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  • Signal Transduction  (84)
  • American Association for the Advancement of Science (AAAS)  (84)
  • American Physical Society (APS)
  • Annual Reviews
  • Blackwell Publishing Ltd
  • De Gruyter
  • Institute of Physics
  • Molecular Diversity Preservation International
  • 2020-2024
  • 2005-2009  (69)
  • 1990-1994  (15)
  • 2007  (69)
  • 1990  (15)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (84)
  • American Physical Society (APS)
  • Annual Reviews
  • Blackwell Publishing Ltd
  • De Gruyter
    • +
Years
  • 2020-2024
  • 2005-2009  (69)
  • 1990-1994  (15)
Year
  • 1
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    The dominant W42 spotting phenotype results from a missense mutation in the c-kit receptor kinase (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-01-12
    Description: The murine white spotting locus (W) is allelic with the proto-oncogene c-kit, which encodes a transmembrane tyrosine protein kinase receptor for an unknown ligand. Mutations at the W locus affect various aspects of hematopoiesis and the proliferation and migration of primordial germ cells and melanoblasts during development to varying degrees of severity. The W42 mutation has a particularly severe effect in both the homozygous and the heterozygous states. The molecular basis of the W42 mutation was determined. The c-kit protein products in homozygous mutant mast cells were expressed normally but displayed a defective tyrosine kinase activity in vitro. Nucleotide sequence analysis of mutant complementary DNAs revealed a missense mutation that replaces aspartic acid with asparagine at position 790 in the c-kit protein product. Aspartic acid-790 is a conserved residue in all protein kinases. These results provide an explanation for the dominant nature of the W42 mutation and provide insight into the mechanism of c-kit-mediated signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tan, J C -- Nocka, K -- Ray, P -- Traktman, P -- Besmer, P -- P01-CA-16599/CA/NCI NIH HHS/ -- R01-CA-32926/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Jan 12;247(4939):209-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Program, Sloan Kettering Institute, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1688471" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cells, Cultured ; DNA/genetics ; Gene Expression ; Homozygote ; Liver/analysis/cytology/embryology ; Mast Cells/metabolism ; Mice ; Molecular Sequence Data ; *Mutation ; *Phenotype ; Polymerase Chain Reaction ; Protein-Tyrosine Kinases/*genetics ; Proto-Oncogene Proteins/*genetics ; Proto-Oncogene Proteins c-kit ; RNA/analysis ; Receptors, Cell Surface/genetics ; Signal Transduction
    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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    PECAM-1 (CD31) cloning and relation to adhesion molecules of the immunoglobulin gene superfamily (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-03-09
    Description: An antibody to a platelet integral membrane glycoprotein was found to cross-react with the previously identified CD31 myelomonocytic differentiation antigen and with hec7, an endothelial cell protein that is enriched at intercellular junctions. This antibody identified a complementary DNA clone from an endothelial cell library. The 130-kilodalton translated sequence contained six extracellular immunoglobulin (Ig)-like domains and was most similar to the cell adhesion molecule (CAM) subgroup of the Ig superfamily. This is the only known member of the CAM family on platelets. Its cell surface distribution suggests participation in cellular recognition events.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Newman, P J -- Berndt, M C -- Gorski, J -- White, G C 2nd -- Lyman, S -- Paddock, C -- Muller, W A -- HL-40926/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Mar 9;247(4947):1219-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Blood Center of Southeastern Wisconsin, Milwaukee 53233.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1690453" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antibodies, Monoclonal ; Antigens, CD31 ; Antigens, Differentiation, Myelomonocytic/*genetics ; Cell Adhesion Molecules/*genetics ; *Cloning, Molecular ; DNA/analysis ; Endothelium, Vascular/analysis/immunology ; Epitopes/immunology ; *Genes, Immunoglobulin ; Humans ; Immunoblotting ; Immunoglobulins ; Immunosorbent Techniques ; Molecular Sequence Data ; Platelet Membrane Glycoproteins/immunology ; Protein Conformation ; Repetitive Sequences, Nucleic Acid ; Sequence Homology, Nucleic Acid ; Signal Transduction
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Common modifications of trimeric G proteins and ras protein: involvement of polyisoprenylation (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-13
    Description: The heterotrimeric guanine nucleotide-binding regulatory proteins act at the inner surface of the plasma membrane to relay information from cell surface receptors to effectors inside the cell. These G proteins are not integral membrane proteins, yet are membrane associated. The processing and function of the gamma subunit of the yeast G protein involved in mating-pheromone signal transduction was found to be affected by the same mutations that block ras processing. The nature of these mutations implied that the gamma subunit was polyisoprenylated and that this modification was necessary for membrane association and biological activity. A microbial screen was developed for pharmacological agents that inhibit polyisoprenylation and that have potential application in cancer therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finegold, A A -- Schafer, W R -- Rine, J -- Whiteway, M -- Tamanoi, F -- CA 41996/CA/NCI NIH HHS/ -- GM 07183/GM/NIGMS NIH HHS/ -- GM 35827/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jul 13;249(4965):165-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, University of Chicago, IL 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1695391" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cell Membrane/metabolism ; Cloning, Molecular ; Epitopes/genetics ; GTP-Binding Proteins/genetics/*metabolism ; Hemagglutinins, Viral/immunology ; Lovastatin/pharmacology ; Mevalonic Acid/pharmacology ; Molecular Sequence Data ; Mutation ; Oncogene Protein p21(ras)/genetics/*metabolism ; Orthomyxoviridae/immunology ; Protein Processing, Post-Translational ; Saccharomyces cerevisiae/*genetics/metabolism ; Signal Transduction ; Suppression, Genetic
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Autophosphorylation of protein kinase C at three separated regions of its primary sequence (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-27
    Description: The major autophosphorylation sites of the rat beta II isozyme of protein kinase C were identified. The modified threonine and serine residues were found in the amino-terminal peptide, the carboxyl-terminal tail, and the hinge region between the regulatory lipid-binding domain and the catalytic kinase domain. Because this autophosphorylation follows an intrapeptide mechanism, extraordinary flexibility of the protein is necessary to phosphorylate the three regions. Comparison of the sequences surrounding the modified residues showed no obvious recognition motif nor any similarity to substrate phosphorylation sites, suggesting that proximity to the active site may be the primary criterion for their phosphorylation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flint, A J -- Paladini, R D -- Koshland, D E Jr -- DK09765/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Jul 27;249(4967):408-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2377895" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Brain/enzymology ; Cloning, Molecular ; Isoenzymes/genetics/*metabolism ; Molecular Sequence Data ; Peptide Fragments/isolation & purification/metabolism ; Phosphorylation ; Protein Conformation ; Protein Kinase C/genetics/*metabolism ; Rats ; Recombinant Proteins/metabolism ; Signal Transduction ; Trypsin
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Evidence for a novel thioredoxin-like catalytic property of gonadotropic hormones (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-01-05
    Description: It has been proposed that dithiol-disulfide interchange and oxidation-reduction reactions may play a role in hormone-induced receptor activation. Inspection of the sequences of the gonadotropic hormones revealed a homologous tetrapeptide (Cys-Gly-Pro-Cys) between the beta subunit of lutropin (LH) and the active site of thioredoxin (TD). The beta subunit of follitropin (FSH) has a similar sequence (Cys-Gly-Lys-Cys). Thioredoxin is a ubiquitous protein serving as an electron donor for ribonucleotide reductase, but it also exhibits disulfide isomerase activity. The catalytic activity of TD was assayed by its ability to reactivate reduced and denatured ribonuclease. In this assay, the purified ovine FSH and bovine LH preparations tested were approximately 60 and approximately 300 times, respectively, as active as TD on a molar basis. This heretofore unsuspected catalytic property of FSH and LH may be important in understanding their mechanism of receptor activation and signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boniface, J J -- Reichert, L E Jr -- HD-13938/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1990 Jan 5;247(4938):61-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Albany Medical College, NY 12208.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2104678" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Bacterial Proteins/*metabolism ; Follicle Stimulating Hormone/*metabolism ; Humans ; Luteinizing Hormone/*metabolism ; Molecular Sequence Data ; Oxidation-Reduction ; Protein Conformation ; Receptors, FSH/metabolism ; Receptors, LH/metabolism ; Ribonucleases/metabolism ; Signal Transduction ; Thioredoxins/*metabolism
    Print ISSN: 0036-8075
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  • 6
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    Structural mutations of the T cell receptor zeta chain and its role in T cell activation (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-13
    Description: T cell hybridomas that express zeta zeta, but not zeta eta, dimers in their T cell receptors (TCRs) produce interleukin-2 (IL-2) and undergo an inhibition of spontaneous growth when activated by antigen, antibodies to the receptor, or antibodies to Thy-1. Hybridomas without zeta and eta were reconstituted with mutated zeta chains. Cytoplasmic truncations of up to 40% of the zeta molecule reconstituted normal surface assembly of TCRs, but antigen-induced IL-2 secretion and growth inhibition were lost. In contrast, cross-linking antibodies to the TCR activated these cells. A point mutation conferred the same signaling phenotype as did the truncations and caused defective antigen-induced tyrosine kinase activation. Thus zeta allows the binding of antigen/major histocompatibility complex (MHC) to alpha beta to effect TCR signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frank, S J -- Niklinska, B B -- Orloff, D G -- Mercep, M -- Ashwell, J D -- Klausner, R D -- New York, N.Y. -- Science. 1990 Jul 13;249(4965):174-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2371564" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cross-Linking Reagents ; Dose-Response Relationship, Immunologic ; Hybridomas ; Immunity, Cellular ; Immunoblotting ; Interleukin-2/*biosynthesis ; Ligands ; *Lymphocyte Activation ; Major Histocompatibility Complex ; Mice ; Molecular Sequence Data ; Mutation ; Peptide Fragments/genetics/*immunology ; Precipitin Tests ; Receptors, Antigen, T-Cell/genetics/*immunology ; Signal Transduction ; T-Lymphocytes/*immunology ; Transfection
    Print ISSN: 0036-8075
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  • 7
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    Activation of polyphosphoinositide hydrolysis in T cells by H-2 alloantigen but not MLS determinants (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-13
    Description: Murine minor lymphocyte-stimulating (Mls) determinants are cell surface antigens that stimulate strong primary T cell responses; the responding T cells display restricted T cell receptor (TCR) V beta gene usage. Interaction of T cells with mitogens or major histocompatibility complex (MHC) antigens activated the polyphosphoinositide (PI) signaling pathway, but this pathway was not triggered by Mls recognition. However, interleukin-2 (IL-2) secretion and proliferation to all three stimuli were comparable. Thus, although recognition of both allo-H-2 and Mls determinants is thought to be mediated by the TCR, these antigens appear to elicit biochemically distinct signal transduction pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Rourke, A M -- Mescher, M F -- Webb, S R -- New York, N.Y. -- Science. 1990 Jul 13;249(4965):171-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Membrane Biology, Medical Biology Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2164711" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Surface/*immunology ; H-2 Antigens/*immunology ; Hybridomas ; Hydrolysis ; Lymphocyte Activation ; Mice ; Mice, Inbred AKR ; Mice, Inbred CBA ; Minor Lymphocyte Stimulatory Antigens ; Phosphatidylinositols/*metabolism ; Receptors, Antigen, T-Cell/genetics/immunology ; Signal Transduction ; T-Lymphocytes/*metabolism
    Print ISSN: 0036-8075
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  • 8
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    New clue to cancer metastasis found (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1990 Aug 3;249(4968):482-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2382130" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Neoplasm Metastasis/*physiopathology ; Neoplasms/*genetics/pathology ; Signal Transduction ; *Suppression, Genetic
    Print ISSN: 0036-8075
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  • 9
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    Inhibition of serum- and ras-stimulated DNA synthesis by antibodies to phospholipase C (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-03-02
    Description: Several immunologically distinct isozymes of inositol phospholipid-specific phospholipase C (PLC) have been purified from bovine brain. Murine NIH 3T3 fibroblasts were found to express PLC-gamma, but the expression of PLC-beta was barely detectable by radioimmunoassay or protein immunoblot. A mixture of monoclonal antibodies was identified that neutralizes the biological activity of both endogenous and injected purified PLC-gamma. When co-injected with oncogenic Ras protein or PLC-gamma, this mixture of antibodies inhibited the induction of DNA synthesis that characteristically results from the injection of these proteins into quiescent 3T3 cells. However, when oncogenic Ras protein or PLC-gamma was co-injected with a neutralizing monoclonal antibody to Ras, only the DNA synthesis induced by the Ras protein was inhibited--that induced by PLC was unaffected. These results suggest that the Ras protein is an upstream effector of PLC activity in phosphoinositide-specific signal transduction and that PLC-gamma activity is necessary for Ras-mediated induction of DNA synthesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, M R -- Liu, Y L -- Kim, H -- Rhee, S G -- Kung, H F -- N01-CO-74102/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Mar 2;247(4946):1074-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biological Carcinogenesis and Development Program, National Cancer Institute-Frederick Cancer Research Facility, MD 21701.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2408147" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Cell Line ; DNA/*biosynthesis ; Fibroblasts ; Growth Substances/pharmacology ; Hybridomas ; Immunoblotting ; Interphase ; Isoenzymes/immunology/*metabolism ; Microinjections ; Oncogene Protein p21(ras)/immunology/*pharmacology ; Radioimmunoassay ; Signal Transduction ; Type C Phospholipases/immunology/*metabolism/pharmacology
    Print ISSN: 0036-8075
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  • 10
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    Specific expression of a tyrosine kinase gene, blk, in B lymphoid cells (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-01-19
    Description: Several pathways of transmembrane signaling in lymphocytes involve protein-tyrosine phosphorylation. With the exception of p56lck, a tyrosine kinase specific to T lymphoid cells that associates with the T cell transmembrane proteins CD4 and CD8, the kinases that function in these pathways are unknown. A murine lymphocyte complementary DNA that represents a new member of the src family has now been isolated and characterized. This complementary DNA, termed blk (for B lymphoid kinase), specifies a polypeptide of 55 kilodaltons that is related to, but distinct from, previously identified retroviral or cellular tyrosine kinases. The protein encoded by blk exhibits tyrosine kinase activity when expressed in bacterial cells. In the mouse and among cell lines, blk is specifically expressed in the B cell lineage. The tyrosine kinase encoded by blk may function in a signal transduction pathway that is restricted to B lymphoid cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dymecki, S M -- Niederhuber, J E -- Desiderio, S V -- New York, N.Y. -- Science. 1990 Jan 19;247(4940):332-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2404338" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; B-Lymphocytes/*enzymology ; Base Sequence ; Codon ; DNA/genetics/isolation & purification ; Escherichia coli/enzymology/genetics ; *Gene Expression ; Mice ; Molecular Sequence Data ; Protein-Tyrosine Kinases/*genetics ; Signal Transduction ; src-Family Kinases/*genetics
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  • 11
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    EGF receptor and erbB-2 tyrosine kinase domains confer cell specificity for mitogenic signaling (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-04-06
    Description: The epidermal growth factor (EGF) receptor (EGFR) can efficiently couple with mitogenic signaling pathways when it is transfected into interleukin-3 (IL-3)-dependent 32D hematopoietic cells. When expression vectors for erbB-2, which is structurally related to EGFR, or its truncated counterpart, delta NerbB-2, were introduced into 32D cells, neither was capable of inducing proliferation. This was despite overexpression and constitutive tyrosine kinase activity of their products at levels associated with potent transformation of fibroblast target cells. Thus, EGFR and erbB-2 couple with distinct mitogenic signaling pathways. The region responsible for the specificity of intracellular signal transduction was localized to a 270-amino acid stretch encompassing their respective tyrosine kinase domains. Thus, tissue- or cell-specific regulation of growth factor receptor signaling can occur at a point after the initial interaction of growth factor with receptor. Such specificity in signal transduction may account for the selection of certain oncogenes in some malignancies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Di Fiore, P P -- Segatto, O -- Taylor, W G -- Aaronson, S A -- Pierce, J H -- New York, N.Y. -- Science. 1990 Apr 6;248(4951):79-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2181668" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Division ; Cell Line ; DNA/genetics ; DNA, Recombinant ; Fibroblasts/cytology/metabolism ; Gene Expression ; Genetic Vectors ; Hematopoietic Stem Cells/cytology/metabolism ; Immunoblotting ; Mice ; *Mitogens ; Molecular Sequence Data ; Protein-Tyrosine Kinases/genetics/*physiology ; Proto-Oncogene Proteins/genetics/*physiology ; Receptor, Epidermal Growth Factor/genetics/*physiology ; Sequence Homology, Nucleic Acid ; Signal Transduction ; Transfection
    Print ISSN: 0036-8075
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  • 12
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    Odor stimuli trigger influx of calcium into olfactory neurons of the channel catfish (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-07
    Description: Olfactory transduction is thought to be mediated by a G protein-coupled increase in intracellular adenosine 3',5'-monophosphate (cAMP) that triggers the opening of cAMP-gated cation channels and results in depolarization of the plasma membrane of olfactory neurons. In olfactory neurons isolated from the channel catfish, Ictalurus punctatus, stimulation with olfactory stimuli (amino acids) elicits an influx of calcium that leads to a rapid increase in intracellular calcium. In addition, in a reconstitution assay a plasma membrane calcium channel has been identified that is gated by inositol-1,4,5-trisphosphate (IP3), which could mediate this calcium influx. Together with previous studies indicating that stimulation with olfactory stimuli leads to stimulation of phosphoinositide turnover in olfactory cilia, these data suggest that an influx of calcium triggered by odor stimulation of phosphoinositide turnover may be an alternate or additional mechanism of olfactory transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Restrepo, D -- Miyamoto, T -- Bryant, B P -- Teeter, J H -- DC00327/DC/NIDCD NIH HHS/ -- DC00566/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 1990 Sep 7;249(4973):1166-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Monell Chemical Senses Center, Philadelphia, PA 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2168580" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids ; Animals ; Calcium/*physiology ; Calcium Channel Blockers/pharmacology ; Calcium Channels/*physiology ; Catfishes/*physiology ; Chemoreceptor Cells/*physiology ; Electric Conductivity ; Ictaluridae/*physiology ; In Vitro Techniques ; Inositol 1,4,5-Trisphosphate/physiology ; Ion Channel Gating ; Signal Transduction ; Smell/*physiology
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  • 13
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    Increase of the catalytic activity of phospholipase C-gamma 1 by tyrosine phosphorylation (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-30
    Description: Phospholipase C-gamma 1 (PLC-gamma 1), an isozyme of the phosphoinositide-specific phospholipase C family, which occupies a central role in hormonal signal transduction pathways, is an excellent substrate for the epidermal growth factor (EGF) receptor tyrosine kinase. Epidermal growth factor elicits tyrosine phosphorylation of PLC-gamma 1 and phosphatidylinositol 4,5-bisphosphate hydrolysis in various cell lines. The ability of tyrosine phosphorylation to activate the catalytic activity of PLC-gamma 1 was tested. Tyrosine phosphorylation in intact cells or in vitro increased the catalytic activity of PLC-gamma 1. Also, treatment of EGF-activated PLC-gamma 1 with a tyrosine-specific phosphatase substantially decreased the catalytic activity of PLC-gamma 1. These results suggest that the EGF-stimulated formation of inositol 1,4,5-trisphosphate and diacylglycerol in intact cells results, at least in part, from catalytic activation of PLC-gamma 1 through tyrosine phosphorylation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nishibe, S -- Wahl, M I -- Hernandez-Sotomayor, S M -- Tonks, N K -- Rhee, S G -- Carpenter, G -- CA43720/CA/NCI NIH HHS/ -- GMO7347/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 30;250(4985):1253-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37232-0146.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1700866" target="_blank"〉PubMed〈/a〉
    Keywords: Catalysis ; Diglycerides/metabolism ; Enzyme Activation/drug effects ; Epidermal Growth Factor/pharmacology ; Immunosorbent Techniques ; Inositol 1,4,5-Trisphosphate/metabolism ; Isoenzymes/*metabolism ; Kinetics ; Phosphatidylinositol 4,5-Diphosphate ; Phosphatidylinositol Diacylglycerol-Lyase ; Phosphatidylinositols/metabolism ; Phosphoric Diester Hydrolases/*metabolism ; Phosphorylation ; Phosphotyrosine ; Protein-Tyrosine Kinases/metabolism ; Receptor, Epidermal Growth Factor ; Signal Transduction ; Tyrosine/*analogs & derivatives/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    Redox regulation of fos and jun DNA-binding activity in vitro (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-07
    Description: The proto-oncogenes c-fos and c-jun function cooperatively as inducible transcription factors in signal transduction processes. Their protein products, Fos and Jun, form a heterodimeric complex that interacts with the DNA regulatory element known as the activator protein-1 (AP-1) binding site. Dimerization occurs via interaction between leucine zipper domains and serves to bring into proper juxtaposition a region in each protein that is rich in basic amino acids and that forms a DNA-binding domain. DNA binding of the Fos-Jun heterodimer was modulated by reduction-oxidation (redox) of a single conserved cysteine residue in the DNA-binding domains of the two proteins. Furthermore, a nuclear protein was identified that reduced Fos and Jun and stimulated DNA-binding activity in vitro. These results suggest that transcriptional activity mediated by AP-1 binding factors may be regulated by a redox mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abate, C -- Patel, L -- Rauscher, F J 3rd -- Curran, T -- New York, N.Y. -- Science. 1990 Sep 7;249(4973):1157-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Oncology and Virology, Roche Institute of Molecular Biology, Nutley, NJ 07110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2118682" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell-Free System ; Cysteine/physiology ; DNA Mutational Analysis ; DNA-Binding Proteins/drug effects/*physiology ; Diamide/pharmacology ; Humans ; In Vitro Techniques ; Molecular Sequence Data ; Oxidation-Reduction ; Proto-Oncogene Proteins/*physiology ; Proto-Oncogene Proteins c-fos ; Proto-Oncogene Proteins c-jun ; Rats ; Recombinant Proteins ; Signal Transduction ; Structure-Activity Relationship ; Sulfhydryl Reagents/pharmacology ; Transcription Factors/*physiology
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  • 15
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    A cell culture model for T lymphocyte clonal anergy (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-15
    Description: T lymphocytes respond to foreign antigens both by producing protein effector molecules known as lymphokines and by multiplying. Complete activation requires two signaling events, one through the antigen-specific receptor and one through the receptor for a costimulatory molecule. In the absence of the latter signal, the T cell makes only a partial response and, more importantly, enters an unresponsive state known as clonal anergy in which the T cell is incapable of producing its own growth hormone, interleukin-2, on restimulation. Our current understanding at the molecular level of this modulatory process and its relevance to T cell tolerance are reviewed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwartz, R H -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1349-56.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2113314" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/immunology ; Antigens, CD4/immunology ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/immunology ; Cells, Cultured ; Clone Cells/*immunology ; Gene Expression Regulation ; Gene Rearrangement, T-Lymphocyte ; *Immune Tolerance ; Interleukin-2/biosynthesis/genetics ; Mice ; *Models, Biological ; Receptors, Antigen, T-Cell/genetics/immunology ; Second Messenger Systems ; Signal Transduction ; T-Lymphocytes/*immunology ; Thymus Gland/immunology
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  • 16
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    The FERONIA receptor-like kinase mediates male-female interactions during pollen tube reception (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-04
    Description: In flowering plants, signaling between the male pollen tube and the synergid cells of the female gametophyte is required for fertilization. In the Arabidopsis thaliana mutant feronia (fer), fertilization is impaired; the pollen tube fails to arrest and thus continues to grow inside the female gametophyte. FER encodes a synergid-expressed, plasma membrane-localized receptor-like kinase. We found that the FER protein accumulates asymmetrically in the synergid membrane at the filiform apparatus. Interspecific crosses using pollen from Arabidopsis lyrata and Cardamine flexuosa on A. thaliana stigmas resulted in a fer-like phenotype that correlates with sequence divergence in the extracellular domain of FER. Our findings show that the female control of pollen tube reception is based on a FER-dependent signaling pathway, which may play a role in reproductive isolation barriers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Escobar-Restrepo, Juan-Miguel -- Huck, Norbert -- Kessler, Sharon -- Gagliardini, Valeria -- Gheyselinck, Jacqueline -- Yang, Wei-Cai -- Grossniklaus, Ueli -- New York, N.Y. -- Science. 2007 Aug 3;317(5838):656-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Plant Biology and Zurich-Basel Plant Science Center, University of Zurich, Zollikerstrasse 107, CH-8008 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17673660" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/enzymology/genetics/*physiology ; Arabidopsis Proteins/chemistry/*genetics/*metabolism ; Brassicaceae/genetics/physiology ; Cell Membrane/enzymology ; Crosses, Genetic ; Evolution, Molecular ; Flowers/cytology/enzymology/*physiology ; Gene Expression ; Genes, Plant ; Germination ; Ligands ; Molecular Sequence Data ; Mutation ; Phosphorylation ; Phosphotransferases/chemistry/*genetics/*metabolism ; Plant Epidermis/enzymology ; Pollen Tube/growth & development/*physiology ; Recombinant Fusion Proteins/metabolism ; Reproduction ; Seeds/growth & development ; Signal Transduction ; Species Specificity
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  • 17
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    Positive regulation of Itk PH domain function by soluble IP4 (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-07
    Description: Pleckstrin homology (PH) domain-mediated protein recruitment to cellular membranes is of paramount importance for signal transduction. The recruitment of many PH domains is controlled through production and turnover of their membrane ligand, phosphatidylinositol 3,4,5-trisphosphate (PIP3). We show that phosphorylation of the second messenger inositol 1,4,5-trisphosphate (IP3) into inositol 1,3,4,5-tetrakisphosphate (IP4) establishes another mode of PH domain regulation through a soluble ligand. At physiological concentrations, IP4 promoted PH domain binding to PIP3. In primary mouse CD4+CD8+ thymocytes, this was required for full activation of the protein tyrosine kinase Itk after T cell receptor engagement. Our data suggest that IP4 establishes a feedback loop of phospholipase C-gamma1 activation through Itk that is essential for T cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Yina H -- Grasis, Juris A -- Miller, Andrew T -- Xu, Ruo -- Soonthornvacharin, Stephen -- Andreotti, Amy H -- Tsoukas, Constantine D -- Cooke, Michael P -- Sauer, Karsten -- AR048848/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2007 May 11;316(5826):886-9. Epub 2007 Apr 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17412921" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; *Amino Acid Motifs ; Animals ; Diglycerides/metabolism ; Feedback, Physiological ; Inositol 1,4,5-Trisphosphate/metabolism ; Inositol Phosphates/*metabolism/pharmacology ; Lymphopoiesis ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Models, Biological ; Organ Culture Techniques ; Phosphatidylinositol Phosphates/metabolism ; Phospholipase C gamma/metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; Protein Structure, Tertiary ; Protein-Tyrosine Kinases/chemistry/*metabolism ; Receptors, Antigen, T-Cell/immunology ; Second Messenger Systems ; Signal Transduction ; Solubility ; T-Lymphocytes/cytology/immunology/*metabolism
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  • 18
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    Forces and bond dynamics in cell adhesion (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-05-26
    Description: Adhesion of a biological cell to another cell or the extracellular matrix involves complex couplings between cell biochemistry, structural mechanics, and surface bonding. The interactions are dynamic and act through association and dissociation of bonds between very large molecules at rates that change considerably under stress. Combining molecular cell biology with single-molecule force spectroscopy provides a powerful tool for exploring the complexity of cell adhesion, that is, how cell signaling processes strengthen adhesion bonds and how forces applied to cell-surface bonds act on intracellular sites to catalyze chemical processes or switch molecular interactions on and off. Probing adhesion receptors on strategically engineered cells with force during functional stimulation can reveal key nodes of communication between the mechanical and chemical circuitry of a cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Evans, Evan A -- Calderwood, David A -- New York, N.Y. -- Science. 2007 May 25;316(5828):1148-53.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biomedical Engineering, Boston University, Boston, MA 02215, USA. evans@physics.ubc.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17525329" target="_blank"〉PubMed〈/a〉
    Keywords: Biomechanical Phenomena ; Cell Adhesion/*physiology ; Humans ; Integrins/chemistry/physiology ; Selectins/chemistry/physiology ; Signal Transduction ; Spectrum Analysis
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  • 19
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    Plant science. Reproductive dialog (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McCormick, Sheila -- New York, N.Y. -- Science. 2007 Aug 3;317(5838):606-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Plant Gene Expression Center, USDA Agricultural Research Service-UC Berkeley, 800 Buchanan Street, Albany, CA 94710, USA. sheilamc@nature.berkeley.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17673644" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/enzymology/genetics/*physiology ; Arabidopsis Proteins/genetics/*metabolism ; Cell Membrane/enzymology ; Crosses, Genetic ; Evolution, Molecular ; Flowers/cytology/enzymology/*physiology ; Genes, Plant ; Ligands ; Models, Biological ; Mutation ; Phosphotransferases/*genetics/*metabolism ; Pollen Tube/growth & development/*physiology ; Reproduction ; Signal Transduction ; Species Specificity
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  • 20
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    Microbiology. Deadly priming (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-10-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kolter, Roberto -- New York, N.Y. -- Science. 2007 Oct 26;318(5850):578-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115, USA. rkolter@hms.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17962544" target="_blank"〉PubMed〈/a〉
    Keywords: *Apoptosis ; Colony Count, Microbial ; Escherichia coli/cytology/*physiology ; Glucosephosphate Dehydrogenase/*metabolism ; Oligopeptides/*metabolism ; *Quorum Sensing ; Signal Transduction
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  • 21
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    Regulation of hepatic stellate cell differentiation by the neurotrophin receptor p75NTR (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-03-31
    Description: Differentiation of hepatic stellate cells (HSCs) to extracellular matrix- and growth factor-producing cells supports liver regeneration through promotion of hepatocyte proliferation. We show that the neurotrophin receptor p75NTR, a tumor necrosis factor receptor superfamily member expressed in HSCs after fibrotic and cirrhotic liver injury in humans, is a regulator of liver repair. In mice, depletion of p75NTR exacerbated liver pathology and inhibited hepatocyte proliferation in vivo. p75NTR-/- HSCs failed to differentiate to myofibroblasts and did not support hepatocyte proliferation. Moreover, inhibition of p75NTR signaling to the small guanosine triphosphatase Rho resulted in impaired HSC differentiation. Our results identify signaling from p75NTR to Rho as a mechanism for the regulation of HSC differentiation to regeneration-promoting cells that support hepatocyte proliferation in the diseased liver.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Passino, Melissa A -- Adams, Ryan A -- Sikorski, Shoana L -- Akassoglou, Katerina -- 5T32-GM07752/GM/NIGMS NIH HHS/ -- NS051470/NS/NINDS NIH HHS/ -- P30-NS047101/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2007 Mar 30;315(5820):1853-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California, San Diego (UCSD), La Jolla, CA 92093-0636, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17395831" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Cell Proliferation ; Cells, Cultured ; Disease Progression ; Extracellular Matrix/metabolism ; Fibroblasts/*cytology ; Hepatocyte Growth Factor/metabolism ; Hepatocytes/*cytology ; Liver/*cytology/metabolism/pathology/physiology ; Liver Diseases/metabolism/*pathology ; *Liver Regeneration ; Mice ; Nerve Growth Factor/pharmacology ; Receptors, Nerve Growth Factor/genetics/*metabolism ; Signal Transduction ; rho GTP-Binding Proteins/metabolism
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  • 22
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    Genetically determined differences in learning from errors (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-12-08
    Description: The role of dopamine in monitoring negative action outcomes and feedback-based learning was tested in a neuroimaging study in humans grouped according to the dopamine D2 receptor gene polymorphism DRD2-TAQ-IA. In a probabilistic learning task, A1-allele carriers with reduced dopamine D2 receptor densities learned to avoid actions with negative consequences less efficiently. Their posterior medial frontal cortex (pMFC), involved in feedback monitoring, responded less to negative feedback than others' did. Dynamically changing interactions between pMFC and hippocampus found to underlie feedback-based learning were reduced in A1-allele carriers. This demonstrates that learning from errors requires dopaminergic signaling. Dopamine D2 receptor reduction seems to decrease sensitivity to negative action consequences, which may explain an increased risk of developing addictive behaviors in A1-allele carriers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Klein, Tilmann A -- Neumann, Jane -- Reuter, Martin -- Hennig, Jurgen -- von Cramon, D Yves -- Ullsperger, Markus -- R01MH74457/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2007 Dec 7;318(5856):1642-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute for Human Cognitive and Brain Sciences, Leipzig, Germany. tklein@cbs.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18063800" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Alleles ; *Avoidance Learning ; Basal Ganglia/physiology ; Brain Mapping ; Dopamine/*physiology ; Feedback, Psychological ; Frontal Lobe/*physiology ; Hippocampus/physiology ; Humans ; *Learning ; Magnetic Resonance Imaging ; Male ; Nucleus Accumbens/physiology ; *Polymorphism, Genetic ; Receptors, Dopamine D2/*genetics/metabolism ; *Reinforcement (Psychology) ; Signal Transduction
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  • 23
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    Comment on "A centrosome-independent role for gamma-TuRC proteins in the spindle assembly checkpoint" (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-19
    Description: Muller et al. (Reports, 27 October 2006, p. 654) proposed a role for microtubule nucleation in mitotic checkpoint signaling. However, their observations of spindle defects and mitotic delay after depletion of gamma-tubulin ring complex (gamma-TuRC) components are fully consistent with activation of the established pathway of checkpoint signaling in response to incomplete or unstable interactions between kinetochores of mitotic chromosomes and spindle microtubules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weaver, Beth A A -- Cleveland, Don W -- New York, N.Y. -- Science. 2007 May 18;316(5827):982; author reply 982.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Institute for Cancer Research and Department of Cellular and Molecular Medicine, University of California at San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0670, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17510348" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Kinetochores/*physiology ; Microtubule-Associated Proteins/*metabolism ; Microtubules/*metabolism/ultrastructure ; *Mitosis ; Signal Transduction ; Spindle Apparatus/*metabolism ; Tubulin/*metabolism
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    Immunology. The shape of things to come (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-06-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fitzgerald, Katherine A -- Golenbock, Douglas T -- New York, N.Y. -- Science. 2007 Jun 15;316(5831):1574-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA 01605, USA. kate.fitzgerald@umassmed.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17569850" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; Adaptor Proteins, Vesicular Transport/metabolism ; *Adjuvants, Immunologic ; Animals ; Crystallography, X-Ray ; Glycolipids/chemistry/metabolism ; Humans ; Hydrophobic and Hydrophilic Interactions ; Ligands ; Lipid A/*analogs & derivatives/chemistry/immunology/metabolism ; Lymphocyte Activation ; Lymphocyte Antigen 96/*chemistry/metabolism ; Mice ; Phosphates/metabolism ; Protein Conformation ; Receptors, Interleukin/metabolism ; Signal Transduction ; T-Lymphocytes/immunology ; Toll-Like Receptor 4/chemistry/*immunology/metabolism
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  • 25
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    Signals from chloroplasts converge to regulate nuclear gene expression (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-03-31
    Description: Plastid-to-nucleus retrograde signaling coordinates nuclear gene expression with chloroplast function and is essential for the photoautotrophic life-style of plants. Three retrograde signals have been described, but little is known of their signaling pathways. We show here that GUN1, a chloroplast-localized pentatricopeptide-repeat protein, and ABI4, an Apetala 2 (AP2)-type transcription factor, are common to all three pathways. ABI4 binds the promoter of a retrograde-regulated gene through a conserved motif found in close proximity to a light-regulatory element. We propose a model in which multiple indicators of aberrant plastid function in Arabidopsis are integrated upstream of GUN1 within plastids, which leads to ABI4-mediated repression of nuclear-encoded genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koussevitzky, Shai -- Nott, Ajit -- Mockler, Todd C -- Hong, Fangxin -- Sachetto-Martins, Gilberto -- Surpin, Marci -- Lim, Jason -- Mittler, Ron -- Chory, Joanne -- DRG-1865-05/PHS HHS/ -- F32 GM 18172/GM/NIGMS NIH HHS/ -- F32 GM 69090/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 May 4;316(5825):715-9. Epub 2007 Mar 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, 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/17395793" target="_blank"〉PubMed〈/a〉
    Keywords: Abscisic Acid ; Amino Acid Motifs ; Amino Acid Sequence ; Arabidopsis/genetics/*metabolism ; Arabidopsis Proteins/chemistry/genetics/*metabolism ; Cell Nucleus/*metabolism/*microbiology ; Chloroplasts/*metabolism ; DNA, Plant/metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Electron Transport ; *Gene Expression Regulation, Plant ; Light-Harvesting Protein Complexes/genetics ; Lincomycin/pharmacology ; Models, Biological ; Molecular Sequence Data ; Oligonucleotide Array Sequence Analysis ; Plants, Genetically Modified ; Promoter Regions, Genetic ; Protoporphyrins/metabolism ; Pyridazines/pharmacology ; Signal Transduction ; Transcription Factors/*metabolism
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    Hardwiring the brain: endocannabinoids shape neuronal connectivity (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-26
    Description: The roles of endocannabinoid signaling during central nervous system development are unknown. We report that CB(1) cannabinoid receptors (CB(1)Rs) are enriched in the axonal growth cones of gamma-aminobutyric acid-containing (GABAergic) interneurons in the rodent cortex during late gestation. Endocannabinoids trigger CB(1)R internalization and elimination from filopodia and induce chemorepulsion and collapse of axonal growth cones of these GABAergic interneurons by activating RhoA. Similarly, endocannabinoids diminish the galvanotropism of Xenopus laevis spinal neurons. These findings, together with the impaired target selection of cortical GABAergic interneurons lacking CB(1)Rs, identify endocannabinoids as axon guidance cues and demonstrate that endocannabinoid signaling regulates synaptogenesis and target selection in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berghuis, Paul -- Rajnicek, Ann M -- Morozov, Yury M -- Ross, Ruth A -- Mulder, Jan -- Urban, Gabriella M -- Monory, Krisztina -- Marsicano, Giovanni -- Matteoli, Michela -- Canty, Alison -- Irving, Andrew J -- Katona, Istvan -- Yanagawa, Yuchio -- Rakic, Pasko -- Lutz, Beat -- Mackie, Ken -- Harkany, Tibor -- DA00286/DA/NIDA NIH HHS/ -- DA015916/DA/NIDA NIH HHS/ -- DA11322/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2007 May 25;316(5828):1212-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, S-17177 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17525344" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Cannabinoid Receptor Modulators/metabolism/*physiology ; Cell Movement ; Cells, Cultured ; Cerebral Cortex/cytology/embryology/ultrastructure ; *Endocannabinoids ; Growth Cones/physiology/ultrasonography ; In Situ Hybridization ; Interneurons/metabolism/*physiology/ultrasonography ; Mice ; Mice, Inbred C57BL ; Microscopy, Confocal ; Rats ; Rats, Sprague-Dawley ; Receptor, Cannabinoid, CB1/agonists/*physiology ; Signal Transduction ; Stem Cells/metabolism ; Synapses/physiology/ultrasonography ; Xenopus Proteins/physiology ; Xenopus laevis ; gamma-Aminobutyric Acid/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The slit receptor EVA-1 coactivates a SAX-3/Robo mediated guidance signal in C. elegans (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-29
    Description: The SAX-3/roundabout (Robo) receptor has SLT-1/Slit-dependent and -independent functions in guiding cell and axon migrations. We identified enhancer of ventral-axon guidance defects of unc-40 mutants (EVA-1) as a Caenorhabditis elegans transmembrane receptor for SLT-1. EVA-1 has two predicted galactose-binding ectodomains, acts cell-autonomously for SLT-1/Slit-dependent axon migration functions of SAX-3/Robo, binds to SLT-1 and SAX-3, colocalizes with SAX-3 on cells, and provides cell specificity to the activation of SAX-3 signaling by SLT-1. Double mutants of eva-1 or slt-1 with sax-3 mutations suggest that SAX-3 can (when slt-1 or eva-1 function is reduced) inhibit a parallel-acting guidance mechanism, which involves UNC-40/deleted in colorectal cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fujisawa, Kazuko -- Wrana, Jeffrey L -- Culotti, Joseph G -- NS41397/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2007 Sep 28;317(5846):1934-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute of Mount Sinai Hospital, 600 University Avenue, Toronto, Ontario M5G 1X5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17901337" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Animals, Genetically Modified ; Axons/*physiology ; Caenorhabditis elegans/cytology/genetics/growth & development/*physiology ; Caenorhabditis elegans Proteins/*chemistry/genetics/*metabolism ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Line ; Cell Movement ; Cloning, Molecular ; Humans ; Molecular Sequence Data ; Mutation ; Nerve Tissue Proteins/*metabolism ; Nervous System/growth & development/metabolism ; Neurons/physiology ; Protein Structure, Tertiary ; Receptors, Immunologic/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction
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  • 28
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    Male and female Drosophila germline stem cells: two versions of immortality (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-21
    Description: Drosophila male and female germline stem cells (GSCs) are sustained by niches and regulatory pathways whose common principles serve as models for understanding mammalian stem cells. Despite striking cellular and genetic similarities that suggest a common evolutionary origin, however, male and female GSCs also display important differences. Comparing these two stem cells and their niches in detail is likely to reveal how a common heritage has been adapted to the differing requirements of male and female gamete production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fuller, Margaret T -- Spradling, Allan C -- P01DK53074/DK/NIDDK NIH HHS/ -- R01GM61986/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2007 Apr 20;316(5823):402-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Developmental Biology and Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17446390" target="_blank"〉PubMed〈/a〉
    Keywords: Adult Stem Cells/*cytology/physiology ; Animals ; Cell Adhesion ; Cell Differentiation ; Cell Division ; Centrosome/physiology ; Drosophila/*cytology/*physiology ; Drosophila Proteins/physiology ; Female ; Germ Cells/*cytology/physiology ; Male ; Ovary/cytology ; Sex Characteristics ; Signal Transduction ; Testis/cytology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 29
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    Physiology. An integrative view of obesity (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wisse, Brent E -- Kim, Francis -- Schwartz, Michael W -- DK073878/DK/NIDDK NIH HHS/ -- DK12829/DK/NIDDK NIH HHS/ -- DK61384/DK/NIDDK NIH HHS/ -- NS3227/NS/NINDS NIH HHS/ -- P01-DK 068384/DK/NIDDK NIH HHS/ -- R01 DK074758/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 9;318(5852):928-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Harborview Medical Center and University of Washington, Seattle, WA 98104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17991852" target="_blank"〉PubMed〈/a〉
    Keywords: Acyl Coenzyme A/metabolism ; Adipose Tissue/metabolism ; Animals ; Diabetes Mellitus, Type 2/metabolism ; Endothelium, Vascular/metabolism ; *Energy Intake ; Energy Metabolism ; Homeostasis ; Humans ; Hypothalamus/metabolism ; Inflammation/metabolism ; Insulin/metabolism/secretion ; Insulin Resistance ; Insulin-Secreting Cells/metabolism ; Leptin/metabolism ; Nitric Oxide/metabolism ; Obesity/etiology/*metabolism ; Oxidative Stress ; Phosphatidylinositol 3-Kinases/metabolism ; Reactive Oxygen Species/metabolism ; Receptor, Insulin/metabolism ; Signal Transduction
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  • 30
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    Sea anemone genome reveals ancestral eumetazoan gene repertoire and genomic organization (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-07-07
    Description: Sea anemones are seemingly primitive animals that, along with corals, jellyfish, and hydras, constitute the oldest eumetazoan phylum, the Cnidaria. Here, we report a comparative analysis of the draft genome of an emerging cnidarian model, the starlet sea anemone Nematostella vectensis. The sea anemone genome is complex, with a gene repertoire, exon-intron structure, and large-scale gene linkage more similar to vertebrates than to flies or nematodes, implying that the genome of the eumetazoan ancestor was similarly complex. Nearly one-fifth of the inferred genes of the ancestor are eumetazoan novelties, which are enriched for animal functions like cell signaling, adhesion, and synaptic transmission. Analysis of diverse pathways suggests that these gene "inventions" along the lineage leading to animals were likely already well integrated with preexisting eukaryotic genes in the eumetazoan progenitor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Putnam, Nicholas H -- Srivastava, Mansi -- Hellsten, Uffe -- Dirks, Bill -- Chapman, Jarrod -- Salamov, Asaf -- Terry, Astrid -- Shapiro, Harris -- Lindquist, Erika -- Kapitonov, Vladimir V -- Jurka, Jerzy -- Genikhovich, Grigory -- Grigoriev, Igor V -- Lucas, Susan M -- Steele, Robert E -- Finnerty, John R -- Technau, Ulrich -- Martindale, Mark Q -- Rokhsar, Daniel S -- 5 P41 LM006252-09/LM/NLM NIH HHS/ -- THL007279F/PHS HHS/ -- New York, N.Y. -- Science. 2007 Jul 6;317(5834):86-94.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Energy Joint Genome Institute, Walnut Creek, CA 94598, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17615350" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Cell Adhesion ; Evolution, Molecular ; Genes ; Genetic Linkage ; *Genome ; Genome, Human ; Genomics ; Humans ; Introns ; Metabolic Networks and Pathways ; Multigene Family ; Muscles/physiology ; Nervous System Physiological Phenomena ; Phylogeny ; Sea Anemones/*genetics/metabolism ; Sequence Analysis, DNA ; Signal Transduction ; Synteny
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    Of aging mice and men (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-10-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Richard -- New York, N.Y. -- Science. 2007 Oct 19;318(5849):390; author reply 390.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17947563" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; Glucuronidase/deficiency/*genetics ; Humans ; Mice ; *Models, Animal ; Signal Transduction ; Vitamin D/*administration & dosage/metabolism ; Wnt Proteins/metabolism
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  • 32
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    Demethylation of H3K27 regulates polycomb recruitment and H2A ubiquitination (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-01
    Description: Methylation of histone H3 lysine 27 (H3K27) is a posttranslational modification that is highly correlated with genomic silencing. Here we show that human UTX, a member of the Jumonji C family of proteins, is a di- and trimethyl H3K27 demethylase. UTX occupies the promoters of HOX gene clusters and regulates their transcriptional output by modulating the recruitment of polycomb repressive complex 1 and the monoubiquitination of histone H2A. Moreover, UTX associates with mixed-lineage leukemia (MLL) 2/3 complexes, and during retinoic acid signaling events, the recruitment of the UTX complex to HOX genes results in H3K27 demethylation and a concomitant methylation of H3K4. Our results suggest a concerted mechanism for transcriptional activation in which cycles of H3K4 methylation by MLL2/3 are linked with the demethylation of H3K27 through UTX.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Min Gyu -- Villa, Raffaella -- Trojer, Patrick -- Norman, Jessica -- Yan, Kai-Ping -- Reinberg, Danny -- Di Croce, Luciano -- Shiekhattar, Ramin -- R01CA090758/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 Oct 19;318(5849):447-50. Epub 2007 Aug 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17761849" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Differentiation ; Cell Line ; Cell Line, Tumor ; DNA-Binding Proteins/metabolism ; Embryonic Stem Cells ; *Genes, Homeobox ; Histone Demethylases ; Histones/*metabolism ; Humans ; Lysine/*metabolism ; Methylation ; Multigene Family ; Neoplasm Proteins/metabolism ; Nuclear Proteins/genetics/*metabolism ; Polycomb-Group Proteins ; Promoter Regions, Genetic ; Protein Processing, Post-Translational ; Recombinant Proteins/metabolism ; Repressor Proteins/*metabolism ; Signal Transduction ; Transcription, Genetic ; Transcriptional Activation ; Tretinoin/metabolism/pharmacology ; Ubiquitin/metabolism
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    Immunology. Eating in to avoid infection (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-03-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reis e Sousa, Caetano -- New York, N.Y. -- Science. 2007 Mar 9;315(5817):1376-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunobiology Laboratory, Cancer Research UK, London Research Institute, Lincoln's Inn Fields Laboratories, 44 Lincoln's Inn Fields, London WC2A 3PX, UK. caetano@cancer.org.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17347432" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autophagy ; Cytokines/metabolism ; Dendritic Cells/*immunology/physiology/*virology ; Endosomes/immunology/virology ; Histocompatibility Antigens Class I/immunology ; Histocompatibility Antigens Class II/immunology ; Membrane Glycoproteins/immunology/physiology ; Mice ; Mice, Transgenic ; RNA, Viral/*immunology/metabolism ; Rhabdoviridae Infections/*immunology ; Signal Transduction ; Toll-Like Receptor 7/immunology/physiology ; Toll-Like Receptor 9/immunology/physiology ; Toll-Like Receptors/immunology/*physiology ; Vesicular stomatitis Indiana virus/*immunology/physiology ; Virus Replication
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    Biochemistry. Signaling across the cell membrane (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-11-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ranganathan, Rama -- New York, N.Y. -- Science. 2007 Nov 23;318(5854):1253-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Green Center for Systems Biology and Department of Pharmacology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. rama.ranganathan@utsouthwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18033872" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic beta-Agonists/chemistry/metabolism ; Adrenergic beta-Antagonists/chemistry/metabolism/pharmacology ; Bacteriophage T4/enzymology ; Binding Sites ; Cell Membrane/chemistry/metabolism ; Immunoglobulin Fab Fragments/metabolism ; Ligands ; Muramidase/chemistry/metabolism ; Propanolamines/chemistry/metabolism ; Protein Conformation ; Protein Folding ; Protein Structure, Secondary ; Receptors, Adrenergic, beta-2/*chemistry/metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Rhodopsin/chemistry/metabolism ; Signal Transduction
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  • 35
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    Legumes symbioses: absence of Nod genes in photosynthetic bradyrhizobia (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-02
    Description: Leguminous plants (such as peas and soybeans) and rhizobial soil bacteria are symbiotic partners that communicate through molecular signaling pathways, resulting in the formation of nodules on legume roots and occasionally stems that house nitrogen-fixing bacteria. Nodule formation has been assumed to be exclusively initiated by the binding of bacterial, host-specific lipochito-oligosaccharidic Nod factors, encoded by the nodABC genes, to kinase-like receptors of the plant. Here we show by complete genome sequencing of two symbiotic, photosynthetic, Bradyrhizobium strains, BTAi1 and ORS278, that canonical nodABC genes and typical lipochito-oligosaccharidic Nod factors are not required for symbiosis in some legumes. Mutational analyses indicated that these unique rhizobia use an alternative pathway to initiate symbioses, where a purine derivative may play a key role in triggering nodule formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giraud, Eric -- Moulin, Lionel -- Vallenet, David -- Barbe, Valerie -- Cytryn, Eddie -- Avarre, Jean-Christophe -- Jaubert, Marianne -- Simon, Damien -- Cartieaux, Fabienne -- Prin, Yves -- Bena, Gilles -- Hannibal, Laure -- Fardoux, Joel -- Kojadinovic, Mila -- Vuillet, Laurie -- Lajus, Aurelie -- Cruveiller, Stephane -- Rouy, Zoe -- Mangenot, Sophie -- Segurens, Beatrice -- Dossat, Carole -- Franck, William L -- Chang, Woo-Suk -- Saunders, Elizabeth -- Bruce, David -- Richardson, Paul -- Normand, Philippe -- Dreyfus, Bernard -- Pignol, David -- Stacey, Gary -- Emerich, David -- Vermeglio, Andre -- Medigue, Claudine -- Sadowsky, Michael -- New York, N.Y. -- Science. 2007 Jun 1;316(5829):1307-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Recherche pour le Developpement, Centre de Cooperation International en Recherche Agronomique pour le Developpement, Institut National de la Recherche Agronomique, Universite Montpellier 2, France. giraud@mpl.ird.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17540897" target="_blank"〉PubMed〈/a〉
    Keywords: Acyltransferases/genetics/metabolism ; Amidohydrolases/genetics/metabolism ; Bacterial Proteins/genetics/metabolism ; Bradyrhizobium/*genetics/growth & development/*physiology ; Cytokinins/metabolism ; Fabaceae/*microbiology ; Genes, Bacterial ; Genome, Bacterial ; Genomics ; Lipopolysaccharides/metabolism ; Molecular Sequence Data ; Mutation ; N-Acetylglucosaminyltransferases/genetics/metabolism ; Photosynthesis ; Plant Roots/microbiology ; Plant Stems/*microbiology ; Purines/biosynthesis ; Root Nodules, Plant/microbiology/*physiology ; Signal Transduction ; *Symbiosis
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    DUBA: a deubiquitinase that regulates type I interferon production (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-10
    Description: Production of type I interferon (IFN-I) is a critical host defense triggered by pattern-recognition receptors (PRRs) of the innate immune system. Deubiquitinating enzyme A (DUBA), an ovarian tumor domain-containing deubiquitinating enzyme, was discovered in a small interfering RNA-based screen as a regulator of IFN-I production. Reduction of DUBA augmented the PRR-induced IFN-I response, whereas ectopic expression of DUBA had the converse effect. DUBA bound tumor necrosis factor receptor-associated factor 3 (TRAF3), an adaptor protein essential for the IFN-I response. TRAF3 is an E3 ubiquitin ligase that preferentially assembled lysine-63-linked polyubiquitin chains. DUBA selectively cleaved the lysine-63-linked polyubiquitin chains on TRAF3, resulting in its dissociation from the downstream signaling complex containing TANK-binding kinase 1. A discrete ubiquitin interaction motif within DUBA was required for efficient deubiquitination of TRAF3 and optimal suppression of IFN-I. Our data identify DUBA as a negative regulator of innate immune responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kayagaki, Nobuhiko -- Phung, Qui -- Chan, Salina -- Chaudhari, Ruchir -- Quan, Casey -- O'Rourke, Karen M -- Eby, Michael -- Pietras, Eric -- Cheng, Genhong -- Bazan, J Fernando -- Zhang, Zemin -- Arnott, David -- Dixit, Vishva M -- New York, N.Y. -- Science. 2007 Dec 7;318(5856):1628-32. Epub 2007 Nov 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiological Chemistry, Genentech, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17991829" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Cell Line ; Endopeptidases/*metabolism ; Humans ; Interferon Type I/*biosynthesis/genetics ; Interferon-alpha/genetics ; Molecular Sequence Data ; NF-kappa B/metabolism ; Protein Structure, Tertiary ; RNA, Small Interfering ; Signal Transduction ; TNF Receptor-Associated Factor 3/metabolism ; Toll-Like Receptor 3/metabolism ; Ubiquitin/metabolism ; Ubiquitination
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    Coactivation of receptor tyrosine kinases affects the response of tumor cells to targeted therapies (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-09-18
    Description: Targeted therapies that inhibit receptor tyrosine kinases (RTKs) and the downstream phosphatidylinositol 3-kinase (PI3K) signaling pathway have shown promising anticancer activity, but their efficacy in the brain tumor glioblastoma multiforme (GBM) and other solid tumors has been modest. We hypothesized that multiple RTKs are coactivated in these tumors and that redundant inputs drive and maintain downstream signaling, thereby limiting the efficacy of therapies targeting single RTKs. Tumor cell lines, xenotransplants, and primary tumors indeed show multiple concomitantly activated RTKs. Combinations of RTK inhibitors and/or RNA interference, but not single agents, decreased signaling, cell survival, and anchorage-independent growth even in glioma cells deficient in PTEN, a frequently inactivated inhibitor of PI3K. Thus, effective GBM therapy may require combined regimens targeting multiple RTKs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stommel, Jayne M -- Kimmelman, Alec C -- Ying, Haoqiang -- Nabioullin, Roustem -- Ponugoti, Aditya H -- Wiedemeyer, Ruprecht -- Stegh, Alexander H -- Bradner, James E -- Ligon, Keith L -- Brennan, Cameron -- Chin, Lynda -- DePinho, Ronald A -- 5P01CA95616/CA/NCI NIH HHS/ -- R01CA99041/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 Oct 12;318(5848):287-90. Epub 2007 Sep 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17872411" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents/*pharmacology ; Antineoplastic Combined Chemotherapy Protocols/pharmacology/therapeutic use ; Brain Neoplasms/drug therapy/*enzymology ; Cell Line, Tumor ; Cell Survival ; Enzyme Activation ; Erlotinib Hydrochloride ; Glioblastoma/drug therapy/*enzymology ; Humans ; Indoles/pharmacology ; PTEN Phosphohydrolase/genetics/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Piperazines/pharmacology ; Protein Kinase Inhibitors/*pharmacology ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-met ; Quinazolines/pharmacology ; Receptor Protein-Tyrosine Kinases/antagonists & inhibitors/*metabolism ; Receptor, Epidermal Growth Factor/antagonists & inhibitors/metabolism ; Receptors, Growth Factor/metabolism ; Signal Transduction ; Sulfonamides/pharmacology
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    Synchrony dynamics during initiation, failure, and rescue of the segmentation clock (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-19
    Description: The "segmentation clock" is thought to coordinate sequential segmentation of the body axis in vertebrate embryos. This clock comprises a multicellular genetic network of synchronized oscillators, coupled by intercellular Delta-Notch signaling. How this synchrony is established and how its loss determines the position of segmentation defects in Delta and Notch mutants are unknown. We analyzed the clock's synchrony dynamics by varying strength and timing of Notch coupling in zebra-fish embryos with techniques for quantitative perturbation of gene function. We developed a physical theory based on coupled phase oscillators explaining the observed onset and rescue of segmentation defects, the clock's robustness against developmental noise, and a critical point beyond which synchrony decays. We conclude that synchrony among these genetic oscillators can be established by simultaneous initiation and self-organization and that the segmentation defect position is determined by the difference between coupling strength and noise.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Riedel-Kruse, Ingmar H -- Muller, Claudia -- Oates, Andrew C -- New York, N.Y. -- Science. 2007 Sep 28;317(5846):1911-5. Epub 2007 Aug 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG), Pfotenhauerstrasse 108, 01307 Dresden, Germany. ingmar@caltech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17702912" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks/*genetics/physiology ; *Body Patterning/genetics ; Dipeptides/pharmacology ; Embryo, Nonmammalian/metabolism ; *Embryonic Development ; Gene Expression Regulation, Developmental ; Gene Regulatory Networks ; Homeodomain Proteins/genetics/metabolism ; Intracellular Signaling Peptides and Proteins ; Mathematics ; Membrane Proteins/genetics/metabolism ; Mesoderm/physiology ; Mutation ; Nerve Tissue Proteins/genetics/metabolism ; Oligonucleotides, Antisense/pharmacology ; RNA Stability ; Receptor, Notch1/genetics/metabolism ; Signal Transduction ; Somites/physiology ; Zebrafish/*embryology/genetics ; Zebrafish Proteins/genetics/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Postreplicative formation of cohesion is required for repair and induced by a single DNA break (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-07-14
    Description: Sister-chromatid cohesion, established during replication by the protein complex cohesin, is essential for both chromosome segregation and double-strand break (DSB) repair. Normally, cohesion formation is strictly limited to the S phase of the cell cycle, but DSBs can trigger cohesion also after DNA replication has been completed. The function of this damage-induced cohesion remains unknown. In this investigation, we show that damage-induced cohesion is essential for repair in postreplicative cells in yeast. Furthermore, it is established genome-wide after induction of a single DSB, and it is controlled by the DNA damage response and cohesin-regulating factors. We thus define a cohesion establishment pathway that is independent of DNA duplication and acts together with cohesion formed during replication in sister chromatid-based DSB repair.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strom, Lena -- Karlsson, Charlotte -- Lindroos, Hanna Betts -- Wedahl, Sara -- Katou, Yuki -- Shirahige, Katsuhiko -- Sjogren, Camilla -- New York, N.Y. -- Science. 2007 Jul 13;317(5835):242-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Molecular Biology, Karolinska Institute, 171 77 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17626884" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/genetics/metabolism ; Cell Cycle Proteins/metabolism ; Cell Division ; Chromatids/*physiology ; Chromosomal Proteins, Non-Histone/metabolism ; *DNA Breaks, Double-Stranded ; *DNA Repair ; DNA Replication ; DNA, Fungal/biosynthesis/*metabolism ; G2 Phase ; Genome, Fungal ; Intracellular Signaling Peptides and Proteins ; Mutation ; Nuclear Proteins/genetics/metabolism ; Protein-Serine-Threonine Kinases ; Saccharomyces cerevisiae/genetics/metabolism/*physiology ; Saccharomyces cerevisiae Proteins/genetics/metabolism ; Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Medicine. The yin-yang of sirtuins (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-07-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dillin, Andrew -- Kelly, Jeffery W -- New York, N.Y. -- Science. 2007 Jul 27;317(5837):461-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA. dillin@salk.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17656709" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Autophagy ; Cell Line, Tumor ; Disease Models, Animal ; Drosophila melanogaster ; Humans ; Neurodegenerative Diseases/physiopathology ; Parkinson Disease/drug therapy/pathology/*physiopathology ; RNA Interference ; Rats ; Signal Transduction ; Sirtuin 1 ; Sirtuin 2 ; Sirtuins/*antagonists & inhibitors/genetics/metabolism/*physiology ; Transfection ; alpha-Synuclein/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 41
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    Comment on "A centrosome-independent role for gamma-TuRC proteins in the spindle assembly checkpoint" (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-19
    Description: Muller et al. (Reports, 27 October 2006, p. 654) showed that inhibition of the gamma-tubulin ring complex (gamma-TuRC) activates the spindle assembly checkpoint (SAC), which led them to suggest that gamma-TuRC proteins play molecular roles in SAC activation. Because gamma-TuRC inhibition leads to pleiotropic spindle defects, which are well known to activate kinetochore-derived checkpoint signaling, we believe that this conclusion is premature.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2590763/" 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/PMC2590763/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taylor, Stephen S -- Hardwick, Kevin G -- Sawin, Kenneth E -- Biggins, Sue -- Piatti, Simonetta -- Khodjakov, Alexey -- Rieder, Conly L -- Salmon, Edward D -- Musacchio, Andrea -- R01 GM059363/GM/NIGMS NIH HHS/ -- R01 GM059363-09/GM/NIGMS NIH HHS/ -- R37 GM040198/GM/NIGMS NIH HHS/ -- R37 GM040198-23/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 May 18;316(5827):982; author reply 982.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Faculty of Life Sciences, University of Manchester, Manchester, UK. stephen.taylor@manchester.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17510347" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Centrosome/physiology ; Kinetochores/*physiology ; Microtubule-Associated Proteins/antagonists & inhibitors/*metabolism ; Microtubules/*metabolism/ultrastructure ; *Mitosis ; Signal Transduction ; Spindle Apparatus/*metabolism ; Tubulin/*metabolism
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  • 42
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    Multiple functions of the IKK-related kinase IKKepsilon in interferon-mediated antiviral immunity (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-03-03
    Description: IKKepsilon is an IKK (inhibitor of nuclear factor kappaBkinase)-related kinase implicated in virus induction of interferon-beta (IFNbeta). We report that, although mice lacking IKKepsilon produce normal amounts of IFNbeta, they are hypersusceptible to viral infection because of a defect in the IFN signaling pathway. Specifically, a subset of type I IFN-stimulated genes are not activated in the absence of IKKepsilon because the interferon-stimulated gene factor 3 complex (ISGF3) does not bind to promoter elements of the affected genes. We demonstrate that IKKepsilon is activated by IFNbeta and that IKKepsilon directly phosphorylates signal transducer and activator of transcription 1 (STAT1), a component of ISGF3. We conclude that IKKepsilon plays a critical role in the IFN-inducible antiviral transcriptional response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tenoever, Benjamin R -- Ng, Sze-Ling -- Chua, Mark A -- McWhirter, Sarah M -- Garcia-Sastre, Adolfo -- Maniatis, Tom -- F31 AI056678/AI/NIAID NIH HHS/ -- P01AI058113/AI/NIAID NIH HHS/ -- R01AI46954/AI/NIAID NIH HHS/ -- U19AI62623/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Mar 2;315(5816):1274-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard University, 7 Divinity Avenue, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17332413" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Deaminase/genetics/metabolism ; Animals ; Cells, Cultured ; Dimerization ; *Gene Expression Regulation ; I-kappa B Kinase/genetics/*metabolism ; *Influenza A Virus, H1N1 Subtype/immunology/physiology ; Interferon-Stimulated Gene Factor 3/metabolism ; Interferon-beta/*immunology/metabolism ; Lung/pathology/virology ; Mice ; Mice, Knockout ; Orthomyxoviridae Infections/*immunology/metabolism/pathology/virology ; Phosphorylation ; Promoter Regions, Genetic ; RNA-Binding Proteins ; STAT1 Transcription Factor/metabolism ; STAT2 Transcription Factor/metabolism ; Signal Transduction ; Transcription, Genetic ; Viral Load ; Virus Replication
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Cysteine redox sensor in PKGIa enables oxidant-induced activation (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-25
    Description: Changes in the concentration of oxidants in cells can regulate biochemical signaling mechanisms that control cell function. We have found that guanosine 3',5'-monophosphate (cGMP)-dependent protein kinase (PKG) functions directly as a redox sensor. The Ialpha isoform, PKGIalpha, formed an interprotein disulfide linking its two subunits in cells exposed to exogenous hydrogen peroxide. This oxidation directly activated the kinase in vitro, and in rat cells and tissues. The affinity of the kinase for substrates it phosphorylates was enhanced by disulfide formation. This oxidation-induced activation represents an alternate mechanism for regulation along with the classical activation involving nitric oxide and cGMP. This mechanism underlies cGMP-independent vasorelaxation in response to oxidants in the cardiovascular system and provides a molecular explantion for how hydrogen peroxide can operate as an endothelium-derived hyperpolarizing factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burgoyne, Joseph R -- Madhani, Melanie -- Cuello, Friederike -- Charles, Rebecca L -- Brennan, Jonathan P -- Schroder, Ewald -- Browning, Darren D -- Eaton, Philip -- G0700320/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Sep 7;317(5843):1393-7. Epub 2007 Aug 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiology, Cardiovascular Division, King's College London, Rayne Institute, St. Thomas' Hospital, London SE1 7EH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17717153" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta ; Cell Line ; Cyclic GMP/metabolism ; Cyclic GMP-Dependent Protein Kinase Type I ; Cyclic GMP-Dependent Protein Kinases/genetics/*metabolism ; Cysteine/*metabolism ; Disulfides/metabolism ; Enzyme Activation ; Humans ; Hydrogen Peroxide/metabolism ; Male ; Nitric Oxide/metabolism ; Oxidants/*metabolism ; Oxidation-Reduction ; Oxidative Stress ; Rats ; Rats, Wistar ; Signal Transduction ; Tissue Culture Techniques ; Transfection ; Vasodilation/physiology
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  • 44
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    Combinatorial ShcA docking interactions support diversity in tissue morphogenesis (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-07-14
    Description: Changes in protein-protein interactions may allow polypeptides to perform unexpected regulatory functions. Mammalian ShcA docking proteins have amino-terminal phosphotyrosine (pTyr) binding (PTB) and carboxyl-terminal Src homology 2 (SH2) domains, which recognize specific pTyr sites on activated receptors, and a central region with two phosphorylated tyrosine-X-asparagine (pYXN) motifs (where X represents any amino acid) that each bind the growth factor receptor-bound protein 2 (Grb2) adaptor. Phylogenetic analysis indicates that ShcA may signal through both pYXN-dependent and -independent pathways. We show that, in mice, cardiomyocyte-expressed ShcA directs mid-gestational heart development by a PTB-dependent mechanism that does not require the pYXN motifs. In contrast, the pYXN motifs are required with PTB and SH2 domains in the same ShcA molecule for the formation of muscle spindles, skeletal muscle sensory organs that regulate motor behavior. Thus, combinatorial differences in ShcA docking interactions may yield multiple signaling mechanisms to support diversity in tissue morphogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2575375/" 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/PMC2575375/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hardy, W Rod -- Li, Lingying -- Wang, Zhi -- Sedy, Jiri -- Fawcett, James -- Frank, Eric -- Kucera, Jan -- Pawson, Tony -- R01 NS024373/NS/NINDS NIH HHS/ -- R01 NS024373-18/NS/NINDS NIH HHS/ -- R01 NS024373-19/NS/NINDS NIH HHS/ -- R01 NS024373-20/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2007 Jul 13;317(5835):251-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute, Mount Sinai Hospital, 600 University Avenue, Toronto, Ontario M5G 1X5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17626887" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/chemistry/genetics/*metabolism ; Amino Acid Motifs ; Animals ; Ataxia ; Excitatory Postsynaptic Potentials ; Genetic Complementation Test ; Heart/*embryology ; Mice ; Mice, Knockout ; *Morphogenesis ; Motor Activity ; Muscle Spindles/*embryology ; Muscle, Skeletal/*embryology/metabolism ; Mutation ; Myocytes, Cardiac/*metabolism ; Neurons, Afferent/physiology ; Phosphorylation ; Protein Structure, Tertiary ; Shc Signaling Adaptor Proteins ; Signal Transduction ; src Homology Domains
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    Materials science. Polymer therapeutics (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-01
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884993/" 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/PMC2884993/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kiick, Kristi L -- P20 RR017716/RR/NCRR NIH HHS/ -- P20 RR017716-010004/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2007 Aug 31;317(5842):1182-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Materials Science and Engineering, University of Delaware, Newark, DE 19716, USA. kiick@udel.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17761873" target="_blank"〉PubMed〈/a〉
    Keywords: B-Lymphocytes/immunology ; Drug Carriers ; Drug Delivery Systems ; Drug Design ; Hydrogels ; L-Selectin/metabolism ; Leukocytes/metabolism ; Ligands ; Peptides/chemistry/metabolism/*therapeutic use ; Polymers/chemistry/metabolism/*therapeutic use ; Receptors, Antigen, B-Cell/immunology/metabolism ; Receptors, Cell Surface/metabolism ; Signal Transduction
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    Plant science. Infectious heresy (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Downie, J Allan -- New York, N.Y. -- Science. 2007 Jun 1;316(5829):1296-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology, John Innes Centre, Norwich NR4 7UH, UK. allan.downie@bbsrc.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17540893" target="_blank"〉PubMed〈/a〉
    Keywords: Acyltransferases/genetics/metabolism ; Bacterial Proteins/genetics/metabolism ; Bradyrhizobium/genetics/growth & development/*physiology ; Cytokinins/metabolism ; Fabaceae/*microbiology ; Genes, Bacterial ; Mutation ; N-Acetylglucosaminyltransferases/genetics/metabolism ; *Nitrogen Fixation ; Photosynthesis ; Plant Roots/microbiology ; Plant Stems/microbiology ; Purines/biosynthesis ; Root Nodules, Plant/microbiology/*physiology ; Signal Transduction ; *Symbiosis
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    Asymmetric T lymphocyte division in the initiation of adaptive immune responses (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-03-03
    Description: A hallmark of mammalian immunity is the heterogeneity of cell fate that exists among pathogen-experienced lymphocytes. We show that a dividing T lymphocyte initially responding to a microbe exhibits unequal partitioning of proteins that mediate signaling, cell fate specification, and asymmetric cell division. Asymmetric segregation of determinants appears to be coordinated by prolonged interaction between the T cell and its antigen-presenting cell before division. Additionally, the first two daughter T cells displayed phenotypic and functional indicators of being differentially fated toward effector and memory lineages. These results suggest a mechanism by which a single lymphocyte can apportion diverse cell fates necessary for adaptive immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, John T -- Palanivel, Vikram R -- Kinjyo, Ichiko -- Schambach, Felix -- Intlekofer, Andrew M -- Banerjee, Arnob -- Longworth, Sarah A -- Vinup, Kristine E -- Mrass, Paul -- Oliaro, Jane -- Killeen, Nigel -- Orange, Jordan S -- Russell, Sarah M -- Weninger, Wolfgang -- Reiner, Steven L -- AI007532/AI/NIAID NIH HHS/ -- AI042370/AI/NIAID NIH HHS/ -- AI053827/AI/NIAID NIH HHS/ -- AI055428/AI/NIAID NIH HHS/ -- AI061699/AI/NIAID NIH HHS/ -- AI069380/AI/NIAID NIH HHS/ -- CA114114/CA/NCI NIH HHS/ -- CA87812/CA/NCI NIH HHS/ -- DK007066/DK/NIDDK NIH HHS/ -- GM007170/GM/NIGMS NIH HHS/ -- R01 AI061699/AI/NIAID NIH HHS/ -- T32 AI055428/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Mar 23;315(5819):1687-91. Epub 2007 Mar 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Abramson Family Cancer Research Institute and Department of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17332376" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Antigen Presentation ; Antigens, CD/analysis ; Antigens, CD8/analysis ; CD8-Positive T-Lymphocytes/*cytology/*immunology ; Cell Differentiation ; *Cell Division ; Cell Lineage ; Cell Polarity ; Dendritic Cells/immunology ; *Immunologic Memory ; Intracellular Signaling Peptides and Proteins/metabolism ; Listeria monocytogenes/immunology ; Listeriosis/immunology ; Lymphocyte Activation ; Membrane Proteins/analysis ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mitosis ; Nerve Tissue Proteins/analysis ; Protein Kinase C/metabolism ; Receptors, Antigen, T-Cell/immunology ; Receptors, Interferon/analysis ; Signal Transduction ; T-Lymphocyte Subsets/*cytology/*immunology ; T-Lymphocytes, Helper-Inducer/immunology
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    Regulation of B versus T lymphoid lineage fate decision by the proto-oncogene LRF (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-15
    Description: Hematopoietic stem cells in the bone marrow give rise to lymphoid progenitors, which subsequently differentiate into B and T lymphocytes. Here we show that the proto-oncogene LRF plays an essential role in the B versus T lymphoid cell-fate decision. We demonstrate that LRF is key for instructing early lymphoid progenitors in mice to develop into B lineage cells by repressing T cell-instructive signals produced by the cell-fate signal protein, Notch. We propose a new model for lymphoid lineage commitment, in which LRF acts as a master regulator of the cell's determination of B versus T lineage.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2978506/" 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/PMC2978506/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maeda, Takahiro -- Merghoub, Taha -- Hobbs, Robin M -- Dong, Lin -- Maeda, Manami -- Zakrzewski, Johannes -- van den Brink, Marcel R M -- Zelent, Arthur -- Shigematsu, Hirokazu -- Akashi, Koichi -- Teruya-Feldstein, Julie -- Cattoretti, Giorgio -- Pandolfi, Pier Paolo -- CA-102142/CA/NCI NIH HHS/ -- R01 CA102142/CA/NCI NIH HHS/ -- R01 CA102142-06A1/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 May 11;316(5826):860-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17495164" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*cytology/physiology ; Bone Marrow Cells/cytology ; Cell Lineage ; Cells, Cultured ; DNA-Binding Proteins/*genetics/physiology ; Gene Deletion ; Hematopoietic Stem Cells/*cytology/physiology ; *Lymphopoiesis ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Models, Biological ; *Proto-Oncogenes ; Receptors, Notch/*metabolism ; Signal Transduction ; T-Lymphocytes/*cytology/physiology ; Thymus Gland/cytology ; Transcription Factors/*genetics/physiology
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    Development. Built to run, not fail (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-03-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oliveri, Paola -- Davidson, Eric H -- HD-37105/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2007 Mar 16;315(5818):1510-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA. poliveri@caltech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17363653" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Embryonic Development/*genetics ; *Gene Regulatory Networks ; Genes, Regulator ; Repressor Proteins/genetics/metabolism ; Signal Transduction ; Transcription Factors/genetics/metabolism
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    Cell biology. Proteins that promote long life (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Stuart K -- New York, N.Y. -- Science. 2007 Aug 3;317(5838):603-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Developmental Biology and Genetics, Stanford University Medical Center, Stanford, CA 94305-5329, USA. kim@cmgm.stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17673641" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; Caenorhabditis elegans/genetics/*physiology ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Gene Expression Regulation ; Genes, Helminth ; Longevity/*physiology ; Mass Spectrometry ; Metabolic Networks and Pathways ; Models, Animal ; Mutation ; RNA Interference ; Receptor, Insulin/genetics/*metabolism ; Signal Transduction
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 51
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    Promotion of tissue inflammation by the immune receptor Tim-3 expressed on innate immune cells (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-17
    Description: CD4+ T helper 1 (TH1) cells are important mediators of inflammation and are regulated by numerous pathways, including the negative immune receptor Tim-3. We found that Tim-3 is constitutively expressed on cells of the innate immune system in both mice and humans, and that it can synergize with Toll-like receptors. Moreover, an antibody agonist of Tim-3 acted as an adjuvant during induced immune responses, and Tim-3 ligation induced distinct signaling events in T cells and dendritic cells; the latter finding could explain the apparent divergent functions of Tim-3 in these cell types. Thus, by virtue of differential expression on innate versus adaptive immune cells, Tim-3 can either promote or terminate TH1 immunity and may be able to influence a range of inflammatory conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, Ana C -- Anderson, David E -- Bregoli, Lisa -- Hastings, William D -- Kassam, Nasim -- Lei, Charles -- Chandwaskar, Rucha -- Karman, Jozsef -- Su, Ee W -- Hirashima, Mitsuomi -- Bruce, Jeffrey N -- Kane, Lawrence P -- Kuchroo, Vijay K -- Hafler, David A -- R01 AI067544/AI/NIAID NIH HHS/ -- R01 AI067544-01A2/AI/NIAID NIH HHS/ -- R56 AI067544/AI/NIAID NIH HHS/ -- R56 AI067544-01A1/AI/NIAID NIH HHS/ -- R56 AI067544-02/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 16;318(5853):1141-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Immunology, Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18006747" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD11b/immunology ; Astrocytes/immunology ; Central Nervous System Neoplasms/immunology ; Dendritic Cells/immunology ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Galectins/immunology ; Glioblastoma/immunology ; Humans ; Immunity, Innate ; Inflammation Mediators/*immunology ; Lipopolysaccharides/immunology ; Macrophages/immunology ; Membrane Proteins/biosynthesis/*immunology ; Mice ; Microglia/immunology ; Multiple Sclerosis/immunology ; Rats ; Receptors, Immunologic/biosynthesis/*immunology ; Receptors, Virus/biosynthesis/*immunology ; Signal Transduction ; T-Lymphocytes/immunology ; Th1 Cells/*immunology ; Toll-Like Receptors
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Cancer. Converging on beta-catenin in Wilms tumor (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nusse, Roel -- New York, N.Y. -- Science. 2007 May 18;316(5827):988-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Howard Hughes Medical Institute, Stanford University, School of Medicine, Stanford, CA 94305-5323, USA. rnusse@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17510350" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Adenomatous Polyposis Coli Protein/metabolism ; Axin Protein ; Cell Nucleus/metabolism ; Chromosomes, Human, X/genetics ; Cytoplasm/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; *Genes, Wilms Tumor ; Humans ; Kidney Neoplasms/*genetics/metabolism ; Male ; Mutation ; Repressor Proteins/metabolism ; Signal Transduction ; Tumor Suppressor Proteins/*genetics/*metabolism ; Wilms Tumor/*genetics/metabolism ; Wnt Proteins/metabolism ; beta Catenin/genetics/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    LRP6 mutation in a family with early coronary disease and metabolic risk factors (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-03-03
    Description: Coronary artery disease (CAD) is the leading cause of death worldwide and is commonly caused by a constellation of risk factors called the metabolic syndrome. We characterized a family with autosomal dominant early CAD, features of the metabolic syndrome (hyperlipidemia, hypertension, and diabetes), and osteoporosis. These traits showed genetic linkage to a short segment of chromosome 12p, in which we identified a missense mutation in LRP6, which encodes a co-receptor in the Wnt signaling pathway. The mutation, which substitutes cysteine for arginine at a highly conserved residue of an epidermal growth factor-like domain, impairs Wnt signaling in vitro. These results link a single gene defect in Wnt signaling to CAD and multiple cardiovascular risk factors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2945222/" 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/PMC2945222/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mani, Arya -- Radhakrishnan, Jayaram -- Wang, He -- Mani, Alaleh -- Mani, Mohammad-Ali -- Nelson-Williams, Carol -- Carew, Khary S -- Mane, Shrikant -- Najmabadi, Hossein -- Wu, Dan -- Lifton, Richard P -- K08 HD041481/HD/NICHD NIH HHS/ -- K08 HD041481-01/HD/NICHD NIH HHS/ -- P01DK68229/DK/NIDDK NIH HHS/ -- P50 HL55007/HL/NHLBI NIH HHS/ -- R01 AR051476/AR/NIAMS NIH HHS/ -- R01 AR051476-01A1/AR/NIAMS NIH HHS/ -- R01 AR051476-02/AR/NIAMS NIH HHS/ -- R01 AR051476-03/AR/NIAMS NIH HHS/ -- R01 AR051476-04/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Mar 2;315(5816):1278-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Howard Hughes Medical Institute and Yale University School of Medicine, New Haven, CT 06510, USA. arya.mani@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17332414" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Aged, 80 and over ; Amino Acid Substitution ; Animals ; Chromosomes, Human, Pair 12/genetics ; Coronary Disease/*genetics/metabolism ; Family Health ; Female ; Genetic Linkage ; *Genetic Predisposition to Disease ; Humans ; LDL-Receptor Related Proteins/*genetics/physiology ; Lipids/blood ; Low Density Lipoprotein Receptor-Related Protein-6 ; Male ; Metabolic Syndrome X/*genetics/metabolism ; Mice ; Middle Aged ; *Mutation, Missense ; NIH 3T3 Cells ; Osteoporosis/genetics ; Pedigree ; Risk Factors ; Signal Transduction ; Wnt Proteins/metabolism
    Print ISSN: 0036-8075
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    Beta-catenin defines head versus tail identity during planarian regeneration and homeostasis (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007
    Description: After amputation, freshwater planarians properly regenerate a head or tail from the resulting anterior or posterior wound. The mechanisms that differentiate anterior from posterior and direct the replacement of the appropriate missing body parts are unknown. We found that in the planarian Schmidtea mediterranea, RNA interference (RNAi) of beta-catenin or dishevelled causes the inappropriate regeneration of a head instead of a tail at posterior amputations. Conversely, RNAi of the beta-catenin antagonist adenomatous polyposis coli results in the regeneration of a tail at anterior wounds. In addition, the silencing of beta-catenin is sufficient to transform the tail of uncut adult animals into a head. We suggest that beta-catenin functions as a molecular switch to specify and maintain anteroposterior identity during regeneration and homeostasis in planarians.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2755502/" 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/PMC2755502/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gurley, Kyle A -- Rink, Jochen C -- Sanchez Alvarado, Alejandro -- F32GM082016/GM/NIGMS NIH HHS/ -- R0-1 GM57260/GM/NIGMS NIH HHS/ -- R01 GM057260/GM/NIGMS NIH HHS/ -- R01 GM057260-08/GM/NIGMS NIH HHS/ -- T32CA093247/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Jan 18;319(5861):323-7. Epub 2007 Dec 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Anatomy, Howard Hughes Medical Institute, University of Utah School of Medicine, 401 MREB, 20N 1900E, Salt Lake City, UT 84132, USA. sanchez@neuro.utah.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18063757" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/chemistry/genetics/physiology ; Adenomatous Polyposis Coli Protein/chemistry/physiology ; Amino Acid Sequence ; Animals ; Body Patterning ; Gene Expression Profiling ; Genes, APC ; Head ; Helminth Proteins/chemistry/genetics/physiology ; Homeostasis ; Molecular Sequence Data ; Phosphoproteins/chemistry/genetics/physiology ; Planarians/genetics/*physiology ; RNA Interference ; *Regeneration ; Signal Transduction ; Tail ; beta Catenin/chemistry/genetics/*physiology
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    Evolutionary dynamics of immune-related genes and pathways in disease-vector mosquitoes (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-26
    Description: Mosquitoes are vectors of parasitic and viral diseases of immense importance for public health. The acquisition of the genome sequence of the yellow fever and Dengue vector, Aedes aegypti (Aa), has enabled a comparative phylogenomic analysis of the insect immune repertoire: in Aa, the malaria vector Anopheles gambiae (Ag), and the fruit fly Drosophila melanogaster (Dm). Analysis of immune signaling pathways and response modules reveals both conservative and rapidly evolving features associated with different functional gene categories and particular aspects of immune reactions. These dynamics reflect in part continuous readjustment between accommodation and rejection of pathogens and suggest how innate immunity may have evolved.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2042107/" 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/PMC2042107/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Waterhouse, Robert M -- Kriventseva, Evgenia V -- Meister, Stephan -- Xi, Zhiyong -- Alvarez, Kanwal S -- Bartholomay, Lyric C -- Barillas-Mury, Carolina -- Bian, Guowu -- Blandin, Stephanie -- Christensen, Bruce M -- Dong, Yuemei -- Jiang, Haobo -- Kanost, Michael R -- Koutsos, Anastasios C -- Levashina, Elena A -- Li, Jianyong -- Ligoxygakis, Petros -- Maccallum, Robert M -- Mayhew, George F -- Mendes, Antonio -- Michel, Kristin -- Osta, Mike A -- Paskewitz, Susan -- Shin, Sang Woon -- Vlachou, Dina -- Wang, Lihui -- Wei, Weiqi -- Zheng, Liangbiao -- Zou, Zhen -- Severson, David W -- Raikhel, Alexander S -- Kafatos, Fotis C -- Dimopoulos, George -- Zdobnov, Evgeny M -- Christophides, George K -- 1 R01 AI059492-01A1/AI/NIAID NIH HHS/ -- 5 R01 AI61576-2/AI/NIAID NIH HHS/ -- G0300170/Medical Research Council/United Kingdom -- GM41247/GM/NIGMS NIH HHS/ -- GR077229MA/Wellcome Trust/United Kingdom -- P01 AI044220-06A1/AI/NIAID NIH HHS/ -- R01 AI037083/AI/NIAID NIH HHS/ -- R01 GM058634/GM/NIGMS NIH HHS/ -- R01 GM058634-09/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Jun 22;316(5832):1738-43.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell and Molecular Biology, Faculty of Natural Sciences, Imperial College London, London SW7 2AZ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17588928" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/*genetics/immunology ; Animals ; Anopheles/*genetics/immunology ; Antimicrobial Cationic Peptides/physiology ; Carrier Proteins/genetics/physiology ; Drosophila melanogaster/genetics/immunology ; *Evolution, Molecular ; Genes, Insect ; Immunity, Innate/*genetics ; Insect Proteins/genetics/physiology ; Insect Vectors/*genetics/immunology ; Malaria/transmission ; Melanins/metabolism ; Multigene Family ; Signal Transduction ; Species Specificity
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    Control of Drosophila gastrulation by apical localization of adherens junctions and RhoGEF2 (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-01-20
    Description: A hallmark of epithelial invagination is the constriction of cells on their apical sides. During Drosophila gastrulation, apical constrictions under the control of the transcription factor Twist lead to the invagination of the mesoderm. Twist-controlled G protein signaling is involved in mediating the invagination but is not sufficient to account for the full activity of Twist. We identified a Twist target, the transmembrane protein T48, which acts in conjunction with G protein signaling to orchestrate shape changes. Together with G protein signaling, T48 recruits adherens junctions and the cytoskeletal regulator RhoGEF2 to the sites of apical constriction, ensuring rapid and intense changes in cell shape.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kolsch, Verena -- Seher, Thomas -- Fernandez-Ballester, Gregorio J -- Serrano, Luis -- Leptin, Maria -- New York, N.Y. -- Science. 2007 Jan 19;315(5810):384-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Genetics, University of Cologne, Zulpicher Strasse 47, 50674 Cologne, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17234948" target="_blank"〉PubMed〈/a〉
    Keywords: Adherens Junctions/*physiology/ultrastructure ; Amino Acid Motifs ; Animals ; Armadillo Domain Proteins/metabolism ; Cell Membrane/metabolism ; Cell Shape ; Drosophila Proteins/*metabolism ; Drosophila melanogaster/*embryology/metabolism ; Embryo, Nonmammalian/cytology/*physiology/ultrastructure ; Embryonic Development ; Gastrula/physiology ; Heterotrimeric GTP-Binding Proteins/metabolism ; Membrane Proteins/*metabolism ; Models, Biological ; Signal Transduction ; Transcription Factors/metabolism ; Twist Transcription Factor/metabolism ; rho GTP-Binding Proteins/*metabolism
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    Rheb activates mTOR by antagonizing its endogenous inhibitor, FKBP38 (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-10
    Description: The mammalian target of rapamycin, mTOR, is a central regulator of cell growth. Its activity is regulated by Rheb, a Ras-like small guanosine triphosphatase (GTPase), in response to growth factor stimulation and nutrient availability. We show that Rheb regulates mTOR through FKBP38, a member of the FK506-binding protein (FKBP) family that is structurally related to FKBP12. FKBP38 binds to mTOR and inhibits its activity in a manner similar to that of the FKBP12-rapamycin complex. Rheb interacts directly with FKBP38 and prevents its association with mTOR in a guanosine 5'-triphosphate (GTP)-dependent manner. Our findings suggest that FKBP38 is an endogenous inhibitor of mTOR, whose inhibitory activity is antagonized by Rheb in response to growth factor stimulation and nutrient availability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bai, Xiaochun -- Ma, Dongzhu -- Liu, Anling -- Shen, Xiaoyun -- Wang, Qiming J -- Liu, Yongjian -- Jiang, Yu -- GM068832/GM/NIGMS NIH HHS/ -- R01 CA129821/CA/NCI NIH HHS/ -- R01 GM068832/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 9;318(5852):977-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Pittsburgh School of Medicine, E1357 Biomedical Science Tower, 200 Lothrop Street, Pittsburgh, PA 15213, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17991864" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/metabolism ; Cell Line ; Culture Media ; Guanosine Triphosphate/metabolism ; Humans ; Insulin/metabolism ; Intercellular Signaling Peptides and Proteins/metabolism ; Monomeric GTP-Binding Proteins/*metabolism ; Multiprotein Complexes ; Mutant Proteins/metabolism ; Neuropeptides/*metabolism ; Phosphorylation ; Protein Binding ; Protein Kinases/chemistry/*metabolism ; Protein Structure, Tertiary ; Proteins ; Recombinant Proteins/metabolism ; Serum ; Signal Transduction ; Sirolimus/metabolism/pharmacology ; TOR Serine-Threonine Kinases ; Tacrolimus Binding Proteins/antagonists & inhibitors/*metabolism ; Transcription Factors/metabolism
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    The vaccine adjuvant monophosphoryl lipid A as a TRIF-biased agonist of TLR4 (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-16
    Description: The inflammatory toxicity of lipopolysaccharide (LPS), a component of bacterial cell walls, is driven by the adaptor proteins myeloid differentiation factor 88 (MyD88) and Toll-interleukin 1 receptor domain-containing adapter inducing interferon-beta (TRIF), which together mediate signaling by the endotoxin receptor Toll-like receptor 4 (TLR4). Monophosphoryl lipid A (MPLA) is a low-toxicity derivative of LPS with useful immunostimulatory properties, which is nearing regulatory approval for use as a human vaccine adjuvant. We report here that, in mice, the low toxicity of MPLA's adjuvant function is associated with a bias toward TRIF signaling, which we suggest is likely caused by the active suppression, rather than passive loss, of proinflammatory activity of this LPS derivative. This finding may have important implications for the development of future vaccine adjuvants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mata-Haro, Veronica -- Cekic, Caglar -- Martin, Michael -- Chilton, Paula M -- Casella, Carolyn R -- Mitchell, Thomas C -- AI059023/AI/NIAID NIH HHS/ -- AI51377/AI/NIAID NIH HHS/ -- K02 AI059023/AI/NIAID NIH HHS/ -- R01 AI051377/AI/NIAID NIH HHS/ -- R01 AI071047/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Jun 15;316(5831):1628-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cellular Therapeutics, University of Louisville, 570 South Preston Street, Louisville, KY 40202, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17569868" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Vesicular Transport/*metabolism ; *Adjuvants, Immunologic/administration & dosage/toxicity ; Adoptive Transfer ; Animals ; Cytokines/biosynthesis ; Immunization ; Lipid A/administration & dosage/*analogs & derivatives/immunology/toxicity ; Lipopolysaccharides/immunology ; Lymphocyte Activation ; Macrophages/immunology ; Mice ; Mice, Inbred C57BL ; Monocytes/immunology ; Myeloid Differentiation Factor 88/metabolism ; Oligonucleotide Array Sequence Analysis ; Ovalbumin/immunology ; Phosphatidylinositol 3-Kinases/metabolism ; Signal Transduction ; T-Lymphocytes/immunology ; Toll-Like Receptor 4/*agonists/*immunology/metabolism
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    Regulation of NF-kappaB activation in T cells via association of the adapter proteins ADAP and CARMA1 (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-05
    Description: The adapter protein ADAP regulates T lymphocyte adhesion and activation. We present evidence for a previously unrecognized function for ADAP in regulating T cell receptor (TCR)-mediated activation of the transcription factor NF-kappaB. Stimulation of ADAP-deficient mouse T cells with antibodies to CD3 and CD28 resulted in impaired nuclear translocation of NF-kappaB, a reduced DNA binding, and delayed degradation and decreased phosphorylation of IkappaB (inhibitor of NF-kappaB). TCR-stimulated assembly of the CARMA1-BCL-10-MALT1 complex was substantially impaired in the absence of ADAP. We further identified a region of ADAP that is required for association with the CARMA1 adapter and NF-kappaB activation but is not required for ADAP-dependent regulation of adhesion. These findings provide new insights into ADAP function and the mechanism by which CARMA1 regulates NF-kappaB activation in T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Medeiros, Ricardo B -- Burbach, Brandon J -- Mueller, Kristen L -- Srivastava, Rupa -- Moon, James J -- Highfill, Sarah -- Peterson, Erik J -- Shimizu, Yoji -- F32 AI063793/AI/NIAID NIH HHS/ -- F32 AI063793-01A1/AI/NIAID NIH HHS/ -- F32AI063793/AI/NIAID NIH HHS/ -- R01AI038474/AI/NIAID NIH HHS/ -- R01AI056016/AI/NIAID NIH HHS/ -- T32DE007288/DE/NIDCR NIH HHS/ -- New York, N.Y. -- Science. 2007 May 4;316(5825):754-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Laboratory Medicine and Pathology, Center for Immunology, Cancer Center, University of Minnesota Medical School, Minneapolis, MN 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17478723" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Adaptor Proteins, Signal Transducing/chemistry/genetics/*metabolism ; Animals ; Antigens, CD28/immunology ; Antigens, CD3/immunology ; Apoptosis Regulatory Proteins/*metabolism ; CARD Signaling Adaptor Proteins/*metabolism ; Caspases/metabolism ; Cell Membrane/metabolism ; Cell Nucleus/metabolism ; Humans ; I-kappa B Proteins/metabolism ; Isoenzymes/metabolism ; Jurkat Cells ; Lymphocyte Activation ; Mice ; Mutation ; Neoplasm Proteins/metabolism ; Protein Kinase C/metabolism ; Protein Structure, Tertiary ; Receptors, Antigen, T-Cell/immunology ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; T-Lymphocytes/*immunology/*metabolism ; Transcription Factor RelA/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Regulation of gammadelta versus alphabeta T lymphocyte differentiation by the transcription factor SOX13 (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-01-16
    Description: alphabeta and gammadelta T cells originate from a common, multipotential precursor population in the thymus, but the molecular mechanisms regulating this lineage-fate decision are unknown. We have identified Sox13 as a gammadelta-specific gene in the immune system. Using Sox13 transgenic mice, we showed that this transcription factor promotes gammadelta T cell development while opposing alphabeta T cell differentiation. Conversely, mice deficient in Sox13 expression exhibited impaired development of gammadelta T cells but not alphabeta T cells. One mechanism of SOX13 function is the inhibition of signaling by the developmentally important Wnt/T cell factor (TCF) pathway. Our data thus reveal a dominant pathway regulating the developmental fate of these two lineages of T lymphocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Melichar, Heather J -- Narayan, Kavitha -- Der, Sandy D -- Hiraoka, Yoshiki -- Gardiol, Noemie -- Jeannet, Gregoire -- Held, Werner -- Chambers, Cynthia A -- Kang, Joonsoo -- R01CA100382/92614/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 Jan 12;315(5809):230-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Graduate Program in Immunology and Virology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17218525" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/genetics ; Autoantigens/genetics/*metabolism ; Cell Line ; Cell Lineage ; Cell Proliferation ; Embryonic Development ; Gene Expression Profiling ; Gene Expression Regulation ; Gene Rearrangement, T-Lymphocyte ; High Mobility Group Proteins/genetics/*metabolism ; Humans ; *Lymphopoiesis ; Mice ; Mice, Transgenic ; Receptors, Antigen, T-Cell, alpha-beta/*analysis ; Receptors, Antigen, T-Cell, gamma-delta/*analysis/genetics ; Signal Transduction ; T Cell Transcription Factor 1/physiology ; T-Lymphocyte Subsets/*cytology/immunology/metabolism ; Wnt Proteins/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    ATM and ATR substrate analysis reveals extensive protein networks responsive to DNA damage (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-26
    Description: Cellular responses to DNA damage are mediated by a number of protein kinases, including ATM (ataxia telangiectasia mutated) and ATR (ATM and Rad3-related). The outlines of the signal transduction portion of this pathway are known, but little is known about the physiological scope of the DNA damage response (DDR). We performed a large-scale proteomic analysis of proteins phosphorylated in response to DNA damage on consensus sites recognized by ATM and ATR and identified more than 900 regulated phosphorylation sites encompassing over 700 proteins. Functional analysis of a subset of this data set indicated that this list is highly enriched for proteins involved in the DDR. This set of proteins is highly interconnected, and we identified a large number of protein modules and networks not previously linked to the DDR. This database paints a much broader landscape for the DDR than was previously appreciated and opens new avenues of investigation into the responses to DNA damage in mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsuoka, Shuhei -- Ballif, Bryan A -- Smogorzewska, Agata -- McDonald, E Robert 3rd -- Hurov, Kristen E -- Luo, Ji -- Bakalarski, Corey E -- Zhao, Zhenming -- Solimini, Nicole -- Lerenthal, Yaniv -- Shiloh, Yosef -- Gygi, Steven P -- Elledge, Stephen J -- 1U19A1067751/PHS HHS/ -- New York, N.Y. -- Science. 2007 May 25;316(5828):1160-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Center for Genetics and Genomics, Brigham and Women's Hospital, Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17525332" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxia Telangiectasia Mutated Proteins ; Binding Sites ; Cell Cycle/physiology ; Cell Cycle Proteins/*physiology ; Cell Line ; Computational Biology ; Consensus Sequence ; *DNA Damage ; *DNA Repair ; DNA Replication/physiology ; DNA-Binding Proteins/*physiology ; Humans ; Immunoprecipitation ; Isotope Labeling ; Mice ; NIH 3T3 Cells ; Phosphorylation ; Protein-Serine-Threonine Kinases/*physiology ; Proteome/isolation & purification/physiology ; RNA, Small Interfering ; Signal Transduction ; Substrate Specificity ; Tumor Suppressor Proteins/*physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Cell signaling. A touching response to damage (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petrini, John H J -- R01 GM059413/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 May 25;316(5828):1138-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA. petrinij@mskcc.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17525326" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxia Telangiectasia Mutated Proteins ; BRCA1 Protein/physiology ; Carrier Proteins/physiology ; Cell Cycle Proteins/physiology ; *DNA Damage ; *DNA Repair ; DNA-Binding Proteins/physiology ; Humans ; Nuclear Proteins/physiology ; Phosphorylation ; Protein-Serine-Threonine Kinases/physiology ; Signal Transduction ; Tumor Suppressor Proteins/physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Neuroscience. A push-me pull-you neural design (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kristan, William B -- New York, N.Y. -- Science. 2007 Jan 19;315(5810):339-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurobiology Section, Division of Biological Sciences, University of California, San Diego, La Jolla, CA 92093-0357, USA. wkristan@ucsd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17234936" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Motor Neurons/*physiology ; Nerve Net/*physiology ; Neural Conduction ; *Neural Inhibition ; Reflex/physiology ; Signal Transduction ; Spinal Cord/cytology/*physiology ; Synaptic Transmission ; Turtles/*physiology
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    Host resistance to lung infection mediated by major vault protein in epithelial cells (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-07-07
    Description: The airway epithelium plays an essential role in innate immunity to lung pathogens. Ribonucleoprotein particles primarily composed of major vault protein (MVP) are highly expressed in cells that encounter xenobiotics. However, a clear biologic function for MVP is not established. We report here that MVP is rapidly recruited to lipid rafts when human lung epithelial cells are infected with Pseudomonas aeruginosa, and maximal recruitment is dependent on bacterial binding to the cystic fibrosis transmembrane conductance regulator. MVP was also essential for optimal epithelial cell internalization and clearance of P. aeruginosa. These results suggest that MVP makes a substantial contribution to epithelial cell-mediated resistance to infection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3685177/" 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/PMC3685177/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kowalski, Michael P -- Dubouix-Bourandy, Anne -- Bajmoczi, Milan -- Golan, David E -- Zaidi, Tanweer -- Coutinho-Sledge, Yamara S -- Gygi, Melanie P -- Gygi, Steven P -- Wiemer, Erik A C -- Pier, Gerald B -- R01 HL 58398-08/HL/NHLBI NIH HHS/ -- R01 HL058398/HL/NHLBI NIH HHS/ -- R37 HL 32854-22/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2007 Jul 6;317(5834):130-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17615361" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cystic Fibrosis Transmembrane Conductance Regulator/genetics/metabolism ; Epithelial Cells/metabolism/microbiology ; Humans ; Immunity, Innate ; Lung/immunology/microbiology ; Lung Diseases/*immunology/metabolism/microbiology ; Membrane Microdomains/metabolism ; Mice ; Pseudomonas Infections/*immunology/metabolism/microbiology ; Pseudomonas aeruginosa/*immunology/metabolism ; RNA, Small Interfering/genetics ; Respiratory Mucosa/immunology/*metabolism/*microbiology ; Signal Transduction ; Vault Ribonucleoprotein Particles/*physiology
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    Cancer. Sex, cytokines, and cancer (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-07-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lawrence, Toby -- Hageman, Thorsten -- Balkwill, Frances -- G0501974/Medical Research Council/United Kingdom -- G0601867/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Jul 6;317(5834):51-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Translational Oncology, Institute of Cancer, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London EC1M 6BQ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17615328" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Colonic Neoplasms/physiopathology ; Disease Progression ; Female ; Humans ; Immunity, Innate ; Interleukin-6/*metabolism ; Kupffer Cells/metabolism ; Liver Neoplasms, Experimental/immunology/physiopathology ; Male ; Mice ; Myeloid Differentiation Factor 88/*physiology ; NF-kappa B/metabolism ; Neoplasms/drug therapy/*physiopathology/prevention & control ; Sex Characteristics ; Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Neuroscience. Synapses here and not everywhere (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, David M -- New York, N.Y. -- Science. 2007 Aug 17;317(5840):907-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, Vanderbilt University, 465 21st Avenue South, Nashville, TN 37232-8240, USA. david.miller@vanderbilt.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17702933" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/growth & development/metabolism/*physiology ; Caenorhabditis elegans Proteins/*metabolism ; Cell Cycle Proteins/*metabolism ; Cues ; Immunoglobulins/*metabolism ; Models, Neurological ; Motor Neurons/*physiology ; Nerve Tissue Proteins/metabolism ; Oviposition ; SKP Cullin F-Box Protein Ligases/*metabolism ; Signal Transduction ; Synapses/*physiology
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    Blurring the boundary: the nuclear envelope extends its reach (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-12-01
    Description: The past decade has seen a complete rethinking of the traditional view of the nuclear envelope as simply a passive enclosure for the chromosomes. The convergence of several lines of clinical and basic research has revealed additional roles in both signaling and mitotic progression. It is becoming apparent that the nuclear envelope defines not only nuclear organization but also that of the cytoskeleton and, in this way, integrates both nuclear and cytoplasmic architecture.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stewart, Colin L -- Roux, Kyle J -- Burke, Brian -- New York, N.Y. -- Science. 2007 Nov 30;318(5855):1408-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Medical Biology, 61 Biopolis Drive, Proteos, Singapore 138668, Singapore.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18048680" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytoplasm/physiology/ultrastructure ; Cytoskeleton/parasitology/physiology/ultrastructure ; Genetic Diseases, Inborn/pathology/physiopathology ; Humans ; Lamins/genetics ; Mitosis ; Mutation ; Nuclear Envelope/*physiology/*ultrastructure ; Nuclear Lamina/physiology/ultrastructure ; Nuclear Pore/physiology/ultrastructure ; Signal Transduction ; Virus Diseases/metabolism/virology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Regulation of the oocyte-to-zygote transition (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-21
    Description: Oocytes, the female germ cells, contain all the messenger RNAs necessary to start a new life but typically wait until fertilization to begin development. The transition from oocyte to fertilized egg (zygote) involves many changes, including protein synthesis, protein and RNA degradation, and organelle remodeling. These changes occur concurrently with the meiotic divisions that produce the haploid maternal genome. Accumulating evidence indicates that the cell-cycle regulators that control the meiotic divisions also regulate the many changes that accompany the oocyte-to-zygote transition. We suggest that the meiotic machinery functions as an internal pacemaker that propels oocytes toward embryogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stitzel, Michael L -- Seydoux, Geraldine -- New York, N.Y. -- Science. 2007 Apr 20;316(5823):407-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics and Howard Hughes Medical Institute, Johns Hopkins School of Medicine, 725 North Wolfe Street, PCTB 706, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17446393" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle ; Female ; Meiosis ; Oocytes/cytology/*physiology ; Organelles ; Protein Biosynthesis ; Proteins/metabolism ; RNA Stability ; RNA, Messenger/metabolism ; RNA, Messenger, Stored/metabolism ; Signal Transduction ; Zygote/cytology/*physiology
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    Division of labor with a workforce of one: challenges in specifying effector and memory T cell fate (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-04
    Description: In the course of the immune response against microbes, naive T cells proliferate and generate varied classes of effector cells, as well as memory cells with distinct properties and functions. Owing to recent technological advances, some of the most imposing questions regarding effector and memory T cell differentiation are now becoming experimentally soluble: How many classes of antigen-specific T cells exist, and how malleable are they in their fate and in their functional state? How might a spectrum of cell fates be imparted to the clonal descendants of a single lymphocyte? Where, when, and how does pathogen-associated information refine the instruction, selection, and direction of newly activated T cells as they perform their tasks in different locations and times? Some surprising new glimpses ahead on these subjects and other yet-unanswered questions are discussed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reiner, Steven L -- Sallusto, Federica -- Lanzavecchia, Antonio -- New York, N.Y. -- Science. 2007 Aug 3;317(5838):622-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Abramson Family Cancer Research Institute of the University of Pennsylvania, Philadelphia, PA 19104, USA. sreiner@mail.med.upenn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17673652" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/immunology ; CD4-Positive T-Lymphocytes/cytology/*immunology ; Cell Differentiation ; Cell Lineage ; Cytokines/immunology ; Humans ; *Immunologic Memory ; Lymphocyte Activation ; Models, Immunological ; Signal Transduction ; T-Lymphocyte Subsets/cytology/*immunology ; T-Lymphocytes, Helper-Inducer/cytology/*immunology
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    Regulation of a cyclin-CDK-CDK inhibitor complex by inositol pyrophosphates (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-04-07
    Description: In budding yeast, phosphate starvation triggers inhibition of the Pho80-Pho85 cyclin-cyclin-dependent kinase (CDK) complex by the CDK inhibitor Pho81, leading to expression of genes involved in nutrient homeostasis. We isolated myo-d-inositol heptakisphosphate (IP7) as a cellular component that stimulates Pho81-dependent inhibition of Pho80-Pho85. IP7 is necessary for Pho81-dependent inhibition of Pho80-Pho85 in vitro. Moreover, intracellular concentrations of IP7 increased upon phosphate starvation, and yeast mutants defective in IP7 production failed to inhibit Pho80-Pho85 in response to phosphate starvation. These observations reveal regulation of a cyclin-CDK complex by a metabolite and suggest that a complex metabolic network mediates signaling of phosphate availability.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2211727/" 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/PMC2211727/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Young-Sam -- Mulugu, Sashidhar -- York, John D -- O'Shea, Erin K -- DK070272/DK/NIDDK NIH HHS/ -- HL055672/HL/NHLBI NIH HHS/ -- R01 GM051377/GM/NIGMS NIH HHS/ -- R01 GM051377-15/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Apr 6;316(5821):109-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Faculty of Arts and Sciences Center for Systems Biology, Department of Molecular and Cellular Biology, Harvard University, 7 Divinity Avenue, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17412959" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Nucleus/metabolism ; Cyclin-Dependent Kinases/*antagonists & inhibitors/metabolism ; Cyclins/*antagonists & inhibitors/metabolism ; DNA-Binding Proteins/metabolism ; Inositol Phosphates/*metabolism ; Phosphotransferases (Phosphate Group Acceptor)/genetics/metabolism ; Recombinant Proteins/metabolism ; Repressor Proteins/*antagonists & inhibitors/*metabolism ; Saccharomyces cerevisiae/genetics/*metabolism ; Saccharomyces cerevisiae Proteins/*antagonists & inhibitors/*metabolism ; Signal Transduction ; Transcription Factors/metabolism
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    Physiology. Sister act (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moore, David D -- New York, N.Y. -- Science. 2007 Jun 8;316(5830):1436-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA. moore@bcm.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17556573" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyl Coenzyme A/metabolism ; Adenosine Monophosphate/metabolism ; Animals ; Body Temperature ; Energy Metabolism ; Fasting ; Fatty Acids/*metabolism ; Fibroblast Growth Factors/genetics/*metabolism/pharmacology ; Glucuronidase/metabolism ; Glycoside Hydrolases/metabolism ; Homeostasis ; Humans ; Ketone Bodies/metabolism ; Lipase/metabolism ; Liver/*metabolism ; Membrane Proteins/*metabolism ; Mice ; Mice, Transgenic ; Motor Activity ; Oxidation-Reduction ; PPAR alpha/*metabolism ; Signal Transduction
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    Genomic minimalism in the early diverging intestinal parasite Giardia lamblia (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-29
    Description: The genome of the eukaryotic protist Giardia lamblia, an important human intestinal parasite, is compact in structure and content, contains few introns or mitochondrial relics, and has simplified machinery for DNA replication, transcription, RNA processing, and most metabolic pathways. Protein kinases comprise the single largest protein class and reflect Giardia's requirement for a complex signal transduction network for coordinating differentiation. Lateral gene transfer from bacterial and archaeal donors has shaped Giardia's genome, and previously unknown gene families, for example, cysteine-rich structural proteins, have been discovered. Unexpectedly, the genome shows little evidence of heterozygosity, supporting recent speculations that this organism is sexual. This genome sequence will not only be valuable for investigating the evolution of eukaryotes, but will also be applied to the search for new therapeutics for this parasite.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morrison, Hilary G -- McArthur, Andrew G -- Gillin, Frances D -- Aley, Stephen B -- Adam, Rodney D -- Olsen, Gary J -- Best, Aaron A -- Cande, W Zacheus -- Chen, Feng -- Cipriano, Michael J -- Davids, Barbara J -- Dawson, Scott C -- Elmendorf, Heidi G -- Hehl, Adrian B -- Holder, Michael E -- Huse, Susan M -- Kim, Ulandt U -- Lasek-Nesselquist, Erica -- Manning, Gerard -- Nigam, Anuranjini -- Nixon, Julie E J -- Palm, Daniel -- Passamaneck, Nora E -- Prabhu, Anjali -- Reich, Claudia I -- Reiner, David S -- Samuelson, John -- Svard, Staffan G -- Sogin, Mitchell L -- AI42488/AI/NIAID NIH HHS/ -- AI43273/AI/NIAID NIH HHS/ -- AI51687/AI/NIAID NIH HHS/ -- R01 AI043273/AI/NIAID NIH HHS/ -- R01 AI048082/AI/NIAID NIH HHS/ -- R01 HG004164/HG/NHGRI NIH HHS/ -- R01 HG004164-01/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2007 Sep 28;317(5846):1921-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Marine Biological Laboratory, Woods Hole, MA 02543-1015, USA. morrison@mbl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17901334" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Biological Evolution ; DNA Replication/genetics ; *Eukaryotic Cells ; Gene Transfer, Horizontal ; Genes, Protozoan ; *Genome, Protozoan ; Genomics ; Giardia lamblia/classification/*genetics/physiology ; Metabolic Networks and Pathways/genetics ; Molecular Sequence Data ; Phylogeny ; Protein Kinases/genetics/metabolism ; Protozoan Proteins/chemistry/genetics/metabolism ; RNA Processing, Post-Transcriptional ; Signal Transduction ; Transcription, Genetic
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    Male germline stem cells: from mice to men (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-21
    Description: The production of functional male gametes is dependent on the continuous activity of germline stem cells. The availability of a transplantation assay system to unequivocally identify male germline stem cells has allowed their in vitro culture, cryopreservation, and genetic modification. Moreover, the system has enabled the identification of conditions and factors involved in stem cell self-renewal, the foundation of spermatogenesis, and the production of spermatozoa. The increased knowledge about these cells is also of great potential practical value, for example, for the possible cryopreservation of stem cells from boys undergoing treatment for cancer to safeguard their germ line.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brinster, Ralph L -- HDO44445/PHS HHS/ -- New York, N.Y. -- Science. 2007 Apr 20;316(5823):404-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17446391" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Culture Techniques ; Cryopreservation ; Gene Expression Regulation, Developmental ; Germ Cells/*cytology/physiology ; Glial Cell Line-Derived Neurotrophic Factor/physiology ; Humans ; Male ; Mice ; Sertoli Cells/cytology/physiology ; Signal Transduction ; Spermatogenesis ; Spermatogonia/*cytology/physiology ; Stem Cell Transplantation ; Stem Cells/*cytology/physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Structure of Galphaq-p63RhoGEF-RhoA complex reveals a pathway for the activation of RhoA by GPCRs (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-12-22
    Description: The guanine nucleotide exchange factor p63RhoGEF is an effector of the heterotrimeric guanine nucleotide-binding protein (G protein) Galphaq and thereby links Galphaq-coupled receptors (GPCRs) to the activation of the small-molecular-weight G protein RhoA. We determined the crystal structure of the Galphaq-p63RhoGEF-RhoA complex, detailing the interactions of Galphaq with the Dbl and pleckstrin homology (DH and PH) domains of p63RhoGEF. These interactions involve the effector-binding site and the C-terminal region of Galphaq and appear to relieve autoinhibition of the catalytic DH domain by the PH domain. Trio, Duet, and p63RhoGEF are shown to constitute a family of Galphaq effectors that appear to activate RhoA both in vitro and in intact cells. We propose that this structure represents the crux of an ancient signal transduction pathway that is expected to be important in an array of physiological processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lutz, Susanne -- Shankaranarayanan, Aruna -- Coco, Cassandra -- Ridilla, Marc -- Nance, Mark R -- Vettel, Christiane -- Baltus, Doris -- Evelyn, Chris R -- Neubig, Richard R -- Wieland, Thomas -- Tesmer, John J G -- HL071818/HL/NHLBI NIH HHS/ -- HL086865/HL/NHLBI NIH HHS/ -- Y1-CO-1020/CO/NCI NIH HHS/ -- Y1-GM-1104/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Dec 21;318(5858):1923-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Experimental and Clinical Pharmacology and Toxicology, Medical Faculty Mannheim, University of Heidelberg, Maybachstrasse 14, D-68169 Mannheim, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18096806" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Binding Sites ; Cell Line ; Crystallography, X-Ray ; GTP-Binding Protein alpha Subunits, Gq-G11/*chemistry/metabolism ; Guanine Nucleotide Exchange Factors/*chemistry/metabolism ; Humans ; Models, Molecular ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Rho Guanine Nucleotide Exchange Factors ; Signal Transduction ; rhoA GTP-Binding Protein/*chemistry/metabolism
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    Blue-light-activated histidine kinases: two-component sensors in bacteria (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-08-25
    Description: Histidine kinases, used for environmental sensing by bacterial two-component systems, are involved in regulation of bacterial gene expression, chemotaxis, phototaxis, and virulence. Flavin-containing domains function as light-sensory modules in plant and algal phototropins and in fungal blue-light receptors. We have discovered that the prokaryotes Brucella melitensis, Brucella abortus, Erythrobacter litoralis, and Pseudomonas syringae contain light-activated histidine kinases that bind a flavin chromophore and undergo photochemistry indicative of cysteinyl-flavin adduct formation. Infection of macrophages by B. abortus was stimulated by light in the wild type but was limited in photochemically inactive and null mutants, indicating that the flavin-containing histidine kinase functions as a photoreceptor regulating B. abortus virulence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Swartz, Trevor E -- Tseng, Tong-Seung -- Frederickson, Marcus A -- Paris, Gaston -- Comerci, Diego J -- Rajashekara, Gireesh -- Kim, Jung-Gun -- Mudgett, Mary Beth -- Splitter, Gary A -- Ugalde, Rodolfo A -- Goldbaum, Fernando A -- Briggs, Winslow R -- Bogomolni, Roberto A -- 1.U54-AI-057153/AI/NIAID NIH HHS/ -- R01 GM068886/GM/NIGMS NIH HHS/ -- R01-GM068886/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Aug 24;317(5841):1090-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, University of California, Santa Cruz, Santa Cruz, CA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17717187" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Brucella abortus/*enzymology/growth & development/pathogenicity ; Brucella melitensis/*enzymology ; Cell Line ; Cloning, Molecular ; Enzyme Activation ; Flavin Mononucleotide/metabolism ; *Light ; Macrophages/*microbiology ; Mice ; Molecular Sequence Data ; Mutation ; Phosphorylation ; Photochemistry ; Protein Kinases/chemistry/genetics/*metabolism ; Protein Structure, Tertiary ; Pseudomonas syringae/*enzymology ; Signal Transduction ; Sphingomonadaceae/*enzymology ; Virulence
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    The Arabidopsis circadian clock incorporates a cADPR-based feedback loop (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-12-18
    Description: Transcriptional feedback loops are a feature of circadian clocks in both animals and plants. We show that the plant circadian clock also incorporates the cytosolic signaling molecule cyclic adenosine diphosphate ribose (cADPR). cADPR modulates the circadian oscillator's transcriptional feedback loops and drives circadian oscillations of Ca2+ release. The effects of antagonists of cADPR signaling, manipulation of cADPR synthesis, and mathematical simulation of the interaction of cADPR with the circadian clock indicate that cADPR forms a feedback loop within the plant circadian clock.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dodd, Antony N -- Gardner, Michael J -- Hotta, Carlos T -- Hubbard, Katharine E -- Dalchau, Neil -- Love, John -- Assie, Jean-Maurice -- Robertson, Fiona C -- Jakobsen, Mia Kyed -- Goncalves, Jorge -- Sanders, Dale -- Webb, Alex A R -- BB/E002692/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- P19207/Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Dec 14;318(5857):1789-92. Epub 2007 Nov 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Sciences, University of Cambridge, Downing Street, Cambridge CB2 3EA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18084825" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/genetics/*metabolism ; Calcium/metabolism ; Calcium Signaling/drug effects ; *Circadian Rhythm/genetics ; Cyclic ADP-Ribose/*metabolism ; *Feedback, Physiological ; Gene Expression Profiling ; Gene Expression Regulation, Plant ; Models, Biological ; Niacinamide/pharmacology ; Plant Leaves/metabolism ; Signal Transduction ; Transcription, Genetic
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    Lymphotoxin beta receptor-dependent control of lipid homeostasis (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-14
    Description: Hyperlipidemia, one of the most important risk factors for coronary heart disease, is often associated with inflammation. We identified lymphotoxin (LT) and LIGHT, tumor necrosis factor cytokine family members that are primarily expressed on lymphocytes, as critical regulators of key enzymes that control lipid metabolism. Dysregulation of LIGHT expression on T cells resulted in hypertriglyceridemia and hypercholesterolemia. In low-density lipoprotein receptor-deficient mice, which lack the ability to control lipid levels in the blood, inhibition of LT and LIGHT signaling with a soluble lymphotoxin beta receptor decoy protein attenuated the dyslipidemia. These results suggest that the immune system directly influences lipid metabolism and that LT modulating agents may represent a novel therapeutic route for the treatment of dyslipidemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lo, James C -- Wang, Yugang -- Tumanov, Alexei V -- Bamji, Michelle -- Yao, Zemin -- Reardon, Catherine A -- Getz, Godfrey S -- Fu, Yang-Xin -- 5 T32 GM07281/GM/NIGMS NIH HHS/ -- AI062026/AI/NIAID NIH HHS/ -- CA097296/CA/NCI NIH HHS/ -- DK58891/DK/NIDDK NIH HHS/ -- HL 85516/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2007 Apr 13;316(5822):285-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Committee on Immunology, University of Chicago, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17431181" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Dyslipidemias/drug therapy/etiology/metabolism ; Female ; Homeostasis ; Humans ; Hypercholesterolemia/etiology ; *Lipid Metabolism ; Lipids/blood ; Liver/*metabolism ; Lymphotoxin beta Receptor/*metabolism/therapeutic use ; Lymphotoxin-alpha/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Signal Transduction ; T-Lymphocytes/metabolism ; Tumor Necrosis Factor Ligand Superfamily Member ; 14/genetics/*metabolism/therapeutic use
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    Genetics. Beta-defensin repertoire expands (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-12-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dorin, Julia R -- Jackson, Ian J -- MC_U127527200/Medical Research Council/United Kingdom -- MC_U127527201/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Nov 30;318(5855):1395.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Human Genetics Unit, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, UK. ian.jackson@hgu.mrc.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18048676" target="_blank"〉PubMed〈/a〉
    Keywords: Agouti Signaling Protein/genetics/metabolism ; Animals ; Dogs/*genetics/metabolism ; Female ; Hair Color/*genetics ; Haplotypes ; Humans ; Male ; Mice ; Mice, Transgenic ; Mutation ; Polymorphism, Genetic ; Receptor, Melanocortin, Type 1/*metabolism ; Sequence Deletion ; Signal Transduction ; Skin/metabolism ; beta-Defensins/chemistry/*genetics/*metabolism
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    A -defensin mutation causes black coat color in domestic dogs (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-10-20
    Description: Genetic analysis of mammalian color variation has provided fundamental insight into human biology and disease. In most vertebrates, two key genes, Agouti and Melanocortin 1 receptor (Mc1r), encode a ligand-receptor system that controls pigment type-switching, but in domestic dogs, a third gene is implicated, the K locus, whose genetic characteristics predict a previously unrecognized component of the melanocortin pathway. We identify the K locus as beta-defensin 103 (CBD103) and show that its protein product binds with high affinity to the Mc1r and has a simple and strong effect on pigment type-switching in domestic dogs and transgenic mice. These results expand the functional role of beta-defensins, a protein family previously implicated in innate immunity, and identify an additional class of ligands for signaling through melanocortin receptors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2906624/" 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/PMC2906624/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Candille, Sophie I -- Kaelin, Christopher B -- Cattanach, Bruce M -- Yu, Bin -- Thompson, Darren A -- Nix, Matthew A -- Kerns, Julie A -- Schmutz, Sheila M -- Millhauser, Glenn L -- Barsh, Gregory S -- R01 DK064265/DK/NIDDK NIH HHS/ -- R01 DK064265-08/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 30;318(5855):1418-23. Epub 2007 Oct 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Genetics and Pediatrics, Stanford University, Stanford, CA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17947548" target="_blank"〉PubMed〈/a〉
    Keywords: Agouti Signaling Protein/genetics/metabolism ; Amino Acid Sequence ; Animals ; Cell Line ; Chromosome Mapping ; Dogs/*genetics/metabolism ; Female ; Hair Color/*genetics ; Haplotypes ; Humans ; Keratinocytes/metabolism ; Male ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Mutation ; Polymorphism, Genetic ; Receptor, Melanocortin, Type 1/*metabolism ; Sequence Analysis, DNA ; Sequence Deletion ; Signal Transduction ; Skin/metabolism ; beta-Defensins/chemistry/*genetics/*metabolism
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    Probing transcription factor dynamics at the single-molecule level in a living cell (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-05-26
    Description: Transcription factors regulate gene expression through their binding to DNA. In a living Escherichia coli cell, we directly observed specific binding of a lac repressor, labeled with a fluorescent protein, to a chromosomal lac operator. Using single-molecule detection techniques, we measured the kinetics of binding and dissociation of the repressor in response to metabolic signals. Furthermore, we characterized the nonspecific binding to DNA, one-dimensional (1D) diffusion along DNA segments, and 3D translocation among segments through cytoplasm at the single-molecule level. In searching for the operator, a lac repressor spends approximately 90% of time nonspecifically bound to and diffusing along DNA with a residence time of 〈5 milliseconds. The methods and findings can be generalized to other nucleic acid binding proteins.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2853898/" 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/PMC2853898/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elf, Johan -- Li, Gene-Wei -- Xie, X Sunney -- DP1 OD000277/OD/NIH HHS/ -- DP1 OD000277-02/OD/NIH HHS/ -- New York, N.Y. -- Science. 2007 May 25;316(5828):1191-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17525339" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/genetics/*metabolism ; DNA, Bacterial/*metabolism ; Diffusion ; Escherichia coli/*genetics ; Escherichia coli Proteins/*metabolism ; Kinetics ; *Lac Operon ; Lac Repressors ; Luminescent Proteins/genetics/metabolism ; Microscopy, Fluorescence ; Operator Regions, Genetic ; Protein Binding ; Repressor Proteins/*metabolism ; Signal Transduction
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    Ethylene modulates stem cell division in the Arabidopsis thaliana root (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-07-28
    Description: The construction of multicellular organisms depends on stem cells-cells that can both regenerate and produce daughter cells that undergo differentiation. Here, we show that the gaseous messenger ethylene modulates cell division in the cells of the quiescent center, which act as a source of stem cells in the seedling root. The cells formed through these ethylene-induced divisions express quiescent center-specific genes and can repress differentiation of surrounding initial cells, showing that quiescence is not required for these cells to signal to adjacent stem cells. We propose that ethylene is part of a signaling pathway that modulates cell division in the quiescent center in the stem cell niche during the postembryonic development of the root system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ortega-Martinez, Olga -- Pernas, Monica -- Carol, Rachel J -- Dolan, Liam -- BBS/E/J/00000168/Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Jul 27;317(5837):507-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, John Innes Centre, Norwich NR4 7UH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17656722" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids, Cyclic/metabolism/pharmacology ; Arabidopsis/*cytology/genetics/growth & development/metabolism ; Arabidopsis Proteins/genetics/metabolism ; Cell Differentiation ; *Cell Division ; Ethylenes/biosynthesis/*metabolism ; Gene Expression ; Genes, Plant ; Glycine/analogs & derivatives/pharmacology ; Indoleacetic Acids/metabolism ; Mutation ; Naphthaleneacetic Acids/pharmacology ; Plant Roots/*cytology/growth & development/metabolism ; Protein Kinases/genetics/metabolism ; Signal Transduction ; Stem Cells/*cytology
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    Control of stress-dependent cardiac growth and gene expression by a microRNA (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-03-24
    Description: The heart responds to diverse forms of stress by hypertrophic growth accompanied by fibrosis and eventual diminution of contractility, which results from down-regulation of alpha-myosin heavy chain (alphaMHC) and up-regulation of betaMHC, the primary contractile proteins of the heart. We found that a cardiac-specific microRNA (miR-208) encoded by an intron of the alphaMHC gene is required for cardiomyocyte hypertrophy, fibrosis, and expression of betaMHC in response to stress and hypothyroidism. Thus, the alphaMHC gene, in addition to encoding a major cardiac contractile protein, regulates cardiac growth and gene expression in response to stress and hormonal signaling through miR-208.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van Rooij, Eva -- Sutherland, Lillian B -- Qi, Xiaoxia -- Richardson, James A -- Hill, Joseph -- Olson, Eric N -- New York, N.Y. -- Science. 2007 Apr 27;316(5824):575-9. Epub 2007 Mar 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9148, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17379774" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cardiac Myosins/genetics/metabolism ; Cardiomegaly/pathology/physiopathology ; Fibrosis ; Gene Deletion ; *Gene Expression Regulation ; Heart/physiopathology ; Heart Diseases/*genetics/pathology/physiopathology ; Hypothyroidism/physiopathology ; Introns ; Mediator Complex ; Mice ; Mice, Transgenic ; MicroRNAs/genetics/*physiology ; Myocardial Contraction ; Myocardium/*metabolism/*pathology ; Myocytes, Cardiac/pathology ; Myosin Heavy Chains/*genetics ; Oligonucleotide Array Sequence Analysis ; Rats ; Signal Transduction ; Stress, Physiological/physiopathology ; Transcription Factors/genetics/metabolism ; Triiodothyronine/metabolism ; Up-Regulation ; Ventricular Myosins/*genetics/metabolism
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    Molecular biology. Cancer's perpetual source? (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, Jean -- New York, N.Y. -- Science. 2007 Aug 24;317(5841):1029-31.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17717165" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/pharmacology/therapeutic use ; Cell Differentiation ; DNA Repair ; Female ; Humans ; Male ; Mice ; Neoplasm Metastasis ; Neoplasm Transplantation ; Neoplasms/*pathology/therapy ; Neoplastic Stem Cells/cytology/drug effects/*physiology ; Neovascularization, Pathologic ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 84
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    Smed-betacatenin-1 is required for anteroposterior blastema polarity in planarian regeneration (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007
    Description: Planarian flatworms can regenerate heads at anterior-facing wounds and tails at posterior-facing wounds throughout the body. How this regeneration polarity is specified has been a classic problem for more than a century. We identified a planarian gene, Smed-betacatenin-1, that controls regeneration polarity. Posterior-facing blastemas regenerate a head instead of a tail in Smed-betacatenin-1(RNAi) animals. Smed-betacatenin-1 is required after wounding and at any posterior-facing wound for polarity. Additionally, intact Smed-betacatenin-1(RNAi) animals display anteriorization during tissue turnover. Five Wnt genes and a secreted Frizzled-related Wnt antagonist-like gene are expressed in domains along the anteroposterior axis that reset to new positions during regeneration, which suggests that Wnts control polarity through Smed-betacatenin-1. Our data suggest that beta-catenin specifies the posterior character of the anteroposterior axis throughout the Bilateria and specifies regeneration polarity in planarians.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petersen, Christian P -- Reddien, Peter W -- New York, N.Y. -- Science. 2008 Jan 18;319(5861):327-30. Epub 2007 Dec 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18063755" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Body Patterning ; Gene Expression ; Genes, Helminth ; Head ; Helminth Proteins/chemistry/genetics/physiology ; Homeostasis ; Molecular Sequence Data ; Photoreceptor Cells, Invertebrate/physiology ; Planarians/cytology/genetics/*physiology ; RNA Interference ; *Regeneration ; Signal Transduction ; Wnt Proteins/genetics/physiology ; beta Catenin/chemistry/genetics/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
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    PAPER CURRENT
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