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  • Cell Line  (64)
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  • American Association for the Advancement of Science (AAAS)  (115)
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  • 1
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-07-01
    Beschreibung: During embryogenesis, stem cells are set aside to fuel the postnatal hair cycle and repair the epidermis after injury. To define how hair follicle stem cells are specified and maintained in an undifferentiated state, we developed a strategy to isolate and transcriptionally profile embryonic hair progenitors in mice. We identified Lhx2 as a transcription factor positioned downstream of signals necessary to specify hair follicle stem cells, but upstream from signals required to drive activated stem cells to terminally differentiate. Using gain- and loss-of-function studies, we uncovered a role for Lhx2 in maintaining the growth and undifferentiated properties of hair follicle progenitors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2405918/" 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/PMC2405918/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rhee, Horace -- Polak, Lisa -- Fuchs, Elaine -- R01 AR031737/AR/NIAMS NIH HHS/ -- R01 AR031737-24/AR/NIAMS NIH HHS/ -- R01 AR050452/AR/NIAMS NIH HHS/ -- R01 AR050452-04/AR/NIAMS NIH HHS/ -- R01-AR050452/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Jun 30;312(5782):1946-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Rockefeller University, 1230 York Avenue, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16809539" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Differentiation ; Cell Lineage ; Cell Proliferation ; Epidermis/cytology/embryology ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Hair/embryology/growth & development ; Hair Follicle/*cytology/embryology/physiology ; Homeodomain Proteins/genetics/*physiology ; LIM-Homeodomain Proteins ; Male ; Mice ; Mice, Knockout ; Mice, Transgenic ; Morphogenesis ; Oligonucleotide Array Sequence Analysis ; Signal Transduction ; Skin Transplantation ; Stem Cells/*physiology ; Transcription Factors/genetics/*physiology ; Up-Regulation
    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
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-09-30
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mustelin, Tomas -- New York, N.Y. -- Science. 2006 Sep 29;313(5795):1902-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program on Inflammatory Disease Research, Infectious and Inflammatory Disease Center, and Program of Signal Transduction, Cancer Center, Burnham Institute for Medical Research, La Jolla, CA 92037, USA. tmustelin@burnham.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17008518" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antigen Presentation ; Antigens, CD ; Antigens, CD28/metabolism ; Antigens, CD80/metabolism ; Antigens, CD86/metabolism ; Antigens, Differentiation/genetics/*physiology ; *Autoimmunity ; CTLA-4 Antigen ; Cell Adhesion ; Cell Movement ; Dendritic Cells/immunology ; Humans ; Integrins/physiology ; Ligands ; Lymph Nodes/*immunology ; Lymphocyte Activation ; Mice ; Receptors, Antigen, T-Cell/immunology/metabolism ; Signal Transduction ; T-Lymphocytes/immunology/*physiology
    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: 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
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    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
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
    Publikationsdatum: 2006-05-20
    Beschreibung: We describe the use of gold nanoparticle-oligonucleotide complexes as intracellular gene regulation agents for the control of protein expression in cells. These oligonucleotide-modified nanoparticles have affinity constants for complementary nucleic acids that are higher than their unmodified oligonucleotide counterparts, are less susceptible to degradation by nuclease activity, exhibit greater than 99% cellular uptake, can introduce oligonucleotides at a higher effective concentration than conventional transfection agents, and are nontoxic to the cells under the conditions studied. By chemically tailoring the density of DNA bound to the surface of gold nanoparticles, we demonstrated a tunable gene knockdown.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosi, Nathaniel L -- Giljohann, David A -- Thaxton, C Shad -- Lytton-Jean, Abigail K R -- Han, Min Su -- Mirkin, Chad A -- New York, N.Y. -- Science. 2006 May 19;312(5776):1027-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and International Institute for Nanotechnology, Northwestern University, 2145 Sheridan Road, Evanston, IL 60208-3113 USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16709779" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; Deoxyribonucleases/metabolism ; *Gene Expression Regulation ; Glutathione/metabolism ; *Gold ; Green Fluorescent Proteins/genetics ; HeLa Cells ; Humans ; Mice ; *Nanostructures ; *Oligodeoxyribonucleotides, Antisense/metabolism ; RNA, Messenger
    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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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-12-16
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Linden, Joel -- New York, N.Y. -- Science. 2006 Dec 15;314(5806):1689-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Virginia, Charlottesville, VA 22908, USA. jlinden@virginia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170280" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adenosine/metabolism ; Adenosine Monophosphate/metabolism ; Adenosine Triphosphate/*metabolism ; Animals ; Apyrase/pharmacology ; *Autocrine Communication ; Blood Platelets/metabolism ; Cell Membrane/metabolism ; *Chemotaxis, Leukocyte/drug effects ; Endothelial Cells/metabolism ; Mice ; Models, Biological ; N-Formylmethionine Leucyl-Phenylalanine ; Neutrophils/drug effects/*metabolism/physiology ; Receptor, Adenosine A3/metabolism ; Receptors, Purinergic/*metabolism ; Receptors, Purinergic P2/metabolism ; Receptors, Purinergic P2Y2 ; Respiratory Burst/drug effects ; 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: 2006-09-09
    Beschreibung: Chromosomal integration enables human immunodeficiency virus (HIV) to establish a permanent reservoir that can be therapeutically suppressed but not eradicated. Participation of cellular proteins in this obligate replication step is poorly understood. We used intensified RNA interference and dominant-negative protein approaches to show that the cellular transcriptional coactivator lens epithelium-derived growth factor (LEDGF)/p75 (p75) is an essential HIV integration cofactor. The mechanism requires both linkages of a molecular tether that p75 forms between integrase and chromatin. Fractionally minute levels of endogenous p75 are sufficient to enable integration, showing that cellular factors that engage HIV after entry may elude identification in less intensive knockdowns. Perturbing the p75-integrase interaction may have therapeutic potential.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Llano, Manuel -- Saenz, Dyana T -- Meehan, Anne -- Wongthida, Phonphimon -- Peretz, Mary -- Walker, William H -- Teo, Wulin -- Poeschla, Eric M -- New York, N.Y. -- Science. 2006 Oct 20;314(5798):461-4. Epub 2006 Sep 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Medicine Program, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16959972" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adaptor Proteins, Signal Transducing/chemistry/genetics/metabolism/*physiology ; CD4-Positive T-Lymphocytes/metabolism/*virology ; Cell Line ; Chromatin/*metabolism ; HIV Integrase/*metabolism ; HIV-1/*physiology ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; RNA Interference ; Recombinant Fusion Proteins/metabolism ; Transcription Factors/chemistry/genetics/metabolism/*physiology ; *Virus Integration ; Virus Replication
    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: 2006-04-08
    Beschreibung: Aortic aneurysm and dissection are manifestations of Marfan syndrome (MFS), a disorder caused by mutations in the gene that encodes fibrillin-1. Selected manifestations of MFS reflect excessive signaling by the transforming growth factor-beta (TGF-beta) family of cytokines. We show that aortic aneurysm in a mouse model of MFS is associated with increased TGF-beta signaling and can be prevented by TGF-beta antagonists such as TGF-beta-neutralizing antibody or the angiotensin II type 1 receptor (AT1) blocker, losartan. AT1 antagonism also partially reversed noncardiovascular manifestations of MFS, including impaired alveolar septation. These data suggest that losartan, a drug already in clinical use for hypertension, merits investigation as a therapeutic strategy for patients with MFS and has the potential to prevent the major life-threatening manifestation of this disorder.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1482474/" 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/PMC1482474/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Habashi, Jennifer P -- Judge, Daniel P -- Holm, Tammy M -- Cohn, Ronald D -- Loeys, Bart L -- Cooper, Timothy K -- Myers, Loretha -- Klein, Erin C -- Liu, Guosheng -- Calvi, Carla -- Podowski, Megan -- Neptune, Enid R -- Halushka, Marc K -- Bedja, Djahida -- Gabrielson, Kathleen -- Rifkin, Daniel B -- Carta, Luca -- Ramirez, Francesco -- Huso, David L -- Dietz, Harry C -- K08 HL067056/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2006 Apr 7;312(5770):117-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16601194" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adrenergic beta-Antagonists/administration & dosage/therapeutic use ; Angiotensin II Type 1 Receptor Blockers/administration & dosage/*therapeutic use ; Animals ; Antibodies/immunology ; Aorta/pathology ; Aortic Aneurysm/etiology/*prevention & control ; *Disease Models, Animal ; Elastic Tissue/pathology ; Female ; Losartan/administration & dosage/*therapeutic use ; Lung/pathology ; Lung Diseases/drug therapy/pathology ; Marfan Syndrome/complications/*drug therapy/metabolism/pathology ; Mice ; Microfilament Proteins/genetics ; Mutation ; Neutralization Tests ; Pregnancy ; Pregnancy Complications/drug therapy ; Propranolol/administration & dosage/therapeutic use ; Pulmonary Alveoli/pathology ; Receptor, Angiotensin, Type 1/metabolism ; Signal Transduction ; Transforming Growth Factor beta/antagonists & inhibitors/immunology/*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: 2006-07-22
    Beschreibung: The surface potential of biological membranes varies according to their lipid composition. We devised genetically encoded probes to assess surface potential in intact cells. These probes revealed marked, localized alterations in the charge of the inner surface of the plasma membrane of macrophages during the course of phagocytosis. Hydrolysis of phosphoinositides and displacement of phosphatidylserine accounted for the change in surface potential at the phagosomal cup. Signaling molecules such as K-Ras, Rac1, and c-Src that are targeted to the membrane by electrostatic interactions were rapidly released from membrane subdomains where the surface charge was altered by lipid remodeling during phagocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yeung, Tony -- Terebiznik, Mauricio -- Yu, Liming -- Silvius, John -- Abidi, Wasif M -- Philips, Mark -- Levine, Tim -- Kapus, Andras -- Grinstein, Sergio -- New York, N.Y. -- Science. 2006 Jul 21;313(5785):347-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell Biology, Hepatology, and Nutrition Department, Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16857939" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Calcium/metabolism ; Cell Line ; Cell Membrane/*physiology ; Fluorescent Dyes/metabolism ; Hydrophobic and Hydrophilic Interactions ; Immunoglobulin G/immunology ; Ionomycin/pharmacology ; Lipid Bilayers/metabolism ; Liposomes/metabolism ; Macrophages/*physiology ; Membrane Potentials ; Mice ; Molecular Probes/metabolism ; Neuropeptides/metabolism ; Opsonin Proteins ; Peptides/metabolism ; *Phagocytosis ; Phagosomes/physiology ; Phospholipids/analysis/metabolism ; Receptors, Fc/immunology/metabolism ; Static Electricity ; rac GTP-Binding Proteins/metabolism ; rac1 GTP-Binding Protein ; 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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  • 10
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-03-18
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉DiCicco-Bloom, Emanuel -- New York, N.Y. -- Science. 2006 Mar 17;311(5767):1560-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience and Cell Biology/Pediatrics (Neurology), University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA. diciccem@umdnj.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16543446" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adherens Junctions/*physiology/ultrastructure ; Animals ; Brain/cytology/*embryology ; *Cell Adhesion ; Cell Count ; Cell Death ; Cell Differentiation ; Cell Movement ; Cell Proliferation ; Central Nervous System/cytology/embryology ; Cytoskeleton/physiology ; Hedgehog Proteins ; Hyperplasia ; Mice ; Mutation ; Neurons/cytology/*physiology ; Signal Transduction ; Stem Cells/cytology/physiology ; Trans-Activators/*metabolism ; alpha Catenin/genetics/*physiology
    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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  • 11
    Publikationsdatum: 2006-12-16
    Beschreibung: Cells must amplify external signals to orient and migrate in chemotactic gradient fields. We find that human neutrophils release adenosine triphosphate (ATP) from the leading edge of the cell surface to amplify chemotactic signals and direct cell orientation by feedback through P2Y2 nucleotide receptors. Neutrophils rapidly hydrolyze released ATP to adenosine that then acts via A3-type adenosine receptors, which are recruited to the leading edge, to promote cell migration. Thus, ATP release and autocrine feedback through P2Y2 and A3 receptors provide signal amplification, controlling gradient sensing and migration of neutrophils.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Yu -- Corriden, Ross -- Inoue, Yoshiaki -- Yip, Linda -- Hashiguchi, Naoyuki -- Zinkernagel, Annelies -- Nizet, Victor -- Insel, Paul A -- Junger, Wolfgang G -- GM-60475/GM/NIGMS NIH HHS/ -- GM-66232/GM/NIGMS NIH HHS/ -- PR043034/PR/OCPHP CDC HHS/ -- R01 GM-51477/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 15;314(5806):1792-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, University of California San Diego, San Diego, CA 92103, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170310" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adenosine/metabolism/pharmacology ; Adenosine A3 Receptor Agonists ; Adenosine A3 Receptor Antagonists ; Adenosine Triphosphate/analogs & derivatives/*metabolism/pharmacology ; Animals ; *Autocrine Communication ; Cell Membrane/metabolism ; *Chemotaxis, Leukocyte/drug effects ; Cytoplasmic Granules/metabolism ; HL-60 Cells ; Humans ; Hydrolysis ; Mice ; Mice, Knockout ; Neutrophils/drug effects/metabolism/*physiology ; Purinergic P2 Receptor Antagonists ; Receptor, Adenosine A3/*metabolism ; Receptors, Purinergic P2/*metabolism ; Receptors, Purinergic P2Y2 ; Signal Transduction ; Suramin/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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  • 12
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-04-29
    Beschreibung: Mutations in the nuclear structural protein lamin A cause the premature aging syndrome Hutchinson-Gilford progeria (HGPS). Whether lamin A plays any role in normal aging is unknown. We show that the same molecular mechanism responsible for HGPS is active in healthy cells. Cell nuclei from old individuals acquire defects similar to those of HGPS patient cells, including changes in histone modifications and increased DNA damage. Age-related nuclear defects are caused by sporadic use, in healthy individuals, of the same cryptic splice site in lamin A whose constitutive activation causes HGPS. Inhibition of this splice site reverses the nuclear defects associated with aging. These observations implicate lamin A in physiological aging.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1855250/" 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/PMC1855250/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scaffidi, Paola -- Misteli, Tom -- Z01 BC010309-07/BC/NCI NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2006 May 19;312(5776):1059-63. Epub 2006 Apr 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Cancer Institute (NCI), NIH, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645051" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Aged, 80 and over ; Aging/*physiology ; Cell Line ; Cell Nucleus/pathology ; DNA Damage ; Exons ; Histones/metabolism ; Humans ; Lamin Type A/genetics/*physiology ; Progeria/genetics/pathology ; RNA Splicing/genetics ; Signal Transduction ; Tumor Suppressor Protein p53/genetics/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 13
    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
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 14
    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
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 15
    Publikationsdatum: 2006-04-01
    Beschreibung: IRAK-4 is a protein kinase that is pivotal in mediating signals for innate immune responses. Here, we report that IRAK-4 signaling is also essential for eliciting adaptive immune responses. Thus, in the absence of IRAK-4, in vivo T cell responses were significantly impaired. Upon T cell receptor stimulation, IRAK-4 is recruited to T cell lipid rafts, where it induces downstream signals, including protein kinase C activation through the association with Zap70. This signaling pathway was found to be required for optimal activation of nuclear factor kappaB. Our findings suggest that T cells use this critical regulator of innate immunity for the development of acquired immunity, suggesting that IRAK-4 may be involved in direct signal cross talk between the two systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suzuki, Nobutaka -- Suzuki, Shinobu -- Millar, Douglas G -- Unno, Midori -- Hara, Hiromitsu -- Calzascia, Thomas -- Yamasaki, Sho -- Yokosuka, Tadashi -- Chen, Nien-Jung -- Elford, Alisha R -- Suzuki, Jun-Ichiro -- Takeuchi, Arata -- Mirtsos, Christine -- Bouchard, Denis -- Ohashi, Pamela S -- Yeh, Wen-Chen -- Saito, Takashi -- New York, N.Y. -- Science. 2006 Mar 31;311(5769):1927-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cell Signaling, RIKEN Research Center for Allergy and Immunology, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama City, Kanagawa 230-0045, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16574867" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Enzyme Activation ; Immunity, Innate ; Interleukin-1 Receptor-Associated Kinases ; Isoenzymes/metabolism ; *Lymphocyte Activation ; Membrane Microdomains/enzymology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Transgenic ; NF-kappa B/metabolism ; Phosphotransferases (Alcohol Group Acceptor)/genetics/*metabolism ; Protein Kinase C/metabolism ; Receptors, Antigen, T-Cell/immunology ; Signal Transduction ; T-Lymphocytes/*immunology ; ZAP-70 Protein-Tyrosine Kinase/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 16
    Publikationsdatum: 2006-01-10
    Beschreibung: The pathophysiology of depression remains enigmatic, although abnormalities in serotonin signaling have been implicated. We have found that the serotonin 1B receptor [5-hydroxytryptamine (5-HT1B) receptor] interacts with p11. p11 increases localization of 5-HT1B receptors at the cell surface. p11 is increased in rodent brains by antidepressants or electroconvulsive therapy, but decreased in an animal model of depression and in brain tissue from depressed patients. Overexpression of p11 increases 5-HT1B receptor function in cells and recapitulates certain behaviors seen after antidepressant treatment in mice. p11 knockout mice exhibit a depression-like phenotype and have reduced responsiveness to 5-HT1B receptor agonists and reduced behavioral reactions to an antidepressant.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Svenningsson, Per -- Chergui, Karima -- Rachleff, Ilan -- Flajolet, Marc -- Zhang, Xiaoqun -- El Yacoubi, Malika -- Vaugeois, Jean-Marie -- Nomikos, George G -- Greengard, Paul -- DA10044/DA/NIDA NIH HHS/ -- MH40899/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2006 Jan 6;311(5757):77-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16400147" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adult ; Aged ; Animals ; Annexin A2/genetics/*metabolism ; Antidepressive Agents/pharmacology ; Behavior, Animal/drug effects ; Brain/drug effects/metabolism ; Cell Membrane/metabolism ; Depression/genetics/*metabolism ; Electroconvulsive Therapy ; Female ; Humans ; Male ; Mice ; Mice, Knockout ; Mice, Transgenic ; Middle Aged ; Neurons/metabolism ; Rats ; Receptor, Serotonin, 5-HT1B/*metabolism ; S100 Proteins/genetics/*metabolism ; Serotonin/metabolism/physiology ; Signal Transduction ; Two-Hybrid System Techniques
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 17
    Publikationsdatum: 2006-10-28
    Beschreibung: The inflammatory bowel diseases Crohn's disease and ulcerative colitis are common, chronic disorders that cause abdominal pain, diarrhea, and gastrointestinal bleeding. To identify genetic factors that might contribute to these disorders, we performed a genome-wide association study. We found a highly significant association between Crohn's disease and the IL23R gene on chromosome 1p31, which encodes a subunit of the receptor for the proinflammatory cytokine interleukin-23. An uncommon coding variant (rs11209026, c.1142G〉A, p.Arg381Gln) confers strong protection against Crohn's disease, and additional noncoding IL23R variants are independently associated. Replication studies confirmed IL23R associations in independent cohorts of patients with Crohn's disease or ulcerative colitis. These results and previous studies on the proinflammatory role of IL-23 prioritize this signaling pathway as a therapeutic target in inflammatory bowel disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4410764/" 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/PMC4410764/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duerr, Richard H -- Taylor, Kent D -- Brant, Steven R -- Rioux, John D -- Silverberg, Mark S -- Daly, Mark J -- Steinhart, A Hillary -- Abraham, Clara -- Regueiro, Miguel -- Griffiths, Anne -- Dassopoulos, Themistocles -- Bitton, Alain -- Yang, Huiying -- Targan, Stephan -- Datta, Lisa Wu -- Kistner, Emily O -- Schumm, L Philip -- Lee, Annette T -- Gregersen, Peter K -- Barmada, M Michael -- Rotter, Jerome I -- Nicolae, Dan L -- Cho, Judy H -- DK62413/DK/NIDDK NIH HHS/ -- DK62420/DK/NIDDK NIH HHS/ -- DK62422/DK/NIDDK NIH HHS/ -- DK62423/DK/NIDDK NIH HHS/ -- DK62429/DK/NIDDK NIH HHS/ -- DK62431/DK/NIDDK NIH HHS/ -- DK62432/DK/NIDDK NIH HHS/ -- P30 DK063491/DK/NIDDK NIH HHS/ -- P30 DK063491-019004/DK/NIDDK NIH HHS/ -- P30 DK063491-029004/DK/NIDDK NIH HHS/ -- P30 DK063491-039004/DK/NIDDK NIH HHS/ -- P30 DK063491-049004/DK/NIDDK NIH HHS/ -- U01 DK062420/DK/NIDDK NIH HHS/ -- U01 DK062422/DK/NIDDK NIH HHS/ -- U01 DK062423/DK/NIDDK NIH HHS/ -- U01 DK062429/DK/NIDDK NIH HHS/ -- U01 DK062432/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 1;314(5804):1461-3. Epub 2006 Oct 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, School of Medicine, University of Pittsburgh, University of Pittsburgh Medical Center Presbyterian, Mezzanine Level, C-Wing, 200 Lothrop Street, Pittsburgh, PA 15213, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17068223" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alleles ; Case-Control Studies ; Chromosomes, Human, Pair 1/genetics ; Cohort Studies ; Colitis, Ulcerative/genetics ; Crohn Disease/*genetics ; Genetic Markers ; Genetic Predisposition to Disease ; Genetic Testing ; Genome, Human ; Haplotypes ; Humans ; Interleukin-23/metabolism ; Jews/genetics ; Linkage Disequilibrium ; *Polymorphism, Single Nucleotide ; Receptors, Interleukin/*genetics/physiology ; Signal Transduction
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 18
    Publikationsdatum: 2006-06-03
    Beschreibung: Checkpoints are evolutionarily conserved signaling mechanisms that arrest cell division and alter cellular stress resistance in response to DNA damage or stalled replication forks. To study the consequences of loss of checkpoint functions in whole animals, checkpoint genes were inactivated in the nematode C. elegans. We show that checkpoint proteins are not only essential for normal development but also determine adult somatic maintenance. Checkpoint proteins play a role in the survival of postmitotic adult cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2568993/" 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/PMC2568993/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olsen, Anders -- Vantipalli, Maithili C -- Lithgow, Gordon J -- AG21069/AG/NIA NIH HHS/ -- AG22868/AG/NIA NIH HHS/ -- NS050789-01/NS/NINDS NIH HHS/ -- R01 AG021069/AG/NIA NIH HHS/ -- R01 AG021069-04/AG/NIA NIH HHS/ -- R01 AG022868/AG/NIA NIH HHS/ -- R01 AG022868-04/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2006 Jun 2;312(5778):1381-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Buck Institute, 8001 Redwood Boulevard, Novato, CA 94945, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16741121" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adaptation, Physiological/genetics/physiology ; Animals ; Caenorhabditis elegans/cytology/growth & development/*physiology ; Caenorhabditis elegans Proteins/genetics/*physiology ; Cell Cycle Proteins/genetics/*physiology ; Cell Survival ; Heat-Shock Proteins/biosynthesis/genetics ; Mitosis/genetics/*physiology ; Mutation ; Protein Kinases/metabolism ; Schizosaccharomyces pombe Proteins ; Signal Transduction ; Stem Cells/cytology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 19
    Publikationsdatum: 2006-02-18
    Beschreibung: Norepinephrine (NE) is widely implicated in opiate withdrawal, but much less is known about its role in opiate-induced locomotion and reward. In mice lacking dopamine beta-hydroxylase (DBH), an enzyme critical for NE synthesis, we found that NE was necessary for morphine-induced conditioned place preference (CPP; a measure of reward) and locomotion. These deficits were rescued by systemic NE restoration. Viral restoration of DBH expression in the nucleus tractus solitarius, but not in the locus coeruleus, restored CPP for morphine. Morphine-induced locomotion was partially restored by DBH expression in either brain region. These data suggest that NE signaling by the nucleus tractus solitarius is necessary for morphine reward.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olson, Valerie G -- Heusner, Carrie L -- Bland, Ross J -- During, Matthew J -- Weinshenker, David -- Palmiter, Richard D -- New York, N.Y. -- Science. 2006 Feb 17;311(5763):1017-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16484499" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Behavior, Animal/drug effects ; Conditioning (Psychology) ; Dopamine beta-Hydroxylase/genetics/metabolism ; Droxidopa/pharmacology ; Locomotion/drug effects ; Locus Coeruleus/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Morphine/*pharmacology ; Motor Activity/drug effects ; Norepinephrine/*physiology ; *Reward ; Signal Transduction ; Solitary Nucleus/*physiology ; *Synaptic Transmission
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 20
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-02-04
    Beschreibung: The aging of organisms is characterized by a gradual functional decline of all organ systems. Mammalian somatic cells in culture display a limited proliferative life span, at the end of which they undergo an irreversible cell cycle arrest known as replicative senescence. Whether cellular senescence contributes to organismal aging has been controversial. We investigated telomere dysfunction, a recently discovered biomarker of cellular senescence, and found that the number of senescent fibroblasts increases exponentially in the skin of aging baboons, reaching 〉15% of all cells in very old individuals. In addition, the same cells contain activated ataxia-telangiectasia mutated kinase and heterochromatinized nuclei, confirming their senescent status.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herbig, Utz -- Ferreira, Mark -- Condel, Laura -- Carey, Dee -- Sedivy, John M -- F32 CA099388/CA/NCI NIH HHS/ -- P01 HL028972/HL/NHLBI NIH HHS/ -- P20 RR015578/RR/NCRR NIH HHS/ -- P51 RR013986/RR/NCRR NIH HHS/ -- R01 AG016694/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2006 Mar 3;311(5765):1257. Epub 2006 Feb 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, RI 02903, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16456035" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Aging/*physiology ; Animals ; Ataxia Telangiectasia Mutated Proteins ; Biomarkers ; Cell Aging/*physiology ; Cell Cycle Proteins/metabolism ; DNA Damage ; DNA Replication ; DNA-Binding Proteins/metabolism ; Dermis/cytology ; Female ; Fibroblasts/cytology/*physiology ; Heterochromatin/metabolism ; Male ; Oxidative Stress ; Papio/*physiology ; Protein-Serine-Threonine Kinases/metabolism ; Signal Transduction ; Telomere/physiology ; Tumor Suppressor Proteins/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 21
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-12-02
    Beschreibung: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4383235/" 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/PMC4383235/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maini, Philip K -- Baker, Ruth E -- Chuong, Cheng-Ming -- R01 AR042177/AR/NIAMS NIH HHS/ -- R01 AR042177-11/AR/NIAMS NIH HHS/ -- R01 AR042177-12/AR/NIAMS NIH HHS/ -- R01 AR047364/AR/NIAMS NIH HHS/ -- R01 AR047364-04/AR/NIAMS NIH HHS/ -- R01 AR047364-05/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 1;314(5804):1397-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Mathematical Biology, University of Oxford, Oxford OX1 3LB, UK. maini@maths.ox.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17138885" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Body Patterning ; Diffusion ; Hair Follicle/*growth & development/metabolism ; Intercellular Signaling Peptides and Proteins/*metabolism ; Mathematics ; Mice ; *Models, Biological ; Signal Transduction ; Wnt Proteins/*metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 22
    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
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 23
    Publikationsdatum: 2006-02-14
    Beschreibung: Plants may "eavesdrop" on volatile organic compounds (VOCs) released by herbivore-attacked neighbors to activate defenses before being attacked themselves. Transcriptome and signal cascade analyses of VOC-exposed plants suggest that plants eavesdrop to prime direct and indirect defenses and to hone competitive abilities. Advances in research on VOC biosynthesis and perception have facilitated the production of plants that are genetically "deaf" to particular VOCs or "mute" in elements of their volatile vocabulary. Such plants, together with advances in VOC analytical instrumentation, will allow researchers to determine whether fluency enhances the fitness of plants in natural communities.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baldwin, Ian T -- Halitschke, Rayko -- Paschold, Anja -- von Dahl, Caroline C -- Preston, Catherine A -- New York, N.Y. -- Science. 2006 Feb 10;311(5762):812-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Ecology, Max Planck Institute for Chemical Ecology, Hans Knoll Strasse 8, Jena 07745, Germany. baldwin@ice.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16469918" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Adaptation, Physiological ; Diffusion ; Gene Expression Regulation, Plant ; Genomics ; Mutation ; Oligonucleotide Array Sequence Analysis ; Organic Chemicals/*metabolism ; Plant Leaves/metabolism ; *Plant Physiological Phenomena ; Plants/*genetics/metabolism ; Signal Transduction ; Volatilization
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 24
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-02-04
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cho, Mildred K -- McGee, Glenn -- Magnus, David -- New York, N.Y. -- Science. 2006 Feb 3;311(5761):614-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stanford Center for Biomedical Ethics, Department of Pediatrics; Palo Alto, CA 94304, USA. micho@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16456065" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Academies and Institutes/ethics/*standards ; Authorship ; Biomedical Research/*ethics/*standards ; Cell Line ; *Ethics, Research ; Female ; Humans ; Korea ; Oocyte Donation/adverse effects ; Research Personnel/*ethics/standards ; Research Support as Topic ; Scientific Misconduct ; Stem Cells ; United States
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 25
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-09-09
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2006 Sep 8;313(5792):1372.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16959980" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Cell Line ; Cloning, Organism/legislation & jurisprudence ; Embryo Research/ethics/*legislation & jurisprudence ; Embryo, Mammalian/cytology ; Humans ; Massachusetts ; Research Embryo Creation/ethics/legislation & jurisprudence ; *Stem Cells
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 26
    Publikationsdatum: 2006-09-16
    Beschreibung: Liver regeneration is an orchestrated cellular response that coordinates cell activation, lipid metabolism, and cell division. We found that caveolin-1 gene-disrupted mice (cav1-/- mice) exhibited impaired liver regeneration and low survival after a partial hepatectomy. Hepatocytes showed dramatically reduced lipid droplet accumulation and did not advance through the cell division cycle. Treatment of cav1-/- mice with glucose (which is a predominant energy substrate when compared to lipids) drastically increased survival and reestablished progression of the cell cycle. Thus, caveolin-1 plays a crucial role in the mechanisms that coordinate lipid metabolism with the proliferative response occurring in the liver after cellular injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fernandez, Manuel A -- Albor, Cecilia -- Ingelmo-Torres, Mercedes -- Nixon, Susan J -- Ferguson, Charles -- Kurzchalia, Teymuras -- Tebar, Francesc -- Enrich, Carlos -- Parton, Robert G -- Pol, Albert -- New York, N.Y. -- Science. 2006 Sep 15;313(5793):1628-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departament de Biologia Cellular, Facultat de Medicina, Institut d'Investigacions Biomediques August Pi i Sunyer, Universitat de Barcelona, Casanova 143, 08036 Barcelona, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16973879" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Caveolae/metabolism ; Caveolin 1/genetics/*physiology ; Cell Cycle ; Cell Division ; Fatty Acids/blood/metabolism ; Glucose/administration & dosage ; Hepatectomy ; Hepatocyte Growth Factor/metabolism ; Hepatocytes/cytology/*metabolism ; *Lipid Metabolism ; Lipids/blood ; Liver/metabolism/ultrastructure ; *Liver Regeneration ; Male ; Mice ; Phosphorylation ; RNA, Small Interfering ; STAT3 Transcription Factor/metabolism ; Signal Transduction ; Triglycerides/blood/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 27
    Publikationsdatum: 2006-10-14
    Beschreibung: The function of cyclin-dependent kinase 2 (CDK2) is often abolished after DNA damage. The inhibition of CDK2 plays a central role in DNA damage-induced cell cycle arrest and DNA repair. However, whether CDK2 also influences the survival of cells under genotoxic stress is unknown. Forkhead box O (FOXO) transcription factors are emerging as key regulators of cell survival. CDK2 specifically phosphorylated FOXO1 at serine-249 (Ser249) in vitro and in vivo. Phosphorylation of Ser249 resulted in cytoplasmic localization and inhibition of FOXO1. This phosphorylation was abrogated upon DNA damage through the cell cycle checkpoint pathway that is dependent on the protein kinases Chk1 and Chk2. Moreover, silencing of FOXO1 by small interfering RNA diminished DNA damage-induced death in both p53-deficient and p53-proficient cells. This effect was reversed by restored expression of FOXO1 in a manner depending on phosphorylation of Ser249. Functional interaction between CDK2 and FOXO1 provides a mechanism that regulates apoptotic cell death after DNA strand breakage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Haojie -- Regan, Kevin M -- Lou, Zhenkun -- Chen, Junjie -- Tindall, Donald J -- CA91956/CA/NCI NIH HHS/ -- DK60920/DK/NIDDK NIH HHS/ -- DK65236/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 13;314(5797):294-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17038621" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Apoptosis ; Camptothecin/pharmacology ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Checkpoint Kinase 2 ; Cyclin-Dependent Kinase 2/antagonists & inhibitors/genetics/*metabolism ; Cytoplasm/metabolism ; *DNA Damage ; Forkhead Transcription Factors/antagonists & inhibitors/*metabolism ; Humans ; Mice ; Phosphorylation ; Phosphoserine/metabolism ; Protein Kinases/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; RNA, Small Interfering ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transcription, Genetic ; Transfection ; Tumor Suppressor Protein p53/metabolism
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  • 28
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-10-14
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2006 Oct 13;314(5797):244-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17038601" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Biological Evolution ; *Brain/physiology ; Brain Chemistry ; Cognition ; Evolution, Molecular ; Gene Expression Profiling ; Humans ; Invertebrates/anatomy & histology/physiology ; Membrane Proteins/*analysis/genetics/metabolism ; Multiprotein Complexes/*analysis/genetics/metabolism ; Nerve Tissue Proteins/*analysis/genetics/metabolism ; Organ Size ; Receptors, Neurotransmitter/analysis/genetics/metabolism ; Signal Transduction ; Synaptic Membranes/*chemistry/physiology ; Synaptic Transmission ; Vertebrates/anatomy & histology/physiology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 29
    Publikationsdatum: 2006-05-06
    Beschreibung: B cells recognize foreign antigens by virtue of cell surface immunoglobulin receptors and are most effectively activated by membrane-bound ligands. Here, we show that in the early stages of this process, B cells exhibit a two-phase response in which they first spread over the antigen-bearing membrane and then contract, thereby collecting bound antigen into a central aggregate. The extent of this response, which is both signaling- and actin-dependent, determines the quantity of antigen accumulated and hence the degree of B cell activation. Brownian dynamic simulations reproduce essential features of the antigen collection process and suggest a possible basis for affinity discrimination. We propose that dynamic spreading is an important step of the immune response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fleire, S J -- Goldman, J P -- Carrasco, Y R -- Weber, M -- Bray, D -- Batista, F D -- G64713/PHS HHS/ -- New York, N.Y. -- Science. 2006 May 5;312(5774):738-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lymphocyte Interaction Laboratory, London Research Institute, Cancer Research UK, 44 Lincoln's Inn Fields, London, WC2A 3PX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16675699" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Actins/physiology ; Algorithms ; Animals ; Antibody Affinity ; Antigen Presentation ; Antigens, Surface/*immunology ; B-Lymphocytes/*immunology/*physiology ; Cell Shape ; Computer Simulation ; Flow Cytometry ; Ligands ; Lipid Bilayers ; *Lymphocyte Activation ; Mice ; Mice, Transgenic ; Microscopy, Fluorescence ; Models, Immunological ; Muramidase/immunology ; Receptors, Antigen, B-Cell/*immunology/metabolism ; Recombinant Fusion Proteins/immunology ; Signal Transduction ; Stochastic Processes ; T-Lymphocytes/immunology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 30
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-11-04
    Beschreibung: Guanosine triphosphatases of the Rab family are key regulators of membrane trafficking, with Rab11 playing a specific role in membrane recycling. We identified a mammalian protein, protrudin, that promoted neurite formation through interaction with the guanosine diphosphate (GDP)-bound form of Rab11. Phosphorylation of protrudin by extracellular signal-regulated kinase (ERK) in response to nerve growth factor promoted protrudin association with Rab11-GDP. Down-regulation of protrudin by RNA interference induced membrane extension in all directions and inhibited neurite formation. Thus, protrudin regulates Rab11-dependent membrane recycling to promote the directional membrane trafficking required for neurite formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shirane, Michiko -- Nakayama, Keiichi I -- New York, N.Y. -- Science. 2006 Nov 3;314(5800):818-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, Fukuoka 812-8582, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17082457" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Adhesion Molecules/metabolism ; Cell Line ; Cell Membrane/*metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Guanosine Diphosphate/metabolism ; HeLa Cells ; Humans ; MAP Kinase Kinase 1/metabolism ; Membrane Proteins ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Nerve Growth Factor/pharmacology/physiology ; Neurites/*physiology ; PC12 Cells ; Phosphorylation ; RNA Interference ; Rats ; Recombinant Fusion Proteins/chemistry/metabolism ; Vesicular Transport Proteins ; rab GTP-Binding Proteins/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 31
    Publikationsdatum: 2006-12-16
    Beschreibung: Antibody class switching in activated B cells uses class switch recombination (CSR), which joins activation-induced cytidine deaminase (AID)-dependent double-strand breaks (DSBs) within two large immunoglobulin heavy chain (IgH) locus switch (S) regions that lie up to 200 kilobases apart. To test postulated roles of S regions and AID in CSR, we generated mutant B cells in which donor Smu and accepter Sgamma1 regions were replaced with yeast I-SceI endonuclease sites. We found that site-specific I-SceI DSBs mediate recombinational IgH locus class switching from IgM to IgG1 without S regions or AID. We propose that CSR evolved to exploit a general DNA repair process that promotes joining of widely separated DSBs within a chromosome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zarrin, Ali A -- Del Vecchio, Catherine -- Tseng, Eva -- Gleason, Megan -- Zarin, Payam -- Tian, Ming -- Alt, Frederick W -- 2P01AI031541-15/AI/NIAID NIH HHS/ -- P01CA092625-05/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 Jan 19;315(5810):377-81. Epub 2006 Dec 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Children's Hospital, CBR Institute for Biomedical Research, and Department of Genetics, Harvard University Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170253" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; B-Lymphocytes/*immunology ; Base Sequence ; Cell Line ; Cytidine Deaminase/*metabolism ; *DNA Breaks, Double-Stranded ; DNA Repair ; Deoxyribonucleases, Type II Site-Specific/genetics/*metabolism ; Embryonic Stem Cells ; Gene Targeting ; Genes, Immunoglobulin Heavy Chain ; Hybridomas ; *Immunoglobulin Class Switching ; Immunoglobulin G/biosynthesis/genetics ; Immunoglobulin M/biosynthesis/genetics ; *Immunoglobulin Switch Region ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Mutation ; Recombination, Genetic ; Saccharomyces cerevisiae/enzymology ; Saccharomyces cerevisiae Proteins
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 32
    Publikationsdatum: 2006-12-16
    Beschreibung: Genetically matched pluripotent embryonic stem (ES) cells generated via nuclear transfer or parthenogenesis (pES cells) are a potential source of histocompatible cells and tissues for transplantation. After parthenogenetic activation of murine oocytes and interruption of meiosis I or II, we isolated and genotyped pES cells and characterized those that carried the full complement of major histocompatibility complex (MHC) antigens of the oocyte donor. Differentiated tissues from these pES cells engrafted in immunocompetent MHC-matched mouse recipients, demonstrating that selected pES cells can serve as a source of histocompatible tissues for transplantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Kitai -- Lerou, Paul -- Yabuuchi, Akiko -- Lengerke, Claudia -- Ng, Kitwa -- West, Jason -- Kirby, Andrew -- Daly, Mark J -- Daley, George Q -- T32: HD07466/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2007 Jan 26;315(5811):482-6. Epub 2006 Dec 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Pediatric Hematology/Oncology, Children's Hospital Boston and Dana Farber Cancer Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170255" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Differentiation ; Cell Line ; Chromosome Segregation ; Embryonic Stem Cells/cytology/*immunology/physiology ; Female ; Genotype ; H-2 Antigens/*genetics/*immunology ; Heterozygote ; *Histocompatibility ; Histocompatibility Antigens Class II/genetics/immunology ; *Major Histocompatibility Complex ; Meiosis ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Oocytes/cytology/immunology ; *Parthenogenesis ; Pluripotent Stem Cells/cytology/*immunology/physiology ; Polymerase Chain Reaction ; Recombination, Genetic ; Stem Cell Transplantation
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  • 33
    Publikationsdatum: 2006-12-23
    Beschreibung: Synonymous single-nucleotide polymorphisms (SNPs) do not produce altered coding sequences, and therefore they are not expected to change the function of the protein in which they occur. We report that a synonymous SNP in the Multidrug Resistance 1 (MDR1) gene, part of a haplotype previously linked to altered function of the MDR1 gene product P-glycoprotein (P-gp), nonetheless results in P-gp with altered drug and inhibitor interactions. Similar mRNA and protein levels, but altered conformations, were found for wild-type and polymorphic P-gp. We hypothesize that the presence of a rare codon, marked by the synonymous polymorphism, affects the timing of cotranslational folding and insertion of P-gp into the membrane, thereby altering the structure of substrate and inhibitor interaction sites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kimchi-Sarfaty, Chava -- Oh, Jung Mi -- Kim, In-Wha -- Sauna, Zuben E -- Calcagno, Anna Maria -- Ambudkar, Suresh V -- Gottesman, Michael M -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2007 Jan 26;315(5811):525-8. Epub 2006 Dec 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA. kimchi@cber.fda.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17185560" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; Cell Membrane/metabolism ; Cercopithecus aethiops ; Codon ; Cyclosporine/pharmacology ; *Genes, MDR ; Haplotypes ; HeLa Cells ; Humans ; Mutagenesis, Site-Directed ; P-Glycoprotein/antagonists & inhibitors/*chemistry/genetics/*metabolism ; *Polymorphism, Single Nucleotide ; Protein Biosynthesis ; Protein Conformation ; *Protein Folding ; Protein Structure, Tertiary ; RNA, Messenger/genetics/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Rhodamine 123/metabolism/pharmacology ; Sirolimus/pharmacology ; Substrate Specificity ; Transfection ; Verapamil/metabolism/pharmacology
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  • 34
    Publikationsdatum: 2006-04-29
    Beschreibung: Store-operated Ca2+ entry is mediated by Ca2+ release-activated Ca2+ (CRAC) channels following Ca2+ release from intracellular stores. We performed a genome-wide RNA interference (RNAi) screen in Drosophila cells to identify proteins that inhibit store-operated Ca2+ influx. A secondary patch-clamp screen identified CRACM1 and CRACM2 (CRAC modulators 1 and 2) as modulators of Drosophila CRAC currents. We characterized the human ortholog of CRACM1, a plasma membrane-resident protein encoded by gene FLJ14466. Although overexpression of CRACM1 did not affect CRAC currents, RNAi-mediated knockdown disrupted its activation. CRACM1 could be the CRAC channel itself, a subunit of it, or a component of the CRAC signaling machinery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vig, M -- Peinelt, C -- Beck, A -- Koomoa, D L -- Rabah, D -- Koblan-Huberson, M -- Kraft, S -- Turner, H -- Fleig, A -- Penner, R -- Kinet, J-P -- 5-R37-GM053950/GM/NIGMS NIH HHS/ -- R01-AI050200/AI/NIAID NIH HHS/ -- R01-GM065360/GM/NIGMS NIH HHS/ -- R01-NS040927/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 May 26;312(5777):1220-3. Epub 2006 Apr 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA. mvig@bidmc.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645049" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Calcium/*metabolism ; Calcium Channels/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Drosophila Proteins/*genetics/*metabolism ; Drosophila melanogaster/*metabolism ; Endoplasmic Reticulum/metabolism ; Humans ; Ion Transport ; Jurkat Cells ; Membrane Proteins/genetics/*metabolism ; Patch-Clamp Techniques ; RNA Interference ; RNA, Small Interfering ; Reverse Transcriptase Polymerase Chain Reaction
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 35
    Publikationsdatum: 2006-08-12
    Beschreibung: We introduce a method for optically imaging intracellular proteins at nanometer spatial resolution. Numerous sparse subsets of photoactivatable fluorescent protein molecules were activated, localized (to approximately 2 to 25 nanometers), and then bleached. The aggregate position information from all subsets was then assembled into a superresolution image. We used this method--termed photoactivated localization microscopy--to image specific target proteins in thin sections of lysosomes and mitochondria; in fixed whole cells, we imaged vinculin at focal adhesions, actin within a lamellipodium, and the distribution of the retroviral protein Gag at the plasma membrane.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Betzig, Eric -- Patterson, George H -- Sougrat, Rachid -- Lindwasser, O Wolf -- Olenych, Scott -- Bonifacino, Juan S -- Davidson, Michael W -- Lippincott-Schwartz, Jennifer -- Hess, Harald F -- New York, N.Y. -- Science. 2006 Sep 15;313(5793):1642-5. Epub 2006 Aug 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Janelia Farm Research Campus, Ashburn, VA 20147, USA. betzige@janelia.hhmi.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16902090" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Actins/analysis ; Algorithms ; Animals ; COS Cells ; Cell Line ; Cell Membrane/*chemistry ; Cercopithecus aethiops ; Fluorescence ; Focal Adhesions/chemistry ; Gene Products, gag/analysis ; Hiv-1 ; Light ; Luminescent Proteins/*analysis ; Lysosomes/chemistry ; Microscopy/*methods ; Mitochondria/chemistry ; *Nanotechnology ; Organelles/*chemistry ; Photobleaching ; Proteins/*analysis ; Pseudopodia/chemistry ; Recombinant Fusion Proteins/*analysis ; Vinculin/analysis
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 36
    Publikationsdatum: 2006-08-12
    Beschreibung: The Arabidopsis CLAVATA3 (CLV3) gene encodes a stem cell-specific protein presumed to be a precursor of a secreted peptide hormone. Matrix-assisted laser desorption/ionization-time-of-flight mass spectrometry (MALDI-TOF MS) applied to in situ Arabidopsis tissues determined the structure of a modified 12-amino acid peptide (MCLV3), which was derived from a conserved motif in the CLV3 sequence. Synthetic MCLV3 induced shoot and root meristem consumption as cells differentiated into other organs, displaying the typical phenotype of transgenic plants overexpressing CLV3. These results suggest that the functional peptide of CLV3 is MCLV3.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kondo, Tatsuhiko -- Sawa, Shinichiro -- Kinoshita, Atsuko -- Mizuno, Satoko -- Kakimoto, Tatsuo -- Fukuda, Hiroo -- Sakagami, Youji -- New York, N.Y. -- Science. 2006 Aug 11;313(5788):845-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate School of Bio-Agricultural Sciences, Nagoya University, Chikusa, Nagoya, 464-8601, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16902141" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Motifs ; Amino Acid Sequence ; Arabidopsis/*cytology/genetics/metabolism ; Arabidopsis Proteins/*chemistry/genetics/*metabolism/pharmacology ; Cell Differentiation ; Cells, Cultured ; Hydroxyproline/chemistry ; Meristem/*cytology/drug effects/metabolism ; Molecular Sequence Data ; Oligopeptides/chemistry/*metabolism/pharmacology ; Plant Roots/growth & development ; Plants, Genetically Modified ; Signal Transduction ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; Stem Cells/cytology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 37
    Publikationsdatum: 2006-06-17
    Beschreibung: Inflammation and trauma lead to enhanced pain sensitivity (hyperalgesia), which is in part due to altered sensory processing in the spinal cord. The synaptic hypothesis of hyperalgesia, which postulates that hyperalgesia is induced by the activity-dependent long-term potentiation (LTP) in the spinal cord, has been challenged, because in previous studies of pain pathways, LTP was experimentally induced by nerve stimulation at high frequencies ( approximately 100 hertz). This does not, however, resemble the real low-frequency afferent barrage that occurs during inflammation. We identified a synaptic amplifier at the origin of an ascending pain pathway that is switched-on by low-level activity in nociceptive nerve fibers. This model integrates known signal transduction pathways of hyperalgesia without contradiction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ikeda, Hiroshi -- Stark, Johanna -- Fischer, Harald -- Wagner, Matthias -- Drdla, Ruth -- Jager, Tino -- Sandkuhler, Jurgen -- P 18129/Austrian Science Fund FWF/Austria -- New York, N.Y. -- Science. 2006 Jun 16;312(5780):1659-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurophysiology, Center for Brain Research, Medical University of Vienna, Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16778058" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Calcium/metabolism ; Electric Stimulation ; Excitatory Postsynaptic Potentials ; Hyperalgesia/*physiopathology ; Inflammation/*physiopathology ; Long-Term Potentiation ; Nerve Fibers, Unmyelinated/*physiology ; Neuronal Plasticity ; Nitric Oxide/physiology ; Pain/*physiopathology ; Patch-Clamp Techniques ; Periaqueductal Gray/physiology ; Posterior Horn Cells/*physiopathology ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Spinal Cord/physiopathology ; Synapses/physiology ; *Synaptic Transmission
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 38
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-05-27
    Beschreibung: Ciona is an emerging model system for elucidating gene networks in development. Comprehensive in situ hybridization assays have identified 76 regulatory genes with localized expression patterns in the early embryo, at the time when naive blastomeres are determined to follow specific cell fates. Systematic gene disruption assays provided more than 3000 combinations of gene expression profiles in mutant backgrounds. Deduced gene circuit diagrams describing the formation of larval tissues were computationally visualized. These diagrams constitute a blueprint for the Ciona embryo and provide a foundation for understanding the evolutionary origins of the chordate body plan.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Imai, Kaoru S -- Levine, Michael -- Satoh, Nori -- Satou, Yutaka -- New York, N.Y. -- Science. 2006 May 26;312(5777):1183-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, Graduate School of Science, Kyoto University, Sakyo-ku, Kyoto, 606-8502, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16728634" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Biological Evolution ; Blastomeres/cytology/physiology ; Body Patterning/genetics ; Cell Differentiation/genetics ; Cell Lineage ; Ciona intestinalis/*embryology/*genetics ; Computational Biology ; Embryo, Nonmammalian/*physiology ; Embryonic Development/*genetics ; Epidermis/cytology ; Gastrula/cytology/physiology ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Genes, Regulator ; In Situ Hybridization ; Intracellular Signaling Peptides and Proteins/*genetics/physiology ; Neurons/cytology ; Nodal Protein ; Notochord/embryology ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Transcription Factors/*genetics/physiology ; Transcription, Genetic ; Transforming Growth Factor beta/genetics/physiology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 39
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-07-15
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2006 Jul 14;313(5784):155-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16840666" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Blastocyst ; Cattle ; Cell Line ; *Cloning, Organism ; Embryo, Mammalian/cytology ; Humans ; Mice ; *Nuclear Transfer Techniques ; *Oocytes ; *Stem Cells ; *Transplantation, Heterologous
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 40
    Publikationsdatum: 2006-08-19
    Beschreibung: Mutations in gld-1 cause lethal germline tumors in the nematode Caenorhabditis elegans. We find that a wide variety of mutations that extend C. elegans' life span confer resistance to these tumors. The long life spans of daf-2/insulin-receptor mutants were not shortened at all by gld-1 mutations; we attribute this finding to decreased cell division and increased DAF-16/p53-dependent apoptosis within the tumors. Mutations that increase life span by restricting food intake or inhibiting respiration did not affect apoptosis but reduced tumor cell division. Unexpectedly, none of these longevity mutations affected mitosis in normal germlines; this finding suggests that cellular changes that lead to longevity preferentially antagonize tumor cell growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pinkston, Julie M -- Garigan, Delia -- Hansen, Malene -- Kenyon, Cynthia -- AG000278/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2006 Aug 18;313(5789):971-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of California, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16917064" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Apoptosis ; Caenorhabditis elegans/*genetics/physiology ; Caenorhabditis elegans Proteins/*genetics/physiology ; Caloric Restriction ; Cell Proliferation ; Forkhead Transcription Factors ; Genes, Helminth ; Germ Cells/cytology ; Insulin/metabolism ; Insulin-Like Growth Factor I/metabolism ; Longevity/*genetics ; Mitochondria/metabolism ; Models, Animal ; *Mutation ; Neoplasms/genetics/*pathology ; Oogenesis ; Receptor, Insulin/*genetics/physiology ; Reproduction ; Signal Transduction ; Transcription Factors/genetics/physiology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 41
    Publikationsdatum: 2006-10-28
    Beschreibung: The spindle assembly checkpoint guards the fidelity of chromosome segregation. It requires the close cooperation of cell cycle regulatory proteins and cytoskeletal elements to sense spindle integrity. The role of the centrosome, the organizing center of the microtubule cytoskeleton, in the spindle checkpoint is unclear. We found that the molecular requirements for a functional spindle checkpoint included components of the large gamma-tubulin ring complex (gamma-TuRC). However, their localization at the centrosome and centrosome integrity were not essential for this function. Thus, the spindle checkpoint can be activated at the level of microtubule nucleation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muller, Hannah -- Fogeron, Marie-Laure -- Lehmann, Verena -- Lehrach, Hans -- Lange, Bodo M H -- New York, N.Y. -- Science. 2006 Oct 27;314(5799):654-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Vertebrate Genomics, Max-Planck Institute for Molecular Genetics, Ihnestrasse 73, D-14195 Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17068266" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Cycle Proteins/metabolism ; Cell Line ; Centrosome/physiology ; Drosophila Proteins/genetics/*metabolism ; Drosophila melanogaster ; Homeodomain Proteins/genetics/metabolism ; Humans ; Kinetochores/metabolism ; Microtubule-Associated Proteins/genetics/*metabolism ; Microtubules/ultrastructure ; *Mitosis ; Protein Kinases/metabolism ; Protein-Serine-Threonine Kinases ; RNA Interference ; Spindle Apparatus/*metabolism/ultrastructure ; Tubulin/*metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 42
    Publikationsdatum: 2006-09-30
    Beschreibung: To pursue a systematic approach to the discovery of functional connections among diseases, genetic perturbation, and drug action, we have created the first installment of a reference collection of gene-expression profiles from cultured human cells treated with bioactive small molecules, together with pattern-matching software to mine these data. We demonstrate that this "Connectivity Map" resource can be used to find connections among small molecules sharing a mechanism of action, chemicals and physiological processes, and diseases and drugs. These results indicate the feasibility of the approach and suggest the value of a large-scale community Connectivity Map project.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamb, Justin -- Crawford, Emily D -- Peck, David -- Modell, Joshua W -- Blat, Irene C -- Wrobel, Matthew J -- Lerner, Jim -- Brunet, Jean-Philippe -- Subramanian, Aravind -- Ross, Kenneth N -- Reich, Michael -- Hieronymus, Haley -- Wei, Guo -- Armstrong, Scott A -- Haggarty, Stephen J -- Clemons, Paul A -- Wei, Ru -- Carr, Steven A -- Lander, Eric S -- Golub, Todd R -- New York, N.Y. -- Science. 2006 Sep 29;313(5795):1929-35.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02142, USA. justin@broad.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17008526" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alzheimer Disease/drug therapy/genetics ; Cell Line ; Cell Line, Tumor ; *Databases, Factual ; Dexamethasone/pharmacology/therapeutic use ; Drug Evaluation, Preclinical/*methods ; Drug Resistance, Neoplasm ; Enzyme Inhibitors/pharmacology ; Estrogens/pharmacology ; Gene Expression/*drug effects ; *Gene Expression Profiling ; HSP90 Heat-Shock Proteins/antagonists & inhibitors ; Histone Deacetylase Inhibitors ; Humans ; Limonins/pharmacology ; Obesity/genetics/physiopathology ; Oligonucleotide Array Sequence Analysis ; Phenothiazines/pharmacology ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug ; therapy/genetics/physiopathology ; Sirolimus/pharmacology/therapeutic use ; Software
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  • 43
    Publikationsdatum: 2006-03-25
    Beschreibung: Innate immunity against bacterial and fungal pathogens is mediated by Toll and immune deficiency (Imd) pathways, but little is known about the antiviral response in Drosophila. Here, we demonstrate that an RNA interference pathway protects adult flies from infection by two evolutionarily diverse viruses. Our work also describes a molecular framework for the viral immunity, in which viral double-stranded RNA produced during infection acts as the pathogen trigger whereas Drosophila Dicer-2 and Argonaute-2 act as host sensor and effector, respectively. These findings establish a Drosophila model for studying the innate immunity against viruses in animals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1509097/" 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/PMC1509097/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Xiao-Hong -- Aliyari, Roghiyh -- Li, Wan-Xiang -- Li, Hong-Wei -- Kim, Kevin -- Carthew, Richard -- Atkinson, Peter -- Ding, Shou-Wei -- AI052447/AI/NIAID NIH HHS/ -- R01 AI052447/AI/NIAID NIH HHS/ -- R01 GM068743/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Apr 21;312(5772):452-4. Epub 2006 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Program for Microbiology, University of California, Riverside, CA 92521, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16556799" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Argonaute Proteins ; Cell Line ; Drosophila Proteins/genetics/metabolism/physiology ; Drosophila melanogaster/embryology/genetics/*immunology/*virology ; Embryo, Nonmammalian/immunology/virology ; Escherichia coli/physiology ; *Immunity, Innate ; Insect Viruses/genetics/*physiology ; Micrococcus luteus/physiology ; Mutation ; Nodaviridae/*physiology ; RNA Helicases/genetics/metabolism ; *RNA Interference ; RNA Viruses/genetics/physiology ; RNA, Double-Stranded/metabolism ; RNA, Small Interfering/metabolism ; RNA, Viral/genetics/metabolism ; RNA-Binding Proteins/genetics/physiology ; RNA-Induced Silencing Complex/genetics/physiology ; Ribonuclease III ; Signal Transduction ; Toll-Like Receptors/physiology ; Transfection ; Virus Replication
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  • 44
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-09-02
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2006 Sep 1;313(5791):1230-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16946049" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Arabidopsis/genetics/*growth & development/metabolism ; Arabidopsis Proteins/chemistry/*metabolism ; Bacteria/metabolism ; Bacterial Physiological Phenomena ; Computer Simulation ; F-Box Proteins/chemistry/*metabolism ; Gene Expression Regulation, Plant ; Indoleacetic Acids/*metabolism ; MicroRNAs/metabolism ; Models, Biological ; *Plant Development ; Plant Growth Regulators/*metabolism ; Plant Proteins/*metabolism ; Plants/genetics/metabolism/microbiology ; RNA Interference ; RNA, Plant/metabolism ; Receptors, Cell Surface/chemistry/*metabolism ; Signal Transduction
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 45
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-08-26
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2006 Aug 25;313(5790):1031.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16931729" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Blastomeres/*cytology ; Cell Culture Techniques ; Cell Division ; Cell Line ; *Embryo Research ; Embryo, Mammalian/cytology ; Humans ; Mice ; *Stem Cells/cytology
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    Standort Signatur Erwartet Verfügbarkeit
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  • 46
    Publikationsdatum: 2006-04-22
    Beschreibung: G protein betagamma subunits have potential as a target for therapeutic treatment of a number of diseases. We performed virtual docking of a small-molecule library to a site on Gbetagamma subunits that mediates protein interactions. We hypothesized that differential targeting of this surface could allow for selective modulation of Gbetagamma subunit functions. Several compounds bound to Gbetagamma subunits with affinities from 0.1 to 60 muM and selectively modulated functional Gbetagamma-protein-protein interactions in vitro, chemotactic peptide signaling pathways in HL-60 leukocytes, and opioid receptor-dependent analgesia in vivo. These data demonstrate an approach for modulation of G protein-coupled receptor signaling that may represent an important therapeutic strategy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonacci, Tabetha M -- Mathews, Jennifer L -- Yuan, Chujun -- Lehmann, David M -- Malik, Sundeep -- Wu, Dianqing -- Font, Jose L -- Bidlack, Jean M -- Smrcka, Alan V -- GM60286/GM/NIGMS NIH HHS/ -- HL-T3207949/HL/NHLBI NIH HHS/ -- HL080706/HL/NHLBI NIH HHS/ -- K05-DA00360/DA/NIDA NIH HHS/ -- R01 CA132317/CA/NCI NIH HHS/ -- R01 GM054597/GM/NIGMS NIH HHS/ -- R01 GM054597-09/GM/NIGMS NIH HHS/ -- R01 HL080706/HL/NHLBI NIH HHS/ -- R01 HL080706-10/HL/NHLBI NIH HHS/ -- R01 HL080706-11/HL/NHLBI NIH HHS/ -- T32DA07232/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2006 Apr 21;312(5772):443-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16627746" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Analgesics/pharmacology ; Animals ; Binding Sites ; Binding, Competitive ; Cell Line ; Computer Simulation ; Cyclohexanes/chemistry/*metabolism/*pharmacology ; Drug Evaluation, Preclinical/*methods ; Enzyme-Linked Immunosorbent Assay ; G-Protein-Coupled Receptor Kinase 2 ; GTP-Binding Protein alpha Subunits/metabolism ; GTP-Binding Protein beta Subunits/chemistry/*metabolism ; GTP-Binding Protein gamma Subunits/chemistry/*metabolism ; HL-60 Cells ; Humans ; Isoenzymes/metabolism ; Mice ; Mice, Inbred ICR ; Mitogen-Activated Protein Kinases/metabolism ; Molecular Structure ; Morphine/pharmacology ; N-Formylmethionine Leucyl-Phenylalanine/metabolism ; Peptide Library ; Peptides/*metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phospholipase C beta ; Protein Binding ; Protein Interaction Mapping ; *Signal Transduction ; Software ; Structure-Activity Relationship ; Type C Phospholipases/metabolism ; Xanthenes/chemistry/*metabolism/*pharmacology ; beta-Adrenergic Receptor Kinases/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 47
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-04-29
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2006 Apr 28;312(5773):516-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645063" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Blastocyst ; Cell Line ; *Cloning, Organism ; Embryo Research/economics ; Embryo, Mammalian/cytology ; Female ; Humans ; Nuclear Transfer Techniques ; Oocyte Donation ; Research Support as Topic ; *Stem Cells
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 48
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-05-27
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lemaire, Patrick -- New York, N.Y. -- Science. 2006 May 26;312(5777):1145-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Biologie du Developpement de Marseille Luminy, UMR6216 CNRS-Universite de la Mediterranee, Campus de Luminy, F-13288 Marseille cedex 9, France. lemaire@ibdm.univ-mrs.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16728621" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Biological Evolution ; Body Patterning/genetics ; Cell Differentiation/genetics ; Ciona intestinalis/*embryology/*genetics ; Embryo, Nonmammalian/physiology ; Embryonic Development/*genetics ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Genes, Regulator ; In Situ Hybridization ; Intracellular Signaling Peptides and Proteins/*genetics/physiology ; Ligands ; Polymerase Chain Reaction ; Signal Transduction ; Transcription Factors/*genetics/physiology ; Transcription, Genetic
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 49
    Publikationsdatum: 2006-07-01
    Beschreibung: Axonal guidance and vascular patterning share several guidance cues, including proteins in the netrin family. We demonstrate that netrins stimulate proliferation, migration, and tube formation of human endothelial cells in vitro and that this stimulation is independent of known netrin receptors. Suppression of netrin1a messenger RNA in zebrafish inhibits vascular sprouting, implying a proangiogenic role for netrins during vertebrate development. We also show that netrins accelerate neovascularization in an in vivo model of ischemia and that they reverse neuropathy and vasculopathy in a diabetic murine model. We propose that the attractive vascular and neural guidance functions of netrins offer a unique therapeutic potential.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2577078/" 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/PMC2577078/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, Brent D -- Ii, Masaaki -- Park, Kye Won -- Suli, Arminda -- Sorensen, Lise K -- Larrieu-Lahargue, Frederic -- Urness, Lisa D -- Suh, Wonhee -- Asai, Jun -- Kock, Gerhardus A H -- Thorne, Tina -- Silver, Marcy -- Thomas, Kirk R -- Chien, Chi-Bin -- Losordo, Douglas W -- Li, Dean Y -- R01 HL068873/HL/NHLBI NIH HHS/ -- R01 HL077671/HL/NHLBI NIH HHS/ -- R01 HL077671-03/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2006 Aug 4;313(5787):640-4. Epub 2006 Jun 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Human Molecular Biology and Genetics, University of Utah, Salt Lake City, UT 84112, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16809490" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Angiogenesis Inducing Agents ; Animals ; Cell Line ; Cell Movement ; Chemotaxis ; DNA, Complementary ; Diabetic Angiopathies/therapy ; Diabetic Neuropathies/therapy ; Embryo, Nonmammalian ; Endothelial Cells/*physiology ; Endothelium, Vascular/cytology ; Genetic Therapy ; Humans ; Ischemia/drug therapy ; Mice ; Muscle, Skeletal/blood supply ; *Neovascularization, Physiologic ; Nerve Growth Factors/genetics/pharmacology/*physiology ; Neural Conduction ; Receptors, Cell Surface/physiology ; Tumor Suppressor Proteins/genetics/pharmacology/*physiology ; Vascular Endothelial Growth Factor A/therapeutic use ; Zebrafish
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  • 50
    facet.materialart.
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-03-04
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Krajick, Kevin -- New York, N.Y. -- Science. 2006 Mar 3;311(5765):1230-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16513956" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Animals, Zoo ; Biodiversity ; *Bufonidae/physiology ; Cell Line ; *Conservation of Natural Resources ; Developed Countries ; *Ecosystem ; Environment ; Population Dynamics ; Rivers ; Tanzania ; Water Movements
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 51
    Publikationsdatum: 2006-09-02
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Laviano, Alessandro -- Meguid, Michael M -- Inui, Akio -- Rossi-Fanelli, Filippo -- New York, N.Y. -- Science. 2006 Sep 1;313(5791):1236-8; author reply 1236-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16946053" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Appetite ; Brain/metabolism ; *Eating ; Humans ; Leucine/*administration & dosage/*physiology ; *Protein Biosynthesis ; Protein Kinases/metabolism ; Rats ; Signal Transduction ; TOR Serine-Threonine Kinases
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    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 52
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-11-11
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fujita, Takashi -- New York, N.Y. -- Science. 2006 Nov 10;314(5801):935-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Genetics, Institute for Virus Research, Kyoto University, Kyoto 606- 8507, Japan. tfujita@virus.kyoto-u.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17095686" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Base Sequence ; Cytoplasm/metabolism/virology ; DEAD-box RNA Helicases/chemistry/*metabolism ; Humans ; Immunity, Innate ; Interferons/biosynthesis ; Nucleic Acid Conformation ; Phosphates/metabolism ; Phosphorylation ; RNA Caps/metabolism ; RNA, Double-Stranded/chemistry/metabolism ; RNA, Viral/chemistry/*metabolism ; Signal Transduction ; Toll-Like Receptors/metabolism ; Viral Nonstructural Proteins/metabolism ; Virus Diseases/immunology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 53
    Publikationsdatum: 2006-09-23
    Beschreibung: Abnormally synchronized synaptic transmission in the brain causes epilepsy. Most inherited forms of epilepsy result from mutations in ion channels. However, one form of epilepsy, autosomal dominant partial epilepsy with auditory features (ADPEAF), is characterized by mutations in a secreted neuronal protein, LGI1. We show that ADAM22, a transmembrane protein that when mutated itself causes seizure, serves as a receptor for LGI1. LGI1 enhances AMPA receptor-mediated synaptic transmission in hippocampal slices. The mutated form of LGI1 fails to bind to ADAM22. ADAM22 is anchored to the postsynaptic density by cytoskeletal scaffolds containing stargazin. These studies in rat brain indicate possible avenues for understanding human epilepsy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fukata, Yuko -- Adesnik, Hillel -- Iwanaga, Tsuyoshi -- Bredt, David S -- Nicoll, Roger A -- Fukata, Masaki -- New York, N.Y. -- Science. 2006 Sep 22;313(5794):1792-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genomics and Proteomics, National Institute for Longevity Sciences, National Center for Geriatrics and Gerontology, Obu, Aichi 474-8522, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16990550" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): ADAM Proteins/chemistry/genetics/*metabolism ; Animals ; Calcium Channels/metabolism ; Cell Line ; Cerebellar Cortex/metabolism ; Cerebral Cortex/metabolism ; Epilepsies, Partial/physiopathology ; Hippocampus/metabolism/*physiology ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Ligands ; Membrane Proteins/metabolism ; Mice ; N-Methylaspartate/metabolism ; Nerve Tissue Proteins/genetics/metabolism ; Protein Binding ; Protein Structure, Tertiary ; Proteins/*metabolism ; Rats ; Receptors, AMPA/*metabolism ; Recombinant Fusion Proteins/metabolism ; Synapses/metabolism ; *Synaptic Transmission ; Transfection ; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 54
    Publikationsdatum: 2006-04-29
    Beschreibung: Wnt proteins function as morphogens that can form long-range concentration gradients to pattern developing tissues. Here, we show that the retromer, a multiprotein complex involved in intracellular protein trafficking, is required for long-range signaling of the Caenorhabditis elegans Wnt ortholog EGL-20. The retromer functions in EGL-20-producing cells to allow the formation of an EGL-20 gradient along the anteroposterior axis. This function is evolutionarily conserved, because Wnt target gene expression is also impaired in the absence of the retromer complex in vertebrates. These results demonstrate that the ability of Wnt to regulate long-range patterning events is dependent on a critical and conserved function of the retromer complex within Wnt-producing cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coudreuse, Damien Y M -- Roel, Giulietta -- Betist, Marco C -- Destree, Olivier -- Korswagen, Hendrik C -- New York, N.Y. -- Science. 2006 May 12;312(5775):921-4. Epub 2006 Apr 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hubrecht Laboratory and Center for Biomedical Genetics, Uppsalalaan 8, 3584 CT, Utrecht, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645052" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Body Patterning ; Caenorhabditis elegans/cytology/genetics/growth & development/*physiology ; Caenorhabditis elegans Proteins/analysis/genetics/*physiology ; Cell Line ; Gene Expression ; Glycoproteins/analysis/genetics/*physiology ; Humans ; Multiprotein Complexes/*physiology ; Mutation ; Neurons/cytology/physiology ; RNA Interference ; *Signal Transduction ; Transgenes ; Vesicular Transport Proteins/genetics/physiology ; Wnt Proteins/*physiology ; Xenopus
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 55
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-12-23
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin, Jennifer -- New York, N.Y. -- Science. 2006 Dec 22;314(5807):1853.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17185568" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Cell Line ; *Embryonic Stem Cells ; Humans ; Periodicals as Topic ; Publishing/standards ; *Scientific Misconduct
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    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 56
    Publikationsdatum: 2006-08-05
    Beschreibung: Immunity-related p47 guanosine triphosphatases (IRG) play a role in defense against intracellular pathogens. We found that the murine Irgm1 (LRG-47) guanosine triphosphatase induced autophagy and generated large autolysosomal organelles as a mechanism for the elimination of intracellular Mycobacterium tuberculosis. We also identified a function for a human IRG protein in the control of intracellular pathogens and report that the human Irgm1 ortholog, IRGM, plays a role in autophagy and in the reduction of intracellular bacillary load.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Singh, Sudha B -- Davis, Alexander S -- Taylor, Gregory A -- Deretic, Vojo -- AI42999/AI/NIAID NIH HHS/ -- AI45148/AI/NIAID NIH HHS/ -- AI57831/AI/NIAID NIH HHS/ -- R01 AI057831/AI/NIAID NIH HHS/ -- T32 AI007538/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2006 Sep 8;313(5792):1438-41. Epub 2006 Aug 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, University of New Mexico School of Medicine, Albuquerque, NM 87131, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16888103" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Autophagy ; Cell Line ; Cytosol/metabolism ; GTP-Binding Proteins/genetics/*physiology ; HeLa Cells ; Humans ; Interferon-gamma/immunology ; Lysosomes/metabolism/microbiology/ultrastructure ; Macrophages/*immunology/*microbiology ; Mice ; Microbial Viability ; Microtubule-Associated Proteins/metabolism ; Mycobacterium bovis/*immunology/physiology ; Phagosomes/metabolism/microbiology/*ultrastructure ; RNA, Small Interfering ; Transfection ; Vacuoles/metabolism/ultrastructure
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 57
    Publikationsdatum: 2006-05-27
    Beschreibung: Yersinia species use a variety of type III effector proteins to target eukaryotic signaling systems. The effector YopJ inhibits mitogen-activated protein kinase (MAPK) and the nuclear factor kappaB (NFkappaB) signaling pathways used in innate immune response by preventing activation of the family of MAPK kinases (MAPKK). We show that YopJ acted as an acetyltransferase, using acetyl-coenzyme A (CoA) to modify the critical serine and threonine residues in the activation loop of MAPKK6 and thereby blocking phosphorylation. The acetylation on MAPKK6 directly competed with phosphorylation, preventing activation of the modified protein. This covalent modification may be used as a general regulatory mechanism in biological signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mukherjee, Sohini -- Keitany, Gladys -- Li, Yan -- Wang, Yong -- Ball, Haydn L -- Goldsmith, Elizabeth J -- Orth, Kim -- R01-AI056404/AI/NIAID NIH HHS/ -- R21-DK072134/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2006 May 26;312(5777):1211-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16728640" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acetyl Coenzyme A/metabolism ; Acetylation ; Acetyltransferases/metabolism ; Bacterial Proteins/*metabolism ; Catalytic Domain ; Cell Line ; Cell-Free System ; Electrophoresis, Polyacrylamide Gel ; Enzyme Activation ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Humans ; I-kappa B Kinase/*metabolism ; MAP Kinase Kinase 6/chemistry/*metabolism ; MAP Kinase Signaling System ; NF-kappa B/metabolism ; Phosphorylation ; Recombinant Proteins/metabolism ; Serine/metabolism ; Signal Transduction ; Threonine/metabolism ; Yersinia/*metabolism/pathogenicity
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 58
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-05-13
    Beschreibung: The interface between an infectious agent and its host represents the ultimate battleground for survival: The microbe must secure a niche for replication, whereas the host must limit the pathogen's advance. Among the host's arsenal of antimicrobial factors, the type 1 interferons (IFNs) induce potent defense mechanisms against viruses and are key in the host-virus standoff. Viruses have evolved multiple tricks to avoid the immediate antiviral effects of IFNs and, in turn, hosts have adapted use of this innate cytokine system to galvanize multiple additional layers of immune defense. The plasticity that exists in these interactions provides us with a lesson in detente.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garcia-Sastre, Adolfo -- Biron, Christine A -- P01AI52106/AI/NIAID NIH HHS/ -- P01AI58113/AI/NIAID NIH HHS/ -- R01AI46954/AI/NIAID NIH HHS/ -- R01AI55677/AI/NIAID NIH HHS/ -- R01CA41268/CA/NCI NIH HHS/ -- U19AI62623/AI/NIAID NIH HHS/ -- U54AI57158/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2006 May 12;312(5775):879-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Mount Sinai School of Medicine, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16690858" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cytokines/physiology ; *Immunity, Innate ; Interferon Regulatory Factors/physiology ; Interferon Type I/biosynthesis/genetics/*physiology ; Models, Biological ; RNA Helicases/metabolism ; Signal Transduction ; Toll-Like Receptors/physiology ; Viral Proteins/metabolism ; *Virus Physiological Phenomena ; Viruses/*immunology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 59
    Publikationsdatum: 2006-11-11
    Beschreibung: We report the sequence and analysis of the 814-megabase genome of the sea urchin Strongylocentrotus purpuratus, a model for developmental and systems biology. The sequencing strategy combined whole-genome shotgun and bacterial artificial chromosome (BAC) sequences. This use of BAC clones, aided by a pooling strategy, overcame difficulties associated with high heterozygosity of the genome. The genome encodes about 23,300 genes, including many previously thought to be vertebrate innovations or known only outside the deuterostomes. This echinoderm genome provides an evolutionary outgroup for the chordates and yields insights into the evolution of deuterostomes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3159423/" 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/PMC3159423/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sea Urchin Genome Sequencing Consortium -- Sodergren, Erica -- Weinstock, George M -- Davidson, Eric H -- Cameron, R Andrew -- Gibbs, Richard A -- Angerer, Robert C -- Angerer, Lynne M -- Arnone, Maria Ina -- Burgess, David R -- Burke, Robert D -- Coffman, James A -- Dean, Michael -- Elphick, Maurice R -- Ettensohn, Charles A -- Foltz, Kathy R -- Hamdoun, Amro -- Hynes, Richard O -- Klein, William H -- Marzluff, William -- McClay, David R -- Morris, Robert L -- Mushegian, Arcady -- Rast, Jonathan P -- Smith, L Courtney -- Thorndyke, Michael C -- Vacquier, Victor D -- Wessel, Gary M -- Wray, Greg -- Zhang, Lan -- Elsik, Christine G -- Ermolaeva, Olga -- Hlavina, Wratko -- Hofmann, Gretchen -- Kitts, Paul -- Landrum, Melissa J -- Mackey, Aaron J -- Maglott, Donna -- Panopoulou, Georgia -- Poustka, Albert J -- Pruitt, Kim -- Sapojnikov, Victor -- Song, Xingzhi -- Souvorov, Alexandre -- Solovyev, Victor -- Wei, Zheng -- Whittaker, Charles A -- Worley, Kim -- Durbin, K James -- Shen, Yufeng -- Fedrigo, Olivier -- Garfield, David -- Haygood, Ralph -- Primus, Alexander -- Satija, Rahul -- Severson, Tonya -- Gonzalez-Garay, Manuel L -- Jackson, Andrew R -- Milosavljevic, Aleksandar -- Tong, Mark -- Killian, Christopher E -- Livingston, Brian T -- Wilt, Fred H -- Adams, Nikki -- Belle, Robert -- Carbonneau, Seth -- Cheung, Rocky -- Cormier, Patrick -- Cosson, Bertrand -- Croce, Jenifer -- Fernandez-Guerra, Antonio -- Geneviere, Anne-Marie -- Goel, Manisha -- Kelkar, Hemant -- Morales, Julia -- Mulner-Lorillon, Odile -- Robertson, Anthony J -- Goldstone, Jared V -- Cole, Bryan -- Epel, David -- Gold, Bert -- Hahn, Mark E -- Howard-Ashby, Meredith -- Scally, Mark -- Stegeman, John J -- Allgood, Erin L -- Cool, Jonah -- Judkins, Kyle M -- McCafferty, Shawn S -- Musante, Ashlan M -- Obar, Robert A -- Rawson, Amanda P -- Rossetti, Blair J -- Gibbons, Ian R -- Hoffman, Matthew P -- Leone, Andrew -- Istrail, Sorin -- Materna, Stefan C -- Samanta, Manoj P -- Stolc, Viktor -- Tongprasit, Waraporn -- Tu, Qiang -- Bergeron, Karl-Frederik -- Brandhorst, Bruce P -- Whittle, James -- Berney, Kevin -- Bottjer, David J -- Calestani, Cristina -- Peterson, Kevin -- Chow, Elly -- Yuan, Qiu Autumn -- Elhaik, Eran -- Graur, Dan -- Reese, Justin T -- Bosdet, Ian -- Heesun, Shin -- Marra, Marco A -- Schein, Jacqueline -- Anderson, Michele K -- Brockton, Virginia -- Buckley, Katherine M -- Cohen, Avis H -- Fugmann, Sebastian D -- Hibino, Taku -- Loza-Coll, Mariano -- Majeske, Audrey J -- Messier, Cynthia -- Nair, Sham V -- Pancer, Zeev -- Terwilliger, David P -- Agca, Cavit -- Arboleda, Enrique -- Chen, Nansheng -- Churcher, Allison M -- Hallbook, F -- Humphrey, Glen W -- Idris, Mohammed M -- Kiyama, Takae -- Liang, Shuguang -- Mellott, Dan -- Mu, Xiuqian -- Murray, Greg -- Olinski, Robert P -- Raible, Florian -- Rowe, Matthew -- Taylor, John S -- Tessmar-Raible, Kristin -- Wang, D -- Wilson, Karen H -- Yaguchi, Shunsuke -- Gaasterland, Terry -- Galindo, Blanca E -- Gunaratne, Herath J -- Juliano, Celina -- Kinukawa, Masashi -- Moy, Gary W -- Neill, Anna T -- Nomura, Mamoru -- Raisch, Michael -- Reade, Anna -- Roux, Michelle M -- Song, Jia L -- Su, Yi-Hsien -- Townley, Ian K -- Voronina, Ekaterina -- Wong, Julian L -- Amore, Gabriele -- Branno, Margherita -- Brown, Euan R -- Cavalieri, Vincenzo -- Duboc, Veronique -- Duloquin, Louise -- Flytzanis, Constantin -- Gache, Christian -- Lapraz, Francois -- Lepage, Thierry -- Locascio, Annamaria -- Martinez, Pedro -- Matassi, Giorgio -- Matranga, Valeria -- Range, Ryan -- Rizzo, Francesca -- Rottinger, Eric -- Beane, Wendy -- Bradham, Cynthia -- Byrum, Christine -- Glenn, Tom -- Hussain, Sofia -- Manning, Gerard -- Miranda, Esther -- Thomason, Rebecca -- Walton, Katherine -- Wikramanayke, Athula -- Wu, Shu-Yu -- Xu, Ronghui -- Brown, C Titus -- Chen, Lili -- Gray, Rachel F -- Lee, Pei Yun -- Nam, Jongmin -- Oliveri, Paola -- Smith, Joel -- Muzny, Donna -- Bell, Stephanie -- Chacko, Joseph -- Cree, Andrew -- Curry, Stacey -- Davis, Clay -- Dinh, Huyen -- Dugan-Rocha, Shannon -- Fowler, Jerry -- Gill, Rachel -- Hamilton, Cerrissa -- Hernandez, Judith -- Hines, Sandra -- Hume, Jennifer -- Jackson, Laronda -- Jolivet, Angela -- Kovar, Christie -- Lee, Sandra -- Lewis, Lora -- Miner, George -- Morgan, Margaret -- Nazareth, Lynne V -- Okwuonu, Geoffrey -- Parker, David -- Pu, Ling-Ling -- Thorn, Rachel -- Wright, Rita -- 2P42 ESO7381/PHS HHS/ -- 5 U54 HG003273/HG/NHGRI NIH HHS/ -- EY11930/EY/NEI NIH HHS/ -- F32 ESO12794/PHS HHS/ -- F32 HD047136/HD/NICHD NIH HHS/ -- F32 HD047136-02/HD/NICHD NIH HHS/ -- F32 HD047136-03/HD/NICHD NIH HHS/ -- F32-HD47136/HD/NICHD NIH HHS/ -- GM058231/GM/NIGMS NIH HHS/ -- GM070840/GM/NIGMS NIH HHS/ -- GM61005/GM/NIGMS NIH HHS/ -- GM61464/GM/NIGMS NIH HHS/ -- HD-37105/HD/NICHD NIH HHS/ -- HD039948/HD/NICHD NIH HHS/ -- HD14483/HD/NICHD NIH HHS/ -- HD66219/HD/NICHD NIH HHS/ -- P30-CA14051/CA/NCI NIH HHS/ -- R01 ES006272/ES/NIEHS NIH HHS/ -- R01 ES006272-13/ES/NIEHS NIH HHS/ -- R01 GM070840/GM/NIGMS NIH HHS/ -- R01 HD028152/HD/NICHD NIH HHS/ -- R01ES006272/ES/NIEHS NIH HHS/ -- R37-HD12896/HD/NICHD NIH HHS/ -- RR-15044/RR/NCRR NIH HHS/ -- S19916/Biotechnology and Biological Sciences Research Council/United Kingdom -- T32 GM007601/GM/NIGMS NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2006 Nov 10;314(5801):941-52.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17095691" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Calcification, Physiologic ; Cell Adhesion Molecules/genetics/physiology ; Complement Activation/genetics ; Computational Biology ; Embryonic Development/genetics ; Evolution, Molecular ; Gene Expression Regulation, Developmental ; Genes ; *Genome ; Immunity, Innate/genetics ; Immunologic Factors/genetics/physiology ; Male ; Nervous System Physiological Phenomena ; Proteins/genetics/physiology ; *Sequence Analysis, DNA ; Signal Transduction ; Strongylocentrotus purpuratus/embryology/*genetics/immunology/physiology ; Transcription Factors/genetics
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 60
    Publikationsdatum: 2006-05-27
    Beschreibung: Genetic mutations that disrupt osteoblast function can result in skeletal dysmorphogenesis or, more rarely, in increased postnatal bone formation. Here we show that Schnurri-3 (Shn3), a mammalian homolog of the Drosophila zinc finger adapter protein Shn, is an essential regulator of adult bone formation. Mice lacking Shn3 display adult-onset osteosclerosis with increased bone mass due to augmented osteoblast activity. Shn3 was found to control protein levels of Runx2, the principal transcriptional regulator of osteoblast differentiation, by promoting its degradation through recruitment of the E3 ubiquitin ligase WWP1 to Runx2. By this means, Runx2-mediated extracellular matrix mineralization was antagonized, revealing an essential role for Shn3 as a central regulator of postnatal bone mass.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, Dallas C -- Wein, Marc N -- Oukka, Mohamed -- Hofstaetter, Jochen G -- Glimcher, Melvin J -- Glimcher, Laurie H -- AI29673/AI/NIAID NIH HHS/ -- AR46983/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2006 May 26;312(5777):1223-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16728642" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Binding Sites ; *Bone Density ; Bone and Bones/*anatomy & histology/chemistry/physiology ; Cell Line ; Cells, Cultured ; Core Binding Factor Alpha 1 Subunit/genetics/metabolism ; DNA-Binding Proteins/analysis/genetics/*metabolism ; Gene Expression Regulation ; Immunoprecipitation ; Mice ; Osteoblasts/chemistry/physiology ; Osteoclasts/physiology ; Osteogenesis ; Protein Binding ; Protein Structure, Tertiary ; RNA Interference ; RNA, Messenger/genetics/metabolism ; Transcriptional Activation ; Transfection ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/chemistry/metabolism ; Zinc Fingers
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 61
    Publikationsdatum: 2006-06-24
    Beschreibung: During fasting, increased concentrations of circulating catecholamines promote the mobilization of lipid stores from adipose tissue in part by phosphorylating and inactivating acetyl-coenzyme A carboxylase (ACC), the rate-limiting enzyme in fatty acid synthesis. Here, we describe a parallel pathway, in which the pseudokinase Tribbles 3 (TRB3), whose abundance is increased during fasting, stimulates lipolysis by triggering the degradation of ACC in adipose tissue. TRB3 promoted ACC ubiquitination through an association with the E3 ubiquitin ligase constitutive photomorphogenic protein 1 (COP1). Indeed, adipocytes deficient in TRB3 accumulated larger amounts of ACC protein than did wild-type cells. Because transgenic mice expressing TRB3 in adipose tissue are protected from diet-induced obesity due to enhanced fatty acid oxidation, these results demonstrate how phosphorylation and ubiquitination pathways converge on a key regulator of lipid metabolism to maintain energy homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Qi, Ling -- Heredia, Jose E -- Altarejos, Judith Y -- Screaton, Robert -- Goebel, Naomi -- Niessen, Sherry -- Macleod, Ian X -- Liew, Chong Wee -- Kulkarni, Rohit N -- Bain, James -- Newgard, Christopher -- Nelson, Michael -- Evans, Ronald M -- Yates, John -- Montminy, Marc -- DK064142/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2006 Jun 23;312(5781):1763-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Peptide Biology Laboratories and Gene Expression Laboratories, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16794074" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 3T3-L1 Cells ; Acetyl-CoA Carboxylase/antagonists & inhibitors/*metabolism ; Adipocytes/metabolism ; Adipose Tissue/cytology/*metabolism ; Adipose Tissue, Brown/cytology/metabolism ; Animals ; Cell Cycle Proteins/*metabolism ; Cell Line ; Dietary Fats/administration & dosage ; Energy Metabolism ; Fasting ; Fatty Acids/metabolism ; Gene Expression ; Humans ; *Lipid Metabolism ; Lipolysis ; Mice ; Mice, Transgenic ; Nuclear Proteins/*metabolism ; Obesity/prevention & control ; Oxidation-Reduction ; Phosphorylation ; Thinness ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/*metabolism ; Weight Gain
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 62
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-03-04
    Beschreibung: The restoration of catalytic activity to mutant enzymes by small molecules is well established for in vitro systems. Here, we show that the protein tyrosine kinase Src arginine-388--〉alanine (R388A) mutant can be rescued in live cells with the use of the small molecule imidazole. Cellular rescue of a viral Src homolog was rapid and reversible and conferred predicted oncogenic properties. Using chemical rescue in combination with mass spectrometry, we confirmed six known Src kinase substrates and identified several new protein targets. Chemical rescue data suggest that cellular Src is active under basal conditions. Rescue of R388A cellular Src provided insights into the mitogen-activated protein kinase pathway. This chemical rescue approach will likely have many applications in cell signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Qiao, Yingfeng -- Molina, Henrik -- Pandey, Akhilesh -- Zhang, Jin -- Cole, Philip A -- New York, N.Y. -- Science. 2006 Mar 3;311(5765):1293-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16513984" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Cell Line ; Cell Transformation, Neoplastic ; Fluorescence Resonance Energy Transfer ; Gene Expression Profiling ; Gene Expression Regulation ; Growth Substances/metabolism/pharmacology ; Humans ; Imidazoles/*metabolism/pharmacology ; Kinetics ; Mice ; Mitogen-Activated Protein Kinases/metabolism ; Mutation ; Nuclear Proteins/metabolism ; Oligonucleotide Array Sequence Analysis ; Phenotype ; Phosphorylation ; Phosphotyrosine/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins pp60(c-src)/*genetics/*metabolism ; Recombinant Proteins/metabolism ; Transfection ; src Homology Domains
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 63
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-04-15
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, Ingrid -- New York, N.Y. -- Science. 2006 Apr 14;312(5771):184-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16614188" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adjuvants, Immunologic ; Animals ; Autoimmune Diseases/drug therapy/*immunology ; Coronary Artery Disease/drug therapy/immunology ; Humans ; Hypersensitivity/drug therapy/*immunology ; *Immunity, Innate ; Infection/drug therapy/*immunology ; Inflammation/drug therapy/*immunology ; Mice ; Mutation ; Sepsis/drug therapy/immunology ; Signal Transduction ; Toll-Like Receptors/antagonists & inhibitors/genetics/*immunology/physiology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 64
    Publikationsdatum: 2006-10-14
    Beschreibung: Double-stranded RNA (dsRNA) produced during viral replication is believed to be the critical trigger for activation of antiviral immunity mediated by the RNA helicase enzymes retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5). We showed that influenza A virus infection does not generate dsRNA and that RIG-I is activated by viral genomic single-stranded RNA (ssRNA) bearing 5'-phosphates. This is blocked by the influenza protein nonstructured protein 1 (NS1), which is found in a complex with RIG-I in infected cells. These results identify RIG-I as a ssRNA sensor and potential target of viral immune evasion and suggest that its ability to sense 5'-phosphorylated RNA evolved in the innate immune system as a means of discriminating between self and nonself.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pichlmair, Andreas -- Schulz, Oliver -- Tan, Choon Ping -- Naslund, Tanja I -- Liljestrom, Peter -- Weber, Friedemann -- Reis e Sousa, Caetano -- New York, N.Y. -- Science. 2006 Nov 10;314(5801):997-1001. Epub 2006 Oct 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunobiology Laboratory, Cancer Research UK, London Research Institute, London WC2A 3PX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17038589" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; Cells, Cultured ; Cytoplasm/metabolism/virology ; DEAD-box RNA Helicases/genetics/*metabolism ; Dendritic Cells/virology ; Encephalomyocarditis virus/genetics/immunology/metabolism ; Genome, Viral ; Humans ; *Immunity, Innate ; Influenza A virus/*genetics/*immunology/metabolism/physiology ; Interferon-alpha/biosynthesis ; Interferon-beta/biosynthesis ; Mice ; Mice, Inbred C57BL ; Phosphates/metabolism ; Phosphorylation ; RNA Caps/metabolism ; RNA, Double-Stranded/metabolism ; RNA, Viral/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Transfection ; Vesicular stomatitis Indiana virus/genetics/immunology/metabolism ; Viral Nonstructural Proteins/genetics/metabolism ; Virus Replication
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 65
    Publikationsdatum: 2006-01-18
    Beschreibung: In contrast to current models, fluorescence resonance energy transfer measurements using a single-cell imaging assay with fluorescent forms of PER and TIM showed that these proteins bind rapidly and persist in the cytoplasm while gradually accumulating in discrete foci. After approximately 6 hours, complexes abruptly dissociated, as PER and TIM independently moved to the nucleus in a narrow time frame. The per(L) mutation delayed nuclear accumulation in vivo and in our cultured cell system, but without affecting rates of PER/TIM assembly or dissociation. This finding points to a previously unrecognized form of temporal regulation that underlies the periodicity of the circadian clock.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyer, Pablo -- Saez, Lino -- Young, Michael W -- GM54339/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Jan 13;311(5758):226-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, 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/16410523" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Active Transport, Cell Nucleus ; Animals ; Cell Line ; Cell Nucleus/metabolism ; Circadian Rhythm/*physiology ; Cytoplasm/metabolism ; Drosophila Proteins/*metabolism ; Drosophila melanogaster ; Fluorescence Resonance Energy Transfer ; Models, Biological ; Nuclear Proteins/*metabolism ; Period Circadian Proteins ; Protein Binding ; Recombinant Fusion Proteins/metabolism ; Time Factors
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 66
    Publikationsdatum: 2006-04-01
    Beschreibung: Kaposi's sarcoma-associated herpesvirus (KSHV, human herpesvirus 8) is the causative agent of Kaposi's sarcoma and other lymphoproliferative syndromes often associated with HIV/AIDS. Functional complementary DNA selection for a receptor mediating KSHV cell fusion identified xCT, the 12-transmembrane light chain of the human cystine/glutamate exchange transporter system x-c. Expression of recombinant xCT rendered otherwise not susceptible target cells permissive for both KSHV cell fusion and virion entry. Antibodies against xCT blocked KSHV fusion and entry with naturally permissive target cells. KSHV target cell permissiveness correlated closely with endogenous expression of xCT messenger RNA and protein in diverse human and nonhuman cell types.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaleeba, Johnan A R -- Berger, Edward A -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2006 Mar 31;311(5769):1921-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16574866" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Transport System y+/genetics/immunology/*metabolism ; Animals ; Cell Fusion ; Cell Line ; Cell Line, Tumor ; DNA, Complementary ; Herpesvirus 8, Human/*metabolism ; Humans ; Immune Sera ; Mice ; RNA, Messenger/analysis/genetics ; Receptors, Virus/genetics/immunology/*metabolism ; Recombinant Proteins/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Transfection
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 67
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-09-23
    Beschreibung: Sleep is a vital, evolutionarily conserved phenomenon, whose function is unclear. Although mounting evidence supports a role for sleep in the consolidation of memories, until now, a molecular connection between sleep, plasticity, and memory formation has been difficult to demonstrate. We establish Drosophila as a model to investigate this relation and demonstrate that the intensity and/or complexity of prior social experience stably modifies sleep need and architecture. Furthermore, this experience-dependent plasticity in sleep need is subserved by the dopaminergic and adenosine 3',5'-monophosphate signaling pathways and a particular subset of 17 long-term memory genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ganguly-Fitzgerald, Indrani -- Donlea, Jeff -- Shaw, Paul J -- R01-NS051305-01A1/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Sep 22;313(5794):1775-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurosciences Institute, 10640 John Jay Hopkins Drive, San Diego, CA 92101, USA. transposase@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16990546" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Brain Chemistry ; Circadian Rhythm ; Cyclic AMP/metabolism ; Dopamine/analysis/metabolism ; Drosophila melanogaster/genetics/growth & development/*physiology ; Female ; Hearing ; Learning ; Male ; Memory ; *Models, Animal ; Mutation ; Sexual Behavior, Animal ; Signal Transduction ; *Sleep ; Smell ; Social Environment ; Social Isolation ; Vision, Ocular
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 68
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-06-03
    Beschreibung: Selector genes modify developmental pathways to sculpt animal body parts. Although body parts differ in size, the ways in which selector genes create size differences are unknown. We have studied how the Drosophila Hox gene Ultrabithorax (Ubx) limits the size of the haltere, which, by the end of larval development, has approximately fivefold fewer cells than the wing. We find that Ubx controls haltere size by restricting both the transcription and the mobility of the morphogen Decapentaplegic (Dpp). Ubx restricts Dpp's distribution in the haltere by increasing the amounts of the Dpp receptor, thickveins. Because morphogens control tissue growth in many contexts, these findings provide a potentially general mechanism for how selector genes modify organ sizes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2628481/" 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/PMC2628481/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Crickmore, Michael A -- Mann, Richard S -- R01 GM054510/GM/NIGMS NIH HHS/ -- R01 GM054510-12/GM/NIGMS NIH HHS/ -- R01 GM054510-13/GM/NIGMS NIH HHS/ -- R01 GM054510-14/GM/NIGMS NIH HHS/ -- R01 GM058575/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Jul 7;313(5783):63-8. Epub 2006 Jun 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Columbia University, New York, NY 10027, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16741075" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Proliferation ; Drosophila Proteins/*genetics/*metabolism/*physiology ; Drosophila melanogaster/anatomy & histology/*genetics/*growth & ; development/metabolism ; Gene Expression Regulation, Developmental ; Genes, Insect ; Homeodomain Proteins/*genetics/*physiology ; Morphogenesis ; Organ Size ; Protein-Serine-Threonine Kinases/genetics/metabolism ; Receptors, Cell Surface/genetics/metabolism ; Signal Transduction ; Transcription Factors/*genetics/*physiology ; Transcription, Genetic ; Up-Regulation ; Wings, Animal/cytology/*growth & development
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 69
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-07-11
    Beschreibung: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2973999/" 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/PMC2973999/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stern, David L -- R01 GM063622/GM/NIGMS NIH HHS/ -- R01 GM063622-01/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Jul 7;313(5783):50-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, Princeton University, Princeton, NJ 08544, USA. dstern@princeton.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16825555" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Biological Evolution ; Body Size ; Cell Proliferation ; Drosophila Proteins/*genetics/*metabolism/physiology ; Drosophila melanogaster/anatomy & histology/*genetics/*growth & ; development/metabolism ; Gene Expression Regulation, Developmental ; Genes, Insect ; Homeodomain Proteins/*genetics/physiology ; Morphogenesis ; Organ Size ; Protein-Serine-Threonine Kinases/metabolism ; Receptors, Cell Surface/metabolism ; Signal Transduction ; Transcription Factors/*genetics/physiology ; Wings, Animal/cytology/*growth & development
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 70
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-04-01
    Beschreibung: A constellation of intrinsic and extrinsic cellular mechanisms regulates the balance of self-renewal and differentiation in all stem cells. Stem cells, their progeny, and elements of their microenvironment make up an anatomical structure that coordinates normal homeostatic production of functional mature cells. Here we discuss the stem cell niche concept, highlight recent progress, and identify important unanswered questions. We focus on three mammalian stem cell systems where large numbers of mature cells must be continuously produced throughout adult life: intestinal epithelium, epidermal structures, and bone marrow.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moore, Kateri A -- Lemischka, Ihor R -- New York, N.Y. -- Science. 2006 Mar 31;311(5769):1880-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Princeton University, Lewis Thomas Laboratory, Princeton, NJ 08544, USA. kamoore@princeton.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16574858" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Bone Marrow Cells/cytology/physiology ; Cell Differentiation ; Cell Division ; Cell Lineage ; Dermis/cytology/physiology ; Epidermis/cytology/physiology ; Hair Follicle/*cytology ; Hematopoietic Stem Cells/*cytology/*physiology ; Homeostasis ; Intestinal Mucosa/*cytology ; Mesoderm/cytology/physiology ; Multipotent Stem Cells/cytology/physiology ; Osteoblasts/physiology ; Signal Transduction ; Stem Cell Transplantation ; Stem Cells/*cytology/*physiology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 71
    Publikationsdatum: 2006-10-21
    Beschreibung: Diverse bacterial and viral pathogens induce actin polymerization in the cytoplasm of host cells to facilitate infection. Here, we describe a pathogenic mechanism for promoting dynamic actin assembly in the nucleus to enable viral replication. The baculovirus Autographa californica multiple nucleopolyhedrovirus induced nuclear actin polymerization by translocating the host actin-nucleating Arp2/3 complex into the nucleus, where it was activated by p78/83, a viral Wiskott-Aldrich syndrome protein (WASP)-like protein. Nuclear actin assembly by p78/83 and Arp2/3 complex was essential for viral progeny production. Recompartmentalizing dynamic host actin may represent a conserved mode of pathogenesis and reflect viral manipulation of normal functions of nuclear actin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goley, Erin D -- Ohkawa, Taro -- Mancuso, Joel -- Woodruff, Jeffrey B -- D'Alessio, Joseph A -- Cande, W Zacheus -- Volkman, Loy E -- Welch, Matthew D -- AI054693/AI/NIAID NIH HHS/ -- GM59609/GM/NIGMS NIH HHS/ -- R01 GM059609/GM/NIGMS NIH HHS/ -- R01 GM059609-07/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 20;314(5798):464-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17053146" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Actin-Related Protein 2-3 Complex/*metabolism ; Actins/*metabolism ; Animals ; Biopolymers/metabolism ; Cell Line ; Cell Nucleus/*metabolism ; Fluorescence Recovery After Photobleaching ; Moths ; Mutation ; Nucleocapsid/metabolism/ultrastructure ; Nucleopolyhedrovirus/genetics/*physiology ; Transfection ; Viral Proteins/chemistry/genetics/isolation & purification/*metabolism ; Virion/ultrastructure ; Virus Replication ; Wiskott-Aldrich Syndrome Protein/chemistry
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 72
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-06-17
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goodnow, Christopher C -- New York, N.Y. -- Science. 2006 Jun 16;312(5780):1606-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉John Curtin School of Medical Research and Australian Phenomics Facility, Australian National University, Post Office Box 334, Canberra, ACT 0200, Australia. chris.goodnow@anu.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16778043" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antigens, Ly/genetics/physiology ; Autoantibodies/biosynthesis ; *Autoimmunity ; B-Lymphocytes/immunology ; Dendritic Cells/immunology ; Gene Dosage ; Gene Duplication ; Humans ; Interferon-alpha/biosynthesis ; Lupus Erythematosus, Systemic/genetics/*immunology ; Lymphocyte Activation ; Membrane Glycoproteins/genetics/*immunology ; Mice ; Multifactorial Inheritance ; RNA Splicing ; Receptors, Antigen, B-Cell/immunology ; Receptors, IgG/genetics/immunology ; Self Tolerance ; Signal Transduction ; Toll-Like Receptor 7/genetics/*immunology ; Toll-Like Receptor 9/*immunology ; Y Chromosome/genetics
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 73
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-05-30
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Worby, Carolyn A -- Dixon, Jack E -- New York, N.Y. -- Science. 2006 May 26;312(5777):1150-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California at San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16731519" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acetylation ; Acetyltransferases/metabolism ; Bacterial Proteins/*metabolism ; Enzyme Activation ; Humans ; I-kappa B Kinase/*metabolism ; MAP Kinase Kinase 1/metabolism ; MAP Kinase Kinase 6/*metabolism ; MAP Kinase Kinase Kinases/metabolism ; MAP Kinase Signaling System ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Models, Biological ; NF-kappa B/metabolism ; Phosphorylation ; SUMO-1 Protein/metabolism ; Serine/metabolism ; Signal Transduction ; Threonine/metabolism ; Yersinia/*metabolism/pathogenicity ; Yersinia pestis/metabolism/pathogenicity ; p38 Mitogen-Activated Protein Kinases/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 74
    Publikationsdatum: 2006-01-21
    Beschreibung: The stable propagation of genetic material during cell division depends on the congression of chromosomes to the spindle equator before the cell initiates anaphase. It is generally assumed that congression requires that chromosomes are connected to the opposite poles of the bipolar spindle ("bioriented"). In mammalian cells, we found that chromosomes can congress before becoming bioriented. By combining the use of reversible chemical inhibitors, live-cell light microscopy, and correlative electron microscopy, we found that monooriented chromosomes could glide toward the spindle equator alongside kinetochore fibers attached to other already bioriented chromosomes. This congression mechanism depended on the kinetochore-associated, plus end-directed microtubule motor CENP-E (kinesin-7).〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4768465/" 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/PMC4768465/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kapoor, Tarun M -- Lampson, Michael A -- Hergert, Polla -- Cameron, Lisa -- Cimini, Daniela -- Salmon, E D -- McEwen, Bruce F -- Khodjakov, Alexey -- GM06627/GM/NIGMS NIH HHS/ -- GM24364/GM/NIGMS NIH HHS/ -- GM59363/GM/NIGMS NIH HHS/ -- GM65933/GM/NIGMS NIH HHS/ -- R01 GM024364/GM/NIGMS NIH HHS/ -- R01 GM059363/GM/NIGMS NIH HHS/ -- R37 GM024364/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Jan 20;311(5759):388-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chemistry and Cell Biology, Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16424343" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Aurora Kinases ; Cell Line ; Chromosomal Proteins, Non-Histone/physiology ; Chromosomes, Mammalian/*physiology/ultrastructure ; HeLa Cells ; Humans ; Indoles/pharmacology ; Kinesin/antagonists & inhibitors ; Kinetochores/*physiology/ultrastructure ; Metaphase ; Microscopy, Confocal ; Microscopy, Electron ; Microscopy, Interference ; Microscopy, Video ; Microtubules/*physiology/ultrastructure ; *Mitosis ; Molecular Motor Proteins/physiology ; Movement ; Potoroidae ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; Pyrimidines/pharmacology ; RNA Interference ; RNA, Small Interfering ; Spindle Apparatus/*physiology/ultrastructure ; Sulfonamides/pharmacology ; Thiones/pharmacology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 75
    Publikationsdatum: 2006-05-20
    Beschreibung: Failure of cells to respond to DNA damage is a primary event associated with mutagenesis and environmental toxicity. To map the transcriptional network controlling the damage response, we measured genomewide binding locations for 30 damage-related transcription factors (TFs) after exposure of yeast to methyl-methanesulfonate (MMS). The resulting 5272 TF-target interactions revealed extensive changes in the pattern of promoter binding and identified damage-specific binding motifs. As systematic functional validation, we identified interactions for which the target changed expression in wild-type cells in response to MMS but was nonresponsive in cells lacking the TF. Validated interactions were assembled into causal pathway models that provide global hypotheses of how signaling, transcription, and phenotype are integrated after damage.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2811083/" 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/PMC2811083/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Workman, Christopher T -- Mak, H Craig -- McCuine, Scott -- Tagne, Jean-Bosco -- Agarwal, Maya -- Ozier, Owen -- Begley, Thomas J -- Samson, Leona D -- Ideker, Trey -- R01 ES014811/ES/NIEHS NIH HHS/ -- R01 ES014811-01A1/ES/NIEHS NIH HHS/ -- R01 GM070743/GM/NIGMS NIH HHS/ -- R01 GM070743-01/GM/NIGMS NIH HHS/ -- R01 GM070743-02/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 May 19;312(5776):1054-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of California San Diego, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16709784" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *DNA Damage ; DNA Repair/genetics/physiology ; DNA, Fungal ; Fungal Proteins/metabolism ; Gene Expression Regulation, Fungal ; Methyl Methanesulfonate ; Promoter Regions, Genetic ; Protein Binding ; Saccharomyces ; Signal Transduction ; Systems Theory ; Transcription Factors/*metabolism ; Transcription, Genetic
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 76
    Publikationsdatum: 2006-10-14
    Beschreibung: The treelike structures of many organs, including the mammary gland, are generated by branching morphogenesis, a reiterative process of branch initiation and invasion from a preexisting epithelium. Using a micropatterning approach to control the initial three-dimensional structure of mouse mammary epithelial tubules in culture, combined with an algorithm to quantify the extent of branching, we found that the geometry of tubules dictates the position of branches. We predicted numerically and confirm experimentally that branches initiate at sites with a local minimum in the concentration of autocrine inhibitory morphogens, such as transforming growth factor-beta. These results reveal that tissue geometry can control organ morphogenesis by defining the local cellular microenvironment, a finding that has relevance to control of invasion and metastasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2933179/" 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/PMC2933179/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, Celeste M -- Vanduijn, Martijn M -- Inman, Jamie L -- Fletcher, Daniel A -- Bissell, Mina J -- CA57621/CA/NCI NIH HHS/ -- CA64786/CA/NCI NIH HHS/ -- GM72736/GM/NIGMS NIH HHS/ -- R01 CA057621/CA/NCI NIH HHS/ -- R01 CA057621-10/CA/NCI NIH HHS/ -- R01 CA064786/CA/NCI NIH HHS/ -- R01 CA064786-10/CA/NCI NIH HHS/ -- R01 GM072736/GM/NIGMS NIH HHS/ -- R01 GM072736-05/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 13;314(5797):298-300.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17038622" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Algorithms ; Animals ; Cell Line ; Diffusion ; Epidermal Growth Factor/pharmacology ; Epithelial Cells/*cytology/metabolism ; Epithelium/growth & development ; Female ; Hepatocyte Growth Factor/pharmacology ; Mammary Glands, Animal/cytology/*growth & development ; Mice ; *Morphogenesis ; Organ Culture Techniques ; Organoids/cytology/*growth & development ; Protein-Serine-Threonine Kinases/antagonists & inhibitors ; Receptors, Transforming Growth Factor beta/metabolism ; Tissue Engineering ; Transforming Growth Factor beta/metabolism ; Transforming Growth Factor beta1
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 77
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-04-22
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉International Stem Cell Forum Ethics Working Party -- New York, N.Y. -- Science. 2006 Apr 21;312(5772):366-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16627723" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Bioethical Issues ; Cell Line ; Cloning, Organism/ethics/legislation & jurisprudence ; Embryo Research/*ethics/legislation & jurisprudence ; Guidelines as Topic ; Humans ; *Internationality ; Research Embryo Creation/ethics/legislation & jurisprudence ; *Stem Cells
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 78
    Publikationsdatum: 2006-04-08
    Beschreibung: We observe that protein kinase C (PKC) is phosphorylated on the activation loop at threonine 538 (Thr-538) before T cell activation. Our results are inconsistent with the conclusions of Lee et al. (Reports, 1 April 2005, p. 114) that the Thr-538 phosphorylation of PKC is regulated by T cell receptor activation. Other mechanisms, such as autophosphorylation of Thr-219, might orchestrate the cellular function of PKC in T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gruber, Thomas -- Freeley, Michael -- Thuille, Nikolaus -- Heit, Isabelle -- Shaw, Stephen -- Long, Aideen -- Baier, Gottfried -- New York, N.Y. -- Science. 2006 Apr 7;312(5770):55; author reply 55.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department for Medical Genetics, Molecular and Clinical Pharmacology, Innsbruck Medical University, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16601177" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 3-Phosphoinositide-Dependent Protein Kinases ; Animals ; Antibodies/immunology ; Antigens, CD28/immunology ; Antigens, CD3/immunology ; Cells, Cultured ; Humans ; Isoenzymes/*metabolism ; Jurkat Cells ; Lymphocyte Activation ; Mice ; NF-kappa B/*metabolism ; Phosphorylation ; Protein Kinase C/*metabolism ; Protein-Serine-Threonine Kinases/*metabolism ; Receptors, Antigen, T-Cell/metabolism ; Signal Transduction ; T-Lymphocytes/enzymology/immunology/*metabolism ; Threonine/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 79
    Publikationsdatum: 2006-06-03
    Beschreibung: The mechanisms underlying induction and suppression of RNA silencing in the ongoing plant-virus arms race are poorly understood. We show here that virus-derived small RNAs produced by Arabidopsis Dicer-like 4 (DCL4) program an effector complex conferring antiviral immunity. Inhibition of DCL4 by a viral-encoded suppressor revealed the subordinate antiviral activity of DCL2. Accordingly, inactivating both DCL2 and DCL4 was necessary and sufficient to restore systemic infection of a suppressor-deficient virus. The effects of DCL2 were overcome by increasing viral dosage in inoculated leaves, but this could not surmount additional, non-cell autonomous effects of DCL4 specifically preventing viral unloading from the vasculature. These findings define a molecular framework for studying antiviral silencing and defense in plants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deleris, Angelique -- Gallego-Bartolome, Javier -- Bao, Jinsong -- Kasschau, Kristin D -- Carrington, James C -- Voinnet, Olivier -- AI43288/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2006 Jul 7;313(5783):68-71. Epub 2006 Jun 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Biologie Moleculaire des Plantes, CNRS Unite Propre de Recherche (UPR) 2357, 12, rue du General Zimmer, 67084 Strasbourg Cedex, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16741077" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Arabidopsis/enzymology/genetics/metabolism/*virology ; Arabidopsis Proteins/antagonists & inhibitors/genetics/*metabolism ; Carmovirus/physiology ; Cell Cycle Proteins/antagonists & inhibitors/genetics/*metabolism ; Green Fluorescent Proteins/metabolism ; Mutation ; Plant Diseases/virology ; Plant Leaves/virology ; Plant Viruses/*physiology ; Plants, Genetically Modified ; *RNA Interference ; RNA Viruses/physiology ; RNA, Double-Stranded/metabolism ; RNA, Small Interfering/*metabolism ; RNA, Viral/*metabolism ; RNA-Induced Silencing Complex/metabolism ; Recombinant Fusion Proteins/metabolism ; Ribonuclease III/antagonists & inhibitors/genetics/*metabolism ; Ribonucleases/antagonists & inhibitors/genetics/*metabolism ; Signal Transduction ; Viral Proteins/*metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 80
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-07-11
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ron, David -- New York, N.Y. -- Science. 2006 Jul 7;313(5783):52-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skirball Institute, New York University Medical Center, 540 First Avenue, New York, NY 10016, USA. ron@saturn.med.nyu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16825557" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; Cytosol/metabolism ; DNA-Binding Proteins/metabolism ; Drosophila Proteins/chemistry/genetics/*metabolism ; Drosophila melanogaster/genetics/metabolism ; Endoplasmic Reticulum/*metabolism ; Endoribonucleases/chemistry/genetics/*metabolism ; Evolution, Molecular ; Gene Expression Regulation ; Membrane Proteins/chemistry/genetics/*metabolism ; Models, Biological ; Protein Biosynthesis ; *Protein Folding ; Protein Sorting Signals/physiology ; Protein Structure, Tertiary ; *RNA Stability ; RNA, Messenger/genetics/*metabolism ; Signal Transduction ; Transcription Factors/metabolism ; Transcription, Genetic
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 81
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-01-21
    Beschreibung: Mammalian X inactivation turns off one female X chromosome to enact dosage compensation between XX and XY individuals. X inactivation is known to be regulated in cis by Xite, Tsix, and Xist, but in principle the two Xs must also be regulated in trans to ensure mutually exclusive silencing. Here, we demonstrate that interchromosomal pairing mediates this communication. Pairing occurs transiently at the onset of X inactivation and is specific to the X-inactivation center. Deleting Xite and Tsix perturbs pairing and counting/choice, whereas their autosomal insertion induces de novo X-autosome pairing. Ectopic X-autosome interactions inhibit endogenous X-X pairing and block the initiation of X-chromosome inactivation. Thus, Tsix and Xite function both in cis and in trans. We propose that Tsix and Xite regulate counting and mutually exclusive choice through X-X pairing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, Na -- Tsai, Chia-Lun -- Lee, Jeannie T -- New York, N.Y. -- Science. 2006 Feb 24;311(5764):1149-52. Epub 2006 Jan 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular Biology, Massachusetts General Hospital, Department of Genetics, Harvard Medical School Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16424298" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Differentiation ; Cell Line ; *Chromosome Pairing ; Female ; In Situ Hybridization, Fluorescence ; Male ; Mice ; Mice, Transgenic ; Models, Genetic ; Mutation ; RNA, Long Noncoding ; RNA, Untranslated/genetics/metabolism ; Regulatory Elements, Transcriptional ; Stem Cells ; Transgenes ; X Chromosome/genetics/*physiology ; *X Chromosome Inactivation
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 82
    Publikationsdatum: 2006-10-07
    Beschreibung: TFII-I is a transcription factor and a target of phosphorylation by Bruton's tyrosine kinase. In humans, deletions spanning the TFII-I locus are associated with a cognitive defect, the Williams-Beuren cognitive profile. We report an unanticipated role of TFII-I outside the nucleus as a negative regulator of agonist-induced calcium entry (ACE) that suppresses surface accumulation of TRPC3 (transient receptor potential C3) channels. Inhibition of ACE by TFII-I requires phosphotyrosine residues that engage the SH2 (Src-homology 2) domains of phospholipase C-g (PLC-g) and an interrupted, pleckstrin homology (PH)-like domain that binds the split PH domain of PLC-g. Our observations suggest a model in which TFII-I suppresses ACE by competing with TRPC3 for binding to PLC-g.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caraveo, Gabriela -- van Rossum, Damian B -- Patterson, Randen L -- Snyder, Solomon H -- Desiderio, Stephen -- New York, N.Y. -- Science. 2006 Oct 6;314(5796):122-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17023658" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Bradykinin/pharmacology ; Calcium/*metabolism ; Calcium Channels/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Cytoplasm/metabolism ; Humans ; Models, Biological ; Molecular Sequence Data ; PC12 Cells ; Phospholipase C gamma/chemistry/*metabolism ; Phosphorylation ; Protein Binding ; Protein Structure, Tertiary ; Rats ; TRPC Cation Channels/*metabolism ; Transcription Factors, TFII/chemistry/*metabolism ; Uridine Triphosphate/pharmacology ; src Homology Domains
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    Standort Signatur Erwartet Verfügbarkeit
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  • 83
    Publikationsdatum: 2006-03-18
    Beschreibung: The parietal-eye photoreceptor is unique because it has two antagonistic light signaling pathways in the same cell-a hyperpolarizing pathway maximally sensitive to blue light and a depolarizing pathway maximally sensitive to green light. Here, we report the molecular components of these two pathways. We found two opsins in the same cell: the blue-sensitive pinopsin and a previously unidentified green-sensitive opsin, which we name parietopsin. Signaling components included gustducin-alpha and Galphao, but not rod or cone transducin-alpha. Single-cell recordings demonstrated that Go mediates the depolarizing response. Gustducin-alpha resembles transducin-alpha functionally and likely mediates the hyperpolarizing response. The parietopsin-Go signaling pair provides clues about how rod and cone phototransduction might have evolved.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Su, Chih-Ying -- Luo, Dong-Gen -- Terakita, Akihisa -- Shichida, Yoshinori -- Liao, Hsi-Wen -- Kazmi, Manija A -- Sakmar, Thomas P -- Yau, King-Wai -- EY06837/EY/NEI NIH HHS/ -- R01 DC006904/DC/NIDCD NIH HHS/ -- R01 DC006904-01/DC/NIDCD NIH HHS/ -- R01 DC006904-02/DC/NIDCD NIH HHS/ -- R01 EY006837/EY/NEI NIH HHS/ -- R01 EY006837-16A1/EY/NEI NIH HHS/ -- R01 EY006837-17/EY/NEI NIH HHS/ -- R01 EY006837-18/EY/NEI NIH HHS/ -- R01 EY006837-19/EY/NEI NIH HHS/ -- R01 EY014596/EY/NEI NIH HHS/ -- R01 EY014596-01/EY/NEI NIH HHS/ -- R01 EY014596-02/EY/NEI NIH HHS/ -- R01 EY014596-03/EY/NEI NIH HHS/ -- R01 EY014596-04/EY/NEI NIH HHS/ -- R37 EY006837/EY/NEI NIH HHS/ -- R37 EY006837-15S1/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2006 Mar 17;311(5767):1617-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. chih-ying.su@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16543463" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 3',5'-Cyclic-GMP Phosphodiesterases/metabolism ; Amino Acid Sequence ; Animals ; *Biological Evolution ; Cell Line ; Cyclic GMP/metabolism ; GTP-Binding Protein alpha Subunits/genetics/physiology ; Humans ; Lizards/genetics/*physiology ; Molecular Sequence Data ; *Ocular Physiological Phenomena ; Patch-Clamp Techniques ; Photoreceptor Cells, Vertebrate/chemistry/*physiology ; Rod Opsins/analysis/genetics/*physiology ; Transducin/genetics/physiology ; *Vision, Ocular
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 84
    Publikationsdatum: 2006-02-18
    Beschreibung: Lithium is commonly used to treat bipolar disorder, which is associated with altered circadian rhythm. Lithium is a potent inhibitor of glycogen synthase kinase 3 (GSK3), which regulates circadian rhythm in several organisms. In experiments with cultured cells, we show here that GSK3beta phosphorylates and stabilizes the orphan nuclear receptor Rev-erbalpha, a negative component of the circadian clock. Lithium treatment of cells leads to rapid proteasomal degradation of Rev-erbalpha and activation of clock gene Bmal1. A form of Rev-erbalpha that is insensitive to lithium interferes with the expression of circadian genes. Control of Rev-erbalpha protein stability is thus a critical component of the peripheral clock and a biological target of lithium therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yin, Lei -- Wang, Jing -- Klein, Peter S -- Lazar, Mitchell A -- DK 19525/DK/NIDDK NIH HHS/ -- DK45586/DK/NIDDK NIH HHS/ -- MH058324/MH/NIMH NIH HHS/ -- R01 MH058324/MH/NIMH NIH HHS/ -- R01 MH058324-07/MH/NIMH NIH HHS/ -- R01 MH058324-08/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 17;311(5763):1002-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Diabetes, and Metabolism, and University of Pennsylvania School of Medicine, 415 Curie Boulevard, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16484495" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): ARNTL Transcription Factors ; Amino Acid Sequence ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism ; Biological Clocks/*physiology ; Cell Line ; Cell Line, Tumor ; Circadian Rhythm/*physiology ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Down-Regulation ; Gene Expression Regulation ; Glycogen Synthase Kinase 3/antagonists & inhibitors/metabolism ; Humans ; Lithium Chloride/*pharmacology ; Mice ; Molecular Sequence Data ; NIH 3T3 Cells ; Nuclear Receptor Subfamily 1, Group D, Member 1 ; Phosphorylation ; Promoter Regions, Genetic ; Proteasome Endopeptidase Complex/metabolism ; Proteasome Inhibitors ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 85
    Publikationsdatum: 2006-05-13
    Beschreibung: The DKC1 gene encodes a pseudouridine synthase that modifies ribosomal RNA (rRNA). DKC1 is mutated in people with X-linked dyskeratosis congenita (X-DC), a disease characterized by bone marrow failure, skin abnormalities, and increased susceptibility to cancer. How alterations in ribosome modification might lead to cancer and other features of the disease remains unknown. Using an unbiased proteomics strategy, we discovered a specific defect in IRES (internal ribosome entry site)-dependent translation in Dkc1(m) mice and in cells from X-DC patients. This defect results in impaired translation of messenger RNAs containing IRES elements, including those encoding the tumor suppressor p27(Kip1) and the antiapoptotic factors Bcl-xL and XIAP (X-linked Inhibitor of Apoptosis Protein). Moreover, Dkc1(m) ribosomes were unable to direct translation from IRES elements present in viral messenger RNAs. These findings reveal a potential mechanism by which defective ribosome activity leads to disease and cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoon, Andrew -- Peng, Guang -- Brandenburger, Yves -- Zollo, Ornella -- Xu, Wei -- Rego, Eduardo -- Ruggero, Davide -- New York, N.Y. -- Science. 2006 May 12;312(5775):902-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genetics Program, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16690864" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *5' Untranslated Regions ; Animals ; Cell Cycle Proteins/chemistry/*genetics/physiology ; Cell Line ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p27/biosynthesis/genetics ; Dyskeratosis Congenita/*genetics ; Humans ; Insect Viruses/genetics ; Lymphocytes/metabolism ; Male ; Mice ; Nuclear Proteins/chemistry/*genetics/physiology ; Oligonucleotide Array Sequence Analysis ; Point Mutation ; Polyribosomes/metabolism ; *Protein Biosynthesis ; Proteomics ; Pseudouridine/metabolism ; RNA Viruses/genetics ; RNA, Messenger/*genetics/metabolism ; RNA, Ribosomal/metabolism ; Transfection ; X-Linked Inhibitor of Apoptosis Protein/biosynthesis/genetics ; bcl-X Protein/biosynthesis/genetics
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 86
    Publikationsdatum: 2006-09-23
    Beschreibung: To resolve the controversy about messengers regulating KCNQ ion channels during phospholipase C-mediated suppression of current, we designed translocatable enzymes that quickly alter the phosphoinositide composition of the plasma membrane after application of a chemical cue. The KCNQ current falls rapidly to zero when phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2 or PI(4,5)P2] is depleted without changing Ca2+, diacylglycerol, or inositol 1,4,5-trisphosphate. Current rises by 30% when PI(4,5)P2 is overproduced and does not change when phosphatidylinositol 3,4,5-trisphosphate is raised. Hence, the depletion of PI(4,5)P2 suffices to suppress current fully, and other second messengers are not needed. Our approach is ideally suited to study biological signaling networks involving membrane phosphoinositides.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3579521/" 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/PMC3579521/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suh, Byung-Chang -- Inoue, Takanari -- Meyer, Tobias -- Hille, Bertil -- AR17803/AR/NIAMS NIH HHS/ -- GM63702/GM/NIGMS NIH HHS/ -- MH64801/MH/NIMH NIH HHS/ -- NS08174/NS/NINDS NIH HHS/ -- R01 GM030179/GM/NIGMS NIH HHS/ -- R01 GM030179-24A1/GM/NIGMS NIH HHS/ -- R01 GM030179-25/GM/NIGMS NIH HHS/ -- R01 GM063702/GM/NIGMS NIH HHS/ -- R01 MH064801/MH/NIMH NIH HHS/ -- R01 NS008174/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 1;314(5804):1454-7. Epub 2006 Sep 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16990515" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Calcium/metabolism ; Cell Line ; Cell Membrane/*metabolism ; Diglycerides/metabolism ; Dimerization ; Humans ; *Ion Channel Gating ; KCNQ Potassium Channels/*metabolism ; KCNQ2 Potassium Channel/metabolism ; KCNQ3 Potassium Channel/metabolism ; Mice ; NIH 3T3 Cells ; Oxotremorine/analogs & derivatives/pharmacology ; Phosphatidylinositol 4,5-Diphosphate/*metabolism ; Phosphoric Monoester Hydrolases/metabolism ; Phosphorylation ; Recombinant Fusion Proteins/metabolism ; Second Messenger Systems ; Sirolimus/analogs & derivatives/pharmacology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 87
    Publikationsdatum: 2006-09-09
    Beschreibung: Yeast is a widely used recombinant protein expression system. We expanded its utility by engineering the yeast Pichia pastoris to secrete human glycoproteins with fully complex terminally sialylated N-glycans. After the knockout of four genes to eliminate yeast-specific glycosylation, we introduced 14 heterologous genes, allowing us to replicate the sequential steps of human glycosylation. The reported cell lines produce complex glycoproteins with greater than 90% terminal sialylation. Finally, to demonstrate the utility of these yeast strains, functional recombinant erythropoietin was produced.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hamilton, Stephen R -- Davidson, Robert C -- Sethuraman, Natarajan -- Nett, Juergen H -- Jiang, Youwei -- Rios, Sandra -- Bobrowicz, Piotr -- Stadheim, Terrance A -- Li, Huijuan -- Choi, Byung-Kwon -- Hopkins, Daniel -- Wischnewski, Harry -- Roser, Jessica -- Mitchell, Teresa -- Strawbridge, Rendall R -- Hoopes, Jack -- Wildt, Stefan -- Gerngross, Tillman U -- New York, N.Y. -- Science. 2006 Sep 8;313(5792):1441-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉GlycoFi Inc., 21 Lafayette Street, Suite 200, Lebanon, NH 03766, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16960007" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; Cloning, Molecular ; Cytidine Monophosphate N-Acetylneuraminic Acid/metabolism ; Erythropoietin/chemistry/genetics/*metabolism ; Genetic Vectors ; Glycosylation ; Humans ; Pichia/*genetics/metabolism ; *Protein Engineering ; Rats ; Recombinant Proteins/biosynthesis/chemistry ; Sialic Acids/metabolism ; Sialoglycoproteins/*biosynthesis/chemistry/genetics ; Transformation, Genetic
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 88
    Publikationsdatum: 2006-09-16
    Beschreibung: Herpes simplex virus-1 (HSV-1) encephalitis (HSE) is the most common form of sporadic viral encephalitis in western countries. Its pathogenesis remains unclear, as it affects otherwise healthy patients and only a small minority of HSV-1-infected individuals. Here, we elucidate a genetic etiology for HSE in two children with autosomal recessive deficiency in the intracellular protein UNC-93B, resulting in impaired cellular interferon-alpha/beta and -lambda antiviral responses. HSE can result from a single-gene immunodeficiency that does not compromise immunity to most pathogens, unlike most known primary immunodeficiencies. Other severe infectious diseases may also reflect monogenic disorders of immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Casrouge, Armanda -- Zhang, Shen-Ying -- Eidenschenk, Celine -- Jouanguy, Emmanuelle -- Puel, Anne -- Yang, Kun -- Alcais, Alexandre -- Picard, Capucine -- Mahfoufi, Nora -- Nicolas, Nathalie -- Lorenzo, Lazaro -- Plancoulaine, Sabine -- Senechal, Brigitte -- Geissmann, Frederic -- Tabeta, Koichi -- Hoebe, Kasper -- Du, Xin -- Miller, Richard L -- Heron, Benedicte -- Mignot, Cyril -- de Villemeur, Thierry Billette -- Lebon, Pierre -- Dulac, Olivier -- Rozenberg, Flore -- Beutler, Bruce -- Tardieu, Marc -- Abel, Laurent -- Casanova, Jean-Laurent -- G0900867/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2006 Oct 13;314(5797):308-12. Epub 2006 Sep 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Genetique Humaine des Maladies Infectieuses, Universite de Paris Rene Descartes, INSERM, U550, Faculte de Medecine Necker, Paris 75015, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16973841" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Child, Preschool ; Cytokines/biosynthesis ; Encephalitis, Herpes Simplex/*genetics/immunology ; Female ; *Genetic Predisposition to Disease ; *Herpesvirus 1, Human/immunology ; Humans ; Infant ; Interferon-alpha/biosynthesis/immunology ; Interferon-beta/biosynthesis/immunology ; Interferon-gamma/biosynthesis/immunology ; Interferons/*biosynthesis/immunology ; Leukocytes, Mononuclear/immunology ; Male ; Membrane Transport Proteins/*deficiency/genetics/*physiology ; Mutation ; Pedigree ; Signal Transduction ; Toll-Like Receptor 3/agonists/physiology ; Toll-Like Receptors/agonists/physiology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 89
    Publikationsdatum: 2006-03-18
    Beschreibung: How the widely used botulinum neurotoxin A (BoNT/A) recognizes and enters neurons is poorly understood. We found that BoNT/A enters neurons by binding to the synaptic vesicle protein SV2 (isoforms A, B, and C). Fragments of SV2 that harbor the toxin interaction domain inhibited BoNT/A from binding to neurons. BoNT/A binding to SV2A and SV2B knockout hippocampal neurons was abolished and was restored by expressing SV2A, SV2B, or SV2C. Reduction of SV2 expression in PC12 and Neuro-2a cells also inhibited entry of BoNT/A, which could be restored by expressing SV2 isoforms. Finally, mice that lacked an SV2 isoform (SV2B) displayed reduced sensitivity to BoNT/A. Thus, SV2 acts as the protein receptor for BoNT/A.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dong, Min -- Yeh, Felix -- Tepp, William H -- Dean, Camin -- Johnson, Eric A -- Janz, Roger -- Chapman, Edwin R -- R01 EY016452/EY/NEI NIH HHS/ -- R01 EY016452-03/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2006 Apr 28;312(5773):592-6. Epub 2006 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Physiology, University of Wisconsin, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16543415" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Botulinum Toxins, Type A/*metabolism/toxicity ; Cell Line ; Cells, Cultured ; Endocytosis ; Hippocampus/cytology ; Membrane Glycoproteins/chemistry/genetics/*metabolism ; Mice ; Mice, Knockout ; Nerve Tissue Proteins/chemistry/genetics/*metabolism ; Neuromuscular Junction/metabolism ; Neurons/*metabolism ; PC12 Cells ; Protein Binding ; Protein Isoforms/chemistry/genetics/metabolism ; Protein Structure, Tertiary ; R-SNARE Proteins/metabolism ; Rats ; Synaptic Vesicles/*metabolism ; Synaptotagmins/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 90
    Publikationsdatum: 2006-09-23
    Beschreibung: The posttranslational modification sumoylation can have multiple effects on its substrate proteins. We studied a patient with isolated cleft lip and palate and a balanced chromosomal translocation that disrupts the SUMO1 (small ubiquitin-related modifier) gene, resulting in haploinsufficiency. In mouse, we found that Sumo1 is expressed in the developing lip and palate and that a Sumo1 hypomorphic allele manifests an incompletely penetrant orofacial clefting phenotype. Products of several genes implicated in clefting are sumoylated, and the Sumo1 hypomorphic allele interacts genetically with a loss-of-function allele for one of these loci. Thus, sumoylation defines a network of genes important for palatogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alkuraya, Fowzan S -- Saadi, Irfan -- Lund, Jennifer J -- Turbe-Doan, Annick -- Morton, Cynthia C -- Maas, Richard L -- DE015246/DE/NIDCR NIH HHS/ -- DE11697/DE/NIDCR NIH HHS/ -- GM061365/GM/NIGMS NIH HHS/ -- HD043430/HD/NICHD NIH HHS/ -- P01 GM061354/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Sep 22;313(5794):1751.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, NRB-458, 77 Louis Pasteur, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16990542" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adult ; Animals ; Cell Line ; Child, Preschool ; Cleft Lip/*genetics ; Cleft Palate/*genetics ; Embryo, Mammalian/cytology/metabolism ; Gene Dosage ; Gene Expression Regulation, Developmental ; Humans ; In Situ Hybridization ; Intracellular Signaling Peptides and Proteins/genetics/metabolism ; Karyotyping ; Mice ; Mice, Inbred C57BL ; Morphogenesis ; Nuclear Proteins/genetics/metabolism ; Palate/embryology/metabolism ; Protein Tyrosine Phosphatases/genetics/metabolism ; SUMO-1 Protein/*genetics/physiology ; Small Ubiquitin-Related Modifier Proteins/*genetics/physiology ; Stem Cells/metabolism ; Translocation, Genetic
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 91
    Publikationsdatum: 2006-12-16
    Beschreibung: Although type 2 immune responses contribute to allergy and asthma, these responses are essential for clearing intestinal helminth infestations by mechanisms that include increased epithelial shedding. We show that T helper 2 cells (T(H)2), but not other T cell subsets, express amphiregulin, a member of the epidermal growth factor (EGF) family. EGF receptor ligands directly induce epithelial cell proliferation, and lack of amphiregulin delayed expulsion of the nematode Trichuris muris. This newly recognized link between T(H)2 cells and epithelial proliferation should help in planning therapeutic interventions for helminth infections and other diseases that involve both cell proliferation and allergy, such as asthma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zaiss, Dietmar M -- Yang, Li -- Shah, Pranav R -- Kobie, James J -- Urban, Joseph F -- Mosmann, Tim R -- AI48604/AI/NIAID NIH HHS/ -- DFG/ZA280/PHS HHS/ -- New York, N.Y. -- Science. 2006 Dec 15;314(5806):1746.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉David H. Smith Center for Vaccine Biology and Immunology and Department of Microbiology and Immunology, University of Rochester, Rochester, NY 14642, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170297" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amphiregulin ; Animals ; Bone Marrow Cells/immunology/metabolism ; Cecum/pathology ; Cell Line ; Cell Proliferation ; Cytokines/biosynthesis/immunology ; EGF Family of Proteins ; Gene Expression Regulation ; Glycoproteins/biosynthesis/genetics/*physiology ; Immunity, Innate ; Intercellular Signaling Peptides and Proteins/biosynthesis/genetics/*physiology ; Intestinal Mucosa/pathology ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; Polymerase Chain Reaction ; Th2 Cells/*immunology/metabolism ; Trichuriasis/*immunology/parasitology/pathology ; Trichuris/immunology/physiology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 92
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-07-29
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Edmunds, John W -- Mahadevan, Louis C -- New York, N.Y. -- Science. 2006 Jul 28;313(5786):449-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nuclear Signalling Laboratory, Department of Biochemistry, University of Oxford, Oxford OX1 3QU, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16873633" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Catalytic Domain ; Chromatin/*metabolism ; Chromatin Immunoprecipitation ; Cyclic AMP-Dependent Protein Kinases/*metabolism ; *Gene Expression Regulation, Fungal ; *Genes, Fungal ; Histones/metabolism ; MAP Kinase Signaling System ; Mitogen-Activated Protein Kinases/*metabolism ; Oligonucleotide Array Sequence Analysis ; Osmotic Pressure ; Promoter Regions, Genetic ; Protein Binding ; RNA Polymerase II/metabolism ; Saccharomyces cerevisiae/enzymology/*genetics ; Saccharomyces cerevisiae Proteins/metabolism ; Signal Transduction ; Transcription Factors/metabolism ; Transcription, Genetic
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 93
    Publikationsdatum: 2006-06-24
    Beschreibung: The formation of the neuromuscular synapse requires muscle-specific receptor kinase (MuSK) to orchestrate postsynaptic differentiation, including the clustering of receptors for the neurotransmitter acetylcholine. Upon innervation, neural agrin activates MuSK to establish the postsynaptic apparatus, although agrin-independent formation of neuromuscular synapses can also occur experimentally in the absence of neurotransmission. Dok-7, a MuSK-interacting cytoplasmic protein, is essential for MuSK activation in cultured myotubes; in particular, the Dok-7 phosphotyrosine-binding domain and its target in MuSK are indispensable. Mice lacking Dok-7 formed neither acetylcholine receptor clusters nor neuromuscular synapses. Thus, Dok-7 is essential for neuromuscular synaptogenesis through its interaction with MuSK.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okada, Kumiko -- Inoue, Akane -- Okada, Momoko -- Murata, Yoji -- Kakuta, Shigeru -- Jigami, Takafumi -- Kubo, Sachiko -- Shiraishi, Hirokazu -- Eguchi, Katsumi -- Motomura, Masakatsu -- Akiyama, Tetsu -- Iwakura, Yoichiro -- Higuchi, Osamu -- Yamanashi, Yuji -- New York, N.Y. -- Science. 2006 Jun 23;312(5781):1802-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Regulation, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16794080" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Agrin/metabolism ; Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Cell Differentiation ; Cell Line ; Down-Regulation ; Enzyme Activation ; Humans ; In Situ Hybridization ; Mice ; Molecular Sequence Data ; Motor Endplate/embryology/metabolism ; Muscle Denervation ; Muscle Fibers, Skeletal/cytology/metabolism ; Muscle Proteins/chemistry/genetics/*metabolism ; Muscle, Skeletal/embryology/*innervation/metabolism ; Mutation ; Neuromuscular Junction/*physiology ; Phosphorylation ; Protein Binding ; Protein Structure, Tertiary ; Receptor Aggregation ; Receptor Protein-Tyrosine Kinases/genetics/*metabolism ; Receptors, Cholinergic/genetics/*metabolism ; Synapses/*physiology ; Synaptic Transmission
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 94
    Publikationsdatum: 2006-11-11
    Beschreibung: Many signaling, cytoskeletal, and transport proteins have to be localized to the plasma membrane (PM) in order to carry out their function. We surveyed PM-targeting mechanisms by imaging the subcellular localization of 125 fluorescent protein-conjugated Ras, Rab, Arf, and Rho proteins. Out of 48 proteins that were PM-localized, 37 contained clusters of positively charged amino acids. To test whether these polybasic clusters bind negatively charged phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] lipids, we developed a chemical phosphatase activation method to deplete PM PI(4,5)P2. Unexpectedly, proteins with polybasic clusters dissociated from the PM only when both PI(4,5)P2 and phosphatidylinositol 3,4,5-trisphosphate [PI(3,4,5)P3] were depleted, arguing that both lipid second messengers jointly regulate PM targeting.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3579512/" 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/PMC3579512/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heo, Won Do -- Inoue, Takanari -- Park, Wei Sun -- Kim, Man Lyang -- Park, Byung Ouk -- Wandless, Thomas J -- Meyer, Tobias -- R01 GM030179/GM/NIGMS NIH HHS/ -- R01 GM030179-24A1/GM/NIGMS NIH HHS/ -- R01 GM030179-25/GM/NIGMS NIH HHS/ -- R01 GM063702/GM/NIGMS NIH HHS/ -- R01 MH064801/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 1;314(5804):1458-61. Epub 2006 Nov 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Pharmacology, 318 Campus Drive, Clark Building, Stanford University Medical School, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17095657" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): ADP-Ribosylation Factors/chemistry/metabolism ; Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Cell Membrane/*metabolism ; GTP Phosphohydrolases/chemistry/*metabolism ; HeLa Cells ; Humans ; Hydrophobic and Hydrophilic Interactions ; Kinetics ; Mice ; Molecular Sequence Data ; NIH 3T3 Cells ; Phosphatidylinositol 4,5-Diphosphate/*metabolism ; Phosphatidylinositol Phosphates/*metabolism ; Second Messenger Systems ; Signal Transduction ; Static Electricity ; rab GTP-Binding Proteins/chemistry/metabolism ; ras Proteins/chemistry/metabolism ; rho GTP-Binding Proteins/metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
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  • 95
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-09-30
    Beschreibung: The heart, an ancient organ and the first to form and function during embryogenesis, evolved by the addition of new structures and functions to a primitive pump. Heart development is controlled by an evolutionarily conserved network of transcription factors that connect signaling pathways with genes for muscle growth, patterning, and contractility. During evolution, this ancestral gene network was expanded through gene duplication and co-option of additional networks. Mutations in components of the cardiac gene network cause congenital heart disease, the most common human birth defect. The consequences of such mutations reveal the logic of organogenesis and the evolutionary origins of morphological complexity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4459601/" 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/PMC4459601/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olson, Eric N -- P01 HL049953/HL/NHLBI NIH HHS/ -- R01 HL053351/HL/NHLBI NIH HHS/ -- R01 HL077439/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2006 Sep 29;313(5795):1922-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, TX 75390, USA. eric.olson@utsouthwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17008524" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Biological Evolution ; Drosophila/embryology/genetics ; Gene Duplication ; *Gene Expression Regulation, Developmental ; *Heart/anatomy & histology/embryology/physiology ; Heart Defects, Congenital/genetics/physiopathology ; Humans ; Morphogenesis/genetics ; Mutation ; Regulatory Sequences, Nucleic Acid ; Signal Transduction ; Transcription Factors/genetics/physiology ; Vertebrates/embryology/genetics
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    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 96
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-03-25
    Beschreibung: Voltage-gated proton channels have been widely observed but have not been identified at a molecular level. Here we report that a four-transmembrane protein similar to the voltage-sensor domain of voltage-gated ion channels is a voltage-gated proton channel. Cells overexpressing this protein showed depolarization-induced outward currents accompanied by tail currents. Current reversal occured at equilibrium potentials for protons. The currents exhibited pH-dependent gating and zinc ion sensitivity, two features which are characteristic of voltage-gated proton channels. Responses of voltage dependence to sequence changes suggest that mouse voltage-sensor domain-only protein is itself a channel, rather than a regulator of another channel protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sasaki, Mari -- Takagi, Masahiro -- Okamura, Yasushi -- New York, N.Y. -- Science. 2006 Apr 28;312(5773):589-92. Epub 2006 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Developmental Neurophysiology, Okazaki Institute for Integrative Bioscience, Higashiyama 5-1, Myodaiji-cho, Okazaki, Aichi 444-8787, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16556803" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; Ciona intestinalis ; Electric Conductivity ; Humans ; Hydrogen-Ion Concentration ; *Ion Channel Gating ; Ion Channels/*chemistry/genetics/*physiology ; Membrane Potentials ; Mice ; Molecular Sequence Data ; Mutation ; Patch-Clamp Techniques ; Protein Structure, Tertiary ; *Protons ; 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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  • 97
    Publikationsdatum: 2006-10-07
    Beschreibung: Because HIV-1 does not infect most nonhuman primates, animal modeling of human HIV infection and AIDS has primarily consisted of experimentally infecting macaques with related simian immunodeficiency viruses (SIVMAC). However, the usefulness of such models is limited by the substantial divergence between SIVMAC and HIV-1. We derived an HIV-1-based virus that includes only small portions of SIVMAC yet replicates robustly in both transformed and primary rhesus macaque T cells. Derivation of simian-tropic HIV-1 (stHIV-1) has important implications for understanding primate lentivirus zoonosis and should allow the development of improved animal models for studies of AIDS and the evaluation of vaccines and treatments.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hatziioannou, Theodora -- Princiotta, Michael -- Piatak, Michael Jr -- Yuan, Fang -- Zhang, Fengwen -- Lifson, Jeffrey D -- Bieniasz, Paul D -- New York, N.Y. -- Science. 2006 Oct 6;314(5796):95.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Aaron Diamond AIDS Research Center and Rockefeller University, 455 First Avenue, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17023652" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Capsid Proteins/genetics ; Cell Line ; Cloning, Molecular ; Cytopathogenic Effect, Viral ; Disease Models, Animal ; Genes, vif ; HIV Infections ; HIV-1/*genetics/*physiology ; Humans ; Lymphocytes/virology ; Macaca mulatta ; Recombination, Genetic ; Simian Immunodeficiency Virus/*genetics ; T-Lymphocytes/*virology ; Virus Replication
    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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  • 98
    Publikationsdatum: 2006-04-29
    Beschreibung: Accumulation of misfolded protein in the endoplasmic reticulum (ER) triggers an adaptive stress response-termed the unfolded protein response (UPR)-mediated by the ER transmembrane protein kinase and endoribonuclease inositol-requiring enzyme-1alpha (IRE1alpha). We investigated UPR signaling events in mice in the absence of the proapoptotic BCL-2 family members BAX and BAK [double knockout (DKO)]. DKO mice responded abnormally to tunicamycin-induced ER stress in the liver, with extensive tissue damage and decreased expression of the IRE1 substrate X-box-binding protein 1 and its target genes. ER-stressed DKO cells showed deficient IRE1alpha signaling. BAX and BAK formed a protein complex with the cytosolic domain of IRE1alpha that was essential for IRE1alpha activation. Thus, BAX and BAK function at the ER membrane to activate IRE1alpha signaling and to provide a physical link between members of the core apoptotic pathway and the UPR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hetz, Claudio -- Bernasconi, Paula -- Fisher, Jill -- Lee, Ann-Hwee -- Bassik, Michael C -- Antonsson, Bruno -- Brandt, Gabriel S -- Iwakoshi, Neal N -- Schinzel, Anna -- Glimcher, Laurie H -- Korsmeyer, Stanley J -- CA100707/CA/NCI NIH HHS/ -- P01 AI56296/AI/NIAID NIH HHS/ -- P01 CA92625/CA/NCI NIH HHS/ -- R01 AI32412/AI/NIAID NIH HHS/ -- R37 CA50239/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2006 Apr 28;312(5773):572-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Dana-Farber Cancer Institute, and Harvard Medical School, Boston, MA 02115, USA. chetz@hsph.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645094" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Apoptosis ; DNA-Binding Proteins/metabolism ; Endoplasmic Reticulum/*metabolism/ultrastructure ; Endoribonucleases/*metabolism ; Gene Expression Regulation ; Heat-Shock Proteins/metabolism ; Humans ; Kidney/cytology/drug effects/metabolism ; Liver/cytology/drug effects/metabolism ; Mice ; Mice, Knockout ; Mitochondria/metabolism ; Molecular Chaperones/metabolism ; Nuclear Proteins/metabolism ; Phosphorylation ; Protein Folding ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/*metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Recombinant Proteins/metabolism ; Signal Transduction ; Transcription Factor CHOP/metabolism ; Transcription Factors ; Tunicamycin/pharmacology ; bcl-2 Homologous Antagonist-Killer Protein/chemistry/genetics/*metabolism ; bcl-2-Associated X Protein/genetics/*metabolism ; eIF-2 Kinase/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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  • 99
    Publikationsdatum: 2006-08-26
    Beschreibung: The coreceptor cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) is pivotal in regulating the threshold of signals during T cell activation, although the underlying mechanism is still not fully understood. Using in vitro migration assays and in vivo two-photon laser scanning microscopy, we showed that CTLA-4 increases T cell motility and overrides the T cell receptor (TCR)-induced stop signal required for stable conjugate formation between T cells and antigen-presenting cells. This event led to reduced contact periods between T cells and antigen-presenting cells that in turn decreased cytokine production and proliferation. These results suggest a fundamentally different model of reverse stop signaling, by which CTLA-4 modulates the threshold for T cell activation and protects against autoimmunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schneider, Helga -- Downey, Jos -- Smith, Andrew -- Zinselmeyer, Bernd H -- Rush, Catherine -- Brewer, James M -- Wei, Bin -- Hogg, Nancy -- Garside, Paul -- Rudd, Christopher E -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2006 Sep 29;313(5795):1972-5. Epub 2006 Aug 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Signalling Section, Division of Immunology, Department of Pathology, University of Cambridge, Cambridge CB2 1QP, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16931720" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antigen Presentation ; Antigens, CD ; Antigens, Differentiation/genetics/*physiology ; Autoimmunity ; B-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/immunology/physiology ; CTLA-4 Antigen ; Cell Adhesion ; Cell Movement ; Dendritic Cells/*immunology ; Humans ; Intercellular Adhesion Molecule-1 ; Lymph Nodes/*immunology ; Lymphocyte Activation ; Mice ; Receptors, Antigen, T-Cell/*metabolism ; Signal Transduction ; T-Lymphocytes/immunology/*physiology ; 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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  • 100
    facet.materialart.
    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2006-02-07
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martin, T John -- New York, N.Y. -- Science. 2006 Feb 3;311(5761):606-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16459361" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Line ; *Editorial Policies ; Embryo, Mammalian/cytology ; Humans ; Peer Review, Research ; Periodicals as Topic ; *Publishing ; *Scientific Misconduct ; Stem Cells
    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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