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  • Articles  (274)
  • Protein Structure, Tertiary  (148)
  • Signal Transduction  (137)
  • Meteorology and Climatology
  • 2005-2009  (274)
  • 1950-1954
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  • 11
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    Solution nuclear magnetic resonance structure of membrane-integral diacylglycerol kinase (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-27
    Description: Escherichia coli diacylglycerol kinase (DAGK) represents a family of integral membrane enzymes that is unrelated to all other phosphotransferases. We have determined the three-dimensional structure of the DAGK homotrimer with the use of solution nuclear magnetic resonance. The third transmembrane helix from each subunit is domain-swapped with the first and second transmembrane segments from an adjacent subunit. Each of DAGK's three active sites resembles a portico. The cornice of the portico appears to be the determinant of DAGK's lipid substrate specificity and overhangs the site of phosphoryl transfer near the water-membrane interface. Mutations to cysteine that caused severe misfolding were located in or near the active site, indicating a high degree of overlap between sites responsible for folding and for catalysis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2764269/" 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/PMC2764269/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Van Horn, Wade D -- Kim, Hak-Jun -- Ellis, Charles D -- Hadziselimovic, Arina -- Sulistijo, Endah S -- Karra, Murthy D -- Tian, Changlin -- Sonnichsen, Frank D -- Sanders, Charles R -- R01 GM047485/GM/NIGMS NIH HHS/ -- R01 GM047485-17/GM/NIGMS NIH HHS/ -- R01 GM47485/GM/NIGMS NIH HHS/ -- T32 NS007491/NS/NINDS NIH HHS/ -- T32 NS007491-09/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 Jun 26;324(5935):1726-9. doi: 10.1126/science.1171716.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Center for Structural Biology, Vanderbilt University, Nashville, TN 37232, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19556511" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Amino Acid Sequence ; Biocatalysis ; Catalytic Domain ; Cell Membrane/enzymology ; Diacylglycerol Kinase/*chemistry/metabolism ; Escherichia coli/*enzymology ; Escherichia coli Proteins/*chemistry/metabolism ; Models, Molecular ; Molecular Sequence Data ; Nuclear Magnetic Resonance, Biomolecular ; Protein Conformation ; Protein Folding ; Protein Multimerization ; Protein Structure, Quaternary ; Protein Structure, Secondary ; Protein Structure, Tertiary
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
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    Genomic minimalism in the early diverging intestinal parasite Giardia lamblia (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-29
    Description: The genome of the eukaryotic protist Giardia lamblia, an important human intestinal parasite, is compact in structure and content, contains few introns or mitochondrial relics, and has simplified machinery for DNA replication, transcription, RNA processing, and most metabolic pathways. Protein kinases comprise the single largest protein class and reflect Giardia's requirement for a complex signal transduction network for coordinating differentiation. Lateral gene transfer from bacterial and archaeal donors has shaped Giardia's genome, and previously unknown gene families, for example, cysteine-rich structural proteins, have been discovered. Unexpectedly, the genome shows little evidence of heterozygosity, supporting recent speculations that this organism is sexual. This genome sequence will not only be valuable for investigating the evolution of eukaryotes, but will also be applied to the search for new therapeutics for this parasite.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morrison, Hilary G -- McArthur, Andrew G -- Gillin, Frances D -- Aley, Stephen B -- Adam, Rodney D -- Olsen, Gary J -- Best, Aaron A -- Cande, W Zacheus -- Chen, Feng -- Cipriano, Michael J -- Davids, Barbara J -- Dawson, Scott C -- Elmendorf, Heidi G -- Hehl, Adrian B -- Holder, Michael E -- Huse, Susan M -- Kim, Ulandt U -- Lasek-Nesselquist, Erica -- Manning, Gerard -- Nigam, Anuranjini -- Nixon, Julie E J -- Palm, Daniel -- Passamaneck, Nora E -- Prabhu, Anjali -- Reich, Claudia I -- Reiner, David S -- Samuelson, John -- Svard, Staffan G -- Sogin, Mitchell L -- AI42488/AI/NIAID NIH HHS/ -- AI43273/AI/NIAID NIH HHS/ -- AI51687/AI/NIAID NIH HHS/ -- R01 AI043273/AI/NIAID NIH HHS/ -- R01 AI048082/AI/NIAID NIH HHS/ -- R01 HG004164/HG/NHGRI NIH HHS/ -- R01 HG004164-01/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2007 Sep 28;317(5846):1921-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Marine Biological Laboratory, Woods Hole, MA 02543-1015, USA. morrison@mbl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17901334" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Biological Evolution ; DNA Replication/genetics ; *Eukaryotic Cells ; Gene Transfer, Horizontal ; Genes, Protozoan ; *Genome, Protozoan ; Genomics ; Giardia lamblia/classification/*genetics/physiology ; Metabolic Networks and Pathways/genetics ; Molecular Sequence Data ; Phylogeny ; Protein Kinases/genetics/metabolism ; Protozoan Proteins/chemistry/genetics/metabolism ; RNA Processing, Post-Transcriptional ; Signal Transduction ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
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    Structure and hydration of membranes embedded with voltage-sensing domains (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-11-27
    Description: Despite the growing number of atomic-resolution membrane protein structures, direct structural information about proteins in their native membrane environment is scarce. This problem is particularly relevant in the case of the highly charged S1-S4 voltage-sensing domains responsible for nerve impulses, where interactions with the lipid bilayer are critical for the function of voltage-activated ion channels. Here we use neutron diffraction, solid-state nuclear magnetic resonance (NMR) spectroscopy and molecular dynamics simulations to investigate the structure and hydration of bilayer membranes containing S1-S4 voltage-sensing domains. Our results show that voltage sensors adopt transmembrane orientations and cause a modest reshaping of the surrounding lipid bilayer, and that water molecules intimately interact with the protein within the membrane. These structural findings indicate that voltage sensors have evolved to interact with the lipid membrane while keeping energetic and structural perturbations to a minimum, and that water penetrates the membrane, to hydrate charged residues and shape the transmembrane electric field.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2784928/" 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/PMC2784928/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Krepkiy, Dmitriy -- Mihailescu, Mihaela -- Freites, J Alfredo -- Schow, Eric V -- Worcester, David L -- Gawrisch, Klaus -- Tobias, Douglas J -- White, Stephen H -- Swartz, Kenton J -- GM74737/GM/NIGMS NIH HHS/ -- GM86685/GM/NIGMS NIH HHS/ -- P01 GM086685/GM/NIGMS NIH HHS/ -- R01 GM074637/GM/NIGMS NIH HHS/ -- R01 RR014812/RR/NCRR NIH HHS/ -- ZIA NS002945-13/Intramural NIH HHS/ -- England -- Nature. 2009 Nov 26;462(7272):473-9. doi: 10.1038/nature08542.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Physiology and Biophysics Section, Porter Neuroscience Research Center, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19940918" target="_blank"〉PubMed〈/a〉
    Keywords: Archaeal Proteins/chemistry/metabolism ; Circular Dichroism ; Lipid Bilayers/*chemistry/*metabolism ; Membrane Lipids/analysis/chemistry/metabolism ; *Membrane Potentials ; Models, Molecular ; Molecular Dynamics Simulation ; Neutron Diffraction ; Nuclear Magnetic Resonance, Biomolecular ; Potassium Channels, Voltage-Gated/*chemistry/metabolism ; Protein Structure, Tertiary ; Spectrometry, Fluorescence ; Water/*analysis/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 14
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    Secreted semaphorins control spine distribution and morphogenesis in the postnatal CNS (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-12-17
    Description: The majority of excitatory synapses in the mammalian CNS (central nervous system) are formed on dendritic spines, and spine morphology and distribution are critical for synaptic transmission, synaptic integration and plasticity. Here, we show that a secreted semaphorin, Sema3F, is a negative regulator of spine development and synaptic structure. Mice with null mutations in genes encoding Sema3F, and its holoreceptor components neuropilin-2 (Npn-2, also known as Nrp2) and plexin A3 (PlexA3, also known as Plxna3), exhibit increased dentate gyrus (DG) granule cell (GC) and cortical layer V pyramidal neuron spine number and size, and also aberrant spine distribution. Moreover, Sema3F promotes loss of spines and excitatory synapses in dissociated neurons in vitro, and in Npn-2(-/-) brain slices cortical layer V and DG GCs exhibit increased mEPSC (miniature excitatory postsynaptic current) frequency. In contrast, a distinct Sema3A-Npn-1/PlexA4 signalling cascade controls basal dendritic arborization in layer V cortical neurons, but does not influence spine morphogenesis or distribution. These disparate effects of secreted semaphorins are reflected in the restricted dendritic localization of Npn-2 to apical dendrites and of Npn-1 (also known as Nrp1) to all dendrites of cortical pyramidal neurons. Therefore, Sema3F signalling controls spine distribution along select dendritic processes, and distinct secreted semaphorin signalling events orchestrate CNS connectivity through the differential control of spine morphogenesis, synapse formation, and the elaboration of dendritic morphology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2842559/" 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/PMC2842559/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tran, Tracy S -- Rubio, Maria E -- Clem, Roger L -- Johnson, Dontais -- Case, Lauren -- Tessier-Lavigne, Marc -- Huganir, Richard L -- Ginty, David D -- Kolodkin, Alex L -- F32 NS051003/NS/NINDS NIH HHS/ -- P50 MH06883/MH/NIMH NIH HHS/ -- R01 DC-006881/DC/NIDCD NIH HHS/ -- R01 MH059199/MH/NIMH NIH HHS/ -- R01 MH059199-07/MH/NIMH NIH HHS/ -- R01 MH059199-08/MH/NIMH NIH HHS/ -- R01 MH059199-09/MH/NIMH NIH HHS/ -- R01 MH059199-10/MH/NIMH NIH HHS/ -- R01 MH59199/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Dec 24;462(7276):1065-9. doi: 10.1038/nature08628. Epub 2009 Dec 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Solomon H. Snyder Department of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20010807" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Central Nervous System/cytology/drug effects/*growth & ; development/*metabolism/ultrastructure ; Female ; Gene Expression Regulation, Developmental ; Male ; Mice ; Mice, Knockout ; Neuropilin-1/metabolism ; Neuropilin-2/metabolism ; Pyramidal Cells/*cytology/drug effects/*growth & development/ultrastructure ; Recombinant Proteins/pharmacology ; Semaphorins/genetics/*metabolism/pharmacology ; Signal Transduction ; Synapses/drug effects/*physiology/ultrastructure
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 15
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    Casein kinase 1alpha governs antigen-receptor-induced NF-kappaB activation and human lymphoma cell survival (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-01-02
    Description: The transcription factor NF-kappaB is required for lymphocyte activation and proliferation as well as the survival of certain lymphoma types. Antigen receptor stimulation assembles an NF-kappaB activating platform containing the scaffold protein CARMA1 (also called CARD11), the adaptor BCL10 and the paracaspase MALT1 (the CBM complex), linked to the inhibitor of NF-kappaB kinase complex, but signal transduction is not fully understood. We conducted parallel screens involving a mass spectrometry analysis of CARMA1 binding partners and an RNA interference screen for growth inhibition of the CBM-dependent 'activated B-cell-like' (ABC) subtype of diffuse large B-cell lymphoma (DLBCL). Here we report that both screens identified casein kinase 1alpha (CK1alpha) as a bifunctional regulator of NF-kappaB. CK1alpha dynamically associates with the CBM complex on T-cell-receptor (TCR) engagement to participate in cytokine production and lymphocyte proliferation. However, CK1alpha kinase activity has a contrasting role by subsequently promoting the phosphorylation and inactivation of CARMA1. CK1alpha has thus a dual 'gating' function which first promotes and then terminates receptor-induced NF-kappaB. ABC DLBCL cells required CK1alpha for constitutive NF-kappaB activity, indicating that CK1alpha functions as a conditionally essential malignancy gene-a member of a new class of potential cancer therapeutic targets.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2688735/" 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/PMC2688735/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bidere, Nicolas -- Ngo, Vu N -- Lee, Jeansun -- Collins, Cailin -- Zheng, Lixin -- Wan, Fengyi -- Davis, R Eric -- Lenz, Georg -- Anderson, D Eric -- Arnoult, Damien -- Vazquez, Aime -- Sakai, Keiko -- Zhang, Jun -- Meng, Zhaojing -- Veenstra, Timothy D -- Staudt, Louis M -- Lenardo, Michael J -- NIH0011349228/PHS HHS/ -- Intramural NIH HHS/ -- England -- Nature. 2009 Mar 5;458(7234):92-6. doi: 10.1038/nature07613. Epub 2008 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Development Section, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19118383" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; CARD Signaling Adaptor Proteins/metabolism ; Casein Kinases/*metabolism ; Caspases/metabolism ; Cell Proliferation ; Cell Survival ; Cells, Cultured ; Feedback, Physiological ; Guanylate Cyclase/metabolism ; Humans ; I-kappa B Kinase/metabolism ; Jurkat Cells ; Lymphoma, Large B-Cell, Diffuse/enzymology/*metabolism/*pathology ; NF-kappa B/*metabolism ; Neoplasm Proteins/metabolism ; Protein Binding ; Receptors, Antigen/*metabolism ; Signal Transduction
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 16
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    XIAP discriminates between type I and type II FAS-induced apoptosis (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-07-25
    Description: FAS (also called APO-1 and CD95) and its physiological ligand, FASL, regulate apoptosis of unwanted or dangerous cells, functioning as a guardian against autoimmunity and cancer development. Distinct cell types differ in the mechanisms by which the 'death receptor' FAS triggers their apoptosis. In type I cells, such as lymphocytes, activation of 'effector caspases' by FAS-induced activation of caspase-8 suffices for cell killing, whereas in type II cells, including hepatocytes and pancreatic beta-cells, caspase cascade amplification through caspase-8-mediated activation of the pro-apoptotic BCL-2 family member BID (BH3 interacting domain death agonist) is essential. Here we show that loss of XIAP (X-chromosome linked inhibitor of apoptosis protein) function by gene targeting or treatment with a second mitochondria-derived activator of caspases (SMAC, also called DIABLO; direct IAP-binding protein with low pI) mimetic drug in mice rendered hepatocytes and beta-cells independent of BID for FAS-induced apoptosis. These results show that XIAP is the critical discriminator between type I and type II apoptosis signalling and suggest that IAP inhibitors should be used with caution in cancer patients with underlying liver conditions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2956120/" 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/PMC2956120/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jost, Philipp J -- Grabow, Stephanie -- Gray, Daniel -- McKenzie, Mark D -- Nachbur, Ueli -- Huang, David C S -- Bouillet, Philippe -- Thomas, Helen E -- Borner, Christoph -- Silke, John -- Strasser, Andreas -- Kaufmann, Thomas -- CA 43540/CA/NCI NIH HHS/ -- CA 80188/CA/NCI NIH HHS/ -- R01 CA043540/CA/NCI NIH HHS/ -- R01 CA043540-09/CA/NCI NIH HHS/ -- R01 CA043540-22/CA/NCI NIH HHS/ -- R01 CA080188-01/CA/NCI NIH HHS/ -- R01 CA080188-08/CA/NCI NIH HHS/ -- England -- Nature. 2009 Aug 20;460(7258):1035-9. doi: 10.1038/nature08229. Epub 2009 Jul 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Walter and Eliza Hall Institute of Medical Research, Melbourne University, Parkville, Victoria 3050, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19626005" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/antagonists & inhibitors/immunology/*metabolism ; *Apoptosis ; BH3 Interacting Domain Death Agonist Protein/deficiency/genetics ; Biomimetic Materials/pharmacology ; Caspase Inhibitors ; Enzyme Activation ; Fas Ligand Protein/metabolism ; Female ; Hepatitis/metabolism/pathology ; Hepatocytes/cytology/drug effects/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Signal Transduction ; Thymus Gland/cytology/drug effects ; X-Linked Inhibitor of Apoptosis Protein/antagonists & ; inhibitors/deficiency/genetics/*metabolism
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 17
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    A phylogeny-driven genomic encyclopaedia of Bacteria and Archaea (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-12-25
    Description: Sequencing of bacterial and archaeal genomes has revolutionized our understanding of the many roles played by microorganisms. There are now nearly 1,000 completed bacterial and archaeal genomes available, most of which were chosen for sequencing on the basis of their physiology. As a result, the perspective provided by the currently available genomes is limited by a highly biased phylogenetic distribution. To explore the value added by choosing microbial genomes for sequencing on the basis of their evolutionary relationships, we have sequenced and analysed the genomes of 56 culturable species of Bacteria and Archaea selected to maximize phylogenetic coverage. Analysis of these genomes demonstrated pronounced benefits (compared to an equivalent set of genomes randomly selected from the existing database) in diverse areas including the reconstruction of phylogenetic history, the discovery of new protein families and biological properties, and the prediction of functions for known genes from other organisms. Our results strongly support the need for systematic 'phylogenomic' efforts to compile a phylogeny-driven 'Genomic Encyclopedia of Bacteria and Archaea' in order to derive maximum knowledge from existing microbial genome data as well as from genome sequences to come.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3073058/" 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/PMC3073058/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Dongying -- Hugenholtz, Philip -- Mavromatis, Konstantinos -- Pukall, Rudiger -- Dalin, Eileen -- Ivanova, Natalia N -- Kunin, Victor -- Goodwin, Lynne -- Wu, Martin -- Tindall, Brian J -- Hooper, Sean D -- Pati, Amrita -- Lykidis, Athanasios -- Spring, Stefan -- Anderson, Iain J -- D'haeseleer, Patrik -- Zemla, Adam -- Singer, Mitchell -- Lapidus, Alla -- Nolan, Matt -- Copeland, Alex -- Han, Cliff -- Chen, Feng -- Cheng, Jan-Fang -- Lucas, Susan -- Kerfeld, Cheryl -- Lang, Elke -- Gronow, Sabine -- Chain, Patrick -- Bruce, David -- Rubin, Edward M -- Kyrpides, Nikos C -- Klenk, Hans-Peter -- Eisen, Jonathan A -- R01 GM054592-09/GM/NIGMS NIH HHS/ -- R01 GM067012-04/GM/NIGMS NIH HHS/ -- England -- Nature. 2009 Dec 24;462(7276):1056-60. doi: 10.1038/nature08656.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉DOE Joint Genome Institute, Walnut Creek, California 94598, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20033048" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/chemistry ; Amino Acid Sequence ; Archaea/*classification/*genetics ; Bacteria/*classification/*genetics ; Bacterial Proteins/chemistry ; Biodiversity ; Databases, Genetic ; Genes, rRNA/genetics ; Genome, Archaeal/*genetics ; Genome, Bacterial/*genetics ; Models, Molecular ; Molecular Sequence Data ; *Phylogeny ; Protein Structure, Tertiary ; Sequence Alignment
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 18
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    WSTF regulates the H2A.X DNA damage response via a novel tyrosine kinase activity (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-12-19
    Description: DNA double-stranded breaks present a serious challenge for eukaryotic cells. The inability to repair breaks leads to genomic instability, carcinogenesis and cell death. During the double-strand break response, mammalian chromatin undergoes reorganization demarcated by H2A.X Ser 139 phosphorylation (gamma-H2A.X). However, the regulation of gamma-H2A.X phosphorylation and its precise role in chromatin remodelling during the repair process remain unclear. Here we report a new regulatory mechanism mediated by WSTF (Williams-Beuren syndrome transcription factor, also known as BAZ1B)-a component of the WICH complex (WSTF-ISWI ATP-dependent chromatin-remodelling complex). We show that WSTF has intrinsic tyrosine kinase activity by means of a domain that shares no sequence homology to any known kinase fold. We show that WSTF phosphorylates Tyr 142 of H2A.X, and that WSTF activity has an important role in regulating several events that are critical for the DNA damage response. Our work demonstrates a new mechanism that regulates the DNA damage response and expands our knowledge of domains that contain intrinsic tyrosine kinase activity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2854499/" 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/PMC2854499/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xiao, Andrew -- Li, Haitao -- Shechter, David -- Ahn, Sung Hee -- Fabrizio, Laura A -- Erdjument-Bromage, Hediye -- Ishibe-Murakami, Satoko -- Wang, Bin -- Tempst, Paul -- Hofmann, Kay -- Patel, Dinshaw J -- Elledge, Stephen J -- Allis, C David -- F32 GM075486/GM/NIGMS NIH HHS/ -- P30 CA08748/CA/NCI NIH HHS/ -- R01 GM040922/GM/NIGMS NIH HHS/ -- R01 GM040922-24/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Jan 1;457(7225):57-62. doi: 10.1038/nature07668. Epub 2008 Dec 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chromatin Biology, The Rockefeller University, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19092802" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/metabolism ; Animals ; Chromatin Assembly and Disassembly ; Chromosomal Proteins, Non-Histone/metabolism ; *DNA Damage ; Histones/genetics/*metabolism ; Humans ; Mice ; NIH 3T3 Cells ; Nucleosomes/metabolism ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein Structure, Tertiary ; Protein-Tyrosine Kinases/*metabolism ; Transcription Factors/chemistry/deficiency/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 19
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    A genome-wide association study identifies IL23R as an inflammatory bowel disease gene (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-28
    Description: 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〉
    Keywords: 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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 20
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    Promotion of tissue inflammation by the immune receptor Tim-3 expressed on innate immune cells (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-17
    Description: CD4+ T helper 1 (TH1) cells are important mediators of inflammation and are regulated by numerous pathways, including the negative immune receptor Tim-3. We found that Tim-3 is constitutively expressed on cells of the innate immune system in both mice and humans, and that it can synergize with Toll-like receptors. Moreover, an antibody agonist of Tim-3 acted as an adjuvant during induced immune responses, and Tim-3 ligation induced distinct signaling events in T cells and dendritic cells; the latter finding could explain the apparent divergent functions of Tim-3 in these cell types. Thus, by virtue of differential expression on innate versus adaptive immune cells, Tim-3 can either promote or terminate TH1 immunity and may be able to influence a range of inflammatory conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, Ana C -- Anderson, David E -- Bregoli, Lisa -- Hastings, William D -- Kassam, Nasim -- Lei, Charles -- Chandwaskar, Rucha -- Karman, Jozsef -- Su, Ee W -- Hirashima, Mitsuomi -- Bruce, Jeffrey N -- Kane, Lawrence P -- Kuchroo, Vijay K -- Hafler, David A -- R01 AI067544/AI/NIAID NIH HHS/ -- R01 AI067544-01A2/AI/NIAID NIH HHS/ -- R56 AI067544/AI/NIAID NIH HHS/ -- R56 AI067544-01A1/AI/NIAID NIH HHS/ -- R56 AI067544-02/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 16;318(5853):1141-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Immunology, Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18006747" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD11b/immunology ; Astrocytes/immunology ; Central Nervous System Neoplasms/immunology ; Dendritic Cells/immunology ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Galectins/immunology ; Glioblastoma/immunology ; Humans ; Immunity, Innate ; Inflammation Mediators/*immunology ; Lipopolysaccharides/immunology ; Macrophages/immunology ; Membrane Proteins/biosynthesis/*immunology ; Mice ; Microglia/immunology ; Multiple Sclerosis/immunology ; Rats ; Receptors, Immunologic/biosynthesis/*immunology ; Receptors, Virus/biosynthesis/*immunology ; Signal Transduction ; T-Lymphocytes/immunology ; Th1 Cells/*immunology ; Toll-Like Receptors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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