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  • Mutation  (380)
  • American Association for the Advancement of Science (AAAS)  (380)
  • 2010-2014  (328)
  • 1980-1984  (52)
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  • 1
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    Molecular biology. Hiding in plain sight (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2010-07-22
    Beschreibung: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3033778/" 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/PMC3033778/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosenberg, Miriam I -- Desplan, Claude -- R01 GM064864/GM/NIGMS NIH HHS/ -- R01 GM064864-07/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Jul 16;329(5989):284-5. doi: 10.1126/science.1192769.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Developmental Genetics, Department of Biology, New York University, New York, NY 10003, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20647453" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Differentiation ; Conserved Sequence ; DNA-Binding Proteins/genetics/*metabolism ; Drosophila Proteins/*genetics/metabolism ; Drosophila melanogaster/embryology/*genetics ; Embryo, Nonmammalian/*metabolism ; Epidermis/cytology ; Evolution, Molecular ; *Gene Expression Regulation, Developmental ; Genes, Insect ; Mutation ; Peptides/*genetics/metabolism ; Protein Processing, Post-Translational ; RNA, Untranslated/*genetics ; Transcription Factors/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)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Arsenic trioxide controls the fate of the PML-RARalpha oncoprotein by directly binding PML (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2010-04-10
    Beschreibung: Arsenic, an ancient drug used in traditional Chinese medicine, has attracted worldwide interest because it shows substantial anticancer activity in patients with acute promyelocytic leukemia (APL). Arsenic trioxide (As2O3) exerts its therapeutic effect by promoting degradation of an oncogenic protein that drives the growth of APL cells, PML-RARalpha (a fusion protein containing sequences from the PML zinc finger protein and retinoic acid receptor alpha). PML and PML-RARalpha degradation is triggered by their SUMOylation, but the mechanism by which As2O3 induces this posttranslational modification is unclear. Here we show that arsenic binds directly to cysteine residues in zinc fingers located within the RBCC domain of PML-RARalpha and PML. Arsenic binding induces PML oligomerization, which increases its interaction with the small ubiquitin-like protein modifier (SUMO)-conjugating enzyme UBC9, resulting in enhanced SUMOylation and degradation. The identification of PML as a direct target of As2O3 provides new insights into the drug's mechanism of action and its specificity for APL.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Xiao-Wei -- Yan, Xiao-Jing -- Zhou, Zi-Ren -- Yang, Fei-Fei -- Wu, Zi-Yu -- Sun, Hong-Bin -- Liang, Wen-Xue -- Song, Ai-Xin -- Lallemand-Breitenbach, Valerie -- Jeanne, Marion -- Zhang, Qun-Ye -- Yang, Huai-Yu -- Huang, Qiu-Hua -- Zhou, Guang-Biao -- Tong, Jian-Hua -- Zhang, Yan -- Wu, Ji-Hui -- Hu, Hong-Yu -- de The, Hugues -- Chen, Sai-Juan -- Chen, Zhu -- New York, N.Y. -- Science. 2010 Apr 9;328(5975):240-3. doi: 10.1126/science.1183424.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Rui Jin Hospital affiliated to Shanghai Jiao Tong University School of Medicine, 197 Rui Jin Road II, Shanghai 200025, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20378816" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Arsenic/*metabolism ; Arsenicals/*metabolism/*pharmacology ; Cell Line ; Humans ; Leukemia, Promyelocytic, Acute/drug therapy/genetics ; Mutant Proteins/chemistry/metabolism ; Mutation ; Nuclear Proteins/chemistry/genetics/*metabolism ; Oncogene Proteins, Fusion/chemistry/genetics/*metabolism ; Oxazines/metabolism ; Oxides/*metabolism/*pharmacology ; Protein Conformation ; Protein Multimerization ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Receptors, Retinoic Acid/metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Small Ubiquitin-Related Modifier Proteins/metabolism ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; Transcription Factors/chemistry/genetics/*metabolism ; Tumor Suppressor Proteins/chemistry/genetics/*metabolism ; Ubiquitination ; Zinc Fingers
    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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  • 3
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    Cytoplasmic partitioning of P granule components is not required to specify the germline in C. elegans (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2010-12-04
    Beschreibung: Asymmetric segregation of P granules during the first four divisions of the Caenorhabditis elegans embryo is a classic example of cytoplasmic partitioning of germline determinants. It is thought that asymmetric partitioning of P granule components during mitosis is essential to distinguish germline from soma. We have identified a mutant (pptr-1) in which P granules become unstable during mitosis and P granule proteins and RNAs are distributed equally to somatic and germline blastomeres. Despite symmetric partitioning of P granule components, pptr-1 mutants segregate a germline that uniquely expresses P granules during postembryonic development. pptr-1 mutants are fertile, except at high temperatures. Hence, asymmetric partitioning of maternal P granules is not essential to specify germ cell fate. Instead, it may serve to protect the nascent germline from stress.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3072820/" 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/PMC3072820/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gallo, Christopher M -- Wang, Jennifer T -- Motegi, Fumio -- Seydoux, Geraldine -- GM080042/GM/NIGMS NIH HHS/ -- HD007276/HD/NICHD NIH HHS/ -- HD037047/HD/NICHD NIH HHS/ -- R01 HD037047/HD/NICHD NIH HHS/ -- R01 HD037047-12/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Dec 17;330(6011):1685-9. doi: 10.1126/science.1193697. Epub 2010 Dec 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Howard Hughes Medical Institute, Center for Cell Dynamics, Johns Hopkins School of Medicine, 725 North Wolfe Street, PCTB 706, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21127218" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Blastomeres/*physiology ; Caenorhabditis elegans/*embryology/genetics/metabolism ; Caenorhabditis elegans Proteins/genetics/*metabolism/physiology ; Cytoplasm/*metabolism ; Cytoplasmic Granules/*physiology/ultrastructure ; Embryo, Nonmammalian/physiology ; Embryonic Development ; Germ Cells/*physiology ; Interphase ; Microscopy, Confocal ; Mitosis ; Mutation ; Nuclear Proteins/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; RNA, Helminth/*metabolism ; RNA-Binding Proteins/metabolism ; Recombinant Fusion Proteins/metabolism ; Zygote/physiology
    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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  • 4
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    Rewiring of genetic networks in response to DNA damage (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2010-12-04
    Beschreibung: Although cellular behaviors are dynamic, the networks that govern these behaviors have been mapped primarily as static snapshots. Using an approach called differential epistasis mapping, we have discovered widespread changes in genetic interaction among yeast kinases, phosphatases, and transcription factors as the cell responds to DNA damage. Differential interactions uncover many gene functions that go undetected in static conditions. They are very effective at identifying DNA repair pathways, highlighting new damage-dependent roles for the Slt2 kinase, Pph3 phosphatase, and histone variant Htz1. The data also reveal that protein complexes are generally stable in response to perturbation, but the functional relations between these complexes are substantially reorganized. Differential networks chart a new type of genetic landscape that is invaluable for mapping cellular responses to stimuli.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3006187/" 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/PMC3006187/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bandyopadhyay, Sourav -- Mehta, Monika -- Kuo, Dwight -- Sung, Min-Kyung -- Chuang, Ryan -- Jaehnig, Eric J -- Bodenmiller, Bernd -- Licon, Katherine -- Copeland, Wilbert -- Shales, Michael -- Fiedler, Dorothea -- Dutkowski, Janusz -- Guenole, Aude -- van Attikum, Haico -- Shokat, Kevan M -- Kolodner, Richard D -- Huh, Won-Ki -- Aebersold, Ruedi -- Keogh, Michael-Christopher -- Krogan, Nevan J -- Ideker, Trey -- P30CA013330/CA/NCI NIH HHS/ -- P50 GM081879/GM/NIGMS NIH HHS/ -- R01 ES014811/ES/NIEHS NIH HHS/ -- R01 ES014811-01A1/ES/NIEHS NIH HHS/ -- R01 ES014811-02/ES/NIEHS NIH HHS/ -- R01 ES014811-02S1/ES/NIEHS NIH HHS/ -- R01 ES014811-03/ES/NIEHS NIH HHS/ -- R01 ES014811-04/ES/NIEHS NIH HHS/ -- R01 ES014811-05/ES/NIEHS NIH HHS/ -- R01 ES014811-05S1/ES/NIEHS NIH HHS/ -- R01 ES014811-06/ES/NIEHS NIH HHS/ -- R01 GM026017/GM/NIGMS NIH HHS/ -- R01 GM084279/GM/NIGMS NIH HHS/ -- R01 GM084279-01A1/GM/NIGMS NIH HHS/ -- R01 GM084279-02/GM/NIGMS NIH HHS/ -- R01 GM084279-02S1/GM/NIGMS NIH HHS/ -- R01 GM084279-03/GM/NIGMS NIH HHS/ -- R01 GM084279-04/GM/NIGMS NIH HHS/ -- R01 GM084448/GM/NIGMS NIH HHS/ -- R01-ES14811/ES/NIEHS NIH HHS/ -- R01-GM084279/GM/NIGMS NIH HHS/ -- R37 GM026017/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Dec 3;330(6009):1385-9. doi: 10.1126/science.1195618.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, 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/21127252" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Chromatin/metabolism ; *DNA Damage ; DNA Repair/*genetics ; DNA, Fungal/genetics ; *Epistasis, Genetic ; *Gene Regulatory Networks ; Genes, Fungal ; Histones/genetics/metabolism ; Methyl Methanesulfonate/pharmacology ; Mitogen-Activated Protein Kinases/genetics/metabolism ; Mutagens/pharmacology ; Mutation ; Phosphoprotein Phosphatases/genetics/metabolism ; Protein Interaction Mapping ; Protein-Serine-Threonine Kinases/genetics/metabolism ; Saccharomyces cerevisiae/*genetics/*metabolism ; Saccharomyces cerevisiae Proteins/genetics/*metabolism ; Signal Transduction ; Transcription Factors/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)
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    Selection at linked sites shapes heritable phenotypic variation in C. elegans (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2010-10-16
    Beschreibung: Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, whereas mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTLs) influencing transcript abundance traits in a cross of two Caenorhabditis elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3138179/" 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/PMC3138179/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rockman, Matthew V -- Skrovanek, Sonja S -- Kruglyak, Leonid -- P50 GM071508/GM/NIGMS NIH HHS/ -- P50 GM071508-01/GM/NIGMS NIH HHS/ -- R01 GM089972/GM/NIGMS NIH HHS/ -- R01 GM089972-02/GM/NIGMS NIH HHS/ -- R01 HG004321/HG/NHGRI NIH HHS/ -- R01 HG004321-01/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Oct 15;330(6002):372-6. doi: 10.1126/science.1194208.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology and Center for Genomics and Systems Biology, New York University, 100 Washington Square East, New York, NY 10003, USA. mrockman@nyu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20947766" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alleles ; Animals ; Caenorhabditis elegans/*genetics/physiology ; Chromosome Mapping ; Chromosomes/*genetics ; Crosses, Genetic ; Evolution, Molecular ; Gene Expression ; Genes, Helminth ; *Genetic Variation ; Logistic Models ; Models, Genetic ; Mutation ; Oligonucleotide Array Sequence Analysis ; Phenotype ; Polymorphism, Single Nucleotide ; Population Density ; *Quantitative Trait Loci ; *Quantitative Trait, Heritable ; Recombination, Genetic ; *Selection, Genetic
    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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    Cell biology. Septins at the nexus (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2010-09-11
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barral, Yves -- New York, N.Y. -- Science. 2010 Sep 10;329(5997):1289-90. doi: 10.1126/science.1195445.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Biochemistry, ETH Zurich, 8093 Zurich, Switzerland. yves.barral@bc.biol.ethz.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20829470" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Membrane/metabolism/ultrastructure ; *Cell Polarity ; Centrioles/metabolism ; Cilia/*metabolism/ultrastructure ; Cytoskeletal Proteins/chemistry/*metabolism ; Diffusion ; GTP-Binding Proteins/chemistry/*metabolism ; Glycoproteins/genetics/metabolism ; Hedgehog Proteins/metabolism ; Humans ; Mutant Proteins/metabolism ; Mutation ; Receptors, Cell Surface/metabolism ; Signal Transduction ; Xenopus Proteins/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)
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
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    Darwinian evolution of prions in cell culture (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2010-01-02
    Beschreibung: Prions are infectious proteins consisting mainly of PrP(Sc), a beta sheet-rich conformer of the normal host protein PrP(C), and occur in different strains. Strain identity is thought to be encoded by PrP(Sc) conformation. We found that biologically cloned prion populations gradually became heterogeneous by accumulating "mutants," and selective pressures resulted in the emergence of different mutants as major constituents of the evolving population. Thus, when transferred from brain to cultured cells, "cell-adapted" prions outcompeted their "brain-adapted" counterparts, and the opposite occurred when prions were returned from cells to brain. Similarly, the inhibitor swainsonine selected for a resistant substrain, whereas, in its absence, the susceptible substrain outgrew its resistant counterpart. Prions, albeit devoid of a nucleic acid genome, are thus subject to mutation and selective amplification.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2848070/" 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/PMC2848070/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Jiali -- Browning, Shawn -- Mahal, Sukhvir P -- Oelschlegel, Anja M -- Weissmann, Charles -- NS059543/NS/NINDS NIH HHS/ -- R01 NS059543/NS/NINDS NIH HHS/ -- R01 NS059543-01/NS/NINDS NIH HHS/ -- R01 NS059543-02/NS/NINDS NIH HHS/ -- R01 NS067214/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2010 Feb 12;327(5967):869-72. doi: 10.1126/science.1183218. Epub 2009 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Infectology, Scripps Florida, 130 Scripps Way, Jupiter, FL 33458, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20044542" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Brain Chemistry ; Cell Line ; Cell Line, Tumor ; Culture Media ; Culture Media, Conditioned ; *Evolution, Molecular ; Mice ; Mice, Inbred C57BL ; Mutation ; *PrPSc Proteins/chemistry/classification/pathogenicity ; Prion Diseases ; Prions/chemistry/classification/*pathogenicity/*physiology ; Protein Conformation ; Swainsonine/pharmacology
    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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  • 8
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    The genetic landscape of a cell (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2010-01-23
    Beschreibung: A genome-scale genetic interaction map was constructed by examining 5.4 million gene-gene pairs for synthetic genetic interactions, generating quantitative genetic interaction profiles for approximately 75% of all genes in the budding yeast, Saccharomyces cerevisiae. A network based on genetic interaction profiles reveals a functional map of the cell in which genes of similar biological processes cluster together in coherent subsets, and highly correlated profiles delineate specific pathways to define gene function. The global network identifies functional cross-connections between all bioprocesses, mapping a cellular wiring diagram of pleiotropy. Genetic interaction degree correlated with a number of different gene attributes, which may be informative about genetic network hubs in other organisms. We also demonstrate that extensive and unbiased mapping of the genetic landscape provides a key for interpretation of chemical-genetic interactions and drug target identification.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Costanzo, Michael -- Baryshnikova, Anastasia -- Bellay, Jeremy -- Kim, Yungil -- Spear, Eric D -- Sevier, Carolyn S -- Ding, Huiming -- Koh, Judice L Y -- Toufighi, Kiana -- Mostafavi, Sara -- Prinz, Jeany -- St Onge, Robert P -- VanderSluis, Benjamin -- Makhnevych, Taras -- Vizeacoumar, Franco J -- Alizadeh, Solmaz -- Bahr, Sondra -- Brost, Renee L -- Chen, Yiqun -- Cokol, Murat -- Deshpande, Raamesh -- Li, Zhijian -- Lin, Zhen-Yuan -- Liang, Wendy -- Marback, Michaela -- Paw, Jadine -- San Luis, Bryan-Joseph -- Shuteriqi, Ermira -- Tong, Amy Hin Yan -- van Dyk, Nydia -- Wallace, Iain M -- Whitney, Joseph A -- Weirauch, Matthew T -- Zhong, Guoqing -- Zhu, Hongwei -- Houry, Walid A -- Brudno, Michael -- Ragibizadeh, Sasan -- Papp, Balazs -- Pal, Csaba -- Roth, Frederick P -- Giaever, Guri -- Nislow, Corey -- Troyanskaya, Olga G -- Bussey, Howard -- Bader, Gary D -- Gingras, Anne-Claude -- Morris, Quaid D -- Kim, Philip M -- Kaiser, Chris A -- Myers, Chad L -- Andrews, Brenda J -- Boone, Charles -- 084314/Wellcome Trust/United Kingdom -- GSP-41567/Canadian Institutes of Health Research/Canada -- R01 HG003224/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2010 Jan 22;327(5964):425-31. doi: 10.1126/science.1180823.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Banting and Best Department of Medical Research, Terrence Donnelly Centre for Cellular and Biomolecular Research, University of Toronto, Toronto, Ontario M5S 3E1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20093466" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Computational Biology ; Gene Duplication ; Gene Expression Regulation, Fungal ; *Gene Regulatory Networks ; Genes, Fungal ; Genetic Fitness ; *Genome, Fungal ; Metabolic Networks and Pathways ; Mutation ; Protein Interaction Mapping ; Saccharomyces cerevisiae/*genetics/*metabolism/physiology ; Saccharomyces cerevisiae Proteins/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)
    Standort Signatur Erwartet Verfügbarkeit
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  • 9
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    Changing face of microglia (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2010-11-06
    Beschreibung: Microglia are resident brain cells that sense pathological tissue alterations. They can develop into brain macrophages and perform immunological functions. However, expression of immune proteins by microglia is not synonymous with inflammation, because these molecules can have central nervous system (CNS)-specific roles. Through their involvement in pain mechanisms, microglia also respond to external threats. Experimental studies support the idea that microglia have a role in the maintenance of synaptic integrity. Analogous to electricians, they are capable of removing defunct axon terminals, thereby helping neuronal connections to stay intact. Microglia in healthy CNS tissue do not qualify as macrophages, and their specific functions are beginning to be explored.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Graeber, Manuel B -- New York, N.Y. -- Science. 2010 Nov 5;330(6005):783-8. doi: 10.1126/science.1190929.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Brain and Mind Research Institute, University of Sydney, Camperdown, NSW 2050, Australia. manuel@graeber.net〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21051630" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Behavior ; Behavior, Animal ; Bone Marrow Transplantation ; Brain/*cytology/pathology/physiology ; Brain Diseases/pathology/physiopathology/therapy ; Humans ; Macrophages/cytology/physiology ; Mental Disorders/physiopathology ; Microglia/immunology/*physiology ; Mutation ; Neuralgia/physiopathology ; Neurodegenerative Diseases/pathology/physiopathology/therapy ; Signal Transduction ; Spinal Cord/*cytology/pathology/physiology ; Synapses/physiology
    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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    The genetic map of Artemisia annua L. identifies loci affecting yield of the antimalarial drug artemisinin (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2010-01-16
    Beschreibung: Artemisinin is a plant natural product produced by Artemisia annua and the active ingredient in the most effective treatment for malaria. Efforts to eradicate malaria are increasing demand for an affordable, high-quality, robust supply of artemisinin. We performed deep sequencing on the transcriptome of A. annua to identify genes and markers for fast-track breeding. Extensive genetic variation enabled us to build a detailed genetic map with nine linkage groups. Replicated field trials resulted in a quantitative trait loci (QTL) map that accounts for a significant amount of the variation in key traits controlling artemisinin yield. Enrichment for positive QTLs in parents of new high-yielding hybrids confirms that the knowledge and tools to convert A. annua into a robust crop are now available.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Graham, Ian A -- Besser, Katrin -- Blumer, Susan -- Branigan, Caroline A -- Czechowski, Tomasz -- Elias, Luisa -- Guterman, Inna -- Harvey, David -- Isaac, Peter G -- Khan, Awais M -- Larson, Tony R -- Li, Yi -- Pawson, Tanya -- Penfield, Teresa -- Rae, Anne M -- Rathbone, Deborah A -- Reid, Sonja -- Ross, Joe -- Smallwood, Margaret F -- Segura, Vincent -- Townsend, Theresa -- Vyas, Darshna -- Winzer, Thilo -- Bowles, Dianna -- New York, N.Y. -- Science. 2010 Jan 15;327(5963):328-31. doi: 10.1126/science.1182612.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Novel Agricultural Products, Department of Biology, University of York, York YO10 5YW, UK. iag1@york.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20075252" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Antimalarials/*metabolism ; Artemisia/*genetics/*metabolism ; Artemisinins/*metabolism ; *Chromosome Mapping ; Crosses, Genetic ; DNA, Complementary ; Gene Expression Profiling ; *Genes, Plant ; Genetic Association Studies ; Humans ; Malaria/drug therapy ; Mutation ; Phenotype ; Polymorphism, Single Nucleotide ; *Quantitative Trait Loci ; Sequence Analysis, DNA
    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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