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  • Transfection  (574)
  • Cells, Cultured  (522)
  • American Association for the Advancement of Science (AAAS)  (1,050)
  • American Meteorological Society
  • 2010-2014  (144)
  • 1995-1999  (474)
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  • 1
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    Structural basis for a Ca2+-sensing function of the metabotropic glutamate receptors (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-28
    Description: The metabotropic glutamate receptors (mGluRs) are widely distributed in the brain and play important roles in synaptic plasticity. Here it is shown that some types of mGluRs are activated not only by glutamate but also by extracellular Ca2+ (Ca2+o). A single amino acid residue was found to determine the sensitivity of mGluRs to Ca2+o. One of the receptors, mGluR1alpha, but not its point mutant with reduced sensitivity to Ca2+o, caused morphological changes when transfected into mammalian cells. Thus, the sensing of Ca2+o by mGluRs may be important in cells under physiological condition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kubo, Y -- Miyashita, T -- Murata, Y -- New York, N.Y. -- Science. 1998 Mar 13;279(5357):1722-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurophysiology, Tokyo Metropolitan Institute for Neuroscience, Musashidai 2-6, Fuchu, Tokyo 183-8526, Japan. ykubo@tmin.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9497291" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/ultrastructure ; Amino Acid Sequence ; Animals ; Binding Sites ; Brain/metabolism ; CHO Cells ; Calcium/*metabolism/pharmacology ; Cell Size ; Cricetinae ; Cyclic AMP/metabolism ; G Protein-Coupled Inwardly-Rectifying Potassium Channels ; Glutamic Acid/metabolism/pharmacology ; Molecular Sequence Data ; Oocytes ; Point Mutation ; Potassium Channels/metabolism ; *Potassium Channels, Inwardly Rectifying ; Rats ; Receptors, Metabotropic Glutamate/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Second Messenger Systems ; Transfection ; Xenopus laevis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Induction of lens differentiation by activation of a bZIP transcription factor, L-Maf (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-04-29
    Description: After the vertebrate lens is induced from head ectoderm, lens-specific genes are expressed. Transcriptional regulation of the lens-specific alphaA-crystallin gene is controlled by an enhancer element, alphaCE2. A gene encoding an alphaCE2-binding protein, L-maf(lens-specific maf), was isolated. L-maf expression is initiated in the lens placode and is restricted to lens cells. The gene product L-Maf regulates the expression of multiple genes expressed in the lens, and ectopic expression of this transcription factor converts chick embryonic ectodermal cells and cultured cells into lens fibers. Thus, vertebrate lens induction and differentiation can be triggered by the activation of L-Maf.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ogino, H -- Yasuda, K -- New York, N.Y. -- Science. 1998 Apr 3;280(5360):115-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate School of Biological Sciences, Nara Institute of Science and Technology, 8916-5 Takayama, Ikoma 630-0101, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9525857" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Basic-Leucine Zipper Transcription Factors ; Cell Differentiation ; Cells, Cultured ; Chick Embryo ; Crystallins/genetics ; DNA, Complementary ; DNA-Binding Proteins/chemistry/genetics ; Ectoderm ; Enhancer Elements, Genetic ; Eye Proteins/genetics ; G-Box Binding Factors ; *Gene Expression Regulation, Developmental ; Genes, Reporter ; Intermediate Filament Proteins/genetics ; Lens, Crystalline/*cytology/*embryology/metabolism ; Maf Transcription Factors ; Molecular Sequence Data ; Promoter Regions, Genetic ; Recombinant Fusion Proteins/metabolism ; Transcription Factors/chemistry/genetics/*metabolism ; *Transcription, Genetic ; Transcriptional Activation ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Coupling of Ras and Rac guanosine triphosphatases through the Ras exchanger Sos (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-07
    Description: The Son of Sevenless (Sos) proteins control receptor-mediated activation of Ras by catalyzing the exchange of guanosine diphosphate for guanosine triphosphate on Ras. The NH2-terminal region of Sos contains a Dbl homology (DH) domain in tandem with a pleckstrin homology (PH) domain. In COS-1 cells, the DH domain of Sos stimulated guanine nucleotide exchange on Rac but not Cdc42 in vitro and in vivo. The tandem DH-PH domain of Sos (DH-PH-Sos) was defective in Rac activation but regained Rac stimulating activity when it was coexpressed with activated Ras. Ras-mediated activation of DH-PH-Sos did not require activation of mitogen-activated protein kinase but it was dependent on activation of phosphoinositide 3-kinase. These results reveal a potential mechanism for coupling of Ras and Rac signaling pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nimnual, A S -- Yatsula, B A -- Bar-Sagi, D -- CA09176/CA/NCI NIH HHS/ -- CA28146/CA/NCI NIH HHS/ -- CA55360/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Jan 23;279(5350):560-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, State University of New York at Stony Brook, Stony Brook, NY 11794, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9438849" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; COS Cells ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Cycle Proteins/metabolism ; Cell Line ; Cell Membrane/ultrastructure ; Enzyme Activation ; GTP Phosphohydrolases/*metabolism ; GTP-Binding Proteins/*metabolism ; Guanine Nucleotide Exchange Factors ; Guanosine Diphosphate/metabolism ; Guanosine Triphosphate/metabolism ; Humans ; JNK Mitogen-Activated Protein Kinases ; Membrane Proteins/chemistry/*metabolism ; *Mitogen-Activated Protein Kinases ; Proteins/metabolism ; Proto-Oncogene Proteins ; Recombinant Fusion Proteins/metabolism ; Retroviridae Proteins, Oncogenic/chemistry ; Signal Transduction ; Son of Sevenless Proteins ; Transfection ; cdc42 GTP-Binding Protein ; rac GTP-Binding Proteins ; ras Guanine Nucleotide Exchange Factors ; ras Proteins/*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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  • 4
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    Essential role of CED-4 oligomerization in CED-3 activation and apoptosis (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-28
    Description: Control of the activation of apoptosis is important both in development and in protection against cancer. In the classic genetic model Caenorhabditis elegans, the pro-apoptotic protein CED-4 activates the CED-3 caspase and is inhibited by the Bcl-2-like protein CED-9. Both processes are mediated by protein-protein interaction. Facilitating the proximity of CED-3 zymogen molecules was found to induce caspase activation and cell death. CED-4 protein oligomerized in cells and in vitro. This oligomerization induced CED-3 proximity and competed with CED-4:CED-9 interaction. Mutations that abolished CED-4 oligomerization inactivated its ability to activate CED-3. Thus, the mechanism of control is that CED-3 in CED-3:CED-4 complexes is activated by CED-4 oligomerization, which is inhibited by binding of CED-9 to CED-4.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, X -- Chang, H Y -- Baltimore, D -- CA51462/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Aug 28;281(5381):1355-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9721101" target="_blank"〉PubMed〈/a〉
    Keywords: *Apoptosis ; Apoptosis Regulatory Proteins ; Biopolymers ; *Caenorhabditis elegans Proteins ; Calcium-Binding Proteins/*chemistry/genetics/*metabolism ; *Caspases ; Cell Line ; Chemistry, Physical ; Cysteine Endopeptidases/*metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Enzyme Activation ; Enzyme Precursors/metabolism ; HeLa Cells ; Helminth Proteins/*chemistry/genetics/*metabolism ; Humans ; Mutation ; Oligopeptides/pharmacology ; Physicochemical Phenomena ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Recombinant Fusion Proteins/metabolism ; Tacrolimus/pharmacology ; Transfection ; bcl-X Protein
    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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    Bid for better beef gives Japan a leg up on cattle (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Normile, D -- New York, N.Y. -- Science. 1998 Dec 11;282(5396):1975-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9874644" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Husbandry/*methods ; Animals ; Blastocyst ; Cattle/embryology/*genetics ; Cell Differentiation ; Cells, Cultured ; *Cloning, Organism ; Embryo Transfer/veterinary ; Fallopian Tubes/cytology ; Female ; Japan ; *Nuclear Transfer Techniques ; Oocytes ; Ovarian Follicle/cytology ; Pregnancy
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Molecular basis of T cell inactivation by CTLA-4 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-12-18
    Description: CTLA-4, a negative regulator of T cell function, was found to associate with the T cell receptor (TCR) complex zeta chain in primary T cells. The association of TCRzeta with CTLA-4, reconstituted in 293 transfectants, was enhanced by p56(lck)-induced tyrosine phosphorylation. Coexpression of the CTLA-4-associated tyrosine phosphatase, SHP-2, resulted in dephosphorylation of TCRzeta bound to CTLA-4 and abolished the p56(lck)-inducible TCRzeta-CTLA-4 interaction. Thus, CTLA-4 inhibits TCR signal transduction by binding to TCRzeta and inhibiting tyrosine phosphorylation after T cell activation. These findings have broad implications for the negative regulation of T cell function and T cell tolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, K M -- Chuang, E -- Griffin, M -- Khattri, R -- Hong, D K -- Zhang, W -- Straus, D -- Samelson, L E -- Thompson, C B -- Bluestone, J A -- P01 AI35294-6/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1998 Dec 18;282(5397):2263-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ben May Institute for Cancer Research, and Committee on Immunology, University of Chicago, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9856951" target="_blank"〉PubMed〈/a〉
    Keywords: Abatacept ; Animals ; Antigens, CD ; Antigens, Differentiation/*metabolism ; CTLA-4 Antigen ; Cell Line ; Cells, Cultured ; Humans ; *Immunoconjugates ; Intracellular Signaling Peptides and Proteins ; *Lymphocyte Activation ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck)/genetics/metabolism ; Membrane Proteins/*metabolism ; Mice ; Mice, Inbred BALB C ; Models, Immunological ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein Tyrosine Phosphatase, Non-Receptor Type 11 ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 ; Protein Tyrosine Phosphatases/genetics/metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Recombinant Fusion Proteins/metabolism ; SH2 Domain-Containing Protein Tyrosine Phosphatases ; *Signal Transduction ; T-Lymphocytes/*immunology ; Transfection ; src Homology Domains
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Triplet-repeat transcripts: a role for DNA in disease (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-05-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Singer, R H -- New York, N.Y. -- Science. 1998 May 1;280(5364):696-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Structural Biology, Institute for Molecular Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, USA. rhsinger@aecom.yu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9599147" target="_blank"〉PubMed〈/a〉
    Keywords: CELF1 Protein ; Cell Nucleus/metabolism ; Exons ; Humans ; Models, Genetic ; Myotonic Dystrophy/*genetics/metabolism ; Myotonin-Protein Kinase ; Protein Binding ; Protein-Serine-Threonine Kinases/*genetics ; *RNA Splicing ; RNA, Messenger/*genetics ; RNA-Binding Proteins/genetics/*metabolism ; Ribonucleoproteins/genetics/*metabolism ; Transcription, Genetic ; Transfection ; *Trinucleotide Repeats ; Troponin/genetics ; Troponin T
    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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    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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  • 9
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    Ribozyme-mediated repair of sickle beta-globin mRNAs in erythrocyte precursors (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-11
    Description: Sickle cell anemia is the most common heritable hematological disease, yet no curative treatment exists for this disorder. Moreover, the intricacies of globin gene expression have made the development of treatments for hemoglobinopathies based on gene therapy difficult. An alternative genetic approach to sickle cell therapy is based on RNA repair. A trans-splicing group I ribozyme was used to alter mutant beta-globin transcripts in erythrocyte precursors derived from peripheral blood from individuals with sickle cell disease. Sickle beta-globin transcripts were converted into messenger RNAs encoding the anti-sickling protein gamma-globin. These results suggest that RNA repair may become a useful approach in the treatment of genetic disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lan, N -- Howrey, R P -- Lee, S W -- Smith, C A -- Sullenger, B A -- HL57606/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1998 Jun 5;280(5369):1593-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Genetic and Cellular Therapies, 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/9616120" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Sickle Cell/*blood/therapy ; Cloning, Molecular ; Erythroid Precursor Cells/*metabolism ; Exons ; Fetal Blood ; Genetic Therapy ; Globins/*genetics ; Humans ; Mutation ; Polymerase Chain Reaction ; *RNA Splicing ; RNA, Catalytic/genetics/*metabolism ; RNA, Messenger/chemistry/*genetics/metabolism ; Transfection ; Uridine/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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  • 10
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    Cloned transgenic calves produced from nonquiescent fetal fibroblasts (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-20
    Description: An efficient system for genetic modification and large-scale cloning of cattle is of importance for agriculture, biotechnology, and human medicine. Here, actively dividing fetal fibroblasts were genetically modified with a marker gene, a clonal line was selected, and the cells were fused to enucleated mature oocytes. Out of 28 embryos transferred to 11 recipient cows, three healthy, identical, transgenic calves were generated. Furthermore, the life-span of near senescent fibroblasts could be extended by nuclear transfer, as indicated by population doublings in fibroblast lines derived from a 40-day-old fetal clone. With the ability to extend the life-span of these primary cultured cells, this system would be useful for inducing complex genetic modifications in cattle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cibelli, J B -- Stice, S L -- Golueke, P J -- Kane, J J -- Jerry, J -- Blackwell, C -- Ponce de Leon, F A -- Robl, J M -- New York, N.Y. -- Science. 1998 May 22;280(5367):1256-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Veterinary and Animal Sciences, University of Massachusetts, Amherst, MA 01003, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9596577" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Animals, Genetically Modified ; Blastocyst ; Cattle/embryology/*genetics ; Cell Aging ; Cell Division ; Cell Nucleus/genetics ; Cells, Cultured ; Clone Cells ; *Cloning, Organism ; Embryo Transfer ; Female ; Fetus/cytology ; Fibroblasts/*cytology ; G1 Phase ; Male ; Nuclear Transfer Techniques ; Oocytes/cytology ; Transfection ; Transgenes
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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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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  • 12
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    Arabidopsis NPH1: a flavoprotein with the properties of a photoreceptor for phototropism (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-30
    Description: The NPH1 gene of Arabidopsis thaliana encodes a 120-kilodalton serine-threonine protein kinase hypothesized to function as a photoreceptor for phototropism. When expressed in insect cells, the NPH1 protein is phosphorylated in response to blue light irradiation. The biochemical and photochemical properties of the photosensitive protein reflect those of the native protein in microsomal membranes. Recombinant NPH1 noncovalently binds flavin mononucleotide, a likely chromophore for light-dependent autophosphorylation. The fluorescence excitation spectrum of the recombinant protein is similar to the action spectrum for phototropism, consistent with the conclusion that NPH1 is an autophosphorylating flavoprotein photoreceptor mediating phototropic responses in higher plants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Christie, J M -- Reymond, P -- Powell, G K -- Bernasconi, P -- Raibekas, A A -- Liscum, E -- Briggs, W R -- New York, N.Y. -- Science. 1998 Nov 27;282(5394):1698-701.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Biology, Carnegie Institution of Washington, 260 Panama Street, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9831559" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arabidopsis/genetics/*physiology ; *Arabidopsis Proteins ; Cell Line ; Cryptochromes ; *Drosophila Proteins ; *Eye Proteins ; Flavin Mononucleotide/metabolism ; Flavoproteins/physiology ; Genes, Plant ; Light ; Mutation ; Phosphoproteins/genetics/*metabolism ; Phosphorylation ; *Photoreceptor Cells, Invertebrate ; *Phototropism ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Receptors, G-Protein-Coupled ; Recombinant Proteins/metabolism ; Spectrometry, Fluorescence ; Spodoptera ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
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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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  • 14
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    Specific covalent labeling of recombinant protein molecules inside live cells (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-07-10
    Description: Recombinant proteins containing four cysteines at the i, i + 1, i + 4, and i + 5 positions of an alpha helix were fluorescently labeled in living cells by extracellular administration of 4',5'-bis(1,3, 2-dithioarsolan-2-yl)fluorescein. This designed small ligand is membrane-permeant and nonfluorescent until it binds with high affinity and specificity to the tetracysteine domain. Such in situ labeling adds much less mass than does green fluorescent protein and offers greater versatility in attachment sites as well as potential spectroscopic and chemical properties. This system provides a recipe for slightly modifying a target protein so that it can be singled out from the many other proteins inside live cells and fluorescently stained by small nonfluorescent dye molecules added from outside the cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Griffin, B A -- Adams, S R -- Tsien, R Y -- NS27177/NS/NINDS NIH HHS/ -- T32 CA09523/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Jul 10;281(5374):269-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, University of California San Diego, La Jolla, CA 92093-0647, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9657724" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Calmodulin/chemistry/genetics/metabolism ; Cell Membrane Permeability ; Cell Survival ; Cysteine/*chemistry ; Energy Transfer ; Ethylene Glycol ; Fluoresceins/chemical synthesis/chemistry/*metabolism ; Fluorescence ; *Fluorescent Dyes ; Green Fluorescent Proteins ; HeLa Cells ; Humans ; Jurkat Cells ; Ligands ; Luminescent Proteins/chemistry/genetics/metabolism ; Molecular Sequence Data ; Organometallic Compounds/chemical synthesis/chemistry/*metabolism ; Peptides/chemistry/*metabolism ; Protein Structure, Secondary ; Recombinant Proteins/chemistry/*metabolism ; Spectrometry, Fluorescence ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    Quantitation of transcription and clonal selection of single living cells with beta-lactamase as reporter (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-01-24
    Description: Gene expression was visualized in single living mammalian cells with beta-lactamase as a reporter that hydrolyzes a substrate loaded intracellularly as a membrane-permeant ester. Each enzyme molecule changed the fluorescence of many substrate molecules from green to blue by disrupting resonance energy transfer. This wavelength shift was detectable by eye or color film in individual cells containing less than 100 beta-lactamase molecules. The robust change in emission ratio reveals quantitative heterogeneity in real-time gene expression, enables clonal selection by flow cytometry, and forms a basis for high-throughput screening of pharmaceutical candidate drugs in living mammalian cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zlokarnik, G -- Negulescu, P A -- Knapp, T E -- Mere, L -- Burres, N -- Feng, L -- Whitney, M -- Roemer, K -- Tsien, R Y -- NS27177/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1998 Jan 2;279(5347):84-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Aurora Biosciences, 11010 Torreyana Road, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9417030" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Separation/methods ; Clone Cells/*metabolism ; DNA-Binding Proteins/genetics/metabolism ; Drug Evaluation, Preclinical ; Energy Transfer ; Flow Cytometry ; Fluoresceins/metabolism ; Fluorescent Dyes/metabolism ; *Gene Expression ; *Genes, Reporter ; Half-Life ; Humans ; *Lactams ; Muscarinic Agonists/pharmacology ; Muscarinic Antagonists/pharmacology ; NFATC Transcription Factors ; *Nuclear Proteins ; Sensitivity and Specificity ; Spectrometry, Fluorescence ; Transcription Factors/genetics/metabolism ; *Transcription, Genetic ; Transfection ; Tumor Cells, Cultured ; Umbelliferones/metabolism ; beta-Lactamases/*genetics/metabolism ; beta-Lactams/metabolism
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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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    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 17
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    Neurons and silicon get intimate (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, R F -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):578-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10328734" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Electric Stimulation ; Electrodes ; Electrodes, Implanted ; *Electronics ; Electrophysiology ; Humans ; Nerve Net/*physiology ; Nervous System Diseases/*therapy ; Neurons/*physiology ; Rats ; Silicon ; *Transistors, Electronic
    Print ISSN: 0036-8075
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  • 18
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    Affinity-driven peptide selection of an NFAT inhibitor more selective than cyclosporin A (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-25
    Description: The flow of information from calcium-mobilizing receptors to nuclear factor of activated T cells (NFAT)-dependent genes is critically dependent on interaction between the phosphatase calcineurin and the transcription factor NFAT. A high-affinity calcineurin-binding peptide was selected from combinatorial peptide libraries based on the calcineurin docking motif of NFAT. This peptide potently inhibited NFAT activation and NFAT-dependent expression of endogenous cytokine genes in T cells, without affecting the expression of other cytokines that require calcineurin but not NFAT. Substitution of the optimized peptide sequence into the natural calcineurin docking site increased the calcineurin responsiveness of NFAT. Compounds that interfere selectively with the calcineurin-NFAT interaction without affecting calcineurin phosphatase activity may be useful as therapeutic agents that are less toxic than current drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aramburu, J -- Yaffe, M B -- Lopez-Rodriguez, C -- Cantley, L C -- Hogan, P G -- Rao, A -- R01 AI 40127/AI/NIAID NIH HHS/ -- R01 GM056203/GM/NIGMS NIH HHS/ -- R01 HL 03601/HL/NHLBI NIH HHS/ -- R43 AI 43726/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Sep 24;285(5436):2129-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10497131" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Binding Sites ; Calcineurin/*metabolism ; Calcineurin Inhibitors ; Cell Nucleus/metabolism ; Cyclosporine/pharmacology ; Cytokines/biosynthesis/genetics ; DNA-Binding Proteins/*antagonists & inhibitors/chemistry/metabolism ; Gene Expression Regulation ; Genes, Reporter ; HeLa Cells ; Humans ; Immunosuppressive Agents/chemistry/metabolism/*pharmacology ; Jurkat Cells ; Molecular Sequence Data ; NFATC Transcription Factors ; *Nuclear Proteins ; Oligopeptides/chemistry/metabolism/*pharmacology ; Peptide Library ; Peptides/chemistry/metabolism/*pharmacology ; Phosphorylation ; Recombinant Fusion Proteins/metabolism ; T-Lymphocytes/*drug effects/immunology ; Transcription Factors/*antagonists & inhibitors/chemistry/metabolism ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 19
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    Filling in the blanks of the GABAB receptor (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):14-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9917254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/metabolism ; Cells, Cultured ; Dimerization ; Drug Design ; Humans ; Neurons/*metabolism ; Potassium Channels/metabolism ; Rats ; Receptors, GABA-B/*chemistry/*metabolism ; Signal Transduction ; gamma-Aminobutyric Acid/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 20
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    Rapid spine delivery and redistribution of AMPA receptors after synaptic NMDA receptor activation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-12
    Description: To monitor changes in alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptor distribution in living neurons, the AMPA receptor subunit GluR1 was tagged with green fluorescent protein (GFP). This protein (GluR1-GFP) was functional and was transiently expressed in hippocampal CA1 neurons. In dendrites visualized with two-photon laser scanning microscopy or electron microscopy, most of the GluR1-GFP was intracellular, mimicking endogenous GluR1 distribution. Tetanic synaptic stimulation induced a rapid delivery of tagged receptors into dendritic spines as well as clusters in dendrites. These postsynaptic trafficking events required synaptic N-methyl-D-aspartate (NMDA) receptor activation and may contribute to the enhanced AMPA receptor-mediatedtransmission observed during long-term potentiation and activity-dependent synaptic maturation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shi, S H -- Hayashi, Y -- Petralia, R S -- Zaman, S H -- Wenthold, R J -- Svoboda, K -- Malinow, R -- New York, N.Y. -- Science. 1999 Jun 11;284(5421):1811-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10364548" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Dendrites/*metabolism/ultrastructure ; Electric Stimulation ; Hippocampus/cytology/physiology ; Humans ; Long-Term Potentiation ; *Neuronal Plasticity ; Neurons/*physiology ; Organ Culture Techniques ; Rats ; Receptor Aggregation ; Receptors, AMPA/*metabolism ; Receptors, N-Methyl-D-Aspartate/*physiology ; Recombinant Fusion Proteins/metabolism ; Synapses/metabolism/*physiology ; Synaptic Transmission ; Tetany
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 21
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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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  • 22
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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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  • 23
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    CD3- and CD28-dependent induction of PDE7 required for T cell activation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-05
    Description: Costimulation of both the CD3 and CD28 receptors is essential for T cell activation. Induction of adenosine 3',5'-monophosphate (cAMP)-specific phosphodiesterase-7 (PDE7) was found to be a consequence of such costimulation. Increased PDE7 in T cells correlated with decreased cAMP, increased interleukin-2 expression, and increased proliferation. Selectively reducing PDE7 expression with a PDE7 antisense oligonucleotide inhibited T cell proliferation; inhibition was reversed by blocking the cAMP signaling pathways that operate through cAMP-dependent protein kinase (PKA). Thus, PDE7 induction and consequent suppression of PKA activity is required for T cell activation, and inhibition of PDE7 could be an approach to treating T cell-dependent disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, L -- Yee, C -- Beavo, J A -- DK21723/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1999 Feb 5;283(5403):848-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Molecular and Cellular Biology Program, Box 357280, University of Washington School of Medicine, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9933169" target="_blank"〉PubMed〈/a〉
    Keywords: 3',5'-Cyclic-AMP Phosphodiesterases/*biosynthesis/genetics/metabolism ; Antibodies ; Antigens, CD28/immunology/*physiology ; Antigens, CD3/immunology/*physiology ; CD4-Positive T-Lymphocytes/enzymology/immunology ; Cells, Cultured ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Cyclic Nucleotide Phosphodiesterases, Type 7 ; Enzyme Induction ; Humans ; Interleukin-2/biosynthesis ; Isoenzymes/*biosynthesis/genetics/metabolism ; *Lymphocyte Activation ; Oligonucleotides, Antisense/pharmacology ; RNA, Messenger/genetics/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; T-Lymphocytes/*enzymology/*immunology/metabolism ; Tumor Cells, Cultured
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  • 24
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    Linear differentiation of cytotoxic effectors into memory T lymphocytes (1999)
    American Association for the Advancement of Science (AAAS)
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    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 25
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    The nature of the principal type 1 interferon-producing cells in human blood (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-12
    Description: Interferons (IFNs) are the most important cytokines in antiviral immune responses. "Natural IFN-producing cells" (IPCs) in human blood express CD4 and major histocompatibility complex class II proteins, but have not been isolated and further characterized because of their rarity, rapid apoptosis, and lack of lineage markers. Purified IPCs are here shown to be the CD4(+)CD11c- type 2 dendritic cell precursors (pDC2s), which produce 200 to 1000 times more IFN than other blood cells after microbial challenge. pDC2s are thus an effector cell type of the immune system, critical for antiviral and antitumor immune responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Siegal, F P -- Kadowaki, N -- Shodell, M -- Fitzgerald-Bocarsly, P A -- Shah, K -- Ho, S -- Antonenko, S -- Liu, Y J -- New York, N.Y. -- Science. 1999 Jun 11;284(5421):1835-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Saint Vincents Hospital and Medical Center, New York, NY 10011, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10364556" target="_blank"〉PubMed〈/a〉
    Keywords: CD40 Ligand ; Cell Lineage ; Cell Separation ; Cells, Cultured ; Dendritic Cells/cytology/*immunology/ultrastructure ; Humans ; Interferon Type I/*biosynthesis ; Interferon-alpha/*biosynthesis/genetics ; Interferon-beta/biosynthesis/genetics ; Interleukin-3/pharmacology ; Leukocytes, Mononuclear/immunology ; Membrane Glycoproteins/pharmacology ; Organelles/ultrastructure ; RNA, Messenger/genetics/metabolism ; Simplexvirus/immunology ; Stem Cells/cytology/immunology
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    Coordinated regulation of iron-controlling genes, H-ferritin and IRP2, by c-MYC (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-29
    Description: The protein encoded by the c-MYC proto-oncogene is a transcription factor that can both activate and repress the expression of target genes, but few of its transcriptional targets have been identified. Here, c-MYC is shown to repress the expression of the heavy subunit of the protein ferritin (H-ferritin), which sequesters intracellular iron, and to stimulate the expression of the iron regulatory protein-2 (IRP2), which increases the intracellular iron pool. Down-regulation of the expression of H-ferritin gene was required for cell transformation by c-MYC. These results indicate that c-MYC coordinately regulates genes controlling intracellular iron concentrations and that this function is essential for the control of cell proliferation and transformation by c-MYC.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, K J -- Polack, A -- Dalla-Favera, R -- CA-37165/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 29;283(5402):676-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Oncology, Department of Pathology, Columbia University, New York, NY 10032, USA. an.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9924025" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cell Line ; Cell Line, Transformed ; Cell Transformation, Neoplastic ; DNA/biosynthesis ; Down-Regulation ; Ferritins/*genetics/metabolism ; *Gene Expression Regulation ; Genes, myc ; Homeostasis ; Iron/*metabolism ; Iron Regulatory Protein 2 ; Iron-Regulatory Proteins ; Iron-Sulfur Proteins/*genetics/metabolism ; Proto-Oncogene Proteins c-myc/*physiology ; RNA/metabolism ; RNA-Binding Proteins/*genetics/metabolism ; Receptors, Transferrin/genetics ; Transcription, Genetic ; Transfection
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  • 27
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    Inhibition of the mitogen-activated protein kinase kinase superfamily by a Yersinia effector (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-18
    Description: The bacterial pathogen Yersinia uses a type III secretion system to inject several virulence factors into target cells. One of the Yersinia virulence factors, YopJ, was shown to bind directly to the superfamily of MAPK (mitogen-activated protein kinase) kinases (MKKs) blocking both phosphorylation and subsequent activation of the MKKs. These results explain the diverse activities of YopJ in inhibiting the extracellular signal-regulated kinase, c-Jun amino-terminal kinase, p38, and nuclear factor kappa B signaling pathways, preventing cytokine synthesis and promoting apoptosis. YopJ-related proteins that are found in a number of bacterial pathogens of animals and plants may function to block MKKs so that host signaling responses can be modulated upon infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Orth, K -- Palmer, L E -- Bao, Z Q -- Stewart, S -- Rudolph, A E -- Bliska, J B -- Dixon, J E -- 18024/PHS HHS/ -- AI35175/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Sep 17;285(5435):1920-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, University of Michigan, Ann Arbor, MI 48109-0606, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10489373" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/*physiology ; Calcium-Calmodulin-Dependent Protein Kinases/*antagonists & inhibitors ; Cell Line ; Enzyme Activation ; Enzyme Inhibitors/*pharmacology ; HeLa Cells ; Humans ; *MAP Kinase Kinase Kinase 1 ; NF-kappa B/metabolism ; Phosphorylation ; Protein Binding ; Protein-Serine-Threonine Kinases/genetics/metabolism ; Recombinant Fusion Proteins/genetics/metabolism ; Transfection ; Virulence ; Yersinia pseudotuberculosis/genetics/metabolism/pathogenicity/*physiology
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  • 28
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    Role of DNA 5-methylcytosine transferase in cell transformation by fos (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-15
    Description: The Fos and Jun oncoproteins form dimeric complexes that stimulate transcription of genes containing activator protein-1 regulatory elements. We found, by representational difference analysis, that expression of DNA 5-methylcytosine transferase (dnmt1) in fos-transformed cells is three times the expression in normal fibroblasts and that fos-transformed cells contain about 20 percent more 5-methylcytosine than normal fibroblasts. Transfection of the gene encoding Dnmt1 induced morphological transformation, whereas inhibition of dnmt1 expression or activity resulted in reversion of fos transformation. Inhibition of histone deacetylase, which associates with methylated DNA, also caused reversion. These results suggest that fos may transform cells through alterations in DNA methylation and in histone deacetylation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bakin, A V -- Curran, T -- P30 CA21765/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 15;283(5400):387-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9888853" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine ; Acetylation ; Animals ; Cell Size ; *Cell Transformation, Neoplastic ; Cytosine/analogs & derivatives/metabolism ; DNA (Cytosine-5-)-Methyltransferase/genetics/*metabolism ; DNA Methylation ; Enzyme Inhibitors/pharmacology ; Gene Expression Regulation, Neoplastic ; *Genes, fos ; Histone Deacetylase Inhibitors ; Histones/metabolism ; Hydroxamic Acids/pharmacology ; Proto-Oncogene Proteins c-fos/*metabolism ; Rats ; Transcription, Genetic ; Transfection
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    Efficient persistence of extrachromosomal KSHV DNA mediated by latency-associated nuclear antigen (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-24
    Description: Primary effusion lymphoma (PEL) cells harbor Kaposi's sarcoma-associated herpesvirus (KSHV) episomes and express a KSHV-encoded latency-associated nuclear antigen (LANA). In PEL cells, LANA and KSHV DNA colocalized in dots in interphase nuclei and along mitotic chromosomes. In the absence of KSHV DNA, LANA was diffusely distributed in the nucleus or on mitotic chromosomes. In lymphoblasts, LANA was necessary and sufficient for the persistence of episomes containing a specific KSHV DNA fragment. Furthermore, LANA colocalized with the artificial KSHV DNA episomes in nuclei and along mitotic chromosomes. These results support a model in which LANA tethers KSHV DNA to chromosomes during mitosis to enable the efficient segregation of KSHV episomes to progeny cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ballestas, M E -- Chatis, P A -- Kaye, K M -- CA67380-04/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):641-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, 181 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10213686" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Viral/analysis/genetics/metabolism ; Cell Nucleus/chemistry ; Chromosomes/chemistry/*metabolism ; Cosmids ; DNA, Viral/analysis/genetics/*metabolism ; Herpesvirus 8, Human/*genetics/physiology ; Humans ; Interphase ; Lymphocytes/chemistry ; Microscopy, Confocal ; *Mitosis ; Nuclear Proteins/analysis/genetics/*metabolism ; *Plasmids ; Transfection ; Tumor Cells, Cultured
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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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    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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    Convergence of transforming growth factor-beta and vitamin D signaling pathways on SMAD transcriptional coactivators (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-26
    Description: Cell proliferation and differentiation are regulated by growth regulatory factors such as transforming growth factor-beta (TGF-beta) and the liphophilic hormone vitamin D. TGF-beta causes activation of SMAD proteins acting as coactivators or transcription factors in the nucleus. Vitamin D controls transcription of target genes through the vitamin D receptor (VDR). Smad3, one of the SMAD proteins downstream in the TGF-beta signaling pathway, was found in mammalian cells to act as a coactivator specific for ligand-induced transactivation of VDR by forming a complex with a member of the steroid receptor coactivator-1 protein family in the nucleus. Thus, Smad3 may mediate cross-talk between vitamin D and TGF-beta signaling pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yanagisawa, J -- Yanagi, Y -- Masuhiro, Y -- Suzawa, M -- Watanabe, M -- Kashiwagi, K -- Toriyabe, T -- Kawabata, M -- Miyazono, K -- Kato, S -- New York, N.Y. -- Science. 1999 Feb 26;283(5406):1317-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10037600" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Morphogenetic Protein Receptors ; Bone Morphogenetic Proteins/pharmacology ; COS Cells ; Calcitriol/*metabolism/pharmacology ; Cell Nucleus/metabolism ; DNA-Binding Proteins/*metabolism ; Histone Acetyltransferases ; Ligands ; Nuclear Receptor Coactivator 1 ; Phosphorylation ; Receptor Cross-Talk ; Receptors, Calcitriol/*metabolism ; Receptors, Cell Surface/metabolism ; *Receptors, Growth Factor ; Receptors, Retinoic Acid/metabolism ; Receptors, Transforming Growth Factor beta/metabolism ; Recombinant Fusion Proteins/metabolism ; Retinoid X Receptors ; Signal Transduction ; Smad3 Protein ; Trans-Activators/*metabolism ; Transcription Factors/metabolism ; *Transcriptional Activation ; Transfection ; Transforming Growth Factor beta/*metabolism
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    Beta-defensins: linking innate and adaptive immunity through dendritic and T cell CCR6 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-16
    Description: Defensins contribute to host defense by disrupting the cytoplasmic membrane of microorganisms. This report shows that human beta-defensins are also chemotactic for immature dendritic cells and memory T cells. Human beta-defensin was selectively chemotactic for cells stably transfected to express human CCR6, a chemokine receptor preferentially expressed by immature dendritic cells and memory T cells. The beta-defensin-induced chemotaxis was sensitive to pertussis toxin and inhibited by antibodies to CCR6. The binding of iodinated LARC, the chemokine ligand for CCR6, to CCR6-transfected cells was competitively displaced by beta-defensin. Thus, beta-defensins may promote adaptive immune responses by recruiting dendritic and T cells to the site of microbial invasion through interaction with CCR6.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, D -- Chertov, O -- Bykovskaia, S N -- Chen, Q -- Buffo, M J -- Shogan, J -- Anderson, M -- Schroder, J M -- Wang, J M -- Howard, O M -- Oppenheim, J J -- N01-CO-56000/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):525-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunoregulation, Division of Basic Sciences, Intramural Research Support Program, SAIC Frederick, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, MD 21702-1201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10521347" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies/immunology ; Binding, Competitive ; Cell Line ; Chemokine CCL20 ; Chemokines, CC/metabolism/pharmacology ; Chemotaxis ; Chemotaxis, Leukocyte ; Defensins ; Dendritic Cells/*immunology ; Humans ; *Immunity, Active ; *Immunity, Innate ; Immunologic Memory ; *Macrophage Inflammatory Proteins ; Pertussis Toxin ; Proteins/pharmacology/*physiology ; Receptors, CCR6 ; Receptors, Chemokine/genetics/*metabolism ; Recombinant Proteins/pharmacology ; T-Lymphocyte Subsets/*immunology ; Transfection ; Virulence Factors, Bordetella/pharmacology ; *beta-Defensins
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  • 34
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    Positive and negative regulation of IkappaB kinase activity through IKKbeta subunit phosphorylation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-09
    Description: IkappaB [inhibitor of nuclear factor kappaB (NF-kappaB)] kinase (IKK) phosphorylates IkappaB inhibitory proteins, causing their degradation and activation of transcription factor NF-kappaB, a master activator of inflammatory responses. IKK is composed of three subunits-IKKalpha and IKKbeta, which are highly similar protein kinases, and IKKgamma, a regulatory subunit. In mammalian cells, phosphorylation of two sites at the activation loop of IKKbeta was essential for activation of IKK by tumor necrosis factor and interleukin-1. Elimination of equivalent sites in IKKalpha, however, did not interfere with IKK activation. Thus, IKKbeta, not IKKalpha, is the target for proinflammatory stimuli. Once activated, IKKbeta autophosphorylated at a carboxyl-terminal serine cluster. Such phosphorylation decreased IKK activity and may prevent prolonged activation of the inflammatory response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Delhase, M -- Hayakawa, M -- Chen, Y -- Karin, M -- R01 AI43477/AI/NIAID NIH HHS/ -- R37 ES04151/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):309-13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0636, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10195894" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Cell Line ; DNA-Binding Proteins/metabolism ; Enzyme Activation ; HeLa Cells ; Helix-Loop-Helix Motifs ; Humans ; I-kappa B Kinase ; I-kappa B Proteins ; Interleukin-1/pharmacology ; Leucine Zippers ; *MAP Kinase Kinase Kinase 1 ; Molecular Sequence Data ; Mutation ; Phosphorylation ; Phosphoserine/metabolism ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Transfection ; Tumor Necrosis Factor-alpha/pharmacology
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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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    Action of DNA repair endonuclease ERCC1/XPF in living cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-13
    Description: To study the nuclear organization and dynamics of nucleotide excision repair (NER), the endonuclease ERCC1/XPF (for excision repair cross complementation group 1/xeroderma pigmentosum group F) was tagged with green fluorescent protein and its mobility was monitored in living Chinese hamster ovary cells. In the absence of DNA damage, the complex moved freely through the nucleus, with a diffusion coefficient (15 +/- 5 square micrometers per second) consistent with its molecular size. Ultraviolet light-induced DNA damage caused a transient dose-dependent immobilization of ERCC1/XPF, likely due to engagement of the complex in a single repair event. After 4 minutes, the complex regained mobility. These results suggest (i) that NER operates by assembly of individual NER factors at sites of DNA damage rather than by preassembly of holocomplexes and (ii) that ERCC1/XPF participates in repair of DNA damage in a distributive fashion rather than by processive scanning of large genome segments.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Houtsmuller, A B -- Rademakers, S -- Nigg, A L -- Hoogstraten, D -- Hoeijmakers, J H -- Vermeulen, W -- New York, N.Y. -- Science. 1999 May 7;284(5416):958-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology (Josephine Nefkens Institute, Erasmus University, Post Office Box 1738, 3000 DR Rotterdam, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10320375" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CHO Cells ; Cell Line, Transformed ; Cell Nucleus/metabolism ; Cricetinae ; *DNA Damage ; *DNA Repair ; DNA-Binding Proteins/*metabolism ; Diffusion ; Endonucleases/*metabolism ; Fluorescence ; Green Fluorescent Proteins ; HeLa Cells ; Humans ; Luminescent Proteins ; Microscopy, Confocal ; Microscopy, Fluorescence ; Proteins/*metabolism ; Recombinant Fusion Proteins/metabolism ; Transfection ; Ultraviolet Rays
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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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    Replication of subgenomic hepatitis C virus RNAs in a hepatoma cell line (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-03
    Description: An estimated 170 million persons worldwide are infected with hepatitis C virus (HCV), a major cause of chronic liver disease. Despite increasing knowledge of genome structure and individual viral proteins, studies on virus replication and pathogenesis have been hampered by the lack of reliable and efficient cell culture systems. A full-length consensus genome was cloned from viral RNA isolated from an infected human liver and used to construct subgenomic selectable replicons. Upon transfection into a human hepatoma cell line, these RNAs were found to replicate to high levels, permitting metabolic radiolabeling of viral RNA and proteins. This work defines the structure of HCV replicons functional in cell culture and provides the basis for a long-sought cellular system that should allow detailed molecular studies of HCV and the development of antiviral drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lohmann, V -- Korner, F -- Koch, J -- Herian, U -- Theilmann, L -- Bartenschlager, R -- New York, N.Y. -- Science. 1999 Jul 2;285(5424):110-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Virology, Johannes-Gutenberg University Mainz, Obere Zahlbacher Strasse 67, 55131 Mainz, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10390360" target="_blank"〉PubMed〈/a〉
    Keywords: Carcinoma, Hepatocellular ; Cloning, Molecular ; Drug Resistance ; *Genome, Viral ; Gentamicins/pharmacology ; Hepacivirus/genetics/*physiology ; Hepatitis C/virology ; Humans ; Liver Neoplasms ; RNA, Viral/*biosynthesis/genetics ; *Replicon ; Transfection ; Tumor Cells, Cultured/*virology ; Viral Nonstructural Proteins/analysis/genetics ; Virus Cultivation ; *Virus Replication
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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)
    Details
    Publication Date: 1999-04-09
    Description: Neuronal death induced by activating N-methyl-D-aspartate (NMDA) receptors has been linked to Ca2+ and Na+ influx through associated channels. Whole-cell recording from cultured mouse cortical neurons revealed a NMDA-evoked outward current, INMDA-K, carried by K+ efflux at membrane potentials positive to -86 millivolts. Cortical neurons exposed to NMDA in medium containing reduced Na+ and Ca2+ (as found in ischemic brain tissue) lost substantial intracellular K+ and underwent apoptosis. Both K+ loss and apoptosis were attenuated by increasing extracellular K+, even when voltage-gated Ca2+ channels were blocked. Thus NMDA receptor-mediated K+ efflux may contribute to neuronal apoptosis after brain ischemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, S P -- Yeh, C -- Strasser, U -- Tian, M -- Choi, D W -- NS 30337/NS/NINDS NIH HHS/ -- NS 32636/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):336-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for the Study of Nervous System Injury and Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10195902" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Calcium/metabolism/pharmacology ; Calcium Channels/metabolism ; Cells, Cultured ; Cerebral Cortex/*cytology/metabolism ; Culture Techniques ; Glutamic Acid/metabolism ; Ion Channel Gating ; Ion Transport ; Membrane Potentials ; Mice ; N-Methylaspartate/pharmacology ; Neocortex/cytology/embryology/metabolism ; Neurons/*cytology/metabolism ; Patch-Clamp Techniques ; Potassium/*metabolism ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Sodium/metabolism/pharmacology
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    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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    Cell survival promoted by the Ras-MAPK signaling pathway by transcription-dependent and -independent mechanisms (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-13
    Description: A mechanism by which the Ras-mitogen-activated protein kinase (MAPK) signaling pathway mediates growth factor-dependent cell survival was characterized. The MAPK-activated kinases, the Rsks, catalyzed the phosphorylation of the pro-apoptotic protein BAD at serine 112 both in vitro and in vivo. The Rsk-induced phosphorylation of BAD at serine 112 suppressed BAD-mediated apoptosis in neurons. Rsks also are known to phosphorylate the transcription factor CREB (cAMP response element-binding protein) at serine 133. Activated CREB promoted cell survival, and inhibition of CREB phosphorylation at serine 133 triggered apoptosis. These findings suggest that the MAPK signaling pathway promotes cell survival by a dual mechanism comprising the posttranslational modification and inactivation of a component of the cell death machinery and the increased transcription of pro-survival genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonni, A -- Brunet, A -- West, A E -- Datta, S R -- Takasu, M A -- Greenberg, M E -- NIHP30-HD18655/HD/NICHD NIH HHS/ -- P01 HD 24926/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 12;286(5443):1358-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, and Department of Neurobiology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10558990" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Brain-Derived Neurotrophic Factor/pharmacology ; Carrier Proteins/genetics/metabolism ; *Cell Survival ; Cells, Cultured ; Cerebellum/cytology ; Cyclic AMP Response Element-Binding Protein/metabolism ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Flavonoids/pharmacology ; Insulin-Like Growth Factor I/pharmacology ; MAP Kinase Kinase 1 ; *MAP Kinase Signaling System ; Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors/metabolism ; Mitogen-Activated Protein Kinases/antagonists & inhibitors/metabolism ; Mutation ; Neurons/*cytology/metabolism ; Phosphorylation ; Phosphoserine/metabolism ; *Protein-Serine-Threonine Kinases ; Rats ; Rats, Long-Evans ; Recombinant Fusion Proteins/metabolism ; Ribosomal Protein S6 Kinases/genetics/*metabolism ; *Transcription, Genetic ; Transfection ; bcl-Associated Death Protein ; ras Proteins/metabolism
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    Gating of BDNF-induced synaptic potentiation by cAMP (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-18
    Description: Neurotrophins have been implicated in activity-dependent synaptic plasticity, but the underlying intracellular mechanisms remain largely unknown. Synaptic potentiation induced by brain-derived neurotrophic factor (BDNF), but not neurotrophin 3, was prevented by blockers of adenosine 3',5'-monophosphate (cAMP) signaling. Activators of cAMP signaling alone were ineffective in modifying synaptic efficacy but greatly enhanced the potentiation effect of BDNF. Blocking cAMP signaling abolished the facilitation of BDNF-induced potentiation by presynaptic activity. Thus synaptic actions of BDNF are gated by cAMP. Activity and other coincident signals that modulate cAMP concentrations may specify the action of secreted neurotrophins on developing nerve terminals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boulanger, L -- Poo, M M -- NS 37831/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jun 18;284(5422):1982-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California at San Diego, La Jolla, CA 92093-0357, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10373115" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain-Derived Neurotrophic Factor/*pharmacology ; *Carbazoles ; Cells, Cultured ; Cyclic AMP/analogs & derivatives/pharmacology/*physiology ; Cycloleucine/analogs & derivatives/pharmacology ; *Excitatory Postsynaptic Potentials/drug effects ; Indoles/pharmacology ; Nerve Growth Factors/pharmacology ; Neuronal Plasticity ; Neurons/cytology/physiology ; Neurotrophin 3 ; Okadaic Acid/pharmacology ; Patch-Clamp Techniques ; Pyrroles/pharmacology ; Signal Transduction ; Synapses/drug effects/*physiology ; *Synaptic Transmission/drug effects ; Thionucleotides/pharmacology ; Xenopus
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    Cancer research. A new way to combat therapy side effects (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferber, D -- New York, N.Y. -- Science. 1999 Sep 10;285(5434):1651, 1653.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10523177" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/*adverse effects ; Apoptosis/*drug effects ; Benzothiazoles ; Cell Division/drug effects/radiation effects ; Cells, Cultured ; Drug Evaluation, Preclinical ; Gamma Rays/*adverse effects ; Humans ; Mice ; Neoplasms/drug therapy/radiotherapy/*therapy ; Radiation Dosage ; Radiation Tolerance/*drug effects ; Thiazoles/*pharmacology ; Toluene/*analogs & derivatives/pharmacology ; Tumor Suppressor Protein p53/*antagonists & inhibitors/physiology
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    A molecular mechanism for electrical tuning of cochlear hair cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-08
    Description: Cochlear frequency selectivity in lower vertebrates arises in part from electrical tuning intrinsic to the sensory hair cells. The resonant frequency is determined largely by the gating kinetics of calcium-activated potassium (BK) channels encoded by the slo gene. Alternative splicing of slo from chick cochlea generated kinetically distinct BK channels. Combination with accessory beta subunits slowed the gating kinetics of alpha splice variants but preserved relative differences between them. In situ hybridization showed that the beta subunit is preferentially expressed by low-frequency (apical) hair cells in the avian cochlea. Interaction of beta with alpha splice variants could provide the kinetic range needed for electrical tuning of cochlear hair cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramanathan, K -- Michael, T H -- Jiang, G J -- Hiel, H -- Fuchs, P A -- DC00276/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 8;283(5399):215-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Hearing Sciences, Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9880252" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Animals ; Calcium/metabolism ; Cell Line ; Electrophysiology ; Gene Expression ; Hair Cells, Auditory/*physiology ; Humans ; In Situ Hybridization ; *Ion Channel Gating ; Kinetics ; Large-Conductance Calcium-Activated Potassium Channel beta Subunits ; Large-Conductance Calcium-Activated Potassium Channels ; Membrane Potentials ; Patch-Clamp Techniques ; Potassium Channels/genetics/*physiology ; *Potassium Channels, Calcium-Activated ; Quail ; RNA, Messenger/genetics/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Transfection
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    Erythropoietin receptor activation by a ligand-induced conformation change (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-12
    Description: Erythropoietin and other cytokine receptors are thought to be activated through hormone-induced dimerization and autophosphorylation of JAK kinases associated with the receptor intracellular domains. An in vivo protein fragment complementation assay was used to obtain evidence for an alternative mechanism in which unliganded erythropoietin receptor dimers exist in a conformation that prevents activation of JAK2 but then undergo a ligand-induced conformation change that allows JAK2 to be activated. These results are consistent with crystallographic evidence of distinct dimeric configurations for unliganded and ligand-bound forms of the erythropoietin receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Remy, I -- Wilson, I A -- Michnick, S W -- GM49497/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Feb 12;283(5404):990-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departement de Biochimie, Universite de Montreal, Casier Postal 6128, succursale Centre-ville, Montreal, Quebec, H3C 3J7, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9974393" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CHO Cells ; COS Cells ; Cricetinae ; Dimerization ; Erythropoietin/metabolism ; Flow Cytometry ; Fluoresceins/metabolism ; Janus Kinase 2 ; Ligands ; Methotrexate/analogs & derivatives/metabolism ; Microscopy, Fluorescence ; Peptides, Cyclic/metabolism ; *Protein Conformation ; Protein-Tyrosine Kinases/metabolism ; *Proto-Oncogene Proteins ; Receptors, Erythropoietin/*chemistry/*metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Tetrahydrofolate Dehydrogenase/chemistry/metabolism ; Transfection
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    The role of local actin instability in axon formation (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-03-19
    Description: The role of localized instability of the actin network in specifying axonal fate was examined with the use of rat hippocampal neurons in culture. During normal neuronal development, actin dynamics and instability polarized to a single growth cone before axon formation. Consistently, global application of actin-depolymerizing drugs and of the Rho-signaling inactivator toxin B to nonpolarized cells produced neurons with multiple axons. Moreover, disruption of the actin network in one individual growth cone induced its neurite to become the axon. Thus, local instability of the actin network restricted to a single growth cone is a physiological signal specifying neuronal polarization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bradke, F -- Dotti, C G -- New York, N.Y. -- Science. 1999 Mar 19;283(5409):1931-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉European Molecular Biology Laboratory, Cell Biology Programme, Meyerhofstrasse 1, 69012 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10082468" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism/*physiology ; Animals ; Axons/*physiology/ultrastructure ; *Bacterial Proteins ; Bacterial Toxins/pharmacology ; Bicyclo Compounds, Heterocyclic/pharmacology ; Cell Polarity ; Cells, Cultured ; Cytochalasin D/pharmacology ; GTP Phosphohydrolases/antagonists & inhibitors/metabolism ; Growth Cones/drug effects/*physiology/ultrastructure ; Hippocampus ; Microtubules/physiology/ultrastructure ; Neurites/*physiology/ultrastructure ; Phenotype ; Pseudopodia/drug effects/ultrastructure ; Rats ; Signal Transduction ; Thiazoles/pharmacology ; Thiazolidines
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    Apaf-1 and caspase-9 in p53-dependent apoptosis and tumor inhibition (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-04-02
    Description: The ability of p53 to promote apoptosis in response to mitogenic oncogenes appears to be critical for its tumor suppressor function. Caspase-9 and its cofactor Apaf-1 were found to be essential downstream components of p53 in Myc-induced apoptosis. Like p53 null cells, mouse embryo fibroblast cells deficient in Apaf-1 and caspase-9, and expressing c-Myc, were resistant to apoptotic stimuli that mimic conditions in developing tumors. Inactivation of Apaf-1 or caspase-9 substituted for p53 loss in promoting the oncogenic transformation of Myc-expressing cells. These results imply a role for Apaf-1 and caspase-9 in controlling tumor development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Soengas, M S -- Alarcon, R M -- Yoshida, H -- Giaccia, A J -- Hakem, R -- Mak, T W -- Lowe, S W -- CA13106/CA/NCI NIH HHS/ -- CA64489/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 2;284(5411):156-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10102818" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptotic Protease-Activating Factor 1 ; Caspase 9 ; Caspases/genetics/*physiology ; Cell Division ; Cell Transformation, Neoplastic ; Cells, Cultured ; Cytochrome c Group/metabolism ; Genes, myc ; *Genes, p53 ; Genes, ras ; Mice ; Mice, Nude ; Mitochondria/metabolism ; Mutation ; Neoplasms, Experimental/genetics/metabolism/*pathology ; Proteins/genetics/*physiology ; Tumor Suppressor Protein p53/metabolism
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    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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    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
    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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    Biological action of leptin as an angiogenic factor (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-11
    Description: Leptin is a hormone that regulates food intake, and its receptor (OB-Rb) is expressed primarily in the hypothalamus. Here, it is shown that OB-Rb is also expressed in human vasculature and in primary cultures of human endothelial cells. In vitro and in vivo assays revealed that leptin has angiogenic activity. In vivo, leptin induced neovascularization in corneas from normal rats but not in corneas from fa/fa Zucker rats, which lack functional leptin receptors. These observations indicate that the vascular endothelium is a target for leptin and suggest a physiological mechanism whereby leptin-induced angiogenesis may facilitate increased energy expenditure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sierra-Honigmann, M R -- Nath, A K -- Murakami, C -- Garcia-Cardena, G -- Papapetropoulos, A -- Sessa, W C -- Madge, L A -- Schechner, J S -- Schwabb, M B -- Polverini, P J -- Flores-Riveros, J R -- New York, N.Y. -- Science. 1998 Sep 11;281(5383):1683-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, CT 06536, USA. rocio_sierra-honigmann@qm.yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9733517" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/metabolism ; Amino Acid Sequence ; Animals ; Carrier Proteins/analysis/*physiology ; Cells, Cultured ; Corneal Neovascularization ; DNA-Binding Proteins/metabolism ; Endothelial Growth Factors/pharmacology ; Endothelium, Vascular/chemistry/cytology/*physiology ; Energy Metabolism ; Humans ; Leptin ; Lipid Metabolism ; Lymphokines/pharmacology ; Molecular Sequence Data ; *Neovascularization, Physiologic ; Phosphorylation ; Proteins/pharmacology/*physiology ; Rats ; Rats, Zucker ; *Receptors, Cell Surface ; Receptors, Leptin ; STAT3 Transcription Factor ; Trans-Activators/metabolism ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
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    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Activation of the ATM kinase by ionizing radiation and phosphorylation of p53 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-11
    Description: The p53 tumor suppressor protein is activated and phosphorylated on serine-15 in response to various DNA damaging agents. The gene product mutated in ataxia telangiectasia, ATM, acts upstream of p53 in a signal transduction pathway initiated by ionizing radiation. Immunoprecipitated ATM had intrinsic protein kinase activity and phosphorylated p53 on serine-15 in a manganese-dependent manner. Ionizing radiation, but not ultraviolet radiation, rapidly enhanced this p53-directed kinase activity of endogenous ATM. These observations, along with the fact that phosphorylation of p53 on serine-15 in response to ionizing radiation is reduced in ataxia telangiectasia cells, suggest that ATM is a protein kinase that phosphorylates p53 in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Canman, C E -- Lim, D S -- Cimprich, K A -- Taya, Y -- Tamai, K -- Sakaguchi, K -- Appella, E -- Kastan, M B -- Siliciano, J D -- CA71387/CA/NCI NIH HHS/ -- ES05777/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1998 Sep 11;281(5383):1677-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Johns Hopkins School of Medicine, Oncology Center, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9733515" target="_blank"〉PubMed〈/a〉
    Keywords: Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins ; Cell Line ; DNA Damage ; DNA-Activated Protein Kinase ; *DNA-Binding Proteins ; Enzyme Activation ; Humans ; Lymphocytes/metabolism/radiation effects ; Mutation ; Nuclear Proteins ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Protein Kinases/*metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Proteins/genetics/*metabolism ; *Radiation, Ionizing ; Recombinant Fusion Proteins/metabolism ; Recombinant Proteins/metabolism ; Signal Transduction ; Transfection ; Tumor Suppressor Protein p53/*metabolism ; Tumor Suppressor Proteins ; Ultraviolet Rays
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  • 53
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    Uncoupling of nonreceptor tyrosine kinases from PLC-gamma1 in an SLP-76-deficient T cell (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-07-17
    Description: Activation of nonreceptor protein tyrosine kinases (PTKs) is essential for T cell receptor (TCR) responsiveness; however, the function of individual PTK substrates is often uncertain. A mutant T cell line was isolated that lacked expression of SLP-76 (SH2 domain-containing leukocyte protein of 76 kilodaltons), a hematopoietically expressed adaptor protein and PTK substrate. SLP-76 was not required for TCR-induced tyrosine phosphorylation of most proteins, but was required for optimal tyrosine phosphorylation and activation of phospholipase C-gamma1 (PLC-gamma1), as well as Ras pathway activation. TCR-inducible gene expression was dependent on SLP-76. Thus, coupling of TCR-regulated PTKs to downstream signaling pathways requires SLP-76.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yablonski, D -- Kuhne, M R -- Kadlecek, T -- Weiss, A -- CA72531/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Jul 17;281(5375):413-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Howard Hughes Medical Institute, Box 0795, University of California, San Francisco, San Francisco, CA 94143-0795, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9665884" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Calcium/metabolism ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Carrier Proteins/metabolism ; Cell Line ; DNA-Binding Proteins/metabolism ; Enzyme Activation ; Gene Expression Regulation ; Humans ; Inositol Phosphates/metabolism ; Interleukin-2/genetics ; Isoenzymes/*metabolism ; Jurkat Cells ; *Membrane Proteins ; Mitogen-Activated Protein Kinase 1 ; NFATC Transcription Factors ; *Nuclear Proteins ; Phospholipase C gamma ; Phosphoproteins/metabolism/*physiology ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein-Tyrosine Kinases/*metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Signal Transduction ; T-Lymphocytes/enzymology/*metabolism ; Transcription Factors/metabolism ; Transcriptional Activation ; Transfection ; Type C Phospholipases/*metabolism ; ras Proteins/metabolism
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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
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  • 55
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    Conversion of neuronal growth cone responses from repulsion to attraction by cyclic nucleotides (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-04
    Description: Nerve growth is regulated by attractive and repulsive factors in the nervous system. Microscopic gradients of Collapsin-1/Semaphorin III/D (Sema III) and myelin-associated glycoprotein trigger repulsive turning responses by growth cones of cultured Xenopus spinal neurons; the repulsion can be converted to attraction by pharmacological activation of the guanosine 3',5'-monophosphate (cGMP) and adenosine 3',5'-monophosphate signaling pathways, respectively. Sema III also causes the collapse of cultured rat sensory growth cones, which can be inhibited by activation of the cGMP pathway. Thus cyclic nucleotides can regulate growth cone behaviors and may be targets for designing treatments to alleviate the inhibition of nerve regeneration by repulsive factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Song, H -- Ming, G -- He, Z -- Lehmann, M -- McKerracher, L -- Tessier-Lavigne, M -- Poo, M -- NS22764/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1998 Sep 4;281(5382):1515-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California at San Diego, La Jolla, CA 92093-0357, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9727979" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Calcium/physiology ; Cells, Cultured ; Cyclic AMP/analogs & derivatives/pharmacology/*physiology ; Cyclic GMP/analogs & derivatives/pharmacology/*physiology ; Ganglia, Spinal/cytology ; Glycoproteins/*physiology ; Myelin-Associated Glycoprotein/physiology ; Nerve Growth Factors/*physiology ; Nerve Tissue Proteins/physiology ; Neurites/*physiology ; Neurons/cytology/*physiology ; Neuropilin-1 ; Rats ; Recombinant Proteins ; Semaphorin-3A ; Spinal Cord/cytology ; Thionucleotides/pharmacology ; Xenopus
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  • 56
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    Sphingosine-1-phosphate as a ligand for the G protein-coupled receptor EDG-1 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-21
    Description: The sphingolipid metabolite sphingosine-1-phosphate (SPP) has been implicated as a second messenger in cell proliferation and survival. However, many of its biological effects are due to binding to unidentified receptors on the cell surface. SPP activated the heterotrimeric guanine nucleotide binding protein (G protein)-coupled orphan receptor EDG-1, originally cloned as Endothelial Differentiation Gene-1. EDG-1 bound SPP with high affinity (dissociation constant = 8.1 nM) and high specificity. Overexpression of EDG-1 induced exaggerated cell-cell aggregation, enhanced expression of cadherins, and formation of well-developed adherens junctions in a manner dependent on SPP and the small guanine nucleotide binding protein Rho.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, M J -- Van Brocklyn, J R -- Thangada, S -- Liu, C H -- Hand, A R -- Menzeleev, R -- Spiegel, S -- Hla, T -- DK45659/DK/NIDDK NIH HHS/ -- GM43880/GM/NIGMS NIH HHS/ -- HL49094/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Mar 6;279(5356):1552-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Connecticut School of Medicine, Farmington, CT 06030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9488656" target="_blank"〉PubMed〈/a〉
    Keywords: Cadherins/*biosynthesis ; *Cell Aggregation ; Cell Differentiation ; Cell Line ; Cloning, Molecular ; GTP-Binding Proteins/metabolism ; Gene Expression ; Genes, Immediate-Early ; Humans ; Immediate-Early Proteins/genetics/*metabolism ; Intercellular Junctions/*ultrastructure ; Ligands ; *Lysophospholipids ; Mitogen-Activated Protein Kinase 1/metabolism ; Morphogenesis ; Receptors, Cell Surface/genetics/*metabolism ; *Receptors, G-Protein-Coupled ; Receptors, Lysophospholipid ; Signal Transduction ; Sphingosine/*analogs & derivatives/metabolism ; Transfection ; rho GTP-Binding Proteins
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  • 57
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    Recognition of stress-induced MHC molecules by intestinal epithelial gammadelta T cells (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-28
    Description: T cells with variable region Vdelta1 gammadelta T cell receptors (TCRs) are distributed throughout the human intestinal epithelium and may function as sentinels that respond to self antigens. The expression of a major histocompatibility complex (MHC) class I-related molecule, MICA, matches this localization. MICA and the closely related MICB were recognized by intestinal epithelial T cells expressing diverse Vdelta1 gammadelta TCRs. These interactions involved the alpha1alpha2 domains of MICA and MICB but were independent of antigen processing. With intestinal epithelial cell lines, the expression and recognition of MICA and MICB could be stress-induced. Thus, these molecules may broadly regulate protective responses by the Vdelta1 gammadelta T cells in the epithelium of the intestinal tract.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Groh, V -- Steinle, A -- Bauer, S -- Spies, T -- P01 CA18221/CA/NCI NIH HHS/ -- R01 AI30581/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1998 Mar 13;279(5357):1737-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fred Hutchinson Cancer Research Center, Clinical Research Division, 1100 Fairview Avenue North, Seattle, WA 98109, USA. vgroh@fred.fhcrc.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9497295" target="_blank"〉PubMed〈/a〉
    Keywords: Antigen Presentation ; Carrier Proteins/analysis/*immunology ; Cell Line ; Cytotoxicity, Immunologic ; Heat-Shock Response ; Histocompatibility Antigens Class I/analysis/*immunology ; Hot Temperature ; Humans ; Immunophenotyping ; Intestinal Mucosa/cytology/*immunology ; Ligands ; Receptors, Antigen, T-Cell, gamma-delta/*immunology ; T-Lymphocyte Subsets/*immunology ; Transfection ; Tumor Cells, Cultured
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    Cloning for profit (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, G B -- Seidel, G E -- New York, N.Y. -- Science. 1998 May 29;280(5368):1400-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Animal Science, University of California at Davis, Davis, CA 95616-8521, USA. gbanderson@ucdavis.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9634416" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Animals, Genetically Modified ; Cell Cycle ; *Cloning, Organism ; Embryo, Mammalian/cytology ; Embryo, Nonmammalian ; Fetus/cytology ; Fibroblasts/cytology ; Genetic Engineering ; *Nuclear Transfer Techniques ; Plants/genetics ; Transfection
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  • 59
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    Regulation of nerve growth mediated by inositol 1,4,5-trisphosphate receptors in growth cones (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-30
    Description: The inositol 1,4,5-trisphosphate (IP3) receptor (IP3R) acts as a Ca2+ release channel on internal Ca2+ stores. Type 1 IP3R (IP3R1) is enriched in growth cones of neurons in chick dorsal root ganglia. Depletion of internal Ca2+ stores and inhibition of IP3 signaling with drugs inhibited neurite extension. Microinjection of heparin, a competitive IP3R blocker, induced neurite retraction. Acute localized loss of function of IP3R1 in the growth cone induced by chromophore-assisted laser inactivation resulted in growth arrest and neurite retraction. IP3-induced Ca2+ release in growth cones appears to have a crucial role in control of nerve growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takei, K -- Shin, R M -- Inoue, T -- Kato, K -- Mikoshiba, K -- New York, N.Y. -- Science. 1998 Nov 27;282(5394):1705-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Calciosignal Net Project, Exploratory Research for Advanced Technology (ERATO), Japan Science and Technology Corporation (JST), Bunkyo-Ku, Tokyo 113-0021, Japan. kohtaro@ims.u-tokyo.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9831561" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Calcium Channels/*metabolism ; Calcium Signaling ; Cells, Cultured ; Cerebellum/metabolism ; Chick Embryo ; Ganglia, Spinal/cytology ; Growth Cones/*metabolism ; Heparin/pharmacology ; Inositol 1,4,5-Trisphosphate/*metabolism ; Inositol 1,4,5-Trisphosphate Receptors ; Lasers ; Lithium Chloride/pharmacology ; Mice ; Microscopy, Video ; Microsomes/metabolism ; Microtubules/metabolism ; Neurites/drug effects/*physiology ; Pseudopodia/drug effects/physiology ; Receptors, Cytoplasmic and Nuclear/*metabolism ; Signal Transduction ; Thapsigargin/pharmacology
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    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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    First components found for new kidney filter (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1999 Oct 8;286(5438):225-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577188" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Cells, Cultured ; Chromosomes, Human, Pair 19/genetics ; Cytoskeletal Proteins ; Humans ; Intercellular Junctions/metabolism/ultrastructure ; Kidney Glomerulus/blood supply/chemistry/*metabolism/*ultrastructure ; Membrane Proteins ; Mice ; Mice, Knockout ; Microscopy, Electron ; Mutation ; Nephrotic Syndrome/congenital/genetics/pathology ; Proteins/chemistry/genetics/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    Dynamic control of CaMKII translocation and localization in hippocampal neurons by NMDA receptor stimulation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-02
    Description: Calcium-calmodulin-dependent protein kinase II (CaMKII) is thought to increase synaptic strength by phosphorylating postsynaptic density (PSD) ion channels and signaling proteins. It is shown that N-methyl-D-aspartate (NMDA) receptor stimulation reversibly translocates green fluorescent protein-tagged CaMKII from an F-actin-bound to a PSD-bound state. The translocation time was controlled by the ratio of expressed beta-CaMKII to alpha-CaMKII isoforms. Although F-actin dissociation into the cytosol required autophosphorylation of or calcium-calmodulin binding to beta-CaMKII, PSD translocation required binding of calcium-calmodulin to either the alpha- or beta-CaMKII subunits. Autophosphorylation of CaMKII indirectly prolongs its PSD localization by increasing the calmodulin-binding affinity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, K -- Meyer, T -- GM-48113/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 2;284(5411):162-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Department of Pharmacology and Cancer Biology, Box 3709, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10102820" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Calcium/pharmacology ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cells, Cultured ; Cytosol/metabolism ; Dendrites/*enzymology ; Electric Stimulation ; Glutamic Acid/pharmacology ; Green Fluorescent Proteins ; Hippocampus/cytology/*enzymology ; Isoenzymes/metabolism ; Luminescent Proteins ; Microscopy, Fluorescence ; Nerve Tissue Proteins/analysis ; Neurons/*enzymology ; Phosphorylation ; Rats ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Synapses/*enzymology ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Perforin gene defects in familial hemophagocytic lymphohistiocytosis (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-03
    Description: Familial hemophagocytic lymphohistiocytosis (FHL) is a rare, rapidly fatal, autosomal recessive immune disorder characterized by uncontrolled activation of T cells and macrophages and overproduction of inflammatory cytokines. Linkage analyses indicate that FHL is genetically heterogeneous and linked to 9q21.3-22, 10q21-22, or another as yet undefined locus. Sequencing of the coding regions of the perforin gene of eight unrelated 10q21-22-linked FHL patients revealed homozygous nonsense mutations in four patients and missense mutations in the other four patients. Cultured lymphocytes from patients had defective cytotoxic activity, and immunostaining revealed little or no perforin in the granules. Thus, defects in perforin are responsible for 10q21-22-linked FHL. Perforin-based effector systems are, therefore, involved not only in the lysis of abnormal cells but also in the down-regulation of cellular immune activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stepp, S E -- Dufourcq-Lagelouse, R -- Le Deist, F -- Bhawan, S -- Certain, S -- Mathew, P A -- Henter, J I -- Bennett, M -- Fischer, A -- de Saint Basile, G -- Kumar, V -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1957-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and the Graduate Program in Immunology, University of Texas Southwestern Medical School, Dallas, TX 75235, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10583959" target="_blank"〉PubMed〈/a〉
    Keywords: Antigen-Presenting Cells/immunology ; Cell Death ; Cell Line ; Cells, Cultured ; Chromosome Mapping ; Chromosomes, Human, Pair 10/*genetics ; Codon, Terminator ; Cytoplasmic Granules/chemistry ; Cytotoxicity, Immunologic ; Frameshift Mutation ; Genetic Linkage ; Granzymes ; Heterozygote ; Histiocytosis, Non-Langerhans-Cell/*genetics/immunology ; Humans ; Lymphocyte Activation ; Membrane Glycoproteins/analysis/*genetics/physiology ; Mutation, Missense ; Perforin ; Point Mutation ; Pore Forming Cytotoxic Proteins ; Serine Endopeptidases/analysis ; T-Lymphocytes, Cytotoxic/chemistry/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Introducing proteins into the body's cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strauss, E -- New York, N.Y. -- Science. 1999 Sep 3;285(5433):1466-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10498525" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/*metabolism ; Cells, Cultured ; Drug Carriers ; *Drug Delivery Systems ; Gene Products, tat/chemistry/*metabolism ; Humans ; Mice ; Protein Denaturation ; Protein Folding ; Recombinant Fusion Proteins/administration & dosage/chemistry/*metabolism ; beta-Galactosidase/administration & dosage/chemistry/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Specific lipopolysaccharide found in cystic fibrosis airway Pseudomonas aeruginosa (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-24
    Description: Cystic fibrosis (CF) patients develop chronic airway infections with Pseudomonas aeruginosa (PA). Pseudomonas aeruginosa synthesized lipopolysaccharide (LPS) with a variety of penta- and hexa-acylated lipid A structures under different environmental conditions. CF patient PA synthesized LPS with specific lipid A structures indicating unique recognition of the CF airway environment. CF-specific lipid A forms containing palmitate and aminoarabinose were associated with resistance to cationic antimicrobial peptides and increased inflammatory responses, indicating that they are likely to be involved in airway disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ernst, R K -- Yi, E C -- Guo, L -- Lim, K B -- Burns, J L -- Hackett, M -- Miller, S I -- R21 R13400/PHS HHS/ -- R55 HL 48888/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1561-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10567263" target="_blank"〉PubMed〈/a〉
    Keywords: Acylation ; Arabinose/analogs & derivatives/analysis/metabolism ; Bacterial Proteins/genetics/physiology ; Cells, Cultured ; Cystic Fibrosis/complications/*microbiology ; Drug Resistance, Microbial ; Humans ; Infant ; Interleukin-8/biosynthesis ; Lipid A/*biosynthesis/*chemistry ; Lipopolysaccharides/chemistry/immunology ; Magnesium/pharmacology ; Mutation ; Palmitates/analysis/metabolism ; Peptides/pharmacology ; Polymyxins/pharmacology ; Pseudomonas Infections/*microbiology ; Pseudomonas aeruginosa/drug effects/genetics/*metabolism/pathogenicity ; Respiratory System/*microbiology ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; Virulence
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    BRCA1 inhibition of estrogen receptor signaling in transfected cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: Mutations of the breast cancer susceptibility gene BRCA1 confer increased risk for breast, ovarian, and prostatic cancers, but it is not clear why the mutations are associated with these particular tumor types. In transient transfection assays, BRCA1 was found to inhibit signaling by the ligand-activated estrogen receptor (ER-alpha) through the estrogen-responsive enhancer element and to block the transcriptional activation function AF-2 of ER-alpha. These results raise the possibility that wild-type BRCA1 suppresses estrogen-dependent transcriptional pathways related to mammary epithelial cell proliferation and that loss of this ability contributes to tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fan, S -- Wang, J -- Yuan, R -- Ma, Y -- Meng, Q -- Erdos, M R -- Pestell, R G -- Yuan, F -- Auborn, K J -- Goldberg, I D -- Rosen, E M -- R01-CA75503/CA/NCI NIH HHS/ -- R01-ES09169/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1999 May 21;284(5418):1354-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Radiation Oncology, Long Island Jewish Medical Center, The Long Island Campus for the Albert Einstein College of Medicine, 270-05 76th Avenue, New Hyde Park, NY 11040, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334989" target="_blank"〉PubMed〈/a〉
    Keywords: BRCA1 Protein/*physiology ; Breast/cytology ; Breast Neoplasms/etiology ; Cell Division ; Enhancer Elements, Genetic ; Epithelial Cells/cytology ; Estradiol/metabolism ; Estrogen Receptor alpha ; Female ; Genes, BRCA1 ; Genes, Reporter ; Humans ; Ligands ; Male ; Receptors, Estrogen/*metabolism ; *Signal Transduction ; Transcription Factors/metabolism ; *Transcriptional Activation ; Transfection ; Tumor Cells, Cultured
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    Regulation of myosin phosphatase by a specific interaction with cGMP- dependent protein kinase Ialpha (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-24
    Description: Contraction and relaxation of smooth muscle are regulated by myosin light-chain kinase and myosin phosphatase through phosphorylation and dephosphorylation of myosin light chains. Cyclic guanosine monophosphate (cGMP)-dependent protein kinase Ialpha (cGKIalpha) mediates physiologic relaxation of vascular smooth muscle in response to nitric oxide and cGMP. It is shown here that cGKIalpha is targeted to the smooth muscle cell contractile apparatus by a leucine zipper interaction with the myosin-binding subunit (MBS) of myosin phosphatase. Uncoupling of the cGKIalpha-MBS interaction prevents cGMP-dependent dephosphorylation of myosin light chain, demonstrating that this interaction is essential to the regulation of vascular smooth muscle cell tone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Surks, H K -- Mochizuki, N -- Kasai, Y -- Georgescu, S P -- Tang, K M -- Ito, M -- Lincoln, T M -- Mendelsohn, M E -- HL09330/HL/NHLBI NIH HHS/ -- HL55309/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1583-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Cardiology Research Institute and Cardiology Division, Department of Medicine, Tufts University School of Medicine and New England Medical Center, Boston, MA 02111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10567269" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Substitution ; Animals ; Cells, Cultured ; Cyclic GMP-Dependent Protein Kinase Type I ; Cyclic GMP-Dependent Protein Kinases/chemistry/genetics/*metabolism ; Histones/metabolism ; Humans ; Isoenzymes/chemistry/metabolism ; Leucine Zippers ; Muscle Contraction ; Muscle Relaxation ; Muscle, Smooth, Vascular/*enzymology/physiology ; Mutagenesis, Site-Directed ; Myosin Light Chains/*metabolism ; Myosin-Light-Chain Phosphatase ; Phosphoprotein Phosphatases/chemistry/*metabolism ; Phosphorylation ; Precipitin Tests ; Rats ; Recombinant Fusion Proteins/metabolism ; Substrate Specificity ; Transfection ; Two-Hybrid System Techniques
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    The role of CCR7 in TH1 and TH2 cell localization and delivery of B cell help in vivo (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-11
    Description: Subsets of murine CD4+ T cells localize to different areas of the spleen after adoptive transfer. Naive and T helper 1 (TH1) cells, which express the chemokine receptor CCR7, are home to the periarteriolar lymphoid sheath, whereas activated TH2 cells, which lack CCR7, form rings at the periphery of the T cell zones near B cell follicles. Retroviral transduction of TH2 cells with CCR7 forces them to localize in a TH1-like pattern and inhibits their participation in B cell help in vivo but not in vitro. Thus, differential expression of chemokine receptors results in unique cellular migration patterns that are important for effective immune responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Randolph, D A -- Huang, G -- Carruthers, C J -- Bromley, L E -- Chaplin, D D -- AI34580/AI/NIAID NIH HHS/ -- T32 GM07200/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Dec 10;286(5447):2159-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Allergy and Immunology, Department of Internal Medicine, Center for Immunology, Washington University School of Medicine. Howard Hughes Medical Institute, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10591648" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; B-Lymphocytes/*immunology ; Calcium/metabolism ; Cell Movement ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; Mice, Transgenic ; Ovalbumin/immunology ; Receptors, CCR7 ; Receptors, Chemokine/*immunology/metabolism ; Signal Transduction ; Spleen/*immunology ; Th1 Cells/*immunology/metabolism ; Th2 Cells/*immunology/metabolism ; Transfection
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    Inhibition of the interferon-inducible protein kinase PKR by HCV E2 protein (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-03
    Description: Most isolates of hepatitis C virus (HCV) infections are resistant to interferon, the only available therapy, but the mechanism underlying this resistance has not been defined. Here it is shown that the HCV envelope protein E2 contains a sequence identical with phosphorylation sites of the interferon-inducible protein kinase PKR and the translation initiation factor eIF2alpha, a target of PKR. E2 inhibited the kinase activity of PKR and blocked its inhibitory effect on protein synthesis and cell growth. This interaction of E2 and PKR may be one mechanism by which HCV circumvents the antiviral effect of interferon.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taylor, D R -- Shi, S T -- Romano, P R -- Barber, G N -- Lai, M M -- AI 40038/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 2;285(5424):107-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology and Immunology and Howard Hughes Medical Institute, University of Southern California, School of Medicine, Los Angeles, CA 90089, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10390359" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Chloramphenicol O-Acetyltransferase/biosynthesis ; Drug Resistance, Microbial ; Endoplasmic Reticulum/metabolism ; Enzyme Induction ; Eukaryotic Initiation Factor-2/chemistry/metabolism ; HeLa Cells ; *Hepacivirus/drug effects ; Humans ; Interferon-alpha/*pharmacology ; Phosphorylation ; Protein Biosynthesis ; Recombinant Fusion Proteins/metabolism/pharmacology ; Saccharomyces cerevisiae/genetics/growth & development/metabolism ; Transfection ; Transformation, Genetic ; Viral Envelope Proteins/chemistry/metabolism/pharmacology/*physiology ; eIF-2 Kinase/*antagonists & inhibitors/chemistry/metabolism
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    Prevention of constitutive TNF receptor 1 signaling by silencer of death domains (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-23
    Description: Tumor necrosis factor receptor type 1 (TNF-R1) contains a cytoplasmic death domain that is required for the signaling of TNF activities such as apoptosis and nuclear factor kappa B (NF-kappaB) activation. Normally, these signals are generated only after TNF-induced receptor aggregation. However, TNF-R1 self-associates and signals independently of ligand when overexpressed. This apparent paradox may be explained by silencer of death domains (SODD), a widely expressed approximately 60-kilodalton protein that was found to be associated with the death domain of TNF-R1. TNF treatment released SODD from TNF-R1, permitting the recruitment of proteins such as TRADD and TRAF2 to the active TNF-R1 signaling complex. SODD also interacted with death receptor-3 (DR3), another member of the TNF receptor superfamily. Thus, SODD association may be representative of a general mechanism for preventing spontaneous signaling by death domain-containing receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jiang, Y -- Woronicz, J D -- Liu, W -- Goeddel, D V -- New York, N.Y. -- Science. 1999 Jan 22;283(5401):543-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tularik, Two Corporate Drive, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9915703" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Antigens, CD/chemistry/genetics/*metabolism ; Apoptosis ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Line ; Fas-Associated Death Domain Protein ; Humans ; Jurkat Cells ; Molecular Sequence Data ; Mutation ; NF-kappa B/metabolism ; Protein Binding ; Proteins/metabolism ; Receptor Aggregation ; Receptor-Interacting Protein Serine-Threonine Kinases ; Receptors, Tumor Necrosis Factor/chemistry/genetics/*metabolism ; Receptors, Tumor Necrosis Factor, Member 25 ; Receptors, Tumor Necrosis Factor, Type I ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; TNF Receptor-Associated Factor 1 ; TNF Receptor-Associated Factor 2 ; Transfection ; Tumor Necrosis Factor-alpha/pharmacology ; U937 Cells
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    Microglial activation resulting from CD40-CD40L interaction after beta-amyloid stimulation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-22
    Description: Alzheimer's disease (AD) has a substantial inflammatory component, and activated microglia may play a central role in neuronal degeneration. CD40 expression was increased on cultured microglia treated with freshly solublized amyloid-beta (Abeta, 500 nanomolar) and on microglia from a transgenic murine model of AD (Tg APPsw). Increased tumor necrosis factor alpha production and induction of neuronal injury occurred when Abeta-stimulated microglia were treated with CD40 ligand (CD40L). Microglia from Tg APPsw mice deficient for CD40L demonstrated reduction in activation, suggesting that the CD40-CD40L interaction is necessary for Abeta-induced microglial activation. Finally, abnormal tau phosphorylation was reduced in Tg APPsw animals deficient for CD40L, suggesting that the CD40-CD40L interaction is an early event in AD pathogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tan, J -- Town, T -- Paris, D -- Mori, T -- Suo, Z -- Crawford, F -- Mattson, M P -- Flavell, R A -- Mullan, M -- New York, N.Y. -- Science. 1999 Dec 17;286(5448):2352-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Roskamp Institute, University of South Florida, 3515 East Fletcher Avenue, Tampa, FL 33613, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10600748" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/metabolism ; Amyloid beta-Peptides/*metabolism/pharmacology ; Animals ; Antigens, CD40/biosynthesis/*metabolism ; CD40 Ligand ; Cell Death ; Cells, Cultured ; Interferon-gamma/pharmacology ; Interleukins/pharmacology ; Ligands ; Membrane Glycoproteins/*metabolism/pharmacology ; Mice ; Mice, Transgenic ; Microglia/cytology/immunology/*metabolism ; Neurons/cytology ; Peptide Fragments/pharmacology ; Phosphorylation ; Signal Transduction ; Tumor Necrosis Factor-alpha/biosynthesis/pharmacology ; tau Proteins/metabolism
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    Beta-arrestin-dependent formation of beta2 adrenergic receptor-Src protein kinase complexes (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-29
    Description: The Ras-dependent activation of mitogen-activated protein (MAP) kinase pathways by many receptors coupled to heterotrimeric guanine nucleotide binding proteins (G proteins) requires the activation of Src family tyrosine kinases. Stimulation of beta2 adrenergic receptors resulted in the assembly of a protein complex containing activated c-Src and the receptor. Src recruitment was mediated by beta-arrestin, which functions as an adapter protein, binding both c-Src and the agonist-occupied receptor. beta-Arrestin 1 mutants, impaired either in c-Src binding or in the ability to target receptors to clathrin-coated pits, acted as dominant negative inhibitors of beta2 adrenergic receptor-mediated activation of the MAP kinases Erk1 and Erk2. These data suggest that beta-arrestin binding, which terminates receptor-G protein coupling, also initiates a second wave of signal transduction in which the "desensitized" receptor functions as a critical structural component of a mitogenic signaling complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luttrell, L M -- Ferguson, S S -- Daaka, Y -- Miller, W E -- Maudsley, S -- Della Rocca, G J -- Lin, F -- Kawakatsu, H -- Owada, K -- Luttrell, D K -- Caron, M G -- Lefkowitz, R J -- DK02352/DK/NIDDK NIH HHS/ -- DK55524/DK/NIDDK NIH HHS/ -- HL16037/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Jan 29;283(5402):655-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9924018" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic beta-Agonists/metabolism/pharmacology ; Animals ; Arrestins/genetics/*metabolism ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Line ; Cell Membrane/metabolism ; Enzyme Activation ; GTP-Binding Proteins/metabolism ; Humans ; Isoproterenol/metabolism/pharmacology ; Mitogen-Activated Protein Kinase 1 ; Mitogen-Activated Protein Kinase 3 ; *Mitogen-Activated Protein Kinases ; Models, Biological ; Phosphorylation ; Point Mutation ; Precipitin Tests ; Proto-Oncogene Proteins pp60(c-src)/*metabolism ; Receptor Cross-Talk ; Receptors, Adrenergic, beta-2/*metabolism ; Receptors, Cell Surface/metabolism ; *Signal Transduction ; Transfection ; src Homology Domains
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    Proapoptotic Bcl-2 relative Bim required for certain apoptotic responses, leukocyte homeostasis, and to preclude autoimmunity (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-27
    Description: Apoptosis can be triggered by members of the Bcl-2 protein family, such as Bim, that share only the BH3 domain with this family. Gene targeting in mice revealed important physiological roles for Bim. Lymphoid and myeloid cells accumulated, T cell development was perturbed, and most older mice accumulated plasma cells and succumbed to autoimmune kidney disease. Lymphocytes were refractory to apoptotic stimuli such as cytokine deprivation, calcium ion flux, and microtubule perturbation but not to others. Thus, Bim is required for hematopoietic homeostasis and as a barrier to autoimmunity. Moreover, particular death stimuli appear to activate apoptosis through distinct BH3-only proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bouillet, P -- Metcalf, D -- Huang, D C -- Tarlinton, D M -- Kay, T W -- Kontgen, F -- Adams, J M -- Strasser, A -- CA43540/CA/NCI NIH HHS/ -- CA80188/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1735-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria 3050, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10576740" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins ; Autoimmune Diseases/etiology ; *Autoimmunity ; B-Lymphocytes/physiology ; Carrier Proteins/*physiology ; Cells, Cultured ; Crosses, Genetic ; Female ; Gene Targeting ; Glomerulonephritis/etiology ; Hematopoietic Stem Cells/physiology ; Homeostasis ; Leukocyte Count ; Leukocytes/*physiology ; Male ; *Membrane Proteins ; Mice ; Mice, Transgenic ; *Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-bcl-2/physiology ; Signal Transduction ; T-Lymphocyte Subsets/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    New clues to how neurons strengthen their connections (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1999 Jun 11;284(5421):1755-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10391789" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/cytology/physiology ; Cells, Cultured ; Dendrites/physiology/ultrastructure ; Glutamic Acid/*physiology ; Long-Term Potentiation/*physiology ; Mice ; Neurons/physiology ; Rats ; Receptors, AMPA/*physiology ; Receptors, N-Methyl-D-Aspartate/*physiology ; Synapses/*physiology
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    Association of BRCA1 with the hRad50-hMre11-p95 complex and the DNA damage response (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: BRCA1 encodes a tumor suppressor that is mutated in familial breast and ovarian cancers. Here, it is shown that BRCA1 interacts in vitro and in vivo with hRad50, which forms a complex with hMre11 and p95/nibrin. Upon irradiation, BRCA1 was detected in discrete foci in the nucleus, which colocalize with hRad50. Formation of irradiation-induced foci positive for BRCA1, hRad50, hMre11, or p95 was dramatically reduced in HCC/1937 breast cancer cells carrying a homozygous mutation in BRCA1 but was restored by transfection of wild-type BRCA1. Ectopic expression of wild-type, but not mutated, BRCA1 in these cells rendered them less sensitive to the DNA damage agent, methyl methanesulfonate. These data suggest that BRCA1 is important for the cellular responses to DNA damage that are mediated by the hRad50-hMre11-p95 complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhong, Q -- Chen, C F -- Li, S -- Chen, Y -- Wang, C C -- Xiao, J -- Chen, P L -- Sharp, Z D -- Lee, W H -- CA 30195/CA/NCI NIH HHS/ -- CA 58183/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):747-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Medicine, Institute of Biotechnology, University of Texas Health Science Center at San Antonio, 15355 Lambda Drive, San Antonio, TX 78245, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426999" target="_blank"〉PubMed〈/a〉
    Keywords: BRCA1 Protein/*metabolism ; Cell Cycle Proteins/*metabolism ; Cell Nucleus/*metabolism ; Cell Survival ; *DNA Damage ; *DNA Repair Enzymes ; DNA-Binding Proteins/*metabolism ; Gamma Rays ; Genes, BRCA1 ; Humans ; Methyl Methanesulfonate/pharmacology ; Mutagens/pharmacology ; Mutation ; *Nuclear Proteins ; Rad51 Recombinase ; Recombination, Genetic ; Transfection ; Tumor Cells, Cultured
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    Identification of a nuclear receptor for bile acids (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-05-21
    Description: Bile acids are essential for the solubilization and transport of dietary lipids and are the major products of cholesterol catabolism. Results presented here show that bile acids are physiological ligands for the farnesoid X receptor (FXR), an orphan nuclear receptor. When bound to bile acids, FXR repressed transcription of the gene encoding cholesterol 7alpha-hydroxylase, which is the rate-limiting enzyme in bile acid synthesis, and activated the gene encoding intestinal bile acid-binding protein, which is a candidate bile acid transporter. These results demonstrate a mechanism by which bile acids transcriptionally regulate their biosynthesis and enterohepatic transport.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Makishima, M -- Okamoto, A Y -- Repa, J J -- Tu, H -- Learned, R M -- Luk, A -- Hull, M V -- Lustig, K D -- Mangelsdorf, D J -- Shan, B -- New York, N.Y. -- Science. 1999 May 21;284(5418):1362-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Pharmacology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235-9050, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334992" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bile Acids and Salts/biosynthesis/*metabolism ; Biological Transport ; Carrier Proteins/*genetics/metabolism ; Cell Line ; Chenodeoxycholic Acid/*metabolism ; Cholesterol/metabolism ; Cholesterol 7-alpha-Hydroxylase/*genetics ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Gene Expression Regulation ; Histone Acetyltransferases ; Homeostasis ; Humans ; *Hydroxysteroid Dehydrogenases ; Ligands ; Liver/metabolism ; *Membrane Glycoproteins ; Mice ; Nuclear Receptor Coactivator 1 ; *Organic Anion Transporters, Sodium-Dependent ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism ; *Symporters ; Transcription Factors/chemistry/genetics/*metabolism ; Transfection ; Tumor Cells, Cultured
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    KDR receptor: a key marker defining hematopoietic stem cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-08
    Description: Studies on pluripotent hematopoietic stem cells (HSCs) have been hindered by lack of a positive marker, comparable to the CD34 marker of hematopoietic progenitor cells (HPCs). In human postnatal hematopoietic tissues, 0.1 to 0.5% of CD34(+) cells expressed vascular endothelial growth factor receptor 2 (VEGFR2, also known as KDR). Pluripotent HSCs were restricted to the CD34+KDR+ cell fraction. Conversely, lineage-committed HPCs were in the CD34+KDR- subset. On the basis of limiting dilution analysis, the HSC frequency in the CD34+KDR+ fraction was 20 percent in bone marrow (BM) by mouse xenograft assay and 25 to 42 percent in BM, peripheral blood, and cord blood by 12-week long-term culture (LTC) assay. The latter values rose to 53 to 63 percent in LTC supplemented with VEGF and to greater than 95 percent for the cell subfraction resistant to growth factor starvation. Thus, KDR is a positive functional marker defining stem cells and distinguishing them from progenitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ziegler, B L -- Valtieri, M -- Porada, G A -- De Maria, R -- Muller, R -- Masella, B -- Gabbianelli, M -- Casella, I -- Pelosi, E -- Bock, T -- Zanjani, E D -- Peschle, C -- New York, N.Y. -- Science. 1999 Sep 3;285(5433):1553-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Hematology and Oncology, University of Tubingen, Otfried-Muller-Strasse 10, D-72076 Tubingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10477517" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD34/*analysis ; Bone Marrow Cells/cytology ; Cell Lineage ; Cell Separation ; Cells, Cultured ; Endothelial Growth Factors/pharmacology ; Female ; Fetal Blood/cytology ; Fetus ; Flow Cytometry ; *Hematopoiesis ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/chemistry/*cytology/drug effects/physiology ; Humans ; Lymphokines/pharmacology ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Phenotype ; Pregnancy ; Receptor Protein-Tyrosine Kinases/*analysis/physiology ; Receptors, Growth Factor/*analysis/physiology ; Receptors, Vascular Endothelial Growth Factor ; Sheep ; Transplantation, Heterologous ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
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    Reciprocal control of T helper cell and dendritic cell differentiation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-02-19
    Description: It is not known whether subsets of dendritic cells provide different cytokine microenvironments that determine the differentiation of either type-1 T helper (TH1) or TH2 cells. Human monocyte (pDC1)-derived dendritic cells (DC1) were found to induce TH1 differentiation, whereas dendritic cells (DC2) derived from CD4+CD3-CD11c- plasmacytoid cells (pDC2) induced TH2 differentiation by use of a mechanism unaffected by interleukin-4 (IL-4) or IL-12. The TH2 cytokine IL-4 enhanced DC1 maturation and killed pDC2, an effect potentiated by IL-10 but blocked by CD40 ligand and interferon-gamma. Thus, a negative feedback loop from the mature T helper cells may selectively inhibit prolonged TH1 or TH2 responses by regulating survival of the appropriate dendritic cell subset.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rissoan, M C -- Soumelis, V -- Kadowaki, N -- Grouard, G -- Briere, F -- de Waal Malefyt, R -- Liu, Y J -- New York, N.Y. -- Science. 1999 Feb 19;283(5405):1183-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Schering-Plough, Laboratory for Immunological Research, 27 chemin des Peupliers, Boite Postale 11, 69571, Dardilly, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10024247" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD40 ; Apoptosis ; CD40 Ligand ; Cell Differentiation ; Cell Lineage ; Cell Survival ; Cells, Cultured ; Coculture Techniques ; Dendritic Cells/*cytology/immunology ; Feedback ; Humans ; Interferon-gamma/biosynthesis/pharmacology ; Interleukin-12/biosynthesis/pharmacology/physiology ; Interleukin-4/biosynthesis/pharmacology/*physiology ; Interleukins/biosynthesis/pharmacology ; Lymphocyte Activation ; Membrane Glycoproteins/pharmacology ; Stem Cells/cytology ; Th1 Cells/*cytology/immunology ; Th2 Cells/*cytology/immunology
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    Differentiation stage-specific inhibition of the Raf-MEK-ERK pathway by Akt (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-27
    Description: Extracellular signals often result in simultaneous activation of both the Raf-MEK-ERK and PI3K-Akt pathways (where ERK is extracellular-regulated kinase, MEK is mitogen-activated protein kinase or ERK kinase, and PI3K is phosphatidylinositol 3-kinase). However, these two signaling pathways were shown to exert opposing effects on muscle cell hypertrophy. Furthermore, the PI3K-Akt pathway was shown to inhibit the Raf-MEK-ERK pathway; this cross-regulation depended on the differentiation state of the cell: Akt activation inhibited the Raf-MEK-ERK pathway in differentiated myotubes, but not in their myoblast precursors. The stage-specific inhibitory action of Akt correlated with its stage-specific ability to form a complex with Raf, suggesting the existence of differentially expressed mediators of an inhibitory Akt-Raf complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rommel, C -- Clarke, B A -- Zimmermann, S -- Nunez, L -- Rossman, R -- Reid, K -- Moelling, K -- Yancopoulos, G D -- Glass, D J -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1738-41.〈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/10576741" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Line ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins/genetics ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Flavonoids/pharmacology ; Insulin-Like Growth Factor I/pharmacology ; MAP Kinase Signaling System/drug effects ; Mice ; Mitogen-Activated Protein Kinases/*antagonists & inhibitors/metabolism ; Muscle, Skeletal/*cytology/*metabolism ; Myogenin/genetics ; Phenotype ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-akt ; Proto-Oncogene Proteins c-raf/*antagonists & inhibitors/metabolism ; Signal Transduction ; Transfection ; Transgenes
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    Molecular identification of a eukaryotic, stretch-activated nonselective cation channel (1999)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1999-08-07
    Description: Calcium-permeable, stretch-activated nonselective cation (SA Cat) channels mediate cellular responses to mechanical stimuli. However, genes encoding such channels have not been identified in eukaryotes. The yeast MID1 gene product (Mid1) is required for calcium influx in the yeast Saccharomyces cerevisiae. Functional expression of Mid1 in Chinese hamster ovary cells conferred sensitivity to mechanical stress that resulted in increases in both calcium conductance and the concentration of cytosolic free calcium. These increases were dependent on the presence of extracellular calcium and were reduced by gadolinium, a blocker of SA Cat channels. Single-channel analyses with cell-attached patches revealed that Mid1 acts as a calcium-permeable, cation-selective stretch-activated channel with a conductance of 32 picosiemens at 150 millimolar cesium chloride in the pipette. Thus, Mid1 appears to be a eukaryotic, SA Cat channel.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kanzaki, M -- Nagasawa, M -- Kojima, I -- Sato, C -- Naruse, K -- Sokabe, M -- Iida, H -- New York, N.Y. -- Science. 1999 Aug 6;285(5429):882-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell Biology, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma 371-8510, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10436155" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; CHO Cells ; Calcium/metabolism ; Calcium Channels/chemistry/genetics/*metabolism ; Cations/*metabolism ; Cell Membrane/metabolism ; Cell Membrane Permeability ; Cesium/metabolism ; Chlorides/pharmacology ; Cricetinae ; Fungal Proteins/chemistry/genetics/*metabolism ; Gadolinium/pharmacology ; Ion Channels/chemistry/genetics/*metabolism ; Membrane Glycoproteins/chemistry/genetics/*metabolism ; Membrane Potentials ; Molecular Sequence Data ; Patch-Clamp Techniques ; Pressure ; Saccharomyces cerevisiae/genetics/metabolism ; *Saccharomyces cerevisiae Proteins ; Stress, Mechanical ; Transfection ; Zinc Compounds/pharmacology
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    UDP-GlcNAc 2-epimerase: a regulator of cell surface sialylation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: Modification of cell surface molecules with sialic acid is crucial for their function in many biological processes, including cell adhesion and signal transduction. Uridine diphosphate-N-acetylglucosamine 2-epimerase (UDP-GlcNAc 2-epimerase) is an enzyme that catalyzes an early, rate-limiting step in the sialic acid biosynthetic pathway. UDP-GlcNAc 2-epimerase was found to be a major determinant of cell surface sialylation in human hematopoietic cell lines and a critical regulator of the function of specific cell surface adhesion molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keppler, O T -- Hinderlich, S -- Langner, J -- Schwartz-Albiez, R -- Reutter, W -- Pawlita, M -- New York, N.Y. -- Science. 1999 May 21;284(5418):1372-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Applied Tumor Virology Program, Tumor Immunology Program, Deutsches Krebsforschungszentrum, Im Neuenheimer Feld 280, D-69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/metabolism ; Antigens, CD14/biosynthesis ; Antigens, CD15/biosynthesis ; Antigens, Differentiation, B-Lymphocyte/metabolism ; Carbohydrate Epimerases/genetics/metabolism ; Cell Adhesion Molecules/metabolism ; Cell Membrane/*metabolism ; Culture Media ; *Escherichia coli Proteins ; Glycoconjugates/*metabolism ; HL-60 Cells ; Histocompatibility Antigens Class I/biosynthesis ; Humans ; Lectins/metabolism ; Oligosaccharides/biosynthesis ; Rats ; Sialic Acid Binding Ig-like Lectin 2 ; Sialic Acids/*biosynthesis ; Transcription, Genetic ; Transfection ; Tumor Cells, Cultured
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    Light-dependent sequestration of TIMELESS by CRYPTOCHROME (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-27
    Description: Most organisms have circadian clocks consisting of negative feedback loops of gene regulation that facilitate adaptation to cycles of light and darkness. In this study, CRYPTOCHROME (CRY), a protein involved in circadian photoperception in Drosophila, is shown to block the function of PERIOD/TIMELESS (PER/TIM) heterodimeric complexes in a light-dependent fashion. TIM degradation does not occur under these conditions; thus, TIM degradation is uncoupled from abrogation of its function by light. CRY and TIM are part of the same complex and directly interact in yeast in a light-dependent fashion. PER/TIM and CRY influence the subcellular distribution of these protein complexes, which reside primarily in the nucleus after the perception of a light signal. Thus, CRY acts as a circadian photoreceptor by directly interacting with core components of the circadian clock.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ceriani, M F -- Darlington, T K -- Staknis, D -- Mas, P -- Petti, A A -- Weitz, C J -- Kay, S A -- MH-51573/MH/NIMH NIH HHS/ -- MH-59943/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 23;285(5427):553-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and NSF Center for Biological Timing, 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/10417378" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Clocks ; Cell Line ; Cell Nucleus/metabolism ; *Circadian Rhythm ; Cryptochromes ; Cytoplasm/metabolism ; Darkness ; Dimerization ; Drosophila ; *Drosophila Proteins ; *Eye Proteins ; Flavoproteins/genetics/*metabolism ; Green Fluorescent Proteins ; Insect Proteins/genetics/*metabolism ; *Light ; Luminescent Proteins ; Mutation ; Nuclear Proteins/genetics/metabolism ; Period Circadian Proteins ; *Photoreceptor Cells, Invertebrate ; Receptors, G-Protein-Coupled ; Recombinant Fusion Proteins/metabolism ; Transfection ; Yeasts/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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  • 84
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    Harnessing the power of stem cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, G -- New York, N.Y. -- Science. 1999 Mar 5;283(5407):1432-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10206866" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Cell Lineage ; Cells, Cultured ; Embryo, Mammalian/cytology ; Endoderm/cytology ; Hematopoietic Stem Cells/cytology ; Humans ; Mesoderm/cytology ; Neurons/cytology ; Stem Cells/*cytology/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 85
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    Transduction of human CD34+ cells that mediate long-term engraftment of NOD/SCID mice by HIV vectors (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-29
    Description: Efficient gene transfer into human hematopoietic stem cells (HSCs) is an important goal in the study of the hematopoietic system as well as for gene therapy of hematopoietic disorders. A lentiviral vector based on the human immunodeficiency virus (HIV) was able to transduce human CD34+ cells capable of stable, long-term reconstitution of nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice. High-efficiency transduction occurred in the absence of cytokine stimulation and resulted in transgene expression in multiple lineages of human hematopoietic cells for up to 22 weeks after transplantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyoshi, H -- Smith, K A -- Mosier, D E -- Verma, I M -- Torbett, B E -- CA44360/CA/NCI NIH HHS/ -- DK49886/DK/NIDDK NIH HHS/ -- HL53670/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 29;283(5402):682-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9924027" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD34/*analysis ; Bone Marrow Cells/cytology ; Cell Division ; Cell Survival ; Colony-Forming Units Assay ; Gene Expression ; *Gene Transfer Techniques ; *Genetic Vectors ; Green Fluorescent Proteins ; HIV/*genetics ; Hematopoiesis ; *Hematopoietic Stem Cell Transplantation ; *Hematopoietic Stem Cells/cytology/immunology ; Humans ; Leukemia Virus, Murine/genetics ; Luminescent Proteins/genetics ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Promoter Regions, Genetic ; Transfection ; Transgenes
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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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    HIV vaccines. Magic of the occult? (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Montefiori, D -- Moore, J P -- New York, N.Y. -- Science. 1999 Jan 15;283(5400):336-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for AIDS Research, Department of Surgery, Duke University Medical Center, Durham, NC 27710, USA. monte005@mc.duke.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9925493" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/*immunology ; Animals ; COS Cells ; Cell Fusion ; Coculture Techniques ; Epitopes/immunology ; HIV Antibodies/biosynthesis/*immunology ; HIV Antigens/*immunology ; HIV Envelope Protein gp120/immunology ; HIV Envelope Protein gp41/immunology ; HIV-1/*immunology/physiology ; Mice ; Neutralization Tests ; Transfection ; Tumor Cells, Cultured
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  • 87
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    Light-independent role of CRY1 and CRY2 in the mammalian circadian clock (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-26
    Description: Cryptochrome (CRY), a photoreceptor for the circadian clock in Drosophila, binds to the clock component TIM in a light-dependent fashion and blocks its function. In mammals, genetic evidence suggests a role for CRYs within the clock, distinct from hypothetical photoreceptor functions. Mammalian CRY1 and CRY2 are here shown to act as light-independent inhibitors of CLOCK-BMAL1, the activator driving Per1 transcription. CRY1 or CRY2 (or both) showed light-independent interactions with CLOCK and BMAL1, as well as with PER1, PER2, and TIM. Thus, mammalian CRYs act as light-independent components of the circadian clock and probably regulate Per1 transcriptional cycling by contacting both the activator and its feedback inhibitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Griffin, E A Jr -- Staknis, D -- Weitz, C J -- MH-59943/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):768-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston, MA 02115 USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10531061" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; ARNTL Transcription Factors ; Animals ; Basic Helix-Loop-Helix Transcription Factors ; *Biological Clocks ; CLOCK Proteins ; Cell Cycle Proteins ; Cells, Cultured ; *Circadian Rhythm ; Cryptochromes ; Dimerization ; *Drosophila Proteins ; *Eye Proteins ; Flavoproteins/metabolism/*physiology ; *Gene Expression Regulation ; Genes, Reporter ; Helix-Loop-Helix Motifs ; Humans ; Intracellular Signaling Peptides and Proteins ; *Light ; Mice ; Nuclear Proteins/antagonists & inhibitors/*genetics/metabolism ; Period Circadian Proteins ; *Photoreceptor Cells, Invertebrate ; Receptors, G-Protein-Coupled ; Trans-Activators/antagonists & inhibitors/metabolism ; Transcription Factors/antagonists & inhibitors/metabolism ; Transcriptional Activation ; Transfection
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  • 88
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    Functional human corneal equivalents constructed from cell lines (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-11
    Description: Human corneal equivalents comprising the three main layers of the cornea (epithelium, stroma, and endothelium) were constructed. Each cellular layer was fabricated from immortalized human corneal cells that were screened for use on the basis of morphological, biochemical, and electrophysiological similarity to their natural counterparts. The resulting corneal equivalents mimicked human corneas in key physical and physiological functions, including morphology, biochemical marker expression, transparency, ion and fluid transport, and gene expression. Morphological and functional equivalents to human corneas that can be produced in vitro have immediate applications in toxicity and drug efficacy testing, and form the basis for future development of implantable tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Griffith, M -- Osborne, R -- Munger, R -- Xiong, X -- Doillon, C J -- Laycock, N L -- Hakim, M -- Song, Y -- Watsky, M A -- New York, N.Y. -- Science. 1999 Dec 10;286(5447):2169-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Ottawa Eye Institute and Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa Hospital-General Campus, Ottawa, Ontario K1H 8L6, Canada. mgriffith@ogh.on.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10591651" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Testing Alternatives ; *Biomedical Engineering ; Cell Line ; Cells, Cultured ; Chondroitin Sulfates ; Collagen ; *Cornea/cytology/growth & development/physiology ; Corneal Opacity/chemically induced ; Corneal Stroma/cytology/growth & development/physiology ; Corneal Transplantation ; Cross-Linking Reagents ; *Culture Techniques ; Electrophysiology ; Endothelium, Corneal/cytology/growth & development ; Epithelium, Corneal/cytology/growth & development ; Gene Expression ; Glutaral ; Humans ; Ion Channels ; Ouabain/pharmacology ; Patch-Clamp Techniques ; Sodium Dodecyl Sulfate/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 89
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    Activity-induced potentiation of developing neuromuscular synapses (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-11
    Description: Electrical activity plays a critical role in shaping the structure and function of synaptic connections in the nervous system. In Xenopus nerve-muscle cultures, a brief burst of action potentials in the presynaptic neuron induced a persistent potentiation of neuromuscular synapses that exhibit immature synaptic functions. Induction of potentiation required an elevation of postsynaptic Ca2+ and expression of potentiation appeared to involve an increased probability of transmitter secretion from the presynaptic nerve terminal. Thus, activity-dependent persistent synaptic enhancement may reflect properties characteristic of immature synaptic connections, and bursting activity in developing spinal neurons may promote functional maturation of the neuromuscular synapse.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wan, J -- Poo, M -- NS22764/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Sep 10;285(5434):1725-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California at San Diego, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10481007" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Animals ; Bungarotoxins/pharmacology ; Calcineurin/physiology ; Calcineurin Inhibitors ; Calcium/metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors/metabolism ; Cells, Cultured ; Chelating Agents/pharmacology ; Egtazic Acid/analogs & derivatives/pharmacology ; Electric Stimulation ; *Excitatory Postsynaptic Potentials/drug effects ; Long-Term Potentiation ; Motor Neurons/*physiology ; Neuromuscular Junction/drug effects/*physiology ; *Neuronal Plasticity/drug effects ; Patch-Clamp Techniques ; Receptors, Cholinergic/physiology ; Spinal Cord ; *Synaptic Transmission ; Xenopus
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  • 90
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    CD1d-restricted immunoglobulin G formation to GPI-anchored antigens mediated by NKT cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-08
    Description: Immunoglobulin G (IgG) responses require major histocompatibility complex (MHC)-restricted recognition of peptide fragments by conventional CD4(+) helper T cells. Immunoglobulin G responses to glycosylphosphatidylinositol (GPI)- anchored protein antigens, however, were found to be regulated in part through CD1d-restricted recognition of the GPI moiety by thymus-dependent, interleukin-4-producing CD4(+), natural killer cell antigen 1.1 [(NK1.1)+] helper T cells. The CD1-NKT cell pathway regulated immunogobulin G responses to the GPI-anchored surface antigens of Plasmodium and Trypanosoma and may be a general mechanism for rapid, MHC-unrestricted antibody responses to diverse pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schofield, L -- McConville, M J -- Hansen, D -- Campbell, A S -- Fraser-Reid, B -- Grusby, M J -- Tachado, S D -- AI-40171/AI/NIAID NIH HHS/ -- GM 41071/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 8;283(5399):225-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, Post Office, Royal Melbourne Hospital, Victoria 3050, Australia. schofield@wehi.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9880256" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Antigen-Presenting Cells/immunology ; Antigens/analysis ; Antigens, CD1/*immunology ; Antigens, Ly ; Antigens, Protozoan/*immunology ; Antigens, Surface ; Cells, Cultured ; Glycosylphosphatidylinositols/*immunology ; Immunoglobulin G/*biosynthesis ; Interleukin-4/biosynthesis ; Lectins, C-Type ; Leishmania mexicana/immunology ; Major Histocompatibility Complex ; Mice ; Mice, Inbred Strains ; NK Cell Lectin-Like Receptor Subfamily B ; Plasmodium/immunology ; Proteins/analysis ; Protozoan Proteins/immunology ; T-Lymphocyte Subsets/*immunology ; T-Lymphocytes, Helper-Inducer/*immunology ; Trypanosoma brucei brucei/immunology ; Variant Surface Glycoproteins, Trypanosoma/immunology
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  • 91
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    HMG-1 as a late mediator of endotoxin lethality in mice (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-10
    Description: Endotoxin, a constituent of Gram-negative bacteria, stimulates macrophages to release large quantities of tumor necrosis factor (TNF) and interleukin-1 (IL-1), which can precipitate tissue injury and lethal shock (endotoxemia). Antagonists of TNF and IL-1 have shown limited efficacy in clinical trials, possibly because these cytokines are early mediators in pathogenesis. Here a potential late mediator of lethality is identified and characterized in a mouse model. High mobility group-1 (HMG-1) protein was found to be released by cultured macrophages more than 8 hours after stimulation with endotoxin, TNF, or IL-1. Mice showed increased serum levels of HMG-1 from 8 to 32 hours after endotoxin exposure. Delayed administration of antibodies to HMG-1 attenuated endotoxin lethality in mice, and administration of HMG-1 itself was lethal. Septic patients who succumbed to infection had increased serum HMG-1 levels, suggesting that this protein warrants investigation as a therapeutic target.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, H -- Bloom, O -- Zhang, M -- Vishnubhakat, J M -- Ombrellino, M -- Che, J -- Frazier, A -- Yang, H -- Ivanova, S -- Borovikova, L -- Manogue, K R -- Faist, E -- Abraham, E -- Andersson, J -- Andersson, U -- Molina, P E -- Abumrad, N N -- Sama, A -- Tracey, K J -- New York, N.Y. -- Science. 1999 Jul 9;285(5425):248-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Emergency Medicine and Department of Surgery, North Shore University Hospital-New York University School of Medicine, Manhasset, NY 11030, USA. hwang@picower.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10398600" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteremia/*blood ; Carrier Proteins/genetics/immunology/*metabolism/toxicity ; Cell Line ; Cells, Cultured ; Endotoxemia/*blood ; Endotoxins/blood/*toxicity ; HMGB1 Protein ; High Mobility Group Proteins/genetics/immunology/*metabolism/toxicity ; Humans ; Immune Sera/immunology ; Immunization, Passive ; Interferon-gamma/pharmacology ; Interleukin-1/pharmacology ; Lethal Dose 50 ; Leukocytes, Mononuclear/metabolism ; Lipopolysaccharides/toxicity ; Macrophages/*metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; RNA, Messenger/genetics/metabolism ; Time Factors ; Tumor Necrosis Factor-alpha/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 92
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    Ca2+-induced apoptosis through calcineurin dephosphorylation of BAD (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-09
    Description: The Ca2+-activated protein phosphatase calcineurin induces apoptosis, but the mechanism is unknown. Calcineurin was found to dephosphorylate BAD, a pro-apoptotic member of the Bcl-2 family, thus enhancing BAD heterodimerization with Bcl-xL and promoting apoptosis. The Ca2+-induced dephosphorylation of BAD correlated with its dissociation from 14-3-3 in the cytosol and translocation to mitochondria where Bcl-xL resides. In hippocampal neurons, L-glutamate, an inducer of Ca2+ influx and calcineurin activation, triggered mitochondrial targeting of BAD and apoptosis, which were both suppressible by coexpression of a dominant-inhibitory mutant of calcineurin or pharmacological inhibitors of this phosphatase. Thus, a Ca2+-inducible mechanism for apoptosis induction operates by regulating BAD phosphorylation and localization in cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, H G -- Pathan, N -- Ethell, I M -- Krajewski, S -- Yamaguchi, Y -- Shibasaki, F -- McKeon, F -- Bobo, T -- Franke, T F -- Reed, J C -- AG-1593/AG/NIA NIH HHS/ -- CA-69381/CA/NCI NIH HHS/ -- HD25938/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):339-43.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10195903" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins ; Animals ; *Apoptosis ; Calcineurin/genetics/*metabolism ; Calcineurin Inhibitors ; Calcium/*metabolism/pharmacology ; Carrier Proteins/chemistry/*metabolism ; Cell Line ; Cells, Cultured ; Dimerization ; Enzyme Inhibitors/pharmacology ; Glutamic Acid/pharmacology ; Hippocampus/cytology ; Humans ; Mitochondria/metabolism ; Neurons/cytology/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/metabolism ; Proteins/metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Rats ; Recombinant Fusion Proteins/metabolism ; Transfection ; *Tyrosine 3-Monooxygenase ; bcl-Associated Death Protein ; bcl-X Protein
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  • 93
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    Cloning genes encoding MHC class II-restricted antigens: mutated CDC27 as a tumor antigen (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: In an effort to identify tumor-specific antigens recognized by CD4(+) T cells, an approach was developed that allows the screening of an invariant chain-complementary DNA fusion library in a genetically engineered cell line expressing the essential components of the major histocompatibility complex (MHC) class II processing and presentation pathway. This led to the identification of a mutated form of human CDC27, which gave rise to an HLA-DR4-restricted melanoma antigen. A mutated form of triosephosphate isomerase, isolated by a biochemical method, was also identified as an HLA-DR1-restricted antigen. Thus, this approach may be generally applicable to the identification of antigens recognized by CD4(+) T cells, which could aid the development of strategies for the treatment of patients with cancer, autoimmune diseases, or infectious diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, R F -- Wang, X -- Atwood, A C -- Topalian, S L -- Rosenberg, S A -- New York, N.Y. -- Science. 1999 May 21;284(5418):1351-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Surgery Branch, National Cancer Institute, National Institutes of Health, Building 10/2B42, 9000 Rockville Pike, Bethesda, MD 20892, USA. rongfu@pop.nci.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334988" target="_blank"〉PubMed〈/a〉
    Keywords: Antigen Presentation ; Antigens, Differentiation, B-Lymphocyte/genetics/immunology ; Antigens, Neoplasm/*immunology ; Apc3 Subunit, Anaphase-Promoting Complex-Cyclosome ; CD4-Positive T-Lymphocytes/immunology ; Cell Cycle Proteins/*genetics/*immunology ; Cell Line, Transformed ; *Cloning, Molecular ; Epitopes/immunology ; HLA-DR1 Antigen/immunology ; HLA-DR4 Antigen/immunology ; Histocompatibility Antigens Class II/genetics/*immunology ; Humans ; Lymphocytes, Tumor-Infiltrating/*immunology ; Melanoma/immunology ; Point Mutation ; Recombinant Fusion Proteins ; Transfection ; Triose-Phosphate Isomerase/genetics/immunology
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  • 94
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    Stimulation of bone formation in vitro and in rodents by statins (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-03
    Description: Osteoporosis and other diseases of bone loss are a major public health problem. Here it is shown that the statins, drugs widely used for lowering serum cholesterol, also enhance new bone formation in vitro and in rodents. This effect was associated with increased expression of the bone morphogenetic protein-2 (BMP-2) gene in bone cells. Lovastatin and simvastatin increased bone formation when injected subcutaneously over the calvaria of mice and increased cancellous bone volume when orally administered to rats. Thus, in appropriate doses, statins may have therapeutic applications for the treatment of osteoporosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mundy, G -- Garrett, R -- Harris, S -- Chan, J -- Chen, D -- Rossini, G -- Boyce, B -- Zhao, M -- Gutierrez, G -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1946-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉OsteoScreen, 2040 Babcock Road, San Antonio, TX 78229, USA. mundy@uthscsa.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10583956" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Density/*drug effects ; Bone Morphogenetic Protein 2 ; Bone Morphogenetic Proteins/biosynthesis/genetics/pharmacology ; Cell Line ; Female ; Fibroblast Growth Factor 1 ; Fibroblast Growth Factor 2/pharmacology ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology ; Lovastatin/*pharmacology ; Male ; Mice ; Mice, Inbred ICR ; Organ Culture Techniques ; Osteoblasts/*drug effects/metabolism ; Osteoclasts/drug effects ; Osteogenesis/*drug effects ; Osteoporosis/drug therapy ; Ovariectomy ; Promoter Regions, Genetic/drug effects ; Rats ; Recombinant Proteins/pharmacology ; Simvastatin/*pharmacology ; Skull ; Transfection ; *Transforming Growth Factor beta
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  • 95
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    Regulation of beta-catenin signaling by the B56 subunit of protein phosphatase 2A (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-26
    Description: Dysregulation of Wnt-beta-catenin signaling disrupts axis formation in vertebrate embryos and underlies multiple human malignancies. The adenomatous polyposis coli (APC) protein, axin, and glycogen synthase kinase 3beta form a Wnt-regulated signaling complex that mediates the phosphorylation-dependent degradation of beta-catenin. A protein phosphatase 2A (PP2A) regulatory subunit, B56, interacted with APC in the yeast two-hybrid system. Expression of B56 reduced the abundance of beta-catenin and inhibited transcription of beta-catenin target genes in mammalian cells and Xenopus embryo explants. The B56-dependent decrease in beta-catenin was blocked by oncogenic mutations in beta-catenin or APC, and by proteasome inhibitors. B56 may direct PP2A to dephosphorylate specific components of the APC-dependent signaling complex and thereby inhibit Wnt signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seeling, J M -- Miller, J R -- Gil, R -- Moon, R T -- White, R -- Virshup, D M -- 3P30CA42014/CA/NCI NIH HHS/ -- R01 CA71074/CA/NCI NIH HHS/ -- T32CA09602/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Mar 26;283(5410):2089-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT 84132, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10092233" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Animals ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Line ; Cysteine Endopeptidases/metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Cytoskeletal Proteins/genetics/*metabolism ; Down-Regulation ; Genes, Reporter ; Glycogen Synthase Kinase 3 ; Glycogen Synthase Kinases ; Humans ; Leupeptins/pharmacology ; Multienzyme Complexes/metabolism ; Mutation ; Phosphoprotein Phosphatases/chemistry/genetics/*metabolism ; Phosphorylation ; Proteasome Endopeptidase Complex ; Protein Phosphatase 2 ; Proto-Oncogene Proteins/*metabolism ; *Signal Transduction ; *Trans-Activators ; Transcriptional Activation ; Transfection ; Tumor Cells, Cultured ; Wnt Proteins ; Xenopus ; Xenopus Proteins ; *Zebrafish Proteins ; beta Catenin
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 96
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    A role for the proteasome in the light response of the timeless clock protein (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-09-11
    Description: The cyclic expression of the period (PER) and timeless (TIM) proteins is critical for the molecular circadian feedback loop in Drosophila. The entrainment by light of the circadian clock is mediated by a reduction in TIM levels. To elucidate the mechanism of this process, the sensitivity of TIM regulation by light was tested in an in vitro assay with inhibitors of candidate proteolytic pathways. The data suggested that TIM is degraded through a ubiquitin-proteasome mechanism. In addition, in cultures from third-instar larvae, TIM degradation was blocked specifically by inhibitors of proteasome activity. Degradation appeared to be preceded by tyrosine phosphorylation. Finally, TIM was ubiquitinated in response to light in cultured cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Naidoo, N -- Song, W -- Hunter-Ensor, M -- Sehgal, A -- New York, N.Y. -- Science. 1999 Sep 10;285(5434):1737-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Neuroscience, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10481010" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcysteine/analogs & derivatives/pharmacology ; Animals ; *Biological Clocks ; Cells, Cultured ; *Circadian Rhythm ; Cysteine Endopeptidases/*physiology ; Cysteine Proteinase Inhibitors/pharmacology ; Darkness ; Drosophila ; *Drosophila Proteins ; Feedback ; Insect Proteins/*metabolism ; Leucine/analogs & derivatives/pharmacology ; Leupeptins/pharmacology ; *Light ; Multienzyme Complexes/*physiology ; Neurons/*metabolism ; Phosphorylation ; Phosphotyrosine/metabolism ; Protease Inhibitors/pharmacology ; Proteasome Endopeptidase Complex ; Ubiquitins/metabolism
    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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  • 97
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    Synergistic signaling in fetal brain by STAT3-Smad1 complex bridged by p300 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-16
    Description: The cytokines LIF (leukemia inhibitory factor) and BMP2 (bone morphogenetic protein-2) signal through different receptors and transcription factors, namely STATs (signal transducers and activators of transcription) and Smads. LIF and BMP2 were found to act in synergy on primary fetal neural progenitor cells to induce astrocytes. The transcriptional coactivator p300 interacts physically with STAT3 at its amino terminus in a cytokine stimulation-independent manner, and with Smad1 at its carboxyl terminus in a cytokine stimulation-dependent manner. The formation of a complex between STAT3 and Smad1, bridged by p300, is involved in the cooperative signaling of LIF and BMP2 and the subsequent induction of astrocytes from neural progenitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakashima, K -- Yanagisawa, M -- Arakawa, H -- Kimura, N -- Hisatsune, T -- Kawabata, M -- Miyazono, K -- Taga, T -- New York, N.Y. -- Science. 1999 Apr 16;284(5413):479-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Cell Biology, Cell Fate Modulation Research Unit, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 101-0062, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10205054" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/cytology ; Bone Morphogenetic Protein 2 ; Bone Morphogenetic Protein Receptors ; Bone Morphogenetic Proteins/metabolism/pharmacology ; COS Cells ; Cell Differentiation ; Cell Nucleus/metabolism ; Cells, Cultured ; Cytokines/*pharmacology ; DNA-Binding Proteins/*metabolism ; E1A-Associated p300 Protein ; Glial Fibrillary Acidic Protein/genetics ; Growth Inhibitors/metabolism/pharmacology ; *Interleukin-6 ; Leukemia Inhibitory Factor ; Leukemia Inhibitory Factor Receptor alpha Subunit ; Lymphokines/metabolism/pharmacology ; Mice ; Nuclear Proteins/*metabolism ; Promoter Regions, Genetic ; Receptors, Cell Surface/metabolism ; Receptors, Cytokine/metabolism ; *Receptors, Growth Factor ; Receptors, OSM-LIF ; STAT3 Transcription Factor ; Sequence Deletion ; *Signal Transduction ; Smad Proteins ; Smad1 Protein ; Stem Cells/cytology/metabolism ; Telencephalon/embryology/metabolism ; Trans-Activators/*metabolism ; *Transcriptional Activation ; *Transforming Growth Factor beta
    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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  • 98
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    Cell activation and apoptosis by bacterial lipoproteins through toll-like receptor-2 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: Apoptosis is implicated in the generation and resolution of inflammation in response to bacterial pathogens. All bacterial pathogens produce lipoproteins (BLPs), which trigger the innate immune response. BLPs were found to induce apoptosis in THP-1 monocytic cells through human Toll-like receptor-2 (hTLR2). BLPs also initiated apoptosis in an epithelial cell line transfected with hTLR2. In addition, BLPs stimulated nuclear factor-kappaB, a transcriptional activator of multiple host defense genes, and activated the respiratory burst through hTLR2. Thus, hTLR2 is a molecular link between microbial products, apoptosis, and host defense mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aliprantis, A O -- Yang, R B -- Mark, M R -- Suggett, S -- Devaux, B -- Radolf, J D -- Klimpel, G R -- Godowski, P -- Zychlinsky, A -- AI 37720-04/AI/NIAID NIH HHS/ -- AI-38894/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):736-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skirball Institute and Department of Microbiology, New York University School of Medicine, 540 First Avenue, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426996" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal ; Antigens, CD14/analysis ; *Apoptosis ; Bacterial Proteins/metabolism/*pharmacology ; Cell Line/metabolism ; Cycloheximide/pharmacology ; Cytotoxicity, Immunologic ; *Drosophila Proteins ; Genes, Reporter ; Humans ; Lipopolysaccharides/immunology ; Lipoproteins/metabolism/*pharmacology ; Membrane Glycoproteins/immunology/*metabolism ; Monocytes/*cytology/immunology/metabolism ; NF-kappa B/metabolism ; Protein Synthesis Inhibitors/pharmacology ; Reactive Oxygen Species/metabolism ; Receptors, Cell Surface/immunology/*metabolism ; Signal Transduction ; Tetradecanoylphorbol Acetate/pharmacology ; Toll-Like Receptor 2 ; Toll-Like Receptors ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
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    STAT5 interaction with the T cell receptor complex and stimulation of T cell proliferation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-08
    Description: The role of STAT (signal transducer and activator of transcription) proteins in T cell receptor (TCR) signaling was analyzed. STAT5 became immediately and transiently phosphorylated on tyrosine 694 in response to TCR stimulation. Expression of the protein tyrosine kinase Lck, a key signaling protein in the TCR complex, activated DNA binding of transfected STAT5A and STAT5B to specific STAT inducible elements. The role of Lck in STAT5 activation was confirmed in a Lck-deficient T cell line in which the activation of STAT5 by TCR stimulation was abolished. Expression of Lck induced specific interaction of STAT5 with the subunits of the TCR, indicating that STAT5 may be directly involved in TCR signaling. Stimulation of T cell clones and primary T cell lines also induced the association of STAT5 with the TCR complex. Inhibition of STAT5 function by expression of a dominant negative mutant STAT5 reduced antigen-stimulated proliferation of T cells. Thus, TCR stimulation appears to directly activate STAT5, which may participate in the regulation of gene transcription and T cell proliferation during immunological responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Welte, T -- Leitenberg, D -- Dittel, B N -- al-Ramadi, B K -- Xie, B -- Chin, Y E -- Janeway, C A Jr -- Bothwell, A L -- Bottomly, K -- Fu, X Y -- AI34522/AI/NIAID NIH HHS/ -- GM46367/GM/NIGMS NIH HHS/ -- GM55590/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Jan 8;283(5399):222-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9880255" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies ; Antigen-Presenting Cells/immunology ; Antigens/immunology ; Cell Division ; Cell Line ; DNA-Binding Proteins/genetics/*metabolism ; Interferon-gamma/pharmacology ; Interleukin-2/pharmacology ; *Lymphocyte Activation ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck)/genetics/metabolism ; Membrane Proteins/genetics/immunology/metabolism ; Mice ; Mice, Transgenic ; *Milk Proteins ; Phosphorylation ; Phosphotyrosine/metabolism ; Receptors, Antigen, T-Cell/genetics/immunology/*metabolism ; STAT5 Transcription Factor ; Signal Transduction ; T-Lymphocytes, Helper-Inducer/cytology/*immunology/metabolism ; Th2 Cells/immunology/metabolism ; Trans-Activators/genetics/*metabolism ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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    Tbx5 and the retinotectum projection (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-30
    Description: Dorsal and ventral aspects of the eye are distinct from the early stages of development. The developing eye cup grows dorsally, and the choroidal fissure is formed on its ventral side. Retinal axons from the dorsal and ventral retina project to the ventral and dorsal tectum, respectively. Misexpression of the Tbx5 gene induced dorsalization of the ventral side of the eye and altered projections of retinal ganglion cell axons. Thus, Tbx5 is involved in eye morphogenesis and is a topographic determinant of the visual projections between retina and tectum.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koshiba-Takeuchi, K -- Takeuchi, J K -- Matsumoto, K -- Momose, T -- Uno, K -- Hoepker, V -- Ogura, K -- Takahashi, N -- Nakamura, H -- Yasuda, K -- Ogura, T -- New York, N.Y. -- Science. 2000 Jan 7;287(5450):134-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate School of Biological Sciences, Nara Institute of Science and Technology, 8916-5, Takayama, Ikoma, Nara, Japan 630-0101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10615048" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Avian Proteins ; Axons/*ultrastructure ; Body Patterning ; Bone Morphogenetic Protein 4 ; Bone Morphogenetic Proteins/genetics/physiology ; Chick Embryo ; DNA-Binding Proteins/genetics ; Electroporation ; Ephrin-B1 ; Ephrin-B2 ; Eye/*embryology ; Gene Expression ; Homeodomain Proteins/genetics ; Membrane Proteins/genetics/physiology ; Morphogenesis ; PAX2 Transcription Factor ; Pigment Epithelium of Eye/embryology/metabolism ; Retina/*embryology/metabolism ; Retinal Ganglion Cells/ultrastructure ; Superior Colliculi/*embryology ; T-Box Domain Proteins/genetics/*physiology ; Transcription Factors/genetics ; Transfection ; Transgenes
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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