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  • Signal Transduction  (39)
  • American Association for the Advancement of Science (AAAS)  (39)
  • MDPI
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  • 1
    Publikationsdatum: 2013-10-26
    Beschreibung: The quiescent center (QC) plays an essential role during root development by creating a microenvironment that preserves the stem cell fate of its surrounding cells. Despite being surrounded by highly mitotic active cells, QC cells self-renew at a low proliferation rate. Here, we identified the ERF115 transcription factor as a rate-limiting factor of QC cell division, acting as a transcriptional activator of the phytosulfokine PSK5 peptide hormone. ERF115 marks QC cell division but is restrained through proteolysis by the APC/C(CCS52A2) ubiquitin ligase, whereas QC proliferation is driven by brassinosteroid-dependent ERF115 expression. Together, these two antagonistic mechanisms delimit ERF115 activity, which is called upon when surrounding stem cells are damaged, revealing a cell cycle regulatory mechanism accounting for stem cell niche longevity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heyman, Jefri -- Cools, Toon -- Vandenbussche, Filip -- Heyndrickx, Ken S -- Van Leene, Jelle -- Vercauteren, Ilse -- Vanderauwera, Sandy -- Vandepoele, Klaas -- De Jaeger, Geert -- Van Der Straeten, Dominique -- De Veylder, Lieven -- New York, N.Y. -- Science. 2013 Nov 15;342(6160):860-3. doi: 10.1126/science.1240667. Epub 2013 Oct 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Systems Biology, VIB, B-9052 Gent, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24158907" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Anaphase-Promoting Complex-Cyclosome/metabolism ; Arabidopsis/*cytology/*growth & development ; Arabidopsis Proteins/genetics/*metabolism ; Cell Cycle/genetics/physiology ; Cell Cycle Proteins/metabolism ; Cell Division/genetics/*physiology ; Mitosis/genetics/physiology ; Peptide Hormones/genetics/metabolism ; Plant Roots/*cytology/*growth & development ; Proteolysis ; Signal Transduction ; Stem Cell Niche ; Stem Cells/*physiology ; Transcription Factors/genetics/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
    Publikationsdatum: 2016-01-23
    Beschreibung: The plant root cap, surrounding the very tip of the growing root, perceives and transmits environmental signals to the inner root tissues. In Arabidopsis thaliana, auxin released by the root cap contributes to the regular spacing of lateral organs along the primary root axis. Here, we show that the periodicity of lateral organ induction is driven by recurrent programmed cell death at the most distal edge of the root cap. We suggest that synchronous bursts of cell death in lateral root cap cells release pulses of auxin to surrounding root tissues, establishing the pattern for lateral root formation. The dynamics of root cap turnover may therefore coordinate primary root growth with root branching in order to optimize the uptake of water and nutrients from the soil.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xuan, Wei -- Band, Leah R -- Kumpf, Robert P -- Van Damme, Daniel -- Parizot, Boris -- De Rop, Gieljan -- Opdenacker, Davy -- Moller, Barbara K -- Skorzinski, Noemi -- Njo, Maria F -- De Rybel, Bert -- Audenaert, Dominique -- Nowack, Moritz K -- Vanneste, Steffen -- Beeckman, Tom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):384-7. doi: 10.1126/science.aad2776.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Systems Biology, Vlaams Instituut voor Biotechnologie (VIB), Technologiepark 927, 9052 Ghent, Belgium. Department of Plant Biotechnology and Bioinformatics, Gent University, Technologiepark 927, 9052 Ghent, Belgium. State Key Laboratory of Crop Genetics and Germplasm Enhancement and MOA Key Laboratory of Plant Nutrition and Fertilization in Lower-Middle Reaches of the Yangtze River, Nanjing Agricultural University, Weigang No. 1, Nanjing 210095, PR China. ; Centre for Plant Integrative Biology, University of Nottingham, Nottingham LE12 5RD, UK. ; Department of Plant Systems Biology, Vlaams Instituut voor Biotechnologie (VIB), Technologiepark 927, 9052 Ghent, Belgium. Department of Plant Biotechnology and Bioinformatics, Gent University, Technologiepark 927, 9052 Ghent, Belgium. ; Max Planck Institute for Developmental Biology, Spemannstrasse 35, 72076 Tubingen, Germany. ; Department of Plant Systems Biology, Vlaams Instituut voor Biotechnologie (VIB), Technologiepark 927, 9052 Ghent, Belgium. Department of Plant Biotechnology and Bioinformatics, Gent University, Technologiepark 927, 9052 Ghent, Belgium. Laboratory of Biochemistry, Wageningen University, Dreijenlaan 3, 6703HA Wageningen, Netherlands. ; Department of Plant Systems Biology, Vlaams Instituut voor Biotechnologie (VIB), Technologiepark 927, 9052 Ghent, Belgium. Department of Plant Biotechnology and Bioinformatics, Gent University, Technologiepark 927, 9052 Ghent, Belgium. tobee@psb.vib-ugent.be.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26798015" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Apoptosis ; Arabidopsis/cytology/*growth & development/metabolism ; Indoleacetic Acids/*metabolism ; Plant Epidermis/cytology/growth & development/metabolism ; Plant Root Cap/cytology/*growth & development/metabolism ; Receptors, TNF-Related Apoptosis-Inducing Ligand/genetics/metabolism ; Signal Transduction ; Soil ; Water/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
    Publikationsdatum: 1998-04-16
    Beschreibung: FADD (also known as Mort-1) is a signal transducer downstream of cell death receptor CD95 (also called Fas). CD95, tumor necrosis factor receptor type 1 (TNFR-1), and death receptor 3 (DR3) did not induce apoptosis in FADD-deficient embryonic fibroblasts, whereas DR4, oncogenes E1A and c-myc, and chemotherapeutic agent adriamycin did. Mice with a deletion in the FADD gene did not survive beyond day 11.5 of embryogenesis; these mice showed signs of cardiac failure and abdominal hemorrhage. Chimeric embryos showing a high contribution of FADD null mutant cells to the heart reproduce the phenotype of FADD-deficient mutants. Thus, not only death receptors, but also receptors that couple to developmental programs, may use FADD for signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yeh, W C -- de la Pompa, J L -- McCurrach, M E -- Shu, H B -- Elia, A J -- Shahinian, A -- Ng, M -- Wakeham, A -- Khoo, W -- Mitchell, K -- El-Deiry, W S -- Lowe, S W -- Goeddel, D V -- Mak, T W -- CA13106/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Mar 20;279(5358):1954-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Amgen Institute, University of Toronto, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9506948" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD95/genetics/physiology ; *Apoptosis ; Carrier Proteins/genetics/*physiology ; Cell Transformation, Neoplastic ; Cells, Cultured ; Doxorubicin/pharmacology ; *Embryonic and Fetal Development ; Endothelium, Vascular/embryology ; Fas-Associated Death Domain Protein ; Female ; Gene Expression ; Gene Targeting ; Heart/*embryology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation ; Oncogenes ; Receptors, Tumor Necrosis Factor/genetics/physiology ; Signal Transduction ; Tumor Necrosis Factor-alpha/pharmacology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1999-03-13
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Lange, T -- DePinho, R A -- CA76027/CA/NCI NIH HHS/ -- HD 348880/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1999 Feb 12;283(5404):947-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cell Biology and Genetics, Rockefeller University, New York, NY 10021, USA. delange@rockvax.rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10075559" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Cell Aging ; *Cell Division ; *Cell Transformation, Neoplastic ; Cyclin-Dependent Kinase Inhibitor p16/metabolism ; Humans ; Neoplasms/enzymology/metabolism/pathology ; Proto-Oncogene Proteins c-myc/metabolism ; Retinoblastoma Protein/metabolism ; Signal Transduction ; Telomerase/genetics/*metabolism ; Telomere/*metabolism ; ras Proteins/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
    Publikationsdatum: 2000-10-20
    Beschreibung: Ectodysplasin, a member of the tumor necrosis factor family, is encoded by the anhidrotic ectodermal dysplasia (EDA) gene. Mutations in EDA give rise to a clinical syndrome characterized by loss of hair, sweat glands, and teeth. EDA-A1 and EDA-A2 are two isoforms of ectodysplasin that differ only by an insertion of two amino acids. This insertion functions to determine receptor binding specificity, such that EDA-A1 binds only the receptor EDAR, whereas EDA-A2 binds only the related, but distinct, X-linked ectodysplasin-A2 receptor (XEDAR). In situ binding and organ culture studies indicate that EDA-A1 and EDA-A2 are differentially expressed and play a role in epidermal morphogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yan, M -- Wang, L C -- Hymowitz, S G -- Schilbach, S -- Lee, J -- Goddard, A -- de Vos, A M -- Gao, W Q -- Dixit, V M -- New York, N.Y. -- Science. 2000 Oct 20;290(5491):523-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Oncology, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11039935" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Binding Sites ; Cell Line ; DNA-Binding Proteins/metabolism ; Ectodermal Dysplasia/genetics ; Ectodysplasins ; Epidermis/embryology/*metabolism ; Humans ; *I-kappa B Proteins ; In Situ Hybridization ; Ligands ; Membrane Proteins/*chemistry/*metabolism ; Mice ; Models, Molecular ; Molecular Sequence Data ; Morphogenesis ; NF-kappa B/metabolism ; Phosphorylation ; Point Mutation ; Protein Conformation ; Proteins/metabolism ; Receptors, Cell Surface/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; TNF Receptor-Associated Factor 6 ; Transfection
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1999-11-05
    Beschreibung: Alzheimer's disease (AD) research has shown that patients with an inherited form of the disease carry mutations in the presenilin proteins or the amyloid precursor protein (APP). These disease-linked mutations result in increased production of the longer form of amyloid-beta (the primary component of the amyloid deposits found in AD brains). However, it is not clear how the presenilins contribute to this increase. New findings now show that the presenilins affect APP processing through their effects on gamma-secretase, an enzyme that cleaves APP. Also, it is known that the presenilins are involved in the cleavage of the Notch receptor, hinting that they either directly regulate gamma-secretase activity or themselves are protease enzymes. These findings suggest that the presenilins may prove to be valuable molecular targets for the development of drugs to combat AD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haass, C -- De Strooper, B -- New York, N.Y. -- Science. 1999 Oct 29;286(5441):916-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Adolf-Butenandt-Institute, Department of Biochemistry, Ludwig-Maximilians University Munich, Germany. chaass@pbm.med.uni-muenchen.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10542139" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alzheimer Disease/drug therapy/enzymology/*metabolism ; Amyloid Precursor Protein Secretases ; Amyloid beta-Protein Precursor/*metabolism ; Animals ; Aspartic Acid Endopeptidases ; Endopeptidases/*metabolism ; Humans ; Membrane Proteins/*metabolism ; Protease Inhibitors/therapeutic use ; Protein Processing, Post-Translational ; Receptors, Notch ; Signal Transduction
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
    Publikationsdatum: 2000-12-16
    Beschreibung: The retinoid X receptor (RXR) is a nuclear receptor that functions as a ligand-activated transcription factor. Little is known about the ligands that activate RXR in vivo. Here, we identified a factor in brain tissue from adult mice that activates RXR in cell-based assays. Purification and analysis of the factor by mass spectrometry revealed that it is docosahexaenoic acid (DHA), a long-chain polyunsaturated fatty acid that is highly enriched in the adult mammalian brain. Previous work has shown that DHA is essential for brain maturation, and deficiency of DHA in both rodents and humans leads to impaired spatial learning and other abnormalities. These data suggest that DHA may influence neural function through activation of an RXR signaling pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Urquiza, A M -- Liu, S -- Sjoberg, M -- Zetterstrom, R H -- Griffiths, W -- Sjovall, J -- Perlmann, T -- New York, N.Y. -- Science. 2000 Dec 15;290(5499):2140-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Institute for Cancer Research, Stockholm Branch, Box 240, S-171 77 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11118147" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Biological Assay ; Brain/growth & development/metabolism ; *Brain Chemistry ; Cell Line ; Chromatography, High Pressure Liquid ; Culture Media, Conditioned ; Dimerization ; Docosahexaenoic Acids/*isolation & purification/*metabolism/pharmacology ; Fatty Acids, Unsaturated/pharmacology ; Histone Acetyltransferases ; Humans ; Ligands ; Male ; Mice ; Nuclear Receptor Coactivator 1 ; Receptors, Retinoic Acid/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Retinoid X Receptors ; Signal Transduction ; Spectrometry, Mass, Electrospray Ionization ; Transcription Factors/genetics/*metabolism ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
    Publikationsdatum: 2001-09-05
    Beschreibung: We report a flexible strategy for transducing ligand-binding events into electrochemical responses for a wide variety of proteins. The method exploits ligand-mediated hinge-bending motions, intrinsic to the bacterial periplasmic binding protein superfamily, to establish allosterically controlled interactions between electrode surfaces and redox-active, Ru(II)-labeled proteins. This approach allows the development of protein-based bioelectronic interfaces that respond to a diverse set of analytes. Families of these interfaces can be generated either by exploiting natural binding diversity within the superfamily or by reengineering the specificity of individual proteins. These proteins may have numerous medical, environmental, and defense applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benson, D E -- Conrad, D W -- de Lorimier, R M -- Trammell, S A -- Hellinga, H W -- New York, N.Y. -- Science. 2001 Aug 31;293(5535):1641-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Box 3711, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11533486" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Allosteric Regulation ; Allosteric Site ; Animals ; Beer ; *Biosensing Techniques ; Blood Glucose/analysis ; Carrier Proteins/*chemistry/genetics/*metabolism ; Electrochemistry ; Electrodes ; Ligands ; Maltose/analysis ; Maltose-Binding Proteins ; Monosaccharide Transport Proteins/chemistry/metabolism ; Mutation ; Oxidation-Reduction ; Protein Conformation ; *Protein Engineering ; Rats ; *Ruthenium ; Signal Transduction ; Thermodynamics ; Zinc/chemistry/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 9
    Publikationsdatum: 2001-12-12
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van Den Brink, G R -- de Santa Barbara, P -- Roberts, D J -- New York, N.Y. -- Science. 2001 Dec 7;294(5549):2115-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Academic Medical Center, Department of Experimental Internal Medicine in the Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11739944" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Apoptosis ; Basic Helix-Loop-Helix Transcription Factors ; *Cell Differentiation ; Cell Division ; Cell Lineage ; Enterocytes/cytology ; Enteroendocrine Cells/cytology ; Epithelial Cells/cytology ; Goblet Cells/cytology ; Helix-Loop-Helix Motifs ; Homeodomain Proteins/metabolism ; Intestinal Mucosa/*cytology/metabolism ; Mice ; Paneth Cells/cytology ; Signal Transduction ; Stem Cells/*cytology ; Transcription Factors/genetics/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 10
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1999-03-26
    Beschreibung: p21-activated kinases (PAKs) are implicated in the cytoskeletal changes induced by the Rho family of guanosine triphosphatases. Cytoskeletal dynamics are primarily modulated by interactions of actin and myosin II that are regulated by myosin light chain kinase (MLCK)-mediated phosphorylation of the regulatory myosin light chain (MLC). p21-activated kinase 1 (PAK1) phosphorylates MLCK, resulting in decreased MLCK activity. MLCK activity and MLC phosphorylation were decreased, and cell spreading was inhibited in baby hamster kidney-21 and HeLa cells expressing constitutively active PAK1. These data indicate that MLCK is a target for PAKs and that PAKs may regulate cytoskeletal dynamics by decreasing MLCK activity and MLC phosphorylation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanders, L C -- Matsumura, F -- Bokoch, G M -- de Lanerolle, P -- New York, N.Y. -- Science. 1999 Mar 26;283(5410):2083-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Immunology and Cell Biology, The 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/10092231" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Adhesion ; Cell Cycle Proteins/metabolism ; Cell Line ; Cell Movement ; Cell Size ; Cricetinae ; Cytoskeleton/*physiology ; Diacetyl/analogs & derivatives/pharmacology ; GTP Phosphohydrolases/metabolism ; GTP-Binding Proteins/metabolism ; HeLa Cells ; Humans ; Intracellular Signaling Peptides and Proteins ; Myosin Light Chains/*metabolism ; Myosin-Light-Chain Kinase/*antagonists & inhibitors/metabolism ; Myosins/physiology ; Phosphorylation ; Phosphoserine/metabolism ; Protein-Serine-Threonine Kinases/*metabolism ; Signal Transduction ; cdc42 GTP-Binding Protein ; p21-Activated Kinases ; rac GTP-Binding Proteins ; rho-Associated Kinases
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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