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  • 1
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    Cross-species genomics matches driver mutations and cell compartments to model ependymoma (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-07-20
    Description: Understanding the biology that underlies histologically similar but molecularly distinct subgroups of cancer has proven difficult because their defining genetic alterations are often numerous, and the cellular origins of most cancers remain unknown. We sought to decipher this heterogeneity by integrating matched genetic alterations and candidate cells of origin to generate accurate disease models. First, we identified subgroups of human ependymoma, a form of neural tumour that arises throughout the central nervous system (CNS). Subgroup-specific alterations included amplifications and homozygous deletions of genes not yet implicated in ependymoma. To select cellular compartments most likely to give rise to subgroups of ependymoma, we matched the transcriptomes of human tumours to those of mouse neural stem cells (NSCs), isolated from different regions of the CNS at different developmental stages, with an intact or deleted Ink4a/Arf locus (that encodes Cdkn2a and b). The transcriptome of human supratentorial ependymomas with amplified EPHB2 and deleted INK4A/ARF matched only that of embryonic cerebral Ink4a/Arf(-/-) NSCs. Notably, activation of Ephb2 signalling in these, but not other, NSCs generated the first mouse model of ependymoma, which is highly penetrant and accurately models the histology and transcriptome of one subgroup of human supratentorial tumour. Further, comparative analysis of matched mouse and human tumours revealed selective deregulation in the expression and copy number of genes that control synaptogenesis, pinpointing disruption of this pathway as a critical event in the production of this ependymoma subgroup. Our data demonstrate the power of cross-species genomics to meticulously match subgroup-specific driver mutations with cellular compartments to model and interrogate cancer subgroups.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2912966/" 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/PMC2912966/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johnson, Robert A -- Wright, Karen D -- Poppleton, Helen -- Mohankumar, Kumarasamypet M -- Finkelstein, David -- Pounds, Stanley B -- Rand, Vikki -- Leary, Sarah E S -- White, Elsie -- Eden, Christopher -- Hogg, Twala -- Northcott, Paul -- Mack, Stephen -- Neale, Geoffrey -- Wang, Yong-Dong -- Coyle, Beth -- Atkinson, Jennifer -- DeWire, Mariko -- Kranenburg, Tanya A -- Gillespie, Yancey -- Allen, Jeffrey C -- Merchant, Thomas -- Boop, Fredrick A -- Sanford, Robert A -- Gajjar, Amar -- Ellison, David W -- Taylor, Michael D -- Grundy, Richard G -- Gilbertson, Richard J -- P01 CA096832/CA/NCI NIH HHS/ -- P01 CA096832-06A18120/CA/NCI NIH HHS/ -- P01 CA096832-078120/CA/NCI NIH HHS/ -- P01CA96832/CA/NCI NIH HHS/ -- P30 CA021765/CA/NCI NIH HHS/ -- P30 CA021765-319030/CA/NCI NIH HHS/ -- P30CA021765/CA/NCI NIH HHS/ -- R01 CA129541/CA/NCI NIH HHS/ -- R01 CA129541-01/CA/NCI NIH HHS/ -- R01 CA129541-02/CA/NCI NIH HHS/ -- R01 CA129541-03/CA/NCI NIH HHS/ -- R01 CA129541-04/CA/NCI NIH HHS/ -- R01CA129541/CA/NCI NIH HHS/ -- T32 CA070089/CA/NCI NIH HHS/ -- England -- Nature. 2010 Jul 29;466(7306):632-6. doi: 10.1038/nature09173. Epub 2010 Jul 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Neurobiology, St Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, Tennessee 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20639864" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Compartmentation ; Central Nervous System/cytology/growth & development ; Central Nervous System Neoplasms/classification/genetics/pathology ; *Disease Models, Animal ; Ependymoma/classification/*genetics/*pathology ; Gene Deletion ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genes, p16 ; *Genomics ; Humans ; Mice ; Models, Biological ; Mutation/*genetics ; Polymorphism, Single Nucleotide/genetics ; Receptor, EphB2/genetics/metabolism ; Species Specificity ; Stem Cells/cytology/metabolism ; Synapses/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    The Amphimedon queenslandica genome and the evolution of animal complexity (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-08-06
    Description: Sponges are an ancient group of animals that diverged from other metazoans over 600 million years ago. Here we present the draft genome sequence of Amphimedon queenslandica, a demosponge from the Great Barrier Reef, and show that it is remarkably similar to other animal genomes in content, structure and organization. Comparative analysis enabled by the sequencing of the sponge genome reveals genomic events linked to the origin and early evolution of animals, including the appearance, expansion and diversification of pan-metazoan transcription factor, signalling pathway and structural genes. This diverse 'toolkit' of genes correlates with critical aspects of all metazoan body plans, and comprises cell cycle control and growth, development, somatic- and germ-cell specification, cell adhesion, innate immunity and allorecognition. Notably, many of the genes associated with the emergence of animals are also implicated in cancer, which arises from defects in basic processes associated with metazoan multicellularity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3130542/" 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/PMC3130542/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Srivastava, Mansi -- Simakov, Oleg -- Chapman, Jarrod -- Fahey, Bryony -- Gauthier, Marie E A -- Mitros, Therese -- Richards, Gemma S -- Conaco, Cecilia -- Dacre, Michael -- Hellsten, Uffe -- Larroux, Claire -- Putnam, Nicholas H -- Stanke, Mario -- Adamska, Maja -- Darling, Aaron -- Degnan, Sandie M -- Oakley, Todd H -- Plachetzki, David C -- Zhai, Yufeng -- Adamski, Marcin -- Calcino, Andrew -- Cummins, Scott F -- Goodstein, David M -- Harris, Christina -- Jackson, Daniel J -- Leys, Sally P -- Shu, Shengqiang -- Woodcroft, Ben J -- Vervoort, Michel -- Kosik, Kenneth S -- Manning, Gerard -- Degnan, Bernard M -- Rokhsar, Daniel S -- R01 HG004164/HG/NHGRI NIH HHS/ -- R01 HG004164-03/HG/NHGRI NIH HHS/ -- R01 HG004164-04/HG/NHGRI NIH HHS/ -- England -- Nature. 2010 Aug 5;466(7307):720-6. doi: 10.1038/nature09201.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Integrative Genomics and Department of Molecular and Cell Biology, University of California, Berkeley, California 94720, USA. mansi@wi.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20686567" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/genetics ; Cell Adhesion/genetics ; Cell Cycle/genetics ; Cell Polarity/genetics ; Cell Proliferation ; *Evolution, Molecular ; Genes/genetics ; Genome/*genetics ; Genomics ; Humans ; Immunity, Innate/genetics ; Models, Biological ; Neurons/metabolism ; Phosphotransferases/chemistry/genetics ; Phylogeny ; Porifera/anatomy & histology/cytology/*genetics/immunology ; Sequence Analysis, DNA ; Signal Transduction/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    A plant-like kinase in Plasmodium falciparum regulates parasite egress from erythrocytes (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-05-15
    Description: Clinical malaria is associated with the proliferation of Plasmodium parasites in human erythrocytes. The coordinated processes of parasite egress from and invasion into erythrocytes are rapid and tightly regulated. We have found that the plant-like calcium-dependent protein kinase PfCDPK5, which is expressed in invasive merozoite forms of Plasmodium falciparum, was critical for egress. Parasites deficient in PfCDPK5 arrested as mature schizonts with intact membranes, despite normal maturation of egress proteases and invasion ligands. Merozoites physically released from stalled schizonts were capable of invading new erythrocytes, separating the pathways of egress and invasion. The arrest was downstream of cyclic guanosine monophosphate-dependent protein kinase (PfPKG) function and independent of protease processing. Thus, PfCDPK5 plays an essential role during the blood stage of malaria replication.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3109083/" 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/PMC3109083/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dvorin, Jeffrey D -- Martyn, Derek C -- Patel, Saurabh D -- Grimley, Joshua S -- Collins, Christine R -- Hopp, Christine S -- Bright, A Taylor -- Westenberger, Scott -- Winzeler, Elizabeth -- Blackman, Michael J -- Baker, David A -- Wandless, Thomas J -- Duraisingh, Manoj T -- 086550/Wellcome Trust/United Kingdom -- G1000779/Medical Research Council/United Kingdom -- GM073046/GM/NIGMS NIH HHS/ -- K08 AI087874/AI/NIAID NIH HHS/ -- K12-HD000850/HD/NICHD NIH HHS/ -- MC_U117532063/Medical Research Council/United Kingdom -- R01 AI057919/AI/NIAID NIH HHS/ -- R01 AI057919-05/AI/NIAID NIH HHS/ -- R01 GM073046/GM/NIGMS NIH HHS/ -- R01AI057919/AI/NIAID NIH HHS/ -- U117532063/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 May 14;328(5980):910-2. doi: 10.1126/science.1188191.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20466936" target="_blank"〉PubMed〈/a〉
    Keywords: Calcium-Binding Proteins/chemistry/genetics/*metabolism ; Cyclic GMP-Dependent Protein Kinases/antagonists & inhibitors/metabolism ; Enzyme Inhibitors/pharmacology ; Erythrocytes/*parasitology ; Host-Parasite Interactions ; Humans ; Ligands ; Merozoites/enzymology/physiology ; Models, Biological ; Morpholines/metabolism ; Plasmodium falciparum/cytology/enzymology/growth & development/*physiology ; Protein Kinases/chemistry/genetics/*metabolism ; Protozoan Proteins/chemistry/genetics/*metabolism ; Pyridines/pharmacology ; Pyrroles/pharmacology ; Recombinant Fusion Proteins/chemistry/metabolism ; Schizonts/cytology/enzymology/physiology
    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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    The mutation spectrum revealed by paired genome sequences from a lung cancer patient (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-05-28
    Description: Lung cancer is the leading cause of cancer-related mortality worldwide, with non-small-cell lung carcinomas in smokers being the predominant form of the disease. Although previous studies have identified important common somatic mutations in lung cancers, they have primarily focused on a limited set of genes and have thus provided a constrained view of the mutational spectrum. Recent cancer sequencing efforts have used next-generation sequencing technologies to provide a genome-wide view of mutations in leukaemia, breast cancer and cancer cell lines. Here we present the complete sequences of a primary lung tumour (60x coverage) and adjacent normal tissue (46x). Comparing the two genomes, we identify a wide variety of somatic variations, including 〉50,000 high-confidence single nucleotide variants. We validated 530 somatic single nucleotide variants in this tumour, including one in the KRAS proto-oncogene and 391 others in coding regions, as well as 43 large-scale structural variations. These constitute a large set of new somatic mutations and yield an estimated 17.7 per megabase genome-wide somatic mutation rate. Notably, we observe a distinct pattern of selection against mutations within expressed genes compared to non-expressed genes and in promoter regions up to 5 kilobases upstream of all protein-coding genes. Furthermore, we observe a higher rate of amino acid-changing mutations in kinase genes. We present a comprehensive view of somatic alterations in a single lung tumour, and provide the first evidence, to our knowledge, of distinct selective pressures present within the tumour environment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, William -- Jiang, Zhaoshi -- Liu, Jinfeng -- Haverty, Peter M -- Guan, Yinghui -- Stinson, Jeremy -- Yue, Peng -- Zhang, Yan -- Pant, Krishna P -- Bhatt, Deepali -- Ha, Connie -- Johnson, Stephanie -- Kennemer, Michael I -- Mohan, Sankar -- Nazarenko, Igor -- Watanabe, Colin -- Sparks, Andrew B -- Shames, David S -- Gentleman, Robert -- de Sauvage, Frederic J -- Stern, Howard -- Pandita, Ajay -- Ballinger, Dennis G -- Drmanac, Radoje -- Modrusan, Zora -- Seshagiri, Somasekar -- Zhang, Zemin -- England -- Nature. 2010 May 27;465(7297):473-7. doi: 10.1038/nature09004.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioinformatics and Computational Biology, Genentech Inc., South San Francisco, California 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20505728" target="_blank"〉PubMed〈/a〉
    Keywords: Carcinoma, Non-Small-Cell Lung/*genetics ; DNA Mutational Analysis ; Genome, Human/*genetics ; Humans ; Lung Neoplasms/*genetics ; Male ; Middle Aged ; Models, Biological ; Point Mutation/*genetics ; Selection, Genetic/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    A novel miRNA processing pathway independent of Dicer requires Argonaute2 catalytic activity (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-05-08
    Description: Dicer is a central enzyme in microRNA (miRNA) processing. We identified a Dicer-independent miRNA biogenesis pathway that uses Argonaute2 (Ago2) slicer catalytic activity. In contrast to other miRNAs, miR-451 levels were refractory to dicer loss of function but were reduced in MZago2 (maternal-zygotic) mutants. We found that pre-miR-451 processing requires Ago2 catalytic activity in vivo. MZago2 mutants showed delayed erythropoiesis that could be rescued by wild-type Ago2 or miR-451-duplex but not by catalytically dead Ago2. Changing the secondary structure of Dicer-dependent miRNAs to mimic that of pre-miR-451 restored miRNA function and rescued developmental defects in MZdicer mutants, indicating that the pre-miRNA secondary structure determines the processing pathway in vivo. We propose that Ago2-mediated cleavage of pre-miRNAs, followed by uridylation and trimming, generates functional miRNAs independently of Dicer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3093307/" 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/PMC3093307/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cifuentes, Daniel -- Xue, Huiling -- Taylor, David W -- Patnode, Heather -- Mishima, Yuichiro -- Cheloufi, Sihem -- Ma, Enbo -- Mane, Shrikant -- Hannon, Gregory J -- Lawson, Nathan D -- Wolfe, Scot A -- Giraldez, Antonio J -- P01 CA013106/CA/NCI NIH HHS/ -- P01 CA013106-38/CA/NCI NIH HHS/ -- R01 GM081602/GM/NIGMS NIH HHS/ -- R01 GM081602-01/GM/NIGMS NIH HHS/ -- R01 GM081602-02/GM/NIGMS NIH HHS/ -- R01 GM081602-03/GM/NIGMS NIH HHS/ -- R01 GM081602-03S1/GM/NIGMS NIH HHS/ -- R01 GM081602-04/GM/NIGMS NIH HHS/ -- R01 GM101108/GM/NIGMS NIH HHS/ -- R01 HL093766/HL/NHLBI NIH HHS/ -- R01 HL093766-04/HL/NHLBI NIH HHS/ -- R01GM081602-03/03S1/GM/NIGMS NIH HHS/ -- R01HL093766/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jun 25;328(5986):1694-8. doi: 10.1126/science.1190809. Epub 2010 May 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20448148" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Argonaute Proteins ; Biocatalysis ; Embryo, Nonmammalian/metabolism ; Embryonic Development ; Erythropoiesis ; Eukaryotic Initiation Factor-2/genetics/*metabolism ; Humans ; MicroRNAs/*chemistry/*metabolism ; Models, Biological ; Morphogenesis ; Nucleic Acid Conformation ; RNA Precursors/metabolism ; RNA Processing, Post-Transcriptional ; Recombinant Proteins/metabolism ; Ribonuclease III/metabolism ; Zebrafish/embryology/genetics/*metabolism ; Zebrafish 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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  • 6
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    Cell type-specific loss of BDNF signaling mimics optogenetic control of cocaine reward (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-10-16
    Description: The nucleus accumbens is a key mediator of cocaine reward, but the distinct roles of the two subpopulations of nucleus accumbens projection neurons, those expressing dopamine D1 versus D2 receptors, are poorly understood. We show that deletion of TrkB, the brain-derived neurotrophic factor (BDNF) receptor, selectively from D1+ or D2+ neurons oppositely affects cocaine reward. Because loss of TrkB in D2+ neurons increases their neuronal excitability, we next used optogenetic tools to control selectively the firing rate of D1+ and D2+ nucleus accumbens neurons and studied consequent effects on cocaine reward. Activation of D2+ neurons, mimicking the loss of TrkB, suppresses cocaine reward, with opposite effects induced by activation of D1+ neurons. These results provide insight into the molecular control of D1+ and D2+ neuronal activity as well as the circuit-level contribution of these cell types to cocaine reward.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3011229/" 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/PMC3011229/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lobo, Mary Kay -- Covington, Herbert E 3rd -- Chaudhury, Dipesh -- Friedman, Allyson K -- Sun, HaoSheng -- Damez-Werno, Diane -- Dietz, David M -- Zaman, Samir -- Koo, Ja Wook -- Kennedy, Pamela J -- Mouzon, Ezekiell -- Mogri, Murtaza -- Neve, Rachael L -- Deisseroth, Karl -- Han, Ming-Hu -- Nestler, Eric J -- P01 DA008227/DA/NIDA NIH HHS/ -- P01 DA008227-20/DA/NIDA NIH HHS/ -- R01 DA007359/DA/NIDA NIH HHS/ -- R01 DA007359-22/DA/NIDA NIH HHS/ -- R01 DA014133/DA/NIDA NIH HHS/ -- R01 DA014133-10/DA/NIDA NIH HHS/ -- R01 DA014133-11/DA/NIDA NIH HHS/ -- R01 DA014133-12/DA/NIDA NIH HHS/ -- R01 MH051399/MH/NIMH NIH HHS/ -- R01 MH051399-19/MH/NIMH NIH HHS/ -- R01 MH051399-20/MH/NIMH NIH HHS/ -- T32 DA007135-26A2/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2010 Oct 15;330(6002):385-90. doi: 10.1126/science.1188472.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20947769" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/drug effects ; Brain-Derived Neurotrophic Factor/*metabolism ; Cocaine/*pharmacology ; Cocaine-Related Disorders/*metabolism ; Conditioning (Psychology) ; Light ; Mice ; Mice, Transgenic ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/metabolism ; Models, Biological ; Motor Activity/drug effects ; Neurons/*metabolism ; Nucleus Accumbens/cytology/*metabolism ; RNA, Messenger/genetics/metabolism ; Receptor, trkB/genetics/*metabolism ; Receptors, Dopamine D1/metabolism ; Receptors, Dopamine D2/metabolism ; *Reward ; Rhodopsin/genetics/metabolism ; *Signal Transduction
    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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  • 7
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    Thousands of chemical starting points for antimalarial lead identification (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-05-21
    Description: Malaria is a devastating infection caused by protozoa of the genus Plasmodium. Drug resistance is widespread, no new chemical class of antimalarials has been introduced into clinical practice since 1996 and there is a recent rise of parasite strains with reduced sensitivity to the newest drugs. We screened nearly 2 million compounds in GlaxoSmithKline's chemical library for inhibitors of P. falciparum, of which 13,533 were confirmed to inhibit parasite growth by at least 80% at 2 microM concentration. More than 8,000 also showed potent activity against the multidrug resistant strain Dd2. Most (82%) compounds originate from internal company projects and are new to the malaria community. Analyses using historic assay data suggest several novel mechanisms of antimalarial action, such as inhibition of protein kinases and host-pathogen interaction related targets. Chemical structures and associated data are hereby made public to encourage additional drug lead identification efforts and further research into this disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gamo, Francisco-Javier -- Sanz, Laura M -- Vidal, Jaume -- de Cozar, Cristina -- Alvarez, Emilio -- Lavandera, Jose-Luis -- Vanderwall, Dana E -- Green, Darren V S -- Kumar, Vinod -- Hasan, Samiul -- Brown, James R -- Peishoff, Catherine E -- Cardon, Lon R -- Garcia-Bustos, Jose F -- England -- Nature. 2010 May 20;465(7296):305-10. doi: 10.1038/nature09107.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tres Cantos Medicines Development Campus, GlaxoSmithKline, Severo Ochoa 2, 28760 Tres Cantos, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20485427" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antimalarials/*analysis/chemistry/*pharmacology/toxicity ; Cell Line, Tumor ; *Drug Discovery ; Drug Resistance, Multiple/drug effects ; Humans ; Malaria, Falciparum/*drug therapy/parasitology ; Models, Biological ; Phylogeny ; Plasmodium falciparum/*drug effects/enzymology/genetics/growth & development ; Small Molecule Libraries/*analysis/chemistry/*pharmacology/toxicity
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    The evolution of maximum body size of terrestrial mammals (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-11-27
    Description: The extinction of dinosaurs at the Cretaceous/Paleogene (K/Pg) boundary was the seminal event that opened the door for the subsequent diversification of terrestrial mammals. Our compilation of maximum body size at the ordinal level by sub-epoch shows a near-exponential increase after the K/Pg. On each continent, the maximum size of mammals leveled off after 40 million years ago and thereafter remained approximately constant. There was remarkable congruence in the rate, trajectory, and upper limit across continents, orders, and trophic guilds, despite differences in geological and climatic history, turnover of lineages, and ecological variation. Our analysis suggests that although the primary driver for the evolution of giant mammals was diversification to fill ecological niches, environmental temperature and land area may have ultimately constrained the maximum size achieved.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, Felisa A -- Boyer, Alison G -- Brown, James H -- Costa, Daniel P -- Dayan, Tamar -- Ernest, S K Morgan -- Evans, Alistair R -- Fortelius, Mikael -- Gittleman, John L -- Hamilton, Marcus J -- Harding, Larisa E -- Lintulaakso, Kari -- Lyons, S Kathleen -- McCain, Christy -- Okie, Jordan G -- Saarinen, Juha J -- Sibly, Richard M -- Stephens, Patrick R -- Theodor, Jessica -- Uhen, Mark D -- New York, N.Y. -- Science. 2010 Nov 26;330(6008):1216-9. doi: 10.1126/science.1194830.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, MSC03 2020, University of New Mexico, Albuquerque, NM 87131, USA. fasmith@unm.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21109666" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atmosphere ; *Biological Evolution ; *Body Size ; Ecosystem ; Environment ; Extinction, Biological ; Fossils ; Geography ; Mammals/*anatomy & histology/classification/growth & development ; Models, Biological ; Oxygen ; Phylogeny ; Temperature
    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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  • 9
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    Target RNA-directed trimming and tailing of small silencing RNAs (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-19
    Description: In Drosophila, microRNAs (miRNAs) typically guide Argonaute1 to repress messenger RNA (mRNA), whereas small interfering RNAs (siRNAs) guide Argonaute2 to destroy viral and transposon RNA. Unlike siRNAs, miRNAs rarely form extensive numbers of base pairs to the mRNAs they regulate. We find that extensive complementarity between a target RNA and an Argonaute1-bound miRNA triggers miRNA tailing and 3'-to-5' trimming. In flies, Argonaute2-bound small RNAs--but not those bound to Argonaute1--bear a 2'-O-methyl group at their 3' ends. This modification blocks target-directed small RNA remodeling: In flies lacking Hen1, the enzyme that adds the 2'-O-methyl group, Argonaute2-associated siRNAs are tailed and trimmed. Target complementarity also affects small RNA stability in human cells. These results provide an explanation for the partial complementarity between animal miRNAs and their targets.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2902985/" 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/PMC2902985/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ameres, Stefan L -- Horwich, Michael D -- Hung, Jui-Hung -- Xu, Jia -- Ghildiyal, Megha -- Weng, Zhiping -- Zamore, Phillip D -- F30AG030283/AG/NIA NIH HHS/ -- GM62862/GM/NIGMS NIH HHS/ -- GM65236/GM/NIGMS NIH HHS/ -- J 2832/Austrian Science Fund FWF/Austria -- R01 GM065236/GM/NIGMS NIH HHS/ -- R01 GM065236-08/GM/NIGMS NIH HHS/ -- R37 GM062862/GM/NIGMS NIH HHS/ -- R37 GM062862-10/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jun 18;328(5985):1534-9. doi: 10.1126/science.1187058.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20558712" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Argonaute Proteins ; *Base Pairing ; Cell Line ; Drosophila Proteins/genetics/metabolism ; Drosophila melanogaster/embryology/genetics ; Eukaryotic Initiation Factors/metabolism ; Green Fluorescent Proteins/genetics ; Humans ; Methylation ; Methyltransferases/genetics/metabolism ; MicroRNAs/chemistry/genetics/*metabolism ; Models, Biological ; RNA Caps ; *RNA Stability ; RNA, Complementary ; RNA, Messenger/chemistry/genetics/*metabolism ; RNA, Small Interfering/chemistry/genetics/*metabolism ; RNA-Induced Silencing Complex/metabolism
    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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    Terrestrial gross carbon dioxide uptake: global distribution and covariation with climate (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-07
    Description: Terrestrial gross primary production (GPP) is the largest global CO(2) flux driving several ecosystem functions. We provide an observation-based estimate of this flux at 123 +/- 8 petagrams of carbon per year (Pg C year(-1)) using eddy covariance flux data and various diagnostic models. Tropical forests and savannahs account for 60%. GPP over 40% of the vegetated land is associated with precipitation. State-of-the-art process-oriented biosphere models used for climate predictions exhibit a large between-model variation of GPP's latitudinal patterns and show higher spatial correlations between GPP and precipitation, suggesting the existence of missing processes or feedback mechanisms which attenuate the vegetation response to climate. Our estimates of spatially distributed GPP and its covariation with climate can help improve coupled climate-carbon cycle process models.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beer, Christian -- Reichstein, Markus -- Tomelleri, Enrico -- Ciais, Philippe -- Jung, Martin -- Carvalhais, Nuno -- Rodenbeck, Christian -- Arain, M Altaf -- Baldocchi, Dennis -- Bonan, Gordon B -- Bondeau, Alberte -- Cescatti, Alessandro -- Lasslop, Gitta -- Lindroth, Anders -- Lomas, Mark -- Luyssaert, Sebastiaan -- Margolis, Hank -- Oleson, Keith W -- Roupsard, Olivier -- Veenendaal, Elmar -- Viovy, Nicolas -- Williams, Christopher -- Woodward, F Ian -- Papale, Dario -- New York, N.Y. -- Science. 2010 Aug 13;329(5993):834-8. doi: 10.1126/science.1184984. Epub 2010 Jul 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biogeochemical Model-Data Integration Group, Max Planck Institute for Biogeochemistry, 07745 Jena, Germany. christian.beer@bgc-jena.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20603496" target="_blank"〉PubMed〈/a〉
    Keywords: Artificial Intelligence ; Atmosphere ; Carbon Dioxide/*metabolism ; *Climate ; Climatic Processes ; *Ecosystem ; Geography ; Models, Biological ; Models, Statistical ; Neural Networks (Computer) ; Oxygen Consumption ; *Photosynthesis ; Plant Leaves/*metabolism ; Plants/*metabolism ; Temperature ; Trees/metabolism ; Uncertainty ; Water
    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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