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  • 1
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    Two-amino acid molecular switch in an epithelial morphogen that regulates binding to two distinct receptors (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-10-20
    Description: 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〉
    Keywords: 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
    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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    Senescence induced by altered telomere state, not telomere loss (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-03-30
    Description: Primary human cells in culture invariably stop dividing and enter a state of growth arrest called replicative senescence. This transition is induced by programmed telomere shortening, but the underlying mechanisms are unclear. Here, we report that overexpression of TRF2, a telomeric DNA binding protein, increased the rate of telomere shortening in primary cells without accelerating senescence. TRF2 reduced the senescence setpoint, defined as telomere length at senescence, from 7 to 4 kilobases. TRF2 protected critically short telomeres from fusion and repressed chromosome-end fusions in presenescent cultures, which explains the ability of TRF2 to delay senescence. Thus, replicative senescence is induced by a change in the protected status of shortened telomeres rather than by a complete loss of telomeric DNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karlseder, Jan -- Smogorzewska, Agata -- de Lange, Titia -- AG16643/AG/NIA NIH HHS/ -- CA76027/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2002 Mar 29;295(5564):2446-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cell Biology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11923537" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Polyomavirus Transforming/genetics/metabolism ; *Cell Aging ; *Cell Division ; Cell Line ; Cells, Cultured ; DNA/*metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Humans ; Oncogene Proteins, Viral/genetics/metabolism ; Papillomavirus E7 Proteins ; *Repressor Proteins ; Retinoblastoma Protein/metabolism ; Retroviridae/genetics ; Telomere/metabolism/*physiology ; Telomeric Repeat Binding Protein 2 ; Transformation, Genetic ; Tumor Suppressor Protein p53/metabolism
    Print ISSN: 0036-8075
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  • 3
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    Transcriptional regulation of cortical neuron migration by POU domain factors (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-02-23
    Description: The identification of pathways mediated by the kinase Cdk5 and the ligand reelin has provided a conceptual framework for exploring the molecular mechanisms underlying proper lamination of the developing mammalian cerebral cortex. In this report, we identify a component of the regulation of Cdk5-mediated cortical lamination by genetic analysis of the roles of the class III POU domain transcription factors, Brn-1 and Brn-2, expressed during the development of the forebrain and coexpressed in most layer II-V cortical neurons. Brn-1 and Brn-2 appear to critically control the initiation of radial migration, redundantly regulating the cell-autonomous expression of the p35 and p39 regulatory subunits of Cdk5 in migrating cortical neurons, with Brn-1(-/-)/Brn-2(-/-) mice exhibiting cortical inversion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McEvilly, Robert J -- de Diaz, Marcela Ortiz -- Schonemann, Marcus D -- Hooshmand, Farideh -- Rosenfeld, Michael G -- New York, N.Y. -- Science. 2002 Feb 22;295(5559):1528-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department and School of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92037-0648, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11859196" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/cytology/embryology/metabolism ; Cell Adhesion Molecules, Neuronal/genetics/metabolism ; Cell Line ; Cell Movement ; Cerebral Cortex/cytology/embryology/*metabolism ; Cyclin-Dependent Kinase 5 ; Cyclin-Dependent Kinases/metabolism ; Extracellular Matrix Proteins/genetics/metabolism ; Female ; Gene Targeting ; Hippocampus/cytology/embryology/metabolism ; Homeodomain Proteins ; In Situ Hybridization ; Male ; Mice ; Mutation ; Nerve Tissue Proteins/genetics/metabolism ; Neurons/*physiology ; Neuropeptides/genetics/*physiology ; POU Domain Factors ; Serine Endopeptidases ; Trans-Activators/genetics/*physiology ; Transcription Factors/genetics/*physiology ; *Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Docosahexaenoic acid, a ligand for the retinoid X receptor in mouse brain (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-16
    Description: 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〉
    Keywords: 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
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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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    Amphiphysin 2 (Bin1) and T-tubule biogenesis in muscle (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-08-17
    Description: In striated muscle, the plasma membrane forms tubular invaginations (transverse tubules or T-tubules) that function in depolarization-contraction coupling. Caveolin-3 and amphiphysin were implicated in their biogenesis. Amphiphysin isoforms have a putative role in membrane deformation at endocytic sites. An isoform of amphiphysin 2 concentrated at T-tubules induced tubular plasma membrane invaginations when expressed in nonmuscle cells. This property required exon 10, a phosphoinositide-binding module. In developing myotubes, amphiphysin 2 and caveolin-3 segregated in tubular and vesicular portions of the T-tubule system, respectively. These findings support a role of the bilayer-deforming properties of amphiphysin at T-tubules and, more generally, a physiological role of amphiphysin in membrane deformation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Eunkyung -- Marcucci, Melissa -- Daniell, Laurie -- Pypaert, Marc -- Weisz, Ora A -- Ochoa, Gian-Carlo -- Farsad, Khashayar -- Wenk, Markus R -- De Camilli, Pietro -- CA46128/CA/NCI NIH HHS/ -- NS36251/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2002 Aug 16;297(5584):1193-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Howard Hughes Medical Institute, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12183633" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CHO Cells ; Caveolin 3 ; Caveolins/metabolism ; Cell Differentiation ; Cell Line ; Cell Membrane/metabolism ; Cell Membrane Structures/metabolism/*ultrastructure ; Cricetinae ; Dynamins ; Exons ; GTP Phosphohydrolases/metabolism ; Liposomes/metabolism ; Mice ; Microscopy, Electron ; Morphogenesis ; *Muscle Development ; Muscle, Skeletal/metabolism/*ultrastructure ; Nerve Tissue Proteins/chemistry/genetics/*metabolism ; Phosphatidylinositol 4,5-Diphosphate/metabolism ; Protein Isoforms ; Protein Structure, Tertiary ; RNA, Small Interfering ; RNA, Untranslated/metabolism ; Recombinant Fusion Proteins/metabolism ; Transfection
    Print ISSN: 0036-8075
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  • 6
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    Cell therapy of alpha-sarcoglycan null dystrophic mice through intra-arterial delivery of mesoangioblasts (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-12
    Description: Preclinical or clinical trials for muscular dystrophies have met with modest success, mainly because of inefficient delivery of viral vectors or donor cells to dystrophic muscles. We report here that intra-arterial delivery of wild-type mesoangioblasts, a class of vessel-associated stem cells, corrects morphologically and functionally the dystrophic phenotype of virtually all downstream muscles in adult immunocompetent alpha-sarcoglycan (alpha-SG) null mice, a model organism for limb-girdle muscular dystrophy. When mesoangioblasts isolated from juvenile dystrophic mice and transduced with a lentiviral vector expressing alpha-SG were injected into the femoral artery of dystrophic mice, they reconstituted skeletal muscle in a manner similar to that seen in wild-type cells. The success of this protocol was mainly due to widespread distribution of donor stem cells through the capillary network, a distinct advantage of this strategy over previous approaches.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sampaolesi, Maurilio -- Torrente, Yvan -- Innocenzi, Anna -- Tonlorenzi, Rossana -- D'Antona, Giuseppe -- Pellegrino, M Antonietta -- Barresi, Rita -- Bresolin, Nereo -- De Angelis, M Gabriella Cusella -- Campbell, Kevin P -- Bottinelli, Roberto -- Cossu, Giulio -- 1322/Telethon/Italy -- 463/BI/Telethon/Italy -- New York, N.Y. -- Science. 2003 Jul 25;301(5632):487-92. Epub 2003 Jul 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cell Research Institute, H. S. Raffaele, Via Olgettina 58, 20132 Milan, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12855815" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Vessels/cytology/embryology ; Cell Differentiation ; Cell Line ; Cell Movement ; Cytoskeletal Proteins/*genetics/*metabolism ; Dystrophin/metabolism ; Endothelium, Vascular/physiology ; Female ; Femoral Artery ; Genetic Vectors ; Lentivirus/genetics ; Locomotion ; Male ; Membrane Glycoproteins/*genetics/*metabolism ; Mesoderm/cytology ; Mice ; Mice, Knockout ; Mice, Transgenic ; Muscle Contraction ; Muscle Fibers, Skeletal/cytology/physiology ; Muscle, Skeletal/cytology/metabolism/pathology/*physiology ; Muscular Dystrophy, Animal/metabolism/pathology/*therapy ; Regeneration ; Sarcoglycans ; *Stem Cell Transplantation ; Stem Cells/*physiology ; Transfection
    Print ISSN: 0036-8075
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  • 7
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    Talin binding to integrin beta tails: a final common step in integrin activation (2003)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2003-10-04
    Description: Control of integrin affinity for ligands (integrin activation) is essential for normal cell adhesion, migration, and assembly of an extracellular matrix. Integrin activation is usually mediated through the integrin beta subunit cytoplasmic tail and can be regulated by many different biochemical signaling pathways. We report that specific binding of the cytoskeletal protein talin to integrin beta subunit cytoplasmic tails leads to the conformational rearrangements of integrin extracellular domains that increase their affinity. Thus, regulated binding of talin to integrin beta tails is a final common element of cellular signaling cascades that control integrin activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tadokoro, Seiji -- Shattil, Sanford J -- Eto, Koji -- Tai, Vera -- Liddington, Robert C -- de Pereda, Jose M -- Ginsberg, Mark H -- Calderwood, David A -- New York, N.Y. -- Science. 2003 Oct 3;302(5642):103-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, The Scripps Research Institute, The Burnham Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14526080" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Antibodies, Monoclonal/immunology ; Antigens, CD29/chemistry/metabolism ; Cell Line ; Fibronectins/metabolism ; Humans ; Integrin beta Chains/chemistry/*metabolism ; Integrin beta3/chemistry/metabolism ; Molecular Sequence Data ; Mutation ; Platelet Glycoprotein GPIIb-IIIa Complex/chemistry/immunology/metabolism ; Protein Binding ; Protein Conformation ; Protein Structure, Tertiary ; RNA, Small Interfering ; Recombinant Proteins/metabolism ; *Signal Transduction ; Talin/*metabolism ; Transfection
    Print ISSN: 0036-8075
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  • 8
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    Legionella effectors that promote nonlytic release from protozoa (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-02-28
    Description: Legionella pneumophila, the bacterial agent of legionnaires' disease, replicates intracellularly within a specialized vacuole of mammalian and protozoan host cells. Little is known about the specialized vacuole except that the Icm/Dot type IV secretion system is essential for its formation and maintenance. The Legionella genome database contains two open reading frames encoding polypeptides (LepA and LepB) with predicted coiled-coil regions and weak homology to SNAREs; these are delivered to host cells by an Icm/Dot-dependent mechanism. Analysis of mutant strains suggests that the Lep proteins may enable the Legionella to commandeer a protozoan exocytic pathway for dissemination of the pathogen.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, John -- de Felipe, Karim Suwwan -- Clarke, Margaret -- Lu, Hao -- Anderson, O Roger -- Segal, Gil -- Shuman, Howard A -- NIH-R01 AI23549/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2004 Feb 27;303(5662):1358-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, College of Physicians and Surgeons, Columbia University, 701 West 168th Street, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14988561" target="_blank"〉PubMed〈/a〉
    Keywords: Acanthamoeba/*microbiology/physiology/ultrastructure ; Animals ; Bacterial Proteins/genetics/metabolism/*physiology ; Cell Line ; Colony Count, Microbial ; Cyclic AMP/metabolism ; Dictyostelium/*microbiology/physiology/ultrastructure ; Exocytosis ; Genome, Bacterial ; Humans ; Legionella pneumophila/*genetics/growth & development/pathogenicity/*physiology ; Lysosomes/physiology ; Macrophages/microbiology/ultrastructure ; Mutation ; Open Reading Frames ; Phagosomes/physiology ; Recombinant Fusion Proteins/metabolism ; Vacuoles/microbiology
    Print ISSN: 0036-8075
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  • 9
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    Calorie restriction promotes mammalian cell survival by inducing the SIRT1 deacetylase (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-06-19
    Description: A major cause of aging is thought to result from the cumulative effects of cell loss over time. In yeast, caloric restriction (CR) delays aging by activating the Sir2 deacetylase. Here we show that expression of mammalian Sir2 (SIRT1) is induced in CR rats as well as in human cells that are treated with serum from these animals. Insulin and insulin-like growth factor 1 (IGF-1) attenuated this response. SIRT1 deacetylates the DNA repair factor Ku70, causing it to sequester the proapoptotic factor Bax away from mitochondria, thereby inhibiting stress-induced apoptotic cell death. Thus, CR could extend life-span by inducing SIRT1 expression and promoting the long-term survival of irreplaceable cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Haim Y -- Miller, Christine -- Bitterman, Kevin J -- Wall, Nathan R -- Hekking, Brian -- Kessler, Benedikt -- Howitz, Konrad T -- Gorospe, Myriam -- de Cabo, Rafael -- Sinclair, David A -- AG19719-03/AG/NIA NIH HHS/ -- AG19972-02/AG/NIA NIH HHS/ -- F32 CA097802/CA/NCI NIH HHS/ -- P01 AG027916/AG/NIA NIH HHS/ -- R01 AG019719/AG/NIA NIH HHS/ -- R01 AG019972/AG/NIA NIH HHS/ -- R01 AG028730/AG/NIA NIH HHS/ -- R01 GM068072/GM/NIGMS NIH HHS/ -- R37 AG028730/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2004 Jul 16;305(5682):390-2. Epub 2004 Jun 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15205477" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Adipose Tissue/metabolism ; Alleles ; Animals ; Antigens, Nuclear/metabolism ; *Apoptosis ; *Caloric Restriction ; Cell Line ; *Cell Survival ; DNA-Binding Proteins/metabolism ; Histone Deacetylases/genetics/*metabolism ; Humans ; Insulin/metabolism/pharmacology ; Insulin-Like Growth Factor I/metabolism/pharmacology ; Kidney/metabolism ; Liver/metabolism ; Male ; Mitochondria/metabolism ; Mutation ; Proto-Oncogene Proteins/metabolism ; *Proto-Oncogene Proteins c-bcl-2 ; RNA, Small Interfering ; Rats ; Rats, Inbred F344 ; Sirtuin 1 ; Sirtuins/genetics/*metabolism ; bcl-2-Associated X Protein
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  • 10
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    Activity-dependent internalization of smoothened mediated by beta-arrestin 2 and GRK2 (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-25
    Description: Binding of Sonic Hedgehog (Shh) to Patched (Ptc) relieves the latter's tonic inhibition of Smoothened (Smo), a receptor that spans the cell membrane seven times. This initiates signaling which, by unknown mechanisms, regulates vertebrate developmental processes. We find that two molecules interact with mammalian Smo in an activation-dependent manner: G protein-coupled receptor kinase 2 (GRK2) leads to phosphorylation of Smo, and beta-arrestin 2 fused to green fluorescent protein interacts with Smo. These two processes promote endocytosis of Smo in clathrin-coated pits. Ptc inhibits association of beta-arrestin 2 with Smo, and this inhibition is relieved in cells treated with Shh. A Smo agonist stimulated and a Smo antagonist (cyclopamine) inhibited both phosphorylation of Smo by GRK2 and interaction of beta-arrestin 2 with Smo. beta-Arrestin 2 and GRK2 are thus potential mediators of signaling by activated Smo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Wei -- Ren, Xiu-Rong -- Nelson, Christopher D -- Barak, Larry S -- Chen, James K -- Beachy, Philip A -- de Sauvage, Frederic -- Lefkowitz, Robert J -- New York, N.Y. -- Science. 2004 Dec 24;306(5705):2257-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA. w.chen@duke.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15618519" target="_blank"〉PubMed〈/a〉
    Keywords: Arrestins/*metabolism ; Cell Line ; Cell Membrane/*metabolism ; Clathrin/metabolism ; Coated Pits, Cell-Membrane/metabolism ; Cyclic AMP-Dependent Protein Kinases/*metabolism ; Cyclohexylamines/pharmacology ; Cytosol/metabolism ; Dynamins/metabolism ; Endocytosis ; Hedgehog Proteins ; Humans ; Membrane Proteins/metabolism ; Phosphorylation ; Receptors, Cell Surface ; Receptors, G-Protein-Coupled/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Thiophenes/pharmacology ; Trans-Activators/metabolism ; Transfection ; Veratrum Alkaloids/pharmacology ; beta-Adrenergic Receptor Kinases
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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