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  • Articles  (16)
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  • American Association for the Advancement of Science (AAAS)  (16)
  • American Association for the Advancement of Science
  • American Chemical Society
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  • 2010-2014  (16)
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  • 1
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    Dysregulated humoral immunity to nontyphoidal Salmonella in HIV-infected African adults (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-04-24
    Description: Nontyphoidal Salmonellae are a major cause of life-threatening bacteremia among HIV-infected individuals. Although cell-mediated immunity controls intracellular infection, antibodies protect against Salmonella bacteremia. We report that high-titer antibodies specific for Salmonella lipopolysaccharide (LPS) are associated with a lack of Salmonella-killing in HIV-infected African adults. Killing was restored by genetically shortening LPS from the target Salmonella or removing LPS-specific antibodies from serum. Complement-mediated killing of Salmonella by healthy serum is shown to be induced specifically by antibodies against outer membrane proteins. This killing is lost when excess antibody against Salmonella LPS is added. Thus, our study indicates that impaired immunity against nontyphoidal Salmonella bacteremia in HIV infection results from excess inhibitory antibodies against Salmonella LPS, whereas serum killing of Salmonella is induced by antibodies against outer membrane proteins.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3772309/" 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/PMC3772309/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉MacLennan, Calman A -- Gilchrist, James J -- Gordon, Melita A -- Cunningham, Adam F -- Cobbold, Mark -- Goodall, Margaret -- Kingsley, Robert A -- van Oosterhout, Joep J G -- Msefula, Chisomo L -- Mandala, Wilson L -- Leyton, Denisse L -- Marshall, Jennifer L -- Gondwe, Esther N -- Bobat, Saeeda -- Lopez-Macias, Constantino -- Doffinger, Rainer -- Henderson, Ian R -- Zijlstra, Eduard E -- Dougan, Gordon -- Drayson, Mark T -- MacLennan, Ian C M -- Molyneux, Malcolm E -- 067321/Wellcome Trust/United Kingdom -- BB/F022778/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0701275/Medical Research Council/United Kingdom -- G108/574/Medical Research Council/United Kingdom -- G8402371/Medical Research Council/United Kingdom -- G9818340/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2010 Apr 23;328(5977):508-12. doi: 10.1126/science.1180346.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Centre for Immune Regulation and Clinical Immunology Service, Institute of Biomedical Research, School of Immunity and Infection, University of Birmingham, Birmingham, UK. c.maclennan@bham.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20413503" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS-Related Opportunistic Infections/immunology ; Adult ; Animals ; Antibodies, Bacterial/blood/*immunology ; Antibodies, Blocking/blood/*immunology ; Bacteremia/immunology ; Bacterial Outer Membrane Proteins/*immunology ; Complement Activation ; Disease Susceptibility ; HIV Infections/complications/*immunology ; Humans ; Immunoglobulin G/blood/immunology ; Lipopolysaccharides/blood/*immunology ; Malawi ; Mice ; Mutation ; O Antigens/*immunology ; Salmonella Infections/*immunology ; Salmonella typhimurium/genetics/*immunology
    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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    The genetic landscape of a cell (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-23
    Description: 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〉
    Keywords: 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
    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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    Analysis of genetic inheritance in a family quartet by whole-genome sequencing (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-12
    Description: We analyzed the whole-genome sequences of a family of four, consisting of two siblings and their parents. Family-based sequencing allowed us to delineate recombination sites precisely, identify 70% of the sequencing errors (resulting in 〉 99.999% accuracy), and identify very rare single-nucleotide polymorphisms. We also directly estimated a human intergeneration mutation rate of approximately 1.1 x 10(-8) per position per haploid genome. Both offspring in this family have two recessive disorders: Miller syndrome, for which the gene was concurrently identified, and primary ciliary dyskinesia, for which causative genes have been previously identified. Family-based genome analysis enabled us to narrow the candidate genes for both of these Mendelian disorders to only four. Our results demonstrate the value of complete genome sequencing in families.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3037280/" 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/PMC3037280/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roach, Jared C -- Glusman, Gustavo -- Smit, Arian F A -- Huff, Chad D -- Hubley, Robert -- Shannon, Paul T -- Rowen, Lee -- Pant, Krishna P -- Goodman, Nathan -- Bamshad, Michael -- Shendure, Jay -- Drmanac, Radoje -- Jorde, Lynn B -- Hood, Leroy -- Galas, David J -- GM076547/GM/NIGMS NIH HHS/ -- P50 GM076547/GM/NIGMS NIH HHS/ -- P50 GM076547-05/GM/NIGMS NIH HHS/ -- R01 HG002939/HG/NHGRI NIH HHS/ -- R01 HG002939-08/HG/NHGRI NIH HHS/ -- R01GM081083/GM/NIGMS NIH HHS/ -- R01HD048895/HD/NICHD NIH HHS/ -- R01HL094976/HL/NHLBI NIH HHS/ -- RC2HG005608/HG/NHGRI NIH HHS/ -- RZ1HG004749/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2010 Apr 30;328(5978):636-9. doi: 10.1126/science.1186802. Epub 2010 Mar 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Systems Biology, Seattle, WA 98103, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20220176" target="_blank"〉PubMed〈/a〉
    Keywords: Abnormalities, Multiple/*genetics ; Algorithms ; Alleles ; Axonemal Dyneins/genetics ; Ciliary Motility Disorders/*genetics ; Crossing Over, Genetic ; Female ; Genes, Dominant ; Genes, Recessive ; Genetic Association Studies ; *Genome, Human ; Humans ; *Inheritance Patterns ; Limb Deformities, Congenital/genetics ; Male ; Mandibulofacial Dysostosis/genetics ; Mutation ; *Nuclear Family ; Oxidoreductases Acting on CH-CH Group Donors/genetics ; Pedigree ; Polymorphism, Single Nucleotide ; *Sequence Analysis, DNA ; Syndrome
    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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    Acetylation of metabolic enzymes coordinates carbon source utilization and metabolic flux (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-02-20
    Description: Lysine acetylation regulates many eukaryotic cellular processes, but its function in prokaryotes is largely unknown. We demonstrated that central metabolism enzymes in Salmonella were acetylated extensively and differentially in response to different carbon sources, concomitantly with changes in cell growth and metabolic flux. The relative activities of key enzymes controlling the direction of glycolysis versus gluconeogenesis and the branching between citrate cycle and glyoxylate bypass were all regulated by acetylation. This modulation is mainly controlled by a pair of lysine acetyltransferase and deacetylase, whose expressions are coordinated with growth status. Reversible acetylation of metabolic enzymes ensure that cells respond environmental changes via promptly sensing cellular energy status and flexibly altering reaction rates or directions. It represents a metabolic regulatory mechanism conserved from bacteria to mammals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4183141/" 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/PMC4183141/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Qijun -- Zhang, Yakun -- Yang, Chen -- Xiong, Hui -- Lin, Yan -- Yao, Jun -- Li, Hong -- Xie, Lu -- Zhao, Wei -- Yao, Yufeng -- Ning, Zhi-Bin -- Zeng, Rong -- Xiong, Yue -- Guan, Kun-Liang -- Zhao, Shimin -- Zhao, Guo-Ping -- R01 CA068377/CA/NCI NIH HHS/ -- R01 CA163834/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Feb 19;327(5968):1004-7. doi: 10.1126/science.1179687.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Genetic Engineering, Department of Microbiology, School of Life Sciences and Institute of Biomedical Sciences, Fudan University, Shanghai 200032, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20167787" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Acetyltransferases/chemistry/genetics/metabolism ; Amino Acid Sequence ; Bacterial Proteins/*metabolism ; Citric Acid/*metabolism ; Energy Metabolism ; Enzymes/*metabolism ; Gene Expression Regulation, Bacterial ; *Gluconeogenesis ; Glucose/*metabolism ; Glyceraldehyde-3-Phosphate Dehydrogenases/metabolism ; *Glycolysis ; Group III Histone Deacetylases/genetics/metabolism ; Isocitrate Lyase/metabolism ; Lysine/metabolism ; Metabolic Networks and Pathways ; Multienzyme Complexes/metabolism ; Mutation ; Protein Processing, Post-Translational ; Protein-Serine-Threonine Kinases/metabolism ; Recombinant Proteins/metabolism ; Salmonella typhimurium/enzymology/genetics/growth & development/*metabolism
    Print ISSN: 0036-8075
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  • 5
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    Peptidomimetic antibiotics target outer-membrane biogenesis in Pseudomonas aeruginosa (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-02-20
    Description: Antibiotics with new mechanisms of action are urgently required to combat the growing health threat posed by resistant pathogenic microorganisms. We synthesized a family of peptidomimetic antibiotics based on the antimicrobial peptide protegrin I. Several rounds of optimization gave a lead compound that was active in the nanomolar range against Gram-negative Pseudomonas spp., but was largely inactive against other Gram-negative and Gram-positive bacteria. Biochemical and genetic studies showed that the peptidomimetics had a non-membrane-lytic mechanism of action and identified a homolog of the beta-barrel protein LptD (Imp/OstA), which functions in outer-membrane biogenesis, as a cellular target. The peptidomimetic showed potent antimicrobial activity in a mouse septicemia infection model. Drug-resistant strains of Pseudomonas are a serious health problem, so this family of antibiotics may have important therapeutic applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Srinivas, Nityakalyani -- Jetter, Peter -- Ueberbacher, Bernhard J -- Werneburg, Martina -- Zerbe, Katja -- Steinmann, Jessica -- Van der Meijden, Benjamin -- Bernardini, Francesca -- Lederer, Alexander -- Dias, Ricardo L A -- Misson, Pauline E -- Henze, Heiko -- Zumbrunn, Jurg -- Gombert, Frank O -- Obrecht, Daniel -- Hunziker, Peter -- Schauer, Stefan -- Ziegler, Urs -- Kach, Andres -- Eberl, Leo -- Riedel, Kathrin -- DeMarco, Steven J -- Robinson, John A -- New York, N.Y. -- Science. 2010 Feb 19;327(5968):1010-3. doi: 10.1126/science.1182749.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Chemistry Department, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20167788" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/chemical synthesis/metabolism/*pharmacology ; Antimicrobial Cationic Peptides/chemistry ; Bacterial Outer Membrane Proteins/chemistry/genetics/*metabolism ; Cell Membrane/*metabolism ; Drug Design ; Drug Resistance, Bacterial/genetics ; Genes, Bacterial ; Lipopolysaccharides/metabolism ; Mice ; Microbial Sensitivity Tests ; Molecular Mimicry ; Mutation ; Peptide Library ; Peptides/chemical synthesis/chemistry/metabolism/*pharmacology ; Protein Structure, Tertiary ; Pseudomonas Infections/drug therapy/microbiology ; Pseudomonas aeruginosa/*drug effects/growth & ; development/*metabolism/ultrastructure ; Sepsis/drug therapy/microbiology
    Print ISSN: 0036-8075
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  • 6
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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
    Publication Date: 2010-10-16
    Description: 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〉
    Keywords: 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
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  • 7
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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
    Publication Date: 2010-01-16
    Description: 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〉
    Keywords: 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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Permissive secondary mutations enable the evolution of influenza oseltamivir resistance (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-05
    Description: The His274--〉Tyr274 (H274Y) mutation confers oseltamivir resistance on N1 influenza neuraminidase but had long been thought to compromise viral fitness. However, beginning in 2007-2008, viruses containing H274Y rapidly became predominant among human seasonal H1N1 isolates. We show that H274Y decreases the amount of neuraminidase that reaches the cell surface and that this defect can be counteracted by secondary mutations that also restore viral fitness. Two such mutations occurred in seasonal H1N1 shortly before the widespread appearance of H274Y. The evolution of oseltamivir resistance was therefore enabled by "permissive" mutations that allowed the virus to tolerate subsequent occurrences of H274Y. An understanding of this process may provide a basis for predicting the evolution of oseltamivir resistance in other influenza strains.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2913718/" 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/PMC2913718/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bloom, Jesse D -- Gong, Lizhi Ian -- Baltimore, David -- P01 CA132681/CA/NCI NIH HHS/ -- P01 CA132681-01A27259/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Jun 4;328(5983):1272-5. doi: 10.1126/science.1187816.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20522774" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; Antiviral Agents/*pharmacology ; Cell Line ; Cell Line, Tumor ; Cell Membrane/metabolism ; Drug Resistance, Viral/*genetics ; *Evolution, Molecular ; Genes, Viral ; Genetic Fitness ; Humans ; Influenza A Virus, H1N1 Subtype/*drug effects/*genetics/growth & development ; Influenza, Human/drug therapy/*virology ; Mutation ; Neuraminidase/antagonists & inhibitors/chemistry/genetics/metabolism ; Oseltamivir/*pharmacology ; Phylogeny ; Selection, Genetic
    Print ISSN: 0036-8075
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  • 9
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    Genotype to phenotype: a complex problem (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-04-24
    Description: We generated a high-resolution whole-genome sequence and individually deleted 5100 genes in Sigma1278b, a Saccharomyces cerevisiae strain closely related to reference strain S288c. Similar to the variation between human individuals, Sigma1278b and S288c average 3.2 single-nucleotide polymorphisms per kilobase. A genome-wide comparison of deletion mutant phenotypes identified a subset of genes that were conditionally essential by strain, including 44 essential genes unique to Sigma1278b and 13 unique to S288c. Genetic analysis indicates the conditional phenotype was most often governed by complex genetic interactions, depending on multiple background-specific modifiers. Our comprehensive analysis suggests that the presence of a complex set of modifiers will often underlie the phenotypic differences between individuals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4412269/" 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/PMC4412269/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dowell, Robin D -- Ryan, Owen -- Jansen, An -- Cheung, Doris -- Agarwala, Sudeep -- Danford, Timothy -- Bernstein, Douglas A -- Rolfe, P Alexander -- Heisler, Lawrence E -- Chin, Brian -- Nislow, Corey -- Giaever, Guri -- Phillips, Patrick C -- Fink, Gerald R -- Gifford, David K -- Boone, Charles -- DK076284/DK/NIDDK NIH HHS/ -- GM035010/GM/NIGMS NIH HHS/ -- GM069676/GM/NIGMS NIH HHS/ -- P01 NS055923/NS/NINDS NIH HHS/ -- R01 GM035010/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Apr 23;328(5977):469. doi: 10.1126/science.1189015.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Computer Science and Artificial Intelligence Laboratory, Department of Electrical Engineering and Computer Science, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20413493" target="_blank"〉PubMed〈/a〉
    Keywords: Crosses, Genetic ; Gene Deletion ; *Gene Expression Regulation, Fungal ; Gene Regulatory Networks ; *Genes, Essential ; *Genes, Fungal ; Genetic Variation ; Genome, Fungal ; Genotype ; Mutation ; Phenotype ; Saccharomyces cerevisiae/*genetics ; Sequence Analysis, DNA
    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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  • 10
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    RTEL-1 enforces meiotic crossover interference and homeostasis (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-06
    Description: Meiotic crossovers (COs) are tightly regulated to ensure that COs on the same chromosome are distributed far apart (crossover interference, COI) and that at least one CO is formed per homolog pair (CO homeostasis). CO formation is controlled in part during meiotic double-strand break (DSB) creation in Caenorhabditis elegans, but a second level of control must also exist because meiotic DSBs outnumber COs. We show that the antirecombinase RTEL-1 is required to prevent excess meiotic COs, probably by promoting meiotic synthesis-dependent strand annealing. Two distinct classes of meiotic COs are increased in rtel-1 mutants, and COI and homeostasis are compromised. We propose that RTEL-1 implements the second level of CO control by promoting noncrossovers.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4770885/" 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/PMC4770885/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Youds, Jillian L -- Mets, David G -- McIlwraith, Michael J -- Martin, Julie S -- Ward, Jordan D -- ONeil, Nigel J -- Rose, Ann M -- West, Stephen C -- Meyer, Barbara J -- Boulton, Simon J -- Canadian Institutes of Health Research/Canada -- Cancer Research UK/United Kingdom -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Mar 5;327(5970):1254-8. doi: 10.1126/science.1183112.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉DNA Damage Response Laboratory, London Research Institute, Cancer Research UK, Clare Hall, South Mimms, EN6 3LD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20203049" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*genetics/physiology ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Chromatids/genetics ; Chromosomal Proteins, Non-Histone/genetics/metabolism ; *Crossing Over, Genetic ; DNA Breaks, Double-Stranded ; DNA Helicases/genetics/*metabolism ; DNA Repair ; DNA, Helminth/genetics/metabolism ; Homeostasis ; *Meiosis ; Mutation ; Polymorphism, Single Nucleotide ; X Chromosome/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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