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  • Mice  (55)
  • Molecular Sequence Data  (28)
  • American Association for the Advancement of Science (AAAS)  (80)
  • 2010-2014
  • 2005-2009  (80)
  • 2006  (80)
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Keywords
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  • American Association for the Advancement of Science (AAAS)  (80)
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  • 2010-2014
  • 2005-2009  (80)
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  • 1
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    Common Kibra alleles are associated with human memory performance (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-21
    Description: Human memory is a polygenic trait. We performed a genome-wide screen to identify memory-related gene variants. A genomic locus encoding the brain protein KIBRA was significantly associated with memory performance in three independent, cognitively normal cohorts from Switzerland and the United States. Gene expression studies showed that KIBRA was expressed in memory-related brain structures. Functional magnetic resonance imaging detected KIBRA allele-dependent differences in hippocampal activations during memory retrieval. Evidence from these experiments suggests a role for KIBRA in human memory.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Papassotiropoulos, Andreas -- Stephan, Dietrich A -- Huentelman, Matthew J -- Hoerndli, Frederic J -- Craig, David W -- Pearson, John V -- Huynh, Kim-Dung -- Brunner, Fabienne -- Corneveaux, Jason -- Osborne, David -- Wollmer, M Axel -- Aerni, Amanda -- Coluccia, Daniel -- Hanggi, Jurgen -- Mondadori, Christian R A -- Buchmann, Andreas -- Reiman, Eric M -- Caselli, Richard J -- Henke, Katharina -- de Quervain, Dominique J-F -- P30AG19610/AG/NIA NIH HHS/ -- R01MH057899/MH/NIMH NIH HHS/ -- U01-HL086528-01/HL/NHLBI NIH HHS/ -- U24NS051872/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 20;314(5798):475-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Psychiatry Research, University of Zurich, Zurich 8057, Switzerland. papas@bli.unizh.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17053149" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Alleles ; Animals ; Attention ; Brain/*physiology ; Brain Chemistry ; Calcium-Binding Proteins/genetics ; Cohort Studies ; Female ; Gene Expression ; Genotype ; Haplotypes ; Hippocampus/chemistry/*physiology ; Humans ; Intracellular Signaling Peptides and Proteins ; Magnetic Resonance Imaging ; Male ; Membrane Proteins/genetics ; *Memory ; Mice ; Middle Aged ; Phosphoproteins ; *Polymorphism, Single Nucleotide ; Proteins/analysis/*genetics/*physiology ; Reverse Transcriptase Polymerase Chain Reaction ; Switzerland ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Losartan, an AT1 antagonist, prevents aortic aneurysm in a mouse model of Marfan syndrome (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-08
    Description: 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〉
    Keywords: 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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Netrins promote developmental and therapeutic angiogenesis (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-01
    Description: 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〉
    Keywords: 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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Sequencing and analysis of Neanderthal genomic DNA (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-11-18
    Description: Our knowledge of Neanderthals is based on a limited number of remains and artifacts from which we must make inferences about their biology, behavior, and relationship to ourselves. Here, we describe the characterization of these extinct hominids from a new perspective, based on the development of a Neanderthal metagenomic library and its high-throughput sequencing and analysis. Several lines of evidence indicate that the 65,250 base pairs of hominid sequence so far identified in the library are of Neanderthal origin, the strongest being the ascertainment of sequence identities between Neanderthal and chimpanzee at sites where the human genomic sequence is different. These results enabled us to calculate the human-Neanderthal divergence time based on multiple randomly distributed autosomal loci. Our analyses suggest that on average the Neanderthal genomic sequence we obtained and the reference human genome sequence share a most recent common ancestor approximately 706,000 years ago, and that the human and Neanderthal ancestral populations split approximately 370,000 years ago, before the emergence of anatomically modern humans. Our finding that the Neanderthal and human genomes are at least 99.5% identical led us to develop and successfully implement a targeted method for recovering specific ancient DNA sequences from metagenomic libraries. This initial analysis of the Neanderthal genome advances our understanding of the evolutionary relationship of Homo sapiens and Homo neanderthalensis and signifies the dawn of Neanderthal genomics.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2583069/" 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/PMC2583069/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Noonan, James P -- Coop, Graham -- Kudaravalli, Sridhar -- Smith, Doug -- Krause, Johannes -- Alessi, Joe -- Chen, Feng -- Platt, Darren -- Paabo, Svante -- Pritchard, Jonathan K -- Rubin, Edward M -- 1-F32-GM074367/GM/NIGMS NIH HHS/ -- HL066681/HL/NHLBI NIH HHS/ -- R01 HG002772/HG/NHGRI NIH HHS/ -- R01 HG002772-01/HG/NHGRI NIH HHS/ -- R01 HG002772-1/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2006 Nov 17;314(5802):1113-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉U.S. Department of Energy Joint Genome Institute, 2800 Mitchell Drive, Walnut Creek, CA 94598, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17110569" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Bone and Bones ; Cell Nucleus ; DNA/*genetics/isolation & purification ; DNA, Mitochondrial ; *Fossils ; Gene Pool ; Genome ; Genome, Human ; Genomic Library ; History, Ancient ; Hominidae/*genetics ; Humans ; Male ; Molecular Sequence Data ; Pan troglodytes/genetics ; Polymerase Chain Reaction ; Sequence Alignment ; *Sequence Analysis, DNA/methods ; Time
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 5
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    Genetic variant BDNF (Val66Met) polymorphism alters anxiety-related behavior (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-07
    Description: A common single-nucleotide polymorphism in the brain-derived neurotrophic factor (BDNF) gene, a methionine (Met) substitution for valine (Val) at codon 66 (Val66Met), is associated with alterations in brain anatomy and memory, but its relevance to clinical disorders is unclear. We generated a variant BDNF mouse (BDNF(Met/Met)) that reproduces the phenotypic hallmarks in humans with the variant allele. BDNF(Met) was expressed in brain at normal levels, but its secretion from neurons was defective. When placed in stressful settings, BDNF(Met/Met) mice exhibited increased anxiety-related behaviors that were not normalized by the antidepressant, fluoxetine. A variant BDNF may thus play a key role in genetic predispositions to anxiety and depressive disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1880880/" 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/PMC1880880/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Zhe-Yu -- Jing, Deqiang -- Bath, Kevin G -- Ieraci, Alessandro -- Khan, Tanvir -- Siao, Chia-Jen -- Herrera, Daniel G -- Toth, Miklos -- Yang, Chingwen -- McEwen, Bruce S -- Hempstead, Barbara L -- Lee, Francis S -- MH060478/MH/NIMH NIH HHS/ -- MH068850/MH/NIMH NIH HHS/ -- NS052819/NS/NINDS NIH HHS/ -- NS30687/NS/NINDS NIH HHS/ -- R01 NS052819/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 6;314(5796):140-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Weill Medical College of Cornell University, New York, NY 10021, USA. zheyuchen@sdu.edu.cn〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17023662" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Anxiety/drug therapy/*genetics ; Behavior, Animal ; Brain-Derived Neurotrophic Factor/*genetics/*physiology ; Conditioning (Psychology) ; Dendrites/ultrastructure ; Dentate Gyrus/cytology ; Fear ; Fluoxetine/administration & dosage/pharmacology ; Hippocampus/anatomy & histology/metabolism ; Memory ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Motor Activity ; Neurons/cytology/metabolism ; Organ Size ; *Polymorphism, Single Nucleotide ; Rats ; Rats, Sprague-Dawley ; Serotonin Uptake Inhibitors/administration & dosage/pharmacology
    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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  • 6
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    A critical role for the innate immune signaling molecule IRAK-4 in T cell activation (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-01
    Description: 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〉
    Keywords: 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
    Print ISSN: 0036-8075
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  • 7
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    Structure of tracheal cytotoxin in complex with a heterodimeric pattern-recognition receptor (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-03-25
    Description: Tracheal cytotoxin (TCT), a naturally occurring fragment of Gram-negative peptidoglycan, is a potent elicitor of innate immune responses in Drosophila. It induces the heterodimerization of its recognition receptors, the peptidoglycan recognition proteins (PGRPs) LCa and LCx, which activates the immune deficiency pathway. The crystal structure at 2.1 angstrom resolution of TCT in complex with the ectodomains of PGRP-LCa and PGRP-LCx shows that TCT is bound to and presented by the LCx ectodomain for recognition by the LCa ectodomain; the latter lacks a canonical peptidoglycan-docking groove conserved in other PGRPs. The interface, revealed in atomic detail, between TCT and the receptor complex highlights the importance of the anhydro-containing disaccharide in bridging the two ectodomains together and the critical role of diaminopimelic acid as the specificity determinant for PGRP interaction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, Chung-I -- Chelliah, Yogarany -- Borek, Dominika -- Mengin-Lecreulx, Dominique -- Deisenhofer, Johann -- New York, N.Y. -- Science. 2006 Mar 24;311(5768):1761-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Texas Southwestern Medical Center at Dallas, 6001 Forest Park Road, Dallas, TX 75390-9050, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16556841" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Carrier Proteins/*chemistry/metabolism ; Crystallization ; Crystallography, X-Ray ; Cytotoxins/*chemistry/metabolism ; Drosophila melanogaster ; Hydrogen Bonding ; Hydrophobic and Hydrophilic Interactions ; Models, Molecular ; Molecular Sequence Data ; Peptidoglycan/*chemistry/metabolism ; Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary
    Print ISSN: 0036-8075
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  • 8
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    Role of noradrenergic signaling by the nucleus tractus solitarius in mediating opiate reward (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-18
    Description: 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〉
    Keywords: 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
    Print ISSN: 0036-8075
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  • 9
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    Crystal structure of a divalent metal ion transporter CorA at 2.9 angstrom resolution (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-22
    Description: CorA family members are ubiquitously distributed transporters of divalent metal cations and are considered to be the primary Mg2+ transporter of Bacteria and Archaea. We have determined a 2.9 angstrom resolution structure of CorA from Thermotoga maritima that reveals a pentameric cone-shaped protein. Two potential regulatory metal binding sites are found in the N-terminal domain that bind both Mg2+ and Co2+. The structure of CorA supports an efflux system involving dehydration and rehydration of divalent metal ions potentially mediated by a ring of conserved aspartate residues at the cytoplasmic entrance and a carbonyl funnel at the periplasmic side of the pore.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eshaghi, Said -- Niegowski, Damian -- Kohl, Andreas -- Martinez Molina, Daniel -- Lesley, Scott A -- Nordlund, Par -- New York, N.Y. -- Science. 2006 Jul 21;313(5785):354-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biophysics, Department of Medical Biochemistry and Biophysics, Karolinska Institute, SE-171 77 Stockholm, Sweden. Said.Eshaghi@ki.se〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16857941" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Bacterial Proteins/*chemistry/metabolism ; Binding Sites ; Cation Transport Proteins/*chemistry/metabolism ; Chlorides/analysis/metabolism ; Cobalt/chemistry/*metabolism ; Crystallography, X-Ray ; Hydrophobic and Hydrophilic Interactions ; Magnesium/chemistry/*metabolism ; Models, Molecular ; Molecular Sequence Data ; Protein Conformation ; Protein Folding ; Protein Structure, Quaternary ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Sequence Alignment ; Thermotoga maritima/*chemistry ; Water/chemistry
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  • 10
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    Genome sequence diversity and clues to the evolution of variola (smallpox) virus (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-29
    Description: Comparative genomics of 45 epidemiologically varied variola virus isolates from the past 30 years of the smallpox era indicate low sequence diversity, suggesting that there is probably little difference in the isolates' functional gene content. Phylogenetic clustering inferred three clades coincident with their geographical origin and case-fatality rate; the latter implicated putative proteins that mediate viral virulence differences. Analysis of the viral linear DNA genome suggests that its evolution involved direct descent and DNA end-region recombination events. Knowing the sequences will help understand the viral proteome and improve diagnostic test precision, therapeutics, and systems for their assessment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Esposito, Joseph J -- Sammons, Scott A -- Frace, A Michael -- Osborne, John D -- Olsen-Rasmussen, Melissa -- Zhang, Ming -- Govil, Dhwani -- Damon, Inger K -- Kline, Richard -- Laker, Miriam -- Li, Yu -- Smith, Geoffrey L -- Meyer, Hermann -- Leduc, James W -- Wohlhueter, Robert M -- G0501257/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2006 Aug 11;313(5788):807-12. Epub 2006 Jul 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biotechnology Core Facility Branch, Division of Scientific Resources, National Center for Preparedness, Detection, and Control of Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30329, USA. jesposito@cdc.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16873609" target="_blank"〉PubMed〈/a〉
    Keywords: DNA, Viral/*genetics ; Disease Outbreaks ; *Evolution, Molecular ; Gene Deletion ; *Genetic Variation ; *Genome, Viral ; Genomics ; Humans ; Molecular Sequence Data ; Open Reading Frames ; Phylogeny ; Proteome/analysis/genetics ; Recombination, Genetic ; Sequence Analysis, DNA ; Smallpox/epidemiology/mortality/*virology ; Variola virus/classification/*genetics/isolation & purification/pathogenicity ; Viral Proteins/chemistry/genetics ; Virulence/genetics
    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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