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  • Mice  (249)
  • Biological Evolution  (68)
  • Time Factors  (67)
  • American Association for the Advancement of Science (AAAS)  (375)
  • 2005-2009  (258)
  • 1980-1984  (117)
  • 2005  (258)
  • 1981  (117)
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  • American Association for the Advancement of Science (AAAS)  (375)
  • Springer  (2)
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  • 2005-2009  (258)
  • 1980-1984  (117)
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  • 1
    Publication Date: 2005-12-03
    Description: Macrophages and dendritic cells (DCs) are crucial for immune and inflammatory responses and belong to a network of cells that has been termed the mononuclear phagocyte system (MPS). However, the origin and lineage of these cells remain poorly understood. Here, we describe the isolation and clonal analysis of a mouse bone marrow progenitor that is specific for monocytes, several macrophage subsets, and resident spleen DCs in vivo. It was also possible to recapitulate this differentiation in vitro by using treatment with the cytokines macrophage colony-stimulating factor and granulocyte-macrophage colony-stimulating factor. Thus, macrophages and DCs appear to renew from a common progenitor, providing a cellular and molecular basis for the concept of the MPS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fogg, Darin K -- Sibon, Claire -- Miled, Chaouki -- Jung, Steffen -- Aucouturier, Pierre -- Littman, Dan R -- Cumano, Ana -- Geissmann, Frederic -- A133856/PHS HHS/ -- G0900867/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2006 Jan 6;311(5757):83-7. Epub 2005 Dec 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM, Laboratory of Mononuclear Phagocyte Biology, Avenir Team, Necker Enfants Malades Institute, 75015 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16322423" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Lineage ; Cell Separation ; Clone Cells ; Colony-Stimulating Factors/pharmacology ; Dendritic Cells/*cytology ; Flow Cytometry ; Granulocyte Colony-Stimulating Factor/pharmacology ; Hematopoietic Stem Cell Transplantation ; Macrophage Colony-Stimulating Factor/pharmacology ; Macrophages/*cytology ; Mice ; Mice, Inbred C57BL ; Myeloid Progenitor Cells/*cytology/immunology ; Proto-Oncogene Proteins c-kit/analysis ; Receptors, Cytokine/analysis ; Receptors, HIV/analysis ; Recombinant Proteins ; Spleen/cytology
    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
    Publication Date: 2005-02-26
    Description: The genomic diversity and relative importance of distinct genotypes within natural bacterial populations have remained largely unknown. Here, we analyze the diversity and annual dynamics of a group of coastal bacterioplankton (greater than 99% 16S ribosomal RNA identity to Vibrio splendidus). We show that this group consists of at least a thousand distinct genotypes, each occurring at extremely low environmental concentrations (on average less than one cell per milliliter). Overall, the genomes show extensive allelic diversity and size variation. Individual genotypes rarely recurred in samples, and allelic distribution did not show spatial or temporal substructure. Ecological considerations suggest that much genotypic and possibly phenotypic variation within natural populations should be considered neutral.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, Janelle R -- Pacocha, Sarah -- Pharino, Chanathip -- Klepac-Ceraj, Vanja -- Hunt, Dana E -- Benoit, Jennifer -- Sarma-Rupavtarm, Ramahi -- Distel, Daniel L -- Polz, Martin F -- New York, N.Y. -- Science. 2005 Feb 25;307(5713):1311-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Civil and Environmental Engineering, 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/15731455" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Chaperonin 60/genetics ; *Ecosystem ; Electrophoresis, Gel, Pulsed-Field ; *Genetic Variation ; Genome, Bacterial ; Genotype ; Molecular Sequence Data ; Plankton/classification/*genetics/growth & development/isolation & purification ; Polymerase Chain Reaction ; Ribotyping ; Seawater/*microbiology ; Time Factors ; Vibrio/classification/*genetics/isolation & purification
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-10-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, Jean -- New York, N.Y. -- Science. 2005 Oct 7;310(5745):43-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16210515" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autophagy ; Brain-Derived Neurotrophic Factor/metabolism ; Cells, Cultured ; Clinical Trials as Topic ; Corpus Striatum/pathology ; Disease Models, Animal ; Gene Expression Regulation ; Humans ; Huntington Disease/*drug therapy/genetics/pathology/*physiopathology ; Mice ; Mitochondria/metabolism ; Mutation ; Nerve Tissue Proteins/chemistry/*genetics/metabolism/*physiology ; Neurons/*physiology ; Nuclear Proteins/chemistry/*genetics/metabolism/*physiology ; Peptides ; Transcription Factors/metabolism ; Trinucleotide Repeat Expansion
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-09-06
    Description: Large numbers of noncoding RNA transcripts (ncRNAs) are being revealed by complementary DNA cloning and genome tiling array studies in animals. The big and as yet largely unanswered question is whether these transcripts are relevant. A paper by Willingham et al. shows the way forward by developing a strategy for large-scale functional screening of ncRNAs, involving small interfering RNA knockdowns in cell-based screens, which identified a previously unidentified ncRNA repressor of the transcription factor NFAT. It appears likely that ncRNAs constitute a critical hidden layer of gene regulation in complex organisms, the understanding of which requires new approaches in functional genomics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mattick, John S -- New York, N.Y. -- Science. 2005 Sep 2;309(5740):1527-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Australian Research Council Special Research Centre for Functional and Applied Genomics, Institute for Molecular Bioscience, University of Queensland, Brisbane, QLD 4072, Australia. j.mattick@imb.uq.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16141063" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Conserved Sequence ; DNA-Binding Proteins/antagonists & inhibitors ; *Genomics ; Humans ; Mice ; NFATC Transcription Factors ; Nuclear Proteins/antagonists & inhibitors ; *RNA Interference ; RNA, Untranslated/antagonists & inhibitors/genetics/*physiology ; Transcription Factors/antagonists & inhibitors ; beta Karyopherins/metabolism
    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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  • 5
    Publication Date: 2005-04-23
    Description: The CLOCK transcription factor is a key component of the molecular circadian clock within pacemaker neurons of the hypothalamic suprachiasmatic nucleus. We found that homozygous Clock mutant mice have a greatly attenuated diurnal feeding rhythm, are hyperphagic and obese, and develop a metabolic syndrome of hyperleptinemia, hyperlipidemia, hepatic steatosis, hyperglycemia, and hypoinsulinemia. Expression of transcripts encoding selected hypothalamic peptides associated with energy balance was attenuated in the Clock mutant mice. These results suggest that the circadian clock gene network plays an important role in mammalian energy balance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3764501/" 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/PMC3764501/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Turek, Fred W -- Joshu, Corinne -- Kohsaka, Akira -- Lin, Emily -- Ivanova, Ganka -- McDearmon, Erin -- Laposky, Aaron -- Losee-Olson, Sue -- Easton, Amy -- Jensen, Dalan R -- Eckel, Robert H -- Takahashi, Joseph S -- Bass, Joseph -- AG11412/AG/NIA NIH HHS/ -- AG18200/AG/NIA NIH HHS/ -- DK02675/DK/NIDDK NIH HHS/ -- DK26356/DK/NIDDK NIH HHS/ -- HL59598/HL/NHLBI NIH HHS/ -- HL75029/HL/NHLBI NIH HHS/ -- K08 DK002675/DK/NIDDK NIH HHS/ -- P01 AG011412/AG/NIA NIH HHS/ -- R01 AG018200/AG/NIA NIH HHS/ -- R01 DK026356/DK/NIDDK NIH HHS/ -- R01 HL059598/HL/NHLBI NIH HHS/ -- R01 HL075029/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2005 May 13;308(5724):1043-5. Epub 2005 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Northwestern University, Evanston, IL 60208, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15845877" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/pathology ; Animals ; Body Weight ; Brain/metabolism ; CLOCK Proteins ; *Circadian Rhythm ; Dietary Fats/administration & dosage ; Energy Intake ; *Energy Metabolism ; *Feeding Behavior ; Hepatocytes/pathology ; Hyperglycemia ; Hyperlipidemias ; Insulin/blood ; Leptin/blood ; Metabolic Syndrome X/genetics/*physiopathology ; Mice ; Mice, Inbred C57BL ; Motor Activity ; Mutation ; Neuropeptides/genetics/metabolism ; Obesity/genetics/*physiopathology ; Trans-Activators/*genetics/*physiology ; Weight Gain
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  • 6
    Publication Date: 2005-10-01
    Description: Monocular deprivation normally alters ocular dominance in the visual cortex only during a postnatal critical period (20 to 32 days postnatal in mice). We find that mutations in the Nogo-66 receptor (NgR) affect cessation of ocular dominance plasticity. In NgR-/- mice, plasticity during the critical period is normal, but it continues abnormally such that ocular dominance at 45 or 120 days postnatal is subject to the same plasticity as at juvenile ages. Thus, physiological NgR signaling from myelin-derived Nogo, MAG, and OMgp consolidates the neural circuitry established during experience-dependent plasticity. After pathological trauma, similar NgR signaling limits functional recovery and axonal regeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2856689/" 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/PMC2856689/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McGee, Aaron W -- Yang, Yupeng -- Fischer, Quentin S -- Daw, Nigel W -- Strittmatter, Stephen M -- R01 NS039962/NS/NINDS NIH HHS/ -- R01 NS039962-10/NS/NINDS NIH HHS/ -- R01 NS042304/NS/NINDS NIH HHS/ -- R01 NS042304-08/NS/NINDS NIH HHS/ -- R01 NS056485/NS/NINDS NIH HHS/ -- R01 NS056485-04/NS/NINDS NIH HHS/ -- R37 NS033020/NS/NINDS NIH HHS/ -- R37 NS033020-15/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2005 Sep 30;309(5744):2222-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16195464" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chondroitin Sulfate Proteoglycans/metabolism ; Darkness ; Dominance, Ocular/*physiology ; Electrophysiology ; GPI-Linked Proteins ; Gene Targeting ; Mice ; Mice, Inbred C57BL ; Mutation ; Myelin Basic Protein/metabolism ; Myelin Proteins/genetics/metabolism/*physiology ; Myelin Sheath/*physiology ; Myelin-Associated Glycoprotein/metabolism ; Neurites/physiology ; Neuronal Plasticity/*physiology ; Neurons/*physiology ; Photic Stimulation ; Receptors, Cell Surface/genetics/*physiology ; Signal Transduction ; Visual Cortex/cytology/growth & development/*physiology ; gamma-Aminobutyric Acid/physiology
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  • 7
    Publication Date: 2005-02-05
    Description: The gene encoding the Nod2 protein is frequently mutated in Crohn's disease (CD) patients, although the physiological function of Nod2 in the intestine remains elusive. Here we show that protective immunity mediated by Nod2 recognition of bacterial muramyl dipeptide is abolished in Nod2-deficient mice. These animals are susceptible to bacterial infection via the oral route but not through intravenous or peritoneal delivery. Nod2 is required for the expression of a subgroup of intestinal anti-microbial peptides, known as cryptdins. The Nod2 protein is thus a critical regulator of bacterial immunity within the intestine, providing a possible mechanism for Nod2 mutations in CD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kobayashi, Koichi S -- Chamaillard, Mathias -- Ogura, Yasunori -- Henegariu, Octavian -- Inohara, Naohiro -- Nunez, Gabriel -- Flavell, Richard A -- New York, N.Y. -- Science. 2005 Feb 4;307(5710):731-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, 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/15692051" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylmuramyl-Alanyl-Isoglutamine/*immunology ; Animals ; *Antibody Formation ; Female ; Gene Expression ; Gene Targeting ; Ileum/*immunology/microbiology ; *Immunity, Innate ; Immunity, Mucosal ; Immunoglobulins/biosynthesis ; Interleukins/biosynthesis ; Intestinal Diseases/immunology/microbiology ; Intestinal Mucosa/immunology/microbiology ; Intracellular Signaling Peptides and Proteins/*physiology ; Ligands ; Lipopolysaccharides/toxicity ; Listeria monocytogenes/growth & development/immunology/isolation & purification ; Listeriosis/*immunology/microbiology ; Liver/microbiology ; Macrophages/immunology ; Male ; Membrane Glycoproteins/physiology ; Mice ; Nod2 Signaling Adaptor Protein ; Oligonucleotide Array Sequence Analysis ; Protein Precursors/biosynthesis/genetics ; Receptors, Cell Surface/physiology ; Serum Albumin/immunology ; Signal Transduction ; Spleen/microbiology ; Toll-Like Receptors ; Tumor Necrosis Factor-alpha/biosynthesis ; alpha-Defensins/*biosynthesis/genetics
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-08-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin, Jennifer -- New York, N.Y. -- Science. 2005 Aug 26;309(5739):1310-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16123271" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*genetics ; Animals ; Blood Glucose/analysis ; Female ; Glucuronidase ; Insulin/blood/metabolism ; Insulin Resistance ; Insulin-Like Growth Factor I/metabolism ; Longevity/*genetics ; Male ; Membrane Proteins/blood/*genetics/*physiology ; Mice ; Mutation ; Signal Transduction
    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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  • 9
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-01-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Payne, Anthony G -- New York, N.Y. -- Science. 2005 Jan 14;307(5707):208-9; author reply 208-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15662728" target="_blank"〉PubMed〈/a〉
    Keywords: Biological Evolution ; Diet ; Edible Grain/chemistry ; Fatty Acids, Unsaturated/analysis ; Humans ; *Inflammation ; *Longevity ; Myocardial Infarction/etiology ; *Nutritional Physiological Phenomena ; Resorcinols/analysis ; Thromboxane A2/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2005-09-17
    Description: The activation dynamics of the transcription factor NF-kappaB exhibit damped oscillatory behavior when cells are stimulated by tumor necrosis factor-alpha (TNFalpha) but stable behavior when stimulated by lipopolysaccharide (LPS). LPS binding to Toll-like receptor 4 (TLR4) causes activation of NF-kappaB that requires two downstream pathways, each of which when isolated exhibits damped oscillatory behavior. Computational modeling of the two TLR4-dependent signaling pathways suggests that one pathway requires a time delay to establish early anti-phase activation of NF-kappaB by the two pathways. The MyD88-independent pathway required Inferon regulatory factor 3-dependent expression of TNFalpha to activate NF-kappaB, and the time required for TNFalpha synthesis established the delay.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Covert, Markus W -- Leung, Thomas H -- Gaston, Jahlionais E -- Baltimore, David -- GM039458-21/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Sep 16;309(5742):1854-7.〈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/16166516" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Adaptor Proteins, Vesicular Transport/deficiency/physiology ; Animals ; Antigens, Differentiation/physiology ; Cell Line ; Cells, Cultured ; Computer Simulation ; Cycloheximide/pharmacology ; DNA-Binding Proteins/genetics/physiology ; Gene Expression Profiling ; Gene Expression Regulation ; I-kappa B Kinase ; I-kappa B Proteins/biosynthesis/genetics/metabolism ; Interferon Regulatory Factor-3 ; Kinetics ; Lipopolysaccharides/*immunology/metabolism ; Mice ; Models, Biological ; Myeloid Differentiation Factor 88 ; NF-kappa B/*metabolism ; Oligonucleotide Array Sequence Analysis ; Protein Synthesis Inhibitors/pharmacology ; Protein-Serine-Threonine Kinases/metabolism ; Receptors, Immunologic/deficiency/metabolism/physiology ; Signal Transduction ; Time Factors ; Toll-Like Receptor 4 ; Transcription Factors/genetics/physiology ; Tumor Necrosis Factor-alpha/biosynthesis/metabolism
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  • 11
    Publication Date: 2005-07-16
    Description: Mutations in mitochondrial DNA (mtDNA) accumulate in tissues of mammalian species and have been hypothesized to contribute to aging. We show that mice expressing a proofreading-deficient version of the mitochondrial DNA polymerase g (POLG) accumulate mtDNA mutations and display features of accelerated aging. Accumulation of mtDNA mutations was not associated with increased markers of oxidative stress or a defect in cellular proliferation, but was correlated with the induction of apoptotic markers, particularly in tissues characterized by rapid cellular turnover. The levels of apoptotic markers were also found to increase during aging in normal mice. Thus, accumulation of mtDNA mutations that promote apoptosis may be a central mechanism driving mammalian aging.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kujoth, G C -- Hiona, A -- Pugh, T D -- Someya, S -- Panzer, K -- Wohlgemuth, S E -- Hofer, T -- Seo, A Y -- Sullivan, R -- Jobling, W A -- Morrow, J D -- Van Remmen, H -- Sedivy, J M -- Yamasoba, T -- Tanokura, M -- Weindruch, R -- Leeuwenburgh, C -- Prolla, T A -- AG021905/AG/NIA NIH HHS/ -- AG16694/AG/NIA NIH HHS/ -- AG17994/AG/NIA NIH HHS/ -- AG18922/AG/NIA NIH HHS/ -- AG21042/AG/NIA NIH HHS/ -- DK48831/DK/NIDDK NIH HHS/ -- RR00095/RR/NCRR NIH HHS/ -- T32 AG00213/AG/NIA NIH HHS/ -- T32 GM07601/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Jul 15;309(5733):481-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Genetics and Medical Genetics, University of Wisconsin, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16020738" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Amino Acid Substitution ; Animals ; *Apoptosis ; Caspase 3 ; Caspases/metabolism ; Cloning, Molecular ; DNA Damage ; DNA Fragmentation ; DNA, Mitochondrial/*genetics ; DNA-Directed DNA Polymerase/genetics ; Gene Targeting ; Humans ; Hydrogen Peroxide/metabolism ; Lipid Peroxidation ; Liver/metabolism ; Mice ; Mitochondria, Heart/metabolism ; Mitochondria, Liver/metabolism ; Muscle, Skeletal/metabolism ; *Mutation ; Myocardium/metabolism ; *Oxidative Stress ; Phenotype ; Presbycusis/etiology ; Reactive Oxygen Species/metabolism
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  • 12
    Publication Date: 2005-10-01
    Description: The oceans are becoming more acidic due to absorption of anthropogenic carbon dioxide from the atmosphere. The impact of ocean acidification on marine ecosystems is unclear, but it will likely depend on species adaptability and the rate of change of seawater pH relative to its natural variability. To constrain the natural variability in reef-water pH, we measured boron isotopic compositions in a approximately 300-year-old massive Porites coral from the southwestern Pacific. Large variations in pH are found over approximately 50-year cycles that covary with the Interdecadal Pacific Oscillation of ocean-atmosphere anomalies, suggesting that natural pH cycles can modulate the impact of ocean acidification on coral reef ecosystems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pelejero, Carles -- Calvo, Eva -- McCulloch, Malcolm T -- Marshall, John F -- Gagan, Michael K -- Lough, Janice M -- Opdyke, Bradley N -- New York, N.Y. -- Science. 2005 Sep 30;309(5744):2204-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research School of Earth Sciences, Australian National University, Canberra, ACT 0200, Australia. pelejero@cmima.csic.es〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16195458" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthozoa/chemistry/*physiology ; Atmosphere ; Boron/analysis ; Carbon Dioxide/analysis ; *Ecosystem ; Hydrogen-Ion Concentration ; Isotopes/analysis ; Pacific Ocean ; Seasons ; *Seawater ; Time Factors
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  • 13
    Publication Date: 2005-08-27
    Description: CD4+ regulatory T (Treg) cells have a profound ability to suppress host immune responses, yet little is understood about how these cells are regulated. We describe a mechanism linking Toll-like receptor (TLR) 8 signaling to the control of Treg cell function, in which synthetic and natural ligands for human TLR8 can reverse Treg cell function. This effect was independent of dendritic cells but required functional TLR8-MyD88-IRAK4 signaling in Treg cells. Adoptive transfer of TLR8 ligand-stimulated Treg cells into tumor-bearing mice enhanced anti-tumor immunity. These results suggest that TLR8 signaling could play a critical role in controlling immune responses to cancer and other diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peng, Guangyong -- Guo, Zhong -- Kiniwa, Yukiko -- Voo, Kui Shin -- Peng, Weiyi -- Fu, Tihui -- Wang, Daniel Y -- Li, Yanchun -- Wang, Helen Y -- Wang, Rong-Fu -- P01CA94237/CA/NCI NIH HHS/ -- P50 CA093459/CA/NCI NIH HHS/ -- P50CA58204/CA/NCI NIH HHS/ -- R01CA101795/CA/NCI NIH HHS/ -- R01CA90327/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2005 Aug 26;309(5739):1380-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cell and Gene Therapy and Department of Immunology, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16123302" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Adoptive Transfer ; Animals ; Antigens, Differentiation/genetics/physiology ; CD4-Positive T-Lymphocytes/*immunology ; Cell Line ; Cell Line, Tumor ; Humans ; Immune Tolerance ; Interleukin-1 Receptor-Associated Kinases ; Killer Cells, Natural/immunology ; Ligands ; Lymphocyte Activation ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Myeloid Differentiation Factor 88 ; Neoplasm Transplantation ; Neoplasms, Experimental/immunology/pathology ; Oligodeoxyribonucleotides/immunology ; Phosphotransferases (Alcohol Group Acceptor)/genetics/physiology ; Poly G/immunology ; RNA Interference ; Receptors, Cell Surface/genetics/*physiology ; Receptors, Immunologic/genetics/physiology ; *Signal Transduction ; T-Lymphocyte Subsets/*immunology ; Toll-Like Receptor 8 ; Toll-Like Receptors
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  • 14
    Publication Date: 2005-02-12
    Description: Most protein phosphatases have little intrinsic substrate specificity, making selective pharmacological inhibition of specific dephosphorylation reactions a challenging problem. In a screen for small molecules that protect cells from endoplasmic reticulum (ER) stress, we identified salubrinal, a selective inhibitor of cellular complexes that dephosphorylate eukaryotic translation initiation factor 2 subunit alpha (eIF2alpha). Salubrinal also blocks eIF2alpha dephosphorylation mediated by a herpes simplex virus protein and inhibits viral replication. These results suggest that selective chemical inhibitors of eIF2alpha dephosphorylation may be useful in diseases involving ER stress or viral infection. More broadly, salubrinal demonstrates the feasibility of selective pharmacological targeting of cellular dephosphorylation events.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boyce, Michael -- Bryant, Kevin F -- Jousse, Celine -- Long, Kai -- Harding, Heather P -- Scheuner, Donalyn -- Kaufman, Randal J -- Ma, Dawei -- Coen, Donald M -- Ron, David -- Yuan, Junying -- AI19838/AI/NIAID NIH HHS/ -- AI26077/AI/NIAID NIH HHS/ -- DDK42394/DK/NIDDK NIH HHS/ -- DK47119/DK/NIDDK NIH HHS/ -- ES08681/ES/NIEHS NIH HHS/ -- GM64703/GM/NIGMS NIH HHS/ -- NS35138/NS/NINDS NIH HHS/ -- R37-AG012859/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2005 Feb 11;307(5711):935-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15705855" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Differentiation ; Apoptosis/*drug effects ; Cell Cycle Proteins ; Cell Line ; Cinnamates/*pharmacology/toxicity ; *Cytoprotection ; Dose-Response Relationship, Drug ; Endoplasmic Reticulum/*metabolism ; Enzyme Inhibitors/pharmacology ; Eukaryotic Initiation Factor-2/*metabolism ; Genes, Reporter ; Herpesvirus 1, Human/drug effects/physiology ; Keratitis, Herpetic/drug therapy/virology ; Male ; Mice ; Oxazoles/pharmacology/toxicity ; PC12 Cells ; Phosphoprotein Phosphatases/metabolism ; Phosphorylation ; Protein Folding ; Protein Kinases/metabolism ; Protein Phosphatase 1 ; Proteins/metabolism ; Rats ; Thiourea/*analogs & derivatives/*pharmacology/toxicity ; Tunicamycin/pharmacology ; Viral Proteins/metabolism ; Virus Replication/drug effects
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  • 15
    Publication Date: 2005-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2005 Dec 16;310(5755):1761.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16357241" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axin Protein ; Body Patterning/drug effects/genetics ; *DNA Methylation ; DNA Transposable Elements ; *Dietary Supplements ; Embryonic Development/drug effects/*genetics ; *Epigenesis, Genetic ; Female ; Folic Acid/*administration & dosage/pharmacology ; Gene Expression Regulation, Developmental/*drug effects ; Mice ; Pregnancy ; Repressor Proteins/genetics ; Tail/embryology ; Vitamin B Complex/*administration & dosage/pharmacology
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  • 16
    Publication Date: 2005-08-20
    Description: The SAR11 clade consists of very small, heterotrophic marine alpha-proteobacteria that are found throughout the oceans, where they account for about 25% of all microbial cells. Pelagibacter ubique, the first cultured member of this clade, has the smallest genome and encodes the smallest number of predicted open reading frames known for a free-living microorganism. In contrast to parasitic bacteria and archaea with small genomes, P. ubique has complete biosynthetic pathways for all 20 amino acids and all but a few cofactors. P. ubique has no pseudogenes, introns, transposons, extrachromosomal elements, or inteins; few paralogs; and the shortest intergenic spacers yet observed for any cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giovannoni, Stephen J -- Tripp, H James -- Givan, Scott -- Podar, Mircea -- Vergin, Kevin L -- Baptista, Damon -- Bibbs, Lisa -- Eads, Jonathan -- Richardson, Toby H -- Noordewier, Michiel -- Rappe, Michael S -- Short, Jay M -- Carrington, James C -- Mathur, Eric J -- New York, N.Y. -- Science. 2005 Aug 19;309(5738):1242-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Oregon State University, Corvallis, OR 97331, USA. steve.giovannoni@oregonstate.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16109880" target="_blank"〉PubMed〈/a〉
    Keywords: Alphaproteobacteria/classification/*genetics/isolation & purification/physiology ; Bacterial Proteins/genetics/metabolism ; Base Composition ; Biological Evolution ; Carbon/metabolism ; Computational Biology ; DNA, Bacterial/chemistry/genetics ; DNA, Intergenic ; Gene Expression Regulation, Bacterial ; Genes, Bacterial ; *Genome, Bacterial ; Membrane Transport Proteins/genetics/metabolism ; Molecular Sequence Data ; Oceans and Seas ; Phosphates/metabolism ; Phylogeny ; Seawater/*microbiology ; Selection, Genetic ; Sigma Factor/genetics ; Thymidylate Synthase/genetics
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  • 17
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-03-19
    Description: After anaphase onset, animal cells build an actomyosin contractile ring that constricts the plasma membrane to generate two daughter cells connected by a cytoplasmic bridge. The bridge is ultimately severed to complete cytokinesis. Myriad techniques have been used to identify proteins that participate in cytokinesis in vertebrates, insects, and nematodes. A conserved core of about 20 proteins are individually involved with cytokinesis in most animal cells. These components are found in the contractile ring, on the central spindle, within the RhoA pathway, and on vesicles that expand the membrane and sever the bridge. Cytokinesis involves additional proteins, but they, or their requirement in cytokinesis, are not conserved among animal cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Glotzer, Michael -- New York, N.Y. -- Science. 2005 Mar 18;307(5716):1735-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Institute of Molecular Pathology, Dr. BohrGasse 7, A-1030 Vienna, Austria. mglotzer@imp.univie.ac.at〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15774750" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/physiology ; Actins/metabolism ; Animals ; Biological Evolution ; Cell Cycle Proteins/*metabolism ; *Cytokinesis/genetics ; Cytoskeletal Proteins/*metabolism ; Genes ; Membrane Fusion/physiology ; Microtubules/physiology ; Models, Biological ; Myosins/metabolism ; Proteins/*metabolism ; Spindle Apparatus/physiology ; rhoA GTP-Binding Protein/metabolism
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  • 18
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-10-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2005 Oct 28;310(5748):602.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16254156" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation/*drug effects ; Ciliary Neurotrophic Factor/*pharmacology ; Humans ; Hypothalamus/cytology/*drug effects ; Mice ; Neurons/cytology/*drug effects ; Weight Loss/*drug effects
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  • 19
    Publication Date: 2005-05-21
    Description: Gene marking with replication-defective retroviral vectors has been used for more than 20 years to track the in vivo fate of cell clones. We demonstrate that retroviral integrations themselves may trigger nonmalignant clonal expansion in murine long-term hematopoiesis. All 29 insertions recovered from clones dominating in serially transplanted recipients affected loci with an established or potential role in the self-renewal or survival of hematopoietic stem cells. Transcriptional dysregulation occurred in all 12 insertion sites analyzed. These findings have major implications for diagnostic gene marking and the discovery of genes regulating stem cell turnover.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kustikova, Olga -- Fehse, Boris -- Modlich, Ute -- Yang, Min -- Dullmann, Jochen -- Kamino, Kenji -- von Neuhoff, Nils -- Schlegelberger, Brigitte -- Li, Zhixiong -- Baum, Christopher -- New York, N.Y. -- Science. 2005 May 20;308(5725):1171-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bone Marrow Transplantation, University Hospital Eppendorf, Martinistrasse 52, 20251 Hamburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15905401" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD34/genetics ; Bone Marrow Transplantation ; DNA-Binding Proteins/genetics ; Down-Regulation ; *Genetic Vectors ; *Hematopoiesis ; *Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*physiology ; Humans ; Ligase Chain Reaction ; Mice ; Mice, Inbred C57BL ; *Mutagenesis, Insertional ; Polymerase Chain Reaction ; Proto-Oncogenes/genetics ; Retroviridae/*genetics ; Transcription Factors/genetics ; Transcription, Genetic ; Transgenes ; Up-Regulation ; *Virus Integration
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  • 20
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-10-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2005 Oct 21;310(5747):416-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16239442" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/cytology ; *Cell Line ; Embryo Implantation ; Embryo Research/economics/*ethics ; Embryo, Mammalian/*cytology ; Female ; Financing, Government ; Humans ; Mice ; Nuclear Transfer Techniques ; *Pluripotent Stem Cells ; Research Support as Topic ; *Stem Cells ; United States
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  • 21
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-04-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Laland, Kevin N -- Coolen, Isabelle -- Kendal, Rachel -- New York, N.Y. -- Science. 2005 Apr 15;308(5720):353-6; author reply 353-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15834975" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Biological ; Animals ; *Behavior, Animal ; Biological Evolution ; *Cultural Evolution ; Feeding Behavior ; Knowledge ; Selection, Genetic ; Smegmamorpha/*physiology ; *Terminology as Topic
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  • 22
    Publication Date: 2005-12-17
    Description: Lighter variations of pigmentation in humans are associated with diminished number, size, and density of melanosomes, the pigmented organelles of melanocytes. Here we show that zebrafish golden mutants share these melanosomal changes and that golden encodes a putative cation exchanger slc24a5 (nckx5) that localizes to an intracellular membrane, likely the melanosome or its precursor. The human ortholog is highly similar in sequence and functional in zebrafish. The evolutionarily conserved ancestral allele of a human coding polymorphism predominates in African and East Asian populations. In contrast, the variant allele is nearly fixed in European populations, is associated with a substantial reduction in regional heterozygosity, and correlates with lighter skin pigmentation in admixed populations, suggesting a key role for the SLC24A5 gene in human pigmentation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamason, Rebecca L -- Mohideen, Manzoor-Ali P K -- Mest, Jason R -- Wong, Andrew C -- Norton, Heather L -- Aros, Michele C -- Jurynec, Michael J -- Mao, Xianyun -- Humphreville, Vanessa R -- Humbert, Jasper E -- Sinha, Soniya -- Moore, Jessica L -- Jagadeeswaran, Pudur -- Zhao, Wei -- Ning, Gang -- Makalowska, Izabela -- McKeigue, Paul M -- O'donnell, David -- Kittles, Rick -- Parra, Esteban J -- Mangini, Nancy J -- Grunwald, David J -- Shriver, Mark D -- Canfield, Victor A -- Cheng, Keith C -- CA73935/CA/NCI NIH HHS/ -- EY11308/EY/NEI NIH HHS/ -- HD37572/HD/NICHD NIH HHS/ -- HD40179/HD/NICHD NIH HHS/ -- HG002154/HG/NHGRI NIH HHS/ -- HL077910/HL/NHLBI NIH HHS/ -- RR017441/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2005 Dec 16;310(5755):1782-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Jake Gittlen Cancer Research Foundation, Department of Pathology, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16357253" target="_blank"〉PubMed〈/a〉
    Keywords: African Americans/genetics ; African Continental Ancestry Group/genetics ; Alanine/genetics ; Alleles ; Amino Acid Sequence ; Animals ; Antiporters/chemistry/*genetics/physiology ; Asian Continental Ancestry Group/genetics ; Biological Evolution ; Calcium/metabolism ; European Continental Ancestry Group/genetics ; Gene Frequency ; Genes ; Genetic Variation ; Haplotypes ; Heterozygote ; Humans ; Ion Transport ; Melanins/analysis ; Melanosomes/chemistry/ultrastructure ; Mice ; Molecular Sequence Data ; Multifactorial Inheritance ; Mutation ; Pigment Epithelium of Eye/chemistry/ultrastructure ; Polymorphism, Single Nucleotide ; Selection, Genetic ; Skin Pigmentation/*genetics ; Threonine/genetics ; Zebrafish/embryology/*genetics/metabolism ; Zebrafish Proteins/chemistry/*genetics/physiology
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  • 23
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-10-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2005 Oct 7;310(5745):28-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16210501" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; Animals ; Bioterrorism ; Chick Embryo/virology ; Containment of Biohazards ; Disease Outbreaks/history ; Editorial Policies ; *Genes, Viral ; Genome, Viral ; Hemagglutinin Glycoproteins, Influenza Virus/chemistry/*metabolism ; History, 20th Century ; Humans ; Influenza A virus/*genetics/*pathogenicity/physiology ; Influenza, Human/epidemiology/history/*virology ; Mice ; Neuraminidase/genetics/metabolism ; Publishing ; RNA Replicase/genetics/metabolism ; United States ; Virulence ; Virus Replication
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  • 24
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-09-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gray, Russell -- New York, N.Y. -- Science. 2005 Sep 23;309(5743):2007-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University of Auckland, Auckland 92019, New Zealand. rd.gray@auckland.ac.nz〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16179464" target="_blank"〉PubMed〈/a〉
    Keywords: Asia ; *Cultural Evolution ; Databases, Factual ; History, Ancient ; Humans ; *Language ; *Linguistics ; Pacific Islands ; Papua New Guinea ; Software ; Time Factors
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  • 25
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-01-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2005 Jan 14;307(5707):194.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15653478" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Birds/anatomy & histology/*embryology/metabolism ; Chick Embryo ; Dinosaurs/*anatomy & histology ; Forelimb/*anatomy & histology ; Homeodomain Proteins/metabolism ; Mice ; Transcription Factors/metabolism ; Wings, Animal/anatomy & histology/*embryology/metabolism
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  • 26
    Publication Date: 2005-04-30
    Description: The clock proteins PERIOD1 (PER1) and PERIOD2 (PER2) play essential roles in a negative transcriptional feedback loop that generates circadian rhythms in mammalian cells. We identified two PER1-associated factors, NONO and WDR5, that modulate PER activity. The reduction of NONO expression by RNA interference (RNAi) attenuated circadian rhythms in mammalian cells, and fruit flies carrying a hypomorphic allele were nearly arrhythmic. WDR5, a subunit of histone methyltransferase complexes, augmented PER-mediated transcriptional repression, and its reduction by RNAi diminished circadian histone methylations at the promoter of a clock gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, Steven A -- Ripperger, Juergen -- Kadener, Sebastian -- Fleury-Olela, Fabienne -- Vilbois, Francis -- Rosbash, Michael -- Schibler, Ueli -- New York, N.Y. -- Science. 2005 Apr 29;308(5722):693-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and National Centres of Competence in Research (NCCR) Frontiers in Genetics, Sciences III, University of Geneva, 30 Quai Ernest Ansermet, CH-1211 Geneva-4, Switzerland. steven.brown@molbio.unige.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15860628" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Carrier Proteins/genetics/*metabolism ; Cell Cycle Proteins ; Cell Line ; *Circadian Rhythm ; DNA-Binding Proteins/genetics/metabolism ; Drosophila/genetics/physiology ; Drosophila Proteins/genetics/physiology ; Female ; Gene Expression Regulation ; Histones/metabolism ; Immunoprecipitation ; Male ; Methylation ; Mice ; Mice, Inbred BALB C ; Nuclear Proteins/genetics/*metabolism/physiology ; Nuclear Receptor Subfamily 1, Group D, Member 1 ; Period Circadian Proteins ; Promoter Regions, Genetic ; Proteins/genetics/*metabolism ; RNA Interference ; Rats ; Receptors, Cytoplasmic and Nuclear/genetics/metabolism ; Transcription Factors ; Transcription, Genetic ; Transfection
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  • 27
    Publication Date: 2005-01-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Timothy M -- Cleveland, Don W -- R37 NS027036/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2005 Jan 21;307(5708):361-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Institute for Cancer Research and the Department of Medicine and Neurosciences, 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/15661995" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/*drug therapy ; Animals ; Anti-Bacterial Agents/pharmacology/*therapeutic use ; Brain/metabolism ; Ceftriaxone/pharmacology/*therapeutic use ; Clinical Trials as Topic ; Drug Evaluation, Preclinical ; Excitatory Amino Acid Transporter 2/genetics/metabolism ; Glutamic Acid/metabolism ; Humans ; Mice ; Motor Neurons/physiology ; Neurodegenerative Diseases/*drug therapy ; Spinal Cord/metabolism ; Synapses/physiology ; Synaptic Transmission ; beta-Lactams/pharmacology/*therapeutic use
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  • 28
    Publication Date: 2005-07-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Ruiter, Peter C -- Wolters, Volkmar -- Moore, John C -- Winemiller, Kirk O -- New York, N.Y. -- Science. 2005 Jul 1;309(5731):68-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Environmental Sciences, Copernicus Research Institute for Sustainable Development and Innovation, Utrecht University, 3508 TC Utrecht, Netherlands. p.deruiter@geo.uu.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15994518" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biodiversity ; Body Size ; *Ecosystem ; Fishes ; *Food Chain ; Population Density ; Population Dynamics ; Predatory Behavior ; Time Factors
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  • 29
    Publication Date: 2005-02-12
    Description: The microenvironments of the thymus are generated by thymic epithelial cells (TECs) and are essential for inducing immune self-tolerance or developing T cells. However, the molecular mechanisms that underlie the differentiation of TECs and thymic compartmentalization are not fully understood. Here we show that deficiency in the tumor necrosis factor receptor-associated factor (TRAF) 6 results in disorganized distribution of medullary TECs (mTECs) and the absence of mature mTECs. Engraftment of thymic stroma of TRAF6(-/-) embryos into athymic nude mice induced autoimmunity. Thus, TRAF6 directs the development of thymic stroma and represents a critical point of regulation for self-tolerance and autoimmunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akiyama, Taishin -- Maeda, Shiori -- Yamane, Sayaka -- Ogino, Kaori -- Kasai, Michiyuki -- Kajiura, Fumiko -- Matsumoto, Mitsuru -- Inoue, Jun-ichiro -- New York, N.Y. -- Science. 2005 Apr 8;308(5719):248-51. Epub 2005 Feb 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cellular and Molecular Biology, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15705807" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmunity ; Cell Line ; Epithelial Cells/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Nude ; Organ Culture Techniques ; Proto-Oncogene Proteins/physiology ; *Self Tolerance ; T-Lymphocytes/immunology ; TNF Receptor-Associated Factor 6/immunology/*physiology ; Thymus Gland/cytology/embryology/*immunology ; Transcription Factor RelB ; Transcription Factors/physiology
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  • 30
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-04-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Delfino, Massimo -- New York, N.Y. -- Science. 2005 Apr 1;308(5718):49-50; author reply 49-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15818797" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; *Amphibians/classification/physiology ; Animals ; *Biodiversity ; Biological Evolution ; Climate ; *Ecosystem ; Environment ; Population Dynamics ; Time
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  • 31
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-03-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2005 Mar 11;307(5715):1544-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15761128" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; Animals ; *Clinical Trials as Topic ; Genetic Diseases, X-Linked/*therapy ; *Genetic Therapy/adverse effects ; Genetic Vectors ; Haplorhini ; Humans ; Infant ; Leukemia, T-Cell/etiology ; Mice ; Oncogenes ; Retroviridae/genetics ; Severe Combined Immunodeficiency/*therapy ; United States
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  • 32
    Publication Date: 2005-07-23
    Description: Many large animal species have a high risk of extinction. This is usually thought to result simply from the way that species traits associated with vulnerability, such as low reproductive rates, scale with body size. In a broad-scale analysis of extinction risk in mammals, we find two additional patterns in the size selectivity of extinction risk. First, impacts of both intrinsic and environmental factors increase sharply above a threshold body mass around 3 kilograms. Second, whereas extinction risk in smaller species is driven by environmental factors, in larger species it is driven by a combination of environmental factors and intrinsic traits. Thus, the disadvantages of large size are greater than generally recognized, and future loss of large mammal biodiversity could be far more rapid than expected.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cardillo, Marcel -- Mace, Georgina M -- Jones, Kate E -- Bielby, Jon -- Bininda-Emonds, Olaf R P -- Sechrest, Wes -- Orme, C David L -- Purvis, Andy -- New York, N.Y. -- Science. 2005 Aug 19;309(5738):1239-41. Epub 2005 Jul 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, Imperial College London, Silwood Park, Ascot SL5 7PY, UK. m.cardillo@imperial.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16037416" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biodiversity ; Biological Evolution ; *Body Size ; Body Weight ; Conservation of Natural Resources ; *Ecosystem ; *Environment ; Female ; Homing Behavior ; Humans ; *Mammals/physiology ; Models, Biological ; Models, Statistical ; Population Density ; Population Dynamics ; Pregnancy ; Pregnancy, Animal ; Regression Analysis ; Risk ; Weaning
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  • 33
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-01-22
    Description: The epidemic of obesity-associated diabetes is a major crisis in modern societies, in which food is plentiful and exercise is optional. The biological basis of this problem has been explored from evolutionary and mechanistic perspectives. Evolutionary theories, focusing on the potential survival advantages of "thrifty" genes that are now maladaptive, are of great interest but are inherently speculative and difficult to prove. Mechanistic studies have revealed numerous fat-derived molecules and a link to inflammation that, together, are hypothesized to underlie the obesity-diabetes connection and thereby represent prospective targets for therapeutic intervention.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lazar, Mitchell A -- New York, N.Y. -- Science. 2005 Jan 21;307(5708):373-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, and The Penn Diabetes Center, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-6149, USA. lazar@mail.med.upenn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15662001" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/metabolism ; Adipose Tissue/metabolism ; Animals ; Biological Evolution ; Cytokines/metabolism ; Diabetes Mellitus, Type 2/epidemiology/*etiology/physiopathology ; Epigenesis, Genetic ; Fetal Nutrition Disorders/physiopathology ; Glucose/metabolism ; Humans ; Immunity, Innate ; Inflammation/physiopathology ; Insulin/physiology ; Insulin Resistance ; Leptin/blood/genetics/physiology ; Lipid Metabolism ; Macrophages/immunology/metabolism ; Obesity/*complications/epidemiology/genetics/physiopathology ; Phenotype ; Proteins/metabolism
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  • 34
    Publication Date: 2005-08-20
    Description: The molecular machinery that governs circadian rhythmicity is based on clock proteins organized in regulatory feedback loops. Although posttranslational modification of clock proteins is likely to finely control their circadian functions, only limited information is available to date. Here, we show that BMAL1, an essential transcription factor component of the clock mechanism, is SUMOylated on a highly conserved lysine residue (Lys259) in vivo. BMAL1 shows a circadian pattern of SUMOylation that parallels its activation in the mouse liver. SUMOylation of BMAL1 requires and is induced by CLOCK, the heterodimerization partner of BMAL1. Ectopic expression of a SUMO-deficient BMAL1 demonstrates that SUMOylation plays an important role in BMAL1 circadian expression and clock rhythmicity. This reveals an additional level of regulation within the core mechanism of the circadian clock.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cardone, Luca -- Hirayama, Jun -- Giordano, Francesca -- Tamaru, Teruya -- Palvimo, Jorma J -- Sassone-Corsi, Paolo -- New York, N.Y. -- Science. 2005 Aug 26;309(5739):1390-4. Epub 2005 Aug 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire, 1 rue Laurent Fries, 67404 Illkirch, Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16109848" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Animals ; Basic Helix-Loop-Helix Transcription Factors ; CLOCK Proteins ; COS Cells ; Cell Cycle Proteins ; Cell Line ; *Circadian Rhythm ; Dimerization ; Ethylmaleimide/pharmacology ; Gene Expression Regulation ; Liver/metabolism ; Lysine/metabolism ; Mice ; Mutation ; Nuclear Proteins/genetics/metabolism ; Period Circadian Proteins ; Phosphorylation ; Recombinant Fusion Proteins/metabolism ; SUMO-1 Protein/*metabolism ; Trans-Activators/genetics/metabolism ; Transcription Factors/chemistry/genetics/*metabolism
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  • 35
    Publication Date: 2005-05-28
    Description: The typical scales for plant and fungal movements vary over many orders of magnitude in time and length, but they are ultimately based on hydraulics and mechanics. We show that quantification of the length and time scales involved in plant and fungal motions leads to a natural classification, whose physical basis can be understood through an analysis of the mechanics of water transport through an elastic tissue. Our study also suggests a design principle for nonmuscular hydraulically actuated structures: Rapid actuation requires either small size or the enhancement of motion on large scales via elastic instabilities.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Skotheim, Jan M -- Mahadevan, L -- New York, N.Y. -- Science. 2005 May 27;308(5726):1308-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Applied Mathematics and Theoretical Physics, Centre for Mathematical Sciences, University of Cambridge, Cambridge CB3 0WA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15919993" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Wall/physiology ; Droseraceae/anatomy & histology/physiology ; Elasticity ; Euphorbiaceae/anatomy & histology/physiology ; Fungi/cytology/*physiology ; Mathematics ; Movement ; Mucorales/cytology/physiology ; Physical Phenomena ; Physics ; Plant Leaves/*physiology ; *Plant Physiological Phenomena ; Plants/anatomy & histology ; Pressure ; Time Factors ; Viscosity ; Water/*physiology
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  • 36
    Publication Date: 2005-09-24
    Description: Mammalian tooth crowns have precise functional requirements but cannot be substantially remodeled after eruption. In developing teeth, epithelial signaling centers, the enamel knots, form at future cusp positions and are the first signs of cusp patterns that distinguish species. We report that ectodin, a secreted bone morphogenetic protein (BMP) inhibitor, is expressed as a "negative" image of mouse enamel knots. Furthermore, we show that ectodin-deficient mice have enlarged enamel knots, highly altered cusp patterns, and extra teeth. Unlike in normal teeth, excess BMP accelerates patterning in ectodin-deficient teeth. We propose that ectodin is critical for robust spatial delineation of enamel knots and cusps.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kassai, Yoshiaki -- Munne, Pauliina -- Hotta, Yuhei -- Penttila, Enni -- Kavanagh, Kathryn -- Ohbayashi, Norihiko -- Takada, Shinji -- Thesleff, Irma -- Jernvall, Jukka -- Itoh, Nobuyuki -- New York, N.Y. -- Science. 2005 Sep 23;309(5743):2067-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetic Biochemistry, Kyoto University Graduate School of Pharmaceutical Sciences, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16179481" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Body Patterning ; Bone Morphogenetic Protein 4 ; Bone Morphogenetic ; Proteins/biosynthesis/genetics/metabolism/pharmacology/*physiology ; Cell Cycle Proteins/biosynthesis/genetics/physiology ; Chimera ; Cyclin-Dependent Kinase Inhibitor p21 ; Dental Enamel/embryology ; Gene Expression Regulation, Developmental ; Hedgehog Proteins ; Heterozygote ; Mice ; Mice, Inbred C57BL ; Microscopy, Confocal ; Molar/embryology/metabolism ; Mutation ; *Odontogenesis ; Organ Culture Techniques ; Tooth Crown/*embryology ; Trans-Activators/biosynthesis/genetics
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  • 37
    Publication Date: 2005-09-17
    Description: A small number of mammalian signaling pathways mediate a myriad of distinct physiological responses to diverse cellular stimuli. Temporal control of the signaling module that contains IkappaB kinase (IKK), its substrate inhibitor of NF-kappaB (IkappaB), and the key inflammatory transcription factor NF-kappaB can allow for selective gene activation. We have demonstrated that different inflammatory stimuli induce distinct IKK profiles, and we examined the underlying molecular mechanisms. Although tumor necrosis factor-alpha (TNFalpha)-induced IKK activity was rapidly attenuated by negative feedback, lipopolysaccharide (LPS) signaling and LPS-specific gene expression programs were dependent on a cytokine-mediated positive feedback mechanism. Thus, the distinct biological responses to LPS and TNFalpha depend on signaling pathway-specific mechanisms that regulate the temporal profile of IKK activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Werner, Shannon L -- Barken, Derren -- Hoffmann, Alexander -- GM071573/GM/NIGMS NIH HHS/ -- GM72024/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Sep 16;309(5742):1857-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Signaling Systems Laboratory, Department of Chemistry and Biochemistry, 9500 Gilman Drive, Mailcode 0375, La Jolla, CA 92093-0375, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16166517" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Autocrine Communication ; Cell Line ; Cells, Cultured ; Computer Simulation ; Cytokines/genetics ; Feedback, Physiological ; Gene Expression Profiling ; *Gene Expression Regulation ; I-kappa B Kinase ; I-kappa B Proteins/metabolism ; Lipopolysaccharides/immunology/metabolism/pharmacology ; Mice ; Models, Biological ; NF-kappa B/deficiency/metabolism ; Oligonucleotide Array Sequence Analysis ; Protein-Serine-Threonine Kinases/*metabolism ; Receptors, Immunologic/metabolism ; Signal Transduction ; Toll-Like Receptor 4 ; Transcriptional Activation ; Tumor Necrosis Factor-alpha/deficiency/immunology/metabolism/pharmacology
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  • 38
    Publication Date: 2005-03-19
    Description: The adherence of Candida glabrata to host cells is mediated, at least in part, by the EPA genes, a family of adhesins encoded at subtelomeric loci, where they are subject to transcriptional silencing. We show that normally silent EPA genes are expressed during murine urinary tract infection (UTI) and that the inducing signal is the limitation of nicotinic acid (NA), a precursor of nicotinamide adenine dinucleotide (NAD+). C. glabrata is an NA auxotroph, and NA-induced EPA expression is likely the result of a reduction in NAD+ availability for the NAD+-dependent histone deacetylase Sir2p. The adaptation of C. glabrata to the host, therefore, involves a loss of metabolic capacity and exploitation of the resulting auxotrophy to signal a particular host environment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Domergue, Renee -- Castano, Irene -- De Las Penas, Alejandro -- Zupancic, Margaret -- Lockatell, Virginia -- Hebel, J Richard -- Johnson, David -- Cormack, Brendan P -- 2PO1DK49720/DK/NIDDK NIH HHS/ -- R01AI46223/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2005 May 6;308(5723):866-70. Epub 2005 Mar 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15774723" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Candida glabrata/*genetics/growth & development/*pathogenicity/physiology ; Candidiasis/*microbiology ; Cell Adhesion ; Culture Media ; Female ; Gene Expression Regulation, Fungal ; *Gene Silencing ; Genes, Fungal ; Histone Deacetylases/genetics/metabolism ; Lectins/*genetics ; Mice ; Mice, Inbred BALB C ; Mice, Inbred CBA ; NAD/metabolism ; Niacin/administration & dosage/*metabolism/pharmacology/urine ; Niacinamide/pharmacology/urine ; Sirtuins/genetics/metabolism ; Transcription, Genetic ; Urinary Bladder/microbiology ; Urinary Tract Infections/*microbiology ; Urine/microbiology ; Urothelium/microbiology ; Virulence
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  • 39
    Publication Date: 2005-02-26
    Description: Many pathogenic bacteria use a type III secretion nanomachine (an injectisome) to deliver virulence proteins into the cytosol of their eukaryotic host cells. Most injectisomes possess a stiff needlelike structure of a genetically defined length. We found that a minimal needle length was required for efficient functioning of the Yersinia enterocolitica injectisome. This minimal needle length correlated with the length of the major adhesin at the bacterial surface. The needle may be required for triggering type III secretion, and its length may have evolved to match specific structures at the bacterial and host cell surfaces.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mota, Luis Jaime -- Journet, Laure -- Sorg, Isabel -- Agrain, Celine -- Cornelis, Guy R -- New York, N.Y. -- Science. 2005 Feb 25;307(5713):1278.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biozentrum, Universitat Basel, 4056 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15731447" target="_blank"〉PubMed〈/a〉
    Keywords: Adhesins, Bacterial/chemistry/*metabolism ; Animals ; Bacterial Outer Membrane Proteins/metabolism ; Bacterial Proteins/chemistry/genetics/metabolism ; Cell Line ; Macrophages/metabolism/microbiology ; Mice ; Plasmids ; Protein-Serine-Threonine Kinases/metabolism ; Virulence ; Virulence Factors/metabolism ; Yersinia enterocolitica/genetics/*metabolism/*pathogenicity
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  • 40
    Publication Date: 2005-08-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anfinrud, Philip -- Schotte, Friedrich -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2005 Aug 19;309(5738):1192-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chemical Physics, National Institutes of Health, Bethesda, MD 20892-0520, USA. anfinrud@nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16109869" target="_blank"〉PubMed〈/a〉
    Keywords: Hydrocarbons, Iodinated/*chemistry ; Molecular Structure ; Scattering, Radiation ; Solutions ; Solvents ; Time Factors ; X-Ray Diffraction/*methods ; X-Rays
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  • 41
    Publication Date: 2005-03-19
    Description: Recognizing a deficiency of indispensable amino acids (IAAs) for protein synthesis is vital for dietary selection in metazoans, including humans. Cells in the brain's anterior piriform cortex (APC) are sensitive to IAA deficiency, signaling diet rejection and foraging for complementary IAA sources, but the mechanism is unknown. Here we report that the mechanism for recognizing IAA-deficient foods follows the conserved general control (GC) system, wherein uncharged transfer RNA induces phosphorylation of eukaryotic initiation factor 2 (eIF2) via the GC nonderepressing 2 (GCN2) kinase. Thus, a basic mechanism of nutritional stress management functions in mammalian brain to guide food selection for survival.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hao, Shuzhen -- Sharp, James W -- Ross-Inta, Catherine M -- McDaniel, Brent J -- Anthony, Tracy G -- Wek, Ronald C -- Cavener, Douglas R -- McGrath, Barbara C -- Rudell, John B -- Koehnle, Thomas J -- Gietzen, Dorothy W -- GM49164/GM/NIGMS NIH HHS/ -- NS043231/NS/NINDS NIH HHS/ -- NS33347/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2005 Mar 18;307(5716):1776-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Veterinary Medicine, Department of Anatomy, Physiology and Cell Biology, University of California, Davis, CA 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15774759" target="_blank"〉PubMed〈/a〉
    Keywords: Acylation ; Amino Acids, Essential/*administration & dosage/analysis/*deficiency ; Animals ; Diet ; Eating ; Eukaryotic Initiation Factor-2/*metabolism ; *Food ; Food Preferences ; Leucine/administration & dosage/*analogs & derivatives/pharmacology ; Mice ; Mice, Inbred C57BL ; Olfactory Pathways/*metabolism ; Phosphorylation ; Protein Kinases/*metabolism ; Protein-Serine-Threonine Kinases ; RNA, Transfer/*metabolism ; Rats ; Stereoisomerism ; Threonine/administration & dosage ; eIF-2 Kinase/metabolism
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  • 42
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-09-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Du Pasquier, Louis -- New York, N.Y. -- Science. 2005 Sep 16;309(5742):1826-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Zoology and Evolutionary Biology, University of Basel, Vesalgasse 1, CH-4051 Basel, Switzerland. dupasquier@dial.eunet.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16166509" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Animals ; Axons/physiology ; Binding Sites ; Biological Evolution ; Cell Adhesion Molecules ; Drosophila Proteins/chemistry/*genetics/*immunology/metabolism ; Drosophila melanogaster/*genetics/*immunology ; Genetic Variation ; Hemocytes/immunology/*metabolism ; Humans ; Immunity, Innate ; Immunoglobulins/chemistry ; Membrane Proteins ; Neurons/metabolism ; Protein Isoforms/chemistry/genetics/metabolism ; Proteins/genetics/physiology ; Receptors, Antigen/immunology/metabolism ; Vertebrates/physiology
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  • 43
    Publication Date: 2005-08-16
    Description: Flowering of Arabidopsis is regulated by several environmental and endogenous signals. An important integrator of these inputs is the FLOWERING LOCUS T (FT) gene, which encodes a small, possibly mobile protein. A primary response to floral induction is the activation of FT RNA expression in leaves. Because flowers form at a distant site, the shoot apex, these data suggest that FT primarily controls the timing of flowering. Integration of temporal and spatial information is mediated in part by the bZIP transcription factor FD, which is already expressed at the shoot apex before floral induction. A complex of FT and FD proteins in turn can activate floral identity genes such as APETALA1 (AP1).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wigge, Philip A -- Kim, Min Chul -- Jaeger, Katja E -- Busch, Wolfgang -- Schmid, Markus -- Lohmann, Jan U -- Weigel, Detlef -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2005 Aug 12;309(5737):1056-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Max Planck Institute for Developmental Biology, 72076 Tubingen, Germany. philip.wigge@bbsrc.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16099980" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/genetics/*growth & development/*metabolism ; Arabidopsis Proteins/genetics/*metabolism ; Chromatin Immunoprecipitation ; DNA-Binding Proteins/genetics/metabolism ; Flowers/*growth & development ; Gene Expression Regulation, Plant ; Homeodomain Proteins/genetics/metabolism ; MADS Domain Proteins ; Models, Biological ; Mutation ; Oligonucleotide Array Sequence Analysis ; Phenotype ; Plant Leaves/metabolism ; Plant Proteins/genetics/metabolism ; Plant Shoots/metabolism ; Protein Interaction Mapping ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Time Factors ; Transcription Factors/genetics/*metabolism ; Transcription, Genetic ; Two-Hybrid System Techniques
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  • 44
    Publication Date: 2005-04-16
    Description: Ebola virus (EboV) causes rapidly fatal hemorrhagic fever in humans and there is currently no effective treatment. We found that the infection of African green monkey kidney (Vero) cells by vesicular stomatitis viruses bearing the EboV glycoprotein (GP) requires the activity of endosomal cysteine proteases. Using selective protease inhibitors and protease-deficient cell lines, we identified an essential role for cathepsin B (CatB) and an accessory role for cathepsin L (CatL) in EboV GP-dependent entry. Biochemical studies demonstrate that CatB and CatL mediate entry by carrying out proteolysis of the EboV GP subunit GP1 and support a multistep mechanism that explains the relative contributions of these enzymes to infection. CatB and CatB/CatL inhibitors diminish the multiplication of infectious EboV-Zaire in cultured cells and may merit investigation as anti-EboV drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chandran, Kartik -- Sullivan, Nancy J -- Felbor, Ute -- Whelan, Sean P -- Cunningham, James M -- R01 AI059371/AI/NIAID NIH HHS/ -- R01 AI059371-01A1/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2005 Jun 10;308(5728):1643-5. Epub 2005 Apr 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15831716" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cathepsin B/antagonists & inhibitors/*metabolism ; Cathepsin L ; Cathepsins/antagonists & inhibitors/*metabolism ; Cell Line ; Cells, Cultured ; Cercopithecus aethiops ; Cysteine Endopeptidases/*metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Ebolavirus/metabolism/*physiology ; Endosomes/*metabolism ; Hydrogen-Ion Concentration ; Mice ; Vero Cells ; Vesicular stomatitis Indiana virus/genetics/physiology ; Viral Envelope Proteins/*metabolism ; Virion/physiology
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  • 45
    Publication Date: 2005-10-22
    Description: Blood calcium concentration is maintained within a narrow range despite large variations in dietary input and body demand. The Transient Receptor Potential ion channel TRPV5 has been implicated in this process. We report here that TRPV5 is stimulated by the mammalian hormone klotho. Klotho, a beta-glucuronidase, hydrolyzes extracellular sugar residues on TRPV5, entrapping the channel in the plasma membrane. This maintains durable calcium channel activity and membrane calcium permeability in kidney. Thus, klotho activates a cell surface channel by hydrolysis of its extracellular N-linked oligosaccharides.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, Q -- Hoefs, S -- van der Kemp, A W -- Topala, C N -- Bindels, R J -- Hoenderop, J G -- New York, N.Y. -- Science. 2005 Oct 21;310(5747):490-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen Medical Centre, 6500 HB Nijmegen, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16239475" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Calcium Channels/genetics/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Cells, Cultured ; Glucuronidase/antagonists & inhibitors/metabolism ; Glycosylation ; Humans ; Hydrolysis ; Kidney/cytology/metabolism ; Membrane Proteins/*metabolism ; Mice ; Mice, Inbred C57BL ; Mutation ; Patch-Clamp Techniques ; Protein Transport ; Rabbits ; Sodium/metabolism ; TRPV Cation Channels/genetics/*metabolism ; Transfection
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  • 46
    Publication Date: 2005-02-19
    Description: We describe several fossils referable to Gomphos elkema from deposits close to the Paleocene-Eocene boundary at Tsagan Khushu, Mongolia. Gomphos shares a suite of cranioskeletal characters with extant rabbits, hares, and pikas but retains a primitive dentition and jaw compared to its modern relatives. Phylogenetic analysis supports the position of Gomphos as a stem lagomorph and excludes Cretaceous taxa from the crown radiation of placental mammals. Our results support the hypothesis that rodents and lagomorphs radiated during the Cenozoic and diverged from other placental mammals close to the Cretaceous-Tertiary boundary.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Asher, Robert J -- Meng, Jin -- Wible, John R -- McKenna, Malcolm C -- Rougier, Guillermo W -- Dashzeveg, Demberlyn -- Novacek, Michael J -- New York, N.Y. -- Science. 2005 Feb 18;307(5712):1091-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Museum fur Naturkunde, Humboldt Universitat, Invalidenstrasse 43, 10115 Berlin, Germany. robert.asher@museum.hu-berlin.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15718468" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Foot Bones/anatomy & histology ; *Fossils ; Jaw/anatomy & histology ; *Lagomorpha/anatomy & histology/classification ; Leg Bones/anatomy & histology ; *Mammals/anatomy & histology/classification ; Mongolia ; Paleodontology ; Phylogeny ; Rodentia/anatomy & histology/classification ; Skull/anatomy & histology ; Spine/anatomy & histology
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  • 47
    Publication Date: 2005-09-06
    Description: Noncoding RNA molecules (ncRNAs) have been implicated in numerous biological processes including transcriptional regulation and the modulation of protein function. Yet, in spite of the apparent abundance of ncRNA, little is known about the biological role of the projected thousands of ncRNA genes present in the human genome. To facilitate functional analysis of these RNAs, we have created an arrayed library of short hairpin RNAs (shRNAs) directed against 512 evolutionarily conserved putative ncRNAs and, via cell-based assays, we have begun to determine their roles in cellular pathways. Using this system, we have identified an ncRNA repressor of the nuclear factor of activated T cells (NFAT), which interacts with multiple proteins including members of the importin-beta superfamily and likely functions as a specific regulator of NFAT nuclear trafficking.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Willingham, A T -- Orth, A P -- Batalov, S -- Peters, E C -- Wen, B G -- Aza-Blanc, P -- Hogenesch, J B -- Schultz, P G -- New York, N.Y. -- Science. 2005 Sep 2;309(5740):1570-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16141075" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; DNA-Binding Proteins/*antagonists & inhibitors ; Humans ; Mice ; NFATC Transcription Factors ; Nuclear Proteins/*antagonists & inhibitors ; *RNA Interference ; RNA, Long Noncoding ; RNA, Untranslated/antagonists & inhibitors/genetics/*physiology ; Transcription Factors/*antagonists & inhibitors ; beta Karyopherins/metabolism
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  • 48
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-04-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kennedy, Donald -- New York, N.Y. -- Science. 2005 Apr 8;308(5719):165.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15821047" target="_blank"〉PubMed〈/a〉
    Keywords: Biological Evolution ; Biomedical Research/*trends ; Christianity ; Education/*trends ; Europe ; Politics ; Public Policy ; *Religion and Science ; Teaching ; United States
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  • 49
    Publication Date: 2005-09-10
    Description: Recent studies have shown multiple differences between humans and apes in sialic acid (Sia) biology, including Siglecs (Sia-recognizing-Ig-superfamily lectins). Comparisons with the chimpanzee genome indicate that human SIGLEC11 emerged through human-specific gene conversion by an adjacent pseudogene. Conversion involved 5 cent untranslated sequences and the Sia-recognition domain. This human protein shows reduced binding relative to the ancestral form but recognizes oligosialic acids, which are enriched in the brain. SIGLEC11 is expressed in human but not in chimpanzee brain microglia. Further studies will determine if this event was related to the evolution of Homo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hayakawa, Toshiyuki -- Angata, Takashi -- Lewis, Amanda L -- Mikkelsen, Tarjei S -- Varki, Nissi M -- Varki, Ajit -- R01GM32373/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Sep 9;309(5741):1693.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Glycobiology Research and Training Center, University of California at San Diego, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16151003" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Brain/*metabolism ; Exons ; *Gene Conversion ; Humans ; Lectins/*genetics/metabolism ; Membrane Proteins/*genetics/metabolism ; Microglia/*metabolism ; Pan troglodytes/genetics/metabolism ; Phylogeny ; Pongo pygmaeus/genetics/metabolism ; Pseudogenes ; Regulatory Sequences, Nucleic Acid ; Sialic Acids/metabolism
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  • 50
    Publication Date: 2005-11-15
    Description: Rapid global warming of 5 degrees to 10 degrees C during the Paleocene-Eocene Thermal Maximum (PETM) coincided with major turnover in vertebrate faunas, but previous studies have found little floral change. Plant fossils discovered in Wyoming, United States, show that PETM floras were a mixture of native and migrant lineages and that plant range shifts were large and rapid (occurring within 10,000 years). Floral composition and leaf shape and size suggest that climate warmed by approximately 5 degrees C during the PETM and that precipitation was low early in the event and increased later. Floral response to warming and/or increased atmospheric CO2 during the PETM was comparable in rate and magnitude to that seen in postglacial floras and to the predicted effects of anthropogenic carbon release and climate change on future vegetation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wing, Scott L -- Harrington, Guy J -- Smith, Francesca A -- Bloch, Jonathan I -- Boyer, Douglas M -- Freeman, Katherine H -- New York, N.Y. -- Science. 2005 Nov 11;310(5750):993-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Paleobiology, Smithsonian Museum of Natural History, 10th Street and Constitution Avenue, NW, Washington, DC 20560, USA. wings@si.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16284173" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biodiversity ; Carbon Isotopes/analysis ; *Climate ; *Ecosystem ; *Fossils ; Geologic Sediments ; *Greenhouse Effect ; Oxygen Isotopes/analysis ; Plant Development ; Plant Leaves/anatomy & histology ; *Plants/anatomy & histology/classification ; Rain ; Temperature ; Time Factors ; Wyoming
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  • 51
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, Martin -- New York, N.Y. -- Science. 2005 Dec 16;310(5755):1758.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16357238" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cricetinae ; Humans ; Mice ; PrPC Proteins/*chemistry ; PrPSc Proteins/*chemistry/*pathogenicity ; Prion Diseases/*etiology ; Protein Folding
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  • 52
    Publication Date: 2005-12-13
    Description: Sir2 (silent information regulator 2) is a nicotinamide adenine dinucleotide-dependent deacetylase required for longevity due to calorie restriction in yeast and Drosophila. In mammals, calorie restriction induces a complex pattern of physiological and behavioral changes. Here we report that the mammalian Sir2 ortholog, Sirt1, is required for the induction of a phenotype by calorie restriction in mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Danica -- Steele, Andrew D -- Lindquist, Susan -- Guarente, Leonard -- AG11119/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2005 Dec 9;310(5754):1641.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16339438" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Caloric Restriction ; Eating ; Mice ; Mice, Knockout ; *Motor Activity ; Movement ; Sirtuin 1 ; Sirtuins/genetics/*physiology
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  • 53
    Publication Date: 2005-04-23
    Description: Obligate Acacia ant plants house mutualistic ants as a defense mechanism and provide them with extrafloral nectar (EFN). Ant/plant mutualisms are widespread, but little is known about the biochemical basis of their species specificity. Despite its importance in these and other plant/animal interactions, little attention has been paid to the control of the chemical composition of nectar. We found high invertase (sucrose-cleaving) activity in Acacia EFN, which thus contained no sucrose. Sucrose, a disaccharide common in other EFNs, usually attracts nonsymbiotic ants. The EFN of the ant acacias was therefore unattractive to such ants. The Pseudomyrmex ants that are specialized to live on Acacia had almost no invertase activity in their digestive tracts and preferred sucrose-free EFN. Our results demonstrate postsecretory regulation of the carbohydrate composition of nectar.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heil, M -- Rattke, J -- Boland, W -- New York, N.Y. -- Science. 2005 Apr 22;308(5721):560-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioorganic Chemistry, Max-Planck-Institute for Chemical Ecology, Hans-Knoll-Strasse 8, D-07745 Jena, Germany. Heil_Martin@web.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15845855" target="_blank"〉PubMed〈/a〉
    Keywords: Acacia/chemistry/*enzymology/physiology ; Animals ; Ants/enzymology/*physiology ; Biological Evolution ; Feeding Behavior ; Hydrolysis ; Species Specificity ; Sucrose/analysis/*metabolism ; *Symbiosis ; beta-Fructofuranosidase/*metabolism
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  • 54
    Publication Date: 2005-07-30
    Description: The open oceans comprise most of the biosphere, yet patterns and trends of species diversity there are enigmatic. Here, we derive worldwide patterns of tuna and billfish diversity over the past 50 years, revealing distinct subtropical "hotspots" that appeared to hold generally for other predators and zooplankton. Diversity was positively correlated with thermal fronts and dissolved oxygen and a nonlinear function of temperature (approximately 25 degrees C optimum). Diversity declined between 10 and 50% in all oceans, a trend that coincided with increased fishing pressure, superimposed on strong El Nino-Southern Oscillation-driven variability across the Pacific. We conclude that predator diversity shows a predictable yet eroding pattern signaling ecosystem-wide changes linked to climate and fishing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Worm, Boris -- Sandow, Marcel -- Oschlies, Andreas -- Lotze, Heike K -- Myers, Ransom A -- New York, N.Y. -- Science. 2005 Aug 26;309(5739):1365-9. Epub 2005 Jul 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biology Department, Dalhousie University, Halifax, NS, Canada B3H 4J1. bworm@dal.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16051749" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biodiversity ; Climate ; *Ecosystem ; Fisheries ; Oceans and Seas ; Oxygen/analysis ; *Perciformes ; Population Density ; *Predatory Behavior ; Regression Analysis ; Seasons ; Temperature ; Time Factors ; *Tuna ; Zooplankton
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  • 55
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-10-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heitman, Joseph -- New York, N.Y. -- Science. 2005 Sep 30;309(5744):2175-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC 27710, USA. heitm001@duke.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16195450" target="_blank"〉PubMed〈/a〉
    Keywords: Antifungal Agents/pharmacology ; Aspergillus/drug effects/genetics ; Benzoquinones ; Biological Evolution ; Calcineurin/*physiology ; Calcineurin Inhibitors ; Candida albicans/drug effects/genetics ; Cyclosporine/pharmacology/therapeutic use ; *Drug Resistance, Fungal ; Drug Therapy, Combination ; Ergosterol/metabolism ; HSP90 Heat-Shock Proteins/antagonists & inhibitors/*physiology ; Humans ; Lactams, Macrocyclic ; Mutation ; Mycoses/drug therapy/microbiology ; Phenotype ; Quinones/pharmacology/therapeutic use ; Saccharomyces cerevisiae/*drug effects/genetics/*metabolism ; Saccharomyces cerevisiae Proteins/antagonists & inhibitors/*physiology ; Tacrolimus/pharmacology/therapeutic use
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  • 56
    Publication Date: 2005-01-18
    Description: Dendritic cells (DCs) and macrophages are critical to innate and adaptive immunity to the intestinal bacterial microbiota. Here, we identify a myeloid-derived mucosal DC in mice, which populates the entire lamina propria of the small intestine. Lamina propria DCs were found to depend on the chemokine receptor CX3CR1 to form transepithelial dendrites, which enable the cells to directly sample luminal antigens. CX3CR1 was also found to control the clearance of entero-invasive pathogens by DCs. Thus, CX3CR1-dependent processes, which control host interactions of specialized DCs with commensal and pathogenic bacteria, may regulate immunological tolerance and inflammation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Niess, Jan Hendrik -- Brand, Stephan -- Gu, Xiubin -- Landsman, Limor -- Jung, Steffen -- McCormick, Beth A -- Vyas, Jatin M -- Boes, Marianne -- Ploegh, Hidde L -- Fox, James G -- Littman, Dan R -- Reinecker, Hans-Christian -- AI33856/AI/NIAID NIH HHS/ -- DK33506/DK/NIDDK NIH HHS/ -- DK54427/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2005 Jan 14;307(5707):254-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gastrointestinal Unit, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15653504" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chemokine CX3CL1 ; Chemokines, CX3C/metabolism ; Dendritic Cells/cytology/*immunology/microbiology ; Escherichia coli/*immunology/isolation & purification ; Gene Deletion ; Green Fluorescent Proteins/metabolism ; Ileum/cytology/immunology ; *Immunity, Mucosal ; Intestinal Mucosa/*immunology/microbiology ; Intestine, Small/immunology/microbiology ; Lymphoid Tissue/cytology/immunology ; Membrane Proteins/metabolism ; Mice ; Mice, Transgenic ; Peyer's Patches/immunology/microbiology ; Phagocytosis ; Receptors, Chemokine/genetics/metabolism/*physiology ; Salmonella Infections, Animal/*immunology/microbiology ; Salmonella typhimurium/*immunology/isolation & purification
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  • 57
    Publication Date: 2005-04-16
    Description: Microglial cells represent the immune system of the mammalian brain and therefore are critically involved in various injuries and diseases. Little is known about their role in the healthy brain and their immediate reaction to brain damage. By using in vivo two-photon imaging in neocortex, we found that microglial cells are highly active in their presumed resting state, continually surveying their microenvironment with extremely motile processes and protrusions. Furthermore, blood-brain barrier disruption provoked immediate and focal activation of microglia, switching their behavior from patroling to shielding of the injured site. Microglia thus are busy and vigilant housekeepers in the adult brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nimmerjahn, Axel -- Kirchhoff, Frank -- Helmchen, Fritjof -- New York, N.Y. -- Science. 2005 May 27;308(5726):1314-8. Epub 2005 Apr 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Abteilung Zellphysiologie, Max Planck Institut fur Medizinische Forschung, Jahnstrasse 29, 69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15831717" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/physiology/ultrastructure ; Bicuculline/pharmacology ; Blood-Brain Barrier ; Brain Injuries/physiopathology ; Capillaries/injuries ; Cell Movement ; Cell Surface Extensions/*physiology/ultrastructure ; GABA Antagonists/pharmacology ; Green Fluorescent Proteins ; Lasers ; Lipopolysaccharides/pharmacology ; Mice ; Mice, Transgenic ; Microglia/cytology/*physiology/*ultrastructure ; Microscopy, Fluorescence ; Neocortex/*cytology/*physiology ; Pseudopodia/physiology ; Sodium Channel Blockers/pharmacology ; Tetrodotoxin/pharmacology
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  • 58
    Publication Date: 2005-10-22
    Description: Infection of mice with an attenuated Creutzfeldt-Jakob disease agent (SY-CJD) interferes with superinfection by a more virulent human-derived CJD agent (FU-CJD) and does not require pathological prion protein (PrPres). Using a rapid coculture system, we found that a neural cell line free of immune system cells similarly supported substantial CJD agent interference without PrPres. In addition, SY-CJD prevented superinfection by sheep-derived Chandler (Ch) and 22L scrapie agents. However, only 22L and not Ch prevented FU-CJD infection, even though both scrapie strains provoked abundant PrPres. This relationship between particular strains of sheep- and human-derived agents is likely to affect their prevalence and epidemic spread.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nishida, Noriuki -- Katamine, Shigeru -- Manuelidis, Laura -- NS12674/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2005 Oct 21;310(5747):493-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Yale Medical School, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16239476" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Coculture Techniques ; *Creutzfeldt-Jakob Syndrome ; Humans ; Mice ; Neurons/metabolism/*physiology ; PrPSc Proteins/metabolism/*pathogenicity ; Prions/metabolism/*pathogenicity/*physiology ; Scrapie ; Sheep ; Species Specificity ; Virulence
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  • 59
    Publication Date: 2005-02-01
    Description: Neuronal gene transcription is repressed in non-neuronal cells by the repressor element 1 (RE-1)-silencing transcription factor/neuron-restrictive silencer factor (REST/NRSF) complex. To understand how this silencing is achieved, we examined a family of class-C RNA polymerase II (RNAPII) carboxyl-terminal domain (CTD) phosphatases [small CTD phosphatases (SCPs) 1 to 3], whose expression is restricted to non-neuronal tissues. We show that REST/NRSF recruits SCPs to neuronal genes that contain RE-1 elements, leading to neuronal gene silencing in non-neuronal cells. Phosphatase-inactive forms of SCP interfere with REST/NRSF function and promote neuronal differentiation of P19 stem cells. Likewise, small interfering RNA directed to the single Drosophila SCP unmasks neuronal gene expression in S2 cells. Thus, SCP activity is an evolutionarily conserved transcriptional regulator that acts globally to silence neuronal genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yeo, Michele -- Lee, Soo-Kyung -- Lee, Bora -- Ruiz, Esmeralda C -- Pfaff, Samuel L -- Gill, Gordon N -- DK13149/DK/NIDDK NIH HHS/ -- NS37116/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2005 Jan 28;307(5709):596-600.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15681389" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors ; Cell Differentiation ; Cell Line ; Chromatin Immunoprecipitation ; DNA-Binding Proteins/metabolism ; Down-Regulation ; Drosophila/genetics/metabolism ; Drosophila Proteins/genetics/metabolism ; Gene Expression Profiling ; Gene Expression Regulation ; *Gene Silencing ; Humans ; In Situ Hybridization ; Mice ; Nerve Tissue Proteins/metabolism ; Neurons/cytology/*physiology ; Nuclear Proteins ; Phosphoprotein Phosphatases/genetics/*metabolism ; Phosphorylation ; RNA Interference ; Regulatory Sequences, Nucleic Acid ; Repressor Proteins/*metabolism ; TCF Transcription Factors ; Transcription Factor 7-Like 1 Protein ; Transcription Factors/*metabolism ; Tretinoin/pharmacology
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  • 60
    Publication Date: 2005-10-29
    Description: Hypothalamic neurons that express neuropeptide Y (NPY) and agouti-related protein (AgRP) are thought to be critical regulators of feeding behavior and body weight. To determine whether NPY/AgRP neurons are essential in mice, we targeted the human diphtheria toxin receptor to the Agrp locus, which allows temporally controlled ablation of NPY/AgRP neurons to occur after an injection of diphtheria toxin. Neonatal ablation of NPY/AgRP neurons had minimal effects on feeding, whereas their ablation in adults caused rapid starvation. These results suggest that network-based compensatory mechanisms can develop after the ablation of NPY/AgRP neurons in neonates but do not readily occur when these neurons become essential in adults.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luquet, Serge -- Perez, Francisco A -- Hnasko, Thomas S -- Palmiter, Richard D -- K01 DA026504/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2005 Oct 28;310(5748):683-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Box 357370, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16254186" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/physiology ; Agouti-Related Protein ; Animals ; Animals, Newborn ; Arcuate Nucleus of Hypothalamus/cytology ; Body Weight/physiology ; Diphtheria Toxin ; Feeding Behavior/*physiology ; Heparin-binding EGF-like Growth Factor ; Humans ; Intercellular Signaling Peptides and Proteins ; Mice ; Neurons/metabolism/*physiology ; Neuropeptide Y/*metabolism ; Proteins/*metabolism ; Receptors, Cell Surface/genetics
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  • 61
    Publication Date: 2005-04-30
    Description: Mammalian Toll-like receptors (TLRs) play an important role in the innate recognition of pathogens by dendritic cells (DCs). Although TLRs are clearly involved in the detection of bacteria and viruses, relatively little is known about their function in the innate response to eukaryotic microorganisms. Here we identify a profilin-like molecule from the protozoan parasite Toxoplasma gondii that generates a potent interleukin-12 (IL-12) response in murine DCs that is dependent on myeloid differentiation factor 88. T. gondii profilin activates DCs through TLR11 and is the first chemically defined ligand for this TLR. Moreover, TLR11 is required in vivo for parasite-induced IL-12 production and optimal resistance to infection, thereby establishing a role for the receptor in host recognition of protozoan pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yarovinsky, Felix -- Zhang, Dekai -- Andersen, John F -- Bannenberg, Gerard L -- Serhan, Charles N -- Hayden, Matthew S -- Hieny, Sara -- Sutterwala, Fayyaz S -- Flavell, Richard A -- Ghosh, Sankar -- Sher, Alan -- 1R01AI045806-01A1/AI/NIAID NIH HHS/ -- AI05093/AI/NIAID NIH HHS/ -- R01-AI59440/AI/NIAID NIH HHS/ -- R01-GM38765/GM/NIGMS NIH HHS/ -- Intramural NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2005 Jun 10;308(5728):1626-9. Epub 2005 Apr 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunobiology Section, Laboratory of Parasitic Diseases; National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. fyarovinsky@niaid.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15860593" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Antigens, Differentiation/genetics/metabolism ; Contractile Proteins/chemistry/*immunology/isolation & purification/metabolism ; Dendritic Cells/*immunology ; Genes, Protozoan ; Immunity, Innate ; Interleukin-12/biosynthesis/blood ; Ligands ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Inbred C57BL ; Microfilament Proteins/chemistry/*immunology/isolation & purification/metabolism ; Molecular Sequence Data ; Myeloid Differentiation Factor 88 ; NF-kappa B/metabolism ; Profilins ; Protozoan Proteins/chemistry/*immunology/isolation & purification/metabolism ; Receptors, Cell Surface/*metabolism ; Receptors, Immunologic/genetics/metabolism ; Recombinant Proteins/immunology ; Signal Transduction ; Toll-Like Receptors ; Toxoplasma/genetics/*immunology ; Toxoplasmosis, Animal/*immunology ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 62
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-03-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yuspa, Stuart H -- Epstein, Ervin H Jr -- New York, N.Y. -- Science. 2005 Mar 18;307(5716):1727-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. sy12j@nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15774745" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinoma, Squamous Cell/etiology/genetics/pathology/*physiopathology ; Cell Adhesion Molecules/metabolism ; Cell Transformation, Neoplastic ; Collagen Type VII/chemistry/*genetics/*physiology ; Disease Susceptibility ; Epidermolysis Bullosa Dystrophica/complications/*genetics/metabolism/pathology ; Genes, ras ; Humans ; I-kappa B Proteins/genetics/metabolism ; Keratinocytes/*metabolism/pathology ; Mice ; Mutation ; Neoplasm Invasiveness ; Protein Structure, Tertiary ; Skin Neoplasms/etiology/genetics/pathology/*physiopathology ; Transduction, Genetic ; Transforming Growth Factor beta/metabolism
    Print ISSN: 0036-8075
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  • 63
    Publication Date: 2005-05-21
    Description: beta-Catenin is a multifunctional protein that mediates Wnt signaling by binding to members of the T cell factor (TCF) family of transcription factors. Here, we report an evolutionarily conserved interaction of beta-catenin with FOXO transcription factors, which are regulated by insulin and oxidative stress signaling. beta-Catenin binds directly to FOXO and enhances FOXO transcriptional activity in mammalian cells. In Caenorhabditis elegans, loss of the beta-catenin BAR-1 reduces the activity of the FOXO ortholog DAF-16 in dauer formation and life span. Association of beta-catenin with FOXO was enhanced in cells exposed to oxidative stress. Furthermore, BAR-1 was required for the oxidative stress-induced expression of the DAF-16 target gene sod-3 and for resistance to oxidative damage. These results demonstrate a role for beta-catenin in regulating FOXO function that is particularly important under conditions of oxidative stress.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Essers, Marieke A G -- de Vries-Smits, Lydia M M -- Barker, Nick -- Polderman, Paulien E -- Burgering, Boudewijn M T -- Korswagen, Hendrik C -- New York, N.Y. -- Science. 2005 May 20;308(5725):1181-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiological Chemistry and Center for Biomedical Genetics, University Medical Center, Universiteitsweg 100, 3584 CG Utrecht, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15905404" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Caenorhabditis elegans/genetics/*metabolism/physiology ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Carrier Proteins/genetics/metabolism ; Cell Cycle ; Cell Line ; Cell Line, Tumor ; Cyclin-Dependent Kinase Inhibitor p27 ; Cytoskeletal Proteins/chemistry/genetics/*metabolism ; DNA-Binding Proteins/metabolism ; Forkhead Transcription Factors ; Humans ; Hydrogen Peroxide/pharmacology ; Immunoprecipitation ; Insulin/pharmacology ; Intracellular Signaling Peptides and Proteins/genetics/metabolism ; Lithium Chloride/pharmacology ; Longevity ; Mice ; Mutation ; *Oxidative Stress ; Receptor, Insulin/genetics/metabolism ; *Signal Transduction ; Superoxide Dismutase/metabolism ; Trans-Activators/chemistry/genetics/*metabolism ; Transcription Factors/*metabolism ; Transfection ; beta Catenin
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  • 64
    Publication Date: 2005-02-26
    Description: Determining what fraction of texts and manuscripts have survived from Antiquity and the Middle Ages has been highly problematic. Analyzing the transmission of texts as the "paleodemography" of their manuscripts yields definite and surprisingly high estimates. Parchment copies of the foremost medieval textbooks on arithmetical and calendrical calculation closely fit age distributions expected for populations with logistic growth and manuscripts with exponential survivorship. The estimated half-lives of copies agree with Bischoff's paleographically based suggestion that roughly one in seven manuscripts survive in some form from ninth-century Carolingian workshops. On this basis, many if not most of the leading technical titles circulating in Latin probably survived, even from late Antiquity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cisne, John L -- New York, N.Y. -- Science. 2005 Feb 25;307(5713):1305-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Earth and Atmospheric Sciences, Cornell University, Ithaca, NY 14853, USA. cisne@geology.cornell.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15731453" target="_blank"〉PubMed〈/a〉
    Keywords: History, 15th Century ; History, 16th Century ; History, Ancient ; History, Medieval ; Logistic Models ; Manuscripts as Topic/*history ; Markov Chains ; Mathematics ; Probability ; Science/*history ; Time Factors
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  • 65
    Publication Date: 2005-12-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zimmerberg, Joshua -- Chernomordik, Leonid V -- New York, N.Y. -- Science. 2005 Dec 9;310(5754):1626-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Biophysics, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892-1855, USA. joshz@helix.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16339436" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Exocytosis ; Fatty Acids/*metabolism ; Hydrolysis ; Lipid Bilayers ; Lysophospholipids/*metabolism ; Membrane Fusion ; Membrane Lipids/analysis/metabolism ; Mice ; Micelles ; Neuromuscular Junction/drug effects/physiology ; Neurotoxins/metabolism/toxicity ; Neurotransmitter Agents/metabolism ; Phospholipases A/*metabolism/toxicity ; Synaptic Membranes/chemistry/*physiology ; Synaptic Vesicles/physiology
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  • 66
    Publication Date: 2005-02-01
    Description: The positive buoyancy of marine fish eggs in sea water, allowed by hydration of the oocyte, is critical for their survival and dispersion in the ocean. We isolated an aquaporin, SaAQP1o, that belongs to a unique subfamily of aquaporin-1-like channels specifically evolved in teleosts and mainly expressed in the ovary. We further show that hormone-induced fish oocyte hydration is a highly controlled process based on the interplay between protein hydrolysis and the translocation of SaAQP1o to the plasma membrane, indicating a specialized physiological role for this aquaporin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fabra, Mercedes -- Raldua, Demetrio -- Power, Deborah M -- Deen, Peter M T -- Cerda, Joan -- New York, N.Y. -- Science. 2005 Jan 28;307(5709):545.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center of Aquaculture-Institut de Recerca i Tecnologia Agroalimentaries, Tarragona, Spain, and Reference Center in Aquaculture, Barcelona, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15681377" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Aquaporin 1 ; Aquaporins/chemistry/classification/genetics/*physiology ; Biological Evolution ; Cell Membrane/metabolism ; Cytoplasm/metabolism ; DNA, Complementary ; Female ; Fishes/genetics/physiology ; Mercuric Chloride/pharmacology ; Microvilli/metabolism ; Molecular Sequence Data ; Oocytes/*physiology ; Ovary ; Permeability ; Phylogeny ; Recombinant Proteins/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Sea Bream/genetics/*physiology ; Water/*metabolism ; Xenopus laevis/genetics
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  • 67
    Publication Date: 2005-08-16
    Description: Mesenchymal stem cells (MSCs) are a pluripotent cell type that can differentiate into several distinct lineages. Two key transcription factors, Runx2 and peroxisome proliferator-activated receptor gamma (PPARgamma), drive MSCs to differentiate into either osteoblasts or adipocytes, respectively. How these two transcription factors are regulated in order to specify these alternate cell fates remains a pivotal question. Here we report that a 14-3-3-binding protein, TAZ (transcriptional coactivator with PDZ-binding motif), coactivates Runx2-dependent gene transcription while repressing PPARgamma-dependent gene transcription. By modulating TAZ expression in model cell lines, mouse embryonic fibroblasts, and primary MSCs in culture and in zebrafish in vivo, we observed alterations in osteogenic versus adipogenic potential. These results indicate that TAZ functions as a molecular rheostat that modulates MSC differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hong, Jeong-Ho -- Hwang, Eun Sook -- McManus, Michael T -- Amsterdam, Adam -- Tian, Yu -- Kalmukova, Ralitsa -- Mueller, Elisabetta -- Benjamin, Thomas -- Spiegelman, Bruce M -- Sharp, Phillip A -- Hopkins, Nancy -- Yaffe, Michael B -- CA042063/CA/NCI NIH HHS/ -- GM60594/GM/NIGMS NIH HHS/ -- GM68762/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Aug 12;309(5737):1074-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cancer Research, Department of Biology, Massachusetts Institute of Technology, 77 Massachusetts Avenue, E18-580, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16099986" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/*cytology ; Animals ; Bone Morphogenetic Protein 2 ; Bone Morphogenetic Proteins/pharmacology ; Cell Differentiation ; Cell Line ; Core Binding Factor Alpha 1 Subunit ; Gene Expression Regulation, Developmental ; Humans ; Mesenchymal Stromal Cells/*cytology/physiology ; Mice ; Neoplasm Proteins/metabolism ; Oligonucleotides, Antisense ; Osteoblasts/*cytology ; Osteocalcin/genetics ; Osteogenesis ; PPAR gamma/metabolism ; Promoter Regions, Genetic ; Protein Structure, Tertiary ; Proteins/chemistry/genetics/*physiology ; RNA, Small Interfering ; Transcription Factors/chemistry/genetics/metabolism/*physiology ; Transcriptional Activation ; Transfection ; Transforming Growth Factor beta/pharmacology ; Zebrafish ; Zebrafish Proteins/genetics/physiology
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  • 68
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-05-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beckman, Mary -- New York, N.Y. -- Science. 2005 May 20;308(5725):1103.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15905376" target="_blank"〉PubMed〈/a〉
    Keywords: Altitude ; Animals ; Biodiversity ; Biological Evolution ; Cercocebus/anatomy & histology/*classification ; Conservation of Natural Resources ; Environment ; Population Density ; Tanzania ; Trees ; Vocalization, Animal
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  • 69
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-09-06
    Description: Recent studies showing that most "messenger" RNAs do not encode proteins finally explain the long-standing discrepancy between the small number of protein-coding genes found in vertebrate genomes and the much larger and ever-increasing number of polyadenylated transcripts identified by tag-sampling or microarray-based methods. Exploring the role and diversity of these numerous noncoding RNAs now constitutes a main challenge in transcription research.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Claverie, Jean-Michel -- New York, N.Y. -- Science. 2005 Sep 2;309(5740):1529-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Structural and Genomics Information Laboratory, CNRS UPR 2589, Institut de Biologie Structurale et Microbiologie, 31 chemin Joseph Aiguier, Marseille 13402, France. jean-michel.claverie@igs.cnrs-mrs.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16141064" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Genes ; *Genome, Human ; Genomics ; Humans ; Mice ; Proteins/genetics ; RNA, Untranslated/*biosynthesis/physiology ; *Transcription, Genetic
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  • 70
    Publication Date: 2005-11-19
    Description: Nodes of Ranvier are regularly placed, nonmyelinated axon segments along myelinated nerves. Here we show that nodal membranes isolated from the central nervous system (CNS) of mammals restricted neurite outgrowth of cultured neurons. Proteomic analysis of these membranes revealed several inhibitors of neurite outgrowth, including the oligodendrocyte myelin glycoprotein (OMgp). In rat spinal cord, OMgp was not localized to compact myelin, as previously thought, but to oligodendroglia-like cells, whose processes converge to form a ring that completely encircles the nodes. In OMgp-null mice, CNS nodes were abnormally wide and collateral sprouting was observed. Nodal ensheathment in the CNS may stabilize the node and prevent axonal sprouting.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Jeffrey K -- Phillips, Greg R -- Roth, Alejandro D -- Pedraza, Liliana -- Shan, Weisong -- Belkaid, Wiam -- Mi, Sha -- Fex-Svenningsen, Asa -- Florens, Laurence -- Yates, John R 3rd -- Colman, David R -- NS20147/NS/NINDS NIH HHS/ -- P41 RR11823/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2005 Dec 16;310(5755):1813-7. Epub 2005 Nov 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fishberg Department of Neuroscience, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16293723" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/analysis ; Axons/*physiology/ultrastructure ; Cattle ; Cell Surface Extensions/chemistry/*physiology/ultrastructure ; Cells, Cultured ; GPI-Linked Proteins ; Ganglia, Spinal/physiology/ultrastructure ; Humans ; Mice ; Myelin Proteins ; Myelin Sheath/chemistry ; Myelin-Associated Glycoprotein/analysis ; Myelin-Oligodendrocyte Glycoprotein ; Neurites/*physiology/ultrastructure ; Neuroglia/chemistry/*physiology/*ultrastructure ; Oligodendroglia/chemistry/physiology/ultrastructure ; Proteoglycans/analysis ; Proteomics ; Ranvier's Nodes/chemistry/*physiology/ultrastructure ; Rats ; Spinal Cord/cytology
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  • 71
    Publication Date: 2005-07-30
    Description: The plague is caused by the bacterium Yersinia pestis. Plague bacteria are thought to inject effector Yop proteins into host cells via the type III pathway. The identity of the host cells targeted for injection during plague infection is unknown. We found, using Yop beta-lactamase hybrids and fluorescent staining of live cells from plague-infected animals, that Y. pestis selected immune cells for injection. In vivo, dendritic cells, macrophages, and neutrophils were injected most frequently, whereas B and T lymphocytes were rarely selected. Thus, it appears that Y. pestis disables these cell populations to annihilate host immune responses during plague.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3210820/" 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/PMC3210820/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marketon, Melanie M -- DePaolo, R William -- DeBord, Kristin L -- Jabri, Bana -- Schneewind, Olaf -- 1-U54-AI-057153/AI/NIAID NIH HHS/ -- U54 AI057153/AI/NIAID NIH HHS/ -- U54 AI057153-01/AI/NIAID NIH HHS/ -- U54 AI057153-02/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2005 Sep 9;309(5741):1739-41. Epub 2005 Jul 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of Chicago, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16051750" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology/metabolism/microbiology ; Bacterial Outer Membrane Proteins/genetics/*metabolism ; Dendritic Cells/immunology/metabolism/*microbiology ; Flow Cytometry ; Fluorescence ; HeLa Cells ; Humans ; Macrophages/immunology/metabolism/*microbiology ; Macrophages, Peritoneal/microbiology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Microscopy, Fluorescence ; Neutrophils/immunology/metabolism/*microbiology ; Plague/immunology/*microbiology ; Recombinant Fusion Proteins/metabolism ; T-Lymphocytes/immunology/metabolism/microbiology ; Transformation, Bacterial ; Yersinia pestis/metabolism/*pathogenicity
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  • 72
    Publication Date: 2005-10-15
    Description: Theoretical and laboratory research suggests that phenotypic plasticity can evolve under selection. However, evidence for its evolutionary potential from the wild is lacking. We present evidence from a Dutch population of great tits (Parus major) for variation in individual plasticity in the timing of reproduction, and we show that this variation is heritable. Selection favoring highly plastic individuals has intensified over a 32-year period. This temporal trend is concurrent with climate change causing a mismatch between the breeding times of the birds and their caterpillar prey. Continued selection on plasticity can act to alleviate this mismatch.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nussey, Daniel H -- Postma, Erik -- Gienapp, Phillip -- Visser, Marcel E -- New York, N.Y. -- Science. 2005 Oct 14;310(5746):304-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Netherlands Institute of Ecology (NIOO-KNAW), Post Office Box 40, 6666 ZG Heteren, Netherlands. d.h.nussey@sms.ed.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16224020" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; Animals ; Animals, Wild ; Biological Evolution ; Climate ; Ecosystem ; Female ; Food ; *Inheritance Patterns ; Passeriformes/genetics/*physiology ; Phenotype ; Reproduction ; *Selection, Genetic
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  • 73
    Publication Date: 2005-04-30
    Description: The capacity to generate and analyze mental visual images is essential for many cognitive abilities. We combined triple-pulse transcranial magnetic stimulation (tpTMS) and repetitive TMS (rTMS) to determine which distinct aspect of mental imagery is carried out by the left and right parietal lobe and to reveal interhemispheric compensatory interactions. The left parietal lobe was predominant in generating mental images, whereas the right parietal lobe was specialized in the spatial comparison of the imagined content. Furthermore, in case of an rTMS-induced left parietal lesion, the right parietal cortex could immediately compensate such a left parietal disruption by taking over the specific function of the left hemisphere.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sack, A T -- Camprodon, J A -- Pascual-Leone, A -- Goebel, R -- K24 RR018875/RR/NCRR NIH HHS/ -- NCRR MO1 RR01032/RR/NCRR NIH HHS/ -- R01MH60734/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2005 Apr 29;308(5722):702-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cognitive Neuroscience, Faculty of Psychology, Maastricht University, Post Office Box 616, 6200 MD Maastricht, Netherlands. a.sack@psychology.unimaas.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15860630" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Brain Mapping ; *Cognition ; Diagnostic Techniques, Neurological ; Functional Laterality ; Humans ; *Imagination ; Magnetics ; Male ; Parietal Lobe/*physiology ; Task Performance and Analysis ; Time Factors
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  • 74
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-04-30
    Description: Nestlings of some brood parasitic birds evict hosts' eggs and young soon after hatching, thereby avoiding discrimination by hosts while monopolizing parental care. Eviction carries a cost, however, because lone parasitic nestlings attract a reduced provisioning rate. Here we describe a form of visual signaling used by the evicting Horsfield's hawk-cuckoo (Cuculus fugax) to obtain sufficient food. The chick displays a gape-colored patch on the wing to the host parents as they deliver food, simulating the gaping display of more than one nestling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tanaka, Keita D -- Ueda, Keisuke -- New York, N.Y. -- Science. 2005 Apr 29;308(5722):653.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Life Sciences, Rikkyo University, 3-34-1 Nishi-Ikebukuro, Toshima, 171-8501 Tokyo, Japan. keita@zaf.att.ne.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15860618" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Biological ; *Animal Communication ; Animals ; *Behavior, Animal ; Biological Evolution ; *Birds/anatomy & histology ; Coloring Agents ; Cues ; *Feeding Behavior ; Linear Models ; *Nesting Behavior ; Pigmentation ; Wings, Animal/*anatomy & histology
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  • 75
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-07-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fetler, Luc -- Amigorena, Sebastian -- New York, N.Y. -- Science. 2005 Jul 15;309(5733):392-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire Physico-Chimie Curie, CNRS UMR 168, Institut Curie, Paris, France. luc.fetler@curie.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16020721" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Astrocytes/metabolism ; Brain/blood supply/*cytology/pathology/*physiology ; Brain Injuries/immunology/pathology/*physiopathology ; Capillaries/injuries ; Cell Surface Extensions/physiology/ultrastructure ; Cells, Cultured ; Mice ; Mice, Transgenic ; Microglia/cytology/*physiology/*ultrastructure ; Microscopy/methods ; Movement ; Phagocytosis ; Photons ; Receptors, Purinergic P2/metabolism
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  • 76
    Publication Date: 2005-12-03
    Description: Taste receptor cells detect chemicals in the oral cavity and transmit this information to taste nerves, but the neurotransmitter(s) have not been identified. We report that adenosine 5'-triphosphate (ATP) is the key neurotransmitter in this system. Genetic elimination of ionotropic purinergic receptors (P2X2 and P2X3) eliminates taste responses in the taste nerves, although the nerves remain responsive to touch, temperature, and menthol. Similarly, P2X-knockout mice show greatly reduced behavioral responses to sweeteners, glutamate, and bitter substances. Finally, stimulation of taste buds in vitro evokes release of ATP. Thus, ATP fulfils the criteria for a neurotransmitter linking taste buds to the nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finger, Thomas E -- Danilova, Vicktoria -- Barrows, Jennell -- Bartel, Dianna L -- Vigers, Alison J -- Stone, Leslie -- Hellekant, Goran -- Kinnamon, Sue C -- P30 DC04657/DC/NIDCD NIH HHS/ -- R01 DC00766/DC/NIDCD NIH HHS/ -- R01 DC06070/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 2005 Dec 2;310(5753):1495-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rocky Mountain Taste and Smell Center, Aurora CO 80045, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16322458" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/*metabolism ; Animals ; Chorda Tympani Nerve/*metabolism ; Glossopharyngeal Nerve/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neurotransmitter Agents/metabolism ; Receptors, Purinergic P2/genetics/metabolism ; Receptors, Purinergic P2X2 ; Receptors, Purinergic P2X3 ; Receptors, Serotonin, 5-HT3/genetics/metabolism ; *Signal Transduction ; Taste Buds/*metabolism
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  • 77
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-07-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ohman, Arne -- New York, N.Y. -- Science. 2005 Jul 29;309(5735):711-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Clinical Neuroscience, Karolinska institutet, SE-17176 Stockholm, Sweden. arne.ohman@cns.ki.se〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16051776" target="_blank"〉PubMed〈/a〉
    Keywords: African Americans/psychology ; Attitude ; Avoidance Learning ; Biological Evolution ; *Conditioning (Psychology) ; Continental Population Groups/*psychology ; Ethnic Groups/*psychology ; European Continental Ancestry Group/psychology ; Face ; Fear/*psychology ; Humans ; Interpersonal Relations ; *Prejudice ; Social Behavior ; Social Distance
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  • 78
    Publication Date: 2005-01-22
    Description: Cell lineage specification depends on both gene activation and gene silencing, and in the differentiation of T helper progenitors to Th1 or Th2 effector cells, this requires the action of two opposing transcription factors, T-bet and GATA-3. T-bet is essential for the development of Th1 cells, and GATA-3 performs an equivalent role in Th2 development. We report that T-bet represses Th2 lineage commitment through tyrosine kinase-mediated interaction between the two transcription factors that interferes with the binding of GATA-3 to its target DNA. These results provide a novel function for tyrosine phosphorylation of a transcription factor in specifying alternate fates of a common progenitor cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hwang, Eun Sook -- Szabo, Susanne J -- Schwartzberg, Pamela L -- Glimcher, Laurie H -- AI48126/AI/NIAID NIH HHS/ -- AI56296/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2005 Jan 21;307(5708):430-3.〈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/15662016" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Lineage ; Cytokines/pharmacology/physiology ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; GATA3 Transcription Factor ; Interleukin-5/genetics ; Mice ; Mice, Inbred BALB C ; Mutation ; Phosphorylation ; Phosphotyrosine/metabolism ; Promoter Regions, Genetic ; Protein Structure, Tertiary ; Protein-Tyrosine Kinases/metabolism ; T-Box Domain Proteins ; T-Lymphocytes, Helper-Inducer/cytology/*physiology ; Th1 Cells/cytology/physiology ; Th2 Cells/cytology/*physiology ; Trans-Activators/chemistry/genetics/*metabolism ; Transcription Factors/chemistry/genetics/*metabolism
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  • 79
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-02-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martin, Thomas -- Luo, Zhe-Xi -- New York, N.Y. -- Science. 2005 Feb 11;307(5711):861-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Forschungsinstitut Senckenberg, D-60325 Frankfurt am Main, Germany. tmartin@senckenberg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15709238" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Ear Ossicles/*anatomy & histology ; *Fossils ; Mammals/*anatomy & histology ; Mandible/*anatomy & histology ; Marsupialia/anatomy & histology ; Monotremata/*anatomy & histology
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  • 80
    Publication Date: 2005-07-16
    Description: Neurofibrillary tangles (NFTs) are the most common intraneuronal inclusion in the brains of patients with neurodegenerative diseases and have been implicated in mediating neuronal death and cognitive deficits. Here, we found that mice expressing a repressible human tau variant developed progressive age-related NFTs, neuronal loss, and behavioral impairments. After the suppression of transgenic tau, memory function recovered, and neuron numbers stabilized, but to our surprise, NFTs continued to accumulate. Thus, NFTs are not sufficient to cause cognitive decline or neuronal death in this model of tauopathy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1574647/" 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/PMC1574647/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Santacruz, K -- Lewis, J -- Spires, T -- Paulson, J -- Kotilinek, L -- Ingelsson, M -- Guimaraes, A -- DeTure, M -- Ramsden, M -- McGowan, E -- Forster, C -- Yue, M -- Orne, J -- Janus, C -- Mariash, A -- Kuskowski, M -- Hyman, B -- Hutton, M -- Ashe, K H -- P01 AG015453/AG/NIA NIH HHS/ -- P01-AG15453/AG/NIA NIH HHS/ -- R01 AG008487/AG/NIA NIH HHS/ -- R01 AG026249/AG/NIA NIH HHS/ -- R01 AG026252/AG/NIA NIH HHS/ -- R01 NS033249/NS/NINDS NIH HHS/ -- R01 NS046355/NS/NINDS NIH HHS/ -- R01-026252/PHS HHS/ -- R01-AG08487/AG/NIA NIH HHS/ -- R01-AG26249/AG/NIA NIH HHS/ -- R01-NS46355/NS/NINDS NIH HHS/ -- T31-AG00277/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2005 Jul 15;309(5733):476-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Laboratory Medicine and Pathology, University of Minnesota Medical School, Minneapolis, MN 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16020737" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Atrophy ; Brain/*metabolism/pathology ; Cognition ; Disease Progression ; Doxycycline/pharmacology ; Hippocampus/metabolism/pathology ; Humans ; Maze Learning ; *Memory ; Mice ; Mice, Transgenic ; Neurodegenerative Diseases/metabolism/*pathology/*physiopathology ; Neurofibrillary Tangles/metabolism/*pathology ; Neuronal Plasticity ; Neurons/metabolism/pathology ; Organ Size ; Phosphorylation ; RNA, Messenger/genetics/metabolism ; Solubility ; tau Proteins/chemistry/genetics/*metabolism
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  • 81
    Publication Date: 2005-07-23
    Description: A key process in organ homeostasis is the mobilization of stem cells out of their niches. We show through analysis of mouse models that telomere length, as well as the catalytic component of telomerase, Tert, are critical determinants in the mobilization of epidermal stem cells. Telomere shortening inhibited mobilization of stem cells out of their niche, impaired hair growth, and resulted in suppression of stem cell proliferative capacity in vitro. In contrast, Tert overexpression in the absence of changes in telomere length promoted stem cell mobilization, hair growth, and stem cell proliferation in vitro. The effects of telomeres and telomerase on stem cell biology anticipate their role in cancer and aging.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flores, Ignacio -- Cayuela, Maria L -- Blasco, Maria A -- New York, N.Y. -- Science. 2005 Aug 19;309(5738):1253-6. Epub 2005 Jul 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Telomeres and Telomerase Group, Molecular Oncology Program, Spanish National Cancer Centre (CNIO), Melchor Fernandez Almagro 3, Madrid E-28029, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16037417" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Count ; Cell Differentiation ; Cell Movement ; Cell Proliferation ; Clone Cells ; Epidermis/*cytology ; Hair Follicle/cytology ; Keratinocytes/*cytology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Multipotent Stem Cells/cytology/*physiology ; Telomerase/genetics/*metabolism ; Telomere/*physiology/ultrastructure ; Tetradecanoylphorbol Acetate/pharmacology ; Up-Regulation
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  • 82
    Publication Date: 2005-04-16
    Description: The Drosophila cuticle is essential for maintaining the surface barrier defenses of the fly. Integral to cuticle resilience is the transcription factor grainy head, which regulates production of the enzyme required for covalent cross-linking of the cuticular structural components. We report that formation and maintenance of the epidermal barrier in mice are dependent on a mammalian homolog of grainy head, Grainy head-like 3. Mice lacking this factor display defective skin barrier function and deficient wound repair, accompanied by reduced expression of transglutaminase 1, the key enzyme involved in cross-linking the structural components of the superficial epidermis. These findings suggest that the functional mechanisms involving protein cross-linking that maintain the epidermal barrier and induce tissue repair are conserved across 700 million years of evolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ting, Stephen B -- Caddy, Jacinta -- Hislop, Nikki -- Wilanowski, Tomasz -- Auden, Alana -- Zhao, Lin-Lin -- Ellis, Sarah -- Kaur, Pritinder -- Uchida, Yoshikazu -- Holleran, Walter M -- Elias, Peter M -- Cunningham, John M -- Jane, Stephen M -- P01 HL53749-03/HL/NHLBI NIH HHS/ -- P01-AR39448/AR/NIAMS NIH HHS/ -- P30 CA 21765/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2005 Apr 15;308(5720):411-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rotary Bone Marrow Research Laboratories, c/o Royal Melbourne Hospital Post Office, Grattan Street, Parkville, Victoria, Australia 3050.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15831758" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Biological Evolution ; DNA-Binding Proteins/*genetics/metabolism/*physiology ; Embryo, Mammalian/physiology ; Embryonic Development ; Epidermis/*embryology/*physiology ; Epithelium/physiology ; Gene Expression ; Kruppel-Like Transcription Factors ; Mice ; Mutation ; Permeability ; Transcription Factors/*genetics/metabolism/*physiology ; Transglutaminases/genetics/metabolism ; Wound Healing/*physiology
    Print ISSN: 0036-8075
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  • 83
    Publication Date: 2005-03-19
    Description: Type VII collagen defects cause recessive dystrophic epidermolysis bullosa (RDEB), a blistering skin disorder often accompanied by epidermal cancers. To study the role of collagen VII in these cancers, we examined Ras-driven tumorigenesis in RDEB keratinocytes. Cells devoid of collagen VII did not form tumors in mice, whereas those retaining a specific collagen VII fragment (the amino-terminal noncollagenous domain NC1) were tumorigenic. Forced NC1 expression restored tumorigenicity to collagen VII-null epidermis in a non-cell-autonomous fashion. Fibronectin-like sequences within NC1 (FNC1) promoted tumor cell invasion in a laminin 5-dependent manner and were required for tumorigenesis. Tumor-stroma interactions mediated by collagen VII thus promote neoplasia, and retention of NC1 sequences in a subset of RDEB patients may contribute to their increased susceptibility to squamous cell carcinoma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ortiz-Urda, Susana -- Garcia, John -- Green, Cheryl L -- Chen, Lei -- Lin, Qun -- Veitch, Dallas P -- Sakai, Lynn Y -- Lee, Hyangkyu -- Marinkovich, M Peter -- Khavari, Paul A -- AR43799/AR/NIAMS NIH HHS/ -- AR44012/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Mar 18;307(5716):1773-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉VA Palo Alto Healthcare System, Palo Alto, CA 94304, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15774758" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Animals ; Antibodies/immunology ; Apoptosis ; Carcinoma, Squamous Cell/etiology/*physiopathology ; Cell Adhesion Molecules/immunology/metabolism ; Cell Proliferation ; Cell Transformation, Neoplastic ; Child ; Collagen Type VII/chemistry/*genetics/immunology/*physiology ; Disease Susceptibility ; Epidermolysis Bullosa Dystrophica/complications/*genetics/metabolism/pathology ; Female ; *Genes, ras ; Humans ; I-kappa B Proteins/genetics/metabolism ; Keratinocytes/*metabolism/pathology ; Male ; Mice ; Mice, SCID ; Middle Aged ; Mutation ; Neoplasm Invasiveness ; Protein Structure, Tertiary ; Skin Neoplasms/etiology/pathology/*physiopathology
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  • 84
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-05-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Forster, Peter -- Matsumura, Shuichi -- New York, N.Y. -- Science. 2005 May 13;308(5724):965-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉McDonald Institute for Archaeological Research, University of Cambridge, Cambridge CB2 3ER, UK. pf223@cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15890867" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Australia ; Biological Evolution ; DNA, Mitochondrial/*genetics ; Emigration and Immigration ; Ethnic Groups/*genetics ; Europe ; Female ; Fossils ; Founder Effect ; Genetic Variation ; Genetics, Population ; History, Ancient ; Humans ; India ; Indian Ocean ; Malaysia ; Male ; *Population Dynamics ; Time
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  • 85
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-10-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koenig, Robert -- New York, N.Y. -- Science. 2005 Oct 28;310(5748):608-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16254161" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Fossils ; History, 20th Century ; History, 21st Century ; Hominidae ; Humans ; Male ; Paleontology/*history ; South Africa
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  • 86
    Publication Date: 2005-10-29
    Description: Ciliary neurotrophic factor (CNTF) induces weight loss in obese rodents and humans, and for reasons that are not understood, its effects persist after the cessation of treatment. Here we demonstrate that centrally administered CNTF induces cell proliferation in feeding centers of the murine hypothalamus. Many of the newborn cells express neuronal markers and show functional phenotypes relevant for energy-balance control, including a capacity for leptin-induced phosphorylation of signal transducer and activator of transcription 3 (STAT3). Coadministration of the mitotic blocker cytosine-beta-d-arabinofuranoside (Ara-C) eliminates the proliferation of neural cells and abrogates the long-term, but not the short-term, effect of CNTF on body weight. These findings link the sustained effect of CNTF on energy balance to hypothalamic neurogenesis and suggest that regulated hypothalamic neurogenesis in adult mice may play a previously unappreciated role in physiology and disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kokoeva, Maia V -- Yin, Huali -- Flier, Jeffrey S -- DKR3728082/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2005 Oct 28;310(5748):679-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, 99 Brookline Avenue, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16254185" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Weight/physiology ; Bromodeoxyuridine/administration & dosage ; Cell Proliferation/drug effects ; Ciliary Neurotrophic Factor/administration & dosage/*physiology ; Cytarabine/pharmacology ; Energy Metabolism ; Hypothalamus/cytology/*physiology ; Injections, Intraventricular ; Leptin/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Microtubule-Associated Proteins/biosynthesis ; Neurons/cytology/drug effects/*physiology ; Neuropeptide Y/metabolism ; Neuropeptides/biosynthesis ; Pro-Opiomelanocortin/metabolism ; RNA, Messenger/metabolism ; Receptor, Ciliary Neurotrophic Factor/genetics/metabolism ; STAT3 Transcription Factor/metabolism
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  • 87
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-05-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Foster, Kevin R -- New York, N.Y. -- Science. 2005 May 27;308(5726):1269-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, Rice University MS 170, 6100 Main Street, Houston, TX 77005, USA. krfoster@rice.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15919984" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteria/classification/growth & development/*pathogenicity ; Bacterial Infections/*microbiology ; Bacteriocins/metabolism ; Biofilms/*growth & development ; Biological Evolution ; Drug Resistance, Bacterial ; Humans ; Pseudomonas aeruginosa/growth & development/pathogenicity ; Siderophores/metabolism ; Virulence
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  • 88
    Publication Date: 2005-02-01
    Description: Lupus, a multigenic autoimmune condition in which a breakdown of tolerance results in the development of autoantibodies, leads to a variety of pathologic outcomes. Despite the heterogeneity of factors influencing disease susceptibility, we demonstrate that the partial restoration of inhibitory Fc receptor (FcgRIIB) levels on B cells in lupus-prone mouse strains is sufficient to restore tolerance and prevent autoimmunity. FcgRIIB regulates a common B cell checkpoint in genetically diverse lupus-prone mouse strains, and modest changes in its expression can result in either tolerance or autoimmunity. Therefore, increasing FcgammaRIIB levels on B cells may be an effective way to treat autoimmune diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McGaha, Tracy L -- Sorrentino, Brian -- Ravetch, Jeffrey V -- New York, N.Y. -- Science. 2005 Jan 28;307(5709):590-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Genetics and Immunology, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15681388" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Antinuclear/blood ; Autoantibodies/blood ; B-Lymphocytes/*immunology ; Bone Marrow Transplantation ; Chromatin/immunology ; Female ; Genetic Vectors ; Kidney/pathology ; Lung/pathology ; Lupus Erythematosus, Systemic/*immunology/pathology/physiopathology/*therapy ; Macrophages/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Myeloid Cells/immunology ; Receptors, IgG/genetics/*metabolism ; Retroviridae/genetics ; *Self Tolerance ; T-Lymphocytes/immunology ; Transduction, Genetic
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  • 89
    Publication Date: 2005-10-01
    Description: Type 2 and type 3 inositol 1,4,5-trisphosphate receptors (IP3R2 and IP3R3) are intracellular calcium-release channels whose physiological roles are unknown. We show exocrine dysfunction in IP3R2 and IP3R3 double knock-out mice, which caused difficulties in nutrient digestion. Severely impaired calcium signaling in acinar cells of the salivary glands and the pancreas in the double mutants ascribed the secretion deficits to a lack of intracellular calcium release. Despite a normal caloric intake, the double mutants were hypoglycemic and lean. These results reveal IP3R2 and IP3R3 as key molecules in exocrine physiology underlying energy metabolism and animal growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Futatsugi, Akira -- Nakamura, Takeshi -- Yamada, Maki K -- Ebisui, Etsuko -- Nakamura, Kyoko -- Uchida, Keiko -- Kitaguchi, Tetsuya -- Takahashi-Iwanaga, Hiromi -- Noda, Tetsuo -- Aruga, Jun -- Mikoshiba, Katsuhiko -- New York, N.Y. -- Science. 2005 Sep 30;309(5744):2232-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Calcium Oscillation, International Cooperative Research Project, Japan Science and Technology Agency, Tokyo 108-0071, Japan. afutatsu@brain.riken.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16195467" target="_blank"〉PubMed〈/a〉
    Keywords: Amylases/secretion ; Animals ; Body Weight ; Calcium/metabolism ; Calcium Channels/genetics/*physiology ; Calcium Signaling ; Carbachol/pharmacology ; Digestion ; Eating ; Energy Intake ; *Energy Metabolism ; Inositol 1,4,5-Trisphosphate Receptors ; Lipase/secretion ; Mice ; Mice, Knockout ; Pancreas, Exocrine/cytology/*secretion ; Receptors, Cytoplasmic and Nuclear/genetics/*physiology ; Saliva/*secretion ; Salivation ; Submandibular Gland/metabolism/secretion ; Trypsinogen/secretion
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  • 90
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-04-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Panksepp, Jaak -- New York, N.Y. -- Science. 2005 Apr 1;308(5718):62-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉J. P. Scott Center for Neuroscience, Mind and Behavior, Department of Psychology, Bowling Green State University, Bowling Green, OH 43403,USA. jpankse@bgnet.bgsu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15802592" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Brain/physiology ; Emotions ; *Happiness ; Humans ; *Laughter ; Play and Playthings ; Rats ; *Vocalization, Animal
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  • 91
    Publication Date: 2005-10-15
    Description: The presence and function of CB2 receptors in central nervous system (CNS) neurons are controversial. We report the expression of CB2 receptor messenger RNA and protein localization on brainstem neurons. These functional CB2 receptors in the brainstem were activated by a CB2 receptor agonist, 2-arachidonoylglycerol, and by elevated endogenous levels of endocannabinoids, which also act at CB1 receptors. CB2 receptors represent an alternative site of action of endocannabinoids that opens the possibility of nonpsychotropic therapeutic interventions using enhanced endocannabinoid levels in localized brain areas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Van Sickle, Marja D -- Duncan, Marnie -- Kingsley, Philip J -- Mouihate, Abdeslam -- Urbani, Paolo -- Mackie, Ken -- Stella, Nephi -- Makriyannis, Alexandros -- Piomelli, Daniele -- Davison, Joseph S -- Marnett, Lawrence J -- Di Marzo, Vincenzo -- Pittman, Quentin J -- Patel, Kamala D -- Sharkey, Keith A -- GM15431/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Oct 14;310(5746):329-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Infection, Immunity, and Inflammation and Hotchkiss Brain Institute, Department of Physiology and Biophysics, University of Calgary, Calgary, AB, Canada T2N 4N1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16224028" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arachidonic Acids/pharmacology ; Blotting, Western ; Brain Stem/*metabolism ; Cannabinoid Receptor Modulators/metabolism ; Cannabinoids/pharmacology ; Cerebellum/metabolism ; Cerebral Cortex/metabolism ; Endocannabinoids ; Ferrets ; Immunohistochemistry ; Mice ; Polyunsaturated Alkamides ; RNA, Messenger/analysis ; Rats ; Receptor, Cannabinoid, CB2/agonists/antagonists & inhibitors/*metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Vomiting/prevention & control
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  • 92
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-10-15
    Description: In his or her Perspective, Blumenthal discusses how plants from high-resource habitats are often poorly defended, nutritious, and strongly regulated by enemies. Consequently, these species may benefit the most by entering new habits to escape their natural enemies. This hypothesis predicts that high-resource invasive species may be particularly susceptible to biological control and that increases in resource availability will favor exotic plants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blumenthal, Dana -- New York, N.Y. -- Science. 2005 Oct 14;310(5746):243-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉U.S. Department of Agriculture-Agricultural Research Service Rangeland Resources Research Unit, Crops Research Laboratory, 1701 Center Avenue, Fort Collins, CO 80526, USA. dana.blumenthal@ars.usda.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16224008" target="_blank"〉PubMed〈/a〉
    Keywords: Biodiversity ; Biological Evolution ; *Ecology ; Ecosystem ; *Environment ; *Plant Physiological Phenomena
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  • 93
    Publication Date: 2005-09-10
    Description: Lymphocyte egress from the thymus and from peripheral lymphoid organs depends on sphingosine 1-phosphate (S1P) receptor-1 and is thought to occur in response to circulatory S1P. However, the existence of an S1P gradient between lymphoid organs and blood or lymph has not been established. To further define egress requirements, we addressed why treatment with the food colorant 2-acetyl-4-tetrahydroxybutylimidazole (THI) induces lymphopenia. We found that S1P abundance in lymphoid tissues of mice is normally low but increases more than 100-fold after THI treatment and that this treatment inhibits the S1P-degrading enzyme S1P lyase. We conclude that lymphocyte egress is mediated by S1P gradients that are established by S1P lyase activity and that the lyase may represent a novel immunosuppressant drug target.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwab, Susan R -- Pereira, Joao P -- Matloubian, Mehrdad -- Xu, Ying -- Huang, Yong -- Cyster, Jason G -- AI40098/AI/NIAID NIH HHS/ -- AI45073/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2005 Sep 9;309(5741):1735-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Microbiology and Immunology, University of California San Francisco, 513 Parnassus Avenue, San Francisco, CA 94143-0414, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16151014" target="_blank"〉PubMed〈/a〉
    Keywords: Aldehyde-Lyases/*antagonists & inhibitors/genetics/metabolism ; Animals ; B-Lymphocytes/immunology/physiology ; Chemotaxis, Leukocyte ; Enzyme Inhibitors/pharmacology ; Food Coloring Agents/pharmacology ; Hematopoietic Stem Cells/physiology ; Imidazoles/*pharmacology ; Immunosuppressive Agents/pharmacology ; Lymph/immunology/metabolism ; Lymph Nodes/immunology ; Lymphoid Tissue/immunology/metabolism ; Lymphopenia/chemically induced ; Lysophospholipids/blood/*metabolism ; Mice ; Mice, Inbred C57BL ; Pyridoxine/analogs & derivatives/pharmacology ; RNA Interference ; Receptors, Lysosphingolipid/metabolism ; Sphingosine/*analogs & derivatives/blood/metabolism ; T-Lymphocytes/*immunology/physiology ; Thymus Gland/immunology/metabolism ; Vitamin B 6/pharmacology
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  • 94
    Publication Date: 2005-03-19
    Description: The mammalian intestine harbors a beneficial microbiota numbering approximately 10(12) organisms per gram of colonic content. The host tolerates this tremendous bacterial load while maintaining the ability to efficiently respond to pathogenic organisms. In this study, we show that the Bacteroides use a mammalian-like pathway to decorate numerous surface capsular polysaccharides and glycoproteins with l-fucose, an abundant surface molecule of intestinal epithelial cells, resulting in the coordinated expression of this surface molecule by host and symbiont. A Bacteroides mutant deficient in the ability to cover its surface with L-fucose is defective in colonizing the mammalian intestine under competitive conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coyne, Michael J -- Reinap, Barbara -- Lee, Martin M -- Comstock, Laurie E -- AI44193/AI/NIAID NIH HHS/ -- AI53694/AI/NIAID NIH HHS/ -- R01 AI044193/AI/NIAID NIH HHS/ -- R01 AI044193-07/AI/NIAID NIH HHS/ -- R01 AI053694/AI/NIAID NIH HHS/ -- R01 AI053694-03/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2005 Mar 18;307(5716):1778-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15774760" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Bacterial Capsules/biosynthesis/chemistry/*metabolism ; Bacterial Proteins/biosynthesis/metabolism ; Bacteroides fragilis/enzymology/genetics/growth & development/*metabolism ; Culture Media ; Feces/microbiology ; Fucose/*metabolism ; Gene Deletion ; Genes, Bacterial ; Glycoproteins/biosynthesis/*metabolism ; Guanosine Diphosphate/metabolism ; Guanosine Triphosphate/metabolism ; Humans ; Hydro-Lyases/genetics/metabolism ; Intestinal Mucosa/metabolism ; Intestines/*microbiology ; Mice ; Molecular Mimicry ; Molecular Sequence Data ; Mutation ; Phosphotransferases (Alcohol Group Acceptor)/genetics/metabolism ; *Symbiosis
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  • 95
    Publication Date: 2005-08-27
    Description: A defect in Klotho gene expression in mice accelerates the degeneration of multiple age-sensitive traits. Here, we show that overexpression of Klotho in mice extends life span. Klotho protein functions as a circulating hormone that binds to a cell-surface receptor and represses intracellular signals of insulin and insulin-like growth factor 1 (IGF1), an evolutionarily conserved mechanism for extending life span. Alleviation of aging-like phenotypes in Klotho-deficient mice was observed by perturbing insulin and IGF1 signaling, suggesting that Klotho-mediated inhibition of insulin and IGF1 signaling contributes to its anti-aging properties. Klotho protein may function as an anti-aging hormone in mammals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2536606/" 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/PMC2536606/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kurosu, Hiroshi -- Yamamoto, Masaya -- Clark, Jeremy D -- Pastor, Johanne V -- Nandi, Animesh -- Gurnani, Prem -- McGuinness, Owen P -- Chikuda, Hirotaka -- Yamaguchi, Masayuki -- Kawaguchi, Hiroshi -- Shimomura, Iichiro -- Takayama, Yoshiharu -- Herz, Joachim -- Kahn, C Ronald -- Rosenblatt, Kevin P -- Kuro-o, Makoto -- R01 AG019712/AG/NIA NIH HHS/ -- R01 AG019712-05/AG/NIA NIH HHS/ -- R01 AG025326/AG/NIA NIH HHS/ -- R01 AG025326-03/AG/NIA NIH HHS/ -- R01AG19712/AG/NIA NIH HHS/ -- R01AG25326/AG/NIA NIH HHS/ -- R37 HL063762/HL/NHLBI NIH HHS/ -- U24 DK059637/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2005 Sep 16;309(5742):1829-33. Epub 2005 Aug 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Texas (UT) Southwestern Medical Center at Dallas, 5323 Harry Hines Bouleuvard, Dallas, TX 75390-9072, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16123266" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/genetics/*physiology ; Animals ; Blood Glucose/analysis ; Cell Line ; Cell Line, Tumor ; Eating ; Female ; Glucuronidase ; Insulin/blood/metabolism ; Insulin Resistance ; Insulin-Like Growth Factor I/metabolism/pharmacology ; Ligands ; Longevity/genetics/*physiology ; Male ; Membrane Proteins/chemistry/*genetics/pharmacology/*physiology ; Mice ; Mice, Transgenic ; Myoblasts/metabolism ; Oxygen Consumption ; Peptide Fragments/chemistry/pharmacology ; Phosphorylation ; Receptor, IGF Type 1/metabolism ; Receptor, Insulin/metabolism ; Receptors, Cell Surface/metabolism ; Recombinant Proteins/chemistry/isolation & purification/metabolism ; Signal Transduction
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  • 96
    Publication Date: 2005-07-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2005 Jul 29;309(5735):678-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16051754" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Cells/*cytology/physiology/transplantation ; Bone Marrow Cells/*cytology ; Bone Marrow Transplantation ; Female ; Gene Expression ; Germ Cells/*cytology/physiology ; Humans ; Infertility, Female/physiopathology/therapy ; Mice ; Oocytes/*cytology/physiology ; *Oogenesis ; Ovary/*cytology/physiology ; Stem Cells/*cytology/physiology
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  • 97
    Publication Date: 2005-08-27
    Description: We have explored the use of embryonic stem cells as an alternative to oocytes for reprogramming human somatic nuclei. Human embryonic stem (hES) cells were fused with human fibroblasts, resulting in hybrid cells that maintain a stable tetraploid DNA content and have morphology, growth rate, and antigen expression patterns characteristic of hES cells. Differentiation of hybrid cells in vitro and in vivo yielded cell types from each embryonic germ layer. Analysis of genome-wide transcriptional activity, reporter gene activation, allele-specific gene expression, and DNA methylation showed that the somatic genome was reprogrammed to an embryonic state. These results establish that hES cells can reprogram the transcriptional state of somatic nuclei and provide a system for investigating the underlying mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cowan, Chad A -- Atienza, Jocelyn -- Melton, Douglas A -- Eggan, Kevin -- New York, N.Y. -- Science. 2005 Aug 26;309(5739):1369-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Harvard Stem Cell Institute, Department of Molecular and Cellular Biology, Harvard University, 7 Divinity Avenue, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16123299" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Biomarkers/analysis ; Cell Cycle ; Cell Differentiation ; *Cell Fusion ; Cell Line ; Cell Nucleus/*physiology ; Cell Shape ; Cell Transplantation ; Chromosomes, Human/genetics ; Embryo, Mammalian/*cytology ; Epigenesis, Genetic ; Female ; Fibroblasts/cytology/*physiology ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Humans ; Hybrid Cells/cytology/*physiology ; Male ; Mice ; Mice, Nude ; Phenotype ; Pluripotent Stem Cells/cytology/*physiology ; Polyploidy ; Teratoma/pathology ; Transcription, Genetic ; Transcriptional Activation ; Transfection
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  • 98
    Publication Date: 2005-08-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gillette, Martha U -- Sejnowski, Terrence J -- New York, N.Y. -- Science. 2005 Aug 19;309(5738):1196-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology and the Neuroscience Program, University of Illinois, Urbana-Champaign, IL 61801, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16109872" target="_blank"〉PubMed〈/a〉
    Keywords: Activity Cycles/genetics/*physiology ; Adaptation, Physiological ; Animals ; Arabidopsis/genetics/physiology ; Biological Clocks/genetics/*physiology ; Brain/physiology ; Cell Cycle/*physiology ; Circadian Rhythm/genetics/*physiology ; Cyanobacteria/cytology/physiology ; Feedback, Physiological ; Gene Expression Regulation ; Homeostasis ; Humans ; Light ; Mice ; Models, Biological ; Protein Biosynthesis ; Seasons ; Sleep ; Transcription, Genetic ; Yeasts/cytology/genetics/metabolism
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  • 99
    Publication Date: 2005-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gilman, Sharon Larimer -- Glaze, Florence Eliza -- New York, N.Y. -- Science. 2005 Feb 25;307(5713):1208-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Coastal Carolina University, Conway, SC 29528, USA. sgilman@coastal.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15731431" target="_blank"〉PubMed〈/a〉
    Keywords: History, Ancient ; History, Medieval ; Logistic Models ; Manuscripts as Topic/*history ; Markov Chains ; Probability ; Science/*history ; Time Factors ; Translations
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  • 100
    Publication Date: 2005-11-15
    Description: The primary event that initiates vision is the light-induced 11-cis to all-trans isomerization of retinal in the visual pigment rhodopsin. Despite decades of study with the traditional tools of chemical reaction dynamics, both the timing and nature of the atomic motions that lead to photoproduct production remain unknown. We used femtosecond-stimulated Raman spectroscopy to obtain time-resolved vibrational spectra of the molecular structures formed along the reaction coordinate. The spectral evolution of the vibrational features from 200 femtoseconds to 1 picosecond after photon absorption reveals the temporal sequencing of the geometric changes in the retinal backbone that activate this receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kukura, Philipp -- McCamant, David W -- Yoon, Sangwoon -- Wandschneider, Daniel B -- Mathies, Richard A -- EY-02051/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2005 Nov 11;310(5750):1006-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16284176" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Chemistry, Physical ; Energy Transfer ; Hydrogen/chemistry ; Isomerism ; *Light ; Models, Chemical ; Models, Molecular ; Photochemistry ; Photons ; Physicochemical Phenomena ; Protein Conformation ; Retinaldehyde/*chemistry ; Rhodopsin/*chemistry ; Spectrum Analysis, Raman ; Time Factors ; *Vision, Ocular
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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