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  • 1
    Publikationsdatum: 2003-05-10
    Beschreibung: 〈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〉
    Schlagwort(e): 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
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-07-05
    Beschreibung: 〈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〉
    Schlagwort(e): 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
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-06-14
    Beschreibung: 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〉
    Schlagwort(e): 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
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
    Publikationsdatum: 2003-08-16
    Beschreibung: 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〉
    Schlagwort(e): 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
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
    Publikationsdatum: 2003-07-05
    Beschreibung: 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〉
    Schlagwort(e): 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
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    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-03-08
    Beschreibung: 〈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〉
    Schlagwort(e): 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
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-03-15
    Beschreibung: 〈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〉
    Schlagwort(e): 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
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-03-22
    Beschreibung: 〈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〉
    Schlagwort(e): 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
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 9
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-11-15
    Beschreibung: 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〉
    Schlagwort(e): 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
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 10
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-09-13
    Beschreibung: 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〉
    Schlagwort(e): 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
    Print ISSN: 0036-8075
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 11
    Publikationsdatum: 2003-06-07
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 12
    Publikationsdatum: 2003-10-25
    Beschreibung: 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〉
    Schlagwort(e): *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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 13
    Publikationsdatum: 2003-02-22
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 14
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-08-09
    Beschreibung: 〈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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 15
    Publikationsdatum: 2003-08-30
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 16
    Publikationsdatum: 2003-09-06
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 17
    Publikationsdatum: 2003-09-23
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 18
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-02-08
    Beschreibung: 〈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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 19
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-12-20
    Beschreibung: 〈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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 20
    Publikationsdatum: 2003-04-12
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 21
    Publikationsdatum: 2003-06-28
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 22
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-11-01
    Beschreibung: 〈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〉
    Schlagwort(e): 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
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 23
    Publikationsdatum: 2003-11-25
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 24
    Publikationsdatum: 2003-10-18
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 25
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-05-06
    Beschreibung: 〈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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 26
    Publikationsdatum: 2003-02-08
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 27
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-09-27
    Beschreibung: 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〉
    Schlagwort(e): Animals ; Biochemical Phenomena ; Biochemistry ; *Biological Evolution ; *Biology ; DNA/metabolism ; Engineering ; *Models, Biological ; Proteins/metabolism ; Signal Transduction ; Systems Theory
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  • 28
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-10-18
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 29
    Publikationsdatum: 2003-03-22
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 30
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-04-05
    Beschreibung: 〈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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 31
    Publikationsdatum: 2003-08-16
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 32
    Publikationsdatum: 2003-11-01
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 33
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-12-06
    Beschreibung: 〈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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 34
    Publikationsdatum: 2003-05-17
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 35
    Publikationsdatum: 2003-03-15
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 36
    Publikationsdatum: 2003-06-07
    Beschreibung: 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〉
    Schlagwort(e): *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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 37
    facet.materialart.
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-02-15
    Beschreibung: 〈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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 38
    Publikationsdatum: 2003-01-04
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 39
    Publikationsdatum: 2003-12-03
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 40
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-06-21
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 41
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-02-22
    Beschreibung: 〈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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 42
    Publikationsdatum: 2003-08-09
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 43
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-01-18
    Beschreibung: 〈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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 44
    Publikationsdatum: 2003-06-28
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 45
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-10-11
    Beschreibung: 〈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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 46
    Publikationsdatum: 2003-08-02
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 47
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-10-04
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 48
    Publikationsdatum: 2003-08-23
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 49
    Publikationsdatum: 2003-09-06
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 50
    Publikationsdatum: 2003-09-13
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 51
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-07-19
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 52
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-01-25
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 53
    Publikationsdatum: 2003-12-06
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 54
    Publikationsdatum: 2003-12-04
    Beschreibung: 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〉
    Schlagwort(e): *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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 55
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-07-19
    Beschreibung: 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〉
    Schlagwort(e): 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
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 56
    Publikationsdatum: 2003-04-12
    Beschreibung: 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〉
    Schlagwort(e): 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
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 57
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-02-15
    Beschreibung: 〈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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 58
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-11-25
    Beschreibung: 〈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〉
    Schlagwort(e): 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
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 59
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-06-07
    Beschreibung: 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〉
    Schlagwort(e): 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
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 60
    Publikationsdatum: 2003-11-08
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 61
    Publikationsdatum: 2003-10-04
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 62
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-06-07
    Beschreibung: 〈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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 63
    Publikationsdatum: 2003-12-04
    Beschreibung: 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〉
    Schlagwort(e): 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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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 64
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-11-25
    Beschreibung: 〈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〉
    Schlagwort(e): Animals ; Glycosphingolipids/analysis ; Leishmania/chemistry ; Membrane Microdomains/metabolism ; Membrane Proteins/*analysis/metabolism ; Phagosomes/*chemistry/parasitology ; *Proteomics ; Signal Transduction
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 65
    Publikationsdatum: 2003-01-11
    Beschreibung: 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〉
    Schlagwort(e): 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
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 66
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-09-27
    Beschreibung: 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〉
    Schlagwort(e): *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
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 67
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-10-25
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cullimore, Julie -- Denarie, Jean -- New York, N.Y. -- Science. 2003 Oct 24;302(5645):575-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire des Interactions Plantes-Microorganismes, CNRS-INRA, 31326 Castanet-Tolosan Cedex, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14576408" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Bacterial Physiological Phenomena ; Fabaceae/genetics/microbiology/*physiology ; Fungi/physiology ; *Genes, Plant ; Lipopolysaccharides/*metabolism ; Lotus/genetics/microbiology/physiology ; Medicago/genetics/microbiology/physiology ; Mutation ; Nitrogen Fixation ; Peas/genetics/microbiology/physiology ; Plant Roots/microbiology ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/chemistry/*genetics/metabolism ; Rhizobium/growth & development/*physiology ; Signal Transduction ; Sinorhizobium meliloti/growth & development/*physiology ; *Symbiosis
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 68
    Publikationsdatum: 2003-02-08
    Beschreibung: The vascular endothelium was once thought to function primarily in nutrient and oxygen delivery, but recent evidence suggests that it may play a broader role in tissue homeostasis. To explore the role of sinusoidal endothelial cells (LSECs) in the adult liver, we studied the effects of vascular endothelial growth factor (VEGF) receptor activation on mouse hepatocyte growth. Delivery of VEGF-A increased liver mass in mice but did not stimulate growth of hepatocytes in vitro, unless LSECs were also present in the culture. Hepatocyte growth factor (HGF) was identified as one of the LSEC-derived paracrine mediators promoting hepatocyte growth. Selective activation of VEGF receptor-1 (VEGFR-1) stimulated hepatocyte but not endothelial proliferation in vivo and reduced liver damage in mice exposed to a hepatotoxin. Thus, VEGFR-1 agonists may have therapeutic potential for preservation of organ function in certain liver disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉LeCouter, Jennifer -- Moritz, Dirk R -- Li, Bing -- Phillips, Gail Lewis -- Liang, Xiao Huan -- Gerber, Hans-Peter -- Hillan, Kenneth J -- Ferrara, Napoleone -- New York, N.Y. -- Science. 2003 Feb 7;299(5608):890-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Molecular Oncology, Protein Engineering, and Pathology, Genentech Inc., 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/12574630" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; CHO Cells ; Carbon Tetrachloride/toxicity ; Cell Division ; Cells, Cultured ; Coculture Techniques ; Cricetinae ; DNA Replication ; Drug-Induced Liver Injury ; Endothelial Growth Factors/genetics/*metabolism/pharmacology ; Endothelium, Vascular/*cytology/physiology ; Gene Expression Regulation ; Growth Substances/genetics/metabolism ; Hepatocyte Growth Factor/genetics/metabolism/pharmacology ; Hepatocytes/cytology/pathology/*physiology ; Humans ; Intercellular Signaling Peptides and Proteins/genetics/*metabolism/pharmacology ; Liver/blood supply/*cytology/pathology/*physiology ; Liver Diseases/metabolism/pathology/prevention & control ; Liver Regeneration ; Lymphokines/genetics/*metabolism/pharmacology ; Mice ; Mice, Nude ; Mitosis ; Mutation ; Necrosis ; Neovascularization, Physiologic ; Paracrine Communication ; RNA, Messenger/genetics/metabolism ; Signal Transduction ; Up-Regulation ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factor Receptor-1/*metabolism ; Vascular Endothelial Growth Factor Receptor-2/metabolism ; Vascular Endothelial Growth Factors
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 69
    Publikationsdatum: 2003-11-08
    Beschreibung: Drosophila melanogaster is a proven model system for many aspects of human biology. Here we present a two-hybrid-based protein-interaction map of the fly proteome. A total of 10,623 predicted transcripts were isolated and screened against standard and normalized complementary DNA libraries to produce a draft map of 7048 proteins and 20,405 interactions. A computational method of rating two-hybrid interaction confidence was developed to refine this draft map to a higher confidence map of 4679 proteins and 4780 interactions. Statistical modeling of the network showed two levels of organization: a short-range organization, presumably corresponding to multiprotein complexes, and a more global organization, presumably corresponding to intercomplex connections. The network recapitulated known pathways, extended pathways, and uncovered previously unknown pathway components. This map serves as a starting point for a systems biology modeling of multicellular organisms, including humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giot, L -- Bader, J S -- Brouwer, C -- Chaudhuri, A -- Kuang, B -- Li, Y -- Hao, Y L -- Ooi, C E -- Godwin, B -- Vitols, E -- Vijayadamodar, G -- Pochart, P -- Machineni, H -- Welsh, M -- Kong, Y -- Zerhusen, B -- Malcolm, R -- Varrone, Z -- Collis, A -- Minto, M -- Burgess, S -- McDaniel, L -- Stimpson, E -- Spriggs, F -- Williams, J -- Neurath, K -- Ioime, N -- Agee, M -- Voss, E -- Furtak, K -- Renzulli, R -- Aanensen, N -- Carrolla, S -- Bickelhaupt, E -- Lazovatsky, Y -- DaSilva, A -- Zhong, J -- Stanyon, C A -- Finley, R L Jr -- White, K P -- Braverman, M -- Jarvie, T -- Gold, S -- Leach, M -- Knight, J -- Shimkets, R A -- McKenna, M P -- Chant, J -- Rothberg, J M -- HG01536/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2003 Dec 5;302(5651):1727-36. Epub 2003 Nov 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CuraGen Corporation, 555 Long Wharf Drive, New Haven, CT 06511, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14605208" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Calcium/metabolism ; Cell Cycle ; Cell Differentiation ; Cloning, Molecular ; Computational Biology ; DNA, Complementary ; Drosophila Proteins/*metabolism ; Drosophila melanogaster/*genetics/*metabolism/physiology ; Genes, Insect ; Immunity, Innate ; Mathematics ; Models, Statistical ; Photoreceptor Cells, Invertebrate/cytology ; Protein Binding ; *Protein Interaction Mapping ; *Proteome ; RNA Splicing ; RNA, Messenger/genetics/metabolism ; Receptor, Epidermal Growth Factor/metabolism ; Signal Transduction ; Transcription, Genetic ; Two-Hybrid System Techniques
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 70
    Publikationsdatum: 2003-09-23
    Beschreibung: Receptors for sex and adrenal steroid hormones are absent from fully sequenced invertebrate genomes and have not been recovered from other invertebrates. Here we report the isolation of an estrogen receptor ortholog from the mollusk Aplysia californica and the reconstruction, synthesis, and experimental characterization of functional domains of the ancestral protein from which all extant steroid receptors (SRs) evolved. Our findings indicate that SRs are extremely ancient and widespread, having diversified from a primordial gene before the origin of bilaterally symmetric animals, and that this ancient receptor had estrogen receptor-like functionality. This gene was lost in the lineage leading to arthropods and nematodes and became independent of hormone regulation in the Aplysia lineage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thornton, Joseph W -- Need, Eleanor -- Crews, David -- 41770/PHS HHS/ -- New York, N.Y. -- Science. 2003 Sep 19;301(5640):1714-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Ecology and Evolutionary Biology, University of Oregon, Eugene, OR 97403, USA. joet@uoregon.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14500980" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Aplysia/chemistry/genetics/*metabolism ; Biological Evolution ; CHO Cells ; Cloning, Molecular ; Cricetinae ; DNA/metabolism ; Estrogens/*metabolism/pharmacology ; *Evolution, Molecular ; Gene Duplication ; Humans ; Ligands ; Likelihood Functions ; Molecular Sequence Data ; Mutation ; *Phylogeny ; Polymerase Chain Reaction ; Protein Structure, Tertiary ; Receptors, Estrogen/chemistry/genetics/isolation & purification/*metabolism ; Receptors, Steroid/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Steroids/metabolism/pharmacology ; Transcription, Genetic ; Transfection
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 71
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-04-26
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maller, James L -- New York, N.Y. -- Science. 2003 Apr 25;300(5619):594-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Pharmacology, University of Colorado School of Medicine, Denver, CO 80262, USA. jim.maller@uchsc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12714732" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adenylyl Cyclase Inhibitors ; Adenylyl Cyclases/metabolism ; Animals ; Cell Membrane/*metabolism ; Cloning, Molecular ; Cyclic AMP/metabolism ; Female ; Fishes/genetics/metabolism ; GTP-Binding Proteins/metabolism ; *MAP Kinase Signaling System ; Mitogen-Activated Protein Kinases/metabolism ; Oocytes/metabolism/physiology ; Ovary/metabolism ; Phylogeny ; Progestins/metabolism ; Receptor Cross-Talk ; Receptors, Cell Surface/chemistry/genetics/*metabolism ; Receptors, Progesterone/chemistry/genetics/*metabolism ; Recombinant Proteins/metabolism ; Signal Transduction
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 72
    Publikationsdatum: 2003-10-25
    Beschreibung: We used a proteomic approach to identify phosphopeptide-binding modules mediating signal transduction events in the DNA damage response pathway. Using a library of partially degenerate phosphopeptides, we identified tandem BRCT (BRCA1 carboxyl-terminal) domains in PTIP (Pax transactivation domain-interacting protein) and in BRCA1 as phosphoserine- or phosphothreonine-specific binding modules that recognize substrates phosphorylated by the kinases ATM (ataxia telangiectasia-mutated) and ATR (ataxia telangiectasia- and RAD3-related) in response to gamma-irradiation. PTIP tandem BRCT domains are responsible for phosphorylation-dependent protein localization into 53BP1- and phospho-H2AX (gamma-H2AX)-containing nuclear foci, a marker of DNA damage. These findings provide a molecular basis for BRCT domain function in the DNA damage response and may help to explain why the BRCA1 BRCT domain mutation Met1775 --〉 Arg, which fails to bind phosphopeptides, predisposes women to breast and ovarian cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Manke, Isaac A -- Lowery, Drew M -- Nguyen, Anhco -- Yaffe, Michael B -- GM60594/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 24;302(5645):636-9.〈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/14576432" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Motifs ; Ataxia Telangiectasia Mutated Proteins ; BRCA1 Protein/*chemistry/*metabolism ; Caffeine/pharmacology ; Calorimetry ; Carrier Proteins/*chemistry/*metabolism ; Cell Cycle Proteins/antagonists & inhibitors/metabolism ; Cell Nucleus/metabolism ; Cytosol/metabolism ; DNA Damage ; DNA-Binding Proteins ; Gamma Rays ; Humans ; Nuclear Proteins/*chemistry/*metabolism ; Peptide Library ; Phosphopeptides/*metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Phosphothreonine/metabolism ; Protein Binding ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; Proteomics ; Signal Transduction ; Tumor Cells, Cultured ; Tumor Suppressor Proteins
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 73
    Publikationsdatum: 2003-02-22
    Beschreibung: Inflammation, trauma, or nerve injury may cause enduring hyperalgesia, an enhanced sensitivity to painful stimuli. Neurons in lamina I of the spinal dorsal horn that express the neurokinin 1 receptor for substance P mediate this abnormal pain sensitivity by an unknown cellular mechanism. We report that in these, but not in other nociceptive lamina I cells, neurokinin 1 receptor-activated signal transduction pathways and activation of low-threshold (T-type) voltage-gated calcium channels synergistically facilitate activity- and calcium-dependent long-term potentiation at synapses from nociceptive nerve fibers. Thereby, memory traces of painful events are retained.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ikeda, Hiroshi -- Heinke, Bernhard -- Ruscheweyh, Ruth -- Sandkuhler, Jurgen -- New York, N.Y. -- Science. 2003 Feb 21;299(5610):1237-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Physiology and Pathophysiology, Heidelberg University, D-69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12595694" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Action Potentials/drug effects ; Animals ; Calcium/metabolism ; Calcium Channels, T-Type/*metabolism ; Excitatory Postsynaptic Potentials ; Hyperalgesia/*physiopathology ; Ion Channel Gating ; *Long-Term Potentiation ; Membrane Potentials ; Nerve Fibers, Unmyelinated/physiology ; Neurokinin-1 Receptor Antagonists ; Nickel/pharmacology ; Patch-Clamp Techniques ; Posterior Horn Cells/metabolism/*physiology ; Quinuclidines/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/metabolism ; Receptors, Neurokinin-1/*metabolism ; Signal Transduction ; Substance P/pharmacology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 74
    Publikationsdatum: 2003-07-12
    Beschreibung: Opiates are widely used analgesics in anesthesiology, but they have serious adverse effects such as depression of breathing. This is caused by direct inhibition of rhythm-generating respiratory neurons in the Pre-Boetzinger complex (PBC) of the brainstem. We report that serotonin 4(a) [5-HT4(a)] receptors are strongly expressed in respiratory PBC neurons and that their selective activation protects spontaneous respiratory activity. Treatment of rats with a 5-HT4 receptor-specific agonist overcame fentanyl-induced respiratory depression and reestablished stable respiratory rhythm without loss of fentanyl's analgesic effect. These findings imply the prospect of a fine-tuned recovery from opioid-induced respiratory depression, through adjustment of intracellular adenosine 3',5'-monophosphate levels through the convergent signaling pathways in neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Manzke, Till -- Guenther, Ulf -- Ponimaskin, Evgeni G -- Haller, Miriam -- Dutschmann, Mathias -- Schwarzacher, Stephan -- Richter, Diethelm W -- New York, N.Y. -- Science. 2003 Jul 11;301(5630):226-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuro- and Sensory Physiology, University of Goettingen, Humboldtallee 23, 37073 Goettingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12855812" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Analgesics, Opioid/*pharmacology/toxicity ; Animals ; Benzimidazoles/pharmacology ; Bicyclo Compounds, Heterocyclic/pharmacology ; Brain Stem/cytology/*metabolism ; Cyclic AMP/metabolism ; Fentanyl/*pharmacology/toxicity ; In Vitro Techniques ; Interneurons/metabolism ; Medulla Oblongata/cytology/metabolism ; Naloxone/pharmacology ; Neurons/*metabolism ; Pain Measurement ; Patch-Clamp Techniques ; RNA, Messenger/genetics/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Neurokinin-1/genetics/metabolism ; Receptors, Opioid, mu/genetics/metabolism ; Receptors, Serotonin/*metabolism ; Receptors, Serotonin, 5-HT4 ; Respiration/*drug effects ; Reverse Transcriptase Polymerase Chain Reaction ; Serotonin Receptor Agonists/pharmacology ; Signal Transduction ; Spinal Cord
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    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 75
    Publikationsdatum: 2003-03-08
    Beschreibung: Photosynthetic organisms adapt to changes in light quality by redistributing light excitation energy between two photosystems through state transition. This reorganization of antenna systems leads to an enhanced photosynthetic yield. Using a genetic approach in Chlamydomonas reinhardtii to dissect the signal transduction pathway of state transition, we identified a chloroplast thylakoid-associated serine-threonine protein kinase, Stt7, that has homologs in land plants. Stt7 is required for the phosphorylation of the major light-harvesting protein (LHCII) and for state transition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Depege, Nathalie -- Bellafiore, Stephane -- Rochaix, Jean-David -- New York, N.Y. -- Science. 2003 Mar 7;299(5612):1572-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Department of Plant Biology, University of Geneva, 30 Quai Ernest Ansermet, 1211 Geneva 4, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12624266" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Algal Proteins/chemistry/genetics/metabolism ; Alleles ; Amino Acid Sequence ; Animals ; Arabidopsis/enzymology/genetics ; Catalytic Domain ; Chlamydomonas reinhardtii/*enzymology/genetics/metabolism ; Chloroplasts/enzymology ; Cosmids ; DNA, Complementary ; Expressed Sequence Tags ; Fluorescence ; Genes ; Genetic Complementation Test ; Light ; Molecular Sequence Data ; Mutation ; Oxidation-Reduction ; Phosphorylation ; Photosynthesis ; Photosynthetic Reaction Center Complex Proteins/*metabolism ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Thylakoids/*enzymology ; Transcription, Genetic ; Transformation, Genetic
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 76
    Publikationsdatum: 2003-12-13
    Beschreibung: Cells exposed to low oxygen concentrations respond by initiating defense mechanisms, including the stabilization of hypoxia-inducible factor (HIF) 1alpha, a transcription factor that upregulates genes such as those involved in glycolysis and angiogenesis. Nitric oxide and other inhibitors of mitochondrial respiration prevent the stabilization of HIF1alpha during hypoxia. In studies of cultured cells, we show that this effect is a result of an increase in prolyl hydroxylase-dependent degradation of HIF1alpha. With the use of Renilla luciferase to detect intracellular oxygen concentrations, we also demonstrate that, upon inhibition of mitochondrial respiration in hypoxia, oxygen is redistributed toward nonrespiratory oxygen-dependent targets such as prolyl hydroxylases so that they do not register hypoxia. Thus, the signaling consequences of hypoxia may be profoundly modified by nitric oxide.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hagen, Thilo -- Taylor, Cormac T -- Lam, Francis -- Moncada, Salvador -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1975-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wolfson Institute for Biomedical Research, University College London, Gower Street, London WC1E 6BT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671307" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Antioxidants/pharmacology ; *Cell Hypoxia ; Cell Line ; *Cell Respiration/drug effects ; Cycloheximide/pharmacology ; Cysteine Proteinase Inhibitors/pharmacology ; HeLa Cells ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit ; Leupeptins/*pharmacology ; Luciferases/metabolism ; Methacrylates ; Mitochondria/*metabolism ; Nitric Oxide/pharmacology/*physiology ; Nitric Oxide Donors/pharmacology ; Oxygen/*metabolism ; Procollagen-Proline Dioxygenase/metabolism ; Protein Synthesis Inhibitors/pharmacology ; Reactive Oxygen Species/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Thiazoles/pharmacology ; Transcription Factors/*metabolism ; Transfection ; Triazenes/pharmacology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 77
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-12-06
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kempermann, Gerd -- Neumann, Harald -- New York, N.Y. -- Science. 2003 Dec 5;302(5651):1689-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuronal Stem Cells Research Group, Max-Delbruck-Centrum fur Molekulare Medizin Berlin-Buch, 13125 Berlin, Germany. gerd.kempermann@mdc-berlin.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14657479" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology ; Brain-Derived Neurotrophic Factor/physiology ; Cell Differentiation ; Hippocampus/cytology/immunology/*physiology/radiation effects ; Immunity, Innate ; Inflammation/drug therapy/*physiopathology ; Inflammation Mediators/physiology ; Interleukin-6/*physiology ; Lipopolysaccharides/pharmacology ; Mice ; Microglia/*physiology ; Minocycline/pharmacology ; Neuronal Plasticity/drug effects ; Neurons/*physiology ; Rats ; Signal Transduction ; Stem Cells/physiology/radiation effects
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 78
    Publikationsdatum: 2003-05-24
    Beschreibung: The phosphorylation of heptahelical receptors by heterotrimeric guanine nucleotide-binding protein (G protein)-coupled receptor kinases (GRKs) is a universal regulatory mechanism that leads to desensitization of G protein signaling and to the activation of alternative signaling pathways. We determined the crystallographic structure of bovine GRK2 in complex with G protein beta1gamma2 subunits. Our results show how the three domains of GRK2-the RGS (regulator of G protein signaling) homology, protein kinase, and pleckstrin homology domains-integrate their respective activities and recruit the enzyme to the cell membrane in an orientation that not only facilitates receptor phosphorylation, but also allows for the simultaneous inhibition of signaling by Galpha and Gbetagamma subunits.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lodowski, David T -- Pitcher, Julie A -- Capel, W Darrell -- Lefkowitz, Robert J -- Tesmer, John J G -- HL16037/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2003 May 23;300(5623):1256-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cellular and Molecular Biology, Department of Chemistry and Biochemistry, University of Texas at Austin, Austin, TX 78712, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12764189" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Cattle ; Cell Membrane/metabolism ; Crystallography, X-Ray ; Cyclic AMP-Dependent Protein Kinases/*chemistry/*metabolism ; *GTP-Binding Protein beta Subunits ; *GTP-Binding Protein gamma Subunits ; Heterotrimeric GTP-Binding Proteins/*chemistry/*metabolism ; Hydrophobic and Hydrophilic Interactions ; Models, Molecular ; Molecular Sequence Data ; Phosphorylation ; Protein Binding ; Protein Conformation ; Protein Structure, Quaternary ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Signal Transduction ; beta-Adrenergic Receptor Kinases
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 79
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-03-01
    Beschreibung: Restriction of the number of calories consumed extends longevity in many organisms. In rodents, caloric restriction decreases the levels of plasma glucose and insulin-like growth factor I (IGF-1) and postpones or attenuates cancer, immunosenescence, and inflammation without irreversible side effects. In organisms ranging from yeast to mice, mutations in glucose or IGF-I-like signaling pathways extend life-span but also cause glycogen or fat accumulation and dwarfism. This information suggests a new category of drugs that could prevent or postpone diseases of aging with few adverse effects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Longo, Valter D -- Finch, Caleb E -- AG 01028/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2003 Feb 28;299(5611):1342-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Andrus Gerontology Center, Division of Biogerontology, and Department of Biological Sciences, University of Southern California, 3715 McClintock Avenue, Los Angeles, CA 90089-0191, USA. vlongo@usc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12610293" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Aging ; Animals ; Biological Evolution ; Caenorhabditis elegans/genetics/physiology ; Caloric Restriction ; Drosophila/genetics/physiology ; Dwarfism/physiopathology ; Gene Expression Regulation ; Glucose/*metabolism ; Growth Hormone/metabolism ; Human Growth Hormone/metabolism ; Humans ; Insulin-Like Growth Factor I/*metabolism ; *Longevity/genetics ; Mice ; Models, Animal ; Mutation ; Signal Transduction ; Yeasts/genetics/physiology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 80
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-11-08
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hatton, Robin D -- Weaver, Casey T -- New York, N.Y. -- Science. 2003 Nov 7;302(5647):993-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14605354" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; CD4-Positive T-Lymphocytes/immunology/*physiology ; CD8-Positive T-Lymphocytes/immunology/*physiology ; DNA-Binding Proteins/metabolism ; GATA3 Transcription Factor ; Gene Expression Regulation ; Interferon-gamma/biosynthesis ; Interleukins/biosynthesis ; Lymphocyte Activation ; Mice ; Mice, Knockout ; Signal Transduction ; T-Box Domain Proteins/genetics/*metabolism ; Th1 Cells/immunology/physiology ; Th2 Cells/immunology/physiology ; Trans-Activators/metabolism ; Transcription Factors/genetics/*metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 81
    Publikationsdatum: 2003-01-11
    Beschreibung: Most gastrointestinal stromal tumors (GISTs) have activating mutations in the KIT receptor tyrosine kinase, and most patients with GISTs respond well to Gleevec, which inhibits KIT kinase activity. Here we show that approximately 35% (14 of 40) of GISTs lacking KIT mutations have intragenic activation mutations in the related receptor tyrosine kinase, platelet-derived growth factor receptor alpha (PDGFRA). Tumors expressing KIT or PDGFRA oncoproteins were indistinguishable with respect to activation of downstream signaling intermediates and cytogenetic changes associated with tumor progression. Thus, KIT and PDGFRA mutations appear to be alternative and mutually exclusive oncogenic mechanisms in GISTs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heinrich, Michael C -- Corless, Christopher L -- Duensing, Anette -- McGreevey, Laura -- Chen, Chang-Jie -- Joseph, Nora -- Singer, Samuel -- Griffith, Diana J -- Haley, Andrea -- Town, Ajia -- Demetri, George D -- Fletcher, Christopher D M -- Fletcher, Jonathan A -- New York, N.Y. -- Science. 2003 Jan 31;299(5607):708-10. Epub 2003 Jan 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Department of Pathology, Oregon Health & Science University Cancer Institute and Portland VA Medical Center, Portland, OR 97201, USA. heinrich@ohsu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12522257" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; CHO Cells ; Chromosome Aberrations ; Cricetinae ; DNA-Binding Proteins/metabolism ; Enzyme Activation ; Exons ; Gastrointestinal Neoplasms/*genetics/metabolism ; Humans ; Karyotyping ; Mitogen-Activated Protein Kinases/metabolism ; Mutation ; Oncogenes ; Phosphorylation ; *Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Proto-Oncogene Proteins c-kit/*genetics/metabolism ; Receptor, Platelet-Derived Growth Factor alpha/*genetics/metabolism ; STAT1 Transcription Factor ; STAT3 Transcription Factor ; Signal Transduction ; Trans-Activators/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 82
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-06-07
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carr, Antony M -- New York, N.Y. -- Science. 2003 Jun 6;300(5625):1512-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genome Damage and Stability Centre, University of Sussex, Falmer, Sussex BN1 9RQ, UK. a.m.carr@sussex.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12791969" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adaptor Proteins, Signal Transducing ; Animals ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins/*metabolism ; DNA/metabolism ; *DNA Damage ; DNA Repair ; DNA Replication ; DNA, Fungal/metabolism ; DNA, Single-Stranded/*metabolism ; DNA-Binding Proteins/*metabolism ; *Exodeoxyribonucleases ; Humans ; Nuclear Proteins ; Nucleic Acid Conformation ; Phosphoproteins/*metabolism ; Phosphorylation ; *Protein-Serine-Threonine Kinases ; Replication Protein A ; Saccharomyces cerevisiae/metabolism ; Saccharomyces cerevisiae Proteins/metabolism ; Signal Transduction
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 83
    Publikationsdatum: 2003-03-29
    Beschreibung: The human gut is colonized with a vast community of indigenous microorganisms that help shape our biology. Here, we present the complete genome sequence of the Gram-negative anaerobe Bacteroides thetaiotaomicron, a dominant member of our normal distal intestinal microbiota. Its 4779-member proteome includes an elaborate apparatus for acquiring and hydrolyzing otherwise indigestible dietary polysaccharides and an associated environment-sensing system consisting of a large repertoire of extracytoplasmic function sigma factors and one- and two-component signal transduction systems. These and other expanded paralogous groups shed light on the molecular mechanisms underlying symbiotic host-bacterial relationships in our intestine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, Jian -- Bjursell, Magnus K -- Himrod, Jason -- Deng, Su -- Carmichael, Lynn K -- Chiang, Herbert C -- Hooper, Lora V -- Gordon, Jeffrey I -- DK30292/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2003 Mar 28;299(5615):2074-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12663928" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adult ; Bacterial Outer Membrane Proteins/genetics/metabolism ; Bacterial Proteins/genetics/physiology ; Bacteroides/*genetics/physiology ; Biological Evolution ; Carbohydrate Metabolism ; Chromosomes, Bacterial/genetics ; Gene Expression Regulation, Bacterial ; Genes, Bacterial ; *Genome, Bacterial ; Humans ; Interspersed Repetitive Sequences ; Intestines/*microbiology ; Physical Chromosome Mapping ; Polysaccharides/metabolism ; Proteome ; *Sequence Analysis, DNA ; Sigma Factor/genetics/physiology ; Signal Transduction ; *Symbiosis
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 84
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-04-19
    Beschreibung: Insulin receptors are abundant in the central nervous system, but their roles remain elusive. Here we show that the insulin receptor functions in axon guidance. The Drosophila insulin receptor (DInR) is required for photoreceptor-cell (R-cell) axons to find their way from the retina to the brain during development of the visual system. DInR functions as a guidance receptor for the adapter protein Dock/Nck. This function is independent of Chico, the Drosophila insulin receptor substrate (IRS) homolog.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Song, Jianbo -- Wu, Lingling -- Chen, Zun -- Kohanski, Ronald A -- Pick, Leslie -- New York, N.Y. -- Science. 2003 Apr 18;300(5618):502-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Brookdale Department for Molecular, Cell, and Developmental Biology, Mount Sinai School of Medicine, One Gustave Levy Place, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12702880" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adaptor Proteins, Signal Transducing ; Animals ; Axons/*physiology ; Binding Sites ; Blotting, Western ; Brain/cytology/growth & development ; Carrier Proteins/genetics/immunology/metabolism/*physiology ; Cell Differentiation ; Cell Size ; Drosophila/genetics/*growth & development/physiology ; Drosophila Proteins/genetics/metabolism ; Eye/cytology/growth & development ; Female ; Growth Cones/physiology ; Insulin Receptor Substrate Proteins ; *Intracellular Signaling Peptides and Proteins ; Male ; Mutation ; Nerve Tissue Proteins/chemistry/genetics/metabolism ; Photoreceptor Cells, Invertebrate/cytology/*physiology ; Precipitin Tests ; Protein-Tyrosine Kinases/genetics/immunology/metabolism/*physiology ; *Receptor Protein-Tyrosine Kinases ; Receptor, Insulin/genetics/immunology/metabolism/*physiology ; Retina/cytology/growth & development ; Signal Transduction ; Two-Hybrid System Techniques ; Visual Pathways ; src Homology Domains
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 85
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-10-25
    Beschreibung: Interferon-gamma (IFN-gamma) provides an essential component of immunity to tuberculosis by activating infected host macrophages to directly inhibit the replication of Mycobacterium tuberculosis (Mtb). IFN-gamma-inducible nitric oxide synthase 2 (NOS2) is considered a principal effector mechanism, although other pathways may also exist. Here, we identify one member of a newly emerging 47-kilodalton (p47) guanosine triphosphatase family, LRG-47, that acts independently of NOS2 to protect against disease. Mice lacking LRG-47 failed to control Mtb replication, unlike those missing the related p47 guanosine triphosphatases IRG-47 or IGTP. Defective bacterial killing in IFN-gamma-activated LRG-47-/- macrophages was associated with impaired maturation of Mtb-containing phagosomes, vesicles that otherwise recruited LRG-47 in wild-type cells. Thus, LRG-47 may serve as a critical vacuolar trafficking component used to dispose of intracellular pathogens like Mtb.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉MacMicking, John D -- Taylor, Gregory A -- McKinney, John D -- R01 A1051702/PHS HHS/ -- New York, N.Y. -- Science. 2003 Oct 24;302(5645):654-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Infection Biology, Rockefeller University, 1230 York Avenue, New York, NY 10021, USA. macmicj@mail.rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14576437" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cells, Cultured ; Computational Biology ; Disease Susceptibility ; Female ; GTP Phosphohydrolases/genetics/physiology ; GTP-Binding Proteins/genetics/*physiology ; Hydrogen-Ion Concentration ; Immunity, Innate ; Interferon-gamma/*immunology ; Macrophage Activation ; Macrophages/immunology/metabolism ; Macrophages, Alveolar/immunology/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mutation ; Mycobacterium tuberculosis/*growth & development ; Nitric Oxide Synthase/genetics/metabolism ; Nitric Oxide Synthase Type II ; Oligonucleotide Array Sequence Analysis ; Phagosomes/microbiology/physiology ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Tuberculosis/*immunology/microbiology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 86
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-07-26
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Engelberg-Kulka, Hanna -- Hazan, Ronen -- New York, N.Y. -- Science. 2003 Jul 25;301(5632):467-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Hebrew University-Hadassah Medical School, Jerusalem 91120, Israel. hanita@cc.huji.ac.il〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12881556" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adenosine Triphosphate/metabolism ; Bacillus subtilis/genetics/metabolism/*physiology ; Bacterial Proteins/genetics/*metabolism ; Bacteriolysis ; *Gene Expression Regulation, Bacterial ; Genes, Bacterial ; Models, Biological ; Mutation ; *Operon ; Sigma Factor/genetics/metabolism ; Signal Transduction ; Spores, Bacterial/*physiology ; Transcription Factors/genetics/metabolism ; Transcription, Genetic
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 87
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-09-23
    Beschreibung: Neuroscientists have long sought to elucidate the molecular underpinnings of the memories needed to learn, for example, a motor task. In his Perspective, Linden discusses new work (Koekkoek et al.) suggesting that long-term depression in Purkinje cells mediated by protein kinase C signaling is responsible for motor memory in a task called associative eyelid conditioning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Linden, David J -- New York, N.Y. -- Science. 2003 Sep 19;301(5640):1682-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. dlinden@jhmi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14500971" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Association Learning ; Blinking ; *Conditioning, Eyelid ; Enzyme Activation ; Hippocampus/physiology ; *Long-Term Synaptic Depression ; *Memory ; Mice ; Mice, Transgenic ; Nerve Fibers/physiology ; Phosphorylation ; Protein Kinase C/metabolism ; Purkinje Cells/*physiology ; Receptors, AMPA/metabolism ; Signal Transduction
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 88
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-12-04
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Li -- Lenardo, Michael J -- New York, N.Y. -- Science. 2003 Nov 28;302(5650):1515-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14645834" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Adaptor Proteins, Signal Transducing ; Animals ; Apoptosis ; B-Lymphocytes/*immunology/metabolism ; Caspases ; Cell Nucleus/metabolism ; Cytokines/metabolism ; Gene Expression Regulation ; I-kappa B Kinase ; Lymphocyte Activation ; Lymphoma, B-Cell, Marginal Zone/chemistry/genetics/*metabolism ; Mice ; NF-kappa B/*metabolism ; Neoplasm Proteins/chemistry/genetics/*metabolism ; Phosphorylation ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/metabolism ; Receptors, Antigen, B-Cell/metabolism ; Receptors, Antigen, T-Cell/metabolism ; Signal Transduction ; T-Lymphocytes/*immunology/metabolism ; Translocation, Genetic
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 89
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2003-12-04
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Savill, John -- Gregory, Chris -- Haslett, Chris -- New York, N.Y. -- Science. 2003 Nov 28;302(5650):1516-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Centre for Inflammation Research, University of Edinburgh College of Medicine and Veterinary Medicine, Edinburgh EH8 9AG, UK. j.savill@ed.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14645835" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Apoptosis ; Autoimmunity ; Brain/abnormalities/embryology ; Caenorhabditis elegans/embryology/metabolism ; Caenorhabditis elegans Proteins/metabolism ; Cell Division ; Cytoskeleton/metabolism ; Embryo, Nonmammalian/cytology/metabolism ; Embryonic Development ; Embryonic and Fetal Development ; Inflammation ; Lung/embryology/metabolism ; Macrophages/physiology ; Mice ; Phagocytes/*physiology ; *Phagocytosis ; Phenotype ; Phosphatidylserines/metabolism ; Receptors, Cell Surface/*metabolism ; Respiratory Insufficiency/etiology ; Signal Transduction
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 90
    Publikationsdatum: 2003-11-15
    Beschreibung: A subset of nonsteroidal anti-inflammatory drugs (NSAIDs) has been shown to preferentially reduce the secretion of the highly amyloidogenic, 42-residue amyloid-beta peptide Abeta42. We found that Rho and its effector, Rho-associated kinase, preferentially regulated the amount of Abeta42 produced in vitro and that only those NSAIDs effective as Rho inhibitors lowered Abeta42. Administration of Y-27632, a selective Rock inhibitor, also preferentially lowered brain levels of Abeta42 in a transgenic mouse model of Alzheimer's disease. Thus, the Rho-Rock pathway may regulate amyloid precursor protein processing, and a subset of NSAIDs can reduce Abeta42 through inhibition of Rho activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Yan -- Su, Yuan -- Li, Baolin -- Liu, Feng -- Ryder, John W -- Wu, Xin -- Gonzalez-DeWhitt, Patricia A -- Gelfanova, Valentina -- Hale, John E -- May, Patrick C -- Paul, Steven M -- Ni, Binhui -- New York, N.Y. -- Science. 2003 Nov 14;302(5648):1215-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience Discovery Research and Bioresearch Technologies and Proteins, Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, IN 46285, USA. zhou_yan_yz@lilly.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14615541" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amides/pharmacology ; Amyloid Precursor Protein Secretases ; Amyloid beta-Peptides/*metabolism ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/*pharmacology ; Aspartic Acid Endopeptidases ; Brain/drug effects/metabolism ; Cell Line, Tumor ; Endopeptidases/metabolism ; Enzyme Inhibitors/pharmacology ; Guanosine Triphosphate/metabolism ; Humans ; Ibuprofen/pharmacology ; Intracellular Signaling Peptides and Proteins ; Mice ; Mice, Transgenic ; Peptide Fragments/*metabolism ; Polyisoprenyl Phosphates/pharmacology ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; Pyridines/pharmacology ; Sesquiterpenes ; Signal Transduction ; Sulindac/*analogs & derivatives/pharmacology ; Transfection ; rho GTP-Binding Proteins/*antagonists & inhibitors/metabolism ; rho-Associated Kinases ; rhoA GTP-Binding Protein/genetics/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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