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  • Signal Transduction  (148)
  • American Association for the Advancement of Science (AAAS)  (148)
  • Nature Publishing Group
  • Wiley
  • 2000-2004  (109)
  • 1995-1999  (39)
  • 2001  (109)
  • 1995  (39)
Collection
Publisher
  • American Association for the Advancement of Science (AAAS)  (148)
  • Nature Publishing Group
  • Wiley
Years
  • 2000-2004  (109)
  • 1995-1999  (39)
Year
  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2001-02-24
    Description: Although the development of the inner ear has been a favorite subject for biologists to study, it is not yet clear exactly which molecules are involved in the induction of the otic placode, the plug of embryonic ectoderm that will become the inner ear. In his Perspective, Graham takes us on an inner ear odyssey, explaining how the signaling molecules FGF-19 and Wnt-8c cooperate to induce formation of the otic placode (Ladher et al.).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Graham, A -- New York, N.Y. -- Science. 2000 Dec 8;290(5498):1904-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Centre for Developmental Neurobiology, Kings College London, London SE1 1UL, UK. anthony.graham@kcl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11187047" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Central Nervous System/embryology/metabolism ; Chick Embryo ; Coculture Techniques ; Culture Techniques ; Ear, Inner/*embryology/metabolism ; Ectoderm/metabolism ; *Embryonic Induction ; Fibroblast Growth Factors/genetics/*metabolism ; Gene Expression ; Mesoderm/metabolism ; Proto-Oncogene Proteins/genetics/metabolism ; Signal Transduction ; Wnt Proteins ; *Zebrafish Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2001-02-24
    Description: The elegant architecture of photoreceptor cells in the retina is dependent on organization of the actin cytoskeleton during eye development. But what drives this organization? In an equally elegant Perspective, Colley explains new findings in fruit flies (Chang and Ready) that point to the photopigment rhodopsin and its signaling molecule the Rho GTPase Drac1 as the orchestrators of actin organization and the consequent assembly of the sensory membrane in the photoreceptor cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Colley, N J -- R01 EY008768/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 8;290(5498):1902-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ophthalmology and Visual Sciences, University of Wisconsin, Madison, WI 53706, USA. njcolley@facstaff.wisc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11187046" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/metabolism/*ultrastructure ; Amino Acid Motifs ; Animals ; Drosophila ; *Drosophila Proteins ; Enzyme Activation ; Humans ; Models, Biological ; Morphogenesis ; Photoreceptor Cells, Invertebrate/cytology/*growth & ; development/metabolism/*ultrastructure ; Retina/growth & development/ultrastructure ; Retinitis Pigmentosa/genetics/metabolism/pathology ; Rhodopsin/chemistry/*metabolism ; Signal Transduction ; rac GTP-Binding Proteins/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2001-02-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kennedy, D -- New York, N.Y. -- Science. 2000 Oct 27;290(5492):709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11184194" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aplysia/physiology ; Congresses as Topic ; Dopamine/physiology ; Learning ; Neurons/physiology ; *Neurosciences ; Neurotransmitter Agents/physiology ; *Nobel Prize ; *Publishing ; Signal Transduction ; Societies, Scientific ; Synapses/physiology ; Synaptic Transmission
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2001-05-31
    Description: Spatially controlled polymerization of actin is at the origin of cell motility and is responsible for the formation of cellular protrusions like lamellipodia. The pathogens Listeria monocytogenes and Shigella flexneri, which undergo actin-based propulsion, are acknowledged models of the leading edge of lamellipodia. Actin-based motility of the bacteria or of functionalized microspheres can be reconstituted in vitro from only five pure proteins. Movement results from the regulated site-directed treadmilling of actin filaments, consistent with observations of actin dynamics in living motile cells and with the biochemical properties of the components of the synthetic motility medium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pantaloni, D -- Le Clainche, C -- Carlier, M F -- New York, N.Y. -- Science. 2001 May 25;292(5521):1502-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dynamique du Cytosquelette, Laboratoire d'Enzymologie et Biochimie Structurales, CNRS, Avenue de la Terrasse, 91198 Gif-sur-Yvette, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11379633" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Depolymerizing Factors ; Actin-Related Protein 2 ; Actin-Related Protein 3 ; Actins/metabolism/*physiology ; Adenosine Triphosphate/metabolism ; Animals ; Bacterial Proteins/metabolism ; Biopolymers ; *Cell Movement ; *Cytoskeletal Proteins ; Destrin ; Listeria monocytogenes/*physiology ; Microfilament Proteins/metabolism ; Models, Biological ; Movement ; Proteins/metabolism ; Pseudopodia/physiology ; Signal Transduction ; Wiskott-Aldrich Syndrome Protein
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2001-12-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 2001 Dec 21;294(5551):2453.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11752547" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks/physiology ; Circadian Rhythm/drug effects/*physiology ; Cricetinae ; Darkness ; Hypothalamus/*metabolism ; Light ; Mice ; *Motor Activity/drug effects ; Mutation ; Neurons/*metabolism ; Receptor, Epidermal Growth Factor/genetics/*metabolism ; Retinal Ganglion Cells/metabolism ; Signal Transduction ; Suprachiasmatic Nucleus/*metabolism ; Transforming Growth Factor alpha/*metabolism/pharmacology
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2001-11-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barres, B A -- Smith, S J -- New York, N.Y. -- Science. 2001 Nov 9;294(5545):1296-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Stanford University School of Medicine, Fairchild Science Building, Stanford, CA 94305-5125, USA. barres@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11701918" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoproteins E/metabolism/pharmacology ; Astrocytes/*metabolism ; Brain/metabolism ; Cells, Cultured ; Cholesterol/*metabolism/pharmacology ; Coculture Techniques ; Mice ; Neuroglia/metabolism ; Neuronal Plasticity ; Neurons/metabolism/*physiology ; Recombinant Proteins/pharmacology ; Signal Transduction ; Synapses/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2001-11-10
    Description: We describe a molecular switch based on the controlled methylation of nucleosome and the transcriptional cofactors, the CREB-binding proteins (CBP)/p300. The CBP/p300 methylation site is localized to an arginine residue that is essential for stabilizing the structure of the KIX domain, which mediates CREB recruitment. Methylation of KIX by coactivator-associated arginine methyltransferase 1 (CARM1) blocks CREB activation by disabling the interaction between KIX and the kinase inducible domain (KID) of CREB. Thus, CARM1 functions as a corepressor in cyclic adenosine monophosphate signaling pathway via its methyltransferase activity while acting as a coactivator for nuclear hormones. These results provide strong in vivo and in vitro evidence that histone methylation plays a key role in hormone-induced gene activation and define cofactor methylation as a new regulatory mechanism in hormone signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, W -- Chen, H -- Du, K -- Asahara, H -- Tini, M -- Emerson, B M -- Montminy, M -- Evans, R M -- 9R01DK57978/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2001 Dec 21;294(5551):2507-11. Epub 2001 Nov 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Expression Laboratory, Department of Biological Chemistry, University of California Davis Cancer Center/Basic Science, Sacramento, CA 95817, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11701890" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/metabolism ; Amino Acid Sequence ; Animals ; Apoptosis ; Cell Line ; Cyclic AMP Response Element-Binding Protein/metabolism ; Dimerization ; E1A-Associated p300 Protein ; *Gene Expression Regulation ; Genes, Reporter ; Histone Acetyltransferases ; Histones/metabolism ; Methylation ; Molecular Sequence Data ; Nerve Growth Factor/pharmacology ; Nuclear Proteins/chemistry/*metabolism ; PC12 Cells ; Protein Structure, Tertiary ; Protein-Arginine N-Methyltransferases/*metabolism ; Rats ; Receptors, Retinoic Acid/*metabolism ; Recombinant Fusion Proteins/metabolism ; Retinoid X Receptors ; *Saccharomyces cerevisiae Proteins ; Signal Transduction ; Somatostatin/genetics ; Trans-Activators/chemistry/*metabolism ; Transcription Factors/metabolism ; *Transcription, Genetic ; Transcriptional Activation ; Transfection ; Tretinoin/metabolism/pharmacology
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  • 8
    Publication Date: 2001-04-17
    Description: A critical step in the infectious cycle of Leishmania is the differentiation of parasites within the sand fly vector to the highly infective metacyclic promastigote stage. Here, we establish tetrahydrobiopterin (H4B) levels as an important factor controlling the extent of metacyclogenesis. H4B levels decline substantially during normal development, and genetic or nutritional manipulations showed that low H4B caused elevated metacyclogenesis. Mutants lacking pteridine reductase 1 (PTR1) had low levels of H4B, remained infectious to mice, and induced larger cutaneous lesions (hypervirulence). Thus, the control of pteridine metabolism has relevance to the mechanism of Leishmania differentiation and the limitation of virulence during evolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cunningham, M L -- Titus, R G -- Turco, S J -- Beverley, S M -- AI21903/AI/NIAID NIH HHS/ -- AI31078/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2001 Apr 13;292(5515):285-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology, 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/11303103" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biopterin/*analogs & derivatives/*metabolism/pharmacology ; Carrier Proteins/genetics/metabolism ; Chromatography, High Pressure Liquid ; Folic Acid/metabolism ; Genes, Protozoan ; Glycosphingolipids/analysis ; Leishmania major/genetics/*growth & development/*metabolism/pathogenicity ; Leishmaniasis, Cutaneous/*parasitology ; *Membrane Transport Proteins ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Mutation ; Oxidoreductases/genetics/metabolism ; *Protozoan Proteins ; Signal Transduction ; Virulence
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  • 9
    Publication Date: 2001-12-12
    Description: The mouse small intestinal epithelium consists of four principal cell types deriving from one multipotent stem cell: enterocytes, goblet, enteroendocrine, and Paneth cells. Previous studies showed that Math1, a basic helix-loop-helix (bHLH) transcription factor, is expressed in the gut. We find that loss of Math1 leads to depletion of goblet, enteroendocrine, and Paneth cells without affecting enterocytes. Colocalization of Math1 with Ki-67 in some proliferating cells suggests that secretory cells (goblet, enteroendocrine, and Paneth cells) arise from a common progenitor that expresses Math1, whereas absorptive cells (enterocytes) arise from a progenitor that is Math1-independent. The continuous rapid renewal of these cells makes the intestinal epithelium a model system for the study of stem cell regeneration and lineage commitment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Q -- Bermingham, N A -- Finegold, M J -- Zoghbi, H Y -- New York, N.Y. -- Science. 2001 Dec 7;294(5549):2155-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, 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/11739954" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Basic Helix-Loop-Helix Transcription Factors ; *Cell Differentiation ; Cell Division ; Cell Lineage ; Enterocytes/cytology ; Enteroendocrine Cells/cytology ; Gene Expression ; Goblet Cells/cytology ; Helix-Loop-Helix Motifs ; Heterozygote ; Homeodomain Proteins/metabolism ; Intestinal Mucosa/*cytology/embryology/*metabolism ; Intestine, Large/cytology/embryology ; Intestine, Small/cytology/embryology ; Ki-67 Antigen/analysis ; Membrane Proteins/metabolism ; Mice ; Paneth Cells/cytology/metabolism ; Protein Precursors/analysis ; Receptors, Notch ; Signal Transduction ; Stem Cells/*cytology ; Transcription Factors/*genetics/*metabolism
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  • 10
    Publication Date: 2001-03-17
    Description: The role of NF-kappaB-inducing kinase (NIK) in cytokine signaling remains controversial. To identify the physiologic functions of NIK, we disrupted the NIK locus by gene targeting. Although NIK-/- mice displayed abnormalities in both lymphoid tissue development and antibody responses, NIK-/- cells manifested normal NF-kappaB DNA binding activity when treated with a variety of cytokines, including tumor necrosis factor (TNF), interleukin-1 (IL-1), and lymphotoxin-beta (LTbeta). However, NIK was selectively required for gene transcription induced through ligation of LTbeta receptor but not TNF receptors. These results reveal that NIK regulates the transcriptional activity of NF-kappaB in a receptor-restricted manner.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yin, L -- Wu, L -- Wesche, H -- Arthur, C D -- White, J M -- Goeddel, D V -- Schreiber, R D -- New York, N.Y. -- Science. 2001 Mar 16;291(5511):2162-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Immunology, Department of Pathology and Immunology, 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/11251123" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; B-Lymphocytes/metabolism ; Cells, Cultured ; DNA/metabolism ; Fibroblasts/metabolism ; Gene Targeting ; Genes, Reporter ; Interleukin-1/metabolism/pharmacology ; Ligands ; Lymphoid Tissue/abnormalities ; Lymphotoxin beta Receptor ; Mice ; Mice, Inbred C57BL ; NF-kappa B/genetics/*metabolism ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Receptors, Tumor Necrosis Factor/immunology/*metabolism ; Signal Transduction ; *Transcription, Genetic ; Tumor Necrosis Factor-alpha/metabolism/pharmacology
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