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  • 1
    Electronic Resource
    Electronic Resource
    Genetic and Developmental Influences on Infant Mouse Ultrasonic Calling. II. Developmental Patterns in the Calls of Mice 2–12 Days of Age (1998)
    Springer
    Behavior genetics 28 (1998), S. 315-325 
    Details
    ISSN: 1573-3297
    Keywords: Mice ; ultrasonic calls ; infants ; individual differences ; signatures
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Psychology
    Notes: Abstract Infant house mice, Mus musculus, produce ultrasonic calls that reliably lead to retrieval by adult mice. While individual differences in calls have been demonstrated both among and within species, the influences of age and sex on call characteristics have not been systematically investigated in mice. This study examined the influences of age, sex, and genotype (inbred versus hybrid) on the rate, length, and frequency characteristics of the calls of 486 male and female mice from 2 to 12 days of age. Rate of calling followed a shallow inverted U-shaped function across days. Call lengths decreased and call frequency characteristics increased, in a linear manner, with age. Females emitted fewer calls, with a smaller bandwidth, at some ages than males. Hybrid pups produced more calls of greater length and a lower frequency than inbred pups. These results indicate the presence of cues that could allow adult mice to behave differentially toward pups as a function of their age and sex.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1021679615792
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  • 2
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    Structural basis of plasticity in T cell receptor recognition of a self peptide-MHC antigen (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-21
    Description: The T cell receptor (TCR) inherently has dual specificity. T cells must recognize self-antigens in the thymus during maturation and then discriminate between foreign pathogens in the periphery. A molecular basis for this cross-reactivity is elucidated by the crystal structure of the alloreactive 2C TCR bound to self peptide-major histocompatibility complex (pMHC) antigen H-2Kb-dEV8 refined against anisotropic 3.0 angstrom resolution x-ray data. The interface between peptide and TCR exhibits extremely poor shape complementarity, and the TCR beta chain complementarity-determining region 3 (CDR3) has minimal interaction with the dEV8 peptide. Large conformational changes in three of the TCR CDR loops are induced upon binding, providing a mechanism of structural plasticity to accommodate a variety of different peptide antigens. Extensive TCR interaction with the pMHC alpha helices suggests a generalized orientation that is mediated by the Valpha domain of the TCR and rationalizes how TCRs can effectively "scan" different peptides bound within a large, low-affinity MHC structural framework for those that provide the slight additional kinetic stabilization required for signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garcia, K C -- Degano, M -- Pease, L R -- Huang, M -- Peterson, P A -- Teyton, L -- Wilson, I A -- AI42266/AI/NIAID NIH HHS/ -- AI42267/AI/NIAID NIH HHS/ -- R01 CA58896/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Feb 20;279(5354):1166-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and the Skaggs Institute of Chemical Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9469799" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Crystallization ; Crystallography, X-Ray ; H-2 Antigens/*chemistry/*immunology/metabolism ; Ligands ; Mice ; Mice, Transgenic ; Models, Molecular ; Mutation ; Oligopeptides/*chemistry/immunology/metabolism ; Protein Conformation ; Protein Structure, Secondary ; Receptors, Antigen, T-Cell, alpha-beta/*chemistry/*immunology/metabolism ; Recombinant Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Identification of alpha-dystroglycan as a receptor for lymphocytic choriomeningitis virus and Lassa fever virus (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-16
    Description: A peripheral membrane protein that is interactive with lymphocytic choriomeningitis virus (LCMV) was purified from cells permissive to infection. Tryptic peptides from this protein were determined to be alpha-dystroglycan (alpha-DG). Several strains of LCMV and other arenaviruses, including Lassa fever virus (LFV), Oliveros, and Mobala, bound to purified alpha-DG protein. Soluble alpha-DG blocked both LCMV and LFV infection. Cells bearing a null mutation of the gene encoding DG were resistant to LCMV infection, and reconstitution of DG expression in null mutant cells restored susceptibility to LCMV infection. Thus, alpha-DG is a cellular receptor for both LCMV and LFV.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cao, W -- Henry, M D -- Borrow, P -- Yamada, H -- Elder, J H -- Ravkov, E V -- Nichol, S T -- Compans, R W -- Campbell, K P -- Oldstone, M B -- AG 00080/AG/NIA NIH HHS/ -- AI 09484/AI/NIAID NIH HHS/ -- DK09712/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Dec 11;282(5396):2079-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Virology, Department of Neuropharmacology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9851928" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Arenavirus/metabolism ; Cell Line ; Cytoskeletal Proteins/chemistry/genetics/*metabolism ; Dystroglycans ; Lassa virus/*metabolism/physiology ; Lymphocytic choriomeningitis virus/*metabolism/physiology ; Membrane Glycoproteins/chemistry/genetics/*metabolism ; Mice ; Molecular Sequence Data ; Mutation ; Receptors, Virus/chemistry/*metabolism ; Recombinant Fusion Proteins/metabolism ; Virus Replication
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Role of IQGAP1, a target of the small GTPases Cdc42 and Rac1, in regulation of E-cadherin- mediated cell-cell adhesion (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-07
    Description: The small guanosine triphosphatases (GTPases) Cdc42 and Rac1 regulate E-cadherin-mediated cell-cell adhesion. IQGAP1, a target of Cdc42 and Rac1, was localized with E-cadherin and beta-catenin at sites of cell-cell contact in mouse L fibroblasts expressing E-cadherin (EL cells), and interacted with E-cadherin and beta-catenin both in vivo and in vitro. IQGAP1 induced the dissociation of alpha-catenin from a cadherin-catenin complex in vitro and in vivo. Overexpression of IQGAP1 in EL cells, but not in L cells expressing an E-cadherin-alpha-catenin chimeric protein, resulted in a decrease in E-cadherin-mediated cell-cell adhesive activity. Thus, IQGAP1, acting downstream of Cdc42 and Rac1, appears to regulate cell-cell adhesion through the cadherin-catenin pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuroda, S -- Fukata, M -- Nakagawa, M -- Fujii, K -- Nakamura, T -- Ookubo, T -- Izawa, I -- Nagase, T -- Nomura, N -- Tani, H -- Shoji, I -- Matsuura, Y -- Yonehara, S -- Kaibuchi, K -- New York, N.Y. -- Science. 1998 Aug 7;281(5378):832-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Signal Transduction, Nara Institute of Science and Technology, Ikoma 630-0101, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9694656" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cadherins/*metabolism ; *Cell Adhesion ; Cell Cycle Proteins/*metabolism ; Cell Membrane/metabolism ; Cytoskeletal Proteins/metabolism ; GTP Phosphohydrolases/*metabolism ; GTP-Binding Proteins/*metabolism ; GTPase-Activating Proteins ; L Cells (Cell Line) ; Mice ; Mutation ; Proteins/*metabolism ; Recombinant Fusion Proteins/metabolism ; Recombinant Proteins/metabolism ; *Trans-Activators ; alpha Catenin ; beta Catenin ; cdc42 GTP-Binding Protein ; rac GTP-Binding Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    A receptor/cytoskeletal movement triggered by costimulation during T cell activation (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-18
    Description: During T cell activation, the engagement of costimulatory molecules is often crucial to the development of an effective immune response, but the mechanism by which this is achieved is not known. Here, it is shown that beads attached to the surface of a T cell translocate toward the interface shortly after the start of T cell activation. This movement appears to depend on myosin motor proteins and requires the engagement of the major costimulatory receptor pairs, B7-CD28 and ICAM-1-LFA-1. This suggests that the engagement of costimulatory receptors triggers an active accumulation of molecules at the interface of the T cell and the antigen-presenting cell, which then increases the overall amplitude and duration of T cell signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wulfing, C -- Davis, M M -- New York, N.Y. -- Science. 1998 Dec 18;282(5397):2266-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Microbiology and Immunology, 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/9856952" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Antigen-Presenting Cells/immunology ; Antigens, CD/*metabolism ; Antigens, CD28/metabolism ; Antigens, CD86 ; Biotinylation ; CHO Cells ; Calcium/metabolism ; Cricetinae ; Cytoskeleton/*physiology ; Intercellular Adhesion Molecule-1/metabolism ; *Lymphocyte Activation ; Lymphocyte Function-Associated Antigen-1/metabolism ; Membrane Glycoproteins/metabolism ; Mice ; Microspheres ; Molecular Motor Proteins/physiology ; Myosins/physiology ; Phosphatidylinositol 3-Kinases/metabolism ; Receptors, Antigen, T-Cell/immunology ; Signal Transduction ; T-Lymphocytes/*immunology/metabolism/ultrastructure ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Automating a mouse (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sikorski, R -- Peters, R -- New York, N.Y. -- Science. 1998 May 15;280(5366):1101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9616082" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gene Library ; Gene Targeting ; *Genetic Techniques ; Genetic Vectors ; Mice ; Mice, Knockout/*genetics ; Mutagenesis, Insertional ; Sequence Analysis, DNA ; *Stem Cells
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Mismatch repair co-opted by hypermutation (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-21
    Description: Mice homozygous for a disrupted allele of the mismatch repair gene Pms2 have a mutator phenotype. When this allele is crossed into quasi-monoclonal (QM) mice, which have a very limited B cell repertoire, homozygotes have fewer somatic mutations at the immunoglobulin heavy chain and lambda chain loci than do heterozygotes or wild-type QM mice. That is, mismatch repair seems to contribute to somatic hypermutation rather than stifling it. It is suggested that at immunoglobulin loci in hypermutable B cells, mismatched base pairs are "corrected" according to the newly synthesized DNA strand, thereby fixing incipient mutations instead of eliminating them.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cascalho, M -- Wong, J -- Steinberg, C -- Wabl, M -- 1R01 GM37699/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Feb 20;279(5354):1207-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of California, San Francisco, CA 94143-0670, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9469811" target="_blank"〉PubMed〈/a〉
    Keywords: *Adenosine Triphosphatases ; Alleles ; Amino Acid Sequence ; Animals ; B-Lymphocytes/immunology ; Base Composition ; Base Sequence ; Cloning, Molecular ; Crosses, Genetic ; *DNA Repair ; *DNA Repair Enzymes ; *DNA-Binding Proteins ; Female ; Gene Rearrangement ; *Genes, Immunoglobulin ; Heterozygote ; Immunoglobulin Heavy Chains/chemistry/genetics ; Immunoglobulin Variable Region/chemistry/*genetics ; Immunoglobulin lambda-Chains/chemistry/genetics ; Male ; Mice ; Mice, Knockout ; Molecular Sequence Data ; *Mutation ; Proteins/*genetics/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    New potential for human embryonic stem cells (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gearhart, J -- New York, N.Y. -- Science. 1998 Nov 6;282(5391):1061-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Gynecology and Obstetrics, Johns Hopkins Medicine, Baltimore, MD 21287, USA. gearhart@jhmi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9841453" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/*cytology ; *Cell Culture Techniques ; Cell Differentiation ; *Cell Line ; Cell Lineage ; *Embryo Research ; Embryo, Mammalian/*cytology ; Federal Government ; Germ Cells/*cytology ; Government Regulation ; Guidelines as Topic ; Humans ; Major Histocompatibility Complex ; Mice ; Research Support as Topic ; Risk Assessment ; Stem Cell Transplantation ; Stem Cells/*cytology ; Transplantation Immunology ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Expansion of the allelic exclusion principle? (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-04-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chess, A -- New York, N.Y. -- Science. 1998 Mar 27;279(5359):2067-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA. chess@wi.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9537917" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Animals ; CD4-Positive T-Lymphocytes/*immunology ; DNA Replication ; *Gene Expression Regulation ; Genes, Immunoglobulin ; Interleukin-2/*genetics ; Lymphocyte Activation ; Mice ; Polymerase Chain Reaction ; Receptors, Antigen, T-Cell/metabolism ; Signal Transduction ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Impaired locomotion and dopamine signaling in retinoid receptor mutant mice (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-28
    Description: In the adult mouse, single and compound null mutations in the genes for retinoic acid receptor beta and retinoid X receptors beta and gamma resulted in locomotor defects related to dysfunction of the mesolimbic dopamine signaling pathway. Expression of the D1 and D2 receptors for dopamine was reduced in the ventral striatum of mutant mice, and the response of double null mutant mice to cocaine, which affects dopamine signaling in the mesolimbic system, was blunted. Thus, retinoid receptors are involved in the regulation of brain functions, and retinoic acid signaling defects may contribute to pathologies such as Parkinson's disease and schizophrenia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Krezel, W -- Ghyselinck, N -- Samad, T A -- Dupe, V -- Kastner, P -- Borrelli, E -- Chambon, P -- New York, N.Y. -- Science. 1998 Feb 6;279(5352):863-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire, CNRS, INSERM, Universite Louis Pasteur, College de France, Boite Postale 163, 67404 Illkirch Cedex, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9452386" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cocaine/pharmacology ; Corpus Striatum/*metabolism ; Dimerization ; Dopamine/*metabolism ; Locomotion ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; *Motor Activity/drug effects ; Muscle, Skeletal/physiology ; Parkinson Disease/etiology ; Peripheral Nervous System/physiology ; Receptors, Dopamine D1/genetics/metabolism ; Receptors, Dopamine D2/genetics/metabolism ; Receptors, Retinoic Acid/genetics/*physiology ; Retinoid X Receptors ; Schizophrenia/etiology ; *Signal Transduction ; Transcription Factors/genetics/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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    Molecular basis of T cell inactivation by CTLA-4 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-18
    Description: CTLA-4, a negative regulator of T cell function, was found to associate with the T cell receptor (TCR) complex zeta chain in primary T cells. The association of TCRzeta with CTLA-4, reconstituted in 293 transfectants, was enhanced by p56(lck)-induced tyrosine phosphorylation. Coexpression of the CTLA-4-associated tyrosine phosphatase, SHP-2, resulted in dephosphorylation of TCRzeta bound to CTLA-4 and abolished the p56(lck)-inducible TCRzeta-CTLA-4 interaction. Thus, CTLA-4 inhibits TCR signal transduction by binding to TCRzeta and inhibiting tyrosine phosphorylation after T cell activation. These findings have broad implications for the negative regulation of T cell function and T cell tolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, K M -- Chuang, E -- Griffin, M -- Khattri, R -- Hong, D K -- Zhang, W -- Straus, D -- Samelson, L E -- Thompson, C B -- Bluestone, J A -- P01 AI35294-6/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1998 Dec 18;282(5397):2263-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ben May Institute for Cancer Research, and Committee on Immunology, University of Chicago, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9856951" target="_blank"〉PubMed〈/a〉
    Keywords: Abatacept ; Animals ; Antigens, CD ; Antigens, Differentiation/*metabolism ; CTLA-4 Antigen ; Cell Line ; Cells, Cultured ; Humans ; *Immunoconjugates ; Intracellular Signaling Peptides and Proteins ; *Lymphocyte Activation ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck)/genetics/metabolism ; Membrane Proteins/*metabolism ; Mice ; Mice, Inbred BALB C ; Models, Immunological ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein Tyrosine Phosphatase, Non-Receptor Type 11 ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 ; Protein Tyrosine Phosphatases/genetics/metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Recombinant Fusion Proteins/metabolism ; SH2 Domain-Containing Protein Tyrosine Phosphatases ; *Signal Transduction ; T-Lymphocytes/*immunology ; Transfection ; src Homology Domains
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
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    FADD: essential for embryo development and signaling from some, but not all, inducers of apoptosis (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-04-16
    Description: FADD (also known as Mort-1) is a signal transducer downstream of cell death receptor CD95 (also called Fas). CD95, tumor necrosis factor receptor type 1 (TNFR-1), and death receptor 3 (DR3) did not induce apoptosis in FADD-deficient embryonic fibroblasts, whereas DR4, oncogenes E1A and c-myc, and chemotherapeutic agent adriamycin did. Mice with a deletion in the FADD gene did not survive beyond day 11.5 of embryogenesis; these mice showed signs of cardiac failure and abdominal hemorrhage. Chimeric embryos showing a high contribution of FADD null mutant cells to the heart reproduce the phenotype of FADD-deficient mutants. Thus, not only death receptors, but also receptors that couple to developmental programs, may use FADD for signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yeh, W C -- de la Pompa, J L -- McCurrach, M E -- Shu, H B -- Elia, A J -- Shahinian, A -- Ng, M -- Wakeham, A -- Khoo, W -- Mitchell, K -- El-Deiry, W S -- Lowe, S W -- Goeddel, D V -- Mak, T W -- CA13106/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Mar 20;279(5358):1954-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Amgen Institute, University of Toronto, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9506948" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD95/genetics/physiology ; *Apoptosis ; Carrier Proteins/genetics/*physiology ; Cell Transformation, Neoplastic ; Cells, Cultured ; Doxorubicin/pharmacology ; *Embryonic and Fetal Development ; Endothelium, Vascular/embryology ; Fas-Associated Death Domain Protein ; Female ; Gene Expression ; Gene Targeting ; Heart/*embryology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation ; Oncogenes ; Receptors, Tumor Necrosis Factor/genetics/physiology ; Signal Transduction ; Tumor Necrosis Factor-alpha/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
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    Progress in progressive hearing loss (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-04-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steel, K P -- New York, N.Y. -- Science. 1998 Mar 20;279(5358):1870-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council, Institute of Hearing Research, Nottingham NG7 2RD, UK. karen@ihr.mrc.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9537904" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Animals ; Carrier Proteins/genetics/physiology ; Cell Differentiation ; Chromosome Mapping ; Chromosomes, Human, Pair 5/genetics ; Deafness/*genetics ; Dyneins ; Female ; Gene Targeting ; Genes, Dominant ; Hair Cells, Auditory/physiology ; Hearing Loss, Sensorineural/*genetics ; Homeodomain Proteins/*genetics/metabolism ; Humans ; Male ; Mice ; Myosins/genetics/physiology ; Pedigree ; Sequence Deletion ; Transcription Factor Brn-3C ; Transcription Factors/*genetics/metabolism/physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    Regulation of the proinflammatory effects of Fas ligand (CD95L) (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-30
    Description: Fas ligand (CD95L) inhibits T cell function in immune-privileged organs such as the eye and testis, yet in most tissues CD95L expression induces potent inflammatory responses. With a stably transfected colon carcinoma cell line, CT26-CD95L, the molecular basis for these divergent responses was defined. When injected subcutaneously, rejection of CT26-CD95L was caused by neutrophils activated by CD95L. CT26-CD95L survived in the intraocular space because of the presence of transforming growth factor-beta (TGF-beta), which inhibited neutrophil activation. Providing TGF-beta to subcutaneous sites protected against tumor rejection. Thus, these cytokines together generate a microenvironment that promotes immunologic tolerance, which may aid in the amelioration of allograft rejection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, J J -- Sun, Y -- Nabel, G J -- New York, N.Y. -- Science. 1998 Nov 27;282(5394):1714-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Michigan Medical Center, Departments of Internal Medicine and Biological Chemistry, 1150 West Medical Center Drive, 4520 Medical Science Research Building I, Ann Arbor, MI 48109-0650, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9831564" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anterior Chamber ; Apoptosis ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors/metabolism ; Cytotoxicity, Immunologic ; Fas Ligand Protein ; Female ; Graft Rejection ; Humans ; Immune Tolerance ; Inflammation/*immunology ; Jurkat Cells ; Membrane Glycoproteins/*physiology ; Mice ; Mice, Inbred BALB C ; *Mitogen-Activated Protein Kinases ; Neoplasm Transplantation ; Neoplasms, Experimental/*immunology/pathology ; *Neutrophil Activation ; Neutrophils/immunology ; Transfection ; Transforming Growth Factor beta/pharmacology ; Tumor Cells, Cultured ; p38 Mitogen-Activated Protein Kinases
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  • 15
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    BSE and prions: uncertainties about the agent (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-01-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chesebro, B -- New York, N.Y. -- Science. 1998 Jan 2;279(5347):42-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Persistent Virus Diseases, Rocky Mountain Laboratories, Hamilton, MT 59840, USA. bchesebro@nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9441410" target="_blank"〉PubMed〈/a〉
    Keywords: Amyloid/chemistry ; Amyloidosis/metabolism ; Animals ; Cattle ; Creutzfeldt-Jakob Syndrome/epidemiology/*etiology/transmission ; Disease Susceptibility ; Encephalopathy, Bovine Spongiform/epidemiology/*etiology/transmission ; Gene Expression ; Great Britain/epidemiology ; Humans ; Mice ; Mice, Transgenic ; Mutation ; Prion Diseases/*etiology/transmission ; Prions/chemistry/genetics/metabolism/*pathogenicity ; Virus Physiological Phenomena ; Viruses/pathogenicity
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    BRCA1 required for transcription-coupled repair of oxidative DNA damage (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-14
    Description: The breast and ovarian cancer susceptibility gene BRCA1 encodes a zinc finger protein of unknown function. Association of the BRCA1 protein with the DNA repair protein Rad51 and changes in the phosphorylation and cellular localization of the protein after exposure to DNA-damaging agents are consistent with a role for BRCA1 in DNA repair. Here, it is shown that mouse embryonic stem cells deficient in BRCA1 are defective in the ability to carry out transcription-coupled repair of oxidative DNA damage, and are hypersensitive to ionizing radiation and hydrogen peroxide. These results suggest that BRCA1 participates, directly or indirectly, in transcription-coupled repair of oxidative DNA damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gowen, L C -- Avrutskaya, A V -- Latour, A M -- Koller, B H -- Leadon, S A -- CA40453/CA/NCI NIH HHS/ -- CA70490/CA/NCI NIH HHS/ -- IP50CA58223/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Aug 14;281(5379):1009-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Curriculum in Genetics and Molecular Biology and Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9703501" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; BRCA1 Protein/genetics/*physiology ; Cell Line ; DNA Damage ; *DNA Repair ; Hydrogen Peroxide ; Mice ; Oxidation-Reduction ; Stem Cells ; Thymine/analogs & derivatives/immunology/metabolism ; Transcription, Genetic ; Ultraviolet Rays
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  • 17
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    Molecular mimicry by herpes simplex virus-type 1: autoimmune disease after viral infection (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-21
    Description: Viral infection is sometimes associated with the initiation or exacerbation of autoimmune disease, although the underlying mechanisms remain unclear. One proposed mechanism is that viral determinants that mimic host antigens trigger self-reactive T cell clones to destroy host tissue. An epitope expressed by a coat protein of herpes simplex virus-type 1 (HSV-1) KOS strain has now been shown to be recognized by autoreactive T cells that target corneal antigens in a murine model of autoimmune herpes stromal keratitis. Mutant HSV-1 viruses that lacked this epitope did not induce autoimmune disease. Thus, expression of molecular mimics can influence the development of autoimmune disease after viral infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhao, Z S -- Granucci, F -- Yeh, L -- Schaffer, P A -- Cantor, H -- AI 37562/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1998 Feb 27;279(5355):1344-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, and Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9478893" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Amino Acid Sequence ; Animals ; Autoantigens/immunology ; Autoimmune Diseases/*immunology ; CD4-Positive T-Lymphocytes/immunology ; Capsid/chemistry/genetics/*immunology ; *Capsid Proteins ; Cornea/*immunology ; Epitopes ; Eye Proteins/immunology ; Herpesvirus 1, Human/*immunology ; Keratitis, Herpetic/*immunology ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Mice, SCID ; *Molecular Mimicry ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Oligopeptides/immunology ; Viral Proteins
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
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    More deafness genes (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steel, K P -- Brown, S D -- New York, N.Y. -- Science. 1998 May 29;280(5368):1403.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council, Institute of Hearing Research, University Park, Nottingham NG7 2RD, UK. karen@ihr.mrc.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9634418" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/physiology ; Animals ; Cilia/physiology ; Deafness/*genetics ; Dyneins ; Extracellular Matrix Proteins/*genetics/physiology ; GPI-Linked Proteins ; Hair Cells, Auditory/physiology/ultrastructure ; Hearing ; Humans ; Membrane Glycoproteins/*genetics/physiology ; Mice ; Mice, Mutant Strains ; Mutation ; Myosin Heavy Chains/genetics/physiology ; Myosins/*genetics/physiology ; Tectorial Membrane/physiology
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  • 19
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    Targeting the receptor-Gq interface to inhibit in vivo pressure overload myocardial hypertrophy (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-05-09
    Description: Hormones and neurotransmitters may mediate common responses through receptors that couple to the same class of heterotrimeric guanine nucleotide-binding (G) protein. For example, several receptors that couple to Gq class proteins can induce cardiomyocyte hypertrophy. Class-specific inhibition of Gq-mediated signaling was produced in the hearts of transgenic mice by targeted expression of a carboxyl-terminal peptide of the alpha subunit Galphaq. When pressure overload was surgically induced, the transgenic mice developed significantly less ventricular hypertrophy than control animals. The data demonstrate the role of myocardial Gq in the initiation of myocardial hypertrophy and indicate a possible strategy for preventing pathophysiological signaling by simultaneously blocking multiple receptors coupled to Gq.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akhter, S A -- Luttrell, L M -- Rockman, H A -- Iaccarino, G -- Lefkowitz, R J -- Koch, W J -- HL-03041/HL/NHLBI NIH HHS/ -- HL-09436/HL/NHLBI NIH HHS/ -- HL-16037/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Apr 24;280(5363):574-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9554846" target="_blank"〉PubMed〈/a〉
    Keywords: Angiotensin II/pharmacology ; Animals ; Atrial Natriuretic Factor/genetics ; COS Cells ; Diglycerides/metabolism ; Enzyme Activation ; GTP-Binding Proteins/antagonists & inhibitors/genetics/*metabolism ; Gene Expression Regulation ; Gene Targeting ; Hypertrophy, Left Ventricular/*metabolism/prevention & control ; Inositol Phosphates/metabolism ; Mice ; Mice, Transgenic ; Mitogen-Activated Protein Kinase 1/metabolism ; Myocardium/*metabolism ; Peptide Fragments/genetics/metabolism ; Phenylephrine/pharmacology ; Receptors, Adrenergic, alpha/*metabolism ; Signal Transduction ; Transfection ; Transgenes ; Ventricular Pressure
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  • 20
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    Control of neonatal tolerance to tissue antigens by peripheral T cell trafficking (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-13
    Description: Self tolerance is acquired by the developing immune system. As reported here, particular properties of the neonatal tissue contribute to this process. Neonatal skin, but not adult skin, was accessible for naive CD8 T cells. In mouse bone marrow chimeras generated at different ages, recent thymic emigrants were tolerized to a skin-expressed major histocompatibility complex class I antigen only during a neonatal period but not during adulthood. Blockade of T cell migration neonatally prevented tolerance induction. Thus, T cell trafficking through nonlymphoid tissues in the neonate is crucial for the establishment of self tolerance to sessile, skin-expressed antigens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alferink, J -- Tafuri, A -- Vestweber, D -- Hallmann, R -- Hammerling, G J -- Arnold, B -- New York, N.Y. -- Science. 1998 Nov 13;282(5392):1338-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tumor Immunology Program, German Cancer Research Center, 69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9812902" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Antigen Presentation ; Bone Marrow Transplantation ; CD8-Positive T-Lymphocytes/*immunology ; Cell Movement ; Graft Rejection ; H-2 Antigens/*immunology ; Keratinocytes/immunology ; Mice ; Mice, Transgenic ; Neoplasm Transplantation ; Neoplasms, Experimental/immunology ; Self Tolerance/*immunology ; Skin/*immunology ; Skin Transplantation ; T-Lymphocytes/*immunology ; Thymus Gland/immunology ; Transplantation Chimera
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 21
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    Reovirus therapy of tumors with activated Ras pathway (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-13
    Description: Human reovirus requires an activated Ras signaling pathway for infection of cultured cells. To investigate whether this property can be exploited for cancer therapy, severe combined immune deficient mice bearing tumors established from v-erbB-transformed murine NIH 3T3 cells or human U87 glioblastoma cells were treated with the virus. A single intratumoral injection of virus resulted in regression of tumors in 65 to 80 percent of the mice. Treatment of immune-competent C3H mice bearing tumors established from ras-transformed C3H-10T1/2 cells also resulted in tumor regression, although a series of injections were required. These results suggest that, with further work, reovirus may have applicability in the treatment of cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coffey, M C -- Strong, J E -- Forsyth, P A -- Lee, P W -- New York, N.Y. -- Science. 1998 Nov 13;282(5392):1332-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Biology Research Group and Department of Microbiology and Infectious Diseases, University of Calgary Health Science Centre, Calgary, Alberta, T2N 4N1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9812900" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Antibodies, Viral/immunology ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Line, Transformed ; Genes, erbB ; *Genes, ras ; Humans ; Male ; Mammalian orthoreovirus 3/immunology/*physiology ; Mice ; Mice, Inbred C3H ; Mice, SCID ; Neoplasm Transplantation ; Neoplasms, Experimental/metabolism/pathology/*therapy/virology ; Signal Transduction ; Tumor Cells, Cultured ; Virus Replication ; ras Proteins/*metabolism
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  • 22
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    Bone marrow cells may provide muscle power (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1998 Mar 6;279(5356):1456.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9508720" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Cells/cytology/*physiology ; Bone Marrow Transplantation ; Cell Differentiation ; Humans ; Mice ; Mice, Transgenic ; Muscle, Skeletal/cytology/pathology/*physiology ; Muscular Dystrophies/pathology/*therapy ; Muscular Dystrophy, Animal/pathology/therapy ; *Regeneration ; Stem Cells/*physiology ; Stromal Cells/physiology
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  • 23
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    Cancer treatment by targeted drug delivery to tumor vasculature in a mouse model (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-07
    Description: In vivo selection of phage display libraries was used to isolate peptides that home specifically to tumor blood vessels. When coupled to the anticancer drug doxorubicin, two of these peptides-one containing an alphav integrin-binding Arg-Gly-Asp motif and the other an Asn-Gly-Arg motif-enhanced the efficacy of the drug against human breast cancer xenografts in nude mice and also reduced its toxicity. These results indicate that it may be possible to develop targeted chemotherapy strategies that are based on selective expression of receptors in tumor vasculature.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arap, W -- Pasqualini, R -- Ruoslahti, E -- CA30199/CA/NCI NIH HHS/ -- CA62042/CA/NCI NIH HHS/ -- CA74238-01/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Jan 16;279(5349):377-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research Center, The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9430587" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/metabolism ; Antineoplastic Agents/*administration & dosage/therapeutic use/toxicity ; Bacteriophages ; Coronary Vessels/drug effects ; Doxorubicin/*administration & dosage/*analogs & ; derivatives/metabolism/therapeutic use/toxicity ; *Drug Carriers ; Heart/drug effects ; Humans ; Integrin alphaV ; Integrins/metabolism ; Liver/blood supply/drug effects ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Neoplasms, Experimental/*blood supply/*drug therapy/pathology ; Oligopeptides/*administration & dosage/metabolism/therapeutic use/toxicity ; Peptide Library ; Random Allocation ; Transplantation, Heterologous ; Tumor Cells, Cultured
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  • 24
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    An essential role for ectodomain shedding in mammalian development (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-13
    Description: The ectodomains of numerous proteins are released from cells by proteolysis to yield soluble intercellular regulators. The responsible protease, tumor necrosis factor-alpha converting enzyme (TACE), has been identified only in the case when tumor necrosis factor-alpha (TNFalpha) is released. Analyses of cells lacking this metalloproteinase-disintegrin revealed an expanded role for TACE in the processing of other cell surface proteins, including a TNF receptor, the L-selectin adhesion molecule, and transforming growth factor-alpha (TGFalpha). The phenotype of mice lacking TACE suggests an essential role for soluble TGFalpha in normal development and emphasizes the importance of protein ectodomain shedding in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peschon, J J -- Slack, J L -- Reddy, P -- Stocking, K L -- Sunnarborg, S W -- Lee, D C -- Russell, W E -- Castner, B J -- Johnson, R S -- Fitzner, J N -- Boyce, R W -- Nelson, N -- Kozlosky, C J -- Wolfson, M F -- Rauch, C T -- Cerretti, D P -- Paxton, R J -- March, C J -- Black, R A -- CA43793/CA/NCI NIH HHS/ -- DK53804/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1998 Nov 13;282(5392):1281-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunex Corporation, Seattle, WA 98101, USA. peschon@immunex.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9812885" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins ; Amino Acid Sequence ; Animals ; Catalytic Domain ; Cell Membrane/*metabolism ; Cells, Cultured ; Crosses, Genetic ; *Embryonic and Fetal Development ; L-Selectin/metabolism ; Ligands ; Membrane Proteins/*metabolism ; Metalloendopeptidases/chemistry/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; Phenotype ; Protein Processing, Post-Translational ; Receptors, Tumor Necrosis Factor/metabolism ; Transforming Growth Factor alpha/metabolism ; Tumor Necrosis Factor-alpha/*metabolism
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  • 25
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    Increased vascularization in mice overexpressing angiopoietin-1 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-10-17
    Description: The angiopoietins and members of the vascular endothelial growth factor (VEGF) family are the only growth factors thought to be largely specific for vascular endothelial cells. Targeted gene inactivation studies in mice have shown that VEGF is necessary for the early stages of vascular development and that angiopoietin-1 is required for the later stages of vascular remodeling. Here it is shown that transgenic overexpression of angiopoietin-1 in the skin of mice produces larger, more numerous, and more highly branched vessels. These results raise the possibility that angiopoietins can be used, alone or in combination with VEGF, to promote therapeutic angiogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suri, C -- McClain, J -- Thurston, G -- McDonald, D M -- Zhou, H -- Oldmixon, E H -- Sato, T N -- Yancopoulos, G D -- HL-24136/HL/NHLBI NIH HHS/ -- HL-59157/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1998 Oct 16;282(5388):468-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals, 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9774272" target="_blank"〉PubMed〈/a〉
    Keywords: Angiopoietin-1 ; Animals ; Capillaries/anatomy & histology/ultrastructure ; Endothelial Growth Factors/genetics/physiology ; Endothelium, Vascular/ultrastructure ; Gene Expression ; Keratinocytes/metabolism ; Lymphokines/genetics/physiology ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Mice, Transgenic ; *Neovascularization, Physiologic ; Skin/*blood supply/metabolism ; Transgenes ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors ; Venules/anatomy & histology/ultrastructure
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 26
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    From mice to maize (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lawler, C -- Erbisch, F -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):33-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9917260" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biotechnology ; Mice ; Mice, Transgenic ; *Patents as Topic ; Plants, Genetically Modified/*genetics ; United States
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  • 27
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    New model for hereditary breast cancer (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hagmann, M -- New York, N.Y. -- Science. 1999 Apr 30;284(5415):723, 725.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10336390" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Breast Neoplasms/*genetics/pathology ; *Disease Models, Animal ; Female ; *Genes, BRCA1 ; Genes, p53 ; Humans ; Mammary Glands, Animal/pathology ; Mammary Neoplasms, Animal/*genetics/pathology ; Mice ; Mice, Knockout ; Mice, Transgenic ; Mutation
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  • 28
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    Stem cells. Rat spinal cord function partially restored (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1826-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610569" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/cytology ; Cell Differentiation ; Cell Survival ; Embryo, Mammalian ; Mice ; Neurons/cytology ; Oligodendroglia/cytology ; Rats ; Spinal Cord/cytology/*physiology ; Spinal Cord Injuries/*therapy ; *Stem Cell Transplantation ; Stem Cells/cytology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Regulation of intestinal alpha-defensin activation by the metalloproteinase matrilysin in innate host defense (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-03
    Description: Precursors of alpha-defensin peptides require activation for bactericidal activity. In mouse small intestine, matrilysin colocalized with alpha-defensins (cryptdins) in Paneth cell granules, and in vitro it cleaved the pro segment from cryptdin precursors. Matrilysin-deficient (MAT-/-) mice lacked mature cryptdins and accumulated precursor molecules. Intestinal peptide preparations from MAT-/- mice had decreased antimicrobial activity. Orally administered bacteria survived in greater numbers and were more virulent in MAT-/- mice than in MAT+/+ mice. Thus, matrilysin functions in intestinal mucosal defense by regulating the activity of defensins, which may be a common role for this metalloproteinase in its numerous epithelial sites of expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, C L -- Ouellette, A J -- Satchell, D P -- Ayabe, T -- Lopez-Boado, Y S -- Stratman, J L -- Hultgren, S J -- Matrisian, L M -- Parks, W C -- New York, N.Y. -- Science. 1999 Oct 1;286(5437):113-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Division of Allergy and Pulmonary Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA. wilson_c@kids.wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10506557" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Catalysis ; Cytoplasmic Granules/enzymology ; Escherichia coli/growth & development ; Escherichia coli Infections/immunology/microbiology ; Female ; Humans ; *Immunity, Innate ; *Immunity, Mucosal ; Intestinal Mucosa/enzymology/immunology/microbiology ; Intestine, Small/enzymology/*immunology/microbiology ; Male ; Matrix Metalloproteinase 7 ; Metalloendopeptidases/genetics/*metabolism ; Mice ; Molecular Sequence Data ; Paneth Cells/enzymology ; Protein Precursors/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Salmonella typhimurium/growth & development/pathogenicity ; Tissue Extracts/pharmacology
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    Perspectives: protein structure. Class-conscious TCR? (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, I A -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1867-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Skaggs Institute for Chemical Biology, The Scripps Research Institute, La Jolla, CA 92037, USA. wilson@scripps.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610577" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/*chemistry/immunology/metabolism ; Binding Sites ; CD4-Positive T-Lymphocytes/immunology/metabolism ; CD8-Positive T-Lymphocytes/immunology/metabolism ; Crystallography, X-Ray ; Histocompatibility Antigens Class I/chemistry/immunology/metabolism ; Histocompatibility Antigens Class II/*chemistry/immunology/metabolism ; Mice ; Models, Molecular ; Peptides/chemistry/immunology/metabolism ; Protein Binding ; Protein Conformation ; Protein Structure, Secondary ; Receptors, Antigen, T-Cell, alpha-beta/*chemistry/immunology/metabolism
    Print ISSN: 0036-8075
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    Control of early viral and bacterial distribution and disease by natural antibodies (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-11
    Description: Natural antibodies are often dismissed from immunological analysis as "background," but they may play an important role in conferring immunity against infections. In antibody-free mice infected with various viruses or with Listeria monocytogenes, viral or bacterial titers in peripheral organs, including the kidney and brain, were 10 to 100 times greater than in antibody-competent mice (and enhanced their susceptibility to some infections), and titers in secondary lymphoid organs were 10 to 100 times lower than in antibody-competent mice. Thus, natural antibodies play a crucial role by preventing pathogen dissemination to vital organs and by improving immunogenicity through enhanced antigen-trapping in secondary lymphoid organs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ochsenbein, A F -- Fehr, T -- Lutz, C -- Suter, M -- Brombacher, F -- Hengartner, H -- Zinkernagel, R M -- New York, N.Y. -- Science. 1999 Dec 10;286(5447):2156-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Experimental Immunology, University Hospital Zurich, Schmelzbergstrasse 12, 8091 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10591647" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Bacterial/blood/immunology ; Antibodies, Viral/blood/immunology ; Bacterial Infections/*immunology/microbiology ; Germ-Free Life ; *Immunity, Innate ; Immunoglobulin M/blood/*immunology ; Kidney/microbiology/virology ; Listeria monocytogenes/immunology/physiology ; Listeriosis/immunology ; Lymphocytic choriomeningitis virus/immunology/physiology ; Lymphoid Tissue/immunology/microbiology/virology ; Mice ; Mice, Inbred C57BL ; Neutralization Tests ; Rhabdoviridae Infections/immunology/virology ; Specific Pathogen-Free Organisms ; Spleen/microbiology/virology ; Vaccinia virus/immunology/physiology ; Vesicular stomatitis Indiana virus/immunology/physiology ; Virus Diseases/*immunology/virology ; Virus Replication
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    Congenital nephrotic syndrome in mice lacking CD2-associated protein (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-09
    Description: CD2-associated protein (CD2AP) is an 80-kilodalton protein that is critical for stabilizing contacts between T cells and antigen-presenting cells. In CD2AP-deficient mice, immune function was compromised, but the mice died at 6 to 7 weeks of age from renal failure. In the kidney, CD2AP was expressed primarily in glomerular epithelial cells. Knockout mice exhibited defects in epithelial cell foot processes, accompanied by mesangial cell hyperplasia and extracellular matrix deposition. Supporting a role for CD2AP in the specialized cell junction known as the slit diaphragm, CD2AP associated with nephrin, the primary component of the slit diaphragm.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shih, N Y -- Li, J -- Karpitskii, V -- Nguyen, A -- Dustin, M L -- Kanagawa, O -- Miner, J H -- Shaw, A S -- New York, N.Y. -- Science. 1999 Oct 8;286(5438):312-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Immunology and Department of Pathology, Washington University, Saint Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10514378" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Basement Membrane/ultrastructure ; Cytoskeletal Proteins ; Epithelial Cells/metabolism/ultrastructure ; Extracellular Matrix Proteins/metabolism ; Glomerular Mesangium/metabolism/ultrastructure ; Intercellular Junctions/metabolism/ultrastructure ; Kidney Glomerulus/blood supply/*metabolism/*ultrastructure ; Lymphocyte Activation ; Membrane Proteins ; Mice ; Mice, Knockout ; Microscopy, Electron ; Nephrotic Syndrome/*congenital/genetics/metabolism/pathology ; Proteins/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; T-Lymphocytes/immunology
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    Calmodulin dependence of presynaptic metabotropic glutamate receptor signaling (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-05
    Description: Glutamatergic neurotransmission is controlled by presynaptic metabotropic glutamate receptors (mGluRs). A subdomain in the intracellular carboxyl-terminal tail of group III mGluRs binds calmodulin and heterotrimeric guanosine triphosphate-binding protein (G protein) betagamma subunits in a mutually exclusive manner. Mutations interfering with calmodulin binding and calmodulin antagonists inhibit G protein-mediated modulation of ionic currents by mGluR 7. Calmodulin antagonists also prevent inhibition of excitatory neurotransmission via presynaptic mGluRs. These results reveal a novel mechanism of presynaptic modulation in which Ca(2+)-calmodulin is required to release G protein betagamma subunits from the C-tail of group III mGluRs in order to mediate glutamatergic autoinhibition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Connor, V -- El Far, O -- Bofill-Cardona, E -- Nanoff, C -- Freissmuth, M -- Karschin, A -- Airas, J M -- Betz, H -- Boehm, S -- New York, N.Y. -- Science. 1999 Nov 5;286(5442):1180-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurochemistry, Max Planck Institute for Brain Research, Deutschordenstrasse 46, 60528 Frankfurt, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10550060" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium/metabolism ; Calmodulin/antagonists & inhibitors/*metabolism ; Cells, Cultured ; Dimerization ; G Protein-Coupled Inwardly-Rectifying Potassium Channels ; GTP-Binding Proteins/*metabolism ; Glutamic Acid/*metabolism ; Hippocampus/cytology/metabolism ; Humans ; Mice ; Molecular Sequence Data ; Neurons/metabolism ; Potassium Channels/metabolism ; *Potassium Channels, Inwardly Rectifying ; Presynaptic Terminals/metabolism ; Propionates/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Metabotropic Glutamate/antagonists & inhibitors/*metabolism ; Recombinant Fusion Proteins/metabolism ; Sesterterpenes ; Signal Transduction ; Swine ; *Synaptic Transmission ; Terpenes/pharmacology
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    Chlamydia infections and heart disease linked through antigenic mimicry (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-26
    Description: Chlamydia infections are epidemiologically linked to human heart disease. A peptide from the murine heart muscle-specific alpha myosin heavy chain that has sequence homology to the 60-kilodalton cysteine-rich outer membrane proteins of Chlamydia pneumoniae, C. psittaci, and C. trachomatis was shown to induce autoimmune inflammatory heart disease in mice. Injection of the homologous Chlamydia peptides into mice also induced perivascular inflammation, fibrotic changes, and blood vessel occlusion in the heart, as well as triggering T and B cell reactivity to the homologous endogenous heart muscle-specific peptide. Chlamydia DNA functioned as an adjuvant in the triggering of peptide-induced inflammatory heart disease. Infection with C. trachomatis led to the production of autoantibodies to heart muscle-specific epitopes. Thus, Chlamydia-mediated heart disease is induced by antigenic mimicry of a heart muscle-specific protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bachmaier, K -- Neu, N -- de la Maza, L M -- Pal, S -- Hessel, A -- Penninger, J M -- New York, N.Y. -- Science. 1999 Feb 26;283(5406):1335-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Amgen Institute, Ontario Cancer Institute, Departments of Medical Biophysics and Immunology, University of Toronto, Toronto, Ontario M5G 2C1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10037605" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Amino Acid Sequence ; Animals ; Antigens, Bacterial/chemistry/immunology ; Autoantibodies/biosynthesis ; Autoimmune Diseases/immunology/*microbiology/pathology ; B-Lymphocytes/immunology ; Bacterial Outer Membrane Proteins/chemistry/*immunology ; CD4-Positive T-Lymphocytes/immunology ; Chlamydia/*immunology ; Chlamydia Infections/complications/*immunology ; Chlamydia trachomatis/immunology ; CpG Islands ; Humans ; Immunization ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; *Molecular Mimicry ; Molecular Sequence Data ; Myocarditis/immunology/*microbiology/pathology ; Myocardium/immunology/pathology ; Myosin Heavy Chains/chemistry/*immunology ; Oligodeoxyribonucleotides/immunology ; Sequence Homology, Amino Acid
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    Defective angiogenesis in mice lacking endoglin (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-29
    Description: Endoglin is a transforming growth factor-beta (TGF-beta) binding protein expressed on the surface of endothelial cells. Loss-of-function mutations in the human endoglin gene ENG cause hereditary hemorrhagic telangiectasia (HHT1), a disease characterized by vascular malformations. Here it is shown that by gestational day 11.5, mice lacking endoglin die from defective vascular development. However, in contrast to mice lacking TGF-beta, vasculogenesis was unaffected. Loss of endoglin caused poor vascular smooth muscle development and arrested endothelial remodeling. These results demonstrate that endoglin is essential for angiogenesis and suggest a pathogenic mechanism for HHT1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, D Y -- Sorensen, L K -- Brooke, B S -- Urness, L D -- Davis, E C -- Taylor, D G -- Boak, B B -- Wendel, D P -- K08 HL03490-03/HL/NHLBI NIH HHS/ -- T35 HL07744-06/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 May 28;284(5419):1534-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Human Molecular Biology and Genetics, Department of Human Genetics, Howard Hughes Medical Institute, University of Utah, Salt Lake City, UT 84112-5330, USA. dean.li@hci.utah.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10348742" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD ; Antigens, CD31/analysis ; Blood Vessels/cytology/*embryology/metabolism ; Cell Differentiation ; Crosses, Genetic ; Endothelium, Vascular/cytology/*embryology/metabolism ; Female ; Gene Targeting ; In Situ Hybridization ; Male ; Mice ; Mice, Inbred C57BL ; Microscopy, Electron ; Muscle, Smooth, Vascular/cytology/*embryology ; *Neovascularization, Physiologic ; Receptors, Cell Surface ; Signal Transduction ; Transforming Growth Factor beta/metabolism ; Vascular Cell Adhesion Molecule-1/genetics/*physiology ; Yolk Sac/ultrastructure
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    Prevention of graft versus host disease by inactivation of host antigen-presenting cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-20
    Description: Graft versus host disease, an alloimmune attack on host tissues mounted by donor T cells, is the most important toxicity of allogeneic bone marrow transplantation. The mechanism by which allogeneic T cells are initially stimulated is unknown. In a murine allogeneic bone marrow transplantation model it was found that, despite the presence of numerous donor antigen-presenting cells, only host-derived antigen-presenting cells initiated graft versus host disease. Thus, strategies for preventing graft versus host disease could be developed that are based on inactivating host antigen-presenting cells. Such strategies could expand the safety and application of allogeneic bone marrow transplantation in treatment of common genetic and neoplastic diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shlomchik, W D -- Couzens, M S -- Tang, C B -- McNiff, J -- Robert, M E -- Liu, J -- Shlomchik, M J -- Emerson, S G -- P50HL-54516/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 16;285(5426):412-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10411505" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/*immunology ; Bone Marrow Transplantation/adverse effects/*immunology ; CD8-Positive T-Lymphocytes/*immunology ; Dendritic Cells/immunology ; Graft vs Host Disease/immunology/*prevention & control ; H-2 Antigens/immunology ; Lymph Nodes/immunology ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Mice, Knockout ; Minor Histocompatibility Antigens/immunology ; Spleen/immunology ; Transplantation Chimera
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    Regulation of maternal behavior and offspring growth by paternally expressed Peg3 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-09
    Description: Imprinted genes display parent-of-origin-dependent monoallelic expression that apparently regulates complex mammalian traits, including growth and behavior. The Peg3 gene is expressed in embryos and the adult brain from the paternal allele only. A mutation in the Peg3 gene resulted in growth retardation, as well as a striking impairment of maternal behavior that frequently resulted in death of the offspring. This result may be partly due to defective neuronal connectivity, as well as reduced oxytocin neurons in the hypothalamus, because mutant mothers were deficient in milk ejection. This study provides further insights on the evolution of epigenetic regulation of imprinted gene dosage in modulating mammalian growth and behavior.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, L -- Keverne, E B -- Aparicio, S A -- Ishino, F -- Barton, S C -- Surani, M A -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):330-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome CRC Institute of Cancer and Developmental Biology, and Physiological Laboratory, University of Cambridge, Tennis Court Road, Cambridge CB2 1QR, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10195900" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Brain/metabolism ; Crosses, Genetic ; Female ; Gene Expression ; Gene Targeting ; *Genomic Imprinting ; *Growth ; Hypothalamus/cytology/metabolism ; Kruppel-Like Transcription Factors ; Lactation ; Male ; *Maternal Behavior ; Mice ; Mutation ; Neural Pathways ; Neurons/metabolism ; Oxytocin/metabolism ; Phenotype ; *Protein Kinases ; Proteins/genetics/*physiology ; *Transcription Factors ; *Weight Gain
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    A role for DNA-PK in retroviral DNA integration (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-24
    Description: Retroviral DNA integration is catalyzed by the viral protein integrase. Here, it is shown that DNA-dependent protein kinase (DNA-PK), a host cell protein, also participates in the reaction. DNA-PK-deficient murine scid cells infected with three different retroviruses showed a substantial reduction in retroviral DNA integration and died by apoptosis. Scid cell killing was not observed after infection with an integrase-defective virus, suggesting that abortive integration is the trigger for death in these DNA repair-deficient cells. These results suggest that the initial events in retroviral integration are detected as DNA damage by the host cell and that completion of the integration process requires the DNA-PK-mediated repair pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Daniel, R -- Katz, R A -- Skalka, A M -- AI40721/AI/NIAID NIH HHS/ -- AI40835/AI/NIAID NIH HHS/ -- CA71515/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):644-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cancer Research, Fox Chase Cancer Center, 7701 Burholme Avenue, Philadelphia, PA 19111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10213687" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; CHO Cells ; Cell Survival ; Cells, Cultured ; Cricetinae ; DNA Damage ; *DNA Repair ; DNA, Viral/*genetics/metabolism ; DNA-Activated Protein Kinase ; *DNA-Binding Proteins ; Genetic Vectors ; HIV-1/genetics ; Integrases/genetics/metabolism ; Mice ; Mutation ; Protein-Serine-Threonine Kinases/*metabolism ; Retroviridae/*genetics/physiology ; *Virus Integration ; Virus Replication
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    An activating immunoreceptor complex formed by NKG2D and DAP10 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: Many immune receptors are composed of separate ligand-binding and signal-transducing subunits. In natural killer (NK) and T cells, DAP10 was identified as a cell surface adaptor protein in an activating receptor complex with NKG2D, a receptor for the stress-inducible and tumor-associated major histocompatibility complex molecule MICA. Within the DAP10 cytoplasmic domain, an Src homology 2 (SH2) domain-binding site was capable of recruiting the p85 subunit of the phosphatidylinositol 3-kinase (PI 3-kinase), providing for NKG2D-dependent signal transduction. Thus, NKG2D-DAP10 receptor complexes may activate NK and T cell responses against MICA-bearing tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, J -- Song, Y -- Bakker, A B -- Bauer, S -- Spies, T -- Lanier, L L -- Phillips, J H -- AI30581/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):730-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉DNAX Research Institute, 901 California Avenue, Palo Alto, CA 94304, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426994" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Cell Line ; Cytotoxicity, Immunologic ; Humans ; Killer Cells, Natural/*immunology/metabolism ; Ligands ; *Lymphocyte Activation ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Molecular Sequence Data ; NK Cell Lectin-Like Receptor Subfamily K ; Neoplasms/immunology ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Phosphotyrosine/metabolism ; Receptors, Immunologic/chemistry/genetics/*metabolism ; Receptors, Natural Killer Cell ; Signal Transduction ; T-Lymphocytes/*immunology/metabolism ; Tumor Cells, Cultured ; src Homology Domains
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    Positive selection of natural autoreactive B cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-03
    Description: Lymphocyte development is critically influenced by self-antigens. T cells are subject to both positive and negative selection, depending on their degree of self-reactivity. Although B cells are subject to negative selection, it has been difficult to test whether self-antigen plays any positive role in B cell development. A murine model system of naturally generated autoreactive B cells with a germ line gene-encoded specificity for the Thy-1 (CD90) glycoprotein was developed, in which the presence of self-antigen promotes B cell accumulation and serum autoantibody secretion. Thus, B cells can be subject to positive selection, generated, and maintained on the basis of their autoreactivity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hayakawa, K -- Asano, M -- Shinton, S A -- Gui, M -- Allman, D -- Stewart, C L -- Silver, J -- Hardy, R R -- New York, N.Y. -- Science. 1999 Jul 2;285(5424):113-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cancer Research, Fox Chase Cancer Center, 7701 Burholme Avenue, Philadelphia, PA 19111, USA. K_Hayakawa@fccc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10390361" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/immunology ; Animals ; Antigens, CD5/analysis ; Antigens, Thy-1/*immunology ; Autoantibodies/*biosynthesis/blood/immunology ; Autoantigens/*immunology ; B-Lymphocyte Subsets/*immunology ; Genes, Immunoglobulin ; Hybridomas ; Immunity, Innate ; Immunologic Surveillance ; Mice ; Mice, SCID ; Mice, Transgenic ; Receptors, Antigen, B-Cell/immunology ; Signal Transduction ; T-Lymphocytes/immunology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Severe liver degeneration in mice lacking the IkappaB kinase 2 gene (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-09
    Description: Phosphorylation of inhibitor of kappa B (IkappaB) proteins is an important step in the activation of the transcription nuclear factor kappa B (NF-kappaB) and requires two IkappaB kinases, IKK1 (IKKalpha) and IKK2 (IKKbeta). Mice that are devoid of the IKK2 gene had extensive liver damage from apoptosis and died as embryos, but these mice could be rescued by the inactivation of the gene encoding tumor necrosis factor receptor 1. Mouse embryonic fibroblast cells that were isolated from IKK2-/- embryos showed a marked reduction in tumor necrosis factor-alpha (TNF-alpha)- and interleukin-1alpha-induced NF-kappaB activity and an enhanced apoptosis in response to TNF-alpha. IKK1 associated with NF-kappaB essential modulator (IKKgamma/IKKAP1), another component of the IKK complex. These results show that IKK2 is essential for mouse development and cannot be substituted with IKK1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Q -- Van Antwerp, D -- Mercurio, F -- Lee, K F -- Verma, I M -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):321-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salk Institute, La Jolla, CA 92037, USA. Signal Pharmaceuticals, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10195897" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Line ; DNA-Binding Proteins/metabolism ; Embryonic and Fetal Development ; Gene Targeting ; I-kappa B Kinase ; I-kappa B Proteins ; Interleukin-1/pharmacology ; Liver/cytology/*embryology ; Mice ; NF-kappa B/metabolism ; Phosphorylation ; Polymerase Chain Reaction ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Receptors, Tumor Necrosis Factor/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Sequence Deletion ; Signal Transduction ; Transcription Factor RelA ; Transcription Factors/metabolism ; Tumor Necrosis Factor-alpha/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 42
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    Linear differentiation of cytotoxic effectors into memory T lymphocytes (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-12
    Description: A central question in immunology is the origin of long-lived T cell memory that confers protection against recurrent infection. The differentiation of naive T cell receptor transgenic CD8+ cells into effector cytotoxic T lymphocytes (CTLs) and memory CD8+ cells was studied. Memory CD8+ cells that were generated after strong antigenic stimulation were the progeny of cytotoxic effectors and retained antigen-specific cytolytic activity 10 weeks after adoptive transfer to antigen-free recipient mice. Thus, potential vaccines based on CTL memory will require the differentiation of naive cells into post-effector memory T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Opferman, J T -- Ober, B T -- Ashton-Rickardt, P G -- 5T32 AI07090/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Mar 12;283(5408):1745-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Committee on Immunology, Department of Pathology, Committee on Developmental Biology, The University of Chicago, Gwen Knapp Center for Lupus and Immunology Research, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10073942" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Apoptosis ; CD8-Positive T-Lymphocytes/*cytology/*immunology ; Cell Differentiation ; Cell Division ; Cell Lineage ; Cells, Cultured ; Cytotoxicity, Immunologic ; Dose-Response Relationship, Immunologic ; H-Y Antigen/immunology ; *Immunologic Memory ; Lymphocyte Activation ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Transgenic ; Perforin ; Pore Forming Cytotoxic Proteins ; T-Lymphocyte Subsets/cytology/*immunology ; T-Lymphocytes, Cytotoxic/cytology/*immunology
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    Cell surgery (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sikorski, R -- Peters, R -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1498.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610553" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Cells/*cytology ; Cell Differentiation ; Cell Separation ; Dystrophin/biosynthesis ; Female ; *Hematopoietic Stem Cell Transplantation ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred mdx ; Muscle, Skeletal/*cytology/metabolism ; *Stem Cell Transplantation ; Stem Cells/*cytology
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  • 44
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    Antiangiogenic activity of the cleaved conformation of the serpin antithrombin (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-18
    Description: Antithrombin, a member of the serpin family, functions as an inhibitor of thrombin and other enzymes. Cleavage of the carboxyl-terminal loop of antithrombin induces a conformational change in the molecule. Here it is shown that the cleaved conformation of antithrombin has potent antiangiogenic and antitumor activity in mouse models. The latent form of intact antithrombin, which is similar in conformation to the cleaved molecule, also inhibited angiogenesis and tumor growth. These data provide further evidence that the clotting and fibrinolytic pathways are directly involved in the regulation of angiogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Reilly, M S -- Pirie-Shepherd, S -- Lane, W S -- Folkman, J -- P01-CA45548/CA/NCI NIH HHS/ -- R01-CA64481/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Sep 17;285(5435):1926-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Children's Hospital, Departments of Surgery and Cellular Biology, Harvard Microchemistry Facility, 16 Divinity Avenue, Cambridge, MA 02138, USA. oreilly@hub.tch.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10489375" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/chemistry/isolation & purification/metabolism/*pharmacology ; Antithrombins/chemistry/isolation & purification/metabolism/*pharmacology ; Carcinoma, Small Cell/blood supply/drug therapy ; Cell Line ; Culture Media, Conditioned ; Drug Screening Assays, Antitumor ; Humans ; Lung Neoplasms/blood supply/drug therapy ; Mice ; Mice, SCID ; Neoplasm Transplantation ; Neovascularization, Pathologic/*drug therapy ; Peptide Fragments/chemistry/metabolism/pharmacology ; Protein Conformation ; Tumor Cells, Cultured
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  • 45
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    Pigment epithelium-derived factor: a potent inhibitor of angiogenesis (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-10
    Description: In the absence of disease, the vasculature of the mammalian eye is quiescent, in part because of the action of angiogenic inhibitors that prevent vessels from invading the cornea and vitreous. Here, an inhibitor responsible for the avascularity of these ocular compartments is identified as pigment epithelium-derived factor (PEDF), a protein previously shown to have neurotrophic activity. The amount of inhibitory PEDF produced by retinal cells was positively correlated with oxygen concentrations, suggesting that its loss plays a permissive role in ischemia-driven retinal neovascularization. These results suggest that PEDF may be of therapeutic use, especially in retinopathies where pathological neovascularization compromises vision and leads to blindness.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dawson, D W -- Volpert, O V -- Gillis, P -- Crawford, S E -- Xu, H -- Benedict, W -- Bouck, N P -- New York, N.Y. -- Science. 1999 Jul 9;285(5425):245-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology-Immunology, Department of Pathology, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Medical School, Chicago, IL 60611, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10398599" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Antibodies/immunology ; Cattle ; Cells, Cultured ; Chemotaxis/drug effects ; Culture Media, Conditioned ; Endothelial Growth Factors/metabolism ; Endothelium, Vascular/cytology/drug effects/physiology ; Eye/blood supply ; *Eye Proteins ; Humans ; Lymphokines/metabolism ; Mice ; Neovascularization, Pathologic/*drug therapy/metabolism/pathology ; Neovascularization, Physiologic/*drug effects ; *Nerve Growth Factors ; Oxygen/physiology ; Proteins/genetics/immunology/*pharmacology/*physiology ; RNA, Messenger/genetics/metabolism ; Rats ; Retina/*metabolism/pathology ; Retinal Neovascularization/*drug therapy ; Retinal Vessels/growth & development ; Serpins/genetics/immunology/*pharmacology/*physiology ; Tumor Cells, Cultured ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
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  • 46
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    An essential role for DNA adenine methylation in bacterial virulence (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-13
    Description: Salmonella typhimurium lacking DNA adenine methylase (Dam) were fully proficient in colonization of mucosal sites but showed severe defects in colonization of deeper tissue sites. These Dam- mutants were totally avirulent and were effective as live vaccines against murine typhoid fever. Dam regulated the expression of at least 20 genes known to be induced during infection; a subset of these genes are among those activated by the PhoP global virulence regulator. PhoP, in turn, affected Dam methylation at specific genomic sites, as evidenced by alterations in DNA methylation patterns. Dam inhibitors are likely to have broad antimicrobial action, and Dam- derivatives of these pathogens may serve as live attenuated vaccines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heithoff, D M -- Sinsheimer, R L -- Low, D A -- Mahan, M J -- AI23348/AI/NIAID NIH HHS/ -- AI36373/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 May 7;284(5416):967-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular, Cellular, and Developmental Biology, University of California, Santa Barbara, CA 93106, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10320378" target="_blank"〉PubMed〈/a〉
    Keywords: Adenine/metabolism ; Animals ; Bacterial Proteins/metabolism ; *Bacterial Vaccines ; *DNA Methylation ; DNA, Bacterial/metabolism ; Gene Expression Regulation, Bacterial ; Genes, Bacterial ; Lethal Dose 50 ; Methylation ; Mice ; Mice, Inbred BALB C ; Mutation ; Peyer's Patches/microbiology ; Salmonella Infections, Animal/immunology/*microbiology/prevention & control ; Salmonella typhimurium/*enzymology/genetics/immunology/*pathogenicity ; Site-Specific DNA-Methyltransferase (Adenine-Specific)/antagonists & ; inhibitors/genetics/*metabolism ; Vaccines, Attenuated ; Virulence/genetics
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  • 47
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    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〉Dawson, G R -- Flint, J -- Wilkinson, L S -- New York, N.Y. -- Science. 1999 Sep 24;285(5436):2068; author reply 2069-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10523201" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Laboratory/genetics ; *Behavior, Animal ; Confounding Factors (Epidemiology) ; Genetics, Behavioral/*methods ; Handling (Psychology) ; Mice ; Reproducibility of Results
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  • 48
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    A molecular pathway revealing a genetic basis for human cardiac and craniofacial defects (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-19
    Description: Microdeletions of chromosome 22q11 are the most common genetic defects associated with cardiac and craniofacial anomalies in humans. A screen for mouse genes dependent on dHAND, a transcription factor implicated in neural crest development, identified Ufd1, which maps to human 22q11 and encodes a protein involved in degradation of ubiquitinated proteins. Mouse Ufd1 was specifically expressed in most tissues affected in patients with 22q11 deletion syndrome. The human UFD1L gene was deleted in all 182 patients studied with 22q11 deletion, and a smaller deletion of approximately 20 kilobases that removed exons 1 to 3 of UFD1L was found in one individual with features typical of 22q11 deletion syndrome. These data suggest that UFD1L haploinsufficiency contributes to the congenital heart and craniofacial defects seen in 22q11 deletion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamagishi, H -- Garg, V -- Matsuoka, R -- Thomas, T -- Srivastava, D -- R01HL57181-01/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 Feb 19;283(5405):1158-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Division of Cardiology, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Room NA8.124, Dallas, TX 75235-9148, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10024240" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta, Thoracic/abnormalities/embryology/metabolism ; Basic Helix-Loop-Helix Transcription Factors ; Cell Cycle Proteins/genetics ; Chromosomes, Human, Pair 22/*genetics ; Craniofacial Abnormalities/*genetics ; DNA-Binding Proteins/genetics/physiology ; Embryo, Mammalian/metabolism ; *Gene Deletion ; Gene Expression Regulation, Developmental ; Heart/embryology ; Heart Defects, Congenital/*genetics ; Humans ; Mice ; Neural Crest/cytology/embryology ; Phenotype ; Proteins/*genetics/physiology ; Transcription Factors/genetics/physiology ; Ubiquitins/metabolism ; Zebrafish Proteins
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  • 49
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    Defective thymocyte maturation in p44 MAP kinase (Erk 1) knockout mice (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-13
    Description: The p42 and p44 mitogen-activated protein kinases (MAPKs), also called Erk2 and Erk1, respectively, have been implicated in proliferation as well as in differentiation programs. The specific role of the p44 MAPK isoform in the whole animal was evaluated by generation of p44 MAPK-deficient mice by homologous recombination in embryonic stem cells. The p44 MAPK-/- mice were viable, fertile, and of normal size. Thus, p44 MAPK is apparently dispensable and p42 MAPK (Erk2) may compensate for its loss. However, in p44 MAPK-/- mice, thymocyte maturation beyond the CD4+CD8+ stage was reduced by half, with a similar diminution in the thymocyte subpopulation expressing high levels of T cell receptor (CD3high). In p44 MAPK-/- thymocytes, proliferation in response to activation with a monoclonal antibody to the T cell receptor in the presence of phorbol myristate acetate was severely reduced even though activation of p42 MAPK was more sustained in these cells. The p44 MAPK apparently has a specific role in thymocyte development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pages, G -- Guerin, S -- Grall, D -- Bonino, F -- Smith, A -- Anjuere, F -- Auberger, P -- Pouyssegur, J -- New York, N.Y. -- Science. 1999 Nov 12;286(5443):1374-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Signaling, Developmental Biology and Cancer Research, CNRS UMR 6543, Centre A. Lacassagne, 33 Avenue de Valombrose, 06189 Nice, France. gpages@unice.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10558995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Antigens, CD/analysis ; Antigens, CD3/immunology ; Cell Differentiation ; Cell Division ; Cells, Cultured ; DNA/biosynthesis ; Enzyme Activation ; Gene Targeting ; Isoenzymes/genetics/metabolism ; Mice ; Mice, Knockout ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3 ; Mitogen-Activated Protein Kinases/deficiency/genetics/*metabolism ; Phosphorylation ; Polymorphism, Restriction Fragment Length ; Receptors, Antigen, T-Cell, alpha-beta/analysis/physiology ; T-Lymphocyte Subsets/*cytology/enzymology/immunology ; Tetradecanoylphorbol Acetate/pharmacology ; Thymus Gland/*cytology
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    Animal testing. One mouse's meat is another one's poison (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Helmuth, L -- New York, N.Y. -- Science. 1999 Aug 20;285(5431):1190-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10484726" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Estradiol/*pharmacology/toxicity ; *Genetic Variation ; Humans ; Litter Size ; Male ; Maximum Allowable Concentration ; Mice ; Mice, Inbred Strains ; Species Specificity ; Spermatogenesis/*drug effects ; Testis/*drug effects ; *Toxicity Tests
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    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〉Hen, R -- New York, N.Y. -- Science. 1999 Sep 24;285(5436):2068-9; author reply 2069-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10523202" target="_blank"〉PubMed〈/a〉
    Keywords: *Alcohol Drinking ; Animals ; Crosses, Genetic ; *Gene Frequency ; Mice ; Mice, Knockout/*genetics ; Receptor, Serotonin, 5-HT1B ; Receptors, Serotonin/genetics/*physiology ; Stem Cells
    Print ISSN: 0036-8075
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    Prions: a lone killer or a vital accomplice? (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balter, M -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):660-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577216" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/chemistry/physiology ; Dendritic Cells, Follicular/chemistry/physiology ; Gene Targeting ; Genetic Predisposition to Disease ; Humans ; Mice ; Mice, Transgenic ; Mutation ; Neurons/chemistry ; Prion Diseases/*etiology/genetics/therapy ; Prions/genetics/metabolism/*pathogenicity
    Print ISSN: 0036-8075
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    Regulated delivery of therapeutic proteins after in vivo somatic cell gene transfer (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999
    Description: Stable delivery of a therapeutic protein under pharmacologic control was achieved through in vivo somatic gene transfer. This system was based on the expression of two chimeric, human-derived proteins that were reconstituted by rapamycin into a transcription factor complex. A mixture of two adeno-associated virus vectors, one expressing the transcription factor chimeras and one containing erythropoietin (Epo) under the control of a promoter responsive to the transcription factor, was injected into skeletal muscle of immune-competent mice. Administration of rapamycin resulted in 200-fold induction of plasma Epo. Stable engraftment of this humanized system in immune-competent mice was achieved for 6 months with similar results for at least 3 months in a rhesus monkey.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ye, X -- Rivera, V M -- Zoltick, P -- Cerasoli, F Jr -- Schnell, M A -- Gao, G -- Hughes, J V -- Gilman, M -- Wilson, J M -- P01 AR/NS43648-03/AR/NIAMS NIH HHS/ -- P30 DK47757-05/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):88-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Human Gene Therapy, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9872748" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytomegalovirus/genetics ; Dependovirus/genetics ; Erythropoietin/administration & dosage/blood/*genetics ; Female ; Gene Expression Regulation ; *Gene Transfer Techniques ; Genetic Therapy/*methods ; Genetic Vectors ; Hematocrit ; Injections, Intramuscular ; Macaca mulatta ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Muscle, Skeletal ; Promoter Regions, Genetic ; Recombinant Fusion Proteins ; Recombinant Proteins ; Sirolimus/*pharmacology ; Transcription Factors/*genetics
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    Requirement for B cell linker protein (BLNK) in B cell development (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-03
    Description: Linker proteins function as molecular scaffolds to localize enzymes with substrates. In B cells, B cell linker protein (BLNK) links the B cell receptor (BCR)-activated Syk kinase to the phosphoinositide and mitogen-activated kinase pathways. To examine the in vivo role of BLNK, mice deficient in BLNK were generated. B cell development in BLNK-/- mice was blocked at the transition from B220+CD43+ progenitor B to B220+CD43- precursor B cells. Only a small percentage of immunoglobulin M++ (IgM++), but not mature IgMloIgDhi, B cells were detected in the periphery. Hence, BLNK is an essential component of BCR signaling pathways and is required to promote B cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pappu, R -- Cheng, A M -- Li, B -- Gong, Q -- Chiu, C -- Griffin, N -- White, M -- Sleckman, B P -- Chan, A C -- AI42787/AI/NIAID NIH HHS/ -- CA71516/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1949-54.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Immunology, Division of Rheumatology, Department of Medicine, Howard Hughes Medical Institute, 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/10583957" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Aging ; Animals ; B-Lymphocyte Subsets/cytology/immunology ; B-Lymphocytes/*cytology/immunology/*metabolism ; Bone Marrow Cells/cytology/immunology ; Carrier Proteins/genetics/*physiology ; Cell Count ; Cell Differentiation ; Cell Separation ; Cell Size ; Flow Cytometry ; Gene Targeting ; Hematopoietic Stem Cells/*cytology/metabolism ; Immunoglobulin M/analysis ; Leukopoiesis ; Lymphoid Tissue/cytology/immunology ; Mice ; Mice, Inbred C57BL ; *Phosphoproteins ; Receptors, Antigen, B-Cell/*metabolism ; Second Messenger Systems ; Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Focal adhesion motility revealed in stationary fibroblasts (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-05
    Description: Focal adhesions (FAs) are clustered integrins and associated proteins that mediate cell adhesion and signaling. A green fluorescent protein-beta1 integrin chimera was used to label FAs in living cells. In stationary cells, FAs were highly motile, moving linearly for several plaque lengths toward the cell center. FA motility was independent of cell density and resulted from contraction of associated actin fibers. In migrating cells, FAs were stationary and only moved in the tail. FA motility in stationary cells suggests that cell movement may be regulated by a clutch-like mechanism by which the affinity of integrins to substrate may be altered in response to migratory cues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smilenov, L B -- Mikhailov, A -- Pelham, R J -- Marcantonio, E E -- Gundersen, G G -- GM42026/GM/NIGMS NIH HHS/ -- GM44585/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 5;286(5442):1172-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10550057" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Actins/physiology ; Animals ; Antigens, CD29/*metabolism ; *Cell Adhesion ; Cell Count ; Cell Line ; *Cell Movement ; Fibroblasts/*cytology/metabolism ; Fluorescence ; Green Fluorescent Proteins ; Luminescent Proteins ; Mice ; Microscopy, Interference ; Rats ; Recombinant Fusion Proteins/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Increased insulin sensitivity and obesity resistance in mice lacking the protein tyrosine phosphatase-1B gene (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-05
    Description: Protein tyrosine phosphatase-1B (PTP-1B) has been implicated in the negative regulation of insulin signaling. Disruption of the mouse homolog of the gene encoding PTP-1B yielded healthy mice that, in the fed state, had blood glucose concentrations that were slightly lower and concentrations of circulating insulin that were one-half those of their PTP-1B+/+ littermates. The enhanced insulin sensitivity of the PTP-1B-/- mice was also evident in glucose and insulin tolerance tests. The PTP-1B-/- mice showed increased phosphorylation of the insulin receptor in liver and muscle tissue after insulin injection in comparison to PTP-1B+/+ mice. On a high-fat diet, the PTP-1B-/- and PTP-1B+/- mice were resistant to weight gain and remained insulin sensitive, whereas the PTP-1B+/+ mice rapidly gained weight and became insulin resistant. These results demonstrate that PTP-1B has a major role in modulating both insulin sensitivity and fuel metabolism, thereby establishing it as a potential therapeutic target in the treatment of type 2 diabetes and obesity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elchebly, M -- Payette, P -- Michaliszyn, E -- Cromlish, W -- Collins, S -- Loy, A L -- Normandin, D -- Cheng, A -- Himms-Hagen, J -- Chan, C C -- Ramachandran, C -- Gresser, M J -- Tremblay, M L -- Kennedy, B P -- New York, N.Y. -- Science. 1999 Mar 5;283(5407):1544-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, McGill University, 3655 Drummond Street, Montreal, Quebec, Canada, H3G 1Y6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10066179" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/metabolism ; Diabetes Mellitus, Type 2/therapy ; Dietary Fats/administration & dosage ; Gene Targeting ; Glucose Tolerance Test ; Insulin/blood/*metabolism/pharmacology ; Insulin Receptor Substrate Proteins ; Insulin Resistance ; Liver/metabolism ; Male ; Mice ; Mice, Knockout ; Muscle, Skeletal/metabolism ; Obesity/*metabolism/therapy ; Phosphoproteins/metabolism ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein Tyrosine Phosphatases/*genetics/*metabolism ; Receptor, Insulin/metabolism ; Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Bile acids: natural ligands for an orphan nuclear receptor (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: Bile acids regulate the transcription of genes that control cholesterol homeostasis through molecular mechanisms that are poorly understood. Physiological concentrations of free and conjugated chenodeoxycholic acid, lithocholic acid, and deoxycholic acid activated the farnesoid X receptor (FXR; NR1H4), an orphan nuclear receptor. As ligands, these bile acids and their conjugates modulated interaction of FXR with a peptide derived from steroid receptor coactivator 1. These results provide evidence for a nuclear bile acid signaling pathway that may regulate cholesterol homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parks, D J -- Blanchard, S G -- Bledsoe, R K -- Chandra, G -- Consler, T G -- Kliewer, S A -- Stimmel, J B -- Willson, T M -- Zavacki, A M -- Moore, D D -- Lehmann, J M -- F32 DK09793/DK/NIDDK NIH HHS/ -- R01 DK53366/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1999 May 21;284(5418):1365-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biochemistry, Glaxo Wellcome Research and Development, Research Triangle Park NC, 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334993" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bile Acids and Salts/chemistry/*metabolism/pharmacology ; Carrier Proteins/metabolism ; Cell Line ; Chenodeoxycholic Acid/*metabolism/pharmacology ; Cholesterol/metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Deoxycholic Acid/metabolism/pharmacology ; Histone Acetyltransferases ; Homeostasis ; Humans ; Ligands ; Lithocholic Acid/metabolism/pharmacology ; Mice ; Nuclear Receptor Coactivator 1 ; *Organic Anion Transporters, Sodium-Dependent ; Protein Conformation ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Structure-Activity Relationship ; *Symporters ; Transcription Factors/chemistry/genetics/*metabolism ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Control of autoimmune diabetes in NOD mice by GAD expression or suppression in beta cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-15
    Description: Glutamic acid decarboxylase (GAD) is a pancreatic beta cell autoantigen in humans and nonobese diabetic (NOD) mice. beta Cell-specific suppression of GAD expression in two lines of antisense GAD transgenic NOD mice prevented autoimmune diabetes, whereas persistent GAD expression in the beta cells in the other four lines of antisense GAD transgenic NOD mice resulted in diabetes, similar to that seen in transgene-negative NOD mice. Complete suppression of beta cell GAD expression blocked the generation of diabetogenic T cells and protected islet grafts from autoimmune injury. Thus, beta cell-specific GAD expression is required for the development of autoimmune diabetes in NOD mice, and modulation of GAD might, therefore, have therapeutic value in type 1 diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoon, J W -- Yoon, C S -- Lim, H W -- Huang, Q Q -- Kang, Y -- Pyun, K H -- Hirasawa, K -- Sherwin, R S -- Jun, H S -- DK 45735/DK/NIDDK NIH HHS/ -- DK 53015-01/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1999 May 14;284(5417):1183-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral and Immunopathogenesis of Diabetes, Julia McFarlane Diabetes Research Centre, Faculty of Medicine, University of Calgary, Calgary, Alberta T2N 4N1, Canada. yoon@ucalgary.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10325232" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Autoantigens/genetics/*immunology/physiology ; Autoimmunity ; DNA, Antisense ; Diabetes Mellitus, Type 1/*enzymology/*immunology/pathology ; Female ; Gene Expression ; Glutamate Decarboxylase/genetics/*immunology/physiology ; Insulin/blood/metabolism ; Islets of Langerhans/*enzymology/immunology/metabolism/pathology ; Islets of Langerhans Transplantation ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Mice, Transgenic ; T-Lymphocytes/immunology ; Transgenes
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Abnormal morphogenesis but intact IKK activation in mice lacking the IKKalpha subunit of IkappaB kinase (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-09
    Description: The oligomeric IkappaB kinase (IKK) is composed of three polypeptides: IKKalpha and IKKbeta, the catalytic subunits, and IKKgamma, a regulatory subunit. IKKalpha and IKKbeta are similar in structure and thought to have similar function-phosphorylation of the IkappaB inhibitors in response to proinflammatory stimuli. Such phosphorylation leads to degradation of IkappaB and activation of nuclear factor kappaB transcription factors. The physiological function of these protein kinases was explored by analysis of IKKalpha-deficient mice. IKKalpha was not required for activation of IKK and degradation of IkappaB by proinflammatory stimuli. Instead, loss of IKKalpha interfered with multiple morphogenetic events, including limb and skeletal patterning and proliferation and differentiation of epidermal keratinocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, Y -- Baud, V -- Delhase, M -- Zhang, P -- Deerinck, T -- Ellisman, M -- Johnson, R -- Karin, M -- R01 AI43477/AI/NIAID NIH HHS/ -- R37 ES04151/ES/NIEHS NIH HHS/ -- RR04050/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):316-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Cancer Center, University of California San Diego, La Jolla, CA 92093-0636, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10195896" target="_blank"〉PubMed〈/a〉
    Keywords: Abnormalities, Multiple/enzymology/genetics ; Animals ; Apoptosis ; Body Patterning ; Bone and Bones/abnormalities/embryology ; Cell Differentiation ; Cell Nucleus/metabolism ; Cells, Cultured ; DNA-Binding Proteins/metabolism ; Dimerization ; *Embryonic and Fetal Development ; Enzyme Activation ; Epidermis/cytology/embryology ; Female ; Gene Targeting ; I-kappa B Kinase ; I-kappa B Proteins ; Keratinocytes ; Limb Deformities, Congenital/enzymology ; Male ; Mice ; *Morphogenesis ; Mutation ; Phosphorylation ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Skin/embryology ; Skin Abnormalities/enzymology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Neuronal protection in stroke by an sLex-glycosylated complement inhibitory protein (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-27
    Description: Glycoprotein adhesion receptors such as selectins contribute to tissue injury in stroke. Ischemic neurons strongly expressed C1q, which may target them for complement-mediated attack or C1qRp-mediated clearance. A hybrid molecule was used to simultaneously inhibit both complement activation and selectin-mediated adhesion. The extracellular domain of soluble complement receptor-1 (sCR1) was sialyl Lewis x glycosylated (sCR1sLex) to inhibit complement activation and endothelial-platelet-leukocyte interactions. sCR1 and sCR1sLex colocalized to ischemic cerebral microvessels and C1q-expressing neurons, inhibited neutrophil and platelet accumulation, and reduced cerebral infarct volumes. Additional benefit was conferred by sialyl Lewis x glycosylation of the unmodified parent sCR1 molecule.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, J -- Kim, L J -- Mealey, R -- Marsh, H C Jr -- Zhang, Y -- Tenner, A J -- Connolly, E S Jr -- Pinsky, D J -- R01 HL55397/HL/NHLBI NIH HHS/ -- R01 HL59488/HL/NHLBI NIH HHS/ -- R01 NS35144/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Jul 23;285(5427):595-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Columbia University, College of Physicians and Surgeons, 630 West 168th Street, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10417391" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Platelets/physiology ; Cell Adhesion ; Cerebral Cortex/blood supply/immunology/metabolism ; Cerebral Infarction/drug therapy ; Cerebrovascular Circulation ; Cerebrovascular Disorders/*drug therapy/immunology/physiopathology ; Complement Activation ; Complement C1q/metabolism ; Glycosylation ; Humans ; Ischemic Attack, Transient/*drug therapy/immunology/physiopathology ; Leukocytes/physiology ; Mice ; Neurons/immunology/metabolism ; Neuroprotective Agents/administration & dosage/adverse ; effects/metabolism/*therapeutic use ; Neutrophils/physiology ; Oligosaccharides/administration & dosage/adverse effects/metabolism/*therapeutic ; use ; Platelet Adhesiveness ; Receptors, Complement/administration & dosage/metabolism/*therapeutic use ; Reperfusion Injury/drug therapy/immunology/metabolism ; Selectins/metabolism ; Time Factors
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Behavioral genetics. Fickle mice highlight test problems (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, M -- New York, N.Y. -- Science. 1999 Jun 4;284(5420):1599-600.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10383330" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Laboratory ; Anxiety ; *Behavior, Animal ; *Environment ; Genetics, Behavioral/*methods ; Mice ; Mice, Inbred Strains ; Mice, Mutant Strains ; Psychological Tests ; Reproducibility of Results
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    Reciprocal inhibitory connections and network synchrony in the mammalian thalamus (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-23
    Description: Neuronal rhythmic activities within thalamocortical circuits range from partially synchronous oscillations during normal sleep to hypersynchrony associated with absence epilepsy. It has been proposed that recurrent inhibition within the thalamic reticular nucleus serves to reduce synchrony and thus prevents seizures. Inhibition and synchrony in slices from mice devoid of the gamma-aminobutyric acid type-A (GABAA) receptor beta3 subunit were examined, because in rodent thalamus, beta3 is largely restricted to reticular nucleus. In beta3 knockout mice, GABAA-mediated inhibition was nearly abolished in reticular nucleus, but was unaffected in relay cells. In addition, oscillatory synchrony was dramatically intensified. Thus, recurrent inhibitory connections within reticular nucleus act as "desynchronizers."〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huntsman, M M -- Porcello, D M -- Homanics, G E -- DeLorey, T M -- Huguenard, J R -- AA10422/AA/NIAAA NIH HHS/ -- NS06477/NS/NINDS NIH HHS/ -- NS34774/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Jan 22;283(5401):541-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Stanford University Medical Center, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9915702" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; GABA Antagonists/pharmacology ; In Vitro Techniques ; Mice ; Mice, Knockout ; Nerve Net/*physiology ; *Neural Inhibition ; Neural Pathways/physiology ; Neurons/*physiology ; Patch-Clamp Techniques ; Picrotoxin/pharmacology ; Receptors, GABA-A/genetics/*physiology ; *Synaptic Transmission ; Thalamic Nuclei/physiology ; Thalamus/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    NMDA receptor-mediated K+ efflux and neuronal apoptosis (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-04-09
    Description: Neuronal death induced by activating N-methyl-D-aspartate (NMDA) receptors has been linked to Ca2+ and Na+ influx through associated channels. Whole-cell recording from cultured mouse cortical neurons revealed a NMDA-evoked outward current, INMDA-K, carried by K+ efflux at membrane potentials positive to -86 millivolts. Cortical neurons exposed to NMDA in medium containing reduced Na+ and Ca2+ (as found in ischemic brain tissue) lost substantial intracellular K+ and underwent apoptosis. Both K+ loss and apoptosis were attenuated by increasing extracellular K+, even when voltage-gated Ca2+ channels were blocked. Thus NMDA receptor-mediated K+ efflux may contribute to neuronal apoptosis after brain ischemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, S P -- Yeh, C -- Strasser, U -- Tian, M -- Choi, D W -- NS 30337/NS/NINDS NIH HHS/ -- NS 32636/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):336-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for the Study of Nervous System Injury and Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10195902" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Calcium/metabolism/pharmacology ; Calcium Channels/metabolism ; Cells, Cultured ; Cerebral Cortex/*cytology/metabolism ; Culture Techniques ; Glutamic Acid/metabolism ; Ion Channel Gating ; Ion Transport ; Membrane Potentials ; Mice ; N-Methylaspartate/pharmacology ; Neocortex/cytology/embryology/metabolism ; Neurons/*cytology/metabolism ; Patch-Clamp Techniques ; Potassium/*metabolism ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Sodium/metabolism/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The mammalian gene collection (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-10-16
    Description: The Mammalian Gene Collection (MGC) project is a new effort by the NIH to generate full-length complementary DNA (cDNA) resources. This project will provide publicly accessible resources to the full research community. The MGC project entails the production of libraries, sequencing, and database and repository development, as well as the support of library construction, sequencing, and analytic technologies dedicated to the goal of obtaining a full set of human and other mammalian full-length (open reading frame) sequences and clones of expressed genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strausberg, R L -- Feingold, E A -- Klausner, R D -- Collins, F S -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):455-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Cancer Institute, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10521335" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Computational Biology ; DNA, Complementary ; Databases, Factual ; Expressed Sequence Tags ; *Gene Library ; *Genome ; *Genome, Human ; Humans ; Mammals/*genetics ; Mice ; National Institutes of Health (U.S.) ; Private Sector ; Public Sector ; *Sequence Analysis, DNA ; United States
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    Nota bene: development. Whirling dervishes (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-12-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, O -- New York, N.Y. -- Science. 1999 Nov 12;286(5443):1311.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10610537" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cilia/*physiology ; Dyneins/genetics/physiology ; Embryo, Mammalian/*cytology ; *Embryonic and Fetal Development ; Mice ; Mice, Mutant Strains ; *Morphogenesis ; Movement ; Proteins/genetics/physiology ; *Transcription Factors
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Requirement for type 2 NO synthase for IL-12 signaling in innate immunity (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-13
    Description: Interleukin-12 (IL-12) and type 2 NO synthase (NOS2) are crucial for defense against bacterial and parasitic pathogens, but their relationship in innate immunity is unknown. In the absence of NOS2 activity, IL-12 was unable to prevent spreading of Leishmania parasites, did not stimulate natural killer (NK) cells for cytotoxicity or interferon-gamma (IFN-gamma) release, and failed to activate Tyk2 kinase and to tyrosine phosphorylate Stat4 (the central signal transducer of IL-12) in NK cells. Activation of Tyk2 in NK cells by IFN-alpha/beta also required NOS2. Thus, NOS2-derived NO is a prerequisite for cytokine signaling and function in innate immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diefenbach, A -- Schindler, H -- Rollinghoff, M -- Yokoyama, W M -- Bogdan, C -- New York, N.Y. -- Science. 1999 May 7;284(5416):951-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Klinische Mikrobiologie, Immunologie und Hygiene, Universitat Erlangen, Wasserturmstrasse 3, D-91054 Erlangen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10320373" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Cyclic GMP/metabolism ; Cytotoxicity, Immunologic ; DNA-Binding Proteins/metabolism ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Immunity, Innate ; Interferon-gamma/biosynthesis/genetics ; Interferons/pharmacology ; Interleukin-12/pharmacology/*physiology ; Janus Kinase 2 ; Killer Cells, Natural/*immunology/metabolism ; *Leishmania major ; Leishmaniasis, Cutaneous/*immunology/metabolism ; Lysine/analogs & derivatives/pharmacology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Nitric Oxide/metabolism ; Nitric Oxide Synthase/antagonists & inhibitors/*metabolism ; Nitric Oxide Synthase Type II ; Phosphorylation ; Protein-Tyrosine Kinases/metabolism ; Proteins/metabolism ; *Proto-Oncogene Proteins ; STAT4 Transcription Factor ; *Signal Transduction ; TYK2 Kinase ; Trans-Activators/metabolism ; Up-Regulation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Nota bene: biomedicine. Pain-killer genes (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, O -- New York, N.Y. -- Science. 1999 Jun 4;284(5420):1634.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10383343" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chronic Disease ; Enkephalin, Methionine/biosynthesis/metabolism ; Enkephalins/*genetics ; Gene Transfer Techniques ; *Genetic Therapy ; Genetic Vectors ; Humans ; Mice ; *Pain Management ; Protein Precursors/*genetics ; Simplexvirus/genetics/physiology ; Spinal Cord/virology ; beta-Endorphin/biosynthesis/cerebrospinal fluid/*genetics
    Print ISSN: 0036-8075
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    Importance of AMPA receptors for hippocampal synaptic plasticity but not for spatial learning (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-12
    Description: Gene-targeted mice lacking the L-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptor subunit GluR-A exhibited normal development, life expectancy, and fine structure of neuronal dendrites and synapses. In hippocampal CA1 pyramidal neurons, GluR-A-/- mice showed a reduction in functional AMPA receptors, with the remaining receptors preferentially targeted to synapses. Thus, the CA1 soma-patch currents were strongly reduced, but glutamatergic synaptic currents were unaltered; and evoked dendritic and spinous Ca2+ transients, Ca2+-dependent gene activation, and hippocampal field potentials were as in the wild type. In adult GluR-A-/- mice, associative long-term potentiation (LTP) was absent in CA3 to CA1 synapses, but spatial learning in the water maze was not impaired. The results suggest that CA1 hippocampal LTP is controlled by the number or subunit composition of AMPA receptors and show a dichotomy between LTP in CA1 and acquisition of spatial memory.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zamanillo, D -- Sprengel, R -- Hvalby, O -- Jensen, V -- Burnashev, N -- Rozov, A -- Kaiser, K M -- Koster, H J -- Borchardt, T -- Worley, P -- Lubke, J -- Frotscher, M -- Kelly, P H -- Sommer, B -- Andersen, P -- Seeburg, P H -- Sakmann, B -- New York, N.Y. -- Science. 1999 Jun 11;284(5421):1805-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Neuroscience, Max-Planck Institute for Medical Research, Jahnstrasse 29, 69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10364547" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Bicuculline/pharmacology ; Calcium/metabolism ; Dendrites/physiology/ultrastructure ; GABA Antagonists/pharmacology ; Gene Expression ; Gene Targeting ; Genes, Immediate-Early ; Glutamic Acid/pharmacology/physiology ; Hippocampus/cytology/physiology ; Long-Term Potentiation/*physiology ; *Maze Learning ; Mice ; Mice, Inbred C57BL ; Pyramidal Cells/*physiology/ultrastructure ; Receptors, AMPA/genetics/*physiology ; Receptors, N-Methyl-D-Aspartate/physiology ; Synapses/*physiology/ultrastructure ; Synaptic Transmission
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Dependence of human stem cell engraftment and repopulation of NOD/SCID mice on CXCR4 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-05
    Description: Stem cell homing and repopulation are not well understood. The chemokine stromal cell-derived factor-1 (SDF-1) and its receptor CXCR4 were found to be critical for murine bone marrow engraftment by human severe combined immunodeficient (SCID) repopulating stem cells. Treatment of human cells with antibodies to CXCR4 prevented engraftment. In vitro CXCR4-dependent migration to SDF-1 of CD34+CD38-/low cells correlated with in vivo engraftment and stem cell function. Stem cell factor and interleukin-6 induced CXCR4 expression on CD34+ cells, which potentiated migration to SDF-1 and engraftment in primary and secondary transplanted mice. Thus, up-regulation of CXCR4 expression may be useful for improving engraftment of repopulating stem cells in clinical transplantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peled, A -- Petit, I -- Kollet, O -- Magid, M -- Ponomaryov, T -- Byk, T -- Nagler, A -- Ben-Hur, H -- Many, A -- Shultz, L -- Lider, O -- Alon, R -- Zipori, D -- Lapidot, T -- A130389/PHS HHS/ -- New York, N.Y. -- Science. 1999 Feb 5;283(5403):845-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, The Weizmann Institute of Science, Rehovot 76100, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9933168" target="_blank"〉PubMed〈/a〉
    Keywords: ADP-ribosyl Cyclase ; Animals ; Antibodies ; *Antigens, CD ; Antigens, CD34/analysis/immunology ; Antigens, CD38 ; Antigens, Differentiation/analysis ; Chemokine CXCL12 ; Chemokines, CXC/pharmacology/*physiology ; Chemotaxis ; Colony-Forming Units Assay ; Fetal Blood ; Hematopoietic Stem Cell Mobilization ; *Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*physiology ; Humans ; Interleukin-6/pharmacology ; Membrane Glycoproteins ; Mice ; Mice, Inbred NOD ; Mice, Knockout ; Mice, SCID ; NAD+ Nucleosidase/analysis ; Receptors, CXCR4/biosynthesis/immunology/*physiology ; Stem Cell Factor/pharmacology ; Tetradecanoylphorbol Acetate/pharmacology ; Up-Regulation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Nota bene: medicine. Fear of flying! (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, O -- New York, N.Y. -- Science. 1999 Apr 2;284(5411):61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10215531" target="_blank"〉PubMed〈/a〉
    Keywords: 2S Albumins, Plant ; Allergens/genetics/*immunology ; Anaphylaxis/*prevention & control/therapy ; Animals ; Antigens, Plant ; Arachis/*adverse effects/immunology ; Food Hypersensitivity/*prevention & control/therapy ; Glycoproteins/genetics/*immunology ; Humans ; Immunoglobulin A/blood ; Immunoglobulin E/blood ; Mice ; Plant Proteins ; T-Lymphocytes, Helper-Inducer/immunology ; *Vaccines, DNA/therapeutic use
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    Cancer research. A new way to combat therapy side effects (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferber, D -- New York, N.Y. -- Science. 1999 Sep 10;285(5434):1651, 1653.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10523177" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/*adverse effects ; Apoptosis/*drug effects ; Benzothiazoles ; Cell Division/drug effects/radiation effects ; Cells, Cultured ; Drug Evaluation, Preclinical ; Gamma Rays/*adverse effects ; Humans ; Mice ; Neoplasms/drug therapy/radiotherapy/*therapy ; Radiation Dosage ; Radiation Tolerance/*drug effects ; Thiazoles/*pharmacology ; Toluene/*analogs & derivatives/pharmacology ; Tumor Suppressor Protein p53/*antagonists & inhibitors/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Apaf-1 and caspase-9 in p53-dependent apoptosis and tumor inhibition (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-02
    Description: The ability of p53 to promote apoptosis in response to mitogenic oncogenes appears to be critical for its tumor suppressor function. Caspase-9 and its cofactor Apaf-1 were found to be essential downstream components of p53 in Myc-induced apoptosis. Like p53 null cells, mouse embryo fibroblast cells deficient in Apaf-1 and caspase-9, and expressing c-Myc, were resistant to apoptotic stimuli that mimic conditions in developing tumors. Inactivation of Apaf-1 or caspase-9 substituted for p53 loss in promoting the oncogenic transformation of Myc-expressing cells. These results imply a role for Apaf-1 and caspase-9 in controlling tumor development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Soengas, M S -- Alarcon, R M -- Yoshida, H -- Giaccia, A J -- Hakem, R -- Mak, T W -- Lowe, S W -- CA13106/CA/NCI NIH HHS/ -- CA64489/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 2;284(5411):156-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10102818" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptotic Protease-Activating Factor 1 ; Caspase 9 ; Caspases/genetics/*physiology ; Cell Division ; Cell Transformation, Neoplastic ; Cells, Cultured ; Cytochrome c Group/metabolism ; Genes, myc ; *Genes, p53 ; Genes, ras ; Mice ; Mice, Nude ; Mitochondria/metabolism ; Mutation ; Neoplasms, Experimental/genetics/metabolism/*pathology ; Proteins/genetics/*physiology ; Tumor Suppressor Protein p53/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Putting stem cells to work (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Solter, D -- Gearhart, J -- New York, N.Y. -- Science. 1999 Mar 5;283(5407):1468-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Max Planck Institute of Immunology, Freiburg, Germany. solter@immunbio.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10206877" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bioethics ; Blastocyst/*cytology ; *Cell Differentiation ; Cell Line ; Cells, Cultured ; Cloning, Organism ; Cytoplasm/physiology ; Embryo, Mammalian/cytology ; Humans ; Mice ; Nuclear Transfer Techniques ; Stem Cells/*cytology
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    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〉Tordoff, M G -- Bachmanov, A A -- Friedman, M I -- Beauchamp, G K -- R01 DC000882/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 1999 Sep 24;285(5436):2069; author reply 2069-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10523203" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Laboratory ; *Behavior, Animal ; *Diet ; Mice
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    Planting the seeds of new antimalarial drugs (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ridley, R G -- New York, N.Y. -- Science. 1999 Sep 3;285(5433):1502-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Drug Discovery Research and the New Medicines for Malaria Venture, Special Programme for Research and Training in Tropical Diseases, World Health Organization, Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10498534" target="_blank"〉PubMed〈/a〉
    Keywords: Aldose-Ketose Isomerases/*antagonists & inhibitors/genetics/metabolism ; Animals ; Antimalarials/pharmacokinetics/*pharmacology ; Drug Design ; Enzyme Inhibitors/pharmacology ; Fosfomycin/analogs & derivatives/pharmacokinetics/pharmacology ; *Hemiterpenes ; Humans ; Malaria/*drug therapy/parasitology ; Malaria, Falciparum/drug therapy ; Mice ; Multienzyme Complexes/*antagonists & inhibitors/genetics/metabolism ; Organelles/drug effects/metabolism ; Organophosphorus Compounds/metabolism ; Oxidoreductases/*antagonists & inhibitors/genetics/metabolism ; Plasmodium falciparum/*drug effects/metabolism ; Steroids/metabolism ; Transferases/antagonists & inhibitors/genetics/metabolism
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    Requirement for diverse, low-abundance peptides in positive selection of T cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-05
    Description: Whether a single major histocompatibility complex (MHC)-bound peptide can drive the positive selection of large numbers of T cells has been a controversial issue. A diverse population of self peptides was shown to be essential for the in vivo development of CD4 T cells. Mice in which all but 5 percent of MHC class II molecules were bound by a single peptide had wild-type numbers of CD4 T cells. However, when the diversity within this 5 percent was lost, CD4 T cell development was impaired. Blocking the major peptide-MHC complex in thymus organ culture had no effect on T cell development, indicating that positive selection occurred on the diverse peptides present at low levels. This requirement for peptide diversity indicates that the interaction between self peptides and T cell receptors during positive selection is highly specific.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barton, G M -- Rudensky, A Y -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):67-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular and Cellular Biology Program of the University of Washington and Fred Hutchinson Cancer Research Center, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9872742" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; CD4-Positive T-Lymphocytes/cytology/*immunology/metabolism ; CD8-Positive T-Lymphocytes/cytology/immunology/metabolism ; Cells, Cultured ; Histocompatibility Antigens Class II/*immunology/metabolism ; Lymphocyte Activation ; Lymphocyte Culture Test, Mixed ; Mice ; Mice, Knockout ; Mice, Transgenic ; Peptides/*immunology/metabolism ; Receptors, Antigen, T-Cell/*immunology ; Recombinant Fusion Proteins/metabolism ; Spleen/immunology ; Thymus Gland/immunology
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    Brain transplants? (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sikorski, R -- Peters, R -- New York, N.Y. -- Science. 1998 Dec 18;282(5397):2213.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9890829" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain Tissue Transplantation ; Cell Differentiation ; Cell Line ; Cell Movement ; Cerebellum/cytology ; Cerebral Ventricles/cytology/embryology ; *Fetal Tissue Transplantation ; Humans ; Mice ; Neuroglia/cytology ; Neurons/cytology ; *Stem Cell Transplantation ; Stem Cells/cytology/enzymology ; beta-N-Acetylhexosaminidases/genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    IEX-1L, an apoptosis inhibitor involved in NF-kappaB-mediated cell survival (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-14
    Description: Transcription factors of the nuclear factor-kappaB/rel (NF-kappaB) family may be important in cell survival by regulating unidentified, anti-apoptotic genes. One such gene that protects cells from apoptosis induced by Fas or tumor necrosis factor type alpha (TNF), IEX-1L, is described here. Its transcription induced by TNF was decreased in cells with defective NF-kappaB activation, rendering them sensitive to TNF-induced apoptosis, which was abolished by transfection with IEX-1L. In support, overexpression of antisense IEX-1L partially blocked TNF-induced expression of IEX-1L and sensitized normal cells to killing. This study demonstrates a key role of IEX-1L in cellular resistance to TNF-induced apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, M X -- Ao, Z -- Prasad, K V -- Wu, R -- Schlossman, S F -- AI12069/AI/NIAID NIH HHS/ -- P30AI28691/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1998 Aug 14;281(5379):998-1001.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Tumor Immunology, Dana-Farber Cancer Institute, and the 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/9703517" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/physiology ; Apoptosis/genetics/*physiology ; Apoptosis Regulatory Proteins ; Cell Line ; Cell Survival ; Cloning, Molecular ; DNA, Antisense/genetics ; Gene Expression Regulation ; Genetic Vectors ; Humans ; Immediate-Early Proteins/genetics/*physiology ; Jurkat Cells ; Membrane Glycoproteins/genetics/*physiology ; Membrane Proteins ; Mice ; NF-kappa B/*physiology ; *Neoplasm Proteins ; Transfection ; Tumor Necrosis Factor-alpha/physiology
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    Cryopreservation. A Frankenstein experiment (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sikorski, R -- Peters, R -- New York, N.Y. -- Science. 1998 Aug 21;281(5380):1163-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9735033" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Fertilization ; *Freeze Drying ; Male ; Mice ; Micromanipulation ; Oocytes/physiology ; Semen Preservation/*methods ; Sperm Head/*physiology
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    Role of MEKK1 in cell survival and activation of JNK and ERK pathways defined by targeted gene disruption (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-04
    Description: Targeted disruption of the gene encoding MEK kinase 1 (MEKK1), a mitogen-activated protein kinase (MAPK) kinase kinase, defined its function in the regulation of MAPK pathways and cell survival. MEKK1(-/-) embryonic stem cells from mice had lost or altered responses of the c-Jun amino-terminal kinase (JNK) to microtubule disruption and cold stress but activated JNK normally in response to heat shock, anisomycin, and ultraviolet irradiation. Activation of JNK was lost and that of extracellular signal-regulated protein kinase (ERK) was diminished in response to hyperosmolarity and serum factors in MEKK1(-/-) cells. Loss of MEKK1 expression resulted in a greater apoptotic response of cells to hyperosmolarity and microtubule disruption. When activated by specific stresses that alter cell shape and the cytoskeleton, MEKK1 signals to protect cells from apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yujiri, T -- Sather, S -- Fanger, G R -- Johnson, G L -- DK37871/DK/NIDDK NIH HHS/ -- GM30324/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Dec 4;282(5395):1911-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Molecular Signal Transduction, Division of Basic Sciences, National Jewish Medical and Research Center, Denver, CO 80206, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9836645" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anisomycin/pharmacology ; Apoptosis ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Line ; Cell Size ; *Cell Survival ; Enzyme Activation ; Gene Targeting ; JNK Mitogen-Activated Protein Kinases ; Lysophospholipids/pharmacology ; *MAP Kinase Kinase 4 ; *MAP Kinase Kinase Kinase 1 ; Mice ; *Mitogen-Activated Protein Kinase Kinases ; *Mitogen-Activated Protein Kinases ; Nocodazole/pharmacology ; Osmolar Concentration ; Phosphorylation ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Protein-Tyrosine Kinases/metabolism ; Recombinant Proteins/metabolism ; Stem Cells ; Temperature ; Transfection ; Ultraviolet Rays
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Role of the CLOCK protein in the mammalian circadian mechanism (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-11
    Description: The mouse Clock gene encodes a bHLH-PAS protein that regulates circadian rhythms and is related to transcription factors that act as heterodimers. Potential partners of CLOCK were isolated in a two-hybrid screen, and one, BMAL1, was coexpressed with CLOCK and PER1 at known circadian clock sites in brain and retina. CLOCK-BMAL1 heterodimers activated transcription from E-box elements, a type of transcription factor-binding site, found adjacent to the mouse per1 gene and from an identical E-box known to be important for per gene expression in Drosophila. Mutant CLOCK from the dominant-negative Clock allele and BMAL1 formed heterodimers that bound DNA but failed to activate transcription. Thus, CLOCK-BMAL1 heterodimers appear to drive the positive component of per transcriptional oscillations, which are thought to underlie circadian rhythmicity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gekakis, N -- Staknis, D -- Nguyen, H B -- Davis, F C -- Wilsbacher, L D -- King, D P -- Takahashi, J S -- Weitz, C J -- New York, N.Y. -- Science. 1998 Jun 5;280(5369):1564-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston MA 02115, USA. 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9616112" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Animals ; Basic Helix-Loop-Helix Transcription Factors ; Biological Clocks ; CLOCK Proteins ; Cell Cycle Proteins ; Circadian Rhythm/genetics/*physiology ; Cloning, Molecular ; Cricetinae ; DNA/metabolism ; Dimerization ; Feedback ; Gene Expression ; Helix-Loop-Helix Motifs ; Male ; Mesocricetus ; Mice ; Mutation ; Nuclear Proteins/*genetics/metabolism ; Period Circadian Proteins ; Promoter Regions, Genetic ; Retina/metabolism ; Suprachiasmatic Nucleus/metabolism ; Trans-Activators/genetics/*metabolism ; Transcription Factors/genetics/*metabolism ; *Transcriptional Activation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 82
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    Fertilization defects in sperm from mice lacking fertilin beta (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-22
    Description: Fertilin, a member of the ADAM family, is found on the plasma membrane of mammalian sperm. Sperm from mice lacking fertilin beta were shown to be deficient in sperm-egg membrane adhesion, sperm-egg fusion, migration from the uterus into the oviduct, and binding to the egg zona pellucida. Egg activation was unaffected. The results are consistent with a direct role of fertilin in sperm-egg plasma membrane interaction. Fertilin could also have a direct role in sperm-zona binding or oviduct migration; alternatively, the effects on these functions could result from the absence of fertilin activity during spermatogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cho, C -- Bunch, D O -- Faure, J E -- Goulding, E H -- Eddy, E M -- Primakoff, P -- Myles, D G -- HD16580/HD/NICHD NIH HHS/ -- U54HD29125/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1998 Sep 18;281(5384):1857-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Molecular and Cellular Biology, University of California, Davis, CA 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9743500" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins ; Animals ; Calcium/metabolism ; Cell Adhesion ; Cell Membrane/physiology ; Fallopian Tubes ; Female ; Male ; Membrane Fusion ; Membrane Glycoproteins/genetics/metabolism/*physiology ; Metalloendopeptidases/genetics/metabolism/*physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Ovum/physiology ; Sperm Capacitation ; *Sperm-Ovum Interactions ; Spermatogenesis ; Spermatozoa/chemistry/*physiology ; Zona Pellucida/physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 83
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    CBP: a signal-regulated transcriptional coactivator controlled by nuclear calcium and CaM kinase IV (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-04
    Description: Recruitment of the coactivator, CREB binding protein (CBP), by signal-regulated transcription factors, such as CREB [adenosine 3', 5'-monophosphate (cAMP) response element binding protein], is critical for stimulation of gene expression. The mouse pituitary cell line AtT20 was used to show that the CBP recruitment step (CREB phosphorylation on serine-133) can be uncoupled from CREB/CBP-activated transcription. CBP was found to contain a signal-regulated transcriptional activation domain that is controlled by nuclear calcium and calcium/calmodulin-dependent (CaM) protein kinase IV and by cAMP. Cytoplasmic calcium signals that stimulate the Ras mitogen-activated protein kinase signaling cascade or expression of the activated form of Ras provided the CBP recruitment signal but did not increase CBP activity and failed to activate CREB- and CBP-mediated transcription. These results identify CBP as a signal-regulated transcriptional coactivator and define a regulatory role for nuclear calcium and cAMP in CBP-dependent gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chawla, S -- Hardingham, G E -- Quinn, D R -- Bading, H -- New York, N.Y. -- Science. 1998 Sep 4;281(5382):1505-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council, Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9727976" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CREB-Binding Protein ; Calcium/*metabolism ; Calcium Channels/metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinase Type 4 ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors/*metabolism ; Cell Line ; Cell Nucleus/*metabolism ; Cyclic AMP/metabolism ; Cyclic AMP Response Element-Binding Protein/metabolism ; Cytoplasm/metabolism ; Genes, Reporter ; Mice ; Models, Genetic ; Nuclear Proteins/*metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Trans-Activators/*metabolism ; Transcription, Genetic ; *Transcriptional Activation ; ras Proteins/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 84
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    Autophosphorylation at Thr286 of the alpha calcium-calmodulin kinase II in LTP and learning (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-28
    Description: The calcium-calmodulin-dependent kinase II (CaMKII) is required for hippocampal long-term potentiation (LTP) and spatial learning. In addition to its calcium-calmodulin (CaM)-dependent activity, CaMKII can undergo autophosphorylation, resulting in CaM-independent activity. A point mutation was introduced into the alphaCaMKII gene that blocked the autophosphorylation of threonine at position 286 (Thr286) of this kinase without affecting its CaM-dependent activity. The mutant mice had no N-methyl-D-aspartate receptor-dependent LTP in the hippocampal CA1 area and showed no spatial learning in the Morris water maze. Thus, the autophosphorylation of alphaCaMKII at Thr286 appears to be required for LTP and learning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giese, K P -- Fedorov, N B -- Filipkowski, R K -- Silva, A J -- AG13622/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1998 Feb 6;279(5352):870-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9452388" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; 6-Cyano-7-nitroquinoxaline-2,3-dione/pharmacology ; Animals ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/genetics/*metabolism ; Calmodulin/metabolism ; Gene Targeting ; Hippocampus/metabolism/*physiology ; *Long-Term Potentiation/drug effects ; *Maze Learning ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Patch-Clamp Techniques ; Phosphorylation ; Phosphothreonine/metabolism ; Picrotoxin/pharmacology ; Point Mutation ; Pyramidal Cells/*physiology ; Receptors, N-Methyl-D-Aspartate/physiology ; Synaptic Transmission
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 85
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    Training viruses to attack cancers (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1998 Nov 13;282(5392):1244-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9867627" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Clinical Trials as Topic ; Combined Modality Therapy ; *Genes, p53 ; *Genes, ras ; Humans ; Mice ; Mutation ; Neoplasms/genetics/pathology/*therapy/virology ; *Virus Physiological Phenomena ; Virus Replication
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 86
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    Axonal swellings and degeneration in mice lacking the major proteolipid of myelin (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-11
    Description: Glial cells produce myelin and contribute to axonal morphology in the nervous system. Two myelin membrane proteolipids, PLP and DM20, were shown to be essential for the integrity of myelinated axons. In the absence of PLP-DM20, mice assembled compact myelin sheaths but subsequently developed widespread axonal swellings and degeneration, associated predominantly with small-caliber nerve fibers. Similar swellings were absent in dysmyelinated shiverer mice, which lack myelin basic protein (MBP), but recurred in MBP*PLP double mutants. Thus, fiber degeneration, which was probably secondary to impaired axonal transport, could indicate that myelinated axons require local oligodendroglial support.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Griffiths, I -- Klugmann, M -- Anderson, T -- Yool, D -- Thomson, C -- Schwab, M H -- Schneider, A -- Zimmermann, F -- McCulloch, M -- Nadon, N -- Nave, K A -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1998 Jun 5;280(5369):1610-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Applied Neurobiology Group, Department of Veterinary Clinical Studies, University of Glasgow, Glasgow G61 1QH, Scotland, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9616125" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axonal Transport ; Axons/*physiology/*ultrastructure ; Cell Communication ; Central Nervous System/*ultrastructure ; Female ; Mice ; Mice, Neurologic Mutants ; Models, Neurological ; Motor Activity ; Myelin Proteolipid Protein/analysis/genetics/*physiology ; Myelin Sheath/chemistry/physiology/ultrastructure ; Nerve Degeneration/*pathology ; *Nerve Tissue Proteins ; Oligodendroglia/physiology ; Optic Nerve/ultrastructure ; Organelles/ultrastructure ; Spinal Cord/ultrastructure ; Transgenes
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Requirement for IL-13 independently of IL-4 in experimental asthma (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-18
    Description: The pathogenesis of asthma reflects, in part, the activity of T cell cytokines. Murine models support participation of interleukin-4 (IL-4) and the IL-4 receptor in asthma. Selective neutralization of IL-13, a cytokine related to IL-4 that also binds to the alpha chain of the IL-4 receptor, ameliorated the asthma phenotype, including airway hyperresponsiveness, eosinophil recruitment, and mucus overproduction. Administration of either IL-13 or IL-4 conferred an asthma-like phenotype to nonimmunized T cell-deficient mice by an IL-4 receptor alpha chain-dependent pathway. This pathway may underlie the genetic associations of asthma with both the human 5q31 locus and the IL-4 receptor.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3897229/" 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/PMC3897229/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grunig, G -- Warnock, M -- Wakil, A E -- Venkayya, R -- Brombacher, F -- Rennick, D M -- Sheppard, D -- Mohrs, M -- Donaldson, D D -- Locksley, R M -- Corry, D B -- 03344/PHS HHS/ -- 47412/PHS HHS/ -- K08 HL003344/HL/NHLBI NIH HHS/ -- T32 HL07185/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Dec 18;282(5397):2261-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, San Francisco General Hospital, University of California San Francisco, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9856950" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Allergens/immunology ; Animals ; Asthma/genetics/*immunology/pathology/physiopathology ; Bronchial Hyperreactivity ; Bronchoalveolar Lavage Fluid/cytology ; Chromosomes, Human, Pair 5 ; Goblet Cells/pathology ; Humans ; Immunoglobulin Fc Fragments ; Interleukin-13/antagonists & inhibitors/genetics/pharmacology/*physiology ; Interleukin-13 Receptor alpha1 Subunit ; Interleukin-4/genetics/pharmacology/*physiology ; Mice ; Mice, Inbred BALB C ; Ovalbumin/immunology ; Phenotype ; Receptors, Interleukin/genetics/immunology/physiology ; Receptors, Interleukin-13 ; Receptors, Interleukin-4/genetics/physiology ; Recombinant Fusion Proteins/pharmacology ; Th2 Cells/immunology
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  • 88
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    Prevention of cardiac hypertrophy in mice by calcineurin inhibition (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-11
    Description: Hypertrophic cardiomyopathy (HCM) is an inherited form of heart disease that affects 1 in 500 individuals. Here it is shown that calcineurin, a calcium-regulated phosphatase, plays a critical role in the pathogenesis of HCM. Administration of the calcineurin inhibitors cyclosporin and FK506 prevented disease in mice that were genetically predisposed to develop HCM as a result of aberrant expression of tropomodulin, myosin light chain-2, or fetal beta-tropomyosin in the heart. Cyclosporin had a similar effect in a rat model of pressure-overload hypertrophy. These results suggest that calcineurin inhibitors merit investigation as potential therapeutics for certain forms of human heart disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sussman, M A -- Lim, H W -- Gude, N -- Taigen, T -- Olson, E N -- Robbins, J -- Colbert, M C -- Gualberto, A -- Wieczorek, D F -- Molkentin, J D -- HL58224-01/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1998 Sep 11;281(5383):1690-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Cardiovascular Biology, Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9733519" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcineurin/metabolism ; *Calcineurin Inhibitors ; Calcium/metabolism ; *Cardiac Myosins ; Cardiomegaly/metabolism/pathology/*prevention & control ; Cardiomyopathy, Dilated/pathology/*prevention & control ; Cardiomyopathy, Hypertrophic/genetics/metabolism/pathology/*prevention & control ; Carrier Proteins/genetics ; Cyclosporine/*pharmacology ; Female ; Mice ; Mice, Transgenic ; *Microfilament Proteins ; Models, Cardiovascular ; Myocardium/*metabolism/pathology ; Myosin Light Chains/genetics/metabolism ; Rats ; Signal Transduction ; Tacrolimus/*pharmacology ; Tropomodulin ; Tropomyosin/genetics
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  • 89
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    Regulation of nerve growth mediated by inositol 1,4,5-trisphosphate receptors in growth cones (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-30
    Description: The inositol 1,4,5-trisphosphate (IP3) receptor (IP3R) acts as a Ca2+ release channel on internal Ca2+ stores. Type 1 IP3R (IP3R1) is enriched in growth cones of neurons in chick dorsal root ganglia. Depletion of internal Ca2+ stores and inhibition of IP3 signaling with drugs inhibited neurite extension. Microinjection of heparin, a competitive IP3R blocker, induced neurite retraction. Acute localized loss of function of IP3R1 in the growth cone induced by chromophore-assisted laser inactivation resulted in growth arrest and neurite retraction. IP3-induced Ca2+ release in growth cones appears to have a crucial role in control of nerve growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takei, K -- Shin, R M -- Inoue, T -- Kato, K -- Mikoshiba, K -- New York, N.Y. -- Science. 1998 Nov 27;282(5394):1705-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Calciosignal Net Project, Exploratory Research for Advanced Technology (ERATO), Japan Science and Technology Corporation (JST), Bunkyo-Ku, Tokyo 113-0021, Japan. kohtaro@ims.u-tokyo.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9831561" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Calcium Channels/*metabolism ; Calcium Signaling ; Cells, Cultured ; Cerebellum/metabolism ; Chick Embryo ; Ganglia, Spinal/cytology ; Growth Cones/*metabolism ; Heparin/pharmacology ; Inositol 1,4,5-Trisphosphate/*metabolism ; Inositol 1,4,5-Trisphosphate Receptors ; Lasers ; Lithium Chloride/pharmacology ; Mice ; Microscopy, Video ; Microsomes/metabolism ; Microtubules/metabolism ; Neurites/drug effects/*physiology ; Pseudopodia/drug effects/physiology ; Receptors, Cytoplasmic and Nuclear/*metabolism ; Signal Transduction ; Thapsigargin/pharmacology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 90
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    p53-independent role of MDM2 in TGF-beta1 resistance (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-18
    Description: Transforming growth factor-beta (TGF-beta) inhibits cell proliferation, and acquisition of TGF-beta resistance has been linked to tumorigenesis. A genetic screen was performed to identify complementary DNAs that abrogated TGF-beta sensitivity in mink lung epithelial cells. Ectopic expression of murine double minute 2 rescued TGF-beta-induced growth arrest in a p53-independent manner by interference with retinoblastoma susceptibility gene product (Rb)/E2F function. In human breast tumor cells, increased MDM2 expression levels correlated with TGF-beta resistance. Thus, MDM2 may confer TGF-beta resistance in a subset of tumors and may promote tumorigenesis by interference with two independent tumor suppressors, p53 and Rb.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, P -- Dong, P -- Dai, K -- Hannon, G J -- Beach, D -- New York, N.Y. -- Science. 1998 Dec 18;282(5397):2270-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9856953" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/genetics/metabolism/pathology ; *Carrier Proteins ; *Cell Cycle Proteins ; *Cell Division ; Cell Line ; Cell Transformation, Neoplastic ; *DNA-Binding Proteins ; Drug Resistance, Neoplasm ; E2F Transcription Factors ; Gene Expression ; Genes, Retinoblastoma ; Genes, p53 ; Genetic Vectors ; Humans ; Mice ; Mink ; *Nuclear Proteins ; Phosphorylation ; Proto-Oncogene Proteins/genetics/*physiology ; Proto-Oncogene Proteins c-mdm2 ; Retinoblastoma Protein/metabolism ; Retinoblastoma-Binding Protein 1 ; Signal Transduction ; Transcription Factor DP1 ; Transcription Factors/genetics/metabolism ; Transcription, Genetic ; Transforming Growth Factor beta/*pharmacology/physiology ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/*physiology
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  • 91
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    Unresponsiveness to cannabinoids and reduced addictive effects of opiates in CB1 receptor knockout mice (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-15
    Description: The function of the central cannabinoid receptor (CB1) was investigated by invalidating its gene. Mutant mice did not respond to cannabinoid drugs, demonstrating the exclusive role of the CB1 receptor in mediating analgesia, reinforcement, hypothermia, hypolocomotion, and hypotension. The acute effects of opiates were unaffected, but the reinforcing properties of morphine and the severity of the withdrawal syndrome were strongly reduced. These observations suggest that the CB1 receptor is involved in the motivational properties of opiates and in the development of physical dependence and extend the concept of an interconnected role of CB1 and opiate receptors in the brain areas mediating addictive behavior.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ledent, C -- Valverde, O -- Cossu, G -- Petitet, F -- Aubert, J F -- Beslot, F -- Bohme, G A -- Imperato, A -- Pedrazzini, T -- Roques, B P -- Vassart, G -- Fratta, W -- Parmentier, M -- New York, N.Y. -- Science. 1999 Jan 15;283(5400):401-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉IRIBHN, Universite libre de Bruxelles, B-1070 Brussels, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9888857" target="_blank"〉PubMed〈/a〉
    Keywords: Analgesics, Opioid/pharmacology ; Animals ; Behavior, Animal/drug effects ; Blood Pressure/drug effects ; Body Temperature/drug effects ; Cannabinoids/metabolism/*pharmacology ; Dronabinol/*pharmacology ; Heart Rate/drug effects ; Mice ; Mice, Knockout ; Morphine/pharmacology ; Motor Activity/drug effects ; Narcotics/*pharmacology ; Opioid-Related Disorders/*physiopathology ; Pain Threshold/drug effects ; Receptors, Cannabinoid ; Receptors, Drug/genetics/*physiology ; Receptors, Opioid, kappa/agonists/physiology ; Reinforcement (Psychology) ; Substance Withdrawal Syndrome/physiopathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 92
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    Genetics of mouse behavior: interactions with laboratory environment (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-05
    Description: Strains of mice that show characteristic patterns of behavior are critical for research in neurobehavioral genetics. Possible confounding influences of the laboratory environment were studied in several inbred strains and one null mutant by simultaneous testing in three laboratories on a battery of six behaviors. Apparatus, test protocols, and many environmental variables were rigorously equated. Strains differed markedly in all behaviors, and despite standardization, there were systematic differences in behavior across labs. For some tests, the magnitude of genetic differences depended upon the specific testing lab. Thus, experiments characterizing mutants may yield results that are idiosyncratic to a particular laboratory.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Crabbe, J C -- Wahlsten, D -- Dudek, B C -- AA00170/AA/NIAAA NIH HHS/ -- AA10760/AA/NIAAA NIH HHS/ -- DA10731/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1999 Jun 4;284(5420):1670-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Portland Alcohol Research Center, Department of Veterans Affairs Medical Center, Portland, OR 97201, USA. crabbe@ohsu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10356397" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Laboratory/genetics ; Anxiety ; *Behavior, Animal ; Confounding Factors (Epidemiology) ; Drinking Behavior ; *Environment ; Female ; Genetics, Behavioral/*methods ; Genotype ; Male ; Mice ; Mice, Inbred Strains/genetics ; Mice, Mutant Strains/genetics ; Motor Activity ; Psychological Tests ; Reproducibility of Results
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 93
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    Gene expression profile of aging and its retardation by caloric restriction (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-28
    Description: The gene expression profile of the aging process was analyzed in skeletal muscle of mice. Use of high-density oligonucleotide arrays representing 6347 genes revealed that aging resulted in a differential gene expression pattern indicative of a marked stress response and lower expression of metabolic and biosynthetic genes. Most alterations were either completely or partially prevented by caloric restriction, the only intervention known to retard aging in mammals. Transcriptional patterns of calorie-restricted animals suggest that caloric restriction retards the aging process by causing a metabolic shift toward increased protein turnover and decreased macromolecular damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, C K -- Klopp, R G -- Weindruch, R -- Prolla, T A -- P01 AG11915/AG/NIA NIH HHS/ -- R01 CA78723/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Aug 27;285(5432):1390-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Environmental Toxicology Center, Institute on Aging, Department of Genetics, University of Wisconsin, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10464095" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*genetics ; Animals ; DNA Damage/genetics ; DNA Repair/genetics ; *Diet ; *Energy Intake ; Energy Metabolism/genetics ; *Gene Expression Regulation ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondria, Muscle/metabolism ; Muscle, Skeletal/innervation/*metabolism ; Oligonucleotide Array Sequence Analysis ; Oxidative Stress/genetics ; Proteins/metabolism ; RNA, Messenger/genetics/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 94
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    Inhibition of cell migration, spreading, and focal adhesions by tumor suppressor PTEN (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-11
    Description: The tumor suppressor PTEN is a phosphatase with sequence similarity to the cytoskeletal protein tensin. Here the cellular roles of PTEN were investigated. Overexpression of PTEN inhibited cell migration, whereas antisense PTEN enhanced migration. Integrin-mediated cell spreading and the formation of focal adhesions were down-regulated by wild-type PTEN but not by PTEN with an inactive phosphatase domain. PTEN interacted with the focal adhesion kinase FAK and reduced its tyrosine phosphorylation. Overexpression of FAK partially antagonized the effects of PTEN. Thus, PTEN phosphatase may function as a tumor suppressor by negatively regulating cell interactions with the extracellular matrix.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tamura, M -- Gu, J -- Matsumoto, K -- Aota, S -- Parsons, R -- Yamada, K M -- New York, N.Y. -- Science. 1998 Jun 5;280(5369):1614-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892-4370, USA. mtamura@yoda.nidr.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9616126" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; *Cell Adhesion ; Cell Adhesion Molecules/metabolism ; Cell Line ; *Cell Movement ; Cell Size ; Concanavalin A ; Down-Regulation ; Ecdysone/pharmacology ; Fibronectins ; Focal Adhesion Kinase 1 ; Focal Adhesion Protein-Tyrosine Kinases ; Genes, Tumor Suppressor ; Humans ; Integrins/physiology ; Mice ; Mutation ; PTEN Phosphohydrolase ; *Phosphoric Monoester Hydrolases ; Phosphorylation ; Polylysine ; Protein Tyrosine Phosphatases/genetics/metabolism/pharmacology/*physiology ; Protein-Tyrosine Kinases/metabolism ; Recombinant Proteins/pharmacology ; Signal Transduction ; Transfection ; Tumor Cells, Cultured ; *Tumor Suppressor Proteins
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 95
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    First components found for new kidney filter (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1999 Oct 8;286(5438):225-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577188" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Cells, Cultured ; Chromosomes, Human, Pair 19/genetics ; Cytoskeletal Proteins ; Humans ; Intercellular Junctions/metabolism/ultrastructure ; Kidney Glomerulus/blood supply/chemistry/*metabolism/*ultrastructure ; Membrane Proteins ; Mice ; Mice, Knockout ; Microscopy, Electron ; Mutation ; Nephrotic Syndrome/congenital/genetics/pathology ; Proteins/chemistry/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 96
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    Contact-dependent inhibition of cortical neurite growth mediated by notch signaling (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-26
    Description: The exuberant growth of neurites during development becomes markedly reduced as cortical neurons mature. In vitro studies of neurons from mouse cerebral cortex revealed that contact-mediated Notch signaling regulates the capacity of neurons to extend and elaborate neurites. Up-regulation of Notch activity was concomitant with an increase in the number of interneuronal contacts and cessation of neurite growth. In neurons with low Notch activity, which readily extend neurites, up-regulation of Notch activity either inhibited extension or caused retraction of neurites. Conversely, in more mature neurons that had ceased their growth after establishing numerous connections and displayed high Notch activity, inhibition of Notch signaling promoted neurite extension. Thus, the formation of neuronal contacts results in activation of Notch receptors, leading to restriction of neuronal growth and a subsequent arrest in maturity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sestan, N -- Artavanis-Tsakonas, S -- Rakic, P -- NS14841/NS/NINDS NIH HHS/ -- NS26084/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):741-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Neurobiology, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10531053" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Communication ; Cell Count ; Cell Differentiation ; Cell Movement ; Cell Nucleus/metabolism ; Cell Size ; Cells, Cultured ; Cerebral Cortex/*cytology/embryology ; Contact Inhibition ; Humans ; Ligands ; Membrane Proteins/*metabolism ; Mice ; Mitosis ; Neurites/chemistry/*physiology ; Neurons/*cytology/metabolism ; Protein Structure, Tertiary ; Receptor, Notch1 ; Receptor, Notch2 ; Receptors, Cell Surface/*metabolism ; Signal Transduction ; *Transcription Factors ; Transcriptional Activation ; Up-Regulation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 97
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    Conserved structures of mediator and RNA polymerase II holoenzyme (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-12
    Description: Single particles of the mediator of transcriptional regulation (Mediator) and of RNA polymerase II holoenzyme were revealed by electron microscopy and image processing. Mediator alone appeared compact, but at high pH or in the presence of RNA polymerase II it displayed an extended conformation. Holoenzyme contained Mediator in a fully extended state, partially enveloping the globular polymerase, with points of apparent contact in the vicinity of the polymerase carboxyl-terminal domain and the DNA-binding channel. A similarity in appearance and conformational behavior of yeast and murine complexes indicates a conservation of Mediator structure among eukaryotes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Asturias, F J -- Jiang, Y W -- Myers, L C -- Gustafsson, C M -- Kornberg, R D -- AI21144/AI/NIAID NIH HHS/ -- GM36659/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Feb 12;283(5404):985-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Structural Biology, Fairchild Building, 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/9974391" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA-Directed RNA Polymerases/*chemistry/metabolism ; Fungal Proteins/*chemistry/metabolism ; Holoenzymes/chemistry/metabolism ; Hydrogen-Ion Concentration ; Mice ; Microscopy, Electron ; *Protein Conformation ; Protein Folding ; Temperature ; Trans-Activators/*chemistry/metabolism ; Transcription Factors/*chemistry/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 98
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    Perspectives: biomedicine. The benefits of recycling (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steel, K P -- New York, N.Y. -- Science. 1999 Aug 27;285(5432):1363-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Institute of Hearing Research, University Park, Nottingham NG7 2RD, UK. karen@ihr.mrc.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10490411" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/genetics/metabolism ; Cochlea/metabolism ; Cochlear Duct/*metabolism/ultrastructure ; *DNA-Binding Proteins ; Deafness/genetics/*metabolism/pathology ; Endolymph/metabolism ; Evoked Potentials, Auditory, Brain Stem ; Extracellular Matrix Proteins ; Eye Proteins/genetics/metabolism ; Genetic Linkage ; Hair Cells, Auditory/cytology/physiology ; Humans ; Ion Transport ; *Membrane Transport Proteins ; Mice ; Mutation ; Nerve Tissue Proteins/genetics/metabolism ; POU Domain Factors ; Potassium/*metabolism ; Potassium Channels/genetics/metabolism ; Proteins/genetics/metabolism ; Transcription Factors/genetics/*metabolism ; X Chromosome
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
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    Identification of a vertebrate sister-chromatid separation inhibitor involved in transformation and tumorigenesis (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-20
    Description: A vertebrate securin (vSecurin) was identified on the basis of its biochemical analogy to the Pds1p protein of budding yeast and the Cut2p protein of fission yeast. The vSecurin protein bound to a vertebrate homolog of yeast separins Esp1p and Cut1p and was degraded by proteolysis mediated by an anaphase-promoting complex in a manner dependent on a destruction motif. Furthermore, expression of a stable Xenopus securin mutant protein blocked sister-chromatid separation but did not block the embryonic cell cycle. The vSecurin proteins share extensive sequence similarity with each other but show no sequence similarity to either of their yeast counterparts. Human securin is identical to the product of the gene called pituitary tumor-transforming gene (PTTG), which is overexpressed in some tumors and exhibits transforming activity in NIH 3T3 cells. The oncogenic nature of increased expression of vSecurin may result from chromosome gain or loss, produced by errors in chromatid separation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zou, H -- McGarry, T J -- Bernal, T -- Kirschner, M W -- GM26875/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 16;285(5426):418-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10411507" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Amino Acid Sequence ; *Anaphase ; Anaphase-Promoting Complex-Cyclosome ; Animals ; CDC2 Protein Kinase/metabolism ; Cell Cycle Proteins/chemistry/metabolism ; *Cell Transformation, Neoplastic ; Chromatids/*physiology ; Conserved Sequence ; Cyclin B/metabolism ; Cyclin B1 ; *Endopeptidases ; Fungal Proteins/chemistry/metabolism ; HeLa Cells ; Humans ; Ligases/metabolism ; Mice ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Neoplasm Proteins/chemistry/genetics/*metabolism ; Neoplasms/etiology ; Nuclear Proteins/chemistry/metabolism ; Oncogene Proteins/chemistry/genetics/*metabolism ; Oncogenes ; *Saccharomyces cerevisiae Proteins ; *Schizosaccharomyces pombe Proteins ; Securin ; Separase ; Spindle Apparatus/metabolism ; *Ubiquitin-Protein Ligase Complexes ; Ubiquitin-Protein Ligases ; Xenopus
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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    Stem cells as potential nerve therapy (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steghaus-Kovac, S -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):650-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10454911" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bioethics ; Diffuse Cerebral Sclerosis of Schilder/*therapy ; Embryo, Mammalian/cytology ; Financing, Government ; Germany ; Humans ; Mice ; Myelin Sheath/*physiology ; Oligodendroglia/*cytology/physiology/transplantation ; Rats ; Research Support as Topic ; Spinal Cord ; Stem Cells/*cytology/physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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