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  • Signal Transduction  (90)
  • Cell Line  (53)
  • American Association for the Advancement of Science (AAAS)  (135)
  • Elsevier
  • Oxford University Press
  • Springer
  • Taylor & Francis
  • 2000-2004  (135)
  • 1980-1984
  • 1935-1939
  • 2003  (135)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (135)
  • Elsevier
  • Oxford University Press
  • Springer
  • Taylor & Francis
Years
  • 2000-2004  (135)
  • 1980-1984
  • 1935-1939
Year
  • 1
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    Stem cells. Setting standards for human embryonic stem cells (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brivanlou, Ali H -- Gage, Fred H -- Jaenisch, Rudolf -- Jessell, Thomas -- Melton, Douglas -- Rossant, Janet -- New York, N.Y. -- Science. 2003 May 9;300(5621):913-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rockefeller University, New York, NY 10021, USA. brvnlou@rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12738841" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Specimen Banks ; Cell Culture Techniques/methods ; Cell Differentiation ; Cell Division ; *Cell Line ; Culture Media ; Culture Media, Conditioned ; Databases, Factual ; *Embryo Research ; Embryo, Mammalian/*cytology ; Humans ; Quality Control ; Registries ; Research/standards ; Signal Transduction ; Stem Cell Transplantation ; *Stem Cells/cytology/physiology ; 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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  • 2
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    Reversing the inactivation of peroxiredoxins caused by cysteine sulfinic acid formation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-26
    Description: The active-site cysteine of peroxiredoxins is selectively oxidized to cysteine sulfinic acid during catalysis, which leads to inactivation of peroxidase activity. This oxidation was thought to be irreversible. However, by metabolic labeling of mammalian cells with 35S, we show that the sulfinic form of peroxiredoxin I, produced during the exposure of cells to H2O2, is rapidly reduced to the catalytically active thiol form. The mammalian cells' ability to reduce protein sulfinic acid might serve as a mechanism to repair oxidatively damaged proteins or represent a new type of cyclic modification by which the function of various proteins is regulated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Woo, Hyun Ae -- Chae, Ho Zoon -- Hwang, Sung Chul -- Yang, Kap-Seok -- Kang, Sang Won -- Kim, Kanghwa -- Rhee, Sue Goo -- New York, N.Y. -- Science. 2003 Apr 25;300(5619):653-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cell Signaling Research and Division of Molecular Life Sciences, Ewha Womans University, Seoul 120-750, Korea.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12714748" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Catalysis ; Cell Line ; Cycloheximide/pharmacology ; Cysteine/*analogs & derivatives/*metabolism ; Dimerization ; HeLa Cells ; Humans ; Hydrogen Peroxide/*metabolism ; Methionine/metabolism ; Mice ; Neurotransmitter Agents ; Oxidation-Reduction ; Peroxidases/chemistry/*metabolism ; Peroxiredoxins ; Protein Synthesis Inhibitors/pharmacology ; Spectrometry, Mass, Electrospray Ionization ; Sulfhydryl Compounds/metabolism ; Sulfinic Acids/metabolism ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Biomedicine. Ataxin-1 regulators in the spotlight (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heintz, Nathaniel -- New York, N.Y. -- Science. 2003 Jul 4;301(5629):59-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Rockefeller University, New York, NY 10021, USA. heintz@rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12843383" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins ; Amino Acid Substitution ; Animals ; Ataxin-1 ; Ataxins ; Cell Nucleus/metabolism ; Disease Progression ; Mice ; Mice, Transgenic ; Mutation ; Nerve Tissue Proteins/*chemistry/genetics/*metabolism ; Nuclear Proteins/*chemistry/genetics/*metabolism ; Peptides ; Phosphorylation ; *Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-akt ; Purkinje Cells/metabolism/ultrastructure ; Signal Transduction ; Spinocerebellar Ataxias/etiology/genetics/pathology/*physiopathology ; *Trinucleotide Repeat Expansion ; Tyrosine 3-Monooxygenase/*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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    Insulin staining of ES cell progeny from insulin uptake (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rajagopal, Jayaraj -- Anderson, William J -- Kume, Shoen -- Martinez, Olga I -- Melton, Douglas A -- New York, N.Y. -- Science. 2003 Jan 17;299(5605):363.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Howard Hughes Medical Institute, Harvard University, 7 Divinity Avenue, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12532008" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/immunology ; Apoptosis ; Cell Differentiation ; Cell Line ; Embryo, Mammalian/*cytology ; Humans ; Insulin/*analysis/genetics/immunology/*metabolism ; Islets of Langerhans/*cytology/metabolism ; Mice ; Microscopy, Confocal ; RNA, Messenger/genetics/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Stem Cells/*cytology/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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  • 5
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    Comprehensive identification of human bZIP interactions with coiled-coil arrays (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-06-14
    Description: In eukaryotes, the combinatorial association of sequence-specific DNA binding proteins is essential for transcription. We have used protein arrays to test 492 pairings of a nearly complete set of coiled-coil strands from human basic-region leucine zipper (bZIP) transcription factors. We find considerable partnering selectivity despite the bZIPs' homologous sequences. The interaction data are of high quality, as assessed by their reproducibility, reciprocity, and agreement with previous observations. Biophysical studies in solution support the relative binding strengths observed with the arrays. New associations provide insights into the circadian clock and the unfolded protein response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Newman, John R S -- Keating, Amy E -- New York, N.Y. -- Science. 2003 Jun 27;300(5628):2097-101. Epub 2003 Jun 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12805554" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Basic-Leucine Zipper Transcription Factors ; Chromatography, High Pressure Liquid ; Circadian Rhythm ; Circular Dichroism ; Cyclic AMP Response Element-Binding Protein/chemistry/metabolism ; DNA-Binding Proteins/chemistry/isolation & purification/*metabolism ; Dimerization ; G-Box Binding Factors ; Humans ; *Leucine Zippers ; Peptides/chemistry/isolation & purification/metabolism ; *Protein Array Analysis ; Protein Binding ; Protein Folding ; Protein Structure, Tertiary ; Signal Transduction ; Temperature ; Thermodynamics ; Transcription Factors/*chemistry/isolation & purification/*metabolism
    Print ISSN: 0036-8075
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  • 6
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    Loss of a callose synthase results in salicylic acid-dependent disease resistance (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-16
    Description: Plants attacked by pathogens rapidly deposit callose, a beta-1,3-glucan, at wound sites. Traditionally, this deposition is thought to reinforce the cell wall and is regarded as a defense response. Surprisingly, here we found that powdery mildew resistant 4 (pmr4), a mutant lacking pathogen-induced callose, became resistant to pathogens, rather than more susceptible. This resistance was due to mutation of a callose synthase, resulting in a loss of the induced callose response. Double-mutant analysis indicated that blocking the salicylic acid (SA) defense signaling pathway was sufficient to restore susceptibility to pmr4 mutants. Thus, callose or callose synthase negatively regulates the SA pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nishimura, Marc T -- Stein, Monica -- Hou, Bi-Huei -- Vogel, John P -- Edwards, Herb -- Somerville, Shauna C -- New York, N.Y. -- Science. 2003 Aug 15;301(5635):969-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Biology, Carnegie Institution, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12920300" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Arabidopsis/cytology/genetics/*metabolism/*microbiology ; Ascomycota/*physiology ; Cell Death ; Gene Expression Profiling ; Gene Expression Regulation, Plant ; Genes, Plant ; Glucans/metabolism ; Glucosyltransferases/*genetics/metabolism ; *Membrane Proteins ; Mutation ; Oligonucleotide Array Sequence Analysis ; Phenotype ; *Plant Diseases ; Plant Leaves/metabolism ; Salicylic Acid/*metabolism ; *Schizosaccharomyces pombe Proteins ; Signal Transduction
    Print ISSN: 0036-8075
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  • 7
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    Role of Raf in vascular protection from distinct apoptotic stimuli (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-05
    Description: Raf kinases have been linked to endothelial cell survival. Here, we show that basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) differentially activate Raf, resulting in protection from distinct pathways of apoptosis in human endothelial cells and chick embryo vasculature. bFGF activated Raf-1 via p21-activated protein kinase-1 (PAK-1) phosphorylation of serines 338 and 339, resulting in Raf-1 mitochondrial translocation and endothelial cell protection from the intrinsic pathway of apoptosis, independent of the mitogen-activated protein kinase kinase-1 (MEK1). In contrast, VEGF activated Raf-1 via Src kinase, leading to phosphorylation of tyrosines 340 and 341 and MEK1-dependent protection from extrinsic-mediated apoptosis. These findings implicate Raf-1 as a pivotal regulator of endothelial cell survival during angiogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alavi, Alireza -- Hood, John D -- Frausto, Ricardo -- Stupack, Dwayne G -- Cheresh, David A -- CA45726/CA/NCI NIH HHS/ -- CA50286/CA/NCI NIH HHS/ -- CA75924/CA/NCI NIH HHS/ -- P01 CA78045/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Jul 4;301(5629):94-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, 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/12843393" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Cell Survival ; Cells, Cultured ; Chick Embryo ; Endothelial Growth Factors/pharmacology ; Endothelium, Vascular/*cytology/drug effects ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Fibroblast Growth Factor 2/pharmacology ; Flavonoids/pharmacology ; Humans ; Intercellular Signaling Peptides and Proteins/pharmacology ; Lymphokines/pharmacology ; MAP Kinase Kinase 1 ; Mitochondria/metabolism ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3 ; Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; Neovascularization, Pathologic ; *Neovascularization, Physiologic/drug effects ; Phosphorylation ; Point Mutation ; Protein Transport ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; Proto-Oncogene Proteins B-raf ; Proto-Oncogene Proteins c-raf/chemistry/genetics/*metabolism ; Signal Transduction ; Umbilical Veins ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors ; p21-Activated Kinases ; src-Family Kinases/antagonists & inhibitors/metabolism
    Print ISSN: 0036-8075
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  • 8
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    Botany. State transitions--a question of balance (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allen, John F -- New York, N.Y. -- Science. 2003 Mar 7;299(5612):1530-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Biochemistry, Center for Chemistry and Chemical Engineering, Box 124, Lund University, SE-221 00 Lund, Sweden. john.allen@plantbio.lu.se〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12624254" target="_blank"〉PubMed〈/a〉
    Keywords: Algal Proteins/chemistry/genetics/isolation & purification/metabolism ; Animals ; Binding Sites ; Chlamydomonas reinhardtii/*enzymology/genetics/metabolism ; Chlorophyll/metabolism ; Electron Transport ; Fluorescence ; Gene Library ; Light ; Light-Harvesting Protein Complexes ; Models, Biological ; Mutation ; Oxidation-Reduction ; Phosphorylation ; Photosynthesis ; Photosynthetic Reaction Center Complex Proteins/*metabolism ; Plastoquinone/metabolism ; Protein-Serine-Threonine Kinases/chemistry/genetics/*isolation & ; purification/*metabolism ; Signal Transduction ; Thylakoids/*enzymology ; Transcription, Genetic
    Print ISSN: 0036-8075
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  • 9
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    Single molecule profiling of alternative pre-mRNA splicing (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-09
    Description: Alternative pre-messenger RNA splicing is an important mechanism for generating protein diversity and may explain in part how mammalian complexity arises from a surprisingly small complement of genes. Here, we describe "digital polony exon profiling,"a single molecule-based technology for studying complex alternative pre-messenger RNA splicing. This technology allows researchers to monitor the combinatorial diversity of exon inclusion in individual transcripts. A minisequencing strategy provides single nucleotide resolution, and the digital nature of the technology allows quantitation of individual splicing variants. Digital polony exon profiling can be used to investigate the physiological and pathological roles of alternately spliced messenger RNAs, as well as the mechanisms by which these messenger RNAs are produced.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, Jun -- Shendure, Jay -- Mitra, Robi D -- Church, George M -- 5U54GM62119/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Aug 8;301(5634):836-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12907803" target="_blank"〉PubMed〈/a〉
    Keywords: Acrylamide ; *Alternative Splicing ; Animals ; Antigens, CD44/genetics ; Brain/metabolism ; Cell Line ; Cell Line, Transformed ; Cyclic AMP Response Element-Binding Protein ; *Exons ; Humans ; Mice ; Microtubule-Associated Proteins/genetics ; Nerve Tissue Proteins/genetics ; Polymerase Chain Reaction/*methods ; Polymorphism, Single Nucleotide ; Protein Isoforms ; RNA Precursors/*genetics/metabolism ; RNA-Binding Proteins ; SMN Complex Proteins
    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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    Virology. Forced entry--or does HTLV-I have the key? (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Derse, David -- Heidecker, Gisela -- New York, N.Y. -- Science. 2003 Mar 14;299(5613):1670-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basic Research Laboratory, National Cancer Institute, Frederick, MD 21702, USA. derse@ncifcrf.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12637723" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Adhesion Molecules/metabolism ; Cell Communication ; Cell Polarity ; Dendritic Cells/virology ; Extracellular Space/virology ; Gene Products, env/metabolism ; Gene Products, tax/physiology ; HTLV-I Infections/virology ; Human T-lymphotropic virus 1/genetics/*physiology ; Humans ; Intercellular Junctions/*physiology/ultrastructure/virology ; Microtubule-Organizing Center/*physiology/ultrastructure ; Receptors, Virus/metabolism ; Signal Transduction ; T-Lymphocytes/*ultrastructure/*virology ; Talin/metabolism ; Virion/physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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    Role of EDEM in the release of misfolded glycoproteins from the calnexin cycle (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-01
    Description: The mechanisms that determine how folding attempts are interrupted to target folding-incompetent proteins for endoplasmic reticulum-associated degradation (ERAD) are poorly defined. Here the alpha-mannosidase I-like protein EDEM was shown to extract misfolded glycoproteins, but not glycoproteins undergoing productive folding, from the calnexin cycle. EDEM overexpression resulted in faster release of folding-incompetent proteins from the calnexin cycle and earlier onset of degradation, whereas EDEM down-regulation prolonged folding attempts and delayed ERAD. Up-regulation of EDEM during ER stress may promote cell recovery by clearing the calnexin cycle and by accelerating ERAD of terminally misfolded polypeptides.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Molinari, Maurizio -- Calanca, Verena -- Galli, Carmela -- Lucca, Paola -- Paganetti, Paolo -- New York, N.Y. -- Science. 2003 Feb 28;299(5611):1397-400.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Research in Biomedicine, CH-6500 Bellinzona, Switzerland. Maurizio.molinari@irb.unisi.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12610306" target="_blank"〉PubMed〈/a〉
    Keywords: Aspartic Acid Endopeptidases/chemistry/*metabolism ; Calnexin/*metabolism ; Cell Line ; Down-Regulation ; Electrophoresis, Polyacrylamide Gel ; Endoplasmic Reticulum/*metabolism ; Glycoproteins/chemistry/*metabolism ; Glycosylation ; Humans ; Kinetics ; Membrane Proteins/*metabolism ; Molecular Weight ; Polysaccharides/metabolism ; Protein Conformation ; Protein Folding ; RNA Interference ; Transfection ; Up-Regulation
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  • 12
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    Botany. Relieving DELLA restraint (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harberd, Nicholas P -- New York, N.Y. -- Science. 2003 Mar 21;299(5614):1853-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉John Innes Centre, Norwich, Norfolk NR4 7UH, UK. nicholas.harberd@bbsrc.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12649470" target="_blank"〉PubMed〈/a〉
    Keywords: Cloning, Molecular ; Genes, Plant ; Gibberellins/*metabolism/pharmacology ; Indoleacetic Acids/metabolism ; Ligases/metabolism ; Models, Biological ; Mutation ; Oryza/genetics/*growth & development/metabolism ; Peptide Hydrolases/metabolism ; Phosphorylation ; Plant Proteins/*genetics/*metabolism ; *Proteasome Endopeptidase Complex ; Signal Transduction ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases
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  • 13
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    A B cell-based sensor for rapid identification of pathogens (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-12
    Description: We report the use of genetically engineered cells in a pathogen identification sensor. This sensor uses B lymphocytes that have been engineered to emit light within seconds of exposure to specific bacteria and viruses. We demonstrated rapid screening of relevant samples and identification of a variety of pathogens at very low levels. Because of its speed, sensitivity, and specificity, this pathogen identification technology could prove useful for medical diagnostics, biowarfare defense, food- and water-quality monitoring, and other applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rider, Todd H -- Petrovick, Martha S -- Nargi, Frances E -- Harper, James D -- Schwoebel, Eric D -- Mathews, Richard H -- Blanchard, David J -- Bortolin, Laura T -- Young, Albert M -- Chen, Jianzhu -- Hollis, Mark A -- New York, N.Y. -- Science. 2003 Jul 11;301(5630):213-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts Institute of Technology Lincoln Laboratory, Lexington, MA 02420, USA. thor@ll.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12855808" target="_blank"〉PubMed〈/a〉
    Keywords: Aequorin/biosynthesis ; Antibodies, Bacterial/immunology ; Antibodies, Viral/immunology ; *B-Lymphocytes/immunology ; Bacillus anthracis/immunology/isolation & purification ; Bacteria/immunology/*isolation & purification ; *Bacteriological Techniques ; *Biosensing Techniques ; Cell Line ; Colony Count, Microbial ; Encephalitis Virus, Venezuelan Equine/immunology/isolation & purification ; Escherichia coli O157/immunology/isolation & purification ; Foot-and-Mouth Disease Virus/immunology/isolation & purification ; Immunoglobulin Variable Region/immunology ; Light ; Receptors, Antigen, B-Cell/immunology ; Sensitivity and Specificity ; Time Factors ; Transfection ; Viruses/immunology/*isolation & purification ; Yersinia pestis/immunology/isolation & purification
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  • 14
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    Inflammatory blockade restores adult hippocampal neurogenesis (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-15
    Description: Cranial radiation therapy causes a progressive decline in cognitive function that is linked to impaired neurogenesis. Chronic inflammation accompanies radiation injury, suggesting that inflammatory processes may contribute to neural stem cell dysfunction. Here, we show that neuroinflammation alone inhibits neurogenesis and that inflammatory blockade with indomethacin, a common nonsteroidal anti-inflammatory drug, restores neurogenesis after endotoxin-induced inflammation and augments neurogenesis after cranial irradiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Monje, Michelle L -- Toda, Hiroki -- Palmer, Theo D -- F30 NS04696701/NS/NINDS NIH HHS/ -- MH20016-05/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2003 Dec 5;302(5651):1760-5. Epub 2003 Nov 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stanford University, Department of Neurosurgery, MSLS P309, Mail Code 5487, 1201 Welch Road, Stanford, CA 94305-5487, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14615545" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology ; Antigens, CD/metabolism ; Apoptosis ; Cell Differentiation ; Cells, Cultured ; Coculture Techniques ; Culture Media, Conditioned ; Cytokine Receptor gp130 ; Cytokines/physiology ; Dentate Gyrus/cytology/drug effects/physiology/radiation effects ; Female ; Gamma Rays ; Hippocampus/cytology/drug effects/*physiology/radiation effects ; In Situ Nick-End Labeling ; Indomethacin/*pharmacology ; Inflammation/drug therapy/*physiopathology ; Interleukin-6/pharmacology/physiology ; Lipopolysaccharides/pharmacology ; Membrane Glycoproteins/metabolism ; Mice ; Microglia/*physiology ; Mitotic Index ; Neurons/drug effects/*physiology/radiation effects ; Rats ; Rats, Inbred F344 ; Receptors, Interleukin-6/metabolism ; Recombinant Proteins/pharmacology ; Signal Transduction ; Stem Cells/physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    Structural basis of a phototropin light switch (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-13
    Description: Phototropins are light-activated kinases important for plant responses to blue light. Light initiates signaling in these proteins by generating a covalent protein-flavin mononucleotide (FMN) adduct within sensory Per-ARNT-Sim (PAS) domains. We characterized the light-dependent changes of a phototropin PAS domain by solution nuclear magnetic resonance spectroscopy and found that an alpha helix located outside the canonical domain plays a key role in this activation process. Although this helix associates with the PAS core in the dark, photoinduced changes in the domain structure disrupt this interaction. We propose that this mechanism couples light-dependent bond formation to kinase activation and identifies a signaling pathway conserved among PAS domains.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harper, Shannon M -- Neil, Lori C -- Gardner, Kevin H -- CA90601/CA/NCI NIH HHS/ -- GM08297/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Sep 12;301(5639):1541-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Biochemistry and Pharmacology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9038, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12970567" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Avena/*chemistry ; Cryptochromes ; Darkness ; *Drosophila Proteins ; *Eye Proteins ; Flavoproteins/*chemistry/metabolism ; *Light ; Models, Molecular ; Molecular Sequence Data ; Nuclear Magnetic Resonance, Biomolecular ; *Photoreceptor Cells, Invertebrate ; *Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Receptors, G-Protein-Coupled ; Signal Transduction
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  • 16
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    TRB3: a tribbles homolog that inhibits Akt/PKB activation by insulin in liver (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-06-07
    Description: Insulin resistance is a major hallmark in the development of type II diabetes, which is characterized by the failure of insulin to promote glucose uptake in muscle and to suppress glucose production in liver. The serine-threonine kinase Akt (PKB) is a principal target of insulin signaling that inhibits hepatic glucose output when glucose is available from food. Here we show that TRB3, a mammalian homolog of Drosophila tribbles, functions as a negative modulator of Akt. TRB3 expression is induced in liver under fasting conditions, and TRB3 disrupts insulin signaling by binding directly to Akt and blocking activation of the kinase. Amounts of TRB3 RNA and protein were increased in livers of db/db diabetic mice compared with those in wild-type mice. Hepatic overexpression of TRB3 in amounts comparable to those in db/db mice promoted hyperglycemia and glucose intolerance. Our results suggest that, by interfering with Akt activation, TRB3 contributes to insulin resistance in individuals with susceptibility to type II diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Du, Keyong -- Herzig, Stephan -- Kulkarni, Rohit N -- Montminy, Marc -- New York, N.Y. -- Science. 2003 Jun 6;300(5625):1574-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Peptide Biology Laboratories, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037-1002, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12791994" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics/physiology ; Amino Acid Substitution ; Animals ; Blood Glucose/metabolism ; Cell Cycle Proteins/genetics/*metabolism ; Cell Line ; Diabetes Mellitus/genetics/metabolism ; Enzyme Activation ; Fasting ; Genetic Vectors ; Glucose/metabolism ; Glucose Intolerance ; Glycogen Synthase Kinase 3/metabolism ; Humans ; Insulin/blood/*metabolism ; Insulin Resistance ; Insulin-Like Growth Factor I/pharmacology ; Liver/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Phosphorylation ; Polymerase Chain Reaction ; Protein-Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-akt ; RNA Interference ; Rats ; Repressor Proteins ; Signal Transduction ; Transfection ; Transgenes ; Tumor Cells, Cultured ; Two-Hybrid System Techniques
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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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    Control of nutrient-sensitive transcription programs by the unconventional prefoldin URI (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-15
    Description: Prefoldins (PFDs) are members of a recently identified, small-molecular weight protein family able to assemble into molecular chaperone complexes. Here we describe an unusually large member of this family, termed URI, that forms complexes with other small-molecular weight PFDs and with RPB5, a shared subunit of all three RNA polymerases. Functional analysis of the yeast and human orthologs of URI revealed that both are targets of nutrient signaling and participate in gene expression controlled by the TOR kinase. Thus, URI is a component of a signaling pathway that coordinates nutrient availability with gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gstaiger, Matthias -- Luke, Brian -- Hess, Daniel -- Oakeley, Edward J -- Wirbelauer, Christiane -- Blondel, Marc -- Vigneron, Marc -- Peter, Matthias -- Krek, Wilhelm -- New York, N.Y. -- Science. 2003 Nov 14;302(5648):1208-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Friedrich Miescher Institut, Maulbeerstrasse 66, CH-4058 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14615539" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acids/*metabolism ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Line ; DNA-Binding Proteins/metabolism ; DNA-Directed RNA Polymerases/metabolism ; GATA Transcription Factors ; *Gene Expression Regulation/drug effects ; Humans ; *Intracellular Signaling Peptides and Proteins ; Molecular Sequence Data ; Phosphorylation ; Protein Kinases/metabolism ; Protein Subunits/metabolism ; RNA Interference ; Repressor Proteins/metabolism ; Saccharomyces cerevisiae/*genetics/metabolism ; Saccharomyces cerevisiae Proteins/metabolism ; *Signal Transduction ; Sirolimus/pharmacology ; TOR Serine-Threonine Kinases ; Trans-Activators/metabolism ; Transcription Factors/metabolism ; *Transcription, Genetic/drug effects ; Transfection
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  • 18
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    A conserved domain in axonal targeting of Kv1 (Shaker) voltage-gated potassium channels (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-02
    Description: Axonal voltage-gated potassium (Kv1) channels regulate action-potential invasion and hence transmitter release. Although evolutionarily conserved, what mediates their axonal targeting is not known. We found that Kv1 axonal targeting required its T1 tetramerization domain. When fused to unpolarized CD4 or dendritic transferrin receptor, T1 promoted their axonal surface expression. Moreover, T1 mutations eliminating Kvbeta association compromised axonal targeting, but not surface expression, of CD4-T1 fusion proteins. Thus, proper association of Kvbeta with the Kv1 T1 domain is essential for axonal targeting.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gu, Chen -- Jan, Yuh Nung -- Jan, Lily Yeh -- New York, N.Y. -- Science. 2003 Aug 1;301(5633):646-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Departments of Physiology and Biochemistry, University of California, San Francisco, CA 94143-0725, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12893943" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Substitution ; Animals ; Antigens, CD4/metabolism ; Axons/*metabolism ; Biopolymers ; COS Cells ; Cell Line ; Cell Membrane/metabolism ; Cell Polarity ; Cells, Cultured ; Dendrites/metabolism ; Endocytosis ; Hippocampus/cytology ; Humans ; Kv1.2 Potassium Channel ; Models, Molecular ; Mutagenesis ; Neurons/metabolism ; Potassium Channels/*chemistry/*metabolism ; *Potassium Channels, Voltage-Gated ; *Protein Structure, Tertiary ; Receptors, Transferrin/metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Shaker Superfamily of Potassium Channels ; Shal Potassium Channels ; 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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    Regulation of NF-kappaB-dependent lymphocyte activation and development by paracaspase (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-25
    Description: Paracaspase (MALT1), a member of an evolutionarily conserved superfamily of caspase-like proteins, has been shown to bind and colocalize with the protein Bcl10 in vitro and, because of this association, has been suggested to be involved in the CARMA1-Bcl10 pathway of antigen-induced nuclear factor kappaB (NF-kappaB) activation. We demonstrate that primary T and B lymphocytes from paracaspase-deficient mice are defective in antigen-receptor-induced NF-kappaB activation, cytokine production, and proliferation. Paracaspase acts downstream of Bcl10 to induce NF-kappaB activation and is required for the normal development of B cells, indicating that paracaspase provides the missing link between Bcl10 and activation of the IkappaB kinase complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ruefli-Brasse, Astrid A -- French, Dorothy M -- Dixit, Vishva M -- New York, N.Y. -- Science. 2003 Nov 28;302(5650):1581-4. Epub 2003 Oct 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Oncology Department, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14576442" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Animals ; Antibody Formation ; Antigens, CD/analysis ; B-Lymphocyte Subsets/immunology/physiology ; B-Lymphocytes/*immunology/metabolism/physiology ; Caspases ; Cell Differentiation ; Cell Division ; Cell Survival ; Cells, Cultured ; Cytokines/metabolism ; Gene Deletion ; Gene Targeting ; Guanylate Kinase ; I-kappa B Kinase ; *Lymphocyte Activation ; Lymphoma, B-Cell, Marginal Zone/chemistry/*metabolism ; Mice ; Mice, Inbred C57BL ; NF-kappa B/*metabolism ; Neoplasm Proteins/chemistry/*metabolism ; Nucleoside-Phosphate Kinase/metabolism ; Phosphorylation ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/metabolism ; Receptors, Antigen, B-Cell/metabolism ; Receptors, Antigen, T-Cell/metabolism ; Signal Transduction ; T-Lymphocyte Subsets/immunology/physiology ; T-Lymphocytes/*immunology/metabolism/physiology ; Transfection
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  • 20
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    Proteomic screen finds pSer/pThr-binding domain localizing Plk1 to mitotic substrates (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-22
    Description: We have developed a proteomic approach for identifying phosphopeptide binding domains that modulate kinase-dependent signaling pathways. An immobilized library of partially degenerate phosphopeptides biased toward a particular protein kinase phosphorylation motif is used to isolate phospho-binding domains that bind to proteins phosphorylated by that kinase. Applying this approach to cyclin-dependent kinases (Cdks), we identified the polo-box domain (PBD) of the mitotic kinase polo-like kinase 1 (Plk1) as a specific phosphoserine (pSer) or phosphothreonine (pThr) binding domain and determined its optimal binding motif. This motif is present in known Plk1 substrates such as Cdc25, and an optimal phosphopeptide containing the motif disrupted PBD-substrate binding and localization of the PBD to centrosomes. This finding reveals how Plk1 can localize to specific sites within cells in response to Cdk phosphorylation at those sites and provides a structural mechanism for targeting the Plk1 kinase domain to its substrates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elia, Andrew E H -- Cantley, Lewis C -- Yaffe, Michael B -- GM52981/GM/NIGMS NIH HHS/ -- GM56203/GM/NIGMS NIH HHS/ -- R01 GM056203/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Feb 21;299(5610):1228-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cancer Research, 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/12595692" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Binding Sites ; Calorimetry ; Cell Cycle Proteins ; Centrosome/metabolism ; HeLa Cells ; Humans ; Ligands ; Mitosis ; Peptide Library ; Phosphopeptides/chemistry/*metabolism ; Phosphorylation ; Phosphoserine/*metabolism ; Phosphothreonine/*metabolism ; Point Mutation ; Protein Binding ; Protein Kinases/*chemistry/genetics/*metabolism ; *Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases ; Proteomics ; Proto-Oncogene Proteins ; Signal Transduction ; cdc25 Phosphatases/chemistry/genetics/*metabolism
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  • 21
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    Development. Longing for ligand: hedgehog, patched, and cell death (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guerrero, Isabel -- Ruiz i Altaba, Ariel -- New York, N.Y. -- Science. 2003 Aug 8;301(5634):774-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centro de Biologia Molecular "Severo Ochoa," CSIC-UAM, Universidad Autonoma de Madrid, Madrid E-28049, Spain. iguerrero@cbm.uam.es〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12907783" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Caspase 3 ; Caspases/metabolism ; Central Nervous System/cytology/*embryology ; Chick Embryo ; Drosophila/growth & development/metabolism ; Drosophila Proteins/metabolism ; Hedgehog Proteins ; Humans ; Intracellular Signaling Peptides and Proteins ; Ligands ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Mutation ; Neoplasms/etiology ; Protein Binding ; Protein Structure, Tertiary ; Receptors, Cell Surface ; Signal Transduction ; Trans-Activators/*metabolism ; Wings, Animal/growth & development
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 22
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    LysM domain receptor kinases regulating rhizobial Nod factor-induced infection (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-30
    Description: The rhizobial infection of legumes has the most stringent demand toward Nod factor structure of all host responses, and therefore a specific Nod factor entry receptor has been proposed. The SYM2 gene identified in certain ecotypes of pea (Pisum sativum) is a good candidate for such an entry receptor. We exploited the close phylogenetic relationship of pea and the model legume Medicago truncatula to identify genes specifically involved in rhizobial infection. The SYM2 orthologous region of M. truncatula contains 15 putative receptor-like genes, of which 7 are LysM domain-containing receptor-like kinases (LYKs). Using reverse genetics in M. truncatula, we show that two LYK genes are specifically involved in infection thread formation. This, as well as the properties of the LysM domains, strongly suggests that they are Nod factor entry receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Limpens, Erik -- Franken, Carolien -- Smit, Patrick -- Willemse, Joost -- Bisseling, Ton -- Geurts, Rene -- New York, N.Y. -- Science. 2003 Oct 24;302(5645):630-3. Epub 2003 Aug 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Biology, Department of Plant Sciences, Wageningen University, Dreijenlaan 3, 6703HA, Wageningen, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12947035" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Gene Expression ; *Genes, Plant ; Ligands ; Lipopolysaccharides/*metabolism ; Medicago/genetics/microbiology/*physiology ; Models, Biological ; Molecular Sequence Data ; Mutation ; Nitrogen Fixation ; Peas ; Phenotype ; Plant Roots/*microbiology/physiology ; Protein Kinases/chemistry/*genetics/*metabolism ; Protein Structure, Tertiary ; RNA Interference ; Signal Transduction ; Sinorhizobium meliloti/chemistry/genetics/growth & development/*physiology ; *Symbiosis
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  • 23
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    Cell therapy of alpha-sarcoglycan null dystrophic mice through intra-arterial delivery of mesoangioblasts (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-12
    Description: Preclinical or clinical trials for muscular dystrophies have met with modest success, mainly because of inefficient delivery of viral vectors or donor cells to dystrophic muscles. We report here that intra-arterial delivery of wild-type mesoangioblasts, a class of vessel-associated stem cells, corrects morphologically and functionally the dystrophic phenotype of virtually all downstream muscles in adult immunocompetent alpha-sarcoglycan (alpha-SG) null mice, a model organism for limb-girdle muscular dystrophy. When mesoangioblasts isolated from juvenile dystrophic mice and transduced with a lentiviral vector expressing alpha-SG were injected into the femoral artery of dystrophic mice, they reconstituted skeletal muscle in a manner similar to that seen in wild-type cells. The success of this protocol was mainly due to widespread distribution of donor stem cells through the capillary network, a distinct advantage of this strategy over previous approaches.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sampaolesi, Maurilio -- Torrente, Yvan -- Innocenzi, Anna -- Tonlorenzi, Rossana -- D'Antona, Giuseppe -- Pellegrino, M Antonietta -- Barresi, Rita -- Bresolin, Nereo -- De Angelis, M Gabriella Cusella -- Campbell, Kevin P -- Bottinelli, Roberto -- Cossu, Giulio -- 1322/Telethon/Italy -- 463/BI/Telethon/Italy -- New York, N.Y. -- Science. 2003 Jul 25;301(5632):487-92. Epub 2003 Jul 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cell Research Institute, H. S. Raffaele, Via Olgettina 58, 20132 Milan, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12855815" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Vessels/cytology/embryology ; Cell Differentiation ; Cell Line ; Cell Movement ; Cytoskeletal Proteins/*genetics/*metabolism ; Dystrophin/metabolism ; Endothelium, Vascular/physiology ; Female ; Femoral Artery ; Genetic Vectors ; Lentivirus/genetics ; Locomotion ; Male ; Membrane Glycoproteins/*genetics/*metabolism ; Mesoderm/cytology ; Mice ; Mice, Knockout ; Mice, Transgenic ; Muscle Contraction ; Muscle Fibers, Skeletal/cytology/physiology ; Muscle, Skeletal/cytology/metabolism/pathology/*physiology ; Muscular Dystrophy, Animal/metabolism/pathology/*therapy ; Regeneration ; Sarcoglycans ; *Stem Cell Transplantation ; Stem Cells/*physiology ; Transfection
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  • 24
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    Dishevelled 2 recruits beta-arrestin 2 to mediate Wnt5A-stimulated endocytosis of Frizzled 4 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-06
    Description: Wnt proteins, regulators of development in many organisms, bind to seven transmembrane-spanning (7TMS) receptors called frizzleds, thereby recruiting the cytoplasmic molecule dishevelled (Dvl) to the plasma membrane.Frizzled-mediated endocytosis of Wg (a Drosophila Wnt protein) and lysosomal degradation may regulate the formation of morphogen gradients. Endocytosis of Frizzled 4 (Fz4) in human embryonic kidney 293 cells was dependent on added Wnt5A protein and was accomplished by the multifunctional adaptor protein beta-arrestin 2 (betaarr2), which was recruited to Fz4 by binding to phosphorylated Dvl2. These findings provide a previously unrecognized mechanism for receptor recruitment of beta-arrestin and demonstrate that Dvl plays an important role in the endocytosis of frizzled, as well as in promoting signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Wei -- ten Berge, Derk -- Brown, Jeff -- Ahn, Seungkirl -- Hu, Liaoyuan A -- Miller, William E -- Caron, Marc G -- Barak, Larry S -- Nusse, Roel -- Lefkowitz, Robert J -- HL 16037/HL/NHLBI NIH HHS/ -- HL 61365/HL/NHLBI NIH HHS/ -- NS 19576/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Sep 5;301(5638):1391-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Departments of Medicine and Biochemistry, 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/12958364" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Arrestins/genetics/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Clathrin/metabolism ; Cytoplasm/metabolism ; *Endocytosis ; Frizzled Receptors ; Humans ; Mice ; Phosphoproteins/metabolism ; Phosphorylation ; Protein Kinase C/antagonists & inhibitors/metabolism ; Proteins/genetics/*metabolism ; Proto-Oncogene Proteins/*metabolism/pharmacology ; RNA, Small Interfering ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Wnt Proteins
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  • 25
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    The BRCT domain is a phospho-protein binding domain (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-25
    Description: The carboxyl-terminal domain (BRCT) of the Breast Cancer Gene 1 (BRCA1) protein is an evolutionarily conserved module that exists in a large number of proteins from prokaryotes to eukaryotes. Although most BRCT domain-containing proteins participate in DNA-damage checkpoint or DNA-repair pathways, or both, the function of the BRCT domain is not fully understood. We show that the BRCA1 BRCT domain directly interacts with phosphorylated BRCA1-Associated Carboxyl-terminal Helicase (BACH1). This specific interaction between BRCA1 and phosphorylated BACH1 is cell cycle regulated and is required for DNA damage-induced checkpoint control during the transition from G2 to M phase of the cell cycle. Further, we show that two other BRCT domains interact with their respective physiological partners in a phosphorylation-dependent manner. Thirteen additional BRCT domains also preferentially bind phospho-peptides rather than nonphosphorylated control peptides. These data imply that the BRCT domain is a phospho-protein binding domain involved in cell cycle control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Xiaochun -- Chini, Claudia Christiano Silva -- He, Miao -- Mer, Georges -- Chen, Junjie -- CA89239/CA/NCI NIH HHS/ -- CA92312/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 24;302(5645):639-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncology, Mayo Clinic and Foundation, Rochester, MN 55905, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14576433" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; BRCA1 Protein/*chemistry/*metabolism ; Carrier Proteins/chemistry/metabolism ; Cell Cycle ; *Cell Cycle Proteins ; Cell Line ; DNA Damage ; DNA Repair ; *DNA-Binding Proteins ; E2F Transcription Factors ; G2 Phase ; Humans ; Mitosis ; Mutation ; Nuclear Proteins ; Peptide Library ; Phosphoprotein Phosphatases/chemistry/metabolism ; Phosphoproteins/chemistry/genetics/*metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Protein Binding ; Protein Structure, Tertiary ; RNA Helicases/chemistry/genetics/*metabolism ; RNA Polymerase II/metabolism ; RNA, Small Interfering ; Recombinant Fusion Proteins/chemistry/metabolism ; Transcription Factors/metabolism ; Transfection ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    VDAC2 inhibits BAK activation and mitochondrial apoptosis (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-26
    Description: The multidomain proapoptotic molecules BAK or BAX are required to initiate the mitochondrial pathway of apoptosis. How cells maintain the potentially lethal proapoptotic effector BAK in a monomeric inactive conformation at mitochondria is unknown. In viable cells, we found BAK complexed with mitochondrial outer-membrane protein VDAC2, a VDAC isoform present in low abundance that interacts specifically with the inactive conformer of BAK. Cells deficient in VDAC2, but not cells lacking the more abundant VDAC1, exhibited enhanced BAK oligomerization and were more susceptible to apoptotic death. Conversely, overexpression of VDAC2 selectively prevented BAK activation and inhibited the mitochondrial apoptotic pathway. Death signals activate "BH3-only" molecules such as tBID, BIM, or BAD, which displace VDAC2 from BAK, enabling homo-oligomerization of BAK and apoptosis. Thus, VDAC2, an isoform restricted to mammals, regulates the activity of BAK and provides a connection between mitochondrial physiology and the core apoptotic pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheng, Emily H Y -- Sheiko, Tatiana V -- Fisher, Jill K -- Craigen, William J -- Korsmeyer, Stanley J -- NS42319/NS/NINDS NIH HHS/ -- R37CA50239/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Jul 25;301(5632):513-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12881569" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; BH3 Interacting Domain Death Agonist Protein ; Biopolymers ; Carrier Proteins/metabolism/pharmacology ; Cell Line ; Cells, Cultured ; Etoposide/pharmacology ; Humans ; Intracellular Membranes/metabolism ; Jurkat Cells ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Mitochondria/*metabolism ; Mitochondria, Liver/metabolism ; Porins/genetics/isolation & purification/*metabolism ; Protein Binding ; Protein Conformation ; Protein Structure, Tertiary ; Proto-Oncogene Proteins/metabolism ; *Proto-Oncogene Proteins c-bcl-2 ; Recombinant Proteins/pharmacology ; Staurosporine/pharmacology ; Voltage-Dependent Anion Channel 1 ; Voltage-Dependent Anion Channel 2 ; Voltage-Dependent Anion Channels ; bcl-2 Homologous Antagonist-Killer Protein ; bcl-2-Associated X Protein
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    Erythrocyte G protein-coupled receptor signaling in malarial infection (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-23
    Description: Erythrocytic mechanisms involved in malarial infection are poorly understood. We have found that signaling via the erythrocyte beta2-adrenergic receptor and heterotrimeric guanine nucleotide-binding protein (Galphas) regulated the entry of the human malaria parasite Plasmodium falciparum. Agonists that stimulate cyclic adenosine 3',5'-monophosphate production led to an increase in malarial infection that could be blocked by specific receptor antagonists. Moreover, peptides designed to inhibit Galphas protein function reduced parasitemia in P. falciparum cultures in vitro, and beta-antagonists reduced parasitemia of P. berghei infections in an in vivo mouse model. Thus, signaling via the erythrocyte beta2-adrenergic receptor and Galphas may regulate malarial infection across parasite species.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harrison, Travis -- Samuel, Benjamin U -- Akompong, Thomas -- Hamm, Heidi -- Mohandas, Narla -- Lomasney, Jon W -- Haldar, Kasturi -- AI39071/AI/NIAID NIH HHS/ -- DK32094/DK/NIDDK NIH HHS/ -- EY06062/EY/NEI NIH HHS/ -- EY10291/EY/NEI NIH HHS/ -- HL03961/HL/NHLBI NIH HHS/ -- HL55591/HL/NHLBI NIH HHS/ -- HL69630/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2003 Sep 19;301(5640):1734-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Feinberg School of Medicine, Northwestern University, 303 Chicago Avenue, Chicago, IL 60611, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14500986" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic beta-2 Receptor Agonists ; Adrenergic beta-2 Receptor Antagonists ; Adrenergic beta-Agonists/pharmacology ; Adrenergic beta-Antagonists/pharmacology ; Alprenolol/pharmacology ; Animals ; Catecholamines/metabolism ; Cyclic AMP/metabolism ; Erythrocyte Membrane/metabolism ; Erythrocytes/metabolism/*parasitology ; GTP-Binding Protein alpha Subunits, Gs/chemistry/*metabolism ; Humans ; Malaria/metabolism/*parasitology ; Membrane Microdomains/metabolism ; Mice ; Parasitemia ; Peptide Fragments/pharmacology ; Plasmodium berghei/*physiology ; Plasmodium falciparum/growth & development/*physiology ; Propranolol/pharmacology ; Purinergic P1 Receptor Agonists ; Purinergic P1 Receptor Antagonists ; Receptors, Adrenergic, beta-2/*metabolism ; Receptors, Purinergic P1/metabolism ; Signal Transduction ; Stereoisomerism ; Vacuoles/parasitology
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    Biomedicine. Love, honor, and protect (your liver) (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davidson, Alan J -- Zon, Leonard I -- New York, N.Y. -- Science. 2003 Feb 7;299(5608):835-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Division of Hematology/Oncology, Children's Hospital, Howard Hughes Medical Institute, Boston, MA 02115, USA. zon@hhmi.tchlab.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12574609" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbon Tetrachloride/toxicity ; Cell Communication ; Cell Division ; Coculture Techniques ; Drug-Induced Liver Injury ; Endothelial Growth Factors/metabolism/*physiology ; Endothelium, Vascular/*cytology/physiology ; Hepatocyte Growth Factor/physiology/secretion ; Hepatocytes/*physiology ; Interleukin-6/physiology/secretion ; Liver/blood supply/*cytology/pathology/*physiology ; Liver Diseases/metabolism/pathology/prevention & control ; *Liver Regeneration ; Mice ; Necrosis ; Signal Transduction ; Up-Regulation ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factor Receptor-1/*metabolism ; Vascular Endothelial Growth Factor Receptor-2/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Neuroscience. ORs rule the roost in the olfactory system (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewcock, Joseph W -- Reed, Randall R -- New York, N.Y. -- Science. 2003 Dec 19;302(5653):2078-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular Biology and Genetics, 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/14684811" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Alleles ; Animals ; Cell Nucleus/metabolism ; Chromosomes, Artificial, Yeast ; Feedback, Physiological ; *Gene Expression Regulation ; Genes, Reporter ; Mice ; Mice, Transgenic ; Multigene Family ; Odors ; Olfactory Receptor Neurons/*metabolism ; Promoter Regions, Genetic ; Pseudogenes ; Receptors, Odorant/*genetics/*metabolism ; Signal Transduction ; Transgenes
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    LRP: role in vascular wall integrity and protection from atherosclerosis (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-12
    Description: Vascular smooth muscle cell (SMC) proliferation and migration are important events in the development of atherosclerosis. The low-density lipoprotein receptor-related protein (LRP1) mediates suppression of SMC migration induced by platelet-derived growth factor (PDGF). Here we show that LRP1 forms a complex with the PDGF receptor (PDGFR). Inactivation of LRP1 in vascular SMCs of mice causes PDGFR overexpression and abnormal activation of PDGFR signaling, resulting in disruption of the elastic layer, SMC proliferation, aneurysm formation, and marked susceptibility to cholesterol-induced atherosclerosis. The development of these abnormalities was reduced by treatment with Gleevec, an inhibitor of PDGF signaling. Thus, LRP1 has a pivotal role in protecting vascular wall integrity and preventing atherosclerosis by controlling PDGFR activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boucher, Philippe -- Gotthardt, Michael -- Li, Wei-Ping -- Anderson, Richard G W -- Herz, Joachim -- GM 52016/GM/NIGMS NIH HHS/ -- HL20948/HL/NHLBI NIH HHS/ -- HL63762/HL/NHLBI NIH HHS/ -- NS43408/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Apr 11;300(5617):329-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9046, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12690199" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta/cytology/metabolism/*pathology ; Arteriosclerosis/*pathology/physiopathology/*prevention & control ; Benzamides ; Cattle ; Cell Division ; Cell Line ; Cholesterol, Dietary/administration & dosage ; Diet, Atherogenic ; Elastin/analysis ; Enzyme Inhibitors/pharmacology ; Imatinib Mesylate ; Ligands ; Low Density Lipoprotein Receptor-Related ; Protein-1/genetics/metabolism/*physiology ; Mesenteric Arteries/cytology/pathology ; Mice ; Mice, Knockout ; Mice, Transgenic ; Muscle, Smooth, Vascular/cytology/*metabolism/pathology ; Myocytes, Smooth Muscle/*metabolism/physiology ; Phosphorylation ; Piperazines/pharmacology ; Platelet-Derived Growth Factor/metabolism/pharmacology ; Proto-Oncogene Proteins c-sis ; Pyrimidines/pharmacology ; Receptor, Platelet-Derived Growth Factor beta/metabolism ; Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Hexameric structure and assembly of the interleukin-6/IL-6 alpha-receptor/gp130 complex (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-06-28
    Description: Interleukin-6 (IL-6) is an immunoregulatory cytokine that activates a cell-surface signaling assembly composed of IL-6, the IL-6 alpha-receptor (IL-6Ralpha), and the shared signaling receptor gp130. The 3.65 angstrom-resolution structure of the extracellular signaling complex reveals a hexameric, interlocking assembly mediated by a total of 10 symmetry-related, thermodynamically coupled interfaces. Assembly of the hexameric complex occurs sequentially: IL-6 is first engaged by IL-6Ralpha and then presented to gp130in the proper geometry to facilitate a cooperative transition into the high-affinity, signaling-competent hexamer. The quaternary structures of other IL-6/IL-12 family signaling complexes are likely constructed by means of a similar topological blueprint.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boulanger, Martin J -- Chow, Dar-chone -- Brevnova, Elena E -- Garcia, K Christopher -- AI51321/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2003 Jun 27;300(5628):2101-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology and Department of Structural Biology, Stanford University School of Medicine, Fairchild D319, 299 Campus Drive, Stanford, CA 94305-5124, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12829785" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD/*chemistry/*metabolism ; Binding Sites ; Crystallography, X-Ray ; Cytokine Receptor gp130 ; Humans ; Interleukin-6/*chemistry/*metabolism ; Macromolecular Substances ; Membrane Glycoproteins/*chemistry/*metabolism ; Models, Molecular ; Protein Binding ; Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Receptors, Interleukin-6/*chemistry/*metabolism ; Signal Transduction ; Thermodynamics
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    Eppendorf 2003 prize-winning essay. Ubiquitin and the deconstruction of synapses (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ehlers, Michael D -- New York, N.Y. -- Science. 2003 Oct 31;302(5646):800-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA. ehlers@neuro.duke.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14593160" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Awards and Prizes ; Carrier Proteins/metabolism ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein/metabolism ; Cysteine Endopeptidases/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; Multienzyme Complexes/metabolism ; Nerve Tissue Proteins/*metabolism ; Neurons/metabolism ; Proteasome Endopeptidase Complex ; Receptors, N-Methyl-D-Aspartate/metabolism ; Signal Transduction ; Synapses/*metabolism/ultrastructure ; Synaptic Membranes/*metabolism/ultrastructure ; *Synaptic Transmission ; Ubiquitin/*metabolism
    Print ISSN: 0036-8075
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    Synchronization of cellular clocks in the suprachiasmatic nucleus (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-25
    Description: Individual cellular clocks in the suprachiasmatic nucleus (SCN), the circadian center, are integrated into a stable and robust pacemaker with a period length of about 24 hours. We used real-time analysis of gene expression to show synchronized rhythms of clock gene transcription across hundreds of neurons within the mammalian SCN in organotypic slice culture. Differentially phased neuronal clocks are topographically arranged across the SCN. A protein synthesis inhibitor set all cell clocks to the same initial phase and, after withdrawal, intrinsic interactions among cell clocks reestablished the stable program of gene expression across the assemblage. Na+-dependent action potentials contributed to establishing cellular synchrony and maintaining spontaneous oscillation across the SCN.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamaguchi, Shun -- Isejima, Hiromi -- Matsuo, Takuya -- Okura, Ryusuke -- Yagita, Kazuhiro -- Kobayashi, Masaki -- Okamura, Hitoshi -- New York, N.Y. -- Science. 2003 Nov 21;302(5649):1408-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Brain Science, Department of Brain Sciences, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14631044" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Action Potentials/drug effects ; Animals ; Basic Helix-Loop-Helix Transcription Factors ; Biological Clocks/*physiology ; CLOCK Proteins ; Cell Cycle Proteins ; Circadian Rhythm/*physiology ; Cycloheximide/pharmacology ; Gene Expression ; Glyceraldehyde-3-Phosphate Dehydrogenases/genetics/metabolism ; Luminescence ; Mice ; Mice, Knockout ; Mice, Transgenic ; Neurons/*physiology ; Nuclear Proteins/genetics/metabolism ; Organ Culture Techniques ; Period Circadian Proteins ; Promoter Regions, Genetic ; Protein Synthesis Inhibitors/pharmacology ; Signal Transduction ; Sodium/metabolism ; Suppression, Genetic ; Suprachiasmatic Nucleus/cytology/*physiology ; Tetrodotoxin/pharmacology ; Trans-Activators/metabolism ; Transcription Factors/metabolism ; Transcription, Genetic
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    Hematopoietic cell regulation by Rac1 and Rac2 guanosine triphosphatases (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-18
    Description: The Rho guanosine triphosphatases (GTPases) Rac1 and Rac2 are critical signaling regulators in mammalian cells. The deletion of both Rac1 and Rac2 murine alleles leads to a massive egress of hematopoietic stem/progenitor cells (HSC/Ps) into the blood from the marrow, whereas Rac1-/- but not Rac2-/- HSC/Ps fail to engraft in the bone marrow of irradiated recipient mice. In contrast, Rac2, but not Rac1, regulates superoxide production and directed migration in neutrophils, and in each cell type, the two GTPases play distinct roles in actin organization, cell survival, and proliferation. Thus, Rac1 and Rac2 regulate unique aspects of hematopoietic development and function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gu, Yi -- Filippi, Marie-Dominique -- Cancelas, Jose A -- Siefring, Jamie E -- Williams, Emily P -- Jasti, Aparna C -- Harris, Chad E -- Lee, Andrew W -- Prabhakar, Rethinasamy -- Atkinson, Simon J -- Kwiatkowski, David J -- Williams, David A -- DK62757/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 17;302(5644):445-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Experimental Hematology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14564009" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Apoptosis ; Bone Marrow Transplantation ; Cell Adhesion ; Cell Cycle ; Cell Movement ; Cell Size ; Colony-Forming Units Assay ; Cyclin D1/metabolism ; Fibronectins/metabolism ; Hematopoiesis ; Hematopoietic Stem Cell Mobilization ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*physiology ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Mitogen-Activated Protein Kinases/metabolism ; Neutrophils/*physiology ; *Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Recombination, Genetic ; Signal Transduction ; Stem Cell Factor/pharmacology ; Superoxides/metabolism ; rac GTP-Binding Proteins/genetics/*metabolism ; rac1 GTP-Binding Protein/genetics/*metabolism
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    Computational biology. Counting on the neuron (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cassman, Marvin -- New York, N.Y. -- Science. 2003 May 2;300(5620):756-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉California Institute for Quantitative Biomedical Research, University of California, San Francisco, CA 94131, USA. mcassman@research.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730591" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aplysia/physiology ; B-Lymphocytes/metabolism ; Calcium/metabolism ; *Cell Physiological Phenomena ; *Computational Biology ; *Computer Simulation ; Electrophysiology ; Gene Expression ; Memory ; *Models, Biological ; *Models, Neurological ; Myocytes, Cardiac/metabolism ; Neurons/*physiology ; Neurons, Afferent/physiology ; Proteins/metabolism ; Signal Transduction
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    Mitochondrial biogenesis in mammals: the role of endogenous nitric oxide (2003)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2003-02-08
    Description: Nitric oxide was found to trigger mitochondrial biogenesis in cells as diverse as brown adipocytes and 3T3-L1, U937, and HeLa cells. This effect of nitric oxide was dependent on guanosine 3',5'-monophosphate (cGMP) and was mediated by the induction of peroxisome proliferator-activated receptor gamma coactivator 1alpha, a master regulator of mitochondrial biogenesis. Moreover, the mitochondrial biogenesis induced by exposure to cold was markedly reduced in brown adipose tissue of endothelial nitric oxide synthase null-mutant (eNOS-/-) mice, which had a reduced metabolic rate and accelerated weight gain as compared to wild-type mice. Thus, a nitric oxide-cGMP-dependent pathway controls mitochondrial biogenesis and body energy balance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nisoli, Enzo -- Clementi, Emilio -- Paolucci, Clara -- Cozzi, Valeria -- Tonello, Cristina -- Sciorati, Clara -- Bracale, Renata -- Valerio, Alessandra -- Francolini, Maura -- Moncada, Salvador -- Carruba, Michele O -- New York, N.Y. -- Science. 2003 Feb 7;299(5608):896-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Preclinical Sciences, Center for Study and Research on Obesity, Luigi Sacco Hospital, University of Milan, Milan 20157, Italy. enzo.nisoli@unimi.it〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12574632" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; 8-Bromo Cyclic Adenosine Monophosphate/pharmacology ; Adipocytes/*metabolism/ultrastructure ; Adipose Tissue, Brown/cytology/metabolism/ultrastructure ; Animals ; Cold Temperature ; Cyclic GMP/metabolism ; DNA, Mitochondrial/metabolism ; DNA-Binding Proteins/metabolism ; Eating ; Energy Metabolism ; Female ; HeLa Cells ; High Mobility Group Proteins ; Humans ; Male ; Mice ; Mice, Knockout ; Mitochondria/*metabolism/ultrastructure ; *Mitochondrial Proteins ; Motor Activity ; NF-E2-Related Factor 1 ; Nitric Oxide/*physiology ; Nitric Oxide Synthase/genetics/*metabolism ; Nitric Oxide Synthase Type II ; Nitric Oxide Synthase Type III ; Nuclear Proteins/metabolism ; Nuclear Respiratory Factors ; Oligonucleotides, Antisense/pharmacology ; Oxadiazoles/pharmacology ; Oxygen Consumption ; Penicillamine/*analogs & derivatives/pharmacology ; Quinoxalines/pharmacology ; RNA, Messenger/genetics/metabolism ; Rats ; Signal Transduction ; Trans-Activators/metabolism ; Transcription Factors/metabolism ; U937 Cells ; Weight Gain
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    Glycosylation restores survival of chilled blood platelets (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-13
    Description: Cooling of blood platelets clusters the von Willebrand factor receptor complex. Macrophage alphaMbeta2 integrins bind to the GPIbalpha subunit of the clustered complex, resulting in rapid clearance of transfused, cooled platelets. This precludes refrigeration of platelets for transfusion, but the current practice of room temperature storage has major drawbacks. We document that alphaMbeta2 is a lectin that recognizes exposed beta-N-acetylglucosamine residues of N-linked glycans on GPIbalpha. Enzymatic galactosylation of chilled platelets blocks alphaMbeta2 recognition, prolonging the circulation of functional cooled platelets. Platelet-associated galactosyltransferase produces efficient galactosylation when uridine diphosphate-galactose is added, affording a potentially simple method for storing platelets in the cold.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffmeister, Karin M -- Josefsson, Emma C -- Isaac, Natasha A -- Clausen, Henrik -- Hartwig, John H -- Stossel, Thomas P -- HL19429/HL/NHLBI NIH HHS/ -- HL56949/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2003 Sep 12;301(5639):1531-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. khoffmeister@rics.bwh.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12970565" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylglucosamine/metabolism/pharmacology ; Animals ; Blood Platelets/metabolism/*physiology ; Blood Preservation ; Carbohydrate Conformation ; Cell Line ; Cell Survival ; *Cold Temperature ; Female ; Galactose/*metabolism ; Galactosyltransferases/metabolism ; Glycosylation ; Humans ; Lectins/metabolism ; Ligands ; Macrophage-1 Antigen/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Monosaccharides/pharmacology ; Phagocytosis/drug effects ; Platelet Aggregation ; Platelet Glycoprotein GPIb-IX Complex/metabolism ; *Platelet Membrane Glycoproteins ; Platelet Transfusion ; Refrigeration ; Uridine Diphosphate Galactose/metabolism ; von Willebrand Factor/metabolism
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    Induction of APOBEC3G ubiquitination and degradation by an HIV-1 Vif-Cul5-SCF complex (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-18
    Description: Human immunodeficiency virus-1 (HIV-1) Vif is essential for viral evasion of host antiviral factor CEM15/APOBEC3G. We report that Vif interacts with cellular proteins Cul5, elongins B and C, and Rbx1 to form an Skp1-cullin-F-box (SCF)-like complex. The ability of Vif to suppress antiviral activity of APOBEC3G was specifically dependent on Cul5-SCF function, allowing Vif to interact with APOBEC3G and induce its ubiquitination and degradation. A Vif mutant that interacted with APOBEC3G but not with Cul5-SCF was functionally inactive. The Cul5-SCF was also required for Vif function in distantly related simian immunodeficiency virus mac. These results indicate that the conserved Cul5-SCF pathway used by Vif is a potential target for antiviral development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Xianghui -- Yu, Yunkai -- Liu, Bindong -- Luo, Kun -- Kong, Wei -- Mao, Panyong -- Yu, Xiao-Fang -- 1S10-RR14702/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2003 Nov 7;302(5647):1056-60. Epub 2003 Oct 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14564014" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/genetics/metabolism ; Cell Line ; Cullin Proteins/genetics/*metabolism ; Cytidine Deaminase ; Gene Products, vif/genetics/*metabolism ; HIV-1/genetics/*physiology ; Humans ; Mutation ; Nucleoside Deaminases ; Proteins/*metabolism ; Repressor Proteins ; Transcription Factors/genetics/metabolism ; Transfection ; Ubiquitin/*metabolism ; Virus Replication ; vif Gene Products, Human Immunodeficiency Virus
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    Biological networks: the tinkerer as an engineer (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-27
    Description: This viewpoint comments on recent advances in understanding the design principles of biological networks. It highlights the surprising discovery of "good-engineering" principles in biochemical circuitry that evolved by random tinkering.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alon, U -- New York, N.Y. -- Science. 2003 Sep 26;301(5641):1866-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel 76100. urialon@weizmann.ac.il〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14512615" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biochemical Phenomena ; Biochemistry ; *Biological Evolution ; *Biology ; DNA/metabolism ; Engineering ; *Models, Biological ; Proteins/metabolism ; Signal Transduction ; Systems Theory
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    Embryonic stem cells. Stem cell programs (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-10
    Description: The availability of human embryonic stem cell lines provides an important tool for scientists to explore the fundamental mechanisms that regulate differentiation into specific cell types. When more is known about the mechanisms that govern these processes, human embryonic stem cells may be clinically useful in generating cell types that have been damaged or depleted by a variety of human diseases. The NIH is actively pursuing a variety of initiatives to promote this developing research field, while continuing and expanding its long-standing investment in adult stem cells and research.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zerhouni, Elias -- New York, N.Y. -- Science. 2003 May 9;300(5621):911-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12738840" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; Cell Culture Techniques ; Cell Line ; Education ; *Embryo Research ; Embryo, Mammalian/*cytology ; Expressed Sequence Tags ; Financing, Government ; Humans ; Internet ; *National Institutes of Health (U.S.) ; Patents as Topic ; Research Support as Topic ; *Stem Cells/cytology/physiology ; United States
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    Disruption of the epithelial apical-junctional complex by Helicobacter pylori CagA (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-31
    Description: Helicobacter pylori translocates the protein CagA into gastric epithelial cells and has been linked to peptic ulcer disease and gastric carcinoma. We show that injected CagA associates with the epithelial tight-junction scaffolding protein ZO-1 and the transmembrane protein junctional adhesion molecule, causing an ectopic assembly of tight-junction components at sites of bacterial attachment, and altering the composition and function of the apical-junctional complex. Long-term CagA delivery to polarized epithelia caused a disruption of the epithelial barrier function and dysplastic alterations in epithelial cell morphology. CagA appears to target H. pylori to host cell intercellular junctions and to disrupt junction-mediated functions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3369828/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3369828/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amieva, Manuel R -- Vogelmann, Roger -- Covacci, Antonello -- Tompkins, Lucy S -- Nelson, W James -- Falkow, Stanley -- AI38459/AI/NIAID NIH HHS/ -- CA92229/CA/NCI NIH HHS/ -- DDC DK56339/DC/NIDCD NIH HHS/ -- R01 GM035527/GM/NIGMS NIH HHS/ -- R01GM35227/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 May 30;300(5624):1430-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA. amieva@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12775840" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Bacterial/genetics/*metabolism ; Bacterial Adhesion ; Bacterial Proteins/genetics/*metabolism ; Cell Adhesion Molecules/metabolism ; Cell Line ; Cell Polarity ; Cell Size ; Dogs ; Epithelial Cells/cytology/metabolism/*microbiology/ultrastructure ; Gastric Mucosa ; Helicobacter pylori/*pathogenicity/physiology ; Humans ; Intracellular Signaling Peptides and Proteins ; Junctional Adhesion Molecules ; Membrane Proteins/metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; Protein Tyrosine Phosphatase, Non-Receptor Type 11 ; Protein Tyrosine Phosphatases/metabolism ; Tight Junctions/*microbiology/physiology/*ultrastructure ; Tumor Cells, Cultured ; Zonula Occludens-1 Protein
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    Talin binding to integrin beta tails: a final common step in integrin activation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-04
    Description: Control of integrin affinity for ligands (integrin activation) is essential for normal cell adhesion, migration, and assembly of an extracellular matrix. Integrin activation is usually mediated through the integrin beta subunit cytoplasmic tail and can be regulated by many different biochemical signaling pathways. We report that specific binding of the cytoskeletal protein talin to integrin beta subunit cytoplasmic tails leads to the conformational rearrangements of integrin extracellular domains that increase their affinity. Thus, regulated binding of talin to integrin beta tails is a final common element of cellular signaling cascades that control integrin activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tadokoro, Seiji -- Shattil, Sanford J -- Eto, Koji -- Tai, Vera -- Liddington, Robert C -- de Pereda, Jose M -- Ginsberg, Mark H -- Calderwood, David A -- New York, N.Y. -- Science. 2003 Oct 3;302(5642):103-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, The Scripps Research Institute, The Burnham Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14526080" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Antibodies, Monoclonal/immunology ; Antigens, CD29/chemistry/metabolism ; Cell Line ; Fibronectins/metabolism ; Humans ; Integrin beta Chains/chemistry/*metabolism ; Integrin beta3/chemistry/metabolism ; Molecular Sequence Data ; Mutation ; Platelet Glycoprotein GPIIb-IIIa Complex/chemistry/immunology/metabolism ; Protein Binding ; Protein Conformation ; Protein Structure, Tertiary ; RNA, Small Interfering ; Recombinant Proteins/metabolism ; *Signal Transduction ; Talin/*metabolism ; Transfection
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    Dilated cardiomyopathy and heart failure caused by a mutation in phospholamban (2003)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2003-03-01
    Description: Molecular etiologies of heart failure, an emerging cardiovascular epidemic affecting 4.7 million Americans and costing 17.8 billion health-care dollars annually, remain poorly understood. Here we report that an inherited human dilated cardiomyopathy with refractory congestive heart failure is caused by a dominant Arg --〉 Cys missense mutation at residue 9 (R9C) in phospholamban (PLN), a transmembrane phosphoprotein that inhibits the cardiac sarcoplasmic reticular Ca2+-adenosine triphosphatase (SERCA2a) pump. Transgenic PLN(R9C) mice recapitulated human heart failure with premature death. Cellular and biochemical studies revealed that, unlike wild-type PLN, PLN(R9C) did not directly inhibit SERCA2a. Rather, PLN(R9C) trapped protein kinase A (PKA), which blocked PKA-mediated phosphorylation of wild-type PLN and in turn delayed decay of calcium transients in myocytes. These results indicate that myocellular calcium dysregulation can initiate human heart failure-a finding that may lead to therapeutic opportunities.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schmitt, Joachim P -- Kamisago, Mitsuhiro -- Asahi, Michio -- Li, Guo Hua -- Ahmad, Ferhaan -- Mende, Ulrike -- Kranias, Evangelia G -- MacLennan, David H -- Seidman, J G -- Seidman, Christine E -- New York, N.Y. -- Science. 2003 Feb 28;299(5611):1410-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School and Howard Hughes Medical Institute, 200 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12610310" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Calcium/metabolism ; Calcium Signaling ; Calcium-Binding Proteins/chemistry/*genetics/*physiology ; Calcium-Transporting ATPases/antagonists & inhibitors/metabolism ; Cardiomegaly ; Cardiomyopathy, Dilated/*genetics/pathology/physiopathology ; Cell Line ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Female ; Heart Failure/*genetics/pathology/physiopathology ; Heart Ventricles/metabolism/pathology ; Humans ; Lod Score ; Male ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Muscle Cells/metabolism/physiology ; *Mutation, Missense ; Myocardial Contraction ; Myocardium/pathology ; Pedigree ; Phosphorylation ; Sarcoplasmic Reticulum Calcium-Transporting ATPases
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    Listeria intracellular growth and virulence require host-derived lipoic acid (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-18
    Description: Listeria monocytogenes is a Gram-positive intracytosolic pathogen that causes severe disease in pregnant and immunocompromised individuals. We found that L. monocytogenes lacking the lipoate protein ligase LplA1 was defective for growth specifically in the host cytosol and was less virulent in animals by a factor of 300. A major target for LplA1, the E2 subunit of pyruvate dehydrogenase (PDH), lacked a critical lipoyl modification when the DeltalplA1 strain was grown intracellularly, which suggests that abortive growth was due to loss of PDH function. Thus, the use of host-derived lipoic acid may be a critical process for in vivo replication of bacterial pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Riordan, Mary -- Moors, Marlena A -- Portnoy, Daniel A -- AI29619/AI/NIAID NIH HHS/ -- R01 AI027655/AI/NIAID NIH HHS/ -- R01 AI27655/AI/NIAID NIH HHS/ -- R37 AI029619/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 17;302(5644):462-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, School of Public Health, University of California, Berkeley, CA 94720-3202, USA. oriordan@umich.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14564012" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Culture Media ; Cytosol/microbiology ; Dihydrolipoyllysine-Residue Acetyltransferase ; Gene Deletion ; Lethal Dose 50 ; Listeria monocytogenes/genetics/*growth & development/metabolism/*pathogenicity ; Listeriosis/microbiology ; Macrophages/metabolism/*microbiology ; Mice ; Mice, Inbred BALB C ; Mutation ; Open Reading Frames ; Peptide Synthases/genetics/metabolism ; Pyruvate Dehydrogenase Complex/metabolism ; Thioctic Acid/*metabolism ; Virulence
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    Bypassing a kinase activity with an ATP-competitive drug (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-18
    Description: Unfolded proteins in the endoplasmic reticulum cause trans-autophosphorylation of the bifunctional transmembrane kinase Ire1, which induces its endoribonuclease activity. The endoribonuclease initiates nonconventional splicing of HAC1 messenger RNA to trigger the unfolded-protein response (UPR). We explored the role of Ire1's kinase domain by sensitizing it through site-directed mutagenesis to the ATP-competitive inhibitor 1NM-PP1. Paradoxically, rather than being inhibited by 1NM-PP1, drug-sensitized Ire1 mutants required 1NM-PP1 as a cofactor for activation. In the presence of 1NM-PP1, drug-sensitized Ire1 bypassed mutations that inactivate its kinase activity and induced a full UPR. Thus, rather than through phosphorylation per se, a conformational change in the kinase domain triggered by occupancy of the active site with a ligand leads to activation of all known downstream functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Papa, Feroz R -- Zhang, Chao -- Shokat, Kevan -- Walter, Peter -- AI44009/AI/NIAID NIH HHS/ -- GM32384/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Nov 28;302(5650):1533-7. Epub 2003 Oct 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Francisco, CA 94143-2200, USA. frpapa@medicine.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14564015" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Diphosphate/pharmacology ; Adenosine Triphosphate/analogs & derivatives/chemistry/*metabolism/pharmacology ; Basic-Leucine Zipper Transcription Factors ; Binding Sites ; Binding, Competitive ; Cytosol/metabolism ; Dithiothreitol/pharmacology ; Endoplasmic Reticulum/*metabolism ; Endoribonucleases/metabolism ; Enzyme Activation ; Ligands ; Membrane Glycoproteins/antagonists & inhibitors/*chemistry/genetics/*metabolism ; Models, Biological ; Mutagenesis, Site-Directed ; Phosphorylation ; Protein Conformation ; *Protein Folding ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/antagonists & ; inhibitors/*chemistry/genetics/*metabolism ; Pyrazoles/chemistry/*metabolism/*pharmacology ; Pyrimidines/chemistry/*metabolism/*pharmacology ; RNA Splicing ; RNA, Messenger/genetics/metabolism ; Repressor Proteins/genetics/metabolism ; Saccharomyces cerevisiae Proteins/antagonists & ; inhibitors/*chemistry/genetics/*metabolism ; Signal Transduction ; Structure-Activity Relationship ; Substrate Specificity ; Transcription Factors/genetics/metabolism ; Up-Regulation
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    Role of EphA4 and EphrinB3 in local neuronal circuits that control walking (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-22
    Description: Local circuits in the spinal cord that generate locomotion are termed central pattern generators (CPGs). These provide coordinated bilateral control over the normal limb alternation that underlies walking. The molecules that organize the mammalian CPG are unknown. Isolated spinal cords from mice lacking either the EphA4 receptor or its ligand ephrinB3 have lost left-right limb alternation and instead exhibit synchrony. We identified EphA4-positive neurons as an excitatory component of the locomotor CPG. Our study shows that dramatic locomotor changes can occur as a consequence of local genetic rewiring and identifies genes required for the development of normal locomotor behavior.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kullander, Klas -- Butt, Simon J B -- Lebret, James M -- Lundfald, Line -- Restrepo, Carlos E -- Rydstrom, Anna -- Klein, Rudiger -- Kiehn, Ole -- New York, N.Y. -- Science. 2003 Mar 21;299(5614):1889-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Biochemistry, Gothenburg University, Medicinaregatan 9 A, 405 30 Gothenburg, Sweden. klas.kullander@medkem.gu.se〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12649481" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Bicuculline/pharmacology ; Carrier Proteins/genetics/metabolism ; Electrophysiology ; Ephrin-B3/genetics/*physiology ; Gait ; In Vitro Techniques ; Interneurons/physiology ; *Membrane Transport Proteins ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Motor Activity ; Neurons/*physiology ; Nipecotic Acids/pharmacology ; Receptor, EphA4/genetics/*physiology ; Sarcosine/pharmacology ; Signal Transduction ; Spinal Cord/*physiology ; Spinal Nerve Roots/physiology ; Strychnine/pharmacology ; Vesicular Glutamate Transport Protein 1 ; Vesicular Glutamate Transport Protein 2 ; *Vesicular Transport Proteins ; *Walking
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    Development. May the force be with you (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martin, Paul -- Parkhurst, Susan M -- New York, N.Y. -- Science. 2003 Apr 4;300(5616):63-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy, University College London, Gower Street, London WC1E 6BT, UK. paul.martin@ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12677046" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Adhesion ; Cell Polarity ; Drosophila/*embryology/genetics ; Embryo, Nonmammalian/*physiology ; Embryonic Development ; Epithelial Cells/physiology ; Epithelium/physiology ; Genes, Insect ; Lasers ; Mathematics ; Microsurgery ; *Models, Biological ; *Morphogenesis ; Mutation ; Signal Transduction
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    Requirement of mammalian Timeless for circadian rhythmicity (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-18
    Description: Despite a central circadian role in Drosophila for the transcriptional regulator Timeless (dTim), the relevance of mammalian Timeless (mTim) remains equivocal. Conditional knockdown of mTim protein expression in the rat suprachiasmatic nucleus (SCN) disrupted SCN neuronal activity rhythms, and altered levels of known core clock elements. Full-length mTim protein (mTIM-fl) exhibited a 24-hour oscillation, where as a truncated isoform (mTIM-s) was constitutively expressed. mTIM-fl associated with the mammalian clock Period proteins (mPERs) in oscillating SCN cells. These data suggest that mTim is required for rhythmicity and is a functional homolog of dTim on the negative-feedback arm of the mammalian molecular clockwork.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnes, Jessica W -- Tischkau, Shelley A -- Barnes, Jeffrey A -- Mitchell, Jennifer W -- Burgoon, Penny W -- Hickok, Jason R -- Gillette, Martha U -- GM07143/GM/NIGMS NIH HHS/ -- HL67007/HL/NHLBI NIH HHS/ -- NS10170/NS/NINDS NIH HHS/ -- NS11134/NS/NINDS NIH HHS/ -- NS11158/NS/NINDS NIH HHS/ -- NS22155/NS/NINDS NIH HHS/ -- NS35859/NS/NINDS NIH HHS/ -- R01 HL067007/HL/NHLBI NIH HHS/ -- R01 NS022155/NS/NINDS NIH HHS/ -- R01 NS035859/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 17;302(5644):439-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Structural Biology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14564007" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks ; Cell Cycle Proteins ; Cell Line ; *Circadian Rhythm ; Cryptochromes ; *Drosophila Proteins ; Electrophysiology ; *Eye Proteins ; Flavoproteins/metabolism ; Humans ; In Vitro Techniques ; Intracellular Signaling Peptides and Proteins ; Neurons/physiology ; Nuclear Proteins/metabolism ; Oligonucleotides, Antisense/pharmacology ; Period Circadian Proteins ; *Photoreceptor Cells, Invertebrate ; RNA Interference ; RNA, Messenger/genetics/metabolism ; Rats ; Rats, Inbred Strains ; Receptors, G-Protein-Coupled ; Reverse Transcriptase Polymerase Chain Reaction ; Suprachiasmatic Nucleus/*physiology ; Transcription Factors/chemistry/genetics/*metabolism ; Transfection
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Hirschsprung disease is linked to defects in neural crest stem cell function (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-16
    Description: Genes associated with Hirschsprung disease, a failure to form enteric ganglia in the hindgut, were highly up-regulated in gut neural crest stem cells relative to whole-fetus RNA. One of these genes, the glial cell line-derived neurotrophic factor (GDNF) receptor Ret, was necessary for neural crest stem cell migration in the gut. GDNF promoted the migration of neural crest stem cells in culture but did not affect their survival or proliferation. Gene expression profiling, combined with reverse genetics and analyses of stem cell function, suggests that Hirschsprung disease is caused by defects in neural crest stem cell function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2614078/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2614078/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iwashita, Toshihide -- Kruger, Genevieve M -- Pardal, Ricardo -- Kiel, Mark J -- Morrison, Sean J -- CA46592/CA/NCI NIH HHS/ -- DK58771/DK/NIDDK NIH HHS/ -- NIH5P60-DK20572/DK/NIDDK NIH HHS/ -- P30 AR48310/AR/NIAMS NIH HHS/ -- P60-AR20557/AR/NIAMS NIH HHS/ -- R01 NS040750/NS/NINDS NIH HHS/ -- R01 NS040750-01/NS/NINDS NIH HHS/ -- R01 NS40750-01/NS/NINDS NIH HHS/ -- R21 HD40760-02/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2003 Aug 15;301(5635):972-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109-0934, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12920301" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cell Movement ; Cell Separation ; Cell Survival ; Cells, Cultured ; Digestive System/cytology/*embryology/innervation/metabolism ; Fetus/metabolism ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Glial Cell Line-Derived Neurotrophic Factor ; Glial Cell Line-Derived Neurotrophic Factor Receptors ; Hirschsprung Disease/*etiology/genetics ; Mice ; Multipotent Stem Cells/*physiology ; Nerve Growth Factors/genetics/metabolism/pharmacology ; Neural Crest/*cytology/physiology ; Oligonucleotide Array Sequence Analysis ; Proto-Oncogene Proteins/*genetics/metabolism ; Proto-Oncogene Proteins c-ret ; Rats ; Rats, Sprague-Dawley ; Receptor Protein-Tyrosine Kinases/*genetics/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Up-Regulation
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Negative feedback regulation ensures the one receptor-one olfactory neuron rule in mouse (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-01
    Description: In the mouse olfactory system, each olfactory sensory neuron (OSN) expresses only one odorant receptor (OR) gene in a monoallelic and mutually exclusive manner. Such expression forms the genetic basis for OR-instructed axonal projection of OSNs to the olfactory bulb of the brain during development. Here, we identify an upstream cis-acting DNA region that activates the OR gene cluster in mouse and allows the expression of only one OR gene within the cluster. Deletion of the coding region of the expressed OR gene or a naturally occurring frame-shift mutation allows a second OR gene to be expressed. We propose that stochastic activation of only one OR gene within the cluster and negative feedback regulation by that OR gene product are necessary to ensure the one receptor-one neuron rule.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Serizawa, Shou -- Miyamichi, Kazunari -- Nakatani, Hiroko -- Suzuki, Misao -- Saito, Michiko -- Yoshihara, Yoshihiro -- Sakano, Hitoshi -- New York, N.Y. -- Science. 2003 Dec 19;302(5653):2088-94. Epub 2003 Oct 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biophysics and Biochemistry, Graduate School of Science, University of Tokyo, Tokyo 113-0032, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14593185" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Axons/physiology ; Chromosomes, Artificial, Yeast ; Conserved Sequence ; *Feedback, Physiological ; Frameshift Mutation ; *Gene Expression Regulation ; Gene Silencing ; In Situ Hybridization ; *Locus Control Region ; Mice ; Mice, Transgenic ; Multigene Family ; Olfactory Bulb/cytology ; Olfactory Receptor Neurons/*metabolism ; Promoter Regions, Genetic ; Pseudogenes ; Receptors, Odorant/*genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transgenes
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Cell biology. Smurfing at the leading edge (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jaffe, Aron B -- Hall, Alan -- New York, N.Y. -- Science. 2003 Dec 5;302(5651):1690-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Laboratory for Molecular Cell Biology and Cell Biology Unit, University College London, London WC1E 6BT, UK. a.jaffe@ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14657480" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/*metabolism ; *Cell Movement ; *Cell Polarity ; GTPase-Activating Proteins/metabolism ; Guanine Nucleotide Exchange Factors/metabolism ; Guanosine Triphosphate/metabolism ; Humans ; Mice ; Protein Kinase C/metabolism ; Pseudopodia/metabolism ; Signal Transduction ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/*metabolism ; cdc42 GTP-Binding Protein/metabolism ; rac GTP-Binding Proteins/metabolism ; rho GTP-Binding Proteins/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Translation of polarity cues into asymmetric spindle positioning in Caenorhabditis elegans embryos (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-17
    Description: Asymmetric divisions are crucial for generating cell diversity; they rely on coupling between polarity cues and spindle positioning, but how this coupling is achieved is poorly understood. In one-cell stage Caenorhabditis elegans embryos, polarity cues set by the PAR proteins mediate asymmetric spindle positioning by governing an imbalance of net pulling forces acting on spindle poles. We found that the GoLoco-containing proteins GPR-1 and GPR-2, as well as the Galpha subunits GOA-1 and GPA-16, were essential for generation of proper pulling forces. GPR-1/2 interacted with guanosine diphosphate-bound GOA-1 and were enriched on the posterior cortex in a par-3- and par-2-dependent manner. Thus, the extent of net pulling forces may depend on cortical Galpha activity, which is regulated by anterior-posterior polarity cues through GPR-1/2.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Colombo, Kelly -- Grill, Stephan W -- Kimple, Randall J -- Willard, Francis S -- Siderovski, David P -- Gonczy, Pierre -- GM62338/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Jun 20;300(5627):1957-61. Epub 2003 May 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Swiss Institute for Experimental Cancer Research (ISREC), 1066 Epalinges/Lausanne, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12750478" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Caenorhabditis elegans/cytology/*embryology/genetics/physiology ; Caenorhabditis elegans Proteins/genetics/*metabolism ; *Cell Division ; *Cell Polarity ; Cues ; GTP-Binding Proteins/genetics/metabolism ; Phenotype ; Protein Subunits/genetics/metabolism ; RNA Interference ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Spindle Apparatus/*physiology/ultrastructure ; Two-Hybrid System Techniques
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    Biotechnology. Stem cells lose market luster (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2003 Mar 21;299(5614):1830-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12649456" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Australia ; Biotechnology/*economics/manpower ; Cell Line ; Clinical Trials as Topic ; Cloning, Organism/*economics ; Commerce ; Embryo Research/*economics ; Embryo, Mammalian/*cytology ; Financing, Government ; Humans ; *Investments ; Research Personnel ; Research Support as Topic ; *Stem Cells ; United States
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  • 54
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    Cleavage of Arabidopsis PBS1 by a bacterial type III effector (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-30
    Description: Plant disease-resistance (R) proteins are thought to function as receptors for ligands produced directly or indirectly by pathogen avirulence (Avr) proteins. The biochemical functions of most Avr proteins are unknown, and the mechanisms by which they activate R proteins have not been determined. In Arabidopsis, resistance to Pseudomonas syringae strains expressing AvrPphB requires RPS5, a member of the class of R proteins that have a predicted nucleotide-binding site and leucine-rich repeats, and PBS1, a protein kinase. AvrPphB was found to proteolytically cleave PBS1, and this cleavage was required for RPS5-mediated resistance, which indicates that AvrPphB is detected indirectly via its enzymatic activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shao, Feng -- Golstein, Catherine -- Ade, Jules -- Stoutemyer, Mark -- Dixon, Jack E -- Innes, Roger W -- DK18849/DK/NIDDK NIH HHS/ -- GM46451/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Aug 29;301(5637):1230-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, Medical School and Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12947197" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Arabidopsis/genetics/*metabolism/microbiology ; Arabidopsis Proteins/chemistry/genetics/*metabolism ; Bacterial Proteins/chemistry/genetics/*metabolism ; Carrier Proteins/genetics/metabolism ; Cell Line ; Cysteine Endopeptidases/chemistry/genetics/*metabolism ; Genes, Bacterial ; Genes, Plant ; Genetic Complementation Test ; Humans ; Models, Biological ; Molecular Sequence Data ; Mutation ; Phosphorylation ; Plant Diseases/*microbiology ; Plant Extracts/metabolism ; Plant Proteins/genetics/metabolism ; Plants, Genetically Modified ; Precipitin Tests ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Pseudomonas/*metabolism ; Recombinant Proteins/metabolism ; Tobacco/genetics/metabolism ; Transformation, Genetic
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    Pyogenic bacterial infections in humans with IRAK-4 deficiency (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-15
    Description: Members of the Toll-like receptor (TLR) and interleukin-1 receptor (IL-1R) superfamily share an intracytoplasmic Toll-IL-1 receptor (TIR) domain, which mediates recruitment of the interleukin-1 receptor-associated kinase (IRAK) complex via TIR-containing adapter molecules. We describe three unrelated children with inherited IRAK-4 deficiency. Their blood and fibroblast cells did not activate nuclear factor kappaB and mitogen-activated protein kinase (MAPK) and failed to induce downstream cytokines in response to any of the known ligands of TIR-bearing receptors. The otherwise healthy children developed infections caused by pyogenic bacteria. These findings suggest that, in humans, the TIR-IRAK signaling pathway is crucial for protective immunity against specific bacteria but is redundant against most other microorganisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Picard, Capucine -- Puel, Anne -- Bonnet, Marion -- Ku, Cheng-Lung -- Bustamante, Jacinta -- Yang, Kun -- Soudais, Claire -- Dupuis, Stephanie -- Feinberg, Jacqueline -- Fieschi, Claire -- Elbim, Carole -- Hitchcock, Remi -- Lammas, David -- Davies, Graham -- Al-Ghonaium, Abdulaziz -- Al-Rayes, Hassan -- Al-Jumaah, Sulaiman -- Al-Hajjar, Sami -- Al-Mohsen, Ibrahim Zaid -- Frayha, Husn H -- Rucker, Rajivi -- Hawn, Thomas R -- Aderem, Alan -- Tufenkeji, Haysam -- Haraguchi, Soichi -- Day, Noorbibi K -- Good, Robert A -- Gougerot-Pocidalo, Marie-Anne -- Ozinsky, Adrian -- Casanova, Jean-Laurent -- New York, N.Y. -- Science. 2003 Mar 28;299(5615):2076-9. Epub 2003 Mar 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Genetique Humaine des Maladies Infectieuses, Universite Rene Descartes-INSERM U550, Faculte Necker, 156 rue de Vaugirard, 75015 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12637671" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Child ; Codon, Terminator ; Cytokines/secretion ; *Drosophila Proteins ; Female ; Fibroblasts/immunology ; Humans ; Interleukin-1 Receptor-Associated Kinases ; Interleukins/immunology/secretion ; Lipopolysaccharides/immunology ; Male ; Membrane Glycoproteins/chemistry/immunology/metabolism ; Monocytes/immunology ; Mutation ; Neutrophils/immunology ; Pedigree ; Phosphotransferases (Alcohol Group Acceptor)/*deficiency/*genetics/metabolism ; Pneumococcal Infections/*immunology/metabolism ; Protein Structure, Tertiary ; Receptors, Cell Surface/chemistry/immunology/metabolism ; Receptors, Interleukin/immunology ; Receptors, Interleukin-1/chemistry ; Signal Transduction ; Staphylococcal Infections/*immunology/metabolism ; Toll-Like Receptors ; Tumor Necrosis Factor-alpha/immunology
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    Hypermutation of HIV-1 DNA in the absence of the Vif protein (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lecossier, Denise -- Bouchonnet, Francine -- Clavel, Francois -- Hance, Allan J -- New York, N.Y. -- Science. 2003 May 16;300(5622):1112.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM U552, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12750511" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Line ; Cytidine Deaminase ; DNA Mutational Analysis ; DNA, Viral/biosynthesis/*genetics ; Gene Products, vif/*physiology ; HIV-1/genetics/*physiology ; HeLa Cells ; Humans ; Molecular Sequence Data ; *Mutation ; Nucleoside Deaminases ; Proteins/physiology ; Repressor Proteins ; Virion/genetics/physiology ; Virus Replication ; vif Gene Products, Human Immunodeficiency Virus
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    Nod1 detects a unique muropeptide from gram-negative bacterial peptidoglycan (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-06-07
    Description: Although the role of Toll-like receptors in extracellular bacterial sensing has been investigated intensively, intracellular detection of bacteria through Nod molecules remains largely uncharacterized. Here, we show that human Nod1 specifically detects a unique diaminopimelate-containing N-acetylglucosamine-N-acetylmuramic acid (GlcNAc-MurNAc) tripeptide motif found in Gram-negative bacterial peptidoglycan, resulting in activation of the transcription factor NF-kappaB pathway. Moreover, we show that in epithelial cells (which represent the first line of defense against invasive pathogens), Nod1is indispensable for intracellular Gram-negative bacterial sensing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Girardin, Stephen E -- Boneca, Ivo G -- Carneiro, Leticia A M -- Antignac, Aude -- Jehanno, Muguette -- Viala, Jerome -- Tedin, Karsten -- Taha, Muhamed-Kheir -- Labigne, Agnes -- Zahringer, Ulrich -- Coyle, Anthony J -- DiStefano, Peter S -- Bertin, John -- Sansonetti, Philippe J -- Philpott, Dana J -- New York, N.Y. -- Science. 2003 Jun 6;300(5625):1584-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite de Pathogenie Microbienne Moleculaire, INSERM U389, Institut Pasteur, 28, Rue du Dr. Roux, 75724Paris Cedex 15, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12791997" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Amino Acid Motifs ; Animals ; Antigens, Differentiation/metabolism ; Carrier Proteins/chemistry/metabolism/*physiology ; Cell Line ; Cytoplasm/microbiology ; Epithelial Cells/metabolism/microbiology ; Gram-Negative Bacteria/*chemistry/immunology ; Gram-Positive Bacteria/chemistry/immunology ; Humans ; Immunity, Innate ; Interleukin-8/metabolism ; *Intracellular Signaling Peptides and Proteins ; Lipopolysaccharides/pharmacology ; Mice ; Myeloid Differentiation Factor 88 ; NF-kappa B/chemistry/metabolism ; Nod1 Signaling Adaptor Protein ; Nod2 Signaling Adaptor Protein ; Oligopeptides/*analysis/chemistry ; Peptidoglycan/*chemistry/pharmacology ; Protein Structure, Tertiary ; Receptors, Immunologic/metabolism ; Signal Transduction ; Trisaccharides/*analysis/chemistry
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    Medicine. Tracing the steps of metastasis, cancer's menacing ballet (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin, Jennifer -- New York, N.Y. -- Science. 2003 Feb 14;299(5609):1002-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12586919" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Neoplasms/secondary ; Breast Neoplasms/pathology ; Cell Adhesion ; Cell Movement ; Chemokines/metabolism ; Embryo, Nonmammalian/cytology ; Gene Expression Profiling ; Genes, Tumor Suppressor ; Humans ; *Neoplasm Metastasis/genetics/pathology/physiopathology ; Neoplasm Seeding ; Neoplastic Cells, Circulating ; Neoplastic Stem Cells/physiology ; Oligonucleotide Array Sequence Analysis ; Receptors, Chemokine/metabolism ; Signal Transduction ; Stem Cells/physiology ; Transforming Growth Factor beta/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Selective trafficking of non-cell-autonomous proteins mediated by NtNCAPP1 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-18
    Description: In plants, cell-to-cell communication is mediated by plasmodesmata and involves the trafficking of non-cell-autonomous proteins (NCAPs). A component in this pathway, Nicotiana tabacum NON-CELL-AUTONOMOUS PATHWAY PROTEIN1 (NtNCAPP1), was affinity purified and cloned. Protein overlay assays and in vivo studies showed that NtNCAPP1 is located on the endoplasmic reticulum at the cell periphery and displays specificity in its interaction with NCAPs. Deletion of the NtNCAPP1 amino-terminal transmembrane domain produced a dominant-negative mutant that blocked the trafficking of specific NCAPs. Transgenic tobacco plants expressing this mutant form of NtNCAPP1 and plants in which the NtNCAPP1 gene was silenced were compromised in their ability to regulate leaf and floral development. These results support a model in which NCAP delivery to plasmodesmata is both selective and regulated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Jung-Youn -- Yoo, Byung-Chun -- Rojas, Maria R -- Gomez-Ospina, Natalia -- Staehelin, L Andrew -- Lucas, William J -- GM18639/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Jan 17;299(5605):392-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Plant Biology, Division of Biological Sciences, University of California, 1 Shields Avenue, Davis, CA 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12532017" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cell Communication ; Cell Line ; Cloning, Molecular ; Cytoplasm/metabolism ; Endoplasmic Reticulum/metabolism ; Flowers/growth & development ; Gene Silencing ; Green Fluorescent Proteins ; Immunohistochemistry ; Luminescent Proteins/metabolism ; Molecular Sequence Data ; Mutation ; Phenotype ; Plant Leaves/growth & development ; Plant Proteins/chemistry/genetics/*isolation & purification/*metabolism ; Plants, Genetically Modified ; Plasmodesmata/*metabolism ; Protein Transport ; Recombinant Fusion Proteins/metabolism ; Tobacco/genetics/growth & development/*metabolism ; Tobacco Mosaic Virus ; Viral Proteins/metabolism
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    Pregnancy-stimulated neurogenesis in the adult female forebrain mediated by prolactin (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-04
    Description: Neurogenesis occurs in the olfactory system of the adult brain throughout life, in both invertebrates and vertebrates, but its physiological regulation is not understood. We show that the production of neuronal progenitors is stimulated in the forebrain subventricular zone of female mice during pregnancy and that this effect is mediated by the hormone prolactin. The progenitors then migrate to produce new olfactory interneurons, a process likely to be important for maternal behavior, because olfactory discrimination is critical for recognition and rearing of offspring. Neurogenesis occurs even in females that mate with sterile males. These findings imply that forebrain olfactory neurogenesis may contribute to adaptive behaviors in mating and pregnancy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shingo, Tetsuro -- Gregg, Christopher -- Enwere, Emeka -- Fujikawa, Hirokazu -- Hassam, Rozina -- Geary, Colleen -- Cross, James C -- Weiss, Samuel -- New York, N.Y. -- Science. 2003 Jan 3;299(5603):117-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genes & Development Research Group, Department of Cell Biology and Anatomy, University of Calgary Faculty of Medicine, Calgary, Alberta, Canada T2N 4N1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12511652" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cell Movement ; Cells, Cultured ; Choroid Plexus/metabolism ; Dentate Gyrus/cytology ; Epidermal Growth Factor/pharmacology ; Estradiol/administration & dosage/pharmacology ; Female ; Interneurons/cytology/*physiology ; Male ; Mice ; Neurons/cytology/*physiology ; Olfactory Bulb/*cytology ; Pregnancy ; Progesterone/administration & dosage/pharmacology ; Prolactin/administration & dosage/blood/pharmacology/*physiology ; Prosencephalon/*cytology/*physiology ; Pseudopregnancy ; Receptors, Prolactin/genetics/metabolism ; Signal Transduction ; Stem Cells/*cytology
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    Mutation of MEF2A in an inherited disorder with features of coronary artery disease (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-03
    Description: The early genetic pathway(s) triggering the pathogenesis of coronary artery disease (CAD) and myocardial infarction (MI) remain largely unknown. Here, we describe an autosomal dominant form of CAD/MI (adCAD1) that is caused by the deletion of seven amino acids in transcription factor MEF2A. The deletion disrupts nuclear localization of MEF2A, reduces MEF2A-mediated transcription activation, and abolishes synergistic activation by MEF2A and by the transcription factor GATA-1 through a dominant-negative mechanism. The MEF2A protein demonstrates strong expression in the endothelium of coronary arteries. These results identify a pathogenic gene for a familial vascular disease with features of CAD and implicate the MEF2A signaling pathway in the pathogenesis of CAD/MI.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1618876/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1618876/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Lejin -- Fan, Chun -- Topol, Sarah E -- Topol, Eric J -- Wang, Qing -- R01 HL065630/HL/NHLBI NIH HHS/ -- R01 HL066251/HL/NHLBI NIH HHS/ -- R01 HL65630/HL/NHLBI NIH HHS/ -- R01 HL66251/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2003 Nov 28;302(5650):1578-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cardiovascular Genetics, Department of Cardiovascular Medicine, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH 44195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14645853" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Amino Acid Sequence ; Animals ; Arteries/metabolism ; Base Sequence ; Cell Nucleus/metabolism ; Chromosomes, Human, Pair 15/genetics ; Coronary Artery Disease/*genetics/metabolism ; Coronary Vessels/metabolism ; DNA-Binding Proteins/chemistry/*genetics/metabolism ; Dimerization ; Endothelium, Vascular/metabolism ; Erythroid-Specific DNA-Binding Factors ; Female ; Fluorescent Antibody Technique ; GATA1 Transcription Factor ; Gene Expression ; Genes, Dominant ; Genetic Linkage ; Genetic Markers ; Genetic Predisposition to Disease ; Humans ; MADS Domain Proteins ; MEF2 Transcription Factors ; Male ; Middle Aged ; Molecular Sequence Data ; Muscle, Smooth/cytology/metabolism ; Myocardial Infarction/*genetics/metabolism ; Myogenic Regulatory Factors ; Pedigree ; Protein Binding ; Protein Conformation ; Protein Structure, Tertiary ; Protein Transport ; Rats ; Risk Factors ; *Sequence Deletion ; Signal Transduction ; Transcription Factors/chemistry/*genetics/metabolism ; Transcriptional Activation
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    Chimeric nucleases stimulate gene targeting in human cells (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Porteus, Matthew H -- Baltimore, David -- R01-GM39458/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 May 2;300(5620):763.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, California Institute of Technology, Pasadena CA 91125, USA. matthew.porteus@UTSouthwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730593" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; DNA/metabolism ; Deoxyribonucleases, Type II Site-Specific/chemistry/genetics/*metabolism ; Dimerization ; Gene Targeting/*methods ; Green Fluorescent Proteins ; Humans ; Luminescent Proteins/genetics ; Mutation ; Nuclear Localization Signals ; Recombinant Fusion Proteins/chemistry/*metabolism ; Recombination, Genetic ; Saccharomyces cerevisiae Proteins ; Transfection ; *Zinc Fingers
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    Cannibalism by sporulating bacteria (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-06-21
    Description: Spore formation by the bacterium Bacillus subtilis is an elaborate developmental process that is triggered by nutrient limitation. Here we report that cells that have entered the pathway to sporulate produce and export a killing factor and a signaling protein that act cooperatively to block sister cells from sporulating and to cause them to lyse. The sporulating cells feed on the nutrients thereby released, which allows them to keep growing rather than to complete morphogenesis. We propose that sporulation is a stress-response pathway of last resort and that B. subtilis delays a commitment to spore formation by cannibalizing its siblings.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gonzalez-Pastor, Jose E -- Hobbs, Errett C -- Losick, Richard -- GM18568/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Jul 25;301(5632):510-3. Epub 2003 Jun 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, The Biological Laboratories, Harvard University, 16 Divinity Avenue, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12817086" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Bacillus subtilis/genetics/metabolism/*physiology ; Bacterial Proteins/genetics/*metabolism ; Bacteriolysis ; Gene Expression Profiling ; *Gene Expression Regulation, Bacterial ; Genes, Bacterial ; Mutation ; Oligonucleotide Array Sequence Analysis ; *Operon ; Sigma Factor/genetics/metabolism ; Signal Transduction ; Spores, Bacterial/*physiology ; Transcription Factors/genetics/metabolism ; Transcription, Genetic
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    Predominant autoantibody production by early human B cell precursors (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-16
    Description: During B lymphocyte development, antibodies are assembled by random gene segment reassortment to produce a vast number of specificities. A potential disadvantage of this process is that some of the antibodies produced are self-reactive. We determined the prevalence of self-reactive antibody formation and its regulation in human B cells. A majority (55 to 75%) of all antibodies expressed by early immature B cells displayed self-reactivity, including polyreactive and anti-nuclear specificities. Most of these autoantibodies were removed from the population at two discrete checkpoints during B cell development. Inefficient checkpoint regulation would lead to substantial increases in circulating autoantibodies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wardemann, Hedda -- Yurasov, Sergey -- Schaefer, Anne -- Young, James W -- Meffre, Eric -- Nussenzweig, Michel C -- New York, N.Y. -- Science. 2003 Sep 5;301(5638):1374-7. Epub 2003 Aug 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12920303" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Antinuclear/biosynthesis/immunology ; Antibody Diversity ; Antibody Specificity ; Autoantibodies/*biosynthesis/immunology ; B-Lymphocytes/cytology/*immunology/physiology ; Cell Differentiation ; Cell Line ; Complementarity Determining Regions/chemistry/immunology ; Cytosol/immunology ; Genes, Immunoglobulin ; Humans ; Immunoglobulin Heavy Chains/chemistry/immunology ; Recombination, Genetic ; Selection, Genetic ; Tumor Cells, Cultured
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    Signal transduction. Capturing polo kinase (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sillje, Herman H W -- Nigg, Erich A -- New York, N.Y. -- Science. 2003 Feb 21;299(5610):1190-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Max Planck Institute of Biochemistry, Am Klopferspitz 18a, D-82152 Martinsried, Germany. sillje@biochem.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12595680" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Binding Sites ; CDC2 Protein Kinase/metabolism ; Catalytic Domain ; Cell Cycle Proteins ; Centrosome/metabolism ; Humans ; Mitosis ; Peptide Library ; Phosphoproteins/*metabolism ; Phosphorylation ; Phosphotransferases/metabolism ; Protein Conformation ; Protein Kinases/*chemistry/*metabolism ; *Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases ; Proteomics ; Proto-Oncogene Proteins ; Signal Transduction ; cdc25 Phosphatases/*metabolism
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    The birth of an alternatively spliced exon: 3' splice-site selection in Alu exons (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-24
    Description: Alu repetitive elements can be inserted into mature messenger RNAs via a splicing-mediated process termed exonization. To understand the molecular basis and the regulation of the process of turning intronic Alus into new exons, we compiled and analyzed a data set of human exonized Alus. We revealed a mechanism that governs 3' splice-site selection in these exons during alternative splicing. On the basis of these findings, we identified mutations that activated the exonization of a silent intronic Alu.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lev-Maor, Galit -- Sorek, Rotem -- Shomron, Noam -- Ast, Gil -- New York, N.Y. -- Science. 2003 May 23;300(5623):1288-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics and Molecular Medicine, Sackler Faculty of Medicine, Tel Aviv University, Ramat Aviv 69978, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12764196" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Deaminase/genetics ; *Alternative Splicing ; Alu Elements/*genetics ; Cell Line ; Cloning, Molecular ; DNA, Antisense ; Dinucleoside Phosphates/genetics ; *Exons ; Genome, Human ; Glucosyltransferases/genetics ; Humans ; Introns ; Mutagenesis, Site-Directed ; Point Mutation ; Polymerase Chain Reaction ; RNA-Binding Proteins ; Ribonucleoproteins, Small Nuclear/genetics/physiology ; Spliceosomes/metabolism ; Transfection ; Tumor Cells, Cultured
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    Inhibition of neuroepithelial patched-induced apoptosis by sonic hedgehog (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-09
    Description: During early development in vertebrates, Sonic hedgehog (Shh) is produced by the notochord and the floor plate. A ventrodorsal gradient of Shh directs ventrodorsal patterning of the neural tube. However, Shh is also required for the survival of neuroepithelial cells. We show that Patched (Ptc) induces apoptotic cell death unless its ligand Shh is present to block the signal. Moreover, the blockade of Ptc-induced cell death partly rescues the chick spinal cord defect provoked by Shh deprivation. Thus, the proapoptotic activity of unbound Ptc and the positive effect of Shh-bound Ptc on cell differentiation probably cooperate to achieve the appropriate spinal cord development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thibert, Chantal -- Teillet, Marie-Aimee -- Lapointe, Francoise -- Mazelin, Laetitia -- Le Douarin, Nicole M -- Mehlen, Patrick -- New York, N.Y. -- Science. 2003 Aug 8;301(5634):843-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Apoptosis/Differentiation Laboratory, "La Ligue," Molecular and Cellular Genetic Center, CNRS Unite Mixte Recherche (UMR) 5534, University of Lyon, 69622 Villeurbanne, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12907805" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Caspase 3 ; Caspases/metabolism ; Cell Differentiation ; Cell Line ; Central Nervous System/cytology/*embryology/metabolism ; Chick Embryo ; Electroporation ; Epithelial Cells/cytology/metabolism ; Hedgehog Proteins ; Humans ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Mutation ; Protein Binding ; Protein Structure, Tertiary ; Rats ; Receptors, Cell Surface ; Signal Transduction ; Spinal Cord/cytology/embryology ; Trans-Activators/genetics/*metabolism ; Transfection
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    Development. What makes an embryo stick? (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fazleabas, Asgerally T -- Kim, J Julie -- New York, N.Y. -- Science. 2003 Jan 17;299(5605):355-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Obstetrics and Gynecology, University of Illinois, Chicago, IL 60612, USA. asgi@uic.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12532005" target="_blank"〉PubMed〈/a〉
    Keywords: Blastocyst/physiology ; Cell Adhesion ; Cell Adhesion Molecules/metabolism ; Cells, Cultured ; Coculture Techniques ; *Embryo Implantation ; Endometrium/cytology/*physiology ; Epithelial Cells/physiology ; Female ; Humans ; L-Selectin/*metabolism ; Ligands ; Oligosaccharides/metabolism ; Pregnancy ; Signal Transduction ; Trophoblasts/*metabolism ; Up-Regulation
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    Melanopsin is required for non-image-forming photic responses in blind mice (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-06-28
    Description: Although mice lacking rod and cone photoreceptors are blind, they retain many eye-mediated responses to light, possibly through photosensitive retinal ganglion cells. These cells express melanopsin, a photopigment that confers this photosensitivity. Mice lacking melanopsin still retain nonvisual photoreception, suggesting that rods and cones could operate in this capacity. We observed that mice with both outer-retinal degeneration and a deficiency in melanopsin exhibited complete loss of photoentrainment of the circadian oscillator, pupillary light responses, photic suppression of arylalkylamine-N-acetyltransferase transcript, and acute suppression of locomotor activity by light. This indicates the importance of both nonvisual and classical visual photoreceptor systems for nonvisual photic responses in mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Panda, Satchidananda -- Provencio, Ignacio -- Tu, Daniel C -- Pires, Susana S -- Rollag, Mark D -- Castrucci, Ana Maria -- Pletcher, Mathew T -- Sato, Trey K -- Wiltshire, Tim -- Andahazy, Mary -- Kay, Steve A -- Van Gelder, Russell N -- Hogenesch, John B -- K08-EY00403/EY/NEI NIH HHS/ -- MH 62405/MH/NIMH NIH HHS/ -- MH51573/MH/NIMH NIH HHS/ -- R01-EY14988/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2003 Jul 25;301(5632):525-7. Epub 2003 Jun 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genomics Institute of the Novartis Research Foundation, 10675 John J. Hopkins Drive, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12829787" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arylamine N-Acetyltransferase/genetics/metabolism ; Blindness/genetics/*physiopathology ; Circadian Rhythm ; *Light ; *Light Signal Transduction ; Mice ; Mice, Inbred C3H ; Motor Activity ; Photoreceptor Cells, Vertebrate/*physiology ; Reflex, Pupillary ; Retinal Degeneration/genetics/physiopathology ; Retinal Ganglion Cells/physiology ; Rod Opsins/deficiency/genetics/*physiology ; Signal Transduction ; Suprachiasmatic Nucleus/physiology
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    Cell biology. How cells step out (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, Jean -- New York, N.Y. -- Science. 2003 Oct 10;302(5643):214-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14551414" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/*physiology/ultrastructure ; Actin Depolymerizing Factors ; Actin-Related Protein 2 ; Actin-Related Protein 3 ; Actins/metabolism/*physiology ; Adenosine Triphosphate/metabolism ; Animals ; *Cell Movement ; Cell Size ; Cytoskeletal Proteins/metabolism ; Humans ; Listeria monocytogenes/*physiology/ultrastructure ; Microfilament Proteins/metabolism ; Movement ; Nerve Tissue Proteins/metabolism ; Signal Transduction ; Wiskott-Aldrich Syndrome Protein, Neuronal ; rho GTP-Binding Proteins/metabolism
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    Screening for nitric oxide-dependent protein-protein interactions (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-02
    Description: Because nitric oxide (NO) may be a ubiquitous regulator of cellular signaling, we have modified the yeast two-hybrid system to explore the possibility of NO-dependent protein-protein interactions. We screened for binding partners of procaspase-3, a protein implicated in apoptotic signaling pathways, and identified multiple NO-dependent interactions.Two such interactions, with acid sphingomyelinase and NO synthase, were shown to occur in mammalian cells dependent on endogenous NO. Nitrosylation may thus provide a broad-based mechanism for regulating interactions between proteins. If so, systematic proteomic analyses in which redox state and NO bioavailability are carefully controlled will reveal a large array of novel interactions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsumoto, Akio -- Comatas, Karrie E -- Liu, Limin -- Stamler, Jonathan S -- New York, N.Y. -- Science. 2003 Aug 1;301(5633):657-61.〈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/12893946" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Caspase 3 ; Caspases/*metabolism ; Cell Line ; Enzyme Inhibitors/pharmacology ; Enzyme Precursors/*metabolism ; Escherichia coli/genetics/growth & development ; Gene Library ; Humans ; Hydrogen Peroxide/metabolism ; Lysosomes/enzymology ; Mitochondria/enzymology ; Nitric Oxide/*metabolism/pharmacology ; Nitric Oxide Donors/pharmacology ; Nitric Oxide Synthase/antagonists & inhibitors/*metabolism ; Nitric Oxide Synthase Type I ; Nitric Oxide Synthase Type II ; Nitric Oxide Synthase Type III ; Oxidation-Reduction ; Precipitin Tests ; *Protein Binding ; Signal Transduction ; Sphingomyelin Phosphodiesterase/*metabolism ; Transfection ; Transformation, Bacterial ; Triazenes/pharmacology ; Two-Hybrid System Techniques ; beta-Galactosidase/metabolism ; omega-N-Methylarginine/pharmacology
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    European Union. E.U. stem cell debate ends in a draw (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1872-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671253" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; *Embryo Research/economics/legislation & jurisprudence ; Embryo, Mammalian/*cytology ; *European Union ; *Guidelines as Topic ; Humans ; Research Support as Topic ; *Stem Cells
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    Stem cells. Visiting German profs could face jail (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2003 Aug 1;301(5633):577.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12893913" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Embryo Research/*legislation & jurisprudence ; Embryo, Mammalian/*cytology ; *Faculty ; Germany ; Government ; Humans ; Jurisprudence ; Private Sector ; Public Sector ; Research Personnel/*legislation & jurisprudence ; *Stem Cells
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    Genome-wide survey of human alternative pre-mRNA splicing with exon junction microarrays (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-20
    Description: Alternative pre-messenger RNA (pre-mRNA) splicing plays important roles in development, physiology, and disease, and more than half of human genes are alternatively spliced. To understand the biological roles and regulation of alternative splicing across different tissues and stages of development, systematic methods are needed. Here, we demonstrate the use of microarrays to monitor splicing at every exon-exon junction in more than 10,000 multi-exon human genes in 52 tissues and cell lines. These genome-wide data provide experimental evidence and tissue distributions for thousands of known and novel alternative splicing events. Adding to previous studies, the results indicate that at least 74% of human multi-exon genes are alternatively spliced.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johnson, Jason M -- Castle, John -- Garrett-Engele, Philip -- Kan, Zhengyan -- Loerch, Patrick M -- Armour, Christopher D -- Santos, Ralph -- Schadt, Eric E -- Stoughton, Roland -- Shoemaker, Daniel D -- New York, N.Y. -- Science. 2003 Dec 19;302(5653):2141-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rosetta Inpharmatics LLC, Merck & Co., Inc., 12040 115th Avenue N.E., Kirkland, WA 98034, USA. jason_johnson@merck.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14684825" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Amyloid beta-Protein Precursor/analysis/genetics ; Cell Line ; DNA, Complementary ; *Exons ; Expressed Sequence Tags ; *Genome, Human ; Humans ; Hydroxymethylglutaryl CoA Reductases/analysis/genetics ; Molecular Sequence Data ; *Oligonucleotide Array Sequence Analysis ; *Phosphoric Monoester Hydrolases ; Protein Isoforms/analysis ; Proteins/analysis/genetics ; RNA Precursors/*genetics ; ROC Curve ; Reverse Transcriptase Polymerase Chain Reaction ; Tissue Distribution
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    Neuroscience. Stout guards of the central nervous system (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-04
    Description: Endocannabinoids have paradoxical effects on the mammalian nervous system: Sometimes they block neuronal excitability and other times they augment it. In their Perspective, Mechoulam and Lichtman discuss new work (Marsicano et al.) showing that activation of the cannabinoid receptor CB1 by the endocannabinoid anandamide protects against excitotoxic damage in a mouse model of kainic acid-induced epilepsy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mechoulam, R -- Lichtman, A H -- New York, N.Y. -- Science. 2003 Oct 3;302(5642):65-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicinal Chemistry and Natural Products, Medical Faculty, Hebrew University, Jerusalem 91120, Israel. mechou@cc.huji.ac.il〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14526067" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anticonvulsants/metabolism ; Arachidonic Acids/*metabolism/pharmacology/therapeutic use ; Brain/drug effects/*metabolism ; Brain Diseases/drug therapy ; Cannabidiol/pharmacology/therapeutic use ; Cannabinoid Receptor Modulators ; Cannabinoids/*metabolism/pharmacology/therapeutic use ; Convulsants/metabolism ; Dronabinol/analogs & derivatives/pharmacology/therapeutic use ; Endocannabinoids ; Epilepsy/drug therapy/*metabolism ; Excitatory Amino Acid Agonists/pharmacology ; Excitatory Amino Acid Antagonists/pharmacology/therapeutic use ; Glutamic Acid/metabolism ; Glycerides/metabolism/pharmacology/therapeutic use ; Humans ; Kainic Acid/pharmacology ; Mice ; Neurons/drug effects/metabolism ; Neuroprotective Agents/*metabolism ; Polyunsaturated Alkamides ; Rats ; Receptors, Cannabinoid ; Receptors, Drug/agonists/antagonists & inhibitors/genetics/*metabolism ; Signal Transduction ; gamma-Aminobutyric Acid/metabolism
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    Helicobacter pylori vacuolating cytotoxin inhibits T lymphocyte activation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-23
    Description: Helicobacter pylori (Hp) vacuolating cytotoxin VacA induces cellular vacuolation in epithelial cells. We found that VacA could efficiently block proliferation of T cells by inducing a G1/S cell cycle arrest. It interfered with the T cell receptor/interleukin-2 (IL-2) signaling pathway at the level of the Ca2+-calmodulin-dependent phosphatase calcineurin. Nuclear translocation of nuclear factor of activated T cells (NFAT), a transcription factor acting as a global regulator of immune response genes, was abrogated, resulting in down-regulation of IL-2 transcription. VacA partially mimicked the activity of the immunosuppressive drug FK506 by possibly inducing a local immune suppression, explaining the extraordinary chronicity of Hp infections.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gebert, Bettina -- Fischer, Wolfgang -- Weiss, Evelyn -- Hoffmann, Reinhard -- Haas, Rainer -- New York, N.Y. -- Science. 2003 Aug 22;301(5636):1099-102.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max von Pettenkofer-Institut fur Hygiene und Medizinische Mikrobiologie, LMU Munchen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12934009" target="_blank"〉PubMed〈/a〉
    Keywords: Apoptosis ; Bacterial Proteins/pharmacology/*physiology ; Bacterial Toxins/pharmacology ; Calcineurin/metabolism ; Calcineurin Inhibitors ; Cyclins/metabolism ; Cytotoxins/pharmacology ; DNA-Binding Proteins/genetics/metabolism ; G1 Phase ; Gene Expression Regulation ; HeLa Cells ; Helicobacter pylori/genetics/*pathogenicity ; Humans ; Interleukin-2/genetics/metabolism ; Jurkat Cells ; *Lymphocyte Activation ; NFATC Transcription Factors ; *Nuclear Proteins ; Oligonucleotide Array Sequence Analysis ; S Phase ; Signal Transduction ; T-Lymphocytes/*immunology/*microbiology/physiology ; Tacrolimus/pharmacology ; Transcription Factors/genetics/metabolism ; Transcription, Genetic ; Transfection
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    Autophagy genes are essential for dauer development and life-span extension in C. elegans (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-06
    Description: Both dauer formation (a stage of developmental arrest) and adult life-span in Caenorhabditis elegans are negatively regulated by insulin-like signaling, but little is known about cellular pathways that mediate these processes. Autophagy, through the sequestration and delivery of cargo to the lysosomes, is the major route for degrading long-lived proteins and cytoplasmic organelles in eukaryotic cells. Using nematodes with a loss-of-function mutation in the insulin-like signaling pathway, we show that bec-1, the C. elegans ortholog of the yeast and mammalian autophagy gene APG6/VPS30/beclin1, is essential for normal dauer morphogenesis and life-span extension. Dauer formation is associated with increased autophagy and also requires C. elegans orthologs of the yeast autophagy genes APG1, APG7, APG8, and AUT10. Thus, autophagy is a cellular pathway essential for dauer development and life-span extension in C. elegans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Melendez, Alicia -- Talloczy, Zsolt -- Seaman, Matthew -- Eskelinen, Eeva-Liisa -- Hall, David H -- Levine, Beth -- CA84254/CA/NCI NIH HHS/ -- RR 12596/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2003 Sep 5;301(5638):1387-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Columbia University College of Physicians & Surgeons, 630 West 168th Street, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12958363" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Apoptosis Regulatory Proteins ; Autophagy/*genetics ; Caenorhabditis elegans/*genetics/*growth & development/metabolism/ultrastructure ; Caenorhabditis elegans Proteins/chemistry/*genetics/metabolism/physiology ; Genes, Fungal ; *Genes, Helminth ; Humans ; Longevity ; Membrane Proteins ; Morphogenesis ; Mutation ; Phagosomes/ultrastructure ; Phenotype ; Proteins/chemistry/genetics/physiology ; RNA Interference ; Receptor, Insulin/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/genetics/physiology ; Signal Transduction ; Vesicular Transport Proteins
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    Triggering the interferon antiviral response through an IKK-related pathway (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-19
    Description: Rapid induction of type I interferon expression, a central event in establishing the innate antiviral response, requires cooperative activation of numerous transcription factors. Although signaling pathways that activate the transcription factors nuclear factor kappaB and ATF-2/c-Jun have been well characterized, activation of the interferon regulatory factors IRF-3 and IRF-7 has remained a critical missing link in understanding interferon signaling. We report here that the IkappaB kinase (IKK)-related kinases IKKepsilon and TANK-binding kinase 1 are components of the virus-activated kinase that phosphorylate IRF-3 and IRF-7. These studies illustrate an essential role for an IKK-related kinase pathway in triggering the host antiviral response to viral infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sharma, Sonia -- tenOever, Benjamin R -- Grandvaux, Nathalie -- Zhou, Guo-Ping -- Lin, Rongtuan -- Hiscott, John -- New York, N.Y. -- Science. 2003 May 16;300(5622):1148-51. Epub 2003 Apr 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lady Davis Institute for Medical Research-Jewish General Hospital, Departments of Microbiology and Immunology and Medicine, McGill University, Montreal, Quebec H3T 1E2, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12702806" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; DNA-Binding Proteins/metabolism ; Enzyme Activation ; Gene Expression Regulation, Viral ; Hepacivirus/immunology/*physiology ; Humans ; I-kappa B Kinase ; Interferon Regulatory Factor-3 ; Interferon Regulatory Factor-7 ; Interferon Type I/*biosynthesis/genetics ; Phosphorylation ; Promoter Regions, Genetic ; Protein-Serine-Threonine Kinases/*metabolism ; RNA, Small Interfering/metabolism ; Transcription Factors/metabolism
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    Transcriptional repression of atherogenic inflammation: modulation by PPARdelta (2003)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2003-09-13
    Description: The formation of an atherosclerotic lesion is mediated by lipid-laden macrophages (foam cells), which also establish chronic inflammation associated with lesion progression. The peroxisome proliferator-activated receptor (PPAR) gamma promotes lipid uptake and efflux in these atherogenic cells. In contrast, we found that the closely related receptor PPARdelta controls the inflammatory status of the macrophage. Deletion of PPARdelta from foam cells increased the availability of inflammatory suppressors, which in turn reduced atherosclerotic lesion area by more than 50%. We propose an unconventional ligand-dependent transcriptional pathway in which PPARdelta controls an inflammatory switch through its association and disassociation with transcriptional repressors. PPARdelta and its ligands may thus serve as therapeutic targets to attenuate inflammation and slow the progression of atherosclerosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Chih-Hao -- Chawla, Ajay -- Urbiztondo, Ned -- Liao, Debbie -- Boisvert, William A -- Evans, Ronald M -- Curtiss, Linda K -- HL69474/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 17;302(5644):453-7. Epub 2003 Sep 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 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/12970571" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arteriosclerosis/drug therapy/*etiology/metabolism ; Bone Marrow Transplantation ; Chemokine CCL2/genetics/metabolism ; Cholesterol/blood/metabolism ; DNA-Binding Proteins/metabolism ; Disease Progression ; Foam Cells/physiology ; Gene Expression Regulation ; Inflammation/*etiology ; Interleukin-1/genetics/metabolism ; Ligands ; Lipid Metabolism ; Lipids/blood ; Macrophages/*physiology ; Matrix Metalloproteinase 9/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-bcl-6 ; Receptors, Cytoplasmic and Nuclear/genetics/*metabolism ; Repressor Proteins/genetics/*metabolism ; Signal Transduction ; Transcription Factors/genetics/*metabolism ; *Transcription, Genetic
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    Phase change and the regulation of developmental timing in plants (2003)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2003-07-19
    Description: Plants produce different types of organs at different times in shoot development. Along with the major changes in organ morphology that take place during developmental transitions, more gradual patterns of variation occur. The identity of organs produced at a particular position on the shoot is determined by interactions between several independently regulated, temporally coordinated processes. Two of these processes are organ production and the specification of organ identity. Coordination of these processes is accomplished in part by a thermal clock and by signal transduction pathways that mediate the response of plants to light.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Poethig, R Scott -- New York, N.Y. -- Science. 2003 Jul 18;301(5631):334-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Plant Science Institute, Department of Biology, University of Pennsylvania, Philadelphia, PA 19104, USA. spoethig@sas.upenn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12869752" target="_blank"〉PubMed〈/a〉
    Keywords: Biological Clocks/*physiology ; Cell Differentiation ; Gene Expression Regulation, Plant ; Genes, Plant ; Light ; Photoperiod ; *Plant Development ; Plant Shoots/*growth & development ; Plants/genetics ; Signal Transduction ; Temperature
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    Extended longevity in mice lacking the insulin receptor in adipose tissue (2003)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2003-01-25
    Description: Caloric restriction has been shown to increase longevity in organisms ranging from yeast to mammals. In some organisms, this has been associated with a decreased fat mass and alterations in insulin/insulin-like growth factor 1 (IGF-1) pathways. To further explore these associations with enhanced longevity, we studied mice with a fat-specific insulin receptor knockout (FIRKO). These animals have reduced fat mass and are protected against age-related obesity and its subsequent metabolic abnormalities, although their food intake is normal. Both male and female FIRKO mice were found to have an increase in mean life-span of approximately 134 days (18%), with parallel increases in median and maximum life-spans. Thus, a reduction of fat mass without caloric restriction can be associated with increased longevity in mice, possibly through effects on insulin signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bluher, Matthias -- Kahn, Barbara B -- Kahn, C Ronald -- DK 30136/DK/NIDDK NIH HHS/ -- DK 43051/DK/NIDDK NIH HHS/ -- DK 56116/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2003 Jan 24;299(5606):572-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Joslin Diabetes Center and Department of Medicine, Harvard Medical School, One Joslin Place, Boston, MA, 02215 USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12543978" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/*anatomy & histology/*metabolism ; Aging ; Animals ; Body Constitution ; Body Weight ; Caloric Restriction ; Eating ; Female ; Insulin/metabolism ; Insulin-Like Growth Factor I/metabolism ; *Longevity ; Male ; Mice ; Mice, Knockout ; Receptor, Insulin/*genetics/metabolism ; Signal Transduction ; *Thinness
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    Regulation of cell polarity and protrusion formation by targeting RhoA for degradation (2003)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2003-12-06
    Description: The Rho family of small guanosine triphosphatases regulates actin cytoskeleton dynamics that underlie cellular functions such as cell shape changes, migration, and polarity. We found that Smurf1, a HECT domain E3 ubiquitin ligase, regulated cell polarity and protrusive activity and was required to maintain the transformed morphology and motility of a tumor cell. Atypical protein kinase C zeta (PKCzeta), an effector of the Cdc42/Rac1-PAR6 polarity complex, recruited Smurf1 to cellular protrusions, where it controlled the local level of RhoA. Smurf1 thus links the polarity complex to degradation of RhoA in lamellipodia and filopodia to prevent RhoA signaling during dynamic membrane movements.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Hong-Rui -- Zhang, Yue -- Ozdamar, Barish -- Ogunjimi, Abiodun A -- Alexandrova, Evguenia -- Thomsen, Gerald H -- Wrana, Jeffrey L -- HD32429/HD/NICHD NIH HHS/ -- R01 HD032429/HD/NICHD NIH HHS/ -- R01 HD032429-06/HD/NICHD NIH HHS/ -- R01 HD032429-07/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2003 Dec 5;302(5651):1775-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Molecular Biology and Cancer, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto M56 1x5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14657501" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Line, Tumor ; Cell Membrane/metabolism/physiology ; *Cell Movement ; *Cell Polarity ; Cell Size ; Cell Transformation, Neoplastic ; Cytoskeleton/ultrastructure ; Guanine Nucleotide Exchange Factors/metabolism ; Humans ; Intercellular Junctions/metabolism ; Mice ; NIH 3T3 Cells ; Protein Kinase C/metabolism ; Protein Structure, Tertiary ; Pseudopodia/*metabolism/ultrastructure ; RNA, Small Interfering ; Signal Transduction ; Transfection ; Ubiquitin-Protein Ligases/chemistry/genetics/*metabolism ; cdc42 GTP-Binding Protein/metabolism ; rhoA GTP-Binding Protein/genetics/*metabolism
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    Cell corpse engulfment mediated by C. elegans phosphatidylserine receptor through CED-5 and CED-12 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-04
    Description: During apoptosis, phosphatidylserine, which is normally restricted to the inner leaflet of the plasma membrane, is exposed on the surface of apoptotic cells and has been suggested to act as an "eat-me" signal to trigger phagocytosis. It is unclear how phagocytes recognize phosphatidylserine. Recently, a putative phosphatidylserine receptor (PSR) was identified and proposed to mediate recognition of phosphatidylserine and phagocytosis. We report that psr-1, the Caenorhabditis elegans homolog of PSR, is important for cell corpse engulfment. In vitro PSR-1 binds preferentially phosphatidylserine or cells with exposed phosphatidylserine. In C. elegans, PSR-1 acts in the same cell corpse engulfment pathway mediated by intracellular signaling molecules CED-2 (homologous to the human CrkII protein), CED-5 (DOCK180), CED-10 (Rac GTPase), and CED-12 (ELMO), possibly through direct interaction with CED-5 and CED-12. Our findings suggest that PSR-1 is likely an upstream receptor for the signaling pathway containing CED-2, CED-5, CED-10, and CED-12 proteins and plays an important role in recognizing phosphatidylserine during phagocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Xiaochen -- Wu, Yi-Chun -- Fadok, Valerie A -- Lee, Ming-Chia -- Gengyo-Ando, Keiko -- Cheng, Li-Chun -- Ledwich, Duncan -- Hsu, Pei-Ken -- Chen, Jia-Yun -- Chou, Bin-Kuan -- Henson, Peter -- Mitani, Shohei -- Xue, Ding -- New York, N.Y. -- Science. 2003 Nov 28;302(5650):1563-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder, CO 80309, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14645848" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; *Apoptosis ; Caenorhabditis elegans/cytology/embryology/metabolism/*physiology ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Carrier Proteins/genetics/*metabolism ; *Cytoskeletal Proteins ; Embryo, Nonmammalian/cytology/metabolism ; Embryonic Development ; Humans ; Jumonji Domain-Containing Histone Demethylases ; Membrane Proteins/genetics/*metabolism ; Molecular Sequence Data ; Mutation ; *Phagocytosis ; Phosphatidylserines/metabolism ; Protein Binding ; Receptors, Cell Surface/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Recombinant Proteins/metabolism ; Signal Transduction ; rac GTP-Binding Proteins/genetics/metabolism
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    The segmentation clock: converting embryonic time into spatial pattern (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-19
    Description: In most animal species, the anteroposterior body axis is generated by the formation of repeated structures called segments. In vertebrate segmentation, a specialized mesodermal structure called the somite gives rise to skeletal muscles, vertebrae, and some dermis. Formation of the somites is a rhythmic process that involves an oscillator--the segmentation clock--driven by Wnt and Notch signaling. The clock ticks in somite precursors and halts when they reach a specific maturation stage defined as the wavefront, established by fibroblast growth factor and Wnt signaling. This process converts the temporal oscillations into the periodic spatial pattern of somite boundaries. The study of somite development provides insights into the spatiotemporal integration of signaling systems in the vertebrate embryo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pourquie, Olivier -- New York, N.Y. -- Science. 2003 Jul 18;301(5631):328-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, MO 64110, USA. olp@stowers-institute.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12869750" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks/*physiology ; *Body Patterning ; *Embryonic Development ; *Embryonic and Fetal Development ; Fibroblast Growth Factor 8 ; Fibroblast Growth Factors/metabolism ; Membrane Proteins/metabolism ; Periodicity ; Proto-Oncogene Proteins/metabolism ; Receptors, Notch ; Signal Transduction ; Somites/*physiology ; Vertebrates/*embryology/genetics/metabolism ; Wnt Proteins ; *Zebrafish Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    DAF-16 target genes that control C. elegans life-span and metabolism (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-12
    Description: Signaling from the DAF-2/insulin receptor to the DAF-16/FOXO transcription factor controls longevity, metabolism, and development in disparate phyla. To identify genes that mediate the conserved biological outputs of daf-2/insulin-like signaling, we used comparative genomics to identify 17 orthologous genes from Caenorhabditis and Drosophila, each of which bears a DAF-16 binding site in the promoter region. One-third of these DAF-16 downstream candidate genes were regulated by daf-2/insulin-like signaling in C. elegans, and RNA interference inactivation of the candidates showed that many of these genes mediate distinct aspects of daf-16 function, including longevity, metabolism, and development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Siu Sylvia -- Kennedy, Scott -- Tolonen, Andrew C -- Ruvkun, Gary -- New York, N.Y. -- Science. 2003 Apr 25;300(5619):644-7. Epub 2003 Apr 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Massachusetts General Hospital, Department of Genetics, Harvard Medical School, 50 Blossom Street, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12690206" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Caenorhabditis/genetics ; Caenorhabditis elegans/*genetics/metabolism/*physiology ; Caenorhabditis elegans Proteins/genetics/physiology ; Computational Biology ; Conserved Sequence ; Down-Regulation ; Drosophila/genetics ; Forkhead Transcription Factors ; Gene Expression Profiling ; Gene Expression Regulation ; *Genes, Helminth ; Genes, Insect ; Genomics ; Insulin/metabolism ; Longevity/genetics ; Mutation ; Promoter Regions, Genetic ; RNA Interference ; Receptor, Insulin/genetics/metabolism ; Signal Transduction ; Transcription Factors/*genetics/*physiology ; Up-Regulation
    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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    Immunology. Regulating the regulators (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Powrie, Fiona -- Maloy, Kevin J -- New York, N.Y. -- Science. 2003 Feb 14;299(5609):1030-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK. fiona.powrie@path. ox.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12586934" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Antigen-Presenting Cells/immunology ; Autoimmune Diseases/immunology/prevention & control ; Cell Differentiation ; DNA-Binding Proteins/genetics/*metabolism ; Dendritic Cells/*immunology ; *Drosophila Proteins ; Forkhead Transcription Factors ; Graft Rejection/immunology ; Humans ; Immune Tolerance ; Immunity, Innate ; Interleukin-10/immunology ; Interleukin-6/immunology/secretion ; Lymphocyte Activation ; Membrane Glycoproteins/*physiology ; Mice ; Models, Immunological ; Mutation ; Receptors, Cell Surface/*physiology ; Receptors, Interleukin-2/analysis ; Signal Transduction ; T-Lymphocyte Subsets/*immunology ; T-Lymphocytes, Regulatory/*immunology ; Thymus Gland/cytology/immunology ; Toll-Like Receptors ; Transduction, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Neuroscience. SPARring with spines (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyer, Guido -- Brose, Nils -- New York, N.Y. -- Science. 2003 Nov 21;302(5649):1341-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Neuroscience, Max Planck Institute for Experimental Medicine, D-37075 Gottingen, Germany. gmeyer@em.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14631024" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; COS Cells ; Cell Cycle ; Cells, Cultured ; Cysteine Endopeptidases/metabolism ; Dendrites/*physiology/ultrastructure ; Down-Regulation ; GTPase-Activating Proteins/chemistry/*metabolism ; Hippocampus/cytology/metabolism ; Multienzyme Complexes/metabolism ; Nerve Tissue Proteins/metabolism ; Neuronal Plasticity/*physiology ; Phosphorylation ; Proteasome Endopeptidase Complex ; Protein Kinases/*metabolism ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases ; Recombinant Proteins/metabolism ; Signal Transduction ; Synapses/*physiology ; Two-Hybrid System Techniques ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/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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    RNA leaching of transcription factors disrupts transcription in myotonic dystrophy (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-06
    Description: Myotonic dystrophy type 1 (DM1) is caused by a CUGn expansion (n approximately 50 to 5000) in the 3' untranslated region of the mRNA of the DM protein kinase gene. We show that mutant RNA binds and sequesters transcription factors (TFs), with up to 90% depletion of selected TFs from active chromatin. Diverse genes are consequently reduced in expression, including the ion transporter CIC-1, which has been implicated in myotonia. When TF specificity protein 1 (Sp1) was overexpressed in DM1-affected cells, low levels of messenger RNA for CIC-1 were restored to normal. Transcription factor leaching from chromatin by mutant RNA provides a potentially unifying pathomechanistic explanation for this disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ebralidze, A -- Wang, Y -- Petkova, V -- Ebralidse, K -- Junghans, R P -- New York, N.Y. -- Science. 2004 Jan 16;303(5656):383-7. Epub 2003 Dec 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biotherapeutics Development Lab, Harvard Institute of Human Genetics, Harvard Medical School and Division of Hematology-Oncology, Beth Israel Deaconess Medical Center, 4 Blackfan Circle, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14657503" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Cell Line ; Cell Nucleus/metabolism ; Chloride Channels/genetics ; Chromatin/metabolism ; DNA-Binding Proteins/genetics/metabolism ; Humans ; Muscle Cells/*metabolism ; Mutation ; Myotonic Dystrophy/*genetics ; Myotonin-Protein Kinase ; Promoter Regions, Genetic ; Protein-Serine-Threonine Kinases/*genetics ; RNA/genetics/*metabolism ; RNA Splicing ; RNA, Messenger/genetics/metabolism ; Receptors, IgG/genetics ; Receptors, Retinoic Acid/genetics/metabolism ; Ribonucleoproteins/metabolism ; STAT1 Transcription Factor ; STAT3 Transcription Factor ; Sp1 Transcription Factor/genetics/metabolism ; Sp3 Transcription Factor ; Trans-Activators/genetics/metabolism ; Transcription Factors/genetics/*metabolism ; *Transcription, Genetic
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    EDEM as an acceptor of terminally misfolded glycoproteins released from calnexin (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-01
    Description: Terminally misfolded proteins in the endoplasmic reticulum (ER) are retrotranslocated to the cytoplasm and degraded by proteasomes through a mechanism known as ER-associated degradation (ERAD). EDEM, a postulated Man8B-binding protein, accelerates the degradation of misfolded proteins in the ER. Here, EDEM was shown to interact with calnexin, but not with calreticulin, through its transmembrane region. Both binding of substrates to calnexin and their release from calnexin were required for ERAD to occur. Overexpression of EDEM accelerated ERAD by promoting the release of terminally misfolded proteins from calnexin. Thus, EDEM appeared to function in the ERAD pathway by accepting substrates from calnexin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oda, Yukako -- Hosokawa, Nobuko -- Wada, Ikuo -- Nagata, Kazuhiro -- New York, N.Y. -- Science. 2003 Feb 28;299(5611):1394-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8397, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12610305" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcysteine/*analogs & derivatives/pharmacology ; Calnexin/*metabolism ; Calreticulin/metabolism ; Cell Line ; Endoplasmic Reticulum/*metabolism ; Glycoproteins/chemistry/*metabolism ; Humans ; Indolizines/pharmacology ; Membrane Proteins/*metabolism ; Precipitin Tests ; Protein Binding ; Protein Conformation ; Protein Folding ; Protein Transport ; Recombinant Fusion Proteins/metabolism ; Transfection ; alpha 1-Antitrypsin/chemistry/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Sensing DNA damage through ATRIP recognition of RPA-ssDNA complexes (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-06-07
    Description: The function of the ATR (ataxia-telangiectasia mutated- and Rad3-related)-ATRIP (ATR-interacting protein) protein kinase complex is crucial for the cellular response to replication stress and DNA damage. Here, we show that replication protein A (RPA), a protein complex that associates with single-stranded DNA (ssDNA), is required for the recruitment of ATR to sites of DNA damage and for ATR-mediated Chk1 activation in human cells. In vitro, RPA stimulates the binding of ATRIP to ssDNA. The binding of ATRIP to RPA-coated ssDNA enables the ATR-ATRIP complex to associate with DNA and stimulates phosphorylation of the Rad17 protein that is bound to DNA. Furthermore, Ddc2, the budding yeast homolog of ATRIP, is specifically recruited to double-strand DNA breaks in an RPA-dependent manner. A checkpoint-deficient mutant of RPA, rfa1-t11, is defective for recruiting Ddc2 to ssDNA both in vivo and in vitro. Our data suggest that RPA-coated ssDNA is the critical structure at sites of DNA damage that recruits the ATR-ATRIP complex and facilitates its recognition of substrates for phosphorylation and the initiation of checkpoint signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zou, Lee -- Elledge, Stephen J -- GM44664/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Jun 6;300(5625):1542-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Verna & Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12791985" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins/*metabolism ; Cell Nucleus/metabolism ; *DNA Damage ; DNA Repair ; DNA Replication ; DNA, Fungal/metabolism ; DNA, Single-Stranded/*metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Enzyme Activation ; *Exodeoxyribonucleases ; HeLa Cells ; Humans ; Mutation ; Phosphoproteins/*metabolism ; Phosphorylation ; Protein Binding ; Protein Kinases/metabolism ; *Protein-Serine-Threonine Kinases ; RNA, Small Interfering ; Radiation, Ionizing ; Recombination, Genetic ; Replication Protein A ; Saccharomyces cerevisiae/genetics/metabolism ; Saccharomyces cerevisiae Proteins/genetics/metabolism ; Signal Transduction ; Transcription Factors/genetics/metabolism ; Transfection ; Tumor Cells, Cultured ; Ultraviolet Rays
    Print ISSN: 0036-8075
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    Design and chemical synthesis of a homogeneous polymer-modified erythropoiesis protein (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-08
    Description: We report the design and total chemical synthesis of "synthetic erythropoiesis protein" (SEP), a 51-kilodalton protein-polymer construct consisting of a 166-amino-acid polypeptide chain and two covalently attached, branched, and monodisperse polymer moieties that are negatively charged. The ability to control the chemistry allowed us to synthesize a macromolecule of precisely defined covalent structure. SEP was homogeneous as shown by high-resolution analytical techniques, with a mass of 50,825 +/-10 daltons by electrospray mass spectrometry, and with a pI of 5.0. In cell and animal assays for erythropoiesis, SEP displayed potent biological activity and had significantly prolonged duration of action in vivo. These chemical methods are a powerful tool in the rational design of protein constructs with potential therapeutic applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kochendoerfer, Gerd G -- Chen, Shiah-Yun -- Mao, Feng -- Cressman, Sonya -- Traviglia, Stacey -- Shao, Haiyan -- Hunter, Christie L -- Low, Donald W -- Cagle, E Neil -- Carnevali, Maia -- Gueriguian, Vincent -- Keogh, Peter J -- Porter, Heather -- Stratton, Stephen M -- Wiedeke, M Con -- Wilken, Jill -- Tang, Jie -- Levy, Jay J -- Miranda, Les P -- Crnogorac, Milan M -- Kalbag, Suresh -- Botti, Paolo -- Schindler-Horvat, Janice -- Savatski, Laura -- Adamson, John W -- Kung, Ada -- Kent, Stephen B H -- Bradburne, James A -- New York, N.Y. -- Science. 2003 Feb 7;299(5608):884-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gryphon Therapeutics, 250 East Grand Avenue, Suite 90, South San Francisco, CA 94080, USA. Gkochendoerfer@gryphonRX.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12574628" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Circular Dichroism ; *Drug Design ; Drug Stability ; Electrophoresis, Polyacrylamide Gel ; *Erythropoiesis ; Erythropoietin/chemistry/pharmacology ; Hematocrit ; Humans ; Isoelectric Point ; Mice ; Molecular Sequence Data ; Molecular Structure ; Molecular Weight ; *Polymers/*chemical synthesis/*chemistry/pharmacokinetics/pharmacology ; Protein Folding ; Proteins/*chemical synthesis/*chemistry/pharmacokinetics/pharmacology ; Rats ; Receptors, Erythropoietin/drug effects/metabolism ; Recombinant Proteins ; Spectrometry, Mass, Electrospray Ionization
    Print ISSN: 0036-8075
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    Mammalian brain morphogenesis and midline axon guidance require heparan sulfate (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-08
    Description: Heparan sulfate (HS) is required for morphogen signaling during Drosophila pattern formation, but little is known about its physiological importance in mammalian development. To define the developmental role of HS in mammalian species, we conditionally disrupted the HS-polymerizing enzyme EXT1 in the embryonic mouse brain. The EXT1-null brain exhibited patterning defects that are composites of those caused by mutations of multiple HS-binding morphogens. Furthermore, the EXT1-null brain displayed severe guidance errors in major commissural tracts, revealing a pivotal role of HS in midline axon guidance. These findings demonstrate that HS is essential for mammalian brain development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Inatani, Masaru -- Irie, Fumitoshi -- Plump, Andrew S -- Tessier-Lavigne, Marc -- Yamaguchi, Yu -- P01 HD25938/HD/NICHD NIH HHS/ -- R01 NS33117/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Nov 7;302(5647):1044-6.〈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/14605369" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Body Patterning ; Brain/abnormalities/*embryology ; Cerebellum/embryology ; Cerebral Cortex/abnormalities/embryology ; Fibroblast Growth Factor 8 ; Fibroblast Growth Factors/metabolism ; Heparitin Sulfate/*physiology ; Homeodomain Proteins/metabolism ; Inferior Colliculi/embryology ; Intercellular Signaling Peptides and Proteins ; Mesencephalon/embryology ; Mice ; Mice, Knockout ; *Morphogenesis ; Mutation ; N-Acetylglucosaminyltransferases/genetics/metabolism ; Nerve Tissue Proteins/genetics/metabolism ; Optic Chiasm/cytology/embryology ; Proto-Oncogene Proteins/metabolism ; Retina/cytology ; Rhombencephalon/embryology ; Signal Transduction ; Wnt Proteins ; *Zebrafish Proteins
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    CB1 cannabinoid receptors and on-demand defense against excitotoxicity (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-04
    Description: Abnormally high spiking activity can damage neurons. Signaling systems to protect neurons from the consequences of abnormal discharge activity have been postulated. We generated conditional mutant mice that lack expression of the cannabinoid receptor type 1 in principal forebrain neurons but not in adjacent inhibitory interneurons. In mutant mice,the excitotoxin kainic acid (KA) induced excessive seizures in vivo. The threshold to KA-induced neuronal excitation in vitro was severely reduced in hippocampal pyramidal neurons of mutants. KA administration rapidly raised hippocampal levels of anandamide and induced protective mechanisms in wild-type principal hippocampal neurons. These protective mechanisms could not be triggered in mutant mice. The endogenous cannabinoid system thus provides on-demand protection against acute excitotoxicity in central nervous system neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marsicano, Giovanni -- Goodenough, Sharon -- Monory, Krisztina -- Hermann, Heike -- Eder, Matthias -- Cannich, Astrid -- Azad, Shahnaz C -- Cascio, Maria Grazia -- Gutierrez, Silvia Ortega -- van der Stelt, Mario -- Lopez-Rodriguez, Maria Luz -- Casanova, Emilio -- Schutz, Gunther -- Zieglgansberger, Walter -- Di Marzo, Vincenzo -- Behl, Christian -- Lutz, Beat -- New York, N.Y. -- Science. 2003 Oct 3;302(5642):84-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Genetics of Behaviour, Max-Planck-Institute of Psychiatry, Kraepelinstrabetae 2-10, 80804 Munich, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14526074" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arachidonic Acids/*metabolism/pharmacology ; Brain/drug effects/*metabolism ; Brain-Derived Neurotrophic Factor/genetics/metabolism ; Cannabinoids/*metabolism ; Endocannabinoids ; Epilepsy/*metabolism/physiopathology ; Excitatory Amino Acid Agonists/pharmacology ; Excitatory Postsynaptic Potentials ; Furans/pharmacology ; Gene Expression Regulation/drug effects ; Genes, Immediate-Early ; Glutamic Acid/metabolism ; Glycerides/metabolism ; Hippocampus/drug effects/metabolism ; In Vitro Techniques ; Kainic Acid/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Mitogen-Activated Protein Kinases/metabolism ; Mutation ; Neurons/drug effects/*metabolism/physiology ; Neuroprotective Agents/metabolism ; Piperidines/pharmacology ; Polyunsaturated Alkamides ; Prosencephalon/drug effects/metabolism ; Pyrazoles/pharmacology ; Receptors, Cannabinoid ; Receptors, Drug/antagonists & inhibitors/genetics/*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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    Heart disease. How to subdue a swelling heart (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-06-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, Jean -- New York, N.Y. -- Science. 2003 Jun 6;300(5625):1492-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12791957" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Calcium/metabolism ; Calcium-Binding Proteins/genetics/metabolism ; Calcium-Transporting ATPases/metabolism ; Cardiac Output, Low/etiology/physiopathology ; *Cardiomyopathy, Dilated/genetics/pathology/physiopathology ; *Cardiomyopathy, Hypertrophic, Familial/genetics/pathology/physiopathology ; Gene Expression Regulation ; Genes ; Heart/physiopathology ; Humans ; Mutation ; Myocardial Contraction ; Myocardium/metabolism ; Signal Transduction
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    Notch-mediated restoration of regenerative potential to aged muscle (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-04
    Description: A hallmark of aging is diminished regenerative potential of tissues, but the mechanism of this decline is unknown. Analysis of injured muscle revealed that, with age, resident precursor cells (satellite cells) had a markedly impaired propensity to proliferate and to produce myoblasts necessary for muscle regeneration. This was due to insufficient up-regulation of the Notch ligand Delta and, thus, diminished activation of Notch in aged, regenerating muscle. Inhibition of Notch impaired regeneration of young muscle, whereas forced activation of Notch restored regenerative potential to old muscle. Thus, Notch signaling is a key determinant of muscle regenerative potential that declines with age.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Conboy, Irina M -- Conboy, Michael J -- Smythe, Gayle M -- Rando, Thomas A -- NRSA-AG05902/NR/NINR NIH HHS/ -- R01-NS36409/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Nov 28;302(5650):1575-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305-5235, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14645852" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; Calcium-Binding Proteins ; Cell Count ; Cell Differentiation ; Cell Division ; Cell Separation ; Culture Techniques ; Hindlimb ; Intercellular Signaling Peptides and Proteins ; Intracellular Signaling Peptides and Proteins ; Male ; Membrane Proteins/*metabolism ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal/cytology/injuries/*physiology ; Myoblasts/*physiology ; Nerve Tissue Proteins/metabolism ; Receptor, Notch1 ; *Receptors, Cell Surface ; Recombinant Fusion Proteins/metabolism ; *Regeneration ; Satellite Cells, Skeletal Muscle/*physiology ; Signal Transduction ; *Transcription Factors ; Up-Regulation
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    Proteomics. A sharper focus (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, Robert F -- New York, N.Y. -- Science. 2003 Nov 21;302(5649):1318.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14631012" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Glycosphingolipids/analysis ; Leishmania/chemistry ; Membrane Microdomains/metabolism ; Membrane Proteins/*analysis/metabolism ; Phagosomes/*chemistry/parasitology ; *Proteomics ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 97
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    Distinctive roles of PHAP proteins and prothymosin-alpha in a death regulatory pathway (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-11
    Description: A small molecule, alpha-(trichloromethyl)-4-pyridineethanol (PETCM), was identified by high-throughput screening as an activator of caspase-3 in extracts of a panel of cancer cells. PETCM was used in combination with biochemical fractionation to identify a pathway that regulates mitochondria-initiated caspase activation. This pathway consists of tumor suppressor putative HLA-DR-associated proteins (PHAP) and oncoprotein prothymosin-alpha (ProT). PHAP proteins promoted caspase-9 activation after apoptosome formation, whereas ProT negatively regulated caspase-9 activation by inhibiting apoptosome formation. PETCM relieved ProT inhibition and allowed apoptosome formation at a physiological concentration of deoxyadenosine triphosphate. Elimination of ProT expression by RNA interference sensitized cells to ultraviolet irradiation-induced apoptosis and negated the requirement of PETCM for caspase activation. Thus, this chemical-biological combinatory approach has revealed the regulatory roles of oncoprotein ProT and tumor suppressor PHAP in apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jiang, Xuejun -- Kim, Hyun-Eui -- Shu, Hongjun -- Zhao, Yingming -- Zhang, Haichao -- Kofron, James -- Donnelly, Jennifer -- Burns, Dave -- Ng, Shi-Chung -- Rosenberg, Saul -- Wang, Xiaodong -- GMRO1-57158/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Jan 10;299(5604):223-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12522243" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Apoptosis ; Apoptotic Protease-Activating Factor 1 ; Caspase 3 ; Caspase 9 ; Caspases/metabolism ; Cell Extracts ; Cytochrome c Group/metabolism ; Deoxyadenine Nucleotides/metabolism/pharmacology ; Enzyme Activation ; HeLa Cells ; Humans ; Intracellular Signaling Peptides and Proteins ; Mitochondria/metabolism ; Molecular Sequence Data ; *Neuropeptides ; Nuclear Proteins/chemistry/isolation & purification/*metabolism/pharmacology ; Protein Precursors/chemistry/isolation & purification/*metabolism/pharmacology ; Proteins/chemistry/isolation & purification/*metabolism/pharmacology ; Pyridines/chemistry/*pharmacology ; RNA Interference ; Recombinant Proteins/metabolism/pharmacology ; Signal Transduction ; Thymosin/*analogs & derivatives/chemistry/isolation & ; purification/*metabolism/pharmacology ; Tumor Suppressor Proteins/chemistry/isolation & purification/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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  • 98
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    A bacterial cell-cycle regulatory network operating in time and space (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-27
    Description: Transcriptional regulatory circuits provide only a fraction of the signaling pathways and regulatory mechanisms that control the bacterial cell cycle. The CtrA regulatory network, important in control of the Caulobacter cell cycle, illustrates the critical role of nontranscriptional pathways and temporally and spatially localized regulatory proteins. The system architecture of Caulobacter cell-cycle control involves top-down control of modular functions by a small number of master regulatory proteins with cross-module signaling coordinating the overall process. Modeling the cell cycle probably requires a top-down modeling approach and a hybrid control system modeling paradigm to treat its combined discrete and continuous characteristics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McAdams, Harley H -- Shapiro, Lucy -- GM32506/5120 M2/GM/NIGMS NIH HHS/ -- GM51426/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Sep 26;301(5641):1874-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Stanford University School of Medicine, B300 Beckman Center, Stanford, CA 94305, USA. hmcadams@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14512618" target="_blank"〉PubMed〈/a〉
    Keywords: *Bacterial Physiological Phenomena ; Bacterial Proteins/metabolism ; Caulobacter/cytology/genetics/growth & development/*physiology ; *Cell Cycle ; Cell Polarity ; DNA-Binding Proteins/genetics/*metabolism ; Flagella/metabolism ; Gene Expression Regulation, Bacterial ; Models, Biological ; Signal Transduction ; Transcription Factors/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
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    FACT facilitates transcription-dependent nucleosome alteration (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-23
    Description: The FACT (facilitates chromatin transcription) complex is required for transcript elongation through nucleosomes by RNA polymerase II (Pol II) in vitro. Here, we show that FACT facilitates Pol II-driven transcription by destabilizing nucleosomal structure so that one histone H2A-H2B dimer is removed during enzyme passage. We also demonstrate that FACT possesses intrinsic histone chaperone activity and can deposit core histones onto DNA. Importantly, FACT activity requires both of its constituent subunits and is dependent on the highly acidic C terminus of its larger subunit, Spt16. These findings define the mechanism by which Pol II can transcribe through chromatin without disrupting its epigenetic status.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Belotserkovskaya, Rimma -- Oh, Sangtaek -- Bondarenko, Vladimir A -- Orphanides, George -- Studitsky, Vasily M -- Reinberg, Danny -- GM37120/GM/NIGMS NIH HHS/ -- GM58650/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Aug 22;301(5636):1090-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biochemistry, Division of Nucleic Acids Enzymology, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, Piscataway, NJ 08854, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12934006" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Cycle Proteins/chemistry/metabolism ; Cell Line ; DNA/metabolism ; DNA-Binding Proteins/chemistry/metabolism ; Dimerization ; HeLa Cells ; High Mobility Group Proteins/chemistry/metabolism ; Histones/metabolism ; Humans ; Models, Genetic ; Molecular Chaperones/chemistry/metabolism ; Molecular Sequence Data ; Nucleosomes/*metabolism ; Protein Binding ; Protein Subunits ; RNA Polymerase II/*metabolism ; Recombinant Proteins/chemistry/metabolism ; Templates, Genetic ; Transcription Factors/chemistry/metabolism ; *Transcription, Genetic ; Transcriptional Elongation Factors/chemistry/*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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  • 100
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    Biochemistry. An overoxidation journey with a return ticket (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Georgiou, George -- Masip, Lluis -- New York, N.Y. -- Science. 2003 Apr 25;300(5619):592-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemical Engineering, Biomedical Engineering and Institute for Cell and Molecular Biology, University of Texas at Austin, Austin, TX 78712, USA. gg@che.utexas.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12714731" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Antioxidants/*metabolism ; Bacteria/enzymology ; Catalysis ; Cell Line ; Cysteine/*analogs & derivatives/metabolism ; Erythrocytes/enzymology ; Evolution, Molecular ; Humans ; Hydrogen Peroxide/*metabolism ; Models, Biological ; Neurotransmitter Agents ; Oxidation-Reduction ; Peroxidases/*chemistry/*metabolism ; Peroxiredoxins ; Protein Conformation ; Protein Structure, Secondary ; *Signal Transduction ; Sulfenic Acids/metabolism ; Sulfinic Acids/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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