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  • Cell Line  (25)
  • *Biological Evolution  (23)
  • American Association for the Advancement of Science (AAAS)  (47)
  • 2005-2009  (47)
  • 2006  (47)
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  • American Association for the Advancement of Science (AAAS)  (47)
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  • 2005-2009  (47)
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  • 1
    Publication Date: 2006-09-02
    Description: Draft genome sequences have been determined for the soybean pathogen Phytophthora sojae and the sudden oak death pathogen Phytophthora ramorum. Oomycetes such as these Phytophthora species share the kingdom Stramenopila with photosynthetic algae such as diatoms, and the presence of many Phytophthora genes of probable phototroph origin supports a photosynthetic ancestry for the stramenopiles. Comparison of the two species' genomes reveals a rapid expansion and diversification of many protein families associated with plant infection such as hydrolases, ABC transporters, protein toxins, proteinase inhibitors, and, in particular, a superfamily of 700 proteins with similarity to known oomycete avirulence genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tyler, Brett M -- Tripathy, Sucheta -- Zhang, Xuemin -- Dehal, Paramvir -- Jiang, Rays H Y -- Aerts, Andrea -- Arredondo, Felipe D -- Baxter, Laura -- Bensasson, Douda -- Beynon, Jim L -- Chapman, Jarrod -- Damasceno, Cynthia M B -- Dorrance, Anne E -- Dou, Daolong -- Dickerman, Allan W -- Dubchak, Inna L -- Garbelotto, Matteo -- Gijzen, Mark -- Gordon, Stuart G -- Govers, Francine -- Grunwald, Niklaus J -- Huang, Wayne -- Ivors, Kelly L -- Jones, Richard W -- Kamoun, Sophien -- Krampis, Konstantinos -- Lamour, Kurt H -- Lee, Mi-Kyung -- McDonald, W Hayes -- Medina, Monica -- Meijer, Harold J G -- Nordberg, Eric K -- Maclean, Donald J -- Ospina-Giraldo, Manuel D -- Morris, Paul F -- Phuntumart, Vipaporn -- Putnam, Nicholas H -- Rash, Sam -- Rose, Jocelyn K C -- Sakihama, Yasuko -- Salamov, Asaf A -- Savidor, Alon -- Scheuring, Chantel F -- Smith, Brian M -- Sobral, Bruno W S -- Terry, Astrid -- Torto-Alalibo, Trudy A -- Win, Joe -- Xu, Zhanyou -- Zhang, Hongbin -- Grigoriev, Igor V -- Rokhsar, Daniel S -- Boore, Jeffrey L -- BB/C509123/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2006 Sep 1;313(5791):1261-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Virginia Bioinformatics Institute, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061, USA. bmtyler@vt.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16946064" target="_blank"〉PubMed〈/a〉
    Keywords: Algal Proteins/genetics/physiology ; *Biological Evolution ; DNA, Algal/*genetics ; Genes ; *Genome ; Hydrolases/genetics/metabolism ; Photosynthesis/genetics ; Phylogeny ; Physical Chromosome Mapping ; Phytophthora/classification/*genetics/*pathogenicity/physiology ; Plant Diseases/microbiology ; Polymorphism, Single Nucleotide ; Repetitive Sequences, Nucleic Acid ; Sequence Analysis, DNA ; Symbiosis ; Toxins, Biological/genetics
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2006-07-01
    Description: Axonal guidance and vascular patterning share several guidance cues, including proteins in the netrin family. We demonstrate that netrins stimulate proliferation, migration, and tube formation of human endothelial cells in vitro and that this stimulation is independent of known netrin receptors. Suppression of netrin1a messenger RNA in zebrafish inhibits vascular sprouting, implying a proangiogenic role for netrins during vertebrate development. We also show that netrins accelerate neovascularization in an in vivo model of ischemia and that they reverse neuropathy and vasculopathy in a diabetic murine model. We propose that the attractive vascular and neural guidance functions of netrins offer a unique therapeutic potential.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2577078/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2577078/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, Brent D -- Ii, Masaaki -- Park, Kye Won -- Suli, Arminda -- Sorensen, Lise K -- Larrieu-Lahargue, Frederic -- Urness, Lisa D -- Suh, Wonhee -- Asai, Jun -- Kock, Gerhardus A H -- Thorne, Tina -- Silver, Marcy -- Thomas, Kirk R -- Chien, Chi-Bin -- Losordo, Douglas W -- Li, Dean Y -- R01 HL068873/HL/NHLBI NIH HHS/ -- R01 HL077671/HL/NHLBI NIH HHS/ -- R01 HL077671-03/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2006 Aug 4;313(5787):640-4. Epub 2006 Jun 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Human Molecular Biology and Genetics, University of Utah, Salt Lake City, UT 84112, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16809490" target="_blank"〉PubMed〈/a〉
    Keywords: Angiogenesis Inducing Agents ; Animals ; Cell Line ; Cell Movement ; Chemotaxis ; DNA, Complementary ; Diabetic Angiopathies/therapy ; Diabetic Neuropathies/therapy ; Embryo, Nonmammalian ; Endothelial Cells/*physiology ; Endothelium, Vascular/cytology ; Genetic Therapy ; Humans ; Ischemia/drug therapy ; Mice ; Muscle, Skeletal/blood supply ; *Neovascularization, Physiologic ; Nerve Growth Factors/genetics/pharmacology/*physiology ; Neural Conduction ; Receptors, Cell Surface/physiology ; Tumor Suppressor Proteins/genetics/pharmacology/*physiology ; Vascular Endothelial Growth Factor A/therapeutic use ; Zebrafish
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2006-11-18
    Description: Our knowledge of Neanderthals is based on a limited number of remains and artifacts from which we must make inferences about their biology, behavior, and relationship to ourselves. Here, we describe the characterization of these extinct hominids from a new perspective, based on the development of a Neanderthal metagenomic library and its high-throughput sequencing and analysis. Several lines of evidence indicate that the 65,250 base pairs of hominid sequence so far identified in the library are of Neanderthal origin, the strongest being the ascertainment of sequence identities between Neanderthal and chimpanzee at sites where the human genomic sequence is different. These results enabled us to calculate the human-Neanderthal divergence time based on multiple randomly distributed autosomal loci. Our analyses suggest that on average the Neanderthal genomic sequence we obtained and the reference human genome sequence share a most recent common ancestor approximately 706,000 years ago, and that the human and Neanderthal ancestral populations split approximately 370,000 years ago, before the emergence of anatomically modern humans. Our finding that the Neanderthal and human genomes are at least 99.5% identical led us to develop and successfully implement a targeted method for recovering specific ancient DNA sequences from metagenomic libraries. This initial analysis of the Neanderthal genome advances our understanding of the evolutionary relationship of Homo sapiens and Homo neanderthalensis and signifies the dawn of Neanderthal genomics.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2583069/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2583069/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Noonan, James P -- Coop, Graham -- Kudaravalli, Sridhar -- Smith, Doug -- Krause, Johannes -- Alessi, Joe -- Chen, Feng -- Platt, Darren -- Paabo, Svante -- Pritchard, Jonathan K -- Rubin, Edward M -- 1-F32-GM074367/GM/NIGMS NIH HHS/ -- HL066681/HL/NHLBI NIH HHS/ -- R01 HG002772/HG/NHGRI NIH HHS/ -- R01 HG002772-01/HG/NHGRI NIH HHS/ -- R01 HG002772-1/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2006 Nov 17;314(5802):1113-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉U.S. Department of Energy Joint Genome Institute, 2800 Mitchell Drive, Walnut Creek, CA 94598, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17110569" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Bone and Bones ; Cell Nucleus ; DNA/*genetics/isolation & purification ; DNA, Mitochondrial ; *Fossils ; Gene Pool ; Genome ; Genome, Human ; Genomic Library ; History, Ancient ; Hominidae/*genetics ; Humans ; Male ; Molecular Sequence Data ; Pan troglodytes/genetics ; Polymerase Chain Reaction ; Sequence Alignment ; *Sequence Analysis, DNA/methods ; Time
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  • 4
    Publication Date: 2006-04-29
    Description: Store-operated Ca2+ entry is mediated by Ca2+ release-activated Ca2+ (CRAC) channels following Ca2+ release from intracellular stores. We performed a genome-wide RNA interference (RNAi) screen in Drosophila cells to identify proteins that inhibit store-operated Ca2+ influx. A secondary patch-clamp screen identified CRACM1 and CRACM2 (CRAC modulators 1 and 2) as modulators of Drosophila CRAC currents. We characterized the human ortholog of CRACM1, a plasma membrane-resident protein encoded by gene FLJ14466. Although overexpression of CRACM1 did not affect CRAC currents, RNAi-mediated knockdown disrupted its activation. CRACM1 could be the CRAC channel itself, a subunit of it, or a component of the CRAC signaling machinery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vig, M -- Peinelt, C -- Beck, A -- Koomoa, D L -- Rabah, D -- Koblan-Huberson, M -- Kraft, S -- Turner, H -- Fleig, A -- Penner, R -- Kinet, J-P -- 5-R37-GM053950/GM/NIGMS NIH HHS/ -- R01-AI050200/AI/NIAID NIH HHS/ -- R01-GM065360/GM/NIGMS NIH HHS/ -- R01-NS040927/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 May 26;312(5777):1220-3. Epub 2006 Apr 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA. mvig@bidmc.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645049" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channels/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Drosophila Proteins/*genetics/*metabolism ; Drosophila melanogaster/*metabolism ; Endoplasmic Reticulum/metabolism ; Humans ; Ion Transport ; Jurkat Cells ; Membrane Proteins/genetics/*metabolism ; Patch-Clamp Techniques ; RNA Interference ; RNA, Small Interfering ; Reverse Transcriptase Polymerase Chain Reaction
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  • 5
    Publication Date: 2006-09-30
    Description: To pursue a systematic approach to the discovery of functional connections among diseases, genetic perturbation, and drug action, we have created the first installment of a reference collection of gene-expression profiles from cultured human cells treated with bioactive small molecules, together with pattern-matching software to mine these data. We demonstrate that this "Connectivity Map" resource can be used to find connections among small molecules sharing a mechanism of action, chemicals and physiological processes, and diseases and drugs. These results indicate the feasibility of the approach and suggest the value of a large-scale community Connectivity Map project.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamb, Justin -- Crawford, Emily D -- Peck, David -- Modell, Joshua W -- Blat, Irene C -- Wrobel, Matthew J -- Lerner, Jim -- Brunet, Jean-Philippe -- Subramanian, Aravind -- Ross, Kenneth N -- Reich, Michael -- Hieronymus, Haley -- Wei, Guo -- Armstrong, Scott A -- Haggarty, Stephen J -- Clemons, Paul A -- Wei, Ru -- Carr, Steven A -- Lander, Eric S -- Golub, Todd R -- New York, N.Y. -- Science. 2006 Sep 29;313(5795):1929-35.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02142, USA. justin@broad.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17008526" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/drug therapy/genetics ; Cell Line ; Cell Line, Tumor ; *Databases, Factual ; Dexamethasone/pharmacology/therapeutic use ; Drug Evaluation, Preclinical/*methods ; Drug Resistance, Neoplasm ; Enzyme Inhibitors/pharmacology ; Estrogens/pharmacology ; Gene Expression/*drug effects ; *Gene Expression Profiling ; HSP90 Heat-Shock Proteins/antagonists & inhibitors ; Histone Deacetylase Inhibitors ; Humans ; Limonins/pharmacology ; Obesity/genetics/physiopathology ; Oligonucleotide Array Sequence Analysis ; Phenothiazines/pharmacology ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug ; therapy/genetics/physiopathology ; Sirolimus/pharmacology/therapeutic use ; Software
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  • 6
    Publication Date: 2006-04-22
    Description: G protein betagamma subunits have potential as a target for therapeutic treatment of a number of diseases. We performed virtual docking of a small-molecule library to a site on Gbetagamma subunits that mediates protein interactions. We hypothesized that differential targeting of this surface could allow for selective modulation of Gbetagamma subunit functions. Several compounds bound to Gbetagamma subunits with affinities from 0.1 to 60 muM and selectively modulated functional Gbetagamma-protein-protein interactions in vitro, chemotactic peptide signaling pathways in HL-60 leukocytes, and opioid receptor-dependent analgesia in vivo. These data demonstrate an approach for modulation of G protein-coupled receptor signaling that may represent an important therapeutic strategy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonacci, Tabetha M -- Mathews, Jennifer L -- Yuan, Chujun -- Lehmann, David M -- Malik, Sundeep -- Wu, Dianqing -- Font, Jose L -- Bidlack, Jean M -- Smrcka, Alan V -- GM60286/GM/NIGMS NIH HHS/ -- HL-T3207949/HL/NHLBI NIH HHS/ -- HL080706/HL/NHLBI NIH HHS/ -- K05-DA00360/DA/NIDA NIH HHS/ -- R01 CA132317/CA/NCI NIH HHS/ -- R01 GM054597/GM/NIGMS NIH HHS/ -- R01 GM054597-09/GM/NIGMS NIH HHS/ -- R01 HL080706/HL/NHLBI NIH HHS/ -- R01 HL080706-10/HL/NHLBI NIH HHS/ -- R01 HL080706-11/HL/NHLBI NIH HHS/ -- T32DA07232/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2006 Apr 21;312(5772):443-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16627746" target="_blank"〉PubMed〈/a〉
    Keywords: Analgesics/pharmacology ; Animals ; Binding Sites ; Binding, Competitive ; Cell Line ; Computer Simulation ; Cyclohexanes/chemistry/*metabolism/*pharmacology ; Drug Evaluation, Preclinical/*methods ; Enzyme-Linked Immunosorbent Assay ; G-Protein-Coupled Receptor Kinase 2 ; GTP-Binding Protein alpha Subunits/metabolism ; GTP-Binding Protein beta Subunits/chemistry/*metabolism ; GTP-Binding Protein gamma Subunits/chemistry/*metabolism ; HL-60 Cells ; Humans ; Isoenzymes/metabolism ; Mice ; Mice, Inbred ICR ; Mitogen-Activated Protein Kinases/metabolism ; Molecular Structure ; Morphine/pharmacology ; N-Formylmethionine Leucyl-Phenylalanine/metabolism ; Peptide Library ; Peptides/*metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phospholipase C beta ; Protein Binding ; Protein Interaction Mapping ; *Signal Transduction ; Software ; Structure-Activity Relationship ; Type C Phospholipases/metabolism ; Xanthenes/chemistry/*metabolism/*pharmacology ; beta-Adrenergic Receptor Kinases/metabolism
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  • 7
    Publication Date: 2006-10-21
    Description: Diverse bacterial and viral pathogens induce actin polymerization in the cytoplasm of host cells to facilitate infection. Here, we describe a pathogenic mechanism for promoting dynamic actin assembly in the nucleus to enable viral replication. The baculovirus Autographa californica multiple nucleopolyhedrovirus induced nuclear actin polymerization by translocating the host actin-nucleating Arp2/3 complex into the nucleus, where it was activated by p78/83, a viral Wiskott-Aldrich syndrome protein (WASP)-like protein. Nuclear actin assembly by p78/83 and Arp2/3 complex was essential for viral progeny production. Recompartmentalizing dynamic host actin may represent a conserved mode of pathogenesis and reflect viral manipulation of normal functions of nuclear actin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goley, Erin D -- Ohkawa, Taro -- Mancuso, Joel -- Woodruff, Jeffrey B -- D'Alessio, Joseph A -- Cande, W Zacheus -- Volkman, Loy E -- Welch, Matthew D -- AI054693/AI/NIAID NIH HHS/ -- GM59609/GM/NIGMS NIH HHS/ -- R01 GM059609/GM/NIGMS NIH HHS/ -- R01 GM059609-07/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 20;314(5798):464-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17053146" target="_blank"〉PubMed〈/a〉
    Keywords: Actin-Related Protein 2-3 Complex/*metabolism ; Actins/*metabolism ; Animals ; Biopolymers/metabolism ; Cell Line ; Cell Nucleus/*metabolism ; Fluorescence Recovery After Photobleaching ; Moths ; Mutation ; Nucleocapsid/metabolism/ultrastructure ; Nucleopolyhedrovirus/genetics/*physiology ; Transfection ; Viral Proteins/chemistry/genetics/isolation & purification/*metabolism ; Virion/ultrastructure ; Virus Replication ; Wiskott-Aldrich Syndrome Protein/chemistry
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  • 8
    Publication Date: 2006-01-21
    Description: The stable propagation of genetic material during cell division depends on the congression of chromosomes to the spindle equator before the cell initiates anaphase. It is generally assumed that congression requires that chromosomes are connected to the opposite poles of the bipolar spindle ("bioriented"). In mammalian cells, we found that chromosomes can congress before becoming bioriented. By combining the use of reversible chemical inhibitors, live-cell light microscopy, and correlative electron microscopy, we found that monooriented chromosomes could glide toward the spindle equator alongside kinetochore fibers attached to other already bioriented chromosomes. This congression mechanism depended on the kinetochore-associated, plus end-directed microtubule motor CENP-E (kinesin-7).〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4768465/" 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/PMC4768465/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kapoor, Tarun M -- Lampson, Michael A -- Hergert, Polla -- Cameron, Lisa -- Cimini, Daniela -- Salmon, E D -- McEwen, Bruce F -- Khodjakov, Alexey -- GM06627/GM/NIGMS NIH HHS/ -- GM24364/GM/NIGMS NIH HHS/ -- GM59363/GM/NIGMS NIH HHS/ -- GM65933/GM/NIGMS NIH HHS/ -- R01 GM024364/GM/NIGMS NIH HHS/ -- R01 GM059363/GM/NIGMS NIH HHS/ -- R37 GM024364/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Jan 20;311(5759):388-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chemistry and Cell Biology, Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16424343" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aurora Kinases ; Cell Line ; Chromosomal Proteins, Non-Histone/physiology ; Chromosomes, Mammalian/*physiology/ultrastructure ; HeLa Cells ; Humans ; Indoles/pharmacology ; Kinesin/antagonists & inhibitors ; Kinetochores/*physiology/ultrastructure ; Metaphase ; Microscopy, Confocal ; Microscopy, Electron ; Microscopy, Interference ; Microscopy, Video ; Microtubules/*physiology/ultrastructure ; *Mitosis ; Molecular Motor Proteins/physiology ; Movement ; Potoroidae ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; Pyrimidines/pharmacology ; RNA Interference ; RNA, Small Interfering ; Spindle Apparatus/*physiology/ultrastructure ; Sulfonamides/pharmacology ; Thiones/pharmacology
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  • 9
    Publication Date: 2006-11-11
    Description: The analysis of Madin et al. (Reports, 12 May 2006, p. 897) of Phanerozoic diversity failed to support expected correlations between carnivores and noncarnivores, leading the authors to reject escalation as an important macroevolutionary process. The test, however, is based on a flawed model of causality, and the ecological groups are improperly delineated with regard to the hypothesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roopnarine, Peter D -- Angielczyk, Kenneth D -- Hertog, Rachel -- New York, N.Y. -- Science. 2006 Nov 10;314(5801):925; author reply 925.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Invertebrate Zoology and Geology, California Academy of Sciences, 875 Howard Street, San Francisco, CA 94103, USA. proopnarine@calacademy.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17095679" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Biological ; Animals ; Biodiversity ; *Biological Evolution ; *Ecosystem ; *Fossils ; *Invertebrates ; Predatory Behavior ; *Seawater ; Statistics as Topic
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  • 10
    Publication Date: 2006-02-04
    Description: An enigmatic stepwise increase in oxygen in the late Precambrian is widely considered a prerequisite for the expansion of animal life. Accumulation of oxygen requires organic matter burial in sediments, which is largely controlled by the sheltering or preservational effects of detrital clay minerals in modern marine continental margin depocenters. Here, we show mineralogical and geochemical evidence for an increase in clay mineral deposition in the Neoproterozoic that immediately predated the first metazoans. Today most clay minerals originate in biologically active soils, so initial expansion of a primitive land biota would greatly enhance production of pedogenic clay minerals (the "clay mineral factory"), leading to increased marine burial of organic carbon via mineral surface preservation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kennedy, Martin -- Droser, Mary -- Mayer, Lawrence M -- Pevear, David -- Mrofka, David -- New York, N.Y. -- Science. 2006 Mar 10;311(5766):1446-9. Epub 2006 Feb 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Earth Science, University of California Riverside, Riverside, CA 92521, USA. martink@mail.ucr.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16456036" target="_blank"〉PubMed〈/a〉
    Keywords: *Aluminum Silicates/analysis ; Animals ; *Atmosphere/chemistry ; *Biological Evolution ; Carbon ; Evolution, Planetary ; Geologic Sediments/chemistry ; *Minerals/analysis/chemistry ; Oxygen/analysis ; Quartz/analysis ; *Soil ; Time
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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