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  • 1
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    Structure of a beta1-adrenergic G-protein-coupled receptor (2008)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2008-07-03
    Beschreibung: G-protein-coupled receptors have a major role in transmembrane signalling in most eukaryotes and many are important drug targets. Here we report the 2.7 A resolution crystal structure of a beta(1)-adrenergic receptor in complex with the high-affinity antagonist cyanopindolol. The modified turkey (Meleagris gallopavo) receptor was selected to be in its antagonist conformation and its thermostability improved by earlier limited mutagenesis. The ligand-binding pocket comprises 15 side chains from amino acid residues in 4 transmembrane alpha-helices and extracellular loop 2. This loop defines the entrance of the ligand-binding pocket and is stabilized by two disulphide bonds and a sodium ion. Binding of cyanopindolol to the beta(1)-adrenergic receptor and binding of carazolol to the beta(2)-adrenergic receptor involve similar interactions. A short well-defined helix in cytoplasmic loop 2, not observed in either rhodopsin or the beta(2)-adrenergic receptor, directly interacts by means of a tyrosine with the highly conserved DRY motif at the end of helix 3 that is essential for receptor activation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2923055/" 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/PMC2923055/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Warne, Tony -- Serrano-Vega, Maria J -- Baker, Jillian G -- Moukhametzianov, Rouslan -- Edwards, Patricia C -- Henderson, Richard -- Leslie, Andrew G W -- Tate, Christopher G -- Schertler, Gebhard F X -- MC_U105178937/Medical Research Council/United Kingdom -- MC_U105184322/Medical Research Council/United Kingdom -- MC_U105184325/Medical Research Council/United Kingdom -- MC_U105197215/Medical Research Council/United Kingdom -- U.1051.04.020(78937)/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2008 Jul 24;454(7203):486-91. doi: 10.1038/nature07101. Epub 2008 Jun 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Laboratory of Molecular Biology, Hills Road, Cambridge CB2 0QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18594507" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adrenergic beta-1 Receptor Agonists ; Adrenergic beta-1 Receptor Antagonists ; Adrenergic beta-Antagonists/chemistry/metabolism ; Amino Acid Motifs ; Animals ; Binding Sites ; Crystallization ; Crystallography, X-Ray ; Ligands ; Models, Molecular ; Mutant Proteins/chemistry/genetics/metabolism ; Mutation ; Pindolol/analogs & derivatives/chemistry/metabolism ; Propanolamines/chemistry/metabolism ; Protein Conformation ; Receptors, Adrenergic, beta-1/*chemistry/metabolism ; Thermodynamics ; Turkeys
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Stem-cell claim gets cold reception (2008)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2008-03-14
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cyranoski, David -- Baker, Monya -- England -- Nature. 2008 Mar 13;452(7184):132. doi: 10.1038/452132a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18337778" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adult ; Adult Stem Cells/*cytology ; Embryonic Stem Cells/*cytology ; Endocytosis ; Genetic Vectors ; Humans ; Male ; *Nanotubes, Carbon/adverse effects ; Peer Review, Research/standards ; Pluripotent Stem Cells/*cytology ; Reproducibility of Results ; Spermatozoa/cytology ; Time Factors ; Transfection/instrumentation/*methods ; Uncertainty
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Nerve cells made from elderly patient's skin cells (2008)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2008-08-08
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baker, Monya -- England -- Nature. 2008 Aug 7;454(7205):675. doi: 10.1038/454675b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18685662" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Aged, 80 and over ; Amyotrophic Lateral Sclerosis/genetics/*pathology/surgery ; Animals ; Cellular Reprogramming ; Disease Models, Animal ; Female ; Humans ; Male ; Mice ; Neurons/*cytology/metabolism/transplantation ; Pluripotent Stem Cells/*cytology/metabolism/transplantation ; Skin/*cytology/metabolism ; Stem Cell Transplantation/contraindications
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    Tumours spark stem-cell review (2009)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2009-02-25
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baker, Monya -- England -- Nature. 2009 Feb 19;457(7232):941. doi: 10.1038/457941a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19238682" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adolescent ; Ataxia Telangiectasia/*surgery ; Brain Neoplasms/*etiology ; Brain Tissue Transplantation/*adverse effects ; Child ; Clinical Trials as Topic/standards/trends ; Fetal Tissue Transplantation/*adverse effects ; Fetus/cytology ; Humans ; Internationality ; Male ; Moscow ; Neurons/cytology/*transplantation ; Spinal Cord Neoplasms/*etiology ; Stem Cell Transplantation/*adverse effects
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    Evolutionary history of Salmonella typhi (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-11-25
    Beschreibung: For microbial pathogens, phylogeographic differentiation seems to be relatively common. However, the neutral population structure of Salmonella enterica serovar Typhi reflects the continued existence of ubiquitous haplotypes over millennia. In contrast, clinical use of fluoroquinolones has yielded at least 15 independent gyrA mutations within a decade and stimulated clonal expansion of haplotype H58 in Asia and Africa. Yet, antibiotic-sensitive strains and haplotypes other than H58 still persist despite selection for antibiotic resistance. Neutral evolution in Typhi appears to reflect the asymptomatic carrier state, and adaptive evolution depends on the rapid transmission of phenotypic changes through acute infections.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2652035/" 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/PMC2652035/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roumagnac, Philippe -- Weill, Francois-Xavier -- Dolecek, Christiane -- Baker, Stephen -- Brisse, Sylvain -- Chinh, Nguyen Tran -- Le, Thi Anh Hong -- Acosta, Camilo J -- Farrar, Jeremy -- Dougan, Gordon -- Achtman, Mark -- 076962/Wellcome Trust/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2006 Nov 24;314(5803):1301-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur Infektionsbiologie, Department of Molecular Biology, Chariteplatz 1, 10117 Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17124322" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adaptation, Physiological ; Africa ; Alleles ; Anti-Bacterial Agents/pharmacology/therapeutic use ; Asia ; *Biological Evolution ; Carrier State/*microbiology ; DNA Gyrase/genetics ; Drug Resistance, Bacterial ; Drug Resistance, Multiple, Bacterial ; Fluoroquinolones/pharmacology/therapeutic use ; *Genes, Bacterial ; Genetic Variation ; Haplotypes ; Humans ; Molecular Sequence Data ; Mutation ; Polymorphism, Genetic ; Polymorphism, Single Nucleotide ; Salmonella typhi/drug effects/*genetics ; Selection, Genetic ; Typhoid Fever/drug therapy/*microbiology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
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    A common variant on chromosome 9p21 affects the risk of myocardial infarction (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2007-05-05
    Beschreibung: The global endemic of cardiovascular diseases calls for improved risk assessment and treatment. Here, we describe an association between myocardial infarction (MI) and a common sequence variant on chromosome 9p21. This study included a total of 4587 cases and 12,767 controls. The identified variant, adjacent to the tumor suppressor genes CDKN2A and CDKN2B, was associated with the disease with high significance. Approximately 21% of individuals in the population are homozygous for this variant, and their estimated risk of suffering myocardial infarction is 1.64 times as great as that of noncarriers. The corresponding risk is 2.02 times as great for early-onset cases. The population attributable risk is 21% for MI in general and 31% for early-onset cases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Helgadottir, Anna -- Thorleifsson, Gudmar -- Manolescu, Andrei -- Gretarsdottir, Solveig -- Blondal, Thorarinn -- Jonasdottir, Aslaug -- Jonasdottir, Adalbjorg -- Sigurdsson, Asgeir -- Baker, Adam -- Palsson, Arnar -- Masson, Gisli -- Gudbjartsson, Daniel F -- Magnusson, Kristinn P -- Andersen, Karl -- Levey, Allan I -- Backman, Valgerdur M -- Matthiasdottir, Sigurborg -- Jonsdottir, Thorbjorg -- Palsson, Stefan -- Einarsdottir, Helga -- Gunnarsdottir, Steinunn -- Gylfason, Arnaldur -- Vaccarino, Viola -- Hooper, W Craig -- Reilly, Muredach P -- Granger, Christopher B -- Austin, Harland -- Rader, Daniel J -- Shah, Svati H -- Quyyumi, Arshed A -- Gulcher, Jeffrey R -- Thorgeirsson, Gudmundur -- Thorsteinsdottir, Unnur -- Kong, Augustine -- Stefansson, Kari -- New York, N.Y. -- Science. 2007 Jun 8;316(5830):1491-3. Epub 2007 May 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉deCODE genetics, Sturlugata 8, IS-101 Reykjavik, Iceland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17478679" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Age of Onset ; Aged ; Case-Control Studies ; Chromosome Mapping ; Chromosomes, Human, Pair 9/*genetics ; Coronary Artery Disease/genetics ; Female ; Genes, p16 ; *Genetic Predisposition to Disease ; *Genetic Variation ; Genotype ; Haplotypes ; Heterozygote ; Homozygote ; Humans ; Linkage Disequilibrium ; Male ; Middle Aged ; Myocardial Infarction/*genetics ; *Polymorphism, Single Nucleotide ; Risk Factors
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
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    Rare structural variants disrupt multiple genes in neurodevelopmental pathways in schizophrenia (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2008-03-29
    Beschreibung: Schizophrenia is a devastating neurodevelopmental disorder whose genetic influences remain elusive. We hypothesize that individually rare structural variants contribute to the illness. Microdeletions and microduplications 〉100 kilobases were identified by microarray comparative genomic hybridization of genomic DNA from 150 individuals with schizophrenia and 268 ancestry-matched controls. All variants were validated by high-resolution platforms. Novel deletions and duplications of genes were present in 5% of controls versus 15% of cases and 20% of young-onset cases, both highly significant differences. The association was independently replicated in patients with childhood-onset schizophrenia as compared with their parents. Mutations in cases disrupted genes disproportionately from signaling networks controlling neurodevelopment, including neuregulin and glutamate pathways. These results suggest that multiple, individually rare mutations altering genes in neurodevelopmental pathways contribute to schizophrenia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walsh, Tom -- McClellan, Jon M -- McCarthy, Shane E -- Addington, Anjene M -- Pierce, Sarah B -- Cooper, Greg M -- Nord, Alex S -- Kusenda, Mary -- Malhotra, Dheeraj -- Bhandari, Abhishek -- Stray, Sunday M -- Rippey, Caitlin F -- Roccanova, Patricia -- Makarov, Vlad -- Lakshmi, B -- Findling, Robert L -- Sikich, Linmarie -- Stromberg, Thomas -- Merriman, Barry -- Gogtay, Nitin -- Butler, Philip -- Eckstrand, Kristen -- Noory, Laila -- Gochman, Peter -- Long, Robert -- Chen, Zugen -- Davis, Sean -- Baker, Carl -- Eichler, Evan E -- Meltzer, Paul S -- Nelson, Stanley F -- Singleton, Andrew B -- Lee, Ming K -- Rapoport, Judith L -- King, Mary-Claire -- Sebat, Jonathan -- HD043569/HD/NICHD NIH HHS/ -- M01 RR000046/RR/NCRR NIH HHS/ -- MH061355/MH/NIMH NIH HHS/ -- MH061464/MH/NIMH NIH HHS/ -- MH061528/MH/NIMH NIH HHS/ -- NS052108/NS/NINDS NIH HHS/ -- R01 HD043569/HD/NICHD NIH HHS/ -- RR000046/RR/NCRR NIH HHS/ -- RR025014/RR/NCRR NIH HHS/ -- U01 MH061355/MH/NIMH NIH HHS/ -- U01 MH061464/MH/NIMH NIH HHS/ -- U01 MH061528/MH/NIMH NIH HHS/ -- U24 NS052108/NS/NINDS NIH HHS/ -- UL1 RR025014/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2008 Apr 25;320(5875):539-43. doi: 10.1126/science.1155174. Epub 2008 Mar 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18369103" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adolescent ; Adult ; Age of Onset ; Amino Acid Sequence ; Brain/cytology/*growth & development/metabolism ; Case-Control Studies ; Child ; Excitatory Amino Acid Transporter 1/chemistry/genetics/physiology ; Female ; *Gene Deletion ; *Gene Duplication ; Genetic Predisposition to Disease ; Genome, Human ; Humans ; Male ; Molecular Sequence Data ; *Mutation ; Neurons/cytology/physiology ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Single Nucleotide ; Receptor, Epidermal Growth Factor/chemistry/genetics/physiology ; Receptor, ErbB-4 ; Schizophrenia/*genetics/physiopathology ; Signal Transduction
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 8
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    The Neurospora checkpoint kinase 2: a regulatory link between the circadian and cell cycles (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2006-07-01
    Beschreibung: The clock gene period-4 (prd-4) in Neurospora was identified by a single allele displaying shortened circadian period and altered temperature compensation. Positional cloning followed by functional tests show that PRD-4 is an ortholog of mammalian checkpoint kinase 2 (Chk2). Expression of prd-4 is regulated by the circadian clock and, reciprocally, PRD-4 physically interacts with the clock component FRQ, promoting its phosphorylation. DNA-damaging agents can reset the clock in a manner that depends on time of day, and this resetting is dependent on PRD-4. Thus, prd-4, the Neurospora Chk2, identifies a molecular link that feeds back conditionally from circadian output to input and the cell cycle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pregueiro, Antonio M -- Liu, Qiuyun -- Baker, Christopher L -- Dunlap, Jay C -- Loros, Jennifer J -- MH44651/MH/NIMH NIH HHS/ -- P01 GM068087/GM/NIGMS NIH HHS/ -- R01 GM034985/GM/NIGMS NIH HHS/ -- R37GM34985/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Aug 4;313(5787):644-9. Epub 2006 Jun 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Dartmouth Medical School, Hanover, NH 03755, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16809488" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; *Cell Cycle ; Checkpoint Kinase 2 ; *Circadian Rhythm ; Cloning, Molecular ; DNA Damage ; Feedback, Physiological ; Fungal Proteins/chemistry/genetics/metabolism ; Gene Expression Regulation, Fungal ; Genes, Fungal ; Methyl Methanesulfonate/pharmacology ; Molecular Sequence Data ; Mutation ; Neurospora/*enzymology/genetics ; Neurospora crassa/cytology/*enzymology/*physiology ; Phosphorylation ; Protein-Serine-Threonine Kinases/chemistry/*genetics/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 9
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    An antifungal agent inhibits an aminoacyl-tRNA synthetase by trapping tRNA in the editing site (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2007-06-26
    Beschreibung: Aminoacyl-transfer RNA (tRNA) synthetases, which catalyze the attachment of the correct amino acid to its corresponding tRNA during translation of the genetic code, are proven antimicrobial drug targets. We show that the broad-spectrum antifungal 5-fluoro-1,3-dihydro-1-hydroxy-2,1-benzoxaborole (AN2690), in development for the treatment of onychomycosis, inhibits yeast cytoplasmic leucyl-tRNA synthetase by formation of a stable tRNA(Leu)-AN2690 adduct in the editing site of the enzyme. Adduct formation is mediated through the boron atom of AN2690 and the 2'- and 3'-oxygen atoms of tRNA's3'-terminal adenosine. The trapping of enzyme-bound tRNA(Leu) in the editing site prevents catalytic turnover, thus inhibiting synthesis of leucyl-tRNA(Leu) and consequentially blocking protein synthesis. This result establishes the editing site as a bona fide target for aminoacyl-tRNA synthetase inhibitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rock, Fernando L -- Mao, Weimin -- Yaremchuk, Anya -- Tukalo, Mikhail -- Crepin, Thibaut -- Zhou, Huchen -- Zhang, Yong-Kang -- Hernandez, Vincent -- Akama, Tsutomu -- Baker, Stephen J -- Plattner, Jacob J -- Shapiro, Lucy -- Martinis, Susan A -- Benkovic, Stephen J -- Cusack, Stephen -- Alley, M R K -- R01 DE16835/DE/NIDCR NIH HHS/ -- New York, N.Y. -- Science. 2007 Jun 22;316(5832):1759-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Anacor Pharmaceuticals, Incorporated, 1060 East Meadow Circle, Palo Alto, CA 94303, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17588934" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Antifungal Agents/chemistry/*pharmacology ; Bicyclo Compounds, Heterocyclic/chemistry/*pharmacology ; Boron/chemistry ; Boron Compounds/chemistry/*pharmacology ; Drug Resistance, Fungal/genetics ; Enzyme Inhibitors/chemistry/*pharmacology ; Leucine-tRNA Ligase/*antagonists & inhibitors/genetics/metabolism ; Mutation ; Protein Synthesis Inhibitors/chemistry/pharmacology ; *RNA Editing/drug effects ; RNA, Transfer, Leu/*antagonists & inhibitors/metabolism ; Saccharomyces cerevisiae/drug effects/enzymology/genetics
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 10
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    An inhibitor of FtsZ with potent and selective anti-staphylococcal activity (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2008-09-20
    Beschreibung: FtsZ is an essential bacterial guanosine triphosphatase and homolog of mammalian beta-tubulin that polymerizes and assembles into a ring to initiate cell division. We have created a class of small synthetic antibacterials, exemplified by PC190723, which inhibits FtsZ and prevents cell division. PC190723 has potent and selective in vitro bactericidal activity against staphylococci, including methicillin- and multi-drug-resistant Staphylococcus aureus. The putative inhibitor-binding site of PC190723 was mapped to a region of FtsZ that is analogous to the Taxol-binding site of tubulin. PC190723 was efficacious in an in vivo model of infection, curing mice infected with a lethal dose of S. aureus. The data validate FtsZ as a target for antibacterial intervention and identify PC190723 as suitable for optimization into a new anti-staphylococcal therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haydon, David J -- Stokes, Neil R -- Ure, Rebecca -- Galbraith, Greta -- Bennett, James M -- Brown, David R -- Baker, Patrick J -- Barynin, Vladimir V -- Rice, David W -- Sedelnikova, Sveta E -- Heal, Jonathan R -- Sheridan, Joseph M -- Aiwale, Sachin T -- Chauhan, Pramod K -- Srivastava, Anil -- Taneja, Amit -- Collins, Ian -- Errington, Jeff -- Czaplewski, Lloyd G -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2008 Sep 19;321(5896):1673-5. doi: 10.1126/science.1159961.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Prolysis, Begbroke Science Park, Oxfordshire OX5 1PF, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18801997" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Anti-Bacterial Agents/*pharmacology/therapeutic use ; Bacillus subtilis/chemistry/*drug effects/genetics ; Bacterial Proteins/*antagonists & inhibitors/chemistry/genetics/metabolism ; Binding Sites ; Cell Division/drug effects ; Crystallography, X-Ray ; Cytoskeletal Proteins/*antagonists & inhibitors/chemistry/genetics/metabolism ; Drug Resistance, Bacterial/genetics ; Drug Resistance, Multiple, Bacterial ; Ligands ; Methicillin Resistance ; Mice ; Microbial Sensitivity Tests ; Models, Molecular ; Molecular Sequence Data ; Mutation ; Protein Conformation ; Pyridines/chemistry/metabolism/*pharmacology/therapeutic use ; Staphylococcal Infections/*drug therapy ; Staphylococcus aureus/chemistry/*drug effects ; Thiazoles/chemistry/metabolism/*pharmacology/therapeutic use ; Tubulin/chemistry/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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