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  • 1
    Publication Date: 2016-07-15
    Description: Calcifying marine phytoplankton—coccolithophores— are some of the most successful yet enigmatic organisms in the ocean and are at risk from global change. To better understand how they will be affected, we need to know "why" coccolithophores calcify. We review coccolithophorid evolutionary history and cell biology as well as insights from recent experiments to provide a critical assessment of the costs and benefits of calcification. We conclude that calcification has high energy demands and that coccolithophores might have calcified initially to reduce grazing pressure but that additional benefits such as protection from photodamage and viral/bacterial attack further explain their high diversity and broad spectrum ecology. The cost-benefit aspect of these traits is illustrated by novel ecosystem modeling, although conclusive observations remain limited. In the future ocean, the trade-off between changing ecological and physiological costs of calcification and their benefits will ultimately decide how this important group is affected by ocean acidification and global warming.
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
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  • 2
    Publication Date: 2019
    Description: 〈p〉Bacteriophage are abundant at sites of bacterial infection, but their effects on mammalian hosts are unclear. We have identified pathogenic roles for filamentous Pf bacteriophage produced by 〈i〉Pseudomonas aeruginosa〈/i〉 (〈i〉Pa〈/i〉) in suppression of immunity against bacterial infection. Pf promote 〈i〉Pa〈/i〉 wound infection in mice and are associated with chronic human 〈i〉Pa〈/i〉 wound infections. Murine and human leukocytes endocytose Pf, and internalization of this single-stranded DNA virus results in phage RNA production. This triggers Toll-like receptor 3 (TLR3)– and TIR domain–containing adapter-inducing interferon-β (TRIF)–dependent type I interferon production, inhibition of tumor necrosis factor (TNF), and the suppression of phagocytosis. Conversely, immunization of mice against Pf prevents 〈i〉Pa〈/i〉 wound infection. Thus, Pf triggers maladaptive innate viral pattern-recognition responses, which impair bacterial clearance. Vaccination against phage virions represents a potential strategy to prevent bacterial infection.〈/p〉
    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
    Publication Date: 1999-01-05
    Description: Recently, GBR1, a seven-transmembrane domain protein with high affinity for gamma-aminobutyric acid (GABA)B receptor antagonists, was identified. Here, a GBR1-related protein, GBR2, was shown to be coexpressed with GBR1 in many brain regions and to interact with it through a short domain in the carboxyl-terminal cytoplasmic tail. Heterologously expressed GBR2 mediated inhibition of adenylyl cyclase; however, inwardly rectifying potassium channels were activated by GABAB receptor agonists only upon coexpression with GBR1 and GBR2. Thus, the interaction of these receptors appears to be crucial for important physiological effects of GABA and provides a mechanism in receptor signaling pathways that involve a heterotrimeric GTP-binding protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuner, R -- Kohr, G -- Grunewald, S -- Eisenhardt, G -- Bach, A -- Kornau, H C -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):74-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉BASF-LYNX Bioscience AG, Department of Neuroscience, Im Neuenheimer Feld 515, D-69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9872744" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclase Inhibitors ; Amino Acid Sequence ; Animals ; Brain/*metabolism ; Cell Line ; Cyclic AMP/metabolism ; Dimerization ; G Protein-Coupled Inwardly-Rectifying Potassium Channels ; GABA-B Receptor Agonists ; Humans ; In Situ Hybridization ; Molecular Sequence Data ; Neurons/metabolism ; Potassium/metabolism ; Potassium Channels/metabolism ; *Potassium Channels, Inwardly Rectifying ; RNA, Messenger/genetics/metabolism ; Rats ; Receptors, GABA/*chemistry/*metabolism ; Receptors, GABA-B/*chemistry/*metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Sequence Alignment
    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
    Publication Date: 2001-12-01
    Description: The mammalian target of rapamycin (mTOR) governs cell growth and proliferation by mediating the mitogen- and nutrient-dependent signal transduction that regulates messenger RNA translation. We identified phosphatidic acid (PA) as a critical component of mTOR signaling. In our study, mitogenic stimulation of mammalian cells led to a phospholipase D-dependent accumulation of cellular PA, which was required for activation of mTOR downstream effectors. PA directly interacted with the domain in mTOR that is targeted by rapamycin, and this interaction was positively correlated with mTOR's ability to activate downstream effectors. The involvement of PA in mTOR signaling reveals an important function of this lipid in signal transduction and protein synthesis, as well as a direct link between mTOR and mitogens. Furthermore, these studies suggest a potential mechanism for the in vivo actions of the immunosuppressant rapamycin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fang, Y -- Vilella-Bach, M -- Bachmann, R -- Flanigan, A -- Chen, J -- GM58064/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2001 Nov 30;294(5548):1942-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Structural Biology, University of Illinois at Urbana-Champaign, 601 South Goodwin Avenue, B107, Urbana, IL 61801, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11729323" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Butanols/pharmacology ; Carrier Proteins/metabolism ; Cell Line ; Culture Media, Serum-Free ; Enzyme Activation/drug effects ; Humans ; Immunosuppressive Agents/pharmacology ; Mitogens/*pharmacology ; Phosphatidic Acids/*metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phospholipase D/metabolism ; Phosphoproteins/metabolism ; Phosphorylation/drug effects ; Protein Binding ; Protein Kinases/chemistry/*metabolism ; Protein Structure, Tertiary ; Ribosomal Protein S6 Kinases/metabolism ; Signal Transduction/*drug effects ; Sirolimus/pharmacology ; TOR Serine-Threonine Kinases ; Time Factors
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    Electronic ISSN: 1095-9203
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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-06-11
    Description: The subunit stoichiometry of several ligand-gated ion channel receptors is still unknown. A counting method was developed to determine the number of subunits in one family of brain glutamate receptors. Successful application of this method in an HEK cell line provides evidence that ionotropic glutamate receptors share a tetrameric structure with the voltage-gated potassium channels. The average conductance of these channels depends on how many subunits are occupied by an agonist.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosenmund, C -- Stern-Bach, Y -- Stevens, C F -- NS 12961/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1998 Jun 5;280(5369):1596-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Workgroup Cellular Neurobiology, Max-Planck-Institute for Biophysical Chemistry, Gottingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9616121" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Cell Line ; Electric Conductivity ; Excitatory Amino Acid Agonists/metabolism ; Excitatory Amino Acid Antagonists/metabolism ; Humans ; Ligands ; Macromolecular Substances ; Models, Biological ; Patch-Clamp Techniques ; Quinoxalines/metabolism ; Quisqualic Acid/metabolism ; Receptors, AMPA/agonists/antagonists & inhibitors/*chemistry/*metabolism ; Receptors, Glutamate/chemistry/metabolism ; Receptors, Kainic Acid/agonists/antagonists & inhibitors/*chemistry/metabolism ; Recombinant Fusion Proteins/chemistry/metabolism
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  • 6
    Publication Date: 1991-09-27
    Description: Serial human immunodeficiency virus type-1 (HIV-1) isolates were obtained from five individuals with acquired immunodeficiency syndrome (AIDS) who changed therapy to 2',3'-dideoxyinosine (ddI) after at least 12 months of treatment with 3'-azido-3'-deoxythymidine (zidovudine, AZT). The in vitro sensitivity to ddI decreased during the 12 months following ddI initiation, whereas AZT sensitivity increased. Analysis of the reverse transcriptase coding region revealed a mutation associated with reduced sensitivity to ddI. When this mutation was present in the same genome as a mutation known to confer AZT resistance, the isolates showed increased sensitivity to AZT. Analysis of HIV-1 variants confirmed that the ddI resistance mutation alone conferred ddI and 2',3'-dideoxycytidine resistance, and suppressed the effect of the AZT resistance mutation. The use of combination therapy for HIV-1 disease may prevent drug-resistant isolates from emerging.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉St Clair, M H -- Martin, J L -- Tudor-Williams, G -- Bach, M C -- Vavro, C L -- King, D M -- Kellam, P -- Kemp, S D -- Larder, B A -- New York, N.Y. -- Science. 1991 Sep 27;253(5027):1557-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Virology, Burroughs Wellcome Co., Research Triangle Park, NC 27709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1716788" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*drug therapy/microbiology ; Base Sequence ; DNA, Viral/*genetics ; Didanosine/*pharmacology/*therapeutic use ; Drug Resistance, Microbial ; Genotype ; HIV-1/*drug effects/enzymology/isolation & purification ; Humans ; Molecular Sequence Data ; *Mutation ; Oligodeoxyribonucleotides ; RNA-Directed DNA Polymerase/*genetics/metabolism ; Zidovudine/pharmacology/*therapeutic use
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 7
    Publication Date: 1990-01-05
    Description: One of the functions of U1 small nuclear ribonucleoprotein (snRNP) in the splicing reaction of pre-mRNA molecules is the recognition of the 5' splice site. U1 snRNP proteins as well as base-pair interactions between U1 snRNA and the 5' splice site are important for the formation of the snRNP-pre-mRNA complex. To determine which proteins are needed for complex formation, the ability of U1 snRNPs gradually depleted of the U1-specific proteins C, A, and 70k to bind to an RNA molecule containing a 5' splice site sequence was studied in a nitrocellulose filter binding assay. The most significant effect was always observed when protein C was removed, either alone or together with other U1-specific proteins; the binding was reduced by 50 to 60%. Complementation of protein C-deficient U1 snRNPs with purified C protein restored their 5' splice site binding activity. These data suggest that protein C may potentiate the base-pair interaction between U1 RNA and the 5' splice site.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heinrichs, V -- Bach, M -- Winkelmann, G -- Luhrmann, R -- New York, N.Y. -- Science. 1990 Jan 5;247(4938):69-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fuer Molekularbiologie und Tumorforschung, Marburg, Federal Republic of Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2136774" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromatography, Affinity ; Electrophoresis, Polyacrylamide Gel ; Introns ; *RNA Splicing ; Ribonucleoproteins/genetics/*physiology ; Ribonucleoproteins, Small Nuclear
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  • 8
    Publication Date: 2010-02-27
    Description: CKAMP44, identified here by a proteomic approach, is a brain-specific type I transmembrane protein that associates with AMPA receptors in synaptic spines. CKAMP44 expressed in Xenopus oocytes reduced GluA1- and A2-mediated steady-state currents, but did not affect kainate- or N-methyl-D-aspartate (NMDA) receptor-mediated currents. Mouse hippocampal CA1 pyramidal neurons expressed CKAMP44 at low abundance, and overexpression of CKAMP44 led to stronger and faster AMPA receptor desensitization, slower recovery from desensitization, and a reduction in the paired-pulse ratio of AMPA currents. By contrast, dentate gyrus granule cells exhibited strong CKAMP44 expression, and CKAMP44 knockout increased the paired-pulse ratio of AMPA currents in lateral and medial perforant path-granule cell synapses. CKAMP44 thus modulates short-term plasticity at specific excitatory synapses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉von Engelhardt, Jakob -- Mack, Volker -- Sprengel, Rolf -- Kavenstock, Netta -- Li, Ka Wan -- Stern-Bach, Yael -- Smit, August B -- Seeburg, Peter H -- Monyer, Hannah -- New York, N.Y. -- Science. 2010 Mar 19;327(5972):1518-22. doi: 10.1126/science.1184178. Epub 2010 Feb 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Clinical Neurobiology, University of Heidelberg, 6910 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20185686" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CA1 Region, Hippocampal/metabolism ; Calcium Channels/metabolism ; Dendritic Spines/metabolism ; Dentate Gyrus/cytology/*metabolism ; Excitatory Postsynaptic Potentials ; Glutamic Acid/metabolism ; Guanylate Kinase ; Intracellular Signaling Peptides and Proteins/metabolism ; Membrane Proteins/metabolism ; Mice ; Mice, Knockout ; Miniature Postsynaptic Potentials ; Molecular Sequence Data ; Nerve Tissue Proteins/chemistry/genetics/*metabolism ; Neural Inhibition ; *Neuronal Plasticity ; Neurons/*metabolism ; Oocytes/metabolism ; Patch-Clamp Techniques ; Perforant Pathway ; Protein Interaction Domains and Motifs ; Protein Isoforms/genetics/metabolism ; Proteomics ; Pyramidal Cells/metabolism ; Receptors, AMPA/chemistry/*metabolism ; Recombinant Fusion Proteins/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Synapses/*physiology ; *Synaptic Transmission ; Xenopus laevis
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  • 9
    Publication Date: 2010-08-14
    Description: Novae are thermonuclear explosions on a white dwarf surface fueled by mass accreted from a companion star. Current physical models posit that shocked expanding gas from the nova shell can produce x-ray emission, but emission at higher energies has not been widely expected. Here, we report the Fermi Large Area Telescope detection of variable gamma-ray emission (0.1 to 10 billion electron volts) from the recently detected optical nova of the symbiotic star V407 Cygni. We propose that the material of the nova shell interacts with the dense ambient medium of the red giant primary and that particles can be accelerated effectively to produce pi(0) decay gamma-rays from proton-proton interactions. Emission involving inverse Compton scattering of the red giant radiation is also considered and is not ruled out.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fermi-LAT Collaboration -- Abdo, A A -- Ackermann, M -- Ajello, M -- Atwood, W B -- Baldini, L -- Ballet, J -- Barbiellini, G -- Bastieri, D -- Bechtol, K -- Bellazzini, R -- Berenji, B -- Blandford, R D -- Bloom, E D -- Bonamente, E -- Borgland, A W -- Bouvier, A -- Brandt, T J -- Bregeon, J -- Brez, A -- Brigida, M -- Bruel, P -- Buehler, R -- Burnett, T H -- Buson, S -- Caliandro, G A -- Cameron, R A -- Caraveo, P A -- Carrigan, S -- Casandjian, J M -- Cecchi, C -- Celik, O -- Charles, E -- Chaty, S -- Chekhtman, A -- Cheung, C C -- Chiang, J -- Ciprini, S -- Claus, R -- Cohen-Tanugi, J -- Conrad, J -- Corbel, S -- Corbet, R -- DeCesar, M E -- den Hartog, P R -- Dermer, C D -- de Palma, F -- Digel, S W -- Donato, D -- do Couto e Silva, E -- Drell, P S -- Dubois, R -- Dubus, G -- Dumora, D -- Favuzzi, C -- Fegan, S J -- Ferrara, E C -- Fortin, P -- Frailis, M -- Fuhrmann, L -- Fukazawa, Y -- Funk, S -- Fusco, P -- Gargano, F -- Gasparrini, D -- Gehrels, N -- Germani, S -- Giglietto, N -- Giordano, F -- Giroletti, M -- Glanzman, T -- Godfrey, G -- Grenier, I A -- Grondin, M-H -- Grove, J E -- Guiriec, S -- Hadasch, D -- Harding, A K -- Hayashida, M -- Hays, E -- Healey, S E -- Hill, A B -- Horan, D -- Hughes, R E -- Itoh, R -- Jean, P -- Johannesson, G -- Johnson, A S -- Johnson, R P -- Johnson, T J -- Johnson, W N -- Kamae, T -- Katagiri, H -- Kataoka, J -- Kerr, M -- Knodlseder, J -- Koerding, E -- Kuss, M -- Lande, J -- Latronico, L -- Lee, S-H -- Lemoine-Goumard, M -- Garde, M Llena -- Longo, F -- Loparco, F -- Lott, B -- Lovellette, M N -- Lubrano, P -- Makeev, A -- Mazziotta, M N -- McConville, W -- McEnery, J E -- Mehault, J -- Michelson, P F -- Mizuno, T -- Moiseev, A A -- Monte, C -- Monzani, M E -- Morselli, A -- Moskalenko, I V -- Murgia, S -- Nakamori, T -- Naumann-Godo, M -- Nestoras, I -- Nolan, P L -- Norris, J P -- Nuss, E -- Ohno, M -- Ohsugi, T -- Okumura, A -- Omodei, N -- Orlando, E -- Ormes, J F -- Ozaki, M -- Paneque, D -- Panetta, J H -- Parent, D -- Pelassa, V -- Pepe, M -- Pesce-Rollins, M -- Piron, F -- Porter, T A -- Raino, S -- Rando, R -- Ray, P S -- Razzano, M -- Razzaque, S -- Rea, N -- Reimer, A -- Reimer, O -- Reposeur, T -- Ripken, J -- Ritz, S -- Romani, R W -- Roth, M -- Sadrozinski, H F-W -- Sander, A -- Parkinson, P M Saz -- Scargle, J D -- Schinzel, F K -- Sgro, C -- Shaw, M S -- Siskind, E J -- Smith, D A -- Smith, P D -- Sokolovsky, K V -- Spandre, G -- Spinelli, P -- Stawarz, L -- Strickman, M S -- Suson, D J -- Takahashi, H -- Takahashi, T -- Tanaka, T -- Tanaka, Y -- Thayer, J B -- Thayer, J G -- Thompson, D J -- Tibaldo, L -- Torres, D F -- Tosti, G -- Tramacere, A -- Uchiyama, Y -- Usher, T L -- Vandenbroucke, J -- Vasileiou, V -- Vilchez, N -- Vitale, V -- Waite, A P -- Wallace, E -- Wang, P -- Winer, B L -- Wolff, M T -- Wood, K S -- Yang, Z -- Ylinen, T -- Ziegler, M -- Maehara, H -- Nishiyama, K -- Kabashima, F -- Bach, U -- Bower, G C -- Falcone, A -- Forster, J R -- Henden, A -- Kawabata, K S -- Koubsky, P -- Mukai, K -- Nelson, T -- Oates, S R -- Sakimoto, K -- Sasada, M -- Shenavrin, V I -- Shore, S N -- Skinner, G K -- Sokoloski, J -- Stroh, M -- Tatarnikov, A M -- Uemura, M -- Wahlgren, G M -- Yamanaka, M -- New York, N.Y. -- Science. 2010 Aug 13;329(5993):817-21. doi: 10.1126/science.1192537.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Space Science Division, Naval Research Laboratory, Washington, DC 20375, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20705855" target="_blank"〉PubMed〈/a〉
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  • 10
    Publication Date: 1996-05-10
    Description: During the Galileo probe's descent through Jupiter's atmosphere, under the ionosphere, the lightning and radio emission detector measured radio frequency signals at levels significantly above the probe's electromagnetic noise. The signal strengths at 3 and 15 kilohertz were relatively large at the beginning of the descent, decreased with depth to a pressure level of about 5 bars, and then increased slowly until the end of the mission. The 15-kilohertz signals show arrival direction anisotropies. Measurements of radio frequency wave forms show that the probe passed through an atmospheric region that did not support lightning within at least 100 kilometers and more likely a few thousand kilometers of the descent trajectory. The apparent opacity of the jovian atmosphere increases sharply at pressures greater than about 4 bars.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lanzerotti -- Rinnert -- Dehmel -- Gliem -- Krider -- Uman -- Bach -- New York, N.Y. -- Science. 1996 May 10;272(5263):858-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉L. J. Lanzerotti, Bell Laboratories, Lucent Technologies, Murray Hill, NJ 07974, and the University of Florida, Gainesville, FL 32611, USA. K. Rinnert, Max-Planck-Institut fur Aeronomy, D-37191 Katlenburg-Lindau, Germany. G. Dehmel, F. O. Gliem, J. Bach, Universitat Braunschweig, D-38106 Braunschweig, Germany. E. P. Krider, University of Arizona, Tucson, AZ 85721, USA. M. A. Uman, University of Florida, Gainesville, FL 32611, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662576" target="_blank"〉PubMed〈/a〉
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