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  • Artikel  (55)
  • Phosphorylation  (55)
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  • 1
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    Sara endosomes and the maintenance of Dpp signaling levels across mitosis (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-11-18
    Beschreibung: During development, cells acquire positional information by reading the concentration of morphogens. In the developing fly wing, a gradient of the transforming growth factor-beta (TGF-beta)-type morphogen decapentaplegic (Dpp) is transduced into a gradient of concentration of the phosphorylated form of the R-Smad transcription factor Mad. The endosomal protein Sara (Smad anchor for receptor activation) recruits R-Smads for phosphorylation by the type I TGF-beta receptor. We found that Sara, Dpp, and its type I receptor Thickveins were targeted to a subpopulation of apical endosomes in the developing wing epithelial cells. During mitosis, the Sara endosomes and the receptors therein associated with the spindle machinery to segregate into the two daughter cells. Daughter cells thereby inherited equal amounts of signaling molecules and thus retained the Dpp signaling levels of the mother cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bokel, Christian -- Schwabedissen, Anja -- Entchev, Eugeni -- Renaud, Olivier -- Gonzalez-Gaitan, Marcos -- New York, N.Y. -- Science. 2006 Nov 17;314(5802):1135-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute of Molecular Cell Biology and Genetics, Pfotenhauerstrasse 108, 01307 Dresden, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17110576" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Cell Division ; DNA-Binding Proteins/metabolism ; Drosophila Proteins/*metabolism ; Drosophila melanogaster/cytology/*metabolism ; Endosomes/*metabolism ; Epithelial Cells/cytology/metabolism ; *Mitosis ; Phosphorylation ; Point Mutation ; Protein-Serine-Threonine Kinases/metabolism ; Receptors, Cell Surface/metabolism ; *Signal Transduction ; Smad Proteins, Receptor-Regulated/metabolism ; Transcription Factors/metabolism ; Transforming Growth Factor beta/*metabolism ; Wings, Animal/cytology/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Molecular linkage between the kinase ATM and NF-kappaB signaling in response to genotoxic stimuli (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-02-25
    Beschreibung: The transcription factor NF-kappaB modulates apoptotic responses induced by genotoxic stress. We show that NF-kappaB essential modulator (NEMO), the regulatory subunit of IkappaB kinase (IKK) (which phosphorylates the NF-kappaB inhibitor IkappaB), associates with activated ataxia telangiectasia mutated (ATM) after the induction of DNA double-strand breaks. ATM phosphorylates serine-85 of NEMO to promote its ubiquitin-dependent nuclear export. ATM is also exported in a NEMO-dependent manner to the cytoplasm, where it associates with and causes the activation of IKK in a manner dependent on another IKK regulator, a protein rich in glutamate, leucine, lysine, and serine (ELKS). Thus, regulated nuclear shuttling of NEMO links two signaling kinases, ATM and IKK, to activate NF-kappaB by genotoxic signals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Zhao-Hui -- Shi, Yuling -- Tibbetts, Randal S -- Miyamoto, Shigeki -- R01-CA77474/CA/NCI NIH HHS/ -- R01-CA81065/CA/NCI NIH HHS/ -- R01-GM067868/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 24;311(5764):1141-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Wisconsin-Madison, 301 SMI, 1300 University Avenue, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16497931" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Active Transport, Cell Nucleus ; Adaptor Proteins, Signal Transducing/genetics/metabolism ; Amino Acid Motifs ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins/*metabolism ; Cell Line ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; *DNA Damage ; DNA-Binding Proteins/*metabolism ; Humans ; I-kappa B Kinase/*metabolism ; I-kappa B Proteins/genetics/metabolism ; NF-kappa B/metabolism ; Nerve Tissue Proteins/genetics/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/*metabolism ; RNA Interference ; Recombinant Fusion Proteins/metabolism ; SUMO-1 Protein/metabolism ; *Signal Transduction ; Tumor Suppressor Proteins/*metabolism ; Ubiquitin/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Cell signaling. A new way to burn fat (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-06-24
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Neels, Jaap G -- Olefsky, Jerrold M -- New York, N.Y. -- Science. 2006 Jun 23;312(5781):1756-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0673, USA. jolefsky@ucsd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16794069" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acetyl-CoA Carboxylase/antagonists & inhibitors/*metabolism ; Adipocytes/metabolism ; Adipose Tissue/*metabolism ; Animals ; Cell Cycle Proteins/*metabolism ; Energy Intake ; Energy Metabolism ; Enzyme Activation ; Fasting ; Fatty Acids/metabolism ; Hepatocytes/metabolism ; Insulin/physiology ; Insulin Resistance ; *Lipid Metabolism ; Lipogenesis ; Liver/metabolism ; Malonyl Coenzyme A/metabolism ; Mice ; Models, Biological ; Nuclear Proteins/*metabolism ; Obesity/therapy ; Oxidation-Reduction ; Phosphorylation ; Proto-Oncogene Proteins c-akt/antagonists & inhibitors/metabolism ; Signal Transduction ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    Transcription. Gene expression needs a break to unwind before carrying on (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-06-24
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haince, Jean-Francois -- Rouleau, Michele -- Poirier, Guy G -- New York, N.Y. -- Science. 2006 Jun 23;312(5781):1752-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Health and Environment Unit, Faculty of Medicine, Laval University Medical Research Center, 2705 Boulevard Laurier, Quebec City, QC, G1V 4G2, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16794066" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Chromatin/chemistry/metabolism ; DNA/*metabolism ; DNA Repair ; DNA Topoisomerases, Type II/*metabolism ; DNA-Activated Protein Kinase/metabolism ; DNA-Binding Proteins/antagonists & inhibitors/*metabolism ; Enzyme Activation ; Gene Expression ; Histones/metabolism ; Humans ; Models, Genetic ; Nucleosomes/metabolism ; Phosphorylation ; Poly Adenosine Diphosphate Ribose/metabolism ; Poly(ADP-ribose) Polymerases/*metabolism ; Response Elements ; Topoisomerase II Inhibitors ; Transcription Factors/metabolism ; *Transcription, Genetic ; *Transcriptional Activation
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    ATM engages autodegradation of the E3 ubiquitin ligase COP1 after DNA damage (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-08-26
    Beschreibung: The ataxia telangiectasia mutated (ATM) protein kinase is a critical component of a DNA-damage response network configured to maintain genomic integrity. The abundance of an essential downstream effecter of this pathway, the tumor suppressor protein p53, is tightly regulated by controlled degradation through COP1 and other E3 ubiquitin ligases, such as MDM2 and Pirh2; however, the signal transduction pathway that regulates the COP1-p53 axis following DNA damage remains enigmatic. We observed that in response to DNA damage, ATM phosphorylated COP1 on Ser(387) and stimulated a rapid autodegradation mechanism. Ionizing radiation triggered an ATM-dependent movement of COP1 from the nucleus to the cytoplasm, and ATM-dependent phosphorylation of COP1 on Ser(387) was both necessary and sufficient to disrupt the COP1-p53 complex and subsequently to abrogate the ubiquitination and degradation of p53. Furthermore, phosphorylation of COP1 on Ser(387) was required to permit p53 to become stabilized and to exert its tumor suppressor properties in response to DNA damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dornan, David -- Shimizu, Harumi -- Mah, Angie -- Dudhela, Tanay -- Eby, Michael -- O'rourke, Karen -- Seshagiri, Somasekar -- Dixit, Vishva M -- New York, N.Y. -- Science. 2006 Aug 25;313(5790):1122-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiological Chemistry, Genentech, Inc., 1 DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16931761" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins/genetics/*metabolism ; Cell Line ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; *DNA Damage ; DNA-Binding Proteins/genetics/*metabolism ; Escherichia coli/genetics/metabolism ; Etoposide/pharmacology ; Humans ; Mutation ; Nuclear Proteins/genetics/*metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Proteasome Endopeptidase Complex/metabolism ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; RNA, Small Interfering ; Radiation, Ionizing ; Recombinant Fusion Proteins/metabolism ; Transfection ; Tumor Suppressor Protein p53/genetics/metabolism ; Tumor Suppressor Proteins/genetics/*metabolism ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/genetics/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
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    S6K1- and betaTRCP-mediated degradation of PDCD4 promotes protein translation and cell growth (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-10-21
    Beschreibung: The tumor suppressor programmed cell death protein 4 (PDCD4) inhibits the translation initiation factor eIF4A, an RNA helicase that catalyzes the unwinding of secondary structure at the 5' untranslated region (5'UTR) of messenger RNAs (mRNAs). In response to mitogens, PDCD4 was rapidly phosphorylated on Ser67 by the protein kinase S6K1 and subsequently degraded via the ubiquitin ligase SCF(betaTRCP). Expression in cultured cells of a stable PDCD4 mutant that is unable to bind betaTRCP inhibited translation of an mRNA with a structured 5'UTR, resulted in smaller cell size, and slowed down cell cycle progression. We propose that regulated degradation of PDCD4 in response to mitogens allows efficient protein synthesis and consequently cell growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dorrello, N Valerio -- Peschiaroli, Angelo -- Guardavaccaro, Daniele -- Colburn, Nancy H -- Sherman, Nicholas E -- Pagano, Michele -- R01-CA76584/CA/NCI NIH HHS/ -- R01-GM57587/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 20;314(5798):467-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 550 First Avenue, MSB 599, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17053147" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 5' Untranslated Regions ; Amino Acid Motifs ; Apoptosis Regulatory Proteins/chemistry/genetics/*metabolism ; Binding Sites ; Cell Line ; Cell Line, Tumor ; *Cell Proliferation ; Cell Size ; Eukaryotic Initiation Factor-4A/antagonists & inhibitors/metabolism ; Eukaryotic Initiation Factor-4F/metabolism ; Eukaryotic Initiation Factor-4G/metabolism ; Eukaryotic Initiation Factors/metabolism ; Humans ; Mitogens/pharmacology ; Phosphorylation ; *Protein Biosynthesis ; RNA, Small Interfering ; RNA-Binding Proteins/chemistry/genetics/*metabolism ; Ribosomal Protein S6 Kinases/metabolism ; SKP Cullin F-Box Protein Ligases/*metabolism ; Serine/metabolism ; Serum ; Signal Transduction ; beta-Transducin Repeat-Containing Proteins/genetics/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 7
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    Cytokinin signaling and its inhibitor AHP6 regulate cell fate during vascular development (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-01-10
    Beschreibung: The cell lineages that form the transporting tissues (xylem and phloem) and the intervening pluripotent procambial tissue originate from stem cells near the root tip. We demonstrate that in Arabidopsis, cytokinin phytohormones negatively regulate protoxylem specification. AHP6, an inhibitory pseudophosphotransfer protein, counteracts cytokinin signaling, allowing protoxylem formation. Conversely, cytokinin signaling negatively regulates the spatial domain of AHP6 expression. Thus, by controlling the identity of cell lineages, the reciprocal interaction of cytokinin signaling and its spatially specific modulator regulates proliferation and differentiation of cell lineages during vascular development, demonstrating a previously unrecognized regulatory circuit underlying meristem organization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mahonen, Ari Pekka -- Bishopp, Anthony -- Higuchi, Masayuki -- Nieminen, Kaisa M -- Kinoshita, Kaori -- Tormakangas, Kirsi -- Ikeda, Yoshihisa -- Oka, Atsuhiro -- Kakimoto, Tatsuo -- Helariutta, Yka -- New York, N.Y. -- Science. 2006 Jan 6;311(5757):94-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Plant Molecular Biology Laboratory, Institute of Biotechnology, POB 56, FI-00014, University of Helsinki, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16400151" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adenosine Triphosphate/metabolism ; Alleles ; Arabidopsis/*cytology/genetics/growth & development/*metabolism ; Arabidopsis Proteins/genetics/*metabolism/physiology ; Cell Differentiation ; Cell Division ; Cell Lineage ; Cloning, Molecular ; Cytokinins/*metabolism ; Genes, Plant ; Kinetin/metabolism/pharmacology ; Meristem/cytology/growth & development/metabolism ; Morphogenesis ; Phenotype ; Phosphorylation ; Plant Growth Regulators/*metabolism ; Plant Roots/*cytology/growth & development/metabolism ; Plant Shoots/metabolism ; Plants, Genetically Modified ; *Signal Transduction ; Suppression, Genetic ; Zeatin/metabolism/pharmacology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 8
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    Escherichia coli induces DNA double-strand breaks in eukaryotic cells (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-08-12
    Beschreibung: Transient infection of eukaryotic cells with commensal and extraintestinal pathogenic Escherichia coli of phylogenetic group B2 blocks mitosis and induces megalocytosis. This trait is linked to a widely spread genomic island that encodes giant modular nonribosomal peptide and polyketide synthases. Contact with E. coli expressing this gene cluster causes DNA double-strand breaks and activation of the DNA damage checkpoint pathway, leading to cell cycle arrest and eventually to cell death. Discovery of hybrid peptide-polyketide genotoxins in E. coli will change our view on pathogenesis and commensalism and open new biotechnological applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nougayrede, Jean-Philippe -- Homburg, Stefan -- Taieb, Frederic -- Boury, Michele -- Brzuszkiewicz, Elzbieta -- Gottschalk, Gerhard -- Buchrieser, Carmen -- Hacker, Jorg -- Dobrindt, Ulrich -- Oswald, Eric -- New York, N.Y. -- Science. 2006 Aug 11;313(5788):848-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INRA, UMR1225, Ecole Nationale Veterinaire de Toulouse, Toulouse F-31076, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16902142" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle ; Cell Cycle Proteins/metabolism ; Cell Death ; Cell Line ; Cell Nucleus/chemistry ; Cytotoxins/*metabolism ; DNA/analysis ; *DNA Damage ; DNA-Binding Proteins/metabolism ; Escherichia coli/genetics/*pathogenicity/*physiology ; G2 Phase ; *Genomic Islands ; HeLa Cells ; Histones/metabolism ; Humans ; Intestinal Mucosa/cytology/microbiology ; Molecular Sequence Data ; Mutagenesis ; Mutagens/*metabolism ; Peptides/*metabolism ; Phosphorylation ; Polyketide Synthases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; Rats ; Signal Transduction ; Tumor Suppressor Proteins/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 9
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    Cell biology. Balancing life-or-death decisions (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-10-14
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bartek, Jiri -- Lukas, Jiri -- New York, N.Y. -- Science. 2006 Oct 13;314(5797):261-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Cancer Biology and Centre for Genotoxic Stress Research, Danish Cancer Society, Strandboulevarden 49, DK-2100 Copenhagen, Denmark. jb@cancer.dk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17038611" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Apoptosis ; BRCA2 Protein/metabolism ; Cell Cycle ; Cell Nucleus/metabolism ; Cell Survival ; Cyclin-Dependent Kinase 2/antagonists & inhibitors/*metabolism ; *DNA Damage ; DNA Repair ; DNA Replication ; Forkhead Transcription Factors/*metabolism ; Gene Expression Regulation ; Humans ; Mice ; Models, Biological ; Phosphorylation ; RNA, Small Interfering ; Transcription, Genetic ; cdc25 Phosphatases/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 10
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    Anaphase inactivation of the spindle checkpoint (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-07-11
    Beschreibung: The spindle checkpoint delays cell cycle progression until microtubules attach each pair of sister chromosomes to opposite poles of the mitotic spindle. Following sister chromatid separation, however, the checkpoint ignores chromosomes whose kinetochores are attached to only one spindle pole, a state that activates the checkpoint prior to metaphase. We demonstrate that, in budding yeast, mutual inhibition between the anaphase-promoting complex (APC) and Mps1, an essential component of the checkpoint, leads to sustained inactivation of the spindle checkpoint. Mps1 protein abundance decreases in anaphase, and Mps1 is a target of the APC. Furthermore, expression of Mps1 in anaphase, or repression of the APC in anaphase, reactivates the spindle checkpoint. This APC-Mps1 feedback circuit allows cells to irreversibly inactivate the checkpoint during anaphase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palframan, William J -- Meehl, Janet B -- Jaspersen, Sue L -- Winey, Mark -- Murray, Andrew W -- GM43987/GM/NIGMS NIH HHS/ -- GM51312/GM/NIGMS NIH HHS/ -- R37 GM043987/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Aug 4;313(5787):680-4. Epub 2006 Jul 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Biological Laboratories, Harvard University, 16 Divinity Avenue, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16825537" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Anaphase/*physiology ; Anaphase-Promoting Complex-Cyclosome ; Cdc20 Proteins ; Cell Cycle Proteins/metabolism ; Chromosomes, Fungal/physiology ; Feedback, Physiological ; GTP-Binding Proteins/metabolism ; Kinetochores/physiology ; Mad2 Proteins ; Mitosis ; Molecular Sequence Data ; Nuclear Proteins/metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Protein-Tyrosine Kinases/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/*cytology/metabolism ; Saccharomyces cerevisiae Proteins/genetics/*metabolism ; Securin ; Spindle Apparatus/*physiology ; Ubiquitin-Protein Ligase Complexes/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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