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  • 1
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    Comment on "On the origin of interictal activity in human temporal lobe epilepsy in vitro" (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wozny, Christian -- Kivi, Anatol -- Lehmann, Thomas-Nicolas -- Dehnicke, Christoph -- Heinemann, Uwe -- Behr, Joachim -- New York, N.Y. -- Science. 2003 Jul 25;301(5632):463; author reply 463.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience Research Center, at the Charite, Humboldt University of Berlin, Schumannstrasse 20/21, 10117 Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12881553" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Electroencephalography ; Epilepsy, Temporal Lobe/pathology/*physiopathology ; Excitatory Amino Acid Antagonists ; Hippocampus/pathology/*physiopathology ; Humans ; In Vitro Techniques ; Neurons/physiology ; Neurons, Afferent/physiology ; Receptors, GABA-A/metabolism ; Receptors, Glutamate/metabolism ; Synaptic Transmission ; Temporal Lobe/physiopathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Bile acids: natural ligands for an orphan nuclear receptor (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: Bile acids regulate the transcription of genes that control cholesterol homeostasis through molecular mechanisms that are poorly understood. Physiological concentrations of free and conjugated chenodeoxycholic acid, lithocholic acid, and deoxycholic acid activated the farnesoid X receptor (FXR; NR1H4), an orphan nuclear receptor. As ligands, these bile acids and their conjugates modulated interaction of FXR with a peptide derived from steroid receptor coactivator 1. These results provide evidence for a nuclear bile acid signaling pathway that may regulate cholesterol homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parks, D J -- Blanchard, S G -- Bledsoe, R K -- Chandra, G -- Consler, T G -- Kliewer, S A -- Stimmel, J B -- Willson, T M -- Zavacki, A M -- Moore, D D -- Lehmann, J M -- F32 DK09793/DK/NIDDK NIH HHS/ -- R01 DK53366/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1999 May 21;284(5418):1365-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biochemistry, Glaxo Wellcome Research and Development, Research Triangle Park NC, 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334993" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bile Acids and Salts/chemistry/*metabolism/pharmacology ; Carrier Proteins/metabolism ; Cell Line ; Chenodeoxycholic Acid/*metabolism/pharmacology ; Cholesterol/metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Deoxycholic Acid/metabolism/pharmacology ; Histone Acetyltransferases ; Homeostasis ; Humans ; Ligands ; Lithocholic Acid/metabolism/pharmacology ; Mice ; Nuclear Receptor Coactivator 1 ; *Organic Anion Transporters, Sodium-Dependent ; Protein Conformation ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Structure-Activity Relationship ; *Symporters ; Transcription Factors/chemistry/genetics/*metabolism ; Transfection
    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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    Orphan nuclear receptors: shifting endocrinology into reverse (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-30
    Description: Steroid and thyroid hormones and vitamin A metabolites (retinoids) regulate the expression of complex gene programs by binding to members of the nuclear receptor family of ligand-activated transcription factors. The nuclear receptor family also includes many "orphan" members that currently lack known ligands but that represent candidate receptors for new hormones. Recently, natural and synthetic ligands have been identified for several orphan receptors and used to dissect their biological roles. This "reverse endocrinology" strategy has resulted in the discovery of unanticipated nuclear signaling pathways for retinoids, fatty acids, eicosanoids, and steroids with important physiological and pharmacological ramifications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kliewer, S A -- Lehmann, J M -- Willson, T M -- New York, N.Y. -- Science. 1999 Apr 30;284(5415):757-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Endocrinology, Glaxo Wellcome Research and Development, Five Moore Drive, Research Triangle Park, NC 27709, USA. sak15922@glaxowellcome.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10221899" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Nucleus/metabolism ; DNA-Binding Proteins/physiology ; Hormones/physiology ; Humans ; Ligands ; Orphan Nuclear Receptors ; Receptors, Cell Surface/*physiology ; Receptors, Cytoplasmic and Nuclear/*physiology ; Receptors, Steroid/*physiology ; *Signal Transduction ; Transcription Factors/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Identification of LFA-1 as a candidate autoantigen in treatment-resistant Lyme arthritis (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-07-31
    Description: Treatment-resistant Lyme arthritis is associated with immune reactivity to outer surface protein A (OspA) of Borrelia burgdorferi, the agent of Lyme disease, and the major histocompatibility complex class II allele DRB1*0401. The immunodominant epitope of OspA for T helper cells was identified. A homology search revealed a peptide from human leukocyte function-associated antigen-1 (hLFA-1) as a candidate autoantigen. Individuals with treatment-resistant Lyme arthritis, but not other forms of arthritis, generated responses to OspA, hLFA-1, and their highly related peptide epitopes. Identification of the initiating bacterial antigen and a cross-reactive autoantigen may provide a model for development of autoimmune disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gross, D M -- Forsthuber, T -- Tary-Lehmann, M -- Etling, C -- Ito, K -- Nagy, Z A -- Field, J A -- Steere, A C -- Huber, B T -- R01 AR20358/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Jul 31;281(5377):703-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Tufts University, Boston, MA 02111 USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9685265" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Algorithms ; Amino Acid Sequence ; Animals ; Antigen Presentation ; Antigens, Surface/immunology/metabolism ; Arthritis, Reactive/drug therapy/*immunology ; Autoantigens/*immunology ; Autoimmune Diseases/*immunology ; Bacterial Outer Membrane Proteins/immunology/metabolism ; Bacterial Vaccines ; Borrelia burgdorferi Group/immunology ; Child ; Cross Reactions ; Female ; HLA-DR Antigens/genetics/immunology/metabolism ; HLA-DRB1 Chains ; Humans ; Immunodominant Epitopes ; *Lipoproteins ; Lyme Disease/drug therapy/*immunology ; Lymphocyte Function-Associated Antigen-1/chemistry/*immunology/metabolism ; Male ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Synovial Fluid/immunology ; T-Lymphocytes, Helper-Inducer/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Link communities reveal multiscale complexity in networks (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-06-22
    Description: Networks have become a key approach to understanding systems of interacting objects, unifying the study of diverse phenomena including biological organisms and human society. One crucial step when studying the structure and dynamics of networks is to identify communities: groups of related nodes that correspond to functional subunits such as protein complexes or social spheres. Communities in networks often overlap such that nodes simultaneously belong to several groups. Meanwhile, many networks are known to possess hierarchical organization, where communities are recursively grouped into a hierarchical structure. However, the fact that many real networks have communities with pervasive overlap, where each and every node belongs to more than one group, has the consequence that a global hierarchy of nodes cannot capture the relationships between overlapping groups. Here we reinvent communities as groups of links rather than nodes and show that this unorthodox approach successfully reconciles the antagonistic organizing principles of overlapping communities and hierarchy. In contrast to the existing literature, which has entirely focused on grouping nodes, link communities naturally incorporate overlap while revealing hierarchical organization. We find relevant link communities in many networks, including major biological networks such as protein-protein interaction and metabolic networks, and show that a large social network contains hierarchically organized community structures spanning inner-city to regional scales while maintaining pervasive overlap. Our results imply that link communities are fundamental building blocks that reveal overlap and hierarchical organization in networks to be two aspects of the same phenomenon.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ahn, Yong-Yeol -- Bagrow, James P -- Lehmann, Sune -- U01 A1070499-01/PHS HHS/ -- England -- Nature. 2010 Aug 5;466(7307):761-4. doi: 10.1038/nature09182. Epub 2010 Jun 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Complex Network Research, Department of Physics, Northeastern University, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20562860" target="_blank"〉PubMed〈/a〉
    Keywords: *Cell Phones/utilization ; Cities ; *Community Networks/statistics & numerical data ; Humans ; *Metabolic Networks and Pathways ; Models, Biological ; *Protein Interaction Mapping
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 6
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    The skeletal muscle chloride channel in dominant and recessive human myotonia (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-07
    Description: Autosomal recessive generalized myotonia (Becker's disease) (GM) and autosomal dominant myotonia congenita (Thomsen's disease) (MC) are characterized by skeletal muscle stiffness that is a result of muscle membrane hyperexcitability. For both diseases, alterations in muscle chloride or sodium currents or both have been observed. A complementary DNA for a human skeletal muscle chloride channel (CLC-1) was cloned, physically localized on chromosome 7, and linked to the T cell receptor beta (TCRB) locus. Tight linkage of these two loci to GM and MC was found in German families. An unusual restriction site in the CLC-1 locus in two GM families identified a mutation associated with that disease, a phenylalanine-to-cysteine substitution in putative transmembrane domain D8. This suggests that different mutations in CLC-1 may cause dominant or recessive myotonia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koch, M C -- Steinmeyer, K -- Lorenz, C -- Ricker, K -- Wolf, F -- Otto, M -- Zoll, B -- Lehmann-Horn, F -- Grzeschik, K H -- Jentsch, T J -- New York, N.Y. -- Science. 1992 Aug 7;257(5071):797-800.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Center for Human Genetics, Marburg University, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1379744" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blotting, Southern ; Chloride Channels ; *Chromosomes, Human, Pair 7 ; Cloning, Molecular ; DNA/genetics ; Female ; *Genes, Dominant ; *Genes, Recessive ; Genetic Linkage ; Humans ; Ion Channels/*genetics ; Lod Score ; Male ; Membrane Proteins/*genetics ; Molecular Sequence Data ; Muscular Dystrophies/*genetics ; Myotonia Congenita/*genetics ; Pedigree ; Polymorphism, Restriction Fragment Length ; Receptors, Antigen, T-Cell/genetics ; Recombination, Genetic ; Sequence Homology, Nucleic Acid
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Modulation of gene expression via disruption of NF-kappaB signaling by a bacterial small molecule (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-06-21
    Description: The control of innate immune responses through activation of the nuclear transcription factor NF-kappaB is essential for the elimination of invading microbial pathogens. We showed that the bacterial N-(3-oxo-dodecanoyl) homoserine lactone (C12) selectively impairs the regulation of NF-kappaB functions in activated mammalian cells. The consequence is specific repression of stimulus-mediated induction of NF-kappaB-responsive genes encoding inflammatory cytokines and other immune regulators. These findings uncover a strategy by which C12-producing opportunistic pathogens, such as Pseudomonas aeruginosa, attenuate the innate immune system to establish and maintain local persistent infection in humans, for example, in cystic fibrosis patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kravchenko, Vladimir V -- Kaufmann, Gunnar F -- Mathison, John C -- Scott, David A -- Katz, Alexander Z -- Grauer, David C -- Lehmann, Mandy -- Meijler, Michael M -- Janda, Kim D -- Ulevitch, Richard J -- New York, N.Y. -- Science. 2008 Jul 11;321(5886):259-63. doi: 10.1126/science.1156499. Epub 2008 Jun 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Microbial Sciences, 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/18566250" target="_blank"〉PubMed〈/a〉
    Keywords: 4-Butyrolactone/*analogs & derivatives/physiology ; Adult ; Animals ; Cyclic AMP Response Element-Binding Protein/metabolism ; Cystic Fibrosis/microbiology ; Female ; *Gene Expression Regulation ; Homoserine/*analogs & derivatives/physiology ; Humans ; I-kappa B Kinase/metabolism ; I-kappa B Proteins/metabolism ; Immunity, Innate ; Interferon-gamma/immunology ; Lipopolysaccharides/immunology ; Macrophage Activation ; Macrophages/*immunology/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Middle Aged ; NF-kappa B/*metabolism ; Phosphorylation ; Pseudomonas Infections/immunology/microbiology ; Pseudomonas aeruginosa/immunology/*pathogenicity/physiology ; *Signal Transduction ; Toll-Like Receptors/metabolism ; Transcription Factor RelA/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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  • 8
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    Modeling human disease (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gitler, Aaron D -- Lehmann, Ruth -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Jul 20;337(6092):269. doi: 10.1126/science.1227179.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22822114" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Disease/*genetics ; *Disease Models, Animal ; Genes/*physiology ; Genetics, Medical/*trends ; Humans ; Sequence Analysis, DNA/*trends
    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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    Ubiquitin-binding domains in Y-family polymerases regulate translesion synthesis (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-12-17
    Description: Translesion synthesis (TLS) is the major pathway by which mammalian cells replicate across DNA lesions. Upon DNA damage, ubiquitination of proliferating cell nuclear antigen (PCNA) induces bypass of the lesion by directing the replication machinery into the TLS pathway. Yet, how this modification is recognized and interpreted in the cell remains unclear. Here we describe the identification of two ubiquitin (Ub)-binding domains (UBM and UBZ), which are evolutionarily conserved in all Y-family TLS polymerases (pols). These domains are required for binding of poleta and poliota to ubiquitin, their accumulation in replication factories, and their interaction with monoubiquitinated PCNA. Moreover, the UBZ domain of poleta is essential to efficiently restore a normal response to ultraviolet irradiation in xeroderma pigmentosum variant (XP-V) fibroblasts. Our results indicate that Ub-binding domains of Y-family polymerases play crucial regulatory roles in TLS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bienko, Marzena -- Green, Catherine M -- Crosetto, Nicola -- Rudolf, Fabian -- Zapart, Grzegorz -- Coull, Barry -- Kannouche, Patricia -- Wider, Gerhard -- Peter, Matthias -- Lehmann, Alan R -- Hofmann, Kay -- Dikic, Ivan -- New York, N.Y. -- Science. 2005 Dec 16;310(5755):1821-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Biochemistry II, Goethe University Medical School, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16357261" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Cell Line ; Computational Biology ; DNA/*biosynthesis ; *DNA Damage ; DNA Repair ; DNA Replication ; DNA-Directed DNA Polymerase/*chemistry/genetics/*metabolism ; Humans ; Hydrophobic and Hydrophilic Interactions ; Models, Molecular ; Molecular Sequence Data ; Mutation ; Nuclear Magnetic Resonance, Biomolecular ; Point Mutation ; Proliferating Cell Nuclear Antigen/metabolism ; Protein Binding ; Protein Conformation ; Protein Interaction Mapping ; Protein Structure, Tertiary ; Recombinant Fusion Proteins/metabolism ; Transfection ; Ubiquitin/*metabolism ; Xeroderma Pigmentosum/genetics ; Zinc Fingers
    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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  • 10
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    A cellular microRNA mediates antiviral defense in human cells (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-04-23
    Description: In eukaryotes, 21- to 24-nucleotide-long RNAs engage in sequence-specific interactions that inhibit gene expression by RNA silencing. This process has regulatory roles involving microRNAs and, in plants and insects, it also forms the basis of a defense mechanism directed by small interfering RNAs that derive from replicative or integrated viral genomes. We show that a cellular microRNA effectively restricts the accumulation of the retrovirus primate foamy virus type 1 (PFV-1) in human cells. PFV-1 also encodes a protein, Tas, that suppresses microRNA-directed functions in mammalian cells and displays cross-kingdom antisilencing activities. Therefore, through fortuitous recognition of foreign nucleic acids, cellular microRNAs have direct antiviral effects in addition to their regulatory functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lecellier, Charles-Henri -- Dunoyer, Patrice -- Arar, Khalil -- Lehmann-Che, Jacqueline -- Eyquem, Stephanie -- Himber, Christophe -- Saib, Ali -- Voinnet, Olivier -- New York, N.Y. -- Science. 2005 Apr 22;308(5721):557-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CNRS Unite Propre de Recherche (UPR) 2357, Institut de Biologie Moleculaire des Plantes, 12 rue du General Zimmer, 67084 Strasbourg Cedex, France. charles.lecellier@infobiogen.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15845854" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antiviral Agents/*physiology ; Arabidopsis/genetics ; Cell Line ; Cricetinae ; DNA-Binding Proteins/genetics/metabolism ; Genes, Reporter ; Green Fluorescent Proteins/genetics ; HeLa Cells ; Humans ; MicroRNAs/*physiology ; Oligonucleotides, Antisense ; Plants, Genetically Modified ; Protein Biosynthesis ; *RNA Interference ; RNA, Viral ; Retroviridae Proteins/genetics/metabolism ; Spumavirus/*genetics/*physiology ; Trans-Activators/genetics/metabolism ; Transfection ; Virus Replication
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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