesting that these molecules play an important nonvasodilatory role in vascular inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2720027/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2720027/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Node, K -- Huo, Y -- Ruan, X -- Yang, B -- Spiecker, M -- Ley, K -- Zeldin, D C -- Liao, J K -- HL-52233/HL/NHLBI NIH HHS/ -- HL-58108/HL/NHLBI NIH HHS/ -- P01 HL048743/HL/NHLBI NIH HHS/ -- P01 HL048743-080008/HL/NHLBI NIH HHS/ -- P01 HL048743-090008/HL/NHLBI NIH HHS/ -- R01 HL052233/HL/NHLBI NIH HHS/ -- R01 HL052233-05/HL/NHLBI NIH HHS/ -- R01 HL052233-06/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 Aug 20;285(5431):1276-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vascular Medicine and Atherosclerosis Unit, Cardiovascular Division, Brigham and Women's Hospital and Harvard Medical School, 221 Longwood Avenue, LMRC-322, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10455056" target="_blank"〉PubMed〈/a〉
    Keywords: 8,11,14-Eicosatrienoic Acid/analogs & derivatives/*metabolism/*pharmacology ; Animals ; *Anti-Inflammatory Agents, Non-Steroidal/metabolism/pharmacology ; Carotid Arteries/cytology ; Cattle ; Cell Adhesion/drug effects ; Cell Adhesion Molecules/biosynthesis ; Cells, Cultured ; Coronary Vessels/enzymology ; Cytochrome P-450 Enzyme System/genetics/*metabolism ; DNA-Binding Proteins/metabolism ; Endothelium, Vascular/enzymology/*metabolism ; Humans ; Hydroxyeicosatetraenoic Acids/pharmacology ; I-kappa B Kinase ; *I-kappa B Proteins ; Mice ; Mice, Inbred C57BL ; NF-kappa B/antagonists & inhibitors/metabolism ; Oxygenases/genetics/*metabolism ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; Tumor Necrosis Factor-alpha/antagonists & inhibitors/pharmacology ; Vascular Cell Adhesion Molecule-1/biosynthesis/genetics
    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
    A gene that scrambles your heart (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hagmann, M -- New York, N.Y. -- Science. 1999 Feb 19;283(5405):1091,1093.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10075562" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors ; Cell Cycle Proteins/genetics ; Chromosomes, Human, Pair 22/genetics ; DNA-Binding Proteins/genetics/physiology ; DiGeorge Syndrome/*genetics ; Gene Deletion ; Heart/embryology ; Heart Defects, Congenital/*genetics ; Humans ; Mice ; Neural Crest/cytology/embryology ; Proteins/*genetics/physiology ; Transcription Factors/genetics/physiology ; Ubiquitins ; 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
  • 132
    facet.materialart.
    Unknown
    Ethical loophole closing up for stem cell researchers (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steghaus-Kovac, S -- New York, N.Y. -- Science. 1999 Oct 1;286(5437):31.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10532887" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bioethics ; Cell Line ; Embryo Research ; Embryo, Mammalian/*cytology ; Female ; Fetus/*cytology ; *Genomic Imprinting ; Germ Cells/*cytology ; Humans ; Male ; Mice ; Stem Cells/*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
  • 133
    facet.materialart.
    Unknown
    Role of bacterial intimin in colonic hyperplasia and inflammation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-27
    Description: Enteropathogenic Escherichia coli (EPEC) cells adhere to gut epithelial cells through intimin alpha: the ligand for a bacterially derived epithelial transmembrane protein called the translocated intimin receptor. Citrobacter rodentium colonizes the mouse colon in a similar fashion and uses a different intimin: intimin beta. Intimin alpha was found to costimulate submitogenic signals through the T cell receptor. Dead intimin beta+ C. rodentium, intimin alpha-transfected C. rodentium or E. coli strain K12, and EPEC induced mucosal hyperplasia identical to that caused by C. rodentium live infection, as well as a massive T helper cell-type 1 immune response in the colonic mucosa. Mutation of cysteine-937 of intimin to alanine reduced costimulatory activity in vitro and prevented immunopathology in vivo. The mucosal changes elicited by C. rodentium were interferon-gamma-dependent. Immunopathology induced by intimin enables the bacteria to promote conditions that are favorable for increased microbial colonization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Higgins, L M -- Frankel, G -- Connerton, I -- Goncalves, N S -- Dougan, G -- MacDonald, T T -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1999 Jul 23;285(5427):588-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Paediatric Gastroenterology, St. Bartholomews and the Royal London School of Medicine and Dentistry, London EC1A 7BE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10417389" target="_blank"〉PubMed〈/a〉
    Keywords: *Adhesins, Bacterial ; Animals ; Bacterial Adhesion ; Bacterial Outer Membrane Proteins/pharmacology/*physiology ; *Carrier Proteins ; Citrobacter/*pathogenicity ; Colitis/immunology/*microbiology/pathology ; Colon/immunology/microbiology/*pathology ; Cytokines/biosynthesis/genetics ; Enterobacteriaceae Infections/immunology/*microbiology/pathology ; Escherichia coli/pathogenicity ; *Escherichia coli Proteins ; Hyperplasia ; Interferon-gamma/physiology ; Intestinal Mucosa/immunology/microbiology/pathology ; Ligands ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; Receptors, Cell Surface/metabolism ; T-Lymphocytes/immunology ; Th1 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
  • 134
    facet.materialart.
    Unknown
    Role of NADH shuttle system in glucose-induced activation of mitochondrial metabolism and insulin secretion (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-12
    Description: Glucose metabolism in glycolysis and in mitochondria is pivotal to glucose-induced insulin secretion from pancreatic beta cells. One or more factors derived from glycolysis other than pyruvate appear to be required for the generation of mitochondrial signals that lead to insulin secretion. The electrons of the glycolysis-derived reduced form of nicotinamide adenine dinucleotide (NADH) are transferred to mitochondria through the NADH shuttle system. By abolishing the NADH shuttle function, glucose-induced increases in NADH autofluorescence, mitochondrial membrane potential, and adenosine triphosphate content were reduced and glucose-induced insulin secretion was abrogated. The NADH shuttle evidently couples glycolysis with activation of mitochondrial energy metabolism to trigger insulin secretion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eto, K -- Tsubamoto, Y -- Terauchi, Y -- Sugiyama, T -- Kishimoto, T -- Takahashi, N -- Yamauchi, N -- Kubota, N -- Murayama, S -- Aizawa, T -- Akanuma, Y -- Aizawa, S -- Kasai, H -- Yazaki, Y -- Kadowaki, T -- New York, N.Y. -- Science. 1999 Feb 12;283(5404):981-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113, Japan. Tokyo〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9974390" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Amino Acid Sequence ; Aminooxyacetic Acid/pharmacology ; Animals ; Aspartate Aminotransferases/antagonists & inhibitors ; Calcium/metabolism ; Citric Acid Cycle ; Enzyme Inhibitors/pharmacology ; Female ; Gene Targeting ; Glucose/metabolism/*pharmacology ; Glycerolphosphate Dehydrogenase/genetics/metabolism ; Glycolysis ; Insulin/*secretion ; Islets of Langerhans/metabolism/*secretion ; Male ; Membrane Potentials ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mitochondria/*metabolism ; Models, Biological ; Molecular Sequence Data ; NAD/*metabolism ; Pyruvic Acid/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
  • 135
    facet.materialart.
    Unknown
    Impaired Fas response and autoimmunity in Pten+/- mice (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-25
    Description: Inactivating mutations in the PTEN tumor suppressor gene, encoding a phosphatase, occur in three related human autosomal dominant disorders characterized by tumor susceptibility. Here it is shown that Pten heterozygous (Pten+/-) mutants develop a lethal polyclonal autoimmune disorder with features reminiscent of those observed in Fas-deficient mutants. Fas-mediated apoptosis was impaired in Pten+/- mice, and T lymphocytes from these mice show reduced activation-induced cell death and increased proliferation upon activation. Phosphatidylinositol (PI) 3-kinase inhibitors restored Fas responsiveness in Pten+/- cells. These results indicate that Pten is an essential mediator of the Fas response and a repressor of autoimmunity and thus implicate the PI 3-kinase/Akt pathway in Fas-mediated apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Di Cristofano, A -- Kotsi, P -- Peng, Y F -- Cordon-Cardo, C -- Elkon, K B -- Pandolfi, P P -- AR45482/AR/NIAMS NIH HHS/ -- CA-08748/CA/NCI NIH HHS/ -- CA-82328/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Sep 24;285(5436):2122-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics-Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, Sloan-Kettering Institute, 1275 York Avenue, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10497129" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Antinuclear/blood ; Antigens, CD95/*physiology ; *Apoptosis ; Autoimmune Diseases/*immunology/pathology ; B-Lymphocytes/immunology/pathology ; Female ; Heterozygote ; Immunoglobulin G/blood ; Kidney Diseases/*immunology/pathology ; Kidney Glomerulus/immunology/pathology ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred C57BL ; PTEN Phosphohydrolase ; Phosphatidylinositol 3-Kinases/antagonists & inhibitors/metabolism ; Phosphoric Monoester Hydrolases/genetics/*physiology ; Phosphorylation ; *Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; T-Lymphocytes/immunology/pathology ; *Tumor Suppressor 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
  • 136
    facet.materialart.
    Unknown
    Testing the genetics of behavior in mice (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Picciotto, M R -- Self, D W -- New York, N.Y. -- Science. 1999 Sep 24;285(5436):2067; author reply 2069-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10523199" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Laboratory/genetics ; *Behavior, Animal ; Confounding Factors (Epidemiology) ; Environment ; Genetics, Behavioral/*methods ; Mice ; Reproducibility of Results
    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
    Redefining rats, mice, and birds. AAA (American Association of Anatomists) Public Affairs Committee (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Besharse, J C -- Carlson, B M -- Jenkins, D P -- Lester, D S -- Olds, J L -- Satir, P -- New York, N.Y. -- Science. 1999 Apr 2;284(5411):49-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10215528" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Rights/*legislation & jurisprudence ; Animal Welfare/*legislation & jurisprudence ; Animals ; *Animals, Laboratory ; Birds ; Mice ; Rats ; Research ; Societies, Scientific ; United States ; United States Department of Agriculture/legislation & jurisprudence
    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
    Xid-like immunodeficiency in mice with disruption of the p85alpha subunit of phosphoinositide 3-kinase (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-15
    Description: Mice with a targeted gene disruption of p85alpha, a regulatory subunit of phosphoinositide 3-kinase, had impaired B cell development at the pro-B cell stage, reduced numbers of mature B cells and peritoneal CD5+ Ly-1 B cells, reduced B cell proliferative responses, and no T cell-independent antibody production. These phenotypes are nearly identical to those of Btk-/- or xid (X-linked immunodeficiency) mice. These results provide evidence that p85alpha is functionally linked to the Btk pathway in antigen receptor-mediated signal transduction and is pivotal in B cell development and functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suzuki, H -- Terauchi, Y -- Fujiwara, M -- Aizawa, S -- Yazaki, Y -- Kadowaki, T -- Koyasu, S -- New York, N.Y. -- Science. 1999 Jan 15;283(5400):390-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9888854" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Formation ; Antigens, CD5/analysis ; Antigens, Ly/analysis ; Antigens, T-Independent/immunology ; B-Lymphocyte Subsets/cytology/immunology ; B-Lymphocytes/cytology/*immunology ; Bone Marrow/immunology ; Cell Survival ; Gene Targeting ; Genetic Linkage ; Immunologic Deficiency Syndromes/*enzymology/genetics/immunology ; Lymphocyte Count ; Lymphoid Tissue/immunology ; Mice ; Mutation ; Phenotype ; Phosphatidylinositol 3-Kinases/genetics/*metabolism ; Protein-Tyrosine Kinases/genetics/metabolism ; Signal Transduction ; T-Lymphocytes/immunology ; X Chromosome
    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
    Class II-independent generation of CD4 memory T cells from effectors (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-13
    Description: The factors required for the generation of memory CD4 T cells remain unclear, and whether there is a continuing requirement for antigen stimulation is critical to design of vaccine strategies. CD4 effectors generated in vitro from naive CD4 T cells of mice efficiently gave rise to small resting memory cells after transfer to class II-deficient hosts, indicating no requirement for further antigen or class II recognition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Swain, S L -- Hu, H -- Huston, G -- New York, N.Y. -- Science. 1999 Nov 12;286(5443):1381-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biomedical Research Laboratories, Trudeau Institute, 100 Algonquin Avenue, Saranac Lake, NY 12983, USA. sswain@northnet.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10558997" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Cell Division ; Cytokines/biosynthesis ; Histocompatibility Antigens Class II/*immunology ; Immunization ; *Immunologic Memory ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocyte Subsets/cytology/*immunology ; Th1 Cells/cytology/*immunology ; Th2 Cells/cytology/*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
  • 140
    facet.materialart.
    Unknown
    Nota bene: neuroscience. For time is the longest distance between two places (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, O -- New York, N.Y. -- Science. 1999 Sep 3;285(5433):1504.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10498536" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Amnesia/physiopathology ; Animals ; Brain Mapping ; Hippocampus/*physiology ; Humans ; Male ; Maze Learning ; Memory/*physiology ; Mice ; Neocortex/*physiology ; Temporal Lobe/*physiology ; 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
  • 141
    facet.materialart.
    Unknown
    New clues found to diabetes and obesity (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferber, D -- New York, N.Y. -- Science. 1999 Mar 5;283(5407):1423, 1425.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10206863" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/metabolism ; Diabetes Mellitus/drug therapy/*metabolism ; Diabetes Mellitus, Type 2/drug therapy/*metabolism ; Humans ; Insulin/*metabolism ; Mice ; Mice, Knockout ; Mutation ; Obesity/drug therapy/*metabolism ; Phosphates/metabolism ; Protein Tyrosine Phosphatases/antagonists & inhibitors/genetics/*metabolism ; Receptor, Insulin/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
  • 142
    facet.materialart.
    Unknown
    Gene skews patterns of inheritance (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1999 Nov 12;286(5443):1269.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610530" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes/*genetics ; Female ; Genes ; Male ; Mice ; Protein Kinases/*genetics/metabolism ; Sperm Motility/*genetics ; Spermatozoa/*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
  • 143
    facet.materialart.
    Unknown
    Arthritis provoked by linked T and B cell recognition of a glycolytic enzyme (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-27
    Description: The hallmark of rheumatoid arthritis (RA) is specific destruction of the synovial joints. In a mouse line that spontaneously develops a disorder with many of the features of human RA, disease is initiated by T cell recognition of a ubiquitously expressed self-antigen; once initiated, pathology is driven almost entirely by immunoglobulins. In this study, the target of both the initiating T cells and pathogenic immunoglobulins was identified as glucose-6-phosphate isomerase, a glycolytic enzyme. Thus, some forms of RA or related arthritides may develop by a mechanism fundamentally different from the currently popular paradigm of a joint-specific T cell response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsumoto, I -- Staub, A -- Benoist, C -- Mathis, D -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1732-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire (CNRS/INSERM/ULP), BP 163, 67404 Illkirch, C.U. de Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10576739" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Antigen-Antibody Complex/immunology/metabolism ; Arthritis, Rheumatoid/*immunology ; Autoantibodies/*immunology ; Autoantigens/*immunology ; B-Lymphocytes/*immunology ; Cross Reactions ; Disease Models, Animal ; Glucose-6-Phosphate Isomerase/chemistry/*immunology ; Humans ; Immunoglobulins/immunology ; Joints/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, Transgenic ; Recombinant Fusion Proteins/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
  • 144
    facet.materialart.
    Unknown
    Adhesive and mammalian transglutaminase substrate properties of Candida albicans Hwp1 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-05
    Description: The pathogenesis of candidiasis involves invasion of host tissues by filamentous forms of the opportunistic yeast Candida albicans. Morphology-specific gene products may confer proinvasive properties. A hypha-specific surface protein, Hwp1, with similarities to mammalian small proline-rich proteins was shown to serve as a substrate for mammalian transglutaminases. Candida albicans strains lacking Hwp1 were unable to form stable attachments to human buccal epithelial cells and had a reduced capacity to cause systemic candidiasis in mice. This represents a paradigm for microbial adhesion that implicates essential host enzymes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Staab, J F -- Bradway, S D -- Fidel, P L -- Sundstrom, P -- 1 R01 DE11375-05A2/DE/NIDCR NIH HHS/ -- AI32556/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Mar 5;283(5407):1535-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Microbiology and Immunology, College of Medicine and Public Health, Ohio State University, 333 West Tenth Avenue, Columbus, OH 43210, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10066176" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Candida albicans/*pathogenicity/physiology ; Candidiasis/microbiology ; Candidiasis, Oral/microbiology ; Cell Adhesion ; Epithelial Cells/enzymology/microbiology ; *Fungal Proteins ; GTP Phosphohydrolases/*metabolism ; *GTP-Binding Proteins ; Genes, Fungal ; Humans ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Mice, Inbred CBA ; Mouth Mucosa/enzymology/*microbiology ; Recombinant Proteins/metabolism ; Transglutaminases/*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
  • 145
    facet.materialart.
    Unknown
    A new look at MHC and autoimmune disease (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ridgway, W M -- Fasso, M -- Fathman, C G -- New York, N.Y. -- Science. 1999 Apr 30;284(5415):749, 751.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10336398" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Antigen-Presenting Cells/immunology ; Autoantigens/*immunology ; Autoimmune Diseases/*immunology ; Diabetes Mellitus, Type 1/*immunology ; Genes, MHC Class II ; Histocompatibility Antigens Class II/*immunology ; Mice ; Mice, Inbred NOD ; Receptors, Antigen, T-Cell/immunology ; Self Tolerance ; T-Lymphocytes/*immunology ; Thymus Gland/*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
  • 146
    facet.materialart.
    Unknown
    Host defense mechanisms triggered by microbial lipoproteins through toll-like receptors (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: The generation of cell-mediated immunity against many infectious pathogens involves the production of interleukin-12 (IL-12), a key signal of the innate immune system. Yet, for many pathogens, the molecules that induce IL-12 production by macrophages and the mechanisms by which they do so remain undefined. Here it is shown that microbial lipoproteins are potent stimulators of IL-12 production by human macrophages, and that induction is mediated by Toll-like receptors (TLRs). Several lipoproteins stimulated TLR-dependent transcription of inducible nitric oxide synthase and the production of nitric oxide, a powerful microbicidal pathway. Activation of TLRs by microbial lipoproteins may initiate innate defense mechanisms against infectious pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brightbill, H D -- Libraty, D H -- Krutzik, S R -- Yang, R B -- Belisle, J T -- Bleharski, J R -- Maitland, M -- Norgard, M V -- Plevy, S E -- Smale, S T -- Brennan, P J -- Bloom, B R -- Godowski, P J -- Modlin, R L -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):732-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Howard Hughes Medical Institute, University of California Los Angeles School of Medicine, Los Anges, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Bacterial/chemistry/*immunology/metabolism ; Cell Line ; *Drosophila Proteins ; Gene Expression Regulation ; Humans ; Interleukin-12/*biosynthesis/genetics ; Lipopolysaccharides/immunology ; Lipoproteins/chemistry/*immunology/metabolism ; Macrophages/*immunology/metabolism ; Membrane Glycoproteins/*metabolism ; Mice ; Monocytes/*immunology/metabolism ; Mycobacterium tuberculosis/*immunology ; NF-kappa B/biosynthesis ; Nitric Oxide Synthase/genetics ; Nitric Oxide Synthase Type II ; Promoter Regions, Genetic ; Receptors, Cell Surface/*metabolism ; Signal Transduction ; Toll-Like Receptors ; Transcription, Genetic ; Transfection ; Tumor Cells, Cultured
    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
    Embryonic stem cell-derived glial precursors: a source of myelinating transplants (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: Self-renewing, totipotent embryonic stem (ES) cells may provide a virtually unlimited donor source for transplantation. A protocol that permits the in vitro generation of precursors for oligodendrocytes and astrocytes from ES cells was devised. Transplantation in a rat model of a human myelin disease shows that these ES cell-derived precursors interact with host neurons and efficiently myelinate axons in brain and spinal cord. Thus, ES cells can serve as a valuable source of cell type-specific somatic precursors for neural transplantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brustle, O -- Jones, K N -- Learish, R D -- Karram, K -- Choudhary, K -- Wiestler, O D -- Duncan, I D -- McKay, R D -- NS33710/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):754-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuropathology, University of Bonn Medical Center, Sigmund-Freud-Strasse 25, 53105 Bonn, Germany. brustle@uni-bonn.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10427001" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*cytology ; Brain/embryology/metabolism ; Cell Differentiation ; Cell Line ; Cell Movement ; Cerebral Ventricles/embryology/surgery ; Diffuse Cerebral Sclerosis of Schilder/genetics/*therapy ; Embryo, Mammalian/cytology ; Growth Substances/pharmacology ; Humans ; Male ; Mice ; Myelin Basic Protein/biosynthesis ; Myelin Proteolipid Protein/biosynthesis/genetics ; Myelin Sheath/*physiology ; Oligodendroglia/*cytology/metabolism/*transplantation/ultrastructure ; Rats ; Spinal Cord ; Stem Cell Transplantation ; Stem Cells/*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
  • 148
    facet.materialart.
    Unknown
    Synergy between tumor suppressor APC and the beta-catenin-Tcf4 target Tcf1 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-18
    Description: Mutations in APC or beta-catenin inappropriately activate the transcription factor Tcf4, thereby transforming intestinal epithelial cells. Here it is shown that one of the target genes of Tcf4 in epithelial cells is Tcf1. The most abundant Tcf1 isoforms lack a beta-catenin interaction domain. Tcf1(-/-) mice develop adenomas in the gut and mammary glands. Introduction of a mutant APC allele into these mice substantially increases the number of these adenomas. Tcf1 may act as a feedback repressor of beta-catenin-Tcf4 target genes and thus may cooperate with APC to suppress malignant transformation of epithelial cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roose, J -- Huls, G -- van Beest, M -- Moerer, P -- van der Horn, K -- Goldschmeding, R -- Logtenberg, T -- Clevers, H -- New York, N.Y. -- Science. 1999 Sep 17;285(5435):1923-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Center for Biomedical Genetics, Department of Pathology, University Medical Center Utrecht, Post Office Box 85500, 3508 GA Utrecht, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10489374" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoma/genetics/metabolism/pathology ; Adenomatous Polyposis Coli Protein ; Animals ; Cytoskeletal Proteins/*metabolism ; DNA-Binding Proteins/*genetics/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Hepatocyte Nuclear Factor 1-alpha ; Humans ; Intestinal Neoplasms/genetics/metabolism/pathology ; Lymphoid Enhancer-Binding Factor 1 ; Male ; Mammary Neoplasms, Experimental/genetics/metabolism/pathology ; Mice ; Neoplasm Proteins/metabolism ; Promoter Regions, Genetic ; T Cell Transcription Factor 1 ; TCF Transcription Factors ; *Trans-Activators ; Transcription Factor 7-Like 2 Protein ; Transcription Factors/*genetics/*metabolism ; Transfection ; Tumor Cells, Cultured ; 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
  • 149
    facet.materialart.
    Unknown
    p53- and ATM-dependent apoptosis induced by telomeres lacking TRF2 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-26
    Description: Although broken chromosomes can induce apoptosis, natural chromosome ends (telomeres) do not trigger this response. It is shown that this suppression of apoptosis involves the telomeric-repeat binding factor 2 (TRF2). Inhibition of TRF2 resulted in apoptosis in a subset of mammalian cell types. The response was mediated by p53 and the ATM (ataxia telangiectasia mutated) kinase, consistent with activation of a DNA damage checkpoint. Apoptosis was not due to rupture of dicentric chromosomes formed by end-to-end fusion, indicating that telomeres lacking TRF2 directly signal apoptosis, possibly because they resemble damaged DNA. Thus, in some cells, telomere shortening may signal cell death rather than senescence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karlseder, J -- Broccoli, D -- Dai, Y -- Hardy, S -- de Lange, T -- GM49046/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Feb 26;283(5406):1321-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cell Biology and Genetics, The Rockefeller University, New York, NY 10021, USA. Cell Genesys, Foster City, CA 94405, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10037601" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics/physiology ; Animals ; *Apoptosis ; Ataxia Telangiectasia/pathology ; Ataxia Telangiectasia Mutated Proteins ; B-Lymphocytes/cytology ; Cell Cycle Proteins ; Cell Line ; Cells, Cultured ; Cloning, Molecular ; DNA Damage ; DNA-Binding Proteins/chemistry/genetics/*physiology ; Genetic Vectors ; Humans ; In Situ Nick-End Labeling ; Mice ; Mitosis ; Phosphorylation ; *Protein-Serine-Threonine Kinases ; Proteins/metabolism ; T-Lymphocytes/cytology ; Telomere/*physiology ; Telomeric Repeat Binding Protein 2 ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/*metabolism ; Tumor Suppressor 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
  • 150
    facet.materialart.
    Unknown
    Nonproteolytic neuroprotection by human recombinant tissue plasminogen activator (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-24
    Description: Human recombinant tissue plasminogen activator (tPA) may benefit ischemic stroke patients by dissolving clots. However, independent of thrombolysis, tPA may also have deleterious effects on neurons by promoting excitotoxicity. Zinc neurotoxicity has been shown to be an additional key mechanism in brain injuries. Hence, if tPA affects zinc neurotoxicity, this may provide additional insights into its effect on neuronal death. Independent of its proteolytic action, tPA markedly attenuated zinc-induced cell death in cortical culture, and, when injected into cerebrospinal fluid, also reduced kainate seizure-induced hippocampal neuronal death in adult rats.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Y H -- Park, J H -- Hong, S H -- Koh, J Y -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):647-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Creative Research Initiative Center for the Study of Central Nervous System Zinc and Department of Neurology, University of Ulsan College of Medicine, 388-1 Poongnap-Dong Songpa-Gu, Seoul 138-736, Korea.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10213688" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Death/drug effects ; Cells, Cultured ; Cerebral Cortex/cytology ; *Cytoprotection ; Fibrinolysin/pharmacology ; Hippocampus/pathology ; Humans ; Kainic Acid/pharmacology ; Male ; Mice ; N-Methylaspartate/pharmacology ; Neurons/*cytology/drug effects ; Neuroprotective Agents/*pharmacology ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley ; Recombinant Proteins/cerebrospinal fluid/pharmacology ; Seizures/chemically induced/pathology ; Tissue Plasminogen Activator/cerebrospinal fluid/*pharmacology ; Zinc/metabolism/*toxicity
    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
    Mouse tumor model for neurofibromatosis type 1 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-11
    Description: Neurofibromatosis type 1 (NF1) is an autosomal dominant disorder characterized by increased incidence of benign and malignant tumors of neural crest origin. Mutations that activate the protooncogene ras, such as loss of Nf1, cooperate with inactivating mutations at the p53 tumor suppressor gene during malignant transformation. One hundred percent of mice harboring null Nf1 and p53 alleles in cis synergize to develop soft tissue sarcomas between 3 and 7 months of age. These sarcomas exhibit loss of heterozygosity at both gene loci and express phenotypic traits characteristic of neural crest derivatives and human NF1 malignancies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3079436/" 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/PMC3079436/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, K S -- Klesse, L J -- Velasco-Miguel, S -- Meyers, K -- Rushing, E J -- Parada, L F -- NS34296/NS/NINDS NIH HHS/ -- R01 NS034296/NS/NINDS NIH HHS/ -- R01 NS034296-04/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Dec 10;286(5447):2176-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Developmental Biology and Department of Pathology, University of Texas Southwestern Medical Center, 6000 Harry Hines Blvd., Dallas, TX 75235-9133, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10591653" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers, Tumor ; Cell Differentiation ; Cell Transformation, Neoplastic ; Crosses, Genetic ; *Disease Models, Animal ; Female ; *Genes, Neurofibromatosis 1 ; *Genes, p53 ; Heterozygote ; Humans ; Loss of Heterozygosity ; Male ; Mice ; Mice, Inbred C57BL ; Mutation ; Neural Crest/metabolism/pathology ; Neurofibromatosis 1/*genetics/*pathology ; Sarcoma/genetics/*pathology ; Schwann Cells/metabolism/pathology ; Tumor Cells, Cultured
    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
    Looking for a few good mutants (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldman, W E -- New York, N.Y. -- Science. 1999 Jul 23;285(5427):539, 541.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology, Washington University, St. Louis, MO 63110, USA. goldman@borcim.wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10447486" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Candida/*genetics/*pathogenicity/physiology ; Cell Adhesion ; DNA Transposable Elements ; Epithelial Cells/*microbiology ; *Fungal Proteins ; Genes, Fungal ; Humans ; Lectins/*genetics/metabolism ; Mice ; *Mutagenesis, Insertional ; Mutation ; Polymerase Chain Reaction ; Tumor Cells, Cultured ; Virulence/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
  • 153
    facet.materialart.
    Unknown
    Requirement of Rsk-2 for epidermal growth factor-activated phosphorylation of histone H3 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-07
    Description: During the immediate-early response of mammalian cells to mitogens, histone H3 is rapidly and transiently phosphorylated by one or more unidentified kinases. Rsk-2, a member of the pp90rsk family of kinases implicated in growth control, was required for epidermal growth factor (EGF)-stimulated phosphorylation of H3. RSK-2 mutations in humans are linked to Coffin-Lowry syndrome (CLS). Fibroblasts derived from a CLS patient failed to exhibit EGF-stimulated phosphorylation of H3, although H3 was phosphorylated during mitosis. Introduction of the wild-type RSK-2 gene restored EGF-stimulated phosphorylation of H3 in CLS cells. In addition, disruption of the RSK-2 gene by homologous recombination in murine embryonic stem cells abolished EGF-stimulated phosphorylation of H3. H3 appears to be a direct or indirect target of Rsk-2, suggesting that chromatin remodeling might contribute to mitogen-activated protein kinase-regulated gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sassone-Corsi, P -- Mizzen, C A -- Cheung, P -- Crosio, C -- Monaco, L -- Jacquot, S -- Hanauer, A -- Allis, C D -- GM40922/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Aug 6;285(5429):886-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire, CNRS, INSERM, ULP, B. P. 163, 67404 Illkirch-Strasbourg, France. paolosc@igbmc.u-strasbg.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10436156" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Abnormalities, Multiple/genetics/metabolism ; Animals ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Line, Transformed ; Cell Nucleus/metabolism ; Cells, Cultured ; Epidermal Growth Factor/*pharmacology ; Gene Expression Regulation ; Gene Targeting ; Histones/*metabolism ; Humans ; Mice ; Mitosis ; Mutation ; Phosphorylation ; Ribosomal Protein S6 Kinases/genetics/*metabolism ; Signal Transduction ; Stem Cells/cytology/metabolism ; Syndrome
    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
    Specific coupling of NMDA receptor activation to nitric oxide neurotoxicity by PSD-95 protein (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-12
    Description: The efficiency with which N-methyl-D-aspartate receptors (NMDARs) trigger intracellular signaling pathways governs neuronal plasticity, development, senescence, and disease. In cultured cortical neurons, suppressing the expression of the NMDAR scaffolding protein PSD-95 (postsynaptic density-95) selectively attenuated excitotoxicity triggered via NMDARs, but not by other glutamate or calcium ion (Ca2+) channels. NMDAR function was unaffected, because receptor expression, NMDA currents, and 45Ca2+ loading were unchanged. Suppressing PSD-95 blocked Ca2+-activated nitric oxide production by NMDARs selectively, without affecting neuronal nitric oxide synthase expression or function. Thus, PSD-95 is required for efficient coupling of NMDAR activity to nitric oxide toxicity, and imparts specificity to excitotoxic Ca2+ signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sattler, R -- Xiong, Z -- Lu, W Y -- Hafner, M -- MacDonald, J F -- Tymianski, M -- NS 39060/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jun 11;284(5421):1845-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Toronto Western Hospital, University of Toronto, Lab 11-416, 399 Bathurst Street, Toronto, Ontario M5T 2S8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10364559" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channels/metabolism ; Cell Survival ; Cells, Cultured ; Enzyme Activation ; Guanylate Kinase ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins ; Mice ; N-Methylaspartate/toxicity ; Nerve Tissue Proteins/genetics/*metabolism ; Neurons/cytology/*metabolism ; Nitric Oxide/*metabolism ; Nitric Oxide Synthase/metabolism ; Nitric Oxide Synthase Type I ; Nucleoside-Phosphate Kinase/metabolism ; Oligodeoxyribonucleotides, Antisense ; Patch-Clamp Techniques ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Second Messenger Systems ; 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
  • 155
    facet.materialart.
    Unknown
    The immunological synapse: a molecular machine controlling T cell activation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-10
    Description: The specialized junction between a T lymphocyte and an antigen-presenting cell, the immunological synapse, consists of a central cluster of T cell receptors surrounded by a ring of adhesion molecules. Immunological synapse formation is now shown to be an active and dynamic mechanism that allows T cells to distinguish potential antigenic ligands. Initially, T cell receptor ligands were engaged in an outermost ring of the nascent synapse. Transport of these complexes into the central cluster was dependent on T cell receptor-ligand interaction kinetics. Finally, formation of a stable central cluster at the heart of the synapse was a determinative event for T cell proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grakoui, A -- Bromley, S K -- Sumen, C -- Davis, M M -- Shaw, A S -- Allen, P M -- Dustin, M L -- New York, N.Y. -- Science. 1999 Jul 9;285(5425):221-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Immunology and the Department of Pathology, 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/10398592" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology/metabolism ; Antigens, CD4/immunology/metabolism ; CHO Cells ; Cell Movement ; Cricetinae ; Cytochrome c Group/immunology/metabolism ; Fluorescence ; Histocompatibility Antigens/immunology/*metabolism ; Intercellular Adhesion Molecule-1/immunology/metabolism ; Ligands ; Lipid Bilayers ; *Lymphocyte Activation ; Mice ; Mice, Transgenic ; Microscopy, Interference ; Models, Immunological ; Peptides/immunology/metabolism ; Receptors, Antigen, T-Cell/immunology/*metabolism ; Signal Transduction ; T-Lymphocytes/*immunology/metabolism ; 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
  • 156
    facet.materialart.
    Unknown
    Stat3-mediated transformation of NIH-3T3 cells by the constitutively active Q205L Galphao protein (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-30
    Description: Expression of Q205L Galphao (Galphao*), an alpha subunit of heterotrimeric guanine nucleotide-binding proteins (G proteins) that lacks guanosine triphosphatase (GTPase) activity in NIH-3T3 cells, results in transformation. Expression of Galphao* in NIH-3T3 cells activated signal transducer and activator of transcription 3 (Stat3) but not mitogen-activated protein (MAP) kinases 1 or 2. Coexpression of dominant negative Stat3 inhibited Galphao*-induced transformation of NIH-3T3 cells and activation of endogenous Stat3. Furthermore, Galphao* expression increased activity of the tyrosine kinase c-Src, and the Galphao*-induced activation of Stat3 was blocked by expression of Csk (carboxyl-terminal Src kinase), which inactivates c-Src. The results indicate that Stat3 can function as a downstream effector for Galphao* and mediate its biological effects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ram, P T -- Horvath, C M -- Iyengar, R -- 1F32 CA79134-01/CA/NCI NIH HHS/ -- DK-38671/DK/NIDDK NIH HHS/ -- GM-54508/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Jan 7;287(5450):142-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Immunobiology Center, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA. ramp01@doc.mssm.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10615050" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Cell Line, Transformed ; *Cell Transformation, Neoplastic ; DNA-Binding Proteins/*metabolism ; Enzyme Activation ; GTP-Binding Protein alpha Subunits ; Genes, Reporter ; Heterotrimeric GTP-Binding Proteins/genetics/*metabolism ; MAP Kinase Signaling System ; Mice ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; Neurites/physiology ; Neuronal Plasticity ; Neurons/metabolism/physiology ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein-Tyrosine Kinases/metabolism ; STAT3 Transcription Factor ; Signal Transduction ; Trans-Activators/*metabolism ; Transfection ; src-Family 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
  • 157
    facet.materialart.
    Unknown
    Sex determination in malaria parasites (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-30
    Description: A century ago, W. G. MacCallum identified distinct male and female forms in malaria parasites of both birds and humans. Since then, scientists have been puzzled by the high female-to-male ratios of parasites in Plasmodium infections and by the mechanism of sex determination. The sex ratio of malaria parasites was shown to become progressively more male as conditions that allow motility and subsequent fertilization by the male parasites become adverse. This resulted from an increased immune response against male gametes, which coincides with intense host erythropoietic activity. Natural and artificial induction of erythropoiesis in vertebrate hosts provoked a shift toward male parasite production. This change in parasite sex ratio led to reduced reproductive success in the parasite, which suggests that sex determination is adaptive and is regulated by the hematologic state of the host.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paul, R E -- Coulson, T N -- Raibaud, A -- Brey, P T -- New York, N.Y. -- Science. 2000 Jan 7;287(5450):128-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Biochimie et Biologie Moleculaire des Insectes, Institut Pasteur, 25 Rue du Dr. Roux, 75724 Paris Cedex 15, France. topotito@pasteur.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10615046" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/parasitology ; Animals ; Chickens ; Erythrocytes/parasitology ; *Erythropoiesis ; Erythropoietin/pharmacology ; Female ; Malaria/*blood/*parasitology ; Malaria, Avian/blood/parasitology ; Male ; Mice ; Plasmodium/growth & development/*physiology ; Plasmodium gallinaceum/growth & development/*physiology ; Recombinant Proteins/pharmacology ; Reproduction ; Reticulocytes/parasitology ; Sex Determination Processes ; Sex Ratio
    Print ISSN: 0036-8075
    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
    Imaging protein kinase Calpha activation in cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-26
    Description: Spatially resolved fluorescence resonance energy transfer (FRET) measured by fluorescence lifetime imaging microscopy (FLIM), provides a method for tracing the catalytic activity of fluorescently tagged proteins inside live cell cultures and enables determination of the functional state of proteins in fixed cells and tissues. Here, a dynamic marker of protein kinase Calpha (PKCalpha) activation is identified and exploited. Activation of PKCalpha is detected through the binding of fluorescently tagged phosphorylation site-specific antibodies; the consequent FRET is measured through the donor fluorophore on PKCalpha by FLIM. This approach enabled the imaging of PKCalpha activation in live and fixed cultured cells and was also applied to pathological samples.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ng, T -- Squire, A -- Hansra, G -- Bornancin, F -- Prevostel, C -- Hanby, A -- Harris, W -- Barnes, D -- Schmidt, S -- Mellor, H -- Bastiaens, P I -- Parker, P J -- New York, N.Y. -- Science. 1999 Mar 26;283(5410):2085-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Protein Phosphorylation Laboratory and Cell Biophysics Laboratory, Imperial Cancer Research Fund (ICRF), 44 Lincoln's Inn Fields, London, WC2A 3PX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10092232" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Breast Neoplasms/enzymology ; COS Cells ; Catalysis ; Cytoplasm/enzymology ; Endoplasmic Reticulum/enzymology ; Energy Transfer ; Enzyme Activation ; Fluorescence ; Fluorescent Dyes ; Golgi Apparatus/enzymology ; Green Fluorescent Proteins ; Humans ; Immune Sera ; Isoenzymes/immunology/*metabolism ; Luminescent Proteins ; Mice ; *Microscopy, Fluorescence ; Phosphorylation ; Phosphothreonine/immunology/metabolism ; Protein Kinase C/immunology/*metabolism ; Protein Kinase C-alpha ; Tetradecanoylphorbol Acetate/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
  • 159
    facet.materialart.
    Unknown
    New leads to cancer, arthritis therapies (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hagmann, M -- New York, N.Y. -- Science. 1999 Jun 4;284(5420):1600-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10383332" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins ; Animals ; Antineoplastic Agents ; Antirheumatic Agents ; Arthritis/*drug therapy ; Binding Sites ; Cloning, Molecular ; Enzyme Precursors/chemistry/metabolism ; Gelatinases/antagonists & inhibitors/*chemistry/metabolism ; Humans ; Matrix Metalloproteinase 2 ; Metalloendopeptidases/antagonists & inhibitors/*chemistry/genetics/metabolism ; Mice ; Models, Molecular ; Neoplasms/*drug therapy ; Procollagen N-Endopeptidase ; Protease Inhibitors/*pharmacology ; Protein Conformation ; Protein Structure, Secondary
    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
    Fertility therapy may aid gene transfer (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hagmann, M -- New York, N.Y. -- Science. 1999 May 14;284(5417):1097-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10366336" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Fertilization in Vitro ; *Gene Transfer Techniques ; Green Fluorescent Proteins ; Luminescent Proteins/genetics ; Male ; Mice ; Mice, Transgenic ; Microinjections ; Sperm Head/*physiology ; *Transgenes
    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
    Use of chemokine receptors by poxviruses (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-03
    Description: Chemokine receptors serve as portals of entry for certain intracellular pathogens, most notably human immunodeficiency virus (HIV). Myxoma virus is a member of the poxvirus family that induces a lethal systemic disease in rabbits, but no poxvirus receptor has ever been defined. Rodent fibroblasts (3T3) that cannot be infected with myxoma virus could be made fully permissive for myxoma virus infection by expression of any one of several human chemokine receptors, including CCR1, CCR5, and CXCR4. Conversely, infection of 3T3-CCR5 cells can be inhibited by RANTES, anti-CCR5 polyclonal antibody, or herbimycin A but not by monoclonal antibodies that block HIV-1 infection or by pertussis toxin. These findings suggest that poxviruses, like HIV, are able to use chemokine receptors to infect specific cell subtypes, notably migratory leukocytes, but that their mechanisms of receptor interactions are distinct.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lalani, A S -- Masters, J -- Zeng, W -- Barrett, J -- Pannu, R -- Everett, H -- Arendt, C W -- McFadden, G -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1968-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The John P. Robarts Research Institute and Department of Immunology, The University of Western Ontario, London, Ontario N6G 2V4, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10583963" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Antibodies/immunology ; Benzoquinones ; Cell Line ; Cercopithecus aethiops ; Chemokine CCL5/pharmacology ; Gene Expression ; Humans ; Lactams, Macrocyclic ; Mice ; Myxoma virus/genetics/*metabolism ; Pertussis Toxin ; Quinones/pharmacology ; Receptors, CCR1 ; Receptors, CCR5/immunology/metabolism ; Receptors, CXCR4/metabolism ; Receptors, Chemokine/*metabolism ; Receptors, Virus/*metabolism ; Rifabutin/analogs & derivatives ; Signal Transduction ; Tumor Cells, Cultured ; Virulence Factors, Bordetella/pharmacology ; beta-Galactosidase/biosynthesis
    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
    Keeping bone marrow grafts in check (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hagmann, M -- New York, N.Y. -- Science. 1999 Jul 16;285(5426):310-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10438289" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/immunology ; Antigen-Presenting Cells/*immunology ; Bone Marrow Transplantation/adverse effects/*immunology ; Graft vs Host Disease/*prevention & control ; Histocompatibility Antigens/immunology ; Humans ; Mice ; 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
  • 163
    facet.materialart.
    Unknown
    A trigger of natural (and other) killers (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hagmann, M -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):645, 647.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10454908" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Histocompatibility Antigens Class I/*metabolism ; Humans ; Killer Cells, Natural/*immunology/metabolism ; Ligands ; Lymphocyte Activation ; Mice ; Neoplasms/immunology ; Receptors, Antigen, T-Cell, gamma-delta/immunology ; Receptors, Immunologic/genetics/*metabolism ; Receptors, Natural Killer Cell ; Signal Transduction ; 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
  • 164
    facet.materialart.
    Unknown
    Postnatal sex reversal of the ovaries in mice lacking estrogen receptors alpha and beta (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-22
    Description: Mice lacking estrogen receptors alpha and beta were generated to clarify the roles of each receptor in the physiology of estrogen target tissues. Both sexes of alphabeta estrogen receptor knockout (alphabetaERKO) mutants exhibit normal reproductive tract development but are infertile. Ovaries of adult alphabetaERKO females exhibit follicle transdifferentiation to structures resembling seminiferous tubules of the testis, including Sertoli-like cells and expression of Mullerian inhibiting substance, sulfated glycoprotein-2, and Sox9. Therefore, loss of both receptors leads to an ovarian phenotype that is distinct from that of the individual ERKO mutants, which indicates that both receptors are required for the maintenance of germ and somatic cells in the postnatal ovary.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couse, J F -- Hewitt, S C -- Bunch, D O -- Sar, M -- Walker, V R -- Davis, B J -- Korach, K S -- New York, N.Y. -- Science. 1999 Dec 17;286(5448):2328-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Receptor Biology Section, Laboratory of Reproductive and Developmental Toxicology, Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10600740" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Mullerian Hormone ; Cell Differentiation ; Clusterin ; *Disorders of Sex Development ; Estradiol/physiology ; Estrogen Receptor alpha ; Estrogen Receptor beta ; Female ; Gene Targeting ; Glycoproteins/analysis ; Growth Inhibitors/analysis ; High Mobility Group Proteins/analysis ; Luteinizing Hormone/blood ; Male ; Mice ; Mice, Knockout ; *Molecular Chaperones ; Ovary/*anatomy & histology/cytology/growth & development/*physiology ; Receptors, Estrogen/genetics/*physiology ; SOX9 Transcription Factor ; Seminiferous Tubules/anatomy & histology/cytology ; Sertoli Cells/cytology ; Signal Transduction ; Testicular Hormones/analysis ; Testis/anatomy & histology/cytology/growth & development/physiology ; Transcription Factors/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
  • 165
    facet.materialart.
    Unknown
    Fas ligand: a sensor for DNA damage critical in skin cancer etiology (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-07
    Description: DNA-damaged cells can either repair the DNA or be eliminated through a homeostatic control mechanism termed "cellular proofreading." Elimination of DNA-damaged cells after ultraviolet radiation (UVR) through sunburn cell (apoptotic keratinocyte) formation is thought to be pivotal for the removal of precancerous skin cells. Sunburn cell formation was found to be dependent on Fas ligand (FasL), a pro-apoptotic protein induced by DNA damage. Chronic exposure to UVR caused 14 of 20 (70 percent) FasL-deficient mice and 1 of 20 (5 percent) wild-type mice to accumulate p53 mutations in the epidermis. Thus, FasL-mediated apoptosis is important for skin homeostasis, suggesting that the dysregulation of Fas-FasL interactions may be central to the development of skin cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hill, L L -- Ouhtit, A -- Loughlin, S M -- Kripke, M L -- Ananthaswamy, H N -- Owen-Schaub, L B -- CA45623/CA/NCI NIH HHS/ -- CA52457/CA/NCI NIH HHS/ -- F32 AI09351/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Aug 6;285(5429):898-900.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, University of Texas, M. D. Anderson Cancer Center, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10436160" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/genetics/physiology ; Apoptosis ; *DNA Damage ; Epidermis/*cytology/metabolism/radiation effects ; Fas Ligand Protein ; *Genes, p53 ; Keratinocytes/*cytology/metabolism/radiation effects ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Mice, Inbred C3H ; Mutation ; Skin Neoplasms/*etiology/pathology ; Ultraviolet Rays ; 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
  • 166
    facet.materialart.
    Unknown
    Inactivation of misselected CD8 T cells by CD8 gene methylation and cell death (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-15
    Description: Misselected CD8 cells that express T cell receptors (TCRs) that do not recognize class I major histocompatibility complex (MHC) protein can emerge from thymic selection. A postthymic quality control mechanism that purges these cells from the repertoire is defined here. The failure of mature CD8 cells to simultaneously engage their TCR and CD8 coreceptor triggers an activation process that begins with inhibition of CD8 gene expression through remethylation and concludes with up-regulation of surface Fas and Fas ligand and cellular apoptosis. Thus, inhibition of a death signal through continued TCR-CD8 coengagement of MHC molecules is a key checkpoint for the continued survival of correctly selected T cells. Molecular defects that prevent delivery of the death signal to mistakenly selected T cells underlie the expansion of double-negative T cells, which is the cellular signature of a subset of systemic autoimmune diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pestano, G A -- Zhou, Y -- Trimble, L A -- Daley, J -- Weber, G F -- Cantor, H -- AI 13600/AI/NIAID NIH HHS/ -- AI 37833/AI/NIAID NIH HHS/ -- CA76176/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 May 14;284(5417):1187-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Immunology and AIDS, Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10325233" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Antigens, CD8/*genetics ; Antigens, CD95/genetics ; *Apoptosis ; CD8-Positive T-Lymphocytes/*cytology/*immunology ; *DNA Methylation ; Fas Ligand Protein ; Gene Expression Regulation ; Granzymes ; Histocompatibility Antigens Class I/immunology ; Kruppel-Like Transcription Factors ; Lymphocyte Count ; Membrane Glycoproteins/genetics ; Mice ; Mice, Inbred C57BL ; Receptors, Antigen, T-Cell/genetics/immunology ; Serine Endopeptidases/genetics ; Thymus Gland/immunology ; Trans-Activators/genetics ; 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
  • 167
    facet.materialart.
    Unknown
    Mammalian transgenesis by intracytoplasmic sperm injection (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-15
    Description: Coinjection of unfertilized mouse oocytes with sperm heads and exogenous DNA encoding either a green fluorescent protein (GFP) or beta-galactosidase reporter produced 64 to 94 percent transgene-expressing embryos, reflecting DNA-sperm head association before coinjection. Nonselective transfer to surrogate mothers of embryos in the GFP series generated about 20 percent offspring expressing the integrated transgene. These data indicate that exogenous DNA can reproducibly be delivered into an oocyte by microinjected spermatozoa and suggest an adaptable method of transgenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Perry, A C -- Wakayama, T -- Kishikawa, H -- Kasai, T -- Okabe, M -- Toyoda, Y -- Yanagimachi, R -- HD-34362/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1999 May 14;284(5417):1180-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Reproductive Biology, University of Hawaii School of Medicine, Honolulu, HI 96822, USA. perry@hawaii.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10325231" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/physiology ; Cell Membrane/physiology ; Culture Techniques ; Embryo Transfer ; Embryonic and Fetal Development ; Female ; *Fertilization in Vitro ; *Gene Transfer Techniques ; Genes, Reporter ; Green Fluorescent Proteins ; Lac Operon ; Luminescent Proteins/genetics ; Male ; Mice ; *Mice, Transgenic/embryology/genetics ; Microinjections ; Morula/physiology ; Oocytes ; Sperm Head/*physiology ; *Transgenes
    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
    Testing the genetics of behavior in mice (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pohorecky, L A -- New York, N.Y. -- Science. 1999 Sep 24;285(5436):2067-8; author reply 2069-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10523200" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Laboratory ; *Behavior, Animal ; Confounding Factors (Epidemiology) ; Genetics, Behavioral/*methods ; Handling (Psychology) ; *Housing, Animal ; Mice ; Rats
    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
    Turning brain into blood: a hematopoietic fate adopted by adult neural stem cells in vivo (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-23
    Description: Stem cells are found in various organs where they participate in tissue homeostasis by replacing differentiated cells lost to physiological turnover or injury. An investigation was performed to determine whether stem cells are restricted to produce specific cell types, namely, those from the tissue in which they reside. After transplantation into irradiated hosts, genetically labeled neural stem cells were found to produce a variety of blood cell types including myeloid and lymphoid cells as well as early hematopoietic cells. Thus, neural stem cells appear to have a wider differentiation potential than previously thought.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bjornson, C R -- Rietze, R L -- Reynolds, B A -- Magli, M C -- Vescovi, A L -- A.116/Telethon/Italy -- New York, N.Y. -- Science. 1999 Jan 22;283(5401):534-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉NeuroSpheres Limited, 3330 Hospital Drive Northwest, Calgary, AB, Canada T2N 4N1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9915700" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Cells/*cytology/immunology ; Bone Marrow Cells/immunology ; Cell Differentiation ; Cells, Cultured ; Colony-Forming Units Assay ; Female ; H-2 Antigens/analysis ; Hematopoiesis ; Hematopoietic Stem Cells/*cytology ; Lac Operon ; Lymphocytes/cytology/immunology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Transgenic ; Prosencephalon/*cytology/embryology ; Spleen/cytology ; Stem Cell Transplantation ; Stem Cells/*cytology/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
  • 170
    facet.materialart.
    Unknown
    Coordinate regulation of RAG1 and RAG2 by cell type-specific DNA elements 5' of RAG2 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-14
    Description: RAG1 and RAG2 are essential for V(D)J recombination and lymphocyte development. These genes are thought to encode a transposase derived from a mobile genetic element that was inserted into the vertebrate genome 450 million years ago. The regulation of RAG1 and RAG2 was investigated in vivo with bacterial artificial chromosome (BAC) transgenes containing a fluorescent indicator. Coordinate expression of RAG1 and RAG2 in B and T cells was found to be regulated by distinct genetic elements found on the 5' side of the RAG2 gene. This observation suggests a mechanism by which asymmetrically disposed cis DNA elements could influence the expression of the primordial transposon and thereby capture RAGs for vertebrate evolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, W -- Misulovin, Z -- Suh, H -- Hardy, R R -- Jankovic, M -- Yannoutsos, N -- Nussenzweig, M C -- GM07739/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Aug 13;285(5430):1080-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, 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/10446057" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*metabolism ; Bacterial Proteins/genetics ; DNA-Binding Proteins/*genetics ; *Gene Expression Regulation ; Genes, Immunoglobulin ; *Genes, RAG-1 ; Green Fluorescent Proteins ; Luminescent Proteins/genetics ; Mice ; Mice, Transgenic ; Recombinant Fusion Proteins ; Recombination, Genetic ; *Regulatory Sequences, Nucleic Acid ; Sequence Deletion ; T-Lymphocytes/*metabolism ; Transcription, Genetic ; Transgenes ; Transposases/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
  • 171
    facet.materialart.
    Unknown
    Math1: an essential gene for the generation of inner ear hair cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-12
    Description: The mammalian inner ear contains the cochlea and vestibular organs, which are responsible for hearing and balance, respectively. The epithelia of these sensory organs contain hair cells that function as mechanoreceptors to transduce sound and head motion. The molecular mechanisms underlying hair cell development and differentiation are poorly understood. Math1, a mouse homolog of the Drosophila proneural gene atonal, is expressed in inner ear sensory epithelia. Embryonic Math1-null mice failed to generate cochlear and vestibular hair cells. This gene is thus required for the genesis of hair cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bermingham, N A -- Hassan, B A -- Price, S D -- Vollrath, M A -- Ben-Arie, N -- Eatock, R A -- Bellen, H J -- Lysakowski, A -- Zoghbi, H Y -- R01 DC002290/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 1999 Jun 11;284(5421):1837-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10364557" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors ; Calbindin 2 ; Cell Differentiation ; Cochlea/embryology/metabolism/ultrastructure ; Ear, Inner/*embryology/metabolism/ultrastructure ; Epithelium/metabolism/ultrastructure ; Gene Expression Regulation, Developmental ; Gene Targeting ; *Genes, Essential ; Hair Cells, Auditory, Inner/*cytology/metabolism ; Mice ; Microscopy, Electron ; Myosin Heavy Chains/biosynthesis ; S100 Calcium Binding Protein G/biosynthesis ; Saccule and Utricle/embryology/metabolism/ultrastructure ; Stem Cells/cytology ; Transcription Factors/*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
  • 172
    facet.materialart.
    Unknown
    Anti-immune trick unveiled in Salmonella (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strauss, E -- New York, N.Y. -- Science. 1999 Jul 16;285(5426):307-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10438287" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/genetics/*physiology ; Biological Transport ; Lysosomes/*microbiology/physiology ; Macrophages/microbiology ; Membrane Fusion ; Mice ; Salmonella enterica/immunology/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
  • 173
    facet.materialart.
    Unknown
    American Society for Cell Biology. Homing in on a sperm receptor (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strauss, E -- New York, N.Y. -- Science. 1999 Jan 8;283(5399):169.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9925473" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins ; Animals ; Female ; Integrin alpha6beta1 ; Integrins/*metabolism ; Male ; Membrane Glycoproteins/*metabolism ; Metalloendopeptidases/*metabolism ; Mice ; Ovum/*metabolism ; Receptors, Cell Surface/*metabolism ; *Sperm-Ovum Interactions ; Spermatozoa/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
  • 174
    facet.materialart.
    Unknown
    Activation of PPARgamma coactivator-1 through transcription factor docking (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-13
    Description: Transcriptional coactivators have been viewed as constitutively active components, using transcription factors mainly to localize their functions. Here, it is shown that PPARgamma coactivator-1 (PGC-1) promotes transcription through the assembly of a complex that includes the histone acetyltransferases steroid receptor coactivator-1 (SRC-1) and CREB binding protein (CBP)/p300. PGC-1 has a low inherent transcriptional activity when it is not bound to a transcription factor. The docking of PGC-1 to peroxisome proliferator-activated receptor gamma (PPARgamma) stimulates an apparent conformational change in PGC-1 that permits binding of SRC-1 and CBP/p300, resulting in a large increase in transcriptional activity. Thus, transcription factor docking switches on the activity of a coactivator protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Puigserver, P -- Adelmant, G -- Wu, Z -- Fan, M -- Xu, J -- O'Malley, B -- Spiegelman, B M -- DK54477/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 12;286(5443):1368-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute and Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10558993" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; COS Cells ; DNA-Binding Proteins/metabolism ; E1A-Associated p300 Protein ; Gene Expression Regulation ; Histone Acetyltransferases ; Mice ; Nuclear Proteins/chemistry/*metabolism ; Nuclear Receptor Coactivator 1 ; Nuclear Respiratory Factors ; Protein Binding ; Protein Conformation ; Receptors, Cytoplasmic and Nuclear/*metabolism ; Recombinant Fusion Proteins/metabolism ; Trans-Activators/chemistry/*metabolism ; Transcription Factors/chemistry/*metabolism ; *Transcription, Genetic ; 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
  • 175
    facet.materialart.
    Unknown
    Limb and skin abnormalities in mice lacking IKKalpha (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-09
    Description: The gene encoding inhibitor of kappa B (IkappaB) kinase alpha (IKKalpha; also called IKK1) was disrupted by gene targeting. IKKalpha-deficient mice died perinatally. In IKKalpha-deficient fetuses, limb outgrowth was severely impaired despite unaffected skeletal development. The epidermal cells in IKKalpha-deficient fetuses were highly proliferative with dysregulated epidermal differentiation. In the basal layer, degradation of IkappaB and nuclear localization of nuclear factor kappa B (NF-kappaB) were not observed. Thus, IKKalpha is essential for NF-kappaB activation in the limb and skin during embryogenesis. In contrast, there was no impairment of NF-kappaB activation induced by either interleukin-1 or tumor necrosis factor-alpha in IKKalpha-deficient embryonic fibroblasts and thymocytes, indicating that IKKalpha is not essential for cytokine-induced activation of NF-kappaB.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takeda, K -- Takeuchi, O -- Tsujimura, T -- Itami, S -- Adachi, O -- Kawai, T -- Sanjo, H -- Yoshikawa, K -- Terada, N -- Akira, S -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):313-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation, Department of Pathology, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo 663-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10195895" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cytoplasm/metabolism ; DNA-Binding Proteins/metabolism ; Epidermis/cytology/*embryology/metabolism ; Extremities/*embryology/growth & development ; Gene Expression Regulation, Developmental ; Gene Targeting ; I-kappa B Kinase ; I-kappa B Proteins ; Interleukin-1/pharmacology ; Keratinocytes/cytology/metabolism ; Limb Buds/enzymology ; Limb Deformities, Congenital/*enzymology/genetics ; Mice ; *Myogenic Regulatory Factors ; NF-kappa B/metabolism ; Nuclear Proteins/genetics ; Phosphorylation ; Protein-Serine-Threonine Kinases/deficiency/genetics/*metabolism ; Skin Abnormalities/*enzymology/genetics ; Transcription Factor RelA ; Tumor Necrosis Factor-alpha/pharmacology ; Twist Transcription Factor
    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
    How stimulant drugs may calm hyperactivity (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1999 Jan 15;283(5400):306.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9925481" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Attention Deficit Disorder with Hyperactivity/drug therapy/physiopathology ; Behavior, Animal/drug effects ; Brain/drug effects/*metabolism ; Carrier Proteins/genetics ; Central Nervous System Stimulants/*pharmacology ; Child ; Disease Models, Animal ; Dopamine/metabolism ; Dopamine Plasma Membrane Transport Proteins ; Humans ; Hyperkinesis/*drug therapy/physiopathology ; Maze Learning ; *Membrane Glycoproteins ; *Membrane Transport Proteins ; Methylphenidate/*pharmacology ; Mice ; Mice, Knockout ; *Nerve Tissue Proteins ; Serotonin/metabolism/*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
  • 177
    facet.materialart.
    Unknown
    Chemokine Up-regulation and activated T cell attraction by maturing dendritic cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-30
    Description: Langerhans' cells migrating from contact-sensitized skin were found to up-regulate expression of macrophage-derived chemokine (MDC) during maturation into lymph node dendritic cells (DCs). Naive T cells did not migrate toward MDC, but antigen-specific T cells rapidly acquired MDC responsiveness in vivo after a subcutaneous injection of antigen. In chemotaxis assays, maturing DCs attracted activated T cells more strongly than naive T cells. These studies identified chemokine up-regulation as part of the Langerhans' cell maturation program to immunogenic T cell-zone DC. Preferential recruitment of activated T cells may be a mechanism used by maturing DCs to promote encounters with antigen-specific T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tang, H L -- Cyster, J G -- AI-40098/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 30;284(5415):819-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of California at San Francisco, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10221917" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Chemokine CCL19 ; Chemokine CCL22 ; Chemokines, CC/*biosynthesis/physiology ; *Chemotaxis, Leukocyte ; Dendritic Cells/cytology/*immunology ; Dermatitis, Contact/immunology ; Fluorescein-5-isothiocyanate ; Langerhans Cells/cytology/immunology ; Lymph Nodes/immunology ; *Lymphocyte Activation ; Mice ; T-Lymphocytes/*immunology/physiology ; 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
  • 178
    facet.materialart.
    Unknown
    The crystal structure of a T cell receptor in complex with peptide and MHC class II (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-03
    Description: The crystal structure of a complex involving the D10 T cell receptor (TCR), 16-residue foreign peptide antigen, and the I-Ak self major histocompatibility complex (MHC) class II molecule is reported at 3.2 angstrom resolution. The D10 TCR is oriented in an orthogonal mode relative to its peptide-MHC (pMHC) ligand, necessitated by the amino-terminal extension of peptide residues projecting from the MHC class II antigen-binding groove as part of a mini beta sheet. Consequently, the disposition of D10 complementarity-determining region loops is altered relative to that of most pMHCI-specific TCRs; the latter TCRs assume a diagonal orientation, although with substantial variability. Peptide recognition, which involves P-1 to P8 residues, is dominated by the Valpha domain, which also binds to the class II MHC beta1 helix. That docking is limited to one segment of MHC-bound peptide offers an explanation for epitope recognition and altered peptide ligand effects, suggests a structural basis for alloreactivity, and illustrates how bacterial superantigens can span the TCR-pMHCII surface.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reinherz, E L -- Tan, K -- Tang, L -- Kern, P -- Liu, J -- Xiong, Y -- Hussey, R E -- Smolyar, A -- Hare, B -- Zhang, R -- Joachimiak, A -- Chang, H C -- Wagner, G -- Wang, J -- AI/CA37581/AI/NIAID NIH HHS/ -- AI19807/AI/NIAID NIH HHS/ -- GM56008/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1913-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunobiology, Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10583947" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/*chemistry/immunology/metabolism ; Binding Sites ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/immunology ; Conalbumin/chemistry/immunology ; Crystallization ; Crystallography, X-Ray ; Histocompatibility Antigens Class I/immunology ; Histocompatibility Antigens Class II/*chemistry/immunology/metabolism ; Hydrogen Bonding ; Ligands ; Mice ; Mice, Inbred AKR ; Models, Molecular ; Oligopeptides/chemistry/immunology/metabolism ; Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Receptors, Antigen, T-Cell, alpha-beta/*chemistry/immunology/metabolism ; Superantigens/immunology/metabolism ; Thymus Gland/cytology/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
  • 179
    facet.materialart.
    Unknown
    Control of hippocampal morphogenesis and neuronal differentiation by the LIM homeobox gene Lhx5 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-15
    Description: The mammalian hippocampus contains the neural circuitry that is crucial for cognitive functions such as learning and memory. The development of such circuitry is dependent on the generation and correct placement of the appropriate number and types of neurons. Mice lacking function of the LIM homeobox gene Lhx5 showed a defect in hippocampus development. Hippocampal neural precursor cells were specified and proliferated, but many of them failed to either exit the cell cycle or to differentiate and migrate properly. Lhx5 is therefore essential for the regulation of precursor cell proliferation and the control of neuronal differentiation and migration during hippocampal development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhao, Y -- Sheng, H Z -- Amini, R -- Grinberg, A -- Lee, E -- Huang, S -- Taira, M -- Westphal, H -- New York, N.Y. -- Science. 1999 May 14;284(5417):1155-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Mammalian Genes and Development, 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/10325223" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Patterning ; Cell Differentiation ; Cell Division ; Cell Movement ; Crosses, Genetic ; Dentate Gyrus/cytology/embryology ; Female ; Gene Deletion ; Gene Expression ; *Genes, Homeobox ; Hippocampus/*cytology/*embryology ; Homeodomain Proteins/*genetics/physiology ; Interneurons/cytology ; LIM-Homeodomain Proteins ; Male ; Mice ; Morphogenesis ; Nerve Tissue Proteins/*genetics/physiology ; Neuroglia/cytology ; Neurons/*cytology ; Pyramidal Cells/cytology ; Stem Cells/*cytology ; 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
  • 180
    facet.materialart.
    Unknown
    Mimicry of CD40 signals by Epstein-Barr virus LMP1 in B lymphocyte responses (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-09
    Description: The effect of the Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1) on the activation and differentiation of normal B cells was investigated. B cells of transgenic mice expressing LMP1 under the control of immunoglobulin promoter/enhancer displayed enhanced expression of activation antigens and spontaneously proliferated and produced antibody. Humoral immune responses of LMP1 transgenic mice in CD40-deficient or normal backgrounds revealed that LMP1 mimics CD40 signals to induce extrafollicular B cell differentiation but, unlike CD40, blocks germinal center formation. Thus, these specific properties of LMP1 may determine the site of primary B cell infection and the state of infection in the natural course of EBV infection, whereas subsequent loss of LMP1 expression may affect the site of persistent latent infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Uchida, J -- Yasui, T -- Takaoka-Shichijo, Y -- Muraoka, M -- Kulwichit, W -- Raab-Traub, N -- Kikutani, H -- CA19014/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Oct 8;286(5438):300-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10514374" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Affinity ; Antigens, CD40/genetics/*metabolism ; B-Lymphocytes/*immunology/metabolism/virology ; Cell Differentiation ; Female ; Germinal Center/immunology/metabolism ; Herpesvirus 4, Human/*metabolism/physiology ; Immunization ; Immunoglobulin Class Switching ; Immunoglobulins/biosynthesis ; Interleukin-4/pharmacology ; *Lymphocyte Activation ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; *Molecular Mimicry ; NF-kappa B/metabolism ; Signal Transduction ; Spleen/immunology ; Viral Matrix Proteins/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
  • 181
    facet.materialart.
    Unknown
    Differences in left-right axis pathways in mouse and chick: functions of FGF8 and SHH (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-20
    Description: A molecular pathway leading to left-right asymmetry in the chick embryo has been described, in which FGF8 is a right determinant and Sonic Hedgehog a left determinant. Here evidence is presented that the Fgf8 and Sonic Hedgehog genes are required for left-right axis determination in the mouse embryo, but that they have different functions from those previously reported in the chick. In the mouse FGF8 is a left determinant and Sonic Hedgehog is required to prevent left determinants from being expressed on the right.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyers, E N -- Martin, G R -- HD01216/HD/NICHD NIH HHS/ -- R01 HD34380/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 16;285(5426):403-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Program in Developmental Biology, School of Medicine, and Department of Pediatrics, School of Medicine, University of California at San Francisco, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10411502" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Body Patterning ; Chick Embryo/*growth & development/metabolism ; Embryo, Mammalian/metabolism ; *Embryonic Induction ; *Embryonic and Fetal Development ; Fibroblast Growth Factor 8 ; Fibroblast Growth Factors/genetics/*physiology ; Gene Expression Regulation, Developmental ; Heart/embryology ; Heart Defects, Congenital/embryology ; Hedgehog Proteins ; Homeodomain Proteins/genetics/physiology ; Left-Right Determination Factors ; Lung/abnormalities/embryology ; Mesoderm/metabolism ; Mice ; Mutation ; Nodal Protein ; *Nuclear Proteins ; Paired Box Transcription Factors ; Proteins/genetics/*physiology ; Recombinant Proteins/metabolism ; *Trans-Activators ; Transcription Factors/genetics/physiology ; Transforming Growth Factor beta/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
  • 182
    facet.materialart.
    Unknown
    Regulation of lineage commitment distinct from positive selection (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-05
    Description: Developing alphabeta T cells diverge into the CD4 and CD8 lineages as they mature in the thymus. It is unclear whether lineage commitment is mechanistically distinct from the process that selects for the survival of T cells with useful T cell receptor (TCR) specificities (positive selection). In HD mice, which lack mature CD4+ T cells, major histocompatibility complex (MHC) class II-restricted T cells are redirected to the CD8 lineage independent of MHC class I expression. However, neither TCR-mediated signaling nor positive selection is impaired. Thus, the HD mutation provides genetic evidence that lineage commitment may be mechanistically distinct from positive selection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keefe, R -- Dave, V -- Allman, D -- Wiest, D -- Kappes, D J -- AI34472/AI/NIAID NIH HHS/ -- CA06927/CA/NCI NIH HHS/ -- CA74620/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 5;286(5442):1149-53.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fox Chase Cancer Center, 7701 Burholme Avenue, Philadelphia, PA 19111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10550051" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD4-Positive T-Lymphocytes/*cytology/immunology ; CD8-Positive T-Lymphocytes/*cytology/immunology ; Cell Differentiation ; *Cell Lineage ; Crosses, Genetic ; Female ; Hematopoietic Stem Cells/cytology/immunology ; Histocompatibility Antigens Class I/immunology ; Histocompatibility Antigens Class II/immunology ; Male ; Mice ; Mice, Mutant Strains ; Mice, Transgenic ; Phenotype ; Phosphorylation ; Radiation Chimera ; Receptors, Antigen, T-Cell, alpha-beta/*metabolism ; Signal Transduction ; T-Lymphocyte Subsets/*cytology/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
    Cutting back the calories (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gerhard, G S -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1679-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610562" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*genetics ; Animals ; Cerebral Cortex/metabolism ; *Energy Intake ; Gene Expression ; *Gene Expression Profiling ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal/*metabolism ; Oligonucleotide Array Sequence Analysis ; Rats ; Research Design
    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
    Breast cancer genes and DNA repair (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Venkitaraman, A R -- New York, N.Y. -- Science. 1999 Nov 5;286(5442):1100-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncology, University of Cambridge, Cambridge CB2 2XY, UK. arv22@cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610523" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxia Telangiectasia Mutated Proteins ; BRCA1 Protein/*metabolism ; BRCA2 Protein ; Breast/metabolism ; Breast Neoplasms/*genetics/metabolism ; Cell Cycle ; Cell Cycle Proteins/metabolism ; DNA Damage ; *DNA Repair ; DNA-Binding Proteins ; Female ; *Genes, BRCA1 ; Humans ; Mice ; Neoplasm Proteins/*genetics/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/genetics/metabolism ; Recombination, Genetic ; Transcription Factors/*genetics/metabolism ; Tumor Suppressor 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
  • 185
    facet.materialart.
    Unknown
    Regulation of transcription by a protein methyltransferase (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-26
    Description: The p160 family of coactivators, SRC-1, GRIP1/TIF2, and p/CIP, mediate transcriptional activation by nuclear hormone receptors. Coactivator-associated arginine methyltransferase 1 (CARM1), a previously unidentified protein that binds to the carboxyl-terminal region of p160 coactivators, enhanced transcriptional activation by nuclear receptors, but only when GRIP1 or SRC-1a was coexpressed. Thus, CARM1 functions as a secondary coactivator through its association with p160 coactivators. CARM1 can methylate histone H3 in vitro, and a mutation in the putative S-adenosylmethionine binding domain of CARM1 substantially reduced both methyltransferase and coactivator activities. Thus, coactivator-mediated methylation of proteins in the transcription machinery may contribute to transcriptional regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, D -- Ma, H -- Hong, H -- Koh, S S -- Huang, S M -- Schurter, B T -- Aswad, D W -- Stallcup, M R -- AG00093/AG/NIA NIH HHS/ -- DK43093/DK/NIDDK NIH HHS/ -- NS17269/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2174-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology HMR 301, University of Southern California, 2011 Zonal Avenue, Los Angeles, CA 90033, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10381882" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Histone Acetyltransferases ; Histones/metabolism ; Methylation ; Mice ; Molecular Sequence Data ; Mutation ; Nuclear Receptor Coactivator 1 ; Nuclear Receptor Coactivator 2 ; Nuclear Receptor Coactivator 3 ; Protein-Arginine N-Methyltransferases/chemistry/genetics/*metabolism ; Receptors, Androgen/metabolism ; Receptors, Estrogen/metabolism ; Receptors, Thyroid Hormone/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Trans-Activators/*metabolism ; Transcription Factors/metabolism ; *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
  • 186
    facet.materialart.
    Unknown
    Altered cochlear fibrocytes in a mouse model of DFN3 nonsyndromic deafness (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-28
    Description: DFN3, an X chromosome-linked nonsyndromic mixed deafness, is caused by mutations in the BRN-4 gene, which encodes a POU transcription factor. Brn-4-deficient mice were created and found to exhibit profound deafness. No gross morphological changes were observed in the conductive ossicles or cochlea, although there was a dramatic reduction in endocochlear potential. Electron microscopy revealed severe ultrastructural alterations in cochlear spiral ligament fibrocytes. The findings suggest that these fibrocytes, which are mesenchymal in origin and for which a role in potassium ion homeostasis has been postulated, may play a critical role in auditory function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Minowa, O -- Ikeda, K -- Sugitani, Y -- Oshima, T -- Nakai, S -- Katori, Y -- Suzuki, M -- Furukawa, M -- Kawase, T -- Zheng, Y -- Ogura, M -- Asada, Y -- Watanabe, K -- Yamanaka, H -- Gotoh, S -- Nishi-Takeshima, M -- Sugimoto, T -- Kikuchi, T -- Takasaka, T -- Noda, T -- New York, N.Y. -- Science. 1999 Aug 27;285(5432):1408-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, The Cancer Institute, Japanese Foundation for Cancer Research, 1-37-1 Kami-ikebukuro, Toshima-ku, Tokyo 170-8455, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10464101" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cochlear Duct/*metabolism/pathology ; *DNA-Binding Proteins ; Deafness/genetics/*metabolism/pathology ; Ear, Inner/metabolism/pathology ; Ear, Middle/pathology ; Endolymph/metabolism ; Evoked Potentials, Auditory, Brain Stem ; Female ; Gene Expression ; Gene Targeting ; Genetic Linkage ; In Situ Hybridization ; Ion Transport ; Male ; Membrane Potentials ; Mice ; Mice, Inbred C57BL ; Mutagenesis ; *Nerve Tissue Proteins ; POU Domain Factors ; Potassium/*metabolism ; Transcription Factors/genetics/*metabolism ; X Chromosome
    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
    BLyS: member of the tumor necrosis factor family and B lymphocyte stimulator (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-10
    Description: The tumor necrosis factor (TNF) superfamily of cytokines includes both soluble and membrane-bound proteins that regulate immune responses. A member of the human TNF family, BLyS (B lymphocyte stimulator), was identified that induced B cell proliferation and immunoglobulin secretion. BLyS expression on human monocytes could be up-regulated by interferon-gamma. Soluble BLyS functioned as a potent B cell growth factor in costimulation assays. Administration of soluble recombinant BLyS to mice disrupted splenic B and T cell zones and resulted in elevated serum immunoglobulin concentrations. The B cell tropism of BLyS is consistent with its receptor expression on B-lineage cells. The biological profile of BLyS suggests it is involved in monocyte-driven B cell activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moore, P A -- Belvedere, O -- Orr, A -- Pieri, K -- LaFleur, D W -- Feng, P -- Soppet, D -- Charters, M -- Gentz, R -- Parmelee, D -- Li, Y -- Galperina, O -- Giri, J -- Roschke, V -- Nardelli, B -- Carrell, J -- Sosnovtseva, S -- Greenfield, W -- Ruben, S M -- Olsen, H S -- Fikes, J -- Hilbert, D M -- New York, N.Y. -- Science. 1999 Jul 9;285(5425):260-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genome Sciences, 9410 Key West Avenue, Rockville, MD 20850, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10398604" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; B-Cell Activating Factor ; B-Cell Activation Factor Receptor ; B-Lymphocyte Subsets/immunology ; B-Lymphocytes/*immunology ; Cell Line ; Cells, Cultured ; Humans ; Immunoglobulins/blood ; Interferon-gamma/pharmacology ; *Lymphocyte Activation ; Membrane Proteins/chemistry/genetics/pharmacology/*physiology ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Monocytes/*immunology ; Receptors, Cytokine/metabolism ; Receptors, Tumor Necrosis Factor/metabolism ; Recombinant Proteins/pharmacology ; Sequence Alignment ; Species Specificity ; Tumor Necrosis Factor-alpha/chemistry/genetics/pharmacology/*physiology ; 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
  • 188
    facet.materialart.
    Unknown
    Organogenic role of B lymphocytes in mucosal immunity (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-03
    Description: Follicle-associated epithelium (FAE) in the intestinal Peyer's patches contains M cells that deliver pathogens to organized lymphoid tissue. Development of Peyer's patches, FAE, and M cells was found to be impaired in mice that had no B cells. Transgenic expression of membrane-bound immunoglobulin M restored B cells and FAE development. The lack of M cells abrogated infection with a milk-borne retrovirus. Thus, in addition to secretion of antibodies and presentation of antigens, B cells are important for organogenesis of the mucosal immune barriers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Golovkina, T V -- Shlomchik, M -- Hannum, L -- Chervonsky, A -- CA34196/CA/NCI NIH HHS/ -- CA65795/CA/NCI NIH HHS/ -- DK53561/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1965-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10583962" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology ; Cell Count ; Genes, Immunoglobulin ; *Immunity, Mucosal ; Immunoglobulin M/genetics/immunology ; Lymphocyte Activation ; Mammary Tumor Virus, Mouse/physiology ; Mice ; Mice, Inbred Strains ; Mice, Knockout ; Mice, Transgenic ; Microscopy, Electron, Scanning ; Peyer's Patches/*cytology/*immunology/ultrastructure ; Retroviridae Infections/immunology/virology ; T-Lymphocytes/immunology ; Tumor Virus Infections/immunology/virology
    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
    Interleukin-13's key role in asthma shown (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, G -- New York, N.Y. -- Science. 1998 Dec 18;282(5397):2168.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9890820" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Asthma/*immunology/physiopathology ; Bronchoconstriction ; Eosinophils/immunology ; Goblet Cells/immunology ; Humans ; Interleukin-13/pharmacology/*physiology ; Interleukin-13 Receptor alpha1 Subunit ; Interleukin-4/pharmacology/physiology ; Lung/immunology/physiopathology ; Mice ; Receptors, Interleukin/metabolism ; Receptors, Interleukin-13 ; Receptors, Interleukin-4/metabolism ; Signal Transduction ; 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
  • 190
    facet.materialart.
    Unknown
    Preliminary Comparison of Skin Friction Measurements with CFD Predictions (1999)
    In:  CASI
    Details
    Publication Date: 2004-12-03
    Description: The work to be described was performed at the NASA Langley UPWT (4-ft supersonic), test section #2, during 21-24 May 1996. The configuration being tested was the 1.675% Ref H controls model; test conditions were Ma = 2.40, Re = 3 million/ft. This was an exploration of a new technique, and it was not intended to provide definitive comparison of measured and computed skin friction results. It is, however, hoped that the experience gained will make such a rigorous comparison possible in the future.
    Keywords: Aerodynamics
    Type: 1997 NASA High-Speed Research Program Aerodynamic Performance; Volume 1; Part 2; 1478-1499; NASA/CP-1999-209691/VOL1/PT2
    Format: text
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    NASA TECHNICAL REPORTS
  • 191
    facet.materialart.
    Unknown
    Preliminary Results of the 1.5% TCA (Modular) Controls Model in the NASA Langley UPWT (1999)
    In:  CASI
    Details
    Publication Date: 2004-12-03
    Description: To summarize the significant highlights in this report: (1) Data quality, determined by multiple repeat runs performed on the TCA baseline configuration, and long-term repeatability, determined by comparing baseline Reference H data from this test to a previous test, have been shown to be good. (2) The longitudinal stability of the TCA is more non-linear than for the Reference H, and while it is similar at normal lift values, the TCA has considerably more pitch-up at higher lift. (3) Longitudinal control effectiveness of the TCA is similar to the Reference H and the ratio of elevator effectiveness to horizontal tail effectiveness is approximately 0.3. 4) The directional stability of the TCA is improved relative to Reference H at higher angles-of attack. The chine is effective for improving directional stability. (5) The directional control effectiveness 'of the TCA rudder is the same as that of the Reference H rudder at low angles-of-attack, after taking factors, such as number of rudder panels deflected and vertical tail volume into account. However, rudder effectiveness was shown to be reduced at higher angles-of-attack. (6) The lateral stability was shown to be reduced relative to the Reference H, which may be beneficial at low speeds for alleviating lateral control saturation. (7) Lateral control effectiveness for the TCA was shown to be similar to the Reference H for negative trailing-edge flap deflections and was reduced by approximately 25% for positive trailing-edge flap deflections.
    Keywords: Aerodynamics
    Type: 1997 NASA High-Speed Research Program Aerodynamic Performance Workshop; Volume 1; Part 1; 612-668; NASA/CP-1999-209691/VOL1/PT1
    Format: text
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    NASA TECHNICAL REPORTS
  • 192
    facet.materialart.
    Unknown
    Turbulence Model Comparisons and Reynolds Number Effects Over a High-Speed Aircraft at Transonic Speeds (1999)
    In:  CASI
    Details
    Publication Date: 2004-12-03
    Description: This paper gives the results of a grid study, a turbulence model study, and a Reynolds number effect study for transonic flows over a high-speed aircraft using the thin-layer, upwind, Navier-Stokes CFL3D code. The four turbulence models evaluated are the algebraic Baldwin-Lomax model with the Degani-Schiff modifications, the one-equation Baldwin-Barth model, the one-equation Spalart-Allmaras model, and Menter's two-equation Shear-Stress-Transport (SST) model. The flow conditions, which correspond to tests performed in the NASA Langley National Transonic Facility (NTF), are a Mach number of 0.90 and a Reynolds number of 30 million based on chord for a range of angle-of-attacks (1 degree to 10 degrees). For the Reynolds number effect study, Reynolds numbers of 10 and 80 million based on chord were also evaluated. Computed forces and surface pressures compare reasonably well with the experimental data for all four of the turbulence models. The Baldwin-Lomax model with the Degani-Schiff modifications and the one-equation Baldwin-Barth model show the best agreement with experiment overall. The Reynolds number effects are evaluated using the Baldwin-Lomax with the Degani-Schiff modifications and the Baldwin-Barth turbulence models. Five angles-of-attack were evaluated for the Reynolds number effect study at three different Reynolds numbers. More work is needed to determine the ability of CFL3D to accurately predict Reynolds number effects.
    Keywords: Aerodynamics
    Type: First NASA/Industry High-Speed Research Configuration Aerodynamics Workshop; Part 3; 1185-1214; NASA/CP-1999-209690/PT3
    Format: text
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    NASA TECHNICAL REPORTS
  • 193
    facet.materialart.
    Unknown
    High Reynolds Number Assessment of Boundary Layer Transition Trip Drag at Mach 2.48 on HSCT Configuration (1999)
    In:  CASI
    Details
    Publication Date: 2004-12-03
    Description: The NASA High Speed Research (HSR) Program is intended to establish a technology base enabling industry development of an economically viable and environmentally acceptable second generation high speed civil transport (HSCT). The HSR program consists of work directed towards several broad technology areas, one of which is aerodynamic performance. The objective of the Configuration Aerodynamics task of the Aerodynamic Performance technology area is the development of aerodynamic drag reduction, stability and control, and propulsion airframe integration technologies required to support the HSCT development process. Towards this goal, computational and empirical based aerodynamic design tools are being developed, evaluated, and validated through ground based experimental testing. In addition, methods for ground to flight scaling are being developed and refined. Successful development of validated design and scaling methodologies will result in improved economy of operation for an HSCT and reduce uncertainty in full-scale flight predictions throughout the development process.
    Keywords: Aerodynamics
    Type: 1998 NASA High-Speed Research Program Aerodynamic Performance Workshop; Volume 1; Part 1; 539-569; NASA/CP-1999-209692/VOL1/PT1
    Format: text
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    NASA TECHNICAL REPORTS
  • 194
    facet.materialart.
    Unknown
    High-Lift CFD Validation (1999)
    In:  CASI
    Details
    Publication Date: 2004-12-03
    Description: It is not unusual when comparing CFD data to experimental data to find discrepancies between the results. Sometimes forces and moments compare well, while surface pressures do not, and vice versa. It is commonplace for the researcher to believe that the flow field has been accurately simulated when these types of measurements compare well. However, being able to routinely predict boundary layer transition and separated flows are not guaranteed. In fact accurate simulation of these types of flow physics has been a challenge to the CFD community. In order to improve Navier-Stokes predictions for complex vortical flow fields, more detailed information about the flow physics is necessary. Unfortunately, the many wind-tunnel tests performed in Langley's NTF and 14x22 facilities as well as in the Ames' 12 ft. Tunnel provided little information about the detailed flow physics, and no priority was given to obtaining any CFD measurements. Using the latest experimental techniques, this information can and should be obtained for present and future use.
    Keywords: Aerodynamics
    Type: 1999 NASA High-Speed Research Program Aerodynamic Performance Workshop; Volume 2; Part 2; 913-948; NASA/CP-1999-209704/VOL2/PT2
    Format: text
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    NASA TECHNICAL REPORTS
  • 195
    facet.materialart.
    Unknown
    Parallel Computation of Sensitivity Derivatives with Application to Aerodynamic Optimization of a Wing (1999)
    In:  CASI
    Details
    Publication Date: 2004-12-03
    Description: This paper focuses on the parallel computation of aerodynamic derivatives via automatic differentiation of the Euler/Navier-Stokes solver CFL3D. The comparison with derivatives obtained by finite differences is presented and the scaling of the time required to obtain the derivatives relative to the number of processors employed for the computation is shown. Finally, the derivative computations are coupled with an optimizer and surface/volume grid deformation tools to perform an optimization to reduce the drag of a three-dimensional wing.
    Keywords: Aerodynamics
    Type: HPCCP/CAS Workshop Proceedings 1998; 219-224; NASA/CP-1999-208757
    Format: text
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    NASA TECHNICAL REPORTS
  • 196
    facet.materialart.
    Unknown
    Aerodynamic Shape Optimization Using A Combined Distributed/Shared Memory Paradigm (1999)
    In:  CASI
    Details
    Publication Date: 2004-12-03
    Description: Current parallel computational approaches involve distributed and shared memory paradigms. In the distributed memory paradigm, each processor has its own independent memory. Message passing typically uses a function library such as MPI or PVM. In the shared memory paradigm, such as that used on the SGI Origin 2000 machine, compiler directives are used to instruct the compiler to schedule multiple threads to perform calculations. In this paradigm, it must be assured that processors (threads) do not simultaneously access regions of memory in such away that errors would occur. This paper utilizes the latest version of the SGI MPI function library to combine the two parallelization paradigms to perform aerodynamic shape optimization of a generic wing/body.
    Keywords: Aerodynamics
    Type: HPCCP/CAS Workshop Proceedings 1998; 207-212; NASA/CP-1999-208757
    Format: text
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    NASA TECHNICAL REPORTS
  • 197
    facet.materialart.
    Unknown
    Prediction and Assessment of Reynolds Number Sensitivities Associated with Wing Leading-Edge Radius Variations (1999)
    In:  CASI
    Details
    Publication Date: 2004-12-03
    Description: The primary objectives of this study were to expand the data base showing the effects of LE radius distribution and corresponding sensitivity to Rn at subsonic and transonic conditions, and to assess the predictive capability of CFD for these effects. Several key elements led to the initiation of this project: 1) the necessity of meeting multipoint design requirements to enable a viable HSCT, 2) the demonstration that blunt supersonic leading-edges can be associated with performance gain at supersonic speeds , and 3) limited data. A test of a modified Reference H model with the TCA planform and 2 LE radius distributions was performed in the NTF, in addition to Navier-Stokes analysis for an additional 3 LE radius distributions. Results indicate that there is a tremendous potential to improve high-lift performance through the use of a blunt LE across the span given an integrated, fully optimized design, and that low Rn data alone is probably not sufficient to demonstrate the benefit.
    Keywords: Aerodynamics
    Type: 1997 NASA High-Speed Research Program Aerodynamic Performance Workshop; Volume 1; Part 1; 588-611; NASA/CP-1999-209691/VOL1/PT1
    Format: text
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    NASA TECHNICAL REPORTS
  • 198
    facet.materialart.
    Unknown
    An Analysis of CFD and Flat Plate Predictions of Friction Drag for the TCA W/B at Supersonic Cruise (1999)
    In:  CASI
    Details
    Publication Date: 2004-12-03
    Description: This paper presents results of a study which attempted to provide some understanding of the relationship between skin friction drag estimates produced by flat plate methods and those produced by Navier-Stokes computations. A brief introduction is followed by analysis, including a flat plate grid study, analysis of the wing flow, an analysis of the fuselage flow. Other results of interest are then presented, including turbulence model sensitivities, and brief analysis of other configurations.
    Keywords: Aerodynamics
    Type: 1997 NASA High-Speed Research Program Aerodynamic Performance; Volume 1; Part 2; 1452-1477; NASA/CP-1999-209691/VOL1/PT2
    Format: text
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    NASA TECHNICAL REPORTS
  • 199
    facet.materialart.
    Unknown
    Boundary Layer Transition in the NTF: HSR Experience and Plans (1999)
    In:  CASI
    Details
    Publication Date: 2004-12-03
    Description: Efforts towards understanding boundary layer transition characteristics on a High Speed Civil Transport (HSCT)-class configuration in the National Transonic Facility (NTF) are ongoing. The majority of the High Speed Research (HSR) data base in the NTF has free transition on the wing, even at low Reynolds numbers (Rn) attainable in conventional facilities. Limited data has been obtained and is described herein showing the effects of a conventional, Braslow method based wing boundary-layer trip on drag. Comparisons are made using force data polars and surface flow visualization at selected angles-of-attack and Mach number. Minimum drag data obtained in this study suggest that boundary layer transition occurred very near the wing leading edge by a chord Rn of 30 million. Sublimating chemicals were used in the air mode of operation only at low Rn and low angles-of-attack with no flap deflections; sublimation results suggest that the forebody and outboard wing panel are the only regions with significant laminar flow. The process and issues related to the sublimating chemical technique as applied in the NTF are discussed. Beyond the existing experience, status of efforts to develop a production transition detection system applicable to both air and cryogenic nitrogen environments is presented.
    Keywords: Aerodynamics
    Type: First NASA/Industry High-Speed Research Configuration Aerodynamics Workshop; Pt. 2; 579-596; NASA/CP-1999-209690/PT2
    Format: text
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    NASA TECHNICAL REPORTS
  • 200
    facet.materialart.
    Unknown
    Model Deformation Measurement Technique NASA Langley HSR Experiences (1999)
    In:  CASI
    Details
    Publication Date: 2004-12-03
    Description: Model deformation measurement techniques have been investigated and developed at NASA's Langley Research Center. The current technique is based upon a single video camera photogrammetric determination of two dimensional coordinates of wing targets with a fixed (and known) third dimensional coordinate, namely the spanwise location. Variations of this technique have been used to measure wing twist and bending at a few selected spanwise locations near the wing tip on HSR models at the National Transonic Facility, the Transonic Dynamics Tunnel, and the Unitary Plan Wind Tunnel. Automated measurements have been made at both the Transonic Dynamics Tunnel and at Unitary Plan Wind Tunnel during the past year. Automated measurements were made for the first time at the NTF during the recently completed HSR Reference H Test 78 in early 1996. A major problem in automation for the NTF has been the need for high contrast targets which do not exceed the stringent surface finish requirements. The advantages and limitations (including targeting) of the technique as well as the rationale for selection of this particular technique are discussed. Wing twist examples from the HSR Reference H model are presented to illustrate the run-to-run and test-to-test repeatability of the technique in air mode at the NTF. Examples of wing twist in cryogenic nitrogen mode at the NTF are also presented.
    Keywords: Aerodynamics
    Type: First NASA/Industry High-Speed Research Configuration Aerodynamics Workshop; Pt. 2; 561-578; NASA/CP-1999-209690/PT2
    Format: text
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    NASA TECHNICAL REPORTS
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...