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  • Mice  (170)
  • Ecosystem
  • American Association for the Advancement of Science (AAAS)  (204)
  • Irkutsk : Ross. Akad. Nauk, Sibirskoe Otd., Inst. Zemnoj Kory
  • Krefeld : Geologischer Dienst Nordhein-Westfalen
  • Wiley
  • 2005-2009  (204)
  • 2005  (204)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (204)
  • Irkutsk : Ross. Akad. Nauk, Sibirskoe Otd., Inst. Zemnoj Kory
  • Krefeld : Geologischer Dienst Nordhein-Westfalen
  • Wiley
Years
  • 2005-2009  (204)
Year
  • 1
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    A clonogenic bone marrow progenitor specific for macrophages and dendritic cells (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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
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    Neurodegeneration. Huntington's research points to possible new therapies (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 3
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    A microbial arsenic cycle in a salt-saturated, extreme environment (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-05-28
    Description: Searles Lake is a salt-saturated, alkaline brine unusually rich in the toxic element arsenic. Arsenic speciation changed from arsenate [As(V)] to arsenite [As(III)] with sediment depth. Incubated anoxic sediment slurries displayed dissimilatory As(V)-reductase activity that was markedly stimulated by H2 or sulfide, whereas aerobic slurries had rapid As(III)-oxidase activity. An anaerobic, extremely haloalkaliphilic bacterium was isolated from the sediment that grew via As(V) respiration, using either lactate or sulfide as its electron donor. Hence, a full biogeochemical cycle of arsenic occurs in Searles Lake, driven in part by inorganic electron donors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oremland, Ronald S -- Kulp, Thomas R -- Blum, Jodi Switzer -- Hoeft, Shelley E -- Baesman, Shaun -- Miller, Laurence G -- Stolz, John F -- New York, N.Y. -- Science. 2005 May 27;308(5726):1305-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉U.S. Geological Survey, ms 480, 345 Middlefield Road, Menlo Park, CA 94025, USA. roremlan@usgs.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15919992" target="_blank"〉PubMed〈/a〉
    Keywords: Aerobiosis ; Anaerobiosis ; Arsenates/*metabolism ; Arsenites/*metabolism ; Bacteria, Anaerobic/classification/growth & development/*isolation & ; purification/*metabolism ; Bicarbonates/metabolism ; California ; Ecosystem ; Electron Transport ; Genes, rRNA ; Geologic Sediments/*microbiology ; Hydrogen-Ion Concentration ; Lactic Acid/metabolism ; Molecular Sequence Data ; Oxidation-Reduction ; Phylogeny ; *Salts ; Sodium Chloride ; Sulfides/metabolism ; Water/chemistry ; *Water Microbiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    The functional genomics of noncoding RNA (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Obesity and metabolic syndrome in circadian Clock mutant mice (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Experience-driven plasticity of visual cortex limited by myelin and Nogo receptor (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 7
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    Nod2-dependent regulation of innate and adaptive immunity in the intestinal tract (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Physiology. Boosting gene extends mouse life span (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Achieving stability of lipopolysaccharide-induced NF-kappaB activation (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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  • 10
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    Mitochondrial DNA mutations, oxidative stress, and apoptosis in mammalian aging (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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  • 11
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    Toll-like receptor 8-mediated reversal of CD4+ regulatory T cell function (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Conservation biology. Hawaii's coral trees feel the sting of foreign wasps (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gramling, Carolyn -- New York, N.Y. -- Science. 2005 Dec 16;310(5755):1759-60.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16357239" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Animals ; Conservation of Natural Resources ; Ecosystem ; Erythrina/growth & development/*parasitology ; Hawaii ; Insecticides ; Pest Control, Biological ; Plant Tumors/*parasitology ; Wasps/*pathogenicity/physiology
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    A selective inhibitor of eIF2alpha dephosphorylation protects cells from ER stress (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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    Environmental epigenomics meeting. Supplements restore gene function via methylation (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Neuroscience. Does brain cell growth drive weight loss? (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Clonal dominance of hematopoietic stem cells triggered by retroviral gene marking (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Stem cells. Deriving 'controversy-free' ES cells is controversial (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    A mouthful of microbes (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-03-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2005 Mar 25;307(5717):1899-901.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15790840" target="_blank"〉PubMed〈/a〉
    Keywords: Antibiosis ; Archaea/genetics/*isolation & purification ; Bacteria/genetics/growth & development/*isolation & purification/metabolism ; Bacterial Infections/*microbiology ; Biofilms/growth & development ; Ecosystem ; Genes, Archaeal ; Genes, Bacterial ; Gingiva/microbiology ; Halitosis/microbiology ; Humans ; Mouth/*microbiology ; Mouth Diseases/*microbiology ; Mouthwashes ; Sequence Analysis, DNA ; Tongue/microbiology ; Tooth/microbiology
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    SLC24A5, a putative cation exchanger, affects pigmentation in zebrafish and humans (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Virology. Resurrected influenza virus yields secrets of deadly 1918 pandemic (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Neutral ecological theory reveals isolation and rapid speciation in a biodiversity hot spot (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-09-10
    Description: South Africa's Mediterranean-climate fynbos shrubland is a hot spot of species diversity, but its diversity patterns contrast strongly with other high-diversity areas, including the Amazon rain forest. With its extremely high levels of endemism and species turnover, fynbos is made up of dissimilar local communities that are species-rich but relatively poor in rare species. Using neutral ecological theory, we show that the relative species-abundance distributions in fynbos can be explained by migration rates that are two orders of magnitude lower than they are in tropical rain forests. Speciation rates, which are indexed by the "biodiversity parameter" Theta, are estimated to be higher than they are in any previously examined plant system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Latimer, Andrew M -- Silander, John A Jr -- Cowling, Richard M -- New York, N.Y. -- Science. 2005 Sep 9;309(5741):1722-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, University of Connecticut, 75 North Eagleville Road, Storrs, CT 06269, USA. latimer@uconn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16151011" target="_blank"〉PubMed〈/a〉
    Keywords: Bayes Theorem ; *Biodiversity ; Climate ; *Ecology ; Ecosystem ; Environment ; Geography ; Likelihood Functions ; Phylogeny ; *Plants/classification ; Rain ; Seasons ; South Africa ; *Trees/classification
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    Developmental biology. Bird wings really are like dinosaurs' hands (2005)
    American Association for the Advancement of Science (AAAS)
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    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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    PERIOD1-associated proteins modulate the negative limb of the mammalian circadian oscillator (2005)
    American Association for the Advancement of Science (AAAS)
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    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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    Taxonomy. Linnaeus's legacy carries on (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2005 Feb 18;307(5712):1038-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15718447" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Population Groups/*classification ; Animals ; *Biodiversity ; Books, Illustrated ; *Classification ; Conservation of Natural Resources ; Diptera/classification ; Ecosystem ; Encyclopedias as Topic ; Hymenoptera/classification ; *Phylogeny ; Plants/*classification ; Sweden ; Terminology as Topic
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    Medicine. Treating neurodegenerative diseases with antibiotics (2005)
    American Association for the Advancement of Science (AAAS)
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    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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    Dependence of self-tolerance on TRAF6-directed development of thymic stroma (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Gene therapy. Panel urges limits on X-SCID trials (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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    Homeward sound (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-04-12
    Description: Despite spending weeks at sea as larvae, potentially scattered over many kilometers, young coral reef fish find suitable settlement habitat and in some cases return to their natal reefs. We report that some dominant families of larval reef fish use the sounds made by fish and shrimp resident on reefs to help them locate and settle on reefs and that some fish groups use specific components of the reef sound to guide their behavior. These findings could offer potential for active management of reef fisheries.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Simpson, Stephen D -- Meekan, Mark -- Montgomery, John -- McCauley, Rob -- Jeffs, Andrew -- New York, N.Y. -- Science. 2005 Apr 8;308(5719):221.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biological Sciences, University of Edinburgh, Edinburgh, EH9 3JT, UK. s.simpson@ed.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15821083" target="_blank"〉PubMed〈/a〉
    Keywords: *Animal Communication ; Animals ; Anthozoa ; Ecosystem ; Fishes/embryology/*physiology ; *Homing Behavior ; Oceans and Seas ; Sound
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    Circadian clock control by SUMOylation of BMAL1 (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Regulation of mammalian tooth cusp patterning by ectodin (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Stimulus specificity of gene expression programs determined by temporal control of IKK activity (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Nicotinic acid limitation regulates silencing of Candida adhesins during UTI (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Bacterial injectisomes: needle length does matter (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Uncharged tRNA and sensing of amino acid deficiency in mammalian piriform cortex (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Problems of studying extinction risks (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-11-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harcourt, A H -- New York, N.Y. -- Science. 2005 Nov 25;310(5752):1276-8; author reply 1276-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16311317" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Size ; *Databases, Factual ; Ecosystem ; Environment ; *Mammals/anatomy & histology/physiology ; Population Density ; Reproduction ; Risk
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    Problems of studying extinction risks (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Putland, David -- New York, N.Y. -- Science. 2005 Nov 25;310(5752):1276-8; author reply 1276-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16315350" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Size ; Conservation of Natural Resources ; Ecosystem ; Environment ; *Mammals/anatomy & histology/classification/physiology ; Phylogeny ; Population Density ; Risk
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    Global impact of recreational fisheries (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-03-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arlinghaus, Robert -- Cooke, Steven J -- New York, N.Y. -- Science. 2005 Mar 11;307(5715):1561-3; author reply 1561-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15765561" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conservation of Natural Resources ; Ecosystem ; *Fisheries ; *Fishes ; Fresh Water ; Internationality ; Population Dynamics ; *Recreation ; Seawater ; United States
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    Endosomal proteolysis of the Ebola virus glycoprotein is necessary for infection (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    The beta-glucuronidase klotho hydrolyzes and activates the TRPV5 channel (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    A strategy for probing the function of noncoding RNAs finds a repressor of NFAT (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Spongiform diseases. Waiting for the final experiment (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Increase in activity during calorie restriction requires Sirt1 (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    CX3CR1-mediated dendritic cell access to the intestinal lumen and bacterial clearance (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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    Biodiversity. Indian activists release disputed report (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bagla, Pallava -- New York, N.Y. -- Science. 2005 Sep 30;309(5744):2146.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16195433" target="_blank"〉PubMed〈/a〉
    Keywords: *Biodiversity ; Ecosystem ; India ; International Cooperation
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    Resting microglial cells are highly dynamic surveillants of brain parenchyma in vivo (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Reciprocal interference between specific CJD and scrapie agents in neural cell cultures (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Small CTD phosphatases function in silencing neuronal gene expression (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    NPY/AgRP neurons are essential for feeding in adult mice but can be ablated in neonates (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    TLR11 activation of dendritic cells by a protozoan profilin-like protein (2005)
    American Association for the Advancement of Science (AAAS)
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    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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    Cancer. An anchor for tumor cell invasion (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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
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    Functional interaction between beta-catenin and FOXO in oxidative stress signaling (2005)
    American Association for the Advancement of Science (AAAS)
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    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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    Neuroscience. Synaptic membranes bend to the will of a neurotoxin (2005)
    American Association for the Advancement of Science (AAAS)
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    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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    TAZ, a transcriptional modulator of mesenchymal stem cell differentiation (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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    Fewer genes, more noncoding RNA (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Glial membranes at the node of Ranvier prevent neurite outgrowth (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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    Plague bacteria target immune cells during infection (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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    Hypoxia, global warming, and terrestrial late Permian extinctions (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-04-16
    Description: A catastrophic extinction occurred at the end of the Permian Period. However, baseline extinction rates appear to have been elevated even before the final catastrophe, suggesting sustained environmental degradation. For terrestrial vertebrates during the Late Permian, the combination of a drop in atmospheric oxygen plus climate warming would have induced hypoxic stress and consequently compressed altitudinal ranges to near sea level. Our simulations suggest that the magnitude of altitudinal compression would have forced extinctions by reducing habitat diversity, fragmenting and isolating populations, and inducing a species-area effect. It also might have delayed ecosystem recovery after the mass extinction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huey, Raymond B -- Ward, Peter D -- New York, N.Y. -- Science. 2005 Apr 15;308(5720):398-401.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Washington, Box 351800, Seattle, WA 98195, USA. hueyrb@u.washington.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15831755" target="_blank"〉PubMed〈/a〉
    Keywords: Altitude ; Animals ; *Atmosphere ; Biodiversity ; Computer Simulation ; Crowding ; Ecosystem ; Environment ; Fossils ; *Greenhouse Effect ; *Oxygen/analysis ; Population Density ; Respiration ; Temperature ; Time ; Vertebrates/*physiology
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    Selection on heritable phenotypic plasticity in a wild bird population (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Neuroscience. Brain under surveillance: the microglia patrol (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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    ATP signaling is crucial for communication from taste buds to gustatory nerves (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    T helper cell fate specified by kinase-mediated interaction of T-bet with GATA-3 (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Tau suppression in a neurodegenerative mouse model improves memory function (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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    Effects of telomerase and telomere length on epidermal stem cell behavior (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    A homolog of Drosophila grainy head is essential for epidermal integrity in mice (2005)
    American Association for the Advancement of Science (AAAS)
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    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
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    Type VII collagen is required for Ras-driven human epidermal tumorigenesis (2005)
    American Association for the Advancement of Science (AAAS)
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    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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    Marked decline in atmospheric carbon dioxide concentrations during the Paleogene (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-06-18
    Description: The relation between the partial pressure of atmospheric carbon dioxide (pCO2) and Paleogene climate is poorly resolved. We used stable carbon isotopic values of di-unsaturated alkenones extracted from deep sea cores to reconstruct pCO2 from the middle Eocene to the late Oligocene (approximately 45 to 25 million years ago). Our results demonstrate that pCO2 ranged between 1000 to 1500 parts per million by volume in the middle to late Eocene, then decreased in several steps during the Oligocene, and reached modern levels by the latest Oligocene. The fall in pCO2 likely allowed for a critical expansion of ice sheets on Antarctica and promoted conditions that forced the onset of terrestrial C4 photosynthesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pagani, Mark -- Zachos, James C -- Freeman, Katherine H -- Tipple, Brett -- Bohaty, Stephen -- New York, N.Y. -- Science. 2005 Jul 22;309(5734):600-3. Epub 2005 Jun 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Geology and Geophysics, Yale University, 210 Whitney Avenue, New Haven, CT 06511, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15961630" target="_blank"〉PubMed〈/a〉
    Keywords: *Atmosphere ; Carbon Dioxide/*analysis/metabolism ; Carbon Isotopes/analysis ; *Climate ; Ecosystem ; Eukaryota/cytology/growth & development/metabolism ; Ice ; *Photosynthesis ; Phytoplankton/cytology/growth & development/metabolism ; Plant Development ; Plants/metabolism ; Poaceae/growth & development/metabolism ; Time
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    Neurogenesis in the hypothalamus of adult mice: potential role in energy balance (2005)
    American Association for the Advancement of Science (AAAS)
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    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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    Restoration of tolerance in lupus by targeted inhibitory receptor expression (2005)
    American Association for the Advancement of Science (AAAS)
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    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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    IP3 receptor types 2 and 3 mediate exocrine secretion underlying energy metabolism (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Trading water for carbon with biological carbon sequestration (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-12-24
    Description: Carbon sequestration strategies highlight tree plantations without considering their full environmental consequences. We combined field research, synthesis of more than 600 observations, and climate and economic modeling to document substantial losses in stream flow, and increased soil salinization and acidification, with afforestation. Plantations decreased stream flow by 227 millimeters per year globally (52%), with 13% of streams drying completely for at least 1 year. Regional modeling of U.S. plantation scenarios suggests that climate feedbacks are unlikely to offset such water losses and could exacerbate them. Plantations can help control groundwater recharge and upwelling but reduce stream flow and salinize and acidify some soils.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jackson, Robert B -- Jobbagy, Esteban G -- Avissar, Roni -- Roy, Somnath Baidya -- Barrett, Damian J -- Cook, Charles W -- Farley, Kathleen A -- le Maitre, David C -- McCarl, Bruce A -- Murray, Brian C -- New York, N.Y. -- Science. 2005 Dec 23;310(5756):1944-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Nicholas School of the Environment and Earth Sciences, and Center on Global Change, Duke University, Durham, NC 27708-1000, USA. jackson@duke.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16373572" target="_blank"〉PubMed〈/a〉
    Keywords: Carbon/*metabolism ; Climate ; Conservation of Natural Resources ; Ecosystem ; *Environment ; Rivers ; Soil ; Trees/*metabolism ; Water/*metabolism
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    Identification and functional characterization of brainstem cannabinoid CB2 receptors (2005)
    American Association for the Advancement of Science (AAAS)
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    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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    Ecology. Interrelated causes of plant invasion (2005)
    American Association for the Advancement of Science (AAAS)
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    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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    Lymphocyte sequestration through S1P lyase inhibition and disruption of S1P gradients (2005)
    American Association for the Advancement of Science (AAAS)
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    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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    Human symbionts use a host-like pathway for surface fucosylation (2005)
    American Association for the Advancement of Science (AAAS)
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    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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    Suppression of aging in mice by the hormone Klotho (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Reproductive biology. Controversial study finds an unexpected source of oocytes (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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    Nuclear reprogramming of somatic cells after fusion with human embryonic stem cells (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Physiology. Biological clocks coordinately keep life on time (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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    The Asian tsunami: a protective role for coastal vegetation (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-29
    Description: The 26 December 2004 Indian Ocean tsunami had major effects on coastal communities and ecosystems. An assessment of coastlines after the tsunami indicates that coastal vegetation such as mangroves and beach forests helped to provide protection and reduce effects on adjacent communities. In recent years, mangroves and other coastal vegetation have been cleared or degraded along many coastlines, increasing their vulnerability to storm and tsunami damage. Establishing or strengthening greenbelts of mangroves and other coastal forests may play a key role in reducing the effect of future extreme events.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Danielsen, Finn -- Sorensen, Mikael K -- Olwig, Mette F -- Selvam, Vaithilingam -- Parish, Faizal -- Burgess, Neil D -- Hiraishi, Tetsuya -- Karunagaran, Vagarappa M -- Rasmussen, Michael S -- Hansen, Lars B -- Quarto, Alfredo -- Suryadiputra, Nyoman -- New York, N.Y. -- Science. 2005 Oct 28;310(5748):643.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉NORDECO, Skindergade 23, Copenhagen DK-1159, Denmark. fd@nordeco.dk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16254180" target="_blank"〉PubMed〈/a〉
    Keywords: Asia ; *Disasters ; Ecosystem ; Indian Ocean ; Rhizophoraceae ; *Trees
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Parasitology. Malaria vaccines: back to the future? (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Waters, A P -- Mota, M M -- van Dijk, M R -- Janse, C J -- New York, N.Y. -- Science. 2005 Jan 28;307(5709):528-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Parasitology, Leiden University Medical Centre, Leiden 2300 RC, Netherlands. a.p.waters @lumc.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15681372" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Genes, Protozoan ; Genetic Engineering ; Hepatocytes/parasitology/physiology ; Humans ; Immunization Schedule ; Immunization, Secondary ; Malaria/*immunology/prevention & control ; *Malaria Vaccines/immunology ; Malaria, Falciparum/immunology/prevention & control ; Mice ; Plasmodium berghei/genetics/growth & development/*immunology ; Plasmodium falciparum/genetics/immunology ; Protozoan Proteins/genetics/physiology ; Sporozoites/genetics/growth & development/*immunology ; Vaccination ; Vaccines, Attenuated/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Immunology. Now presenting: gammadelta T cells (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-07-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Modlin, Robert L -- Sieling, Peter A -- New York, N.Y. -- Science. 2005 Jul 8;309(5732):252-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Dermatology and Department of Microbiology, Immunology and Molecular Genetics, David Geffen School of Medicine, University of California-Los Angeles, Los Angeles, CA 90095, USA. rmodlin@mednet.ucla.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16002604" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; Antigen-Presenting Cells/*immunology ; Dendritic Cells/immunology ; Genes, T-Cell Receptor ; Histocompatibility Antigens Class II/immunology/metabolism ; Humans ; Immunity, Active ; Immunity, Innate ; Immunologic Memory ; Lymphocyte Activation ; Mice ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; Receptors, Antigen, T-Cell, gamma-delta/*immunology ; T-Lymphocyte Subsets/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Treatment of autoimmune neuroinflammation with a synthetic tryptophan metabolite (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-11-08
    Description: Local catabolism of the amino acid tryptophan (Trp) by indoleamine 2,3-dioxygenase (IDO) is considered an important mechanism of regulating T cell immunity. We show that IDO transcription was increased when myelin-specific T cells were stimulated with tolerogenic altered self-peptides. Catabolites of Trp suppressed proliferation of myelin-specific T cells and inhibited production of proinflammatory T helper-1 (T(H)1) cytokines. N-(3,4,-Dimethoxycinnamoyl) anthranilic acid (3,4-DAA), an orally active synthetic derivative of the Trp metabolite anthranilic acid, reversed paralysis in mice with experimental autoimmune encephalomyelitis, a model of multiple sclerosis (MS). Trp catabolites and their derivatives offer a new strategy for treating T(H)1-mediated autoimmune diseases such as MS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Platten, Michael -- Ho, Peggy P -- Youssef, Sawsan -- Fontoura, Paulo -- Garren, Hideki -- Hur, Eun Mi -- Gupta, Rohit -- Lee, Lowen Y -- Kidd, Brian A -- Robinson, William H -- Sobel, Raymond A -- Selley, Michael L -- Steinman, Lawrence -- New York, N.Y. -- Science. 2005 Nov 4;310(5749):850-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Beckman Center for Molecular Medicine, Stanford University, Stanford, CA 94305, USA. michael.platten@uni-tuebingen.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16272121" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/administration & ; dosage/pharmacology/*therapeutic use ; Antigen-Presenting Cells/drug effects/immunology ; Brain/pathology ; Cell Line ; Cytokines/biosynthesis ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental/*drug therapy/immunology ; Female ; Histocompatibility Antigens Class II/immunology/metabolism ; Immune Tolerance ; Immunosuppressive Agents/pharmacology/therapeutic use ; Indoleamine-Pyrrole 2,3,-Dioxygenase/genetics/metabolism ; Interferon-gamma/immunology ; Lymphocyte Activation ; Mice ; Mice, Transgenic ; Microglia/drug effects/immunology ; Multiple Sclerosis/drug therapy/immunology/pathology ; Myelin Proteins/immunology ; Signal Transduction ; Spinal Cord/pathology ; T-Lymphocytes/immunology ; Th1 Cells/immunology ; Th2 Cells/immunology ; Tryptophan/*metabolism ; ortho-Aminobenzoates/administration & dosage/pharmacology/*therapeutic use
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    Bone marrow stromal cells generate muscle cells and repair muscle degeneration (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-07-09
    Description: Bone marrow stromal cells (MSCs) have great potential as therapeutic agents. We report a method for inducing skeletal muscle lineage cells from human and rat general adherent MSCs with an efficiency of 89%. Induced cells differentiated into muscle fibers upon transplantation into degenerated muscles of rats and mdx-nude mice. The induced population contained Pax7-positive cells that contributed to subsequent regeneration of muscle upon repetitive damage without additional transplantation of cells. These MSCs represent a more ready supply of myogenic cells than do the rare myogenic stem cells normally found in muscle and bone marrow.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dezawa, Mari -- Ishikawa, Hiroto -- Itokazu, Yutaka -- Yoshihara, Tomoyuki -- Hoshino, Mikio -- Takeda, Shin-ichi -- Ide, Chizuka -- Nabeshima, Yo-ichi -- New York, N.Y. -- Science. 2005 Jul 8;309(5732):314-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Kyoto University Graduate School of Medicine, Yoshidakonoecho, Sakyo-ku, Kyoto, 606-8501 Japan. dezawa@anat2.med.kyoto-u.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16002622" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Cells/*cytology/physiology ; Bone Marrow Transplantation ; *Cell Differentiation ; Cell Fusion ; Cell Lineage ; Cell Proliferation ; Cell Separation ; Cells, Cultured ; Colforsin/pharmacology ; Fibroblast Growth Factor 2/pharmacology ; Gene Expression Profiling ; Homeodomain Proteins/analysis ; Humans ; Mice ; Mice, Inbred mdx ; Mice, Nude ; Muscle Cells/*cytology ; Muscle Development/genetics ; Muscle Fibers, Skeletal/*cytology ; Muscle Proteins/analysis ; Muscle, Skeletal/cytology ; Muscular Diseases/*therapy ; Muscular Dystrophy, Duchenne/therapy ; Neuregulins/pharmacology ; PAX7 Transcription Factor ; Platelet-Derived Growth Factor/pharmacology ; Rats ; Regeneration ; Satellite Cells, Skeletal Muscle/cytology/physiology ; Stem Cells/cytology/physiology ; Stromal Cells/*cytology/physiology/transplantation ; Transfection
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    Applied physics. Subsurface imaging with scanning ultrasound holography (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-08
    Description: Every new microscopic imaging technique reveals hidden features but also new challenges. To capture information about substructure features, especially defects and voids, in the next generation of integrated circuits, higher resolution methods of surface imaging will be required. In his Perspective, Diebold discusses results reported in the same issue by Shekhawat and Dravid in which an acoustic scanning holographic imaging technique has been extended to unprecedented spatial resolution. The method has also been used on biological cells, and the hope is that it can be developed further to obtain detailed information about the depth and elastic properties of buried features.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diebold, Alain C -- New York, N.Y. -- Science. 2005 Oct 7;310(5745):61-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉SEMATECH, Austin, TX 78741, USA. .diebold@sematech.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16210522" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Copper ; Fibroblasts/ultrastructure ; Holography/*methods ; Mice ; Microscopy, Acoustic ; Microscopy, Atomic Force/*instrumentation ; *Nanostructures ; *Nanotechnology ; Polymers ; *Ultrasonography
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    Developmental biology. Rac1 up for epidermal stem cells (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-08-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dotto, G Paolo -- Cotsarelis, George -- New York, N.Y. -- Science. 2005 Aug 5;309(5736):890-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Biochemistry, University of Lausanne, Chemin de Bovaresses 155, CH-1066 Epalinges, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16081726" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Homeostasis ; Mice ; Neuropeptides/*physiology ; Skin/*cytology ; Skin Physiological Phenomena ; Stem Cells/*physiology ; rac GTP-Binding Proteins/*physiology ; rac1 GTP-Binding Protein
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    Altered TCR signaling from geometrically repatterned immunological synapses (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-11-19
    Description: The immunological synapse is a specialized cell-cell junction that is defined by large-scale spatial patterns of receptors and signaling molecules yet remains largely enigmatic in terms of formation and function. We used supported bilayer membranes and nanometer-scale structures fabricated onto the underlying substrate to impose geometric constraints on immunological synapse formation. Analysis of the resulting alternatively patterned synapses revealed a causal relation between the radial position of T cell receptors (TCRs) and signaling activity, with prolonged signaling from TCR microclusters that had been mechanically trapped in the peripheral regions of the synapse. These results are consistent with a model of the synapse in which spatial translocation of TCRs represents a direct mechanism of signal regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mossman, Kaspar D -- Campi, Gabriele -- Groves, Jay T -- Dustin, Michael L -- GM64900/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Nov 18;310(5751):1191-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biophysics Graduate Group, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16293763" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Antigen-Presenting Cells/metabolism ; Cells, Cultured ; Lipid Bilayers ; Mice ; Models, Immunological ; Receptors, Antigen, T-Cell/chemistry/*metabolism ; *Signal Transduction ; Structure-Activity Relationship ; T-Lymphocytes/immunology/*metabolism
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    Evolution. Life on the early Earth: a sedimentary view (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-04-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Westall, Frances -- New York, N.Y. -- Science. 2005 Apr 15;308(5720):366-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre de Biophysique Moleculaire, CNRS, Rue Charles Sadron 45071 Orleans cedex 2, France. westall@cnrs-orleans.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15831746" target="_blank"〉PubMed〈/a〉
    Keywords: *Archaea ; Australia ; *Bacteria ; Biofilms ; *Biological Evolution ; Ecosystem ; Environment ; *Fossils ; Geologic Sediments/*microbiology ; *Life ; Microbiological Techniques/instrumentation ; South Africa
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    Cell biology. Of grainy heads and broken skins (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-04-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harden, Nicholas -- New York, N.Y. -- Science. 2005 Apr 15;308(5720):364-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Biochemistry, Simon Fraser University, Burnaby, BC, V5A 1S6 Canada. nharden@sfu.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15831745" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Biological Evolution ; DNA-Binding Proteins/chemistry/*metabolism ; Dopa Decarboxylase/genetics/metabolism ; Drosophila/*embryology/genetics/metabolism ; Drosophila Proteins/genetics/metabolism ; Embryo, Mammalian/physiology ; Embryo, Nonmammalian/physiology ; Enhancer Elements, Genetic ; Epidermis/cytology/*embryology/physiology ; Epithelium/physiology ; Extracellular Signal-Regulated MAP Kinases/metabolism ; *Gene Expression Regulation ; Genes, Reporter ; JNK Mitogen-Activated Protein Kinases/metabolism ; MAP Kinase Signaling System ; Mice ; Mutation ; Nuclear Proteins ; *Signal Transduction ; Transcription Factor AP-1/metabolism ; Transcription Factors/chemistry/*metabolism ; Transcription, Genetic ; Transglutaminases/metabolism ; Tyrosine 3-Monooxygenase/genetics/metabolism ; *Wound Healing
    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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  • 89
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    A role for the phagosome in cytokine secretion (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-11-12
    Description: Membrane traffic in activated macrophages is required for two critical events in innate immunity: proinflammatory cytokine secretion and phagocytosis of pathogens. We found a joint trafficking pathway linking both actions, which may economize membrane transport and augment the immune response. Tumor necrosis factor alpha (TNFalpha) is trafficked from the Golgi to the recycling endosome (RE), where vesicle-associated membrane protein 3 mediates its delivery to the cell surface at the site of phagocytic cup formation. Fusion of the RE at the cup simultaneously allows rapid release of TNFalpha and expands the membrane for phagocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murray, Rachael Z -- Kay, Jason G -- Sangermani, Daniele G -- Stow, Jennifer L -- New York, N.Y. -- Science. 2005 Dec 2;310(5753):1492-5. Epub 2005 Nov 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular Bioscience, University of Queensland, Brisbane, Queensland 4072, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16282525" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Candida albicans/immunology ; Cell Line ; Cell Membrane/metabolism ; Cytoplasmic Vesicles/metabolism ; Endosomes/metabolism ; Interferon-gamma/metabolism ; Macrophage Activation ; Macrophages/immunology/*secretion ; Mice ; Phagocytosis ; Phagosomes/*physiology ; Qa-SNARE Proteins/metabolism ; Tumor Necrosis Factor-alpha/*secretion ; Vesicle-Associated Membrane Protein 3/physiology ; rab GTP-Binding Proteins/biosynthesis
    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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  • 90
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    Akt-mediated phosphorylation of EZH2 suppresses methylation of lysine 27 in histone H3 (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-15
    Description: Enhancer of Zeste homolog 2 (EZH2) is a methyltransferase that plays an important role in many biological processes through its ability to trimethylate lysine 27 in histone H3. Here, we show that Akt phosphorylates EZH2 at serine 21 and suppresses its methyltransferase activity by impeding EZH2 binding to histone H3, which results in a decrease of lysine 27 trimethylation and derepression of silenced genes. Our results imply that Akt regulates the methylation activity, through phosphorylation of EZH2, which may contribute to oncogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cha, Tai-Lung -- Zhou, Binhua P -- Xia, Weiya -- Wu, Yadi -- Yang, Cheng-Chieh -- Chen, Chun-Te -- Ping, Bo -- Otte, Arie P -- Hung, Mien-Chie -- P01 099031/PHS HHS/ -- R01 109311/PHS HHS/ -- New York, N.Y. -- Science. 2005 Oct 14;310(5746):306-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Oncology, the University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16224021" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; COS Cells ; Cell Line ; Cell Transformation, Neoplastic ; Cercopithecus aethiops ; Chromones/pharmacology ; DNA-Binding Proteins ; Enzyme Inhibitors/pharmacology ; Gene Expression Regulation ; HeLa Cells ; Histone-Lysine N-Methyltransferase/metabolism ; Histones/*metabolism ; Homeodomain Proteins/genetics ; Humans ; Lysine/*metabolism ; Methylation ; Mice ; Molecular Sequence Data ; Morpholines/pharmacology ; Phosphorylation ; Polycomb Repressive Complex 2 ; Protein Binding ; Protein Methyltransferases ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/*metabolism ; Proteins/*metabolism ; Proto-Oncogene Proteins/antagonists & inhibitors/*metabolism ; Proto-Oncogene Proteins c-akt ; Serine/metabolism ; Transcription Factors
    Print ISSN: 0036-8075
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  • 91
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    Axonopathy and transport deficits early in the pathogenesis of Alzheimer's disease (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-26
    Description: We identified axonal defects in mouse models of Alzheimer's disease that preceded known disease-related pathology by more than a year; we observed similar axonal defects in the early stages of Alzheimer's disease in humans. Axonal defects consisted of swellings that accumulated abnormal amounts of microtubule-associated and molecular motor proteins, organelles, and vesicles. Impairing axonal transport by reducing the dosage of a kinesin molecular motor protein enhanced the frequency of axonal defects and increased amyloid-beta peptide levels and amyloid deposition. Reductions in microtubule-dependent transport may stimulate proteolytic processing of beta-amyloid precursor protein, resulting in the development of senile plaques and Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stokin, Gorazd B -- Lillo, Concepcion -- Falzone, Tomas L -- Brusch, Richard G -- Rockenstein, Edward -- Mount, Stephanie L -- Raman, Rema -- Davies, Peter -- Masliah, Eliezer -- Williams, David S -- Goldstein, Lawrence S B -- EY12598/EY/NEI NIH HHS/ -- EY13408/EY/NEI NIH HHS/ -- P50 AG05131/AG/NIA NIH HHS/ -- R01 EY007042/EY/NEI NIH HHS/ -- R01 EY007042-19/EY/NEI NIH HHS/ -- R01 EY013408/EY/NEI NIH HHS/ -- R01 EY013408-02/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2005 Feb 25;307(5713):1282-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Cellular and Molecular Medicine, School of Medicine, University of California San Diego (UCSD), 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/15731448" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Aged, 80 and over ; Alzheimer Disease/genetics/*metabolism/*pathology ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/metabolism ; Animals ; *Axonal Transport ; Axons/*pathology/physiology ; Basal Nucleus of Meynert/pathology ; Brain/*metabolism/*pathology ; Cells, Cultured ; Cytoplasmic Vesicles/ultrastructure ; Female ; Hippocampus ; Humans ; Kinesin/metabolism ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Microtubule-Associated Proteins/genetics/metabolism ; Neurons/metabolism ; Organelles/ultrastructure ; Plaque, Amyloid/pathology ; Time Factors
    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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  • 92
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    Immunology. Decoding calcium signaling (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-01-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Winslow, Monte M -- Crabtree, Gerald R -- New York, N.Y. -- Science. 2005 Jan 7;307(5706):56-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology Program, Stanford University, Stanford, CA 94305, USA〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15637261" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channels/metabolism ; Calcium Channels, L-Type/genetics/*metabolism ; *Calcium Signaling ; Cation Transport Proteins/metabolism ; DNA-Binding Proteins/metabolism ; Lymphocyte Activation ; Membrane Potentials ; Mice ; Models, Biological ; Mutation ; NFATC Transcription Factors ; Nuclear Proteins/metabolism ; Phosphorylation ; Potassium/metabolism ; Potassium Channels/metabolism ; Protein Subunits/metabolism ; Receptors, Antigen, T-Cell/metabolism ; T-Lymphocytes/*immunology/metabolism ; TRPM Cation Channels ; Transcription Factors/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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  • 93
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    Chronic lymphocytic inflammation specifies the organ tropism of prions (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-01-22
    Description: Prions typically accumulate in nervous and lymphoid tissues. Because proinflammatory cytokines and immune cells are required for lymphoid prion replication, we tested whether inflammatory conditions affect prion pathogenesis. We administered prions to mice with five inflammatory diseases of the kidney, pancreas, or liver. In all cases, chronic lymphocytic inflammation enabled prion accumulation in otherwise prion-free organs. Inflammatory foci consistently correlated with lymphotoxin up-regulation and ectopic induction of FDC-M1+ cells expressing the normal cellular prion protein PrPC. By contrast, inflamed organs of mice lacking lymphotoxin-alpha or its receptor did not accumulate the abnormal isoform PrPSc, nor did they display infectivity upon prion inoculation. By expanding the tissue distribution of prions, chronic inflammatory conditions may act as modifiers of natural and iatrogenic prion transmission.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heikenwalder, Mathias -- Zeller, Nicolas -- Seeger, Harald -- Prinz, Marco -- Klohn, Peter-Christian -- Schwarz, Petra -- Ruddle, Nancy H -- Weissmann, Charles -- Aguzzi, Adriano -- R01 CA 16885/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2005 Feb 18;307(5712):1107-10. Epub 2005 Jan 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neuropathology, University Hospital of Zurich, CH-8091 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15661974" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chemokine CCL21 ; Chemokines, CC/metabolism ; Hepatitis/immunology/metabolism/pathology ; Inflammation/immunology/*metabolism/pathology ; Islets of Langerhans/immunology/metabolism ; Kidney/immunology/*metabolism/pathology ; Liver/immunology/*metabolism/pathology ; Lymphocytes/*immunology ; Lymphotoxin-alpha/metabolism ; Lymphotoxin-beta ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Nephritis/immunology/metabolism/pathology ; Pancreas/immunology/*metabolism/pathology ; Pancreatitis/immunology/metabolism/pathology ; PrPC Proteins/metabolism ; PrPSc Proteins/analysis/*metabolism ; Scrapie/immunology/*metabolism/pathology ; Spleen/immunology/metabolism ; Tissue Distribution
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  • 94
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    Immunology. Tipping the scales toward more effective antibodies (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-12-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Woof, Jenny M -- New York, N.Y. -- Science. 2005 Dec 2;310(5753):1442-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Pathology and Neuroscience, University of Dundee Medical School, Ninewells Hospital, Dundee DD1 9SY, UK. j.m.woof@dundee.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16322444" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/*immunology/therapeutic use ; Antibodies, Monoclonal/immunology/therapeutic use ; Antigen-Antibody Reactions ; Antigens, Neoplasm/immunology ; Blood Platelets/immunology ; Humans ; Immunoglobulin G/immunology/*therapeutic use ; Lung Neoplasms/immunology/prevention & control ; Mice ; Models, Immunological ; Receptors, IgG/immunology ; Signal Transduction
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  • 95
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    Dependence of olfactory bulb neurogenesis on prokineticin 2 signaling (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-06-25
    Description: Neurogenesis persists in the olfactory bulb (OB) of the adult mammalian brain. New interneurons are continually added to the OB from the subventricular zone (SVZ) via the rostral migratory stream (RMS). Here we show that secreted prokineticin 2 (PK2) functions as a chemoattractant for SVZ-derived neuronal progenitors. Within the OB, PK2 may also act as a detachment signal for chain-migrating progenitors arriving from the RMS. PK2 deficiency in mice leads to a marked reduction in OB size, loss of normal OB architecture, and the accumulation of neuronal progenitors in the RMS. These findings define an essential role for G protein-coupled PK2 signaling in postnatal and adult OB neurogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ng, Kwan L -- Li, Jia-Da -- Cheng, Michelle Y -- Leslie, Frances M -- Lee, Alex G -- Zhou, Qun-Yong -- New York, N.Y. -- Science. 2005 Jun 24;308(5730):1923-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California-Irvine (UCI), Irvine, CA 92697, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15976302" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Brain/cytology/growth & development/metabolism ; Cell Adhesion ; Cell Count ; Cell Line ; Cell Proliferation ; Cerebral Ventricles/cytology/*physiology ; Chemotactic Factors/physiology ; Chemotaxis ; Coculture Techniques ; Dopamine/physiology ; Gastrointestinal Hormones/*metabolism ; Gene Expression ; Interneurons/cytology/*physiology ; Mice ; Mice, Inbred C57BL ; Neurons/cytology/*physiology ; Neuropeptides/*metabolism ; Olfactory Bulb/*cytology/growth & development/*metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, G-Protein-Coupled/genetics/metabolism ; *Signal Transduction ; Stem Cells/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 96
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    Host-bacterial mutualism in the human intestine (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-03-26
    Description: The distal human intestine represents an anaerobic bioreactor programmed with an enormous population of bacteria, dominated by relatively few divisions that are highly diverse at the strain/subspecies level. This microbiota and its collective genomes (microbiome) provide us with genetic and metabolic attributes we have not been required to evolve on our own, including the ability to harvest otherwise inaccessible nutrients. New studies are revealing how the gut microbiota has coevolved with us and how it manipulates and complements our biology in ways that are mutually beneficial. We are also starting to understand how certain keystone members of the microbiota operate to maintain the stability and functional adaptability of this microbial organ.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Backhed, Fredrik -- Ley, Ruth E -- Sonnenburg, Justin L -- Peterson, Daniel A -- Gordon, Jeffrey I -- New York, N.Y. -- Science. 2005 Mar 25;307(5717):1915-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Genome Sciences, Washington University School of Medicine, St. Louis, MO 63108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15790844" target="_blank"〉PubMed〈/a〉
    Keywords: Anaerobiosis ; Bacteria/classification ; *Bacterial Physiological Phenomena ; Bacteroides/genetics/physiology ; Biodiversity ; Biological Evolution ; Ecosystem ; Energy Intake ; Energy Metabolism ; Gastrointestinal Tract/*microbiology/physiology ; Genome, Bacterial ; Humans ; Intestines/*microbiology/physiology ; Obesity/etiology ; Selection, Genetic
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  • 97
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    Requirement of voltage-gated calcium channel beta4 subunit for T lymphocyte functions (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-01-08
    Description: Calcium is known to play vital roles in diverse physiological processes, and it is known that voltage-gated calcium channels (Cav) mediate calcium influx in excitable cells. However, no consensus exists on the molecular identity of the calcium channels present in nonexcitable cells such as T lymphocytes. Here, we demonstrate that T lymphocytes express both regulatory beta4 and poreforming Cav1 alpha1 subunits of Cav channels. Cav beta4-mutant T lymphocytes fail to acquire normal functions and display impairment in the calcium response, activation of the transcription factor NFAT, and cytokine production. Although Cav1 channels of lymphocytes retain their voltage dependency, T cell receptor stimulation dramatically increases channel opening, providing a new mechanism for calcium entry in lymphocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Badou, Abdallah -- Basavappa, Srisaila -- Desai, Rooma -- Peng, You-Qing -- Matza, Didi -- Mehal, Wajahat Z -- Kaczmarek, Leonard K -- Boulpaep, Emile L -- Flavell, Richard A -- New York, N.Y. -- Science. 2005 Jan 7;307(5706):117-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, Howard Hughes Medical Institute, 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/15637280" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD4-Positive T-Lymphocytes/*immunology/*metabolism ; Calcium/*metabolism ; Calcium Channels, L-Type/*metabolism ; *Calcium Signaling ; Cytokines/biosynthesis ; DNA-Binding Proteins/metabolism ; Ion Channel Gating ; Lymphocyte Activation ; Membrane Potentials ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mutation ; NFATC Transcription Factors ; Nuclear Proteins/metabolism ; Patch-Clamp Techniques ; Phosphorylation ; Protein Subunits/metabolism ; Receptors, Antigen, T-Cell/metabolism ; T-Lymphocytes/immunology/metabolism ; Transcription Factors/metabolism
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  • 98
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    Anchorless prion protein results in infectious amyloid disease without clinical scrapie (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-06-04
    Description: In prion and Alzheimer's diseases, the roles played by amyloid versus nonamyloid deposits in brain damage remain unresolved. In scrapie-infected transgenic mice expressing prion protein (PrP) lacking the glycosylphosphatidylinositol (GPI) membrane anchor, abnormal protease-resistant PrPres was deposited as amyloid plaques, rather than the usual nonamyloid form of PrPres. Although PrPres amyloid plaques induced brain damage reminiscent of Alzheimer's disease, clinical manifestations were minimal. In contrast, combined expression of anchorless and wild-type PrP produced accelerated clinical scrapie. Thus, the PrP GPI anchor may play a role in the pathogenesis of prion diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chesebro, Bruce -- Trifilo, Matthew -- Race, Richard -- Meade-White, Kimberly -- Teng, Chao -- LaCasse, Rachel -- Raymond, Lynne -- Favara, Cynthia -- Baron, Gerald -- Priola, Suzette -- Caughey, Byron -- Masliah, Eliezer -- Oldstone, Michael -- AG004342/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2005 Jun 3;308(5727):1435-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, Hamilton, MT 59840, USA. bchesebro@niaid.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15933194" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/metabolism/pathology/ultrastructure ; Glycosylphosphatidylinositols/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Plaque, Amyloid/metabolism/pathology ; PrPSc Proteins/chemistry/metabolism ; Prion Diseases/etiology/metabolism/pathology ; Prions/biosynthesis/chemistry/genetics/*metabolism ; Scrapie/*etiology/metabolism/pathology
    Print ISSN: 0036-8075
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  • 99
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    Divergent immunoglobulin g subclass activity through selective Fc receptor binding (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-12-03
    Description: Subclasses of immunoglobulin G (IgG) display substantial differences in their ability to mediate effector responses, contributing to variable activity of antibodies against microbes and tumors. We demonstrate that the mechanism underlying this long-standing observation of subclass dominance in function is provided by the differential affinities of IgG subclasses for specific activating IgG Fc receptors compared with their affinities for the inhibitory IgG Fc receptor. The significant differences in the ratios of activating-to-inhibitory receptor binding predicted the in vivo activity. We suggest that these highly predictable functions assigned by Fc binding will be an important consideration in the design of therapeutic antibodies and vaccines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nimmerjahn, Falk -- Ravetch, Jeffrey V -- New York, N.Y. -- Science. 2005 Dec 2;310(5753):1510-2.〈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/16322460" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Platelets/immunology ; Cell Line ; Female ; Immunoglobulin G/*immunology/*metabolism ; Melanosomes/immunology ; Mice ; Mice, Inbred C57BL ; Protein Binding ; Receptors, IgG/classification/*metabolism
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  • 100
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    Immunology. Dietary factors and immunological consequences (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-09-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hla, Timothy -- HL67330/HL/NHLBI NIH HHS/ -- HL70694/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2005 Sep 9;309(5741):1682-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Vascular Biology, Department of Cell Biology, University of Connecticut Health Center, Farmington, CT 06030, USA. hla@nso2.uchc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16150998" target="_blank"〉PubMed〈/a〉
    Keywords: Aldehyde-Lyases/*antagonists & inhibitors/metabolism ; Animals ; Cell Movement ; Chemotaxis, Leukocyte ; *Diet ; Enzyme Inhibitors/pharmacology ; Fingolimod Hydrochloride ; Food Coloring Agents/administration & dosage/pharmacology ; Imidazoles/administration & dosage/*pharmacology ; Immunosuppressive Agents/pharmacology ; Lymphoid Tissue/immunology ; Lysophospholipids/blood/*metabolism ; Mice ; Propylene Glycols/pharmacology ; Receptors, Lysosphingolipid/metabolism ; Sphingosine/*analogs & derivatives/blood/metabolism ; T-Lymphocytes/*immunology/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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