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  • 11
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    Genome sequence of the radioresistant bacterium Deinococcus radiodurans R1 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-24
    Description: The complete genome sequence of the radiation-resistant bacterium Deinococcus radiodurans R1 is composed of two chromosomes (2,648,638 and 412,348 base pairs), a megaplasmid (177,466 base pairs), and a small plasmid (45,704 base pairs), yielding a total genome of 3,284, 156 base pairs. Multiple components distributed on the chromosomes and megaplasmid that contribute to the ability of D. radiodurans to survive under conditions of starvation, oxidative stress, and high amounts of DNA damage were identified. Deinococcus radiodurans represents an organism in which all systems for DNA repair, DNA damage export, desiccation and starvation recovery, and genetic redundancy are present in one cell.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4147723/" 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/PMC4147723/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉White, O -- Eisen, J A -- Heidelberg, J F -- Hickey, E K -- Peterson, J D -- Dodson, R J -- Haft, D H -- Gwinn, M L -- Nelson, W C -- Richardson, D L -- Moffat, K S -- Qin, H -- Jiang, L -- Pamphile, W -- Crosby, M -- Shen, M -- Vamathevan, J J -- Lam, P -- McDonald, L -- Utterback, T -- Zalewski, C -- Makarova, K S -- Aravind, L -- Daly, M J -- Minton, K W -- Fleischmann, R D -- Ketchum, K A -- Nelson, K E -- Salzberg, S -- Smith, H O -- Venter, J C -- Fraser, C M -- R01 CA077712/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1571-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genomic Research, 9712 Medical Center Drive, Rockville, MD 20850, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10567266" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/biosynthesis/chemistry/genetics ; Catalase/genetics ; Chromosomes, Bacterial/genetics ; DNA Damage ; DNA Repair/genetics ; DNA, Bacterial/genetics ; Energy Metabolism ; Genes, Bacterial ; *Genome, Bacterial ; Gram-Positive Cocci/chemistry/classification/*genetics/radiation effects ; Molecular Sequence Data ; Open Reading Frames ; Oxidative Stress ; *Physical Chromosome Mapping ; Plasmids ; Radiation Tolerance ; Repetitive Sequences, Nucleic Acid ; *Sequence Analysis, DNA ; Superoxide Dismutase/genetics ; Thermus/chemistry/genetics ; Ultraviolet Rays
    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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  • 12
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    5'-Deoxyribose phosphate lyase activity of human DNA polymerase iota in vitro (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-03-17
    Description: DNA polymerase iota (pol iota) is one of several recently discovered DNA polymerases in mammalian cells whose function is unknown. We report here that human pol iota has an intrinsic 5'-deoxyribose phosphate (dRP) lyase activity. In reactions reconstituted with uracil-DNA glycosylase (UDG), apurinic/apyrimidinic (AP) endonuclease and DNA ligase I, pol iota can use its dRP lyase and polymerase activities to repair G*U and A*U pairs in DNA. These data and three distinct catalytic properties of pol iota implicate it in specialized forms of base excision repair (BER).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bebenek, K -- Tissier, A -- Frank, E G -- McDonald, J P -- Prasad, R -- Wilson, S H -- Woodgate, R -- Kunkel, T A -- New York, N.Y. -- Science. 2001 Mar 16;291(5511):2156-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Genetics and, Laboratory of Structural Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11251121" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Pairing ; Base Sequence ; Carbon-Oxygen Lyases/metabolism ; DNA/*metabolism ; *DNA Glycosylases ; DNA Ligases/metabolism ; *DNA Repair ; DNA-(Apurinic or Apyrimidinic Site) Lyase ; DNA-Directed DNA Polymerase/chemistry/*metabolism ; Deoxyribonuclease IV (Phage T4-Induced) ; Humans ; Molecular Sequence Data ; N-Glycosyl Hydrolases/metabolism ; Phosphorus-Oxygen Lyases/*metabolism ; Recombinant Fusion Proteins/metabolism ; Ribosemonophosphates/*metabolism ; Schiff Bases ; Uracil/metabolism ; Uracil-DNA Glycosidase
    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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  • 13
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    Beta-arrestin 2: a receptor-regulated MAPK scaffold for the activation of JNK3 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-11-25
    Description: beta-Arrestins, originally discovered in the context of heterotrimeric guanine nucleotide binding protein-coupled receptor (GPCR) desensitization, also function in internalization and signaling of these receptors. We identified c-Jun amino-terminal kinase 3 (JNK3) as a binding partner of beta-arrestin 2 using a yeast two-hybrid screen and by coimmunoprecipitation from mouse brain extracts or cotransfected COS-7 cells. The upstream JNK activators apoptosis signal-regulating kinase 1 (ASK1) and mitogen-activated protein kinase (MAPK) kinase 4 were also found in complex with beta-arrestin 2. Cellular transfection of beta-arrestin 2 caused cytosolic retention of JNK3 and enhanced JNK3 phosphorylation stimulated by ASK1. Moreover, stimulation of the angiotensin II type 1A receptor activated JNK3 and triggered the colocalization of beta-arrestin 2 and active JNK3 to intracellular vesicles. Thus, beta-arrestin 2 acts as a scaffold protein, which brings the spatial distribution and activity of this MAPK module under the control of a GPCR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDonald, P H -- Chow, C W -- Miller, W E -- Laporte, S A -- Field, M E -- Lin, F T -- Davis, R J -- Lefkowitz, R J -- CA65861/CA/NCI NIH HHS/ -- CA85422/CA/NCI NIH HHS/ -- HL16037/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2000 Nov 24;290(5496):1574-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Medicine, Duke University Medical Center, Box 3821, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11090355" target="_blank"〉PubMed〈/a〉
    Keywords: Angiotensin II/metabolism/pharmacology ; Animals ; Arrestins/genetics/*metabolism ; COS Cells ; Cell Line ; Cell Nucleus/metabolism ; Cytosol/enzymology/metabolism ; Endosomes/enzymology/metabolism ; Enzyme Activation ; Humans ; *MAP Kinase Kinase 4 ; MAP Kinase Kinase Kinase 5 ; MAP Kinase Kinase Kinases/*metabolism ; *MAP Kinase Signaling System ; Mice ; Mitogen-Activated Protein Kinase 10 ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Mitogen-Activated Protein Kinases/*metabolism ; Mutation ; Phosphorylation ; Protein-Tyrosine Kinases/*metabolism ; Proto-Oncogene Proteins c-jun/metabolism ; Rats ; Receptor, Angiotensin, Type 1 ; Receptors, Angiotensin/*metabolism ; Recombinant Fusion Proteins/metabolism ; Transfection ; Two-Hybrid System Techniques
    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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  • 14
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    Multisensory integration and crossmodal attention effects in the human brain (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-06-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDonald, J J -- Teder-Salejarvi, W A -- Ward, L M -- New York, N.Y. -- Science. 2001 Jun 8;292(5523):1791.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, Simon Fraser University, 8888 University Drive, Burnaby, BC V5A 1S6, Canada. jmcd@sfu.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11397913" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Attention/*physiology ; Brain Mapping ; Cues ; Functional Laterality ; Humans ; Light ; Magnetic Resonance Imaging ; Neural Pathways/physiology ; Photic Stimulation ; Touch/*physiology ; Visual Cortex/*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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  • 15
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    Role of Rpn11 metalloprotease in deubiquitination and degradation by the 26S proteasome (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-08-17
    Description: The 26S proteasome mediates degradation of ubiquitin-conjugated proteins. Although ubiquitin is recycled from proteasome substrates, the molecular basis of deubiquitination at the proteasome and its relation to substrate degradation remain unknown. The Rpn11 subunit of the proteasome lid subcomplex contains a highly conserved Jab1/MPN domain-associated metalloisopeptidase (JAMM) motif-EX(n)HXHX(10)D. Mutation of the predicted active-site histidines to alanine (rpn11AXA) was lethal and stabilized ubiquitin pathway substrates in yeast. Rpn11(AXA) mutant proteasomes assembled normally but failed to either deubiquitinate or degrade ubiquitinated Sic1 in vitro. Our findings reveal an unexpected coupling between substrate deubiquitination and degradation and suggest a unifying rationale for the presence of the lid in eukaryotic proteasomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Verma, Rati -- Aravind, L -- Oania, Robert -- McDonald, W Hayes -- Yates, John R 3rd -- Koonin, Eugene V -- Deshaies, Raymond J -- RR11823-05-01/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2002 Oct 18;298(5593):611-5. Epub 2002 Aug 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology and Howard Hughes Medical Institute, 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/12183636" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Amino Acid Motifs ; Amino Acid Sequence ; Binding Sites ; Carbon-Nitrogen Lyases/chemistry/*metabolism ; Cyclin-Dependent Kinase Inhibitor Proteins ; Cysteine Endopeptidases/metabolism ; DNA-Binding Proteins/chemistry ; Endopeptidases/chemistry/*metabolism ; Fungal Proteins/*metabolism ; Metalloendopeptidases/chemistry/*metabolism ; Molecular Sequence Data ; Multienzyme Complexes/metabolism ; Mutation ; Oligopeptides/pharmacology ; Peptide Hydrolases/*metabolism ; Proteasome Endopeptidase Complex ; Saccharomyces cerevisiae Proteins/chemistry/*metabolism ; Transcription Factors/chemistry ; Ubiquitins/*metabolism ; Yeasts/metabolism ; Zinc/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 16
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    Scale-invariant magnetoresistance in a cuprate superconductor (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-08-03
    Description: The anomalous metallic state in the high-temperature superconducting cuprates is masked by superconductivity near a quantum critical point. Applying high magnetic fields to suppress superconductivity has enabled detailed studies of the normal state, yet the direct effect of strong magnetic fields on the metallic state is poorly understood. We report the high-field magnetoresistance of thin-film La 2– x Sr x CuO 4 cuprate in the vicinity of the critical doping, 0.161 ≤ p ≤ 0.190. We find that the metallic state exposed by suppressing superconductivity is characterized by magnetoresistance that is linear in magnetic fields up to 80 tesla. The magnitude of the linear-in-field resistivity mirrors the magnitude and doping evolution of the well-known linear-in-temperature resistivity that has been associated with quantum criticality in high-temperature superconductors.
    Keywords: Physics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 17
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    Unlocking P(V): Reagents for chiral phosphorothioate synthesis (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-09-21
    Description: Phosphorothioate nucleotides have emerged as powerful pharmacological substitutes of their native phosphodiester analogs with important translational applications in antisense oligonucleotide (ASO) therapeutics and cyclic dinucleotide (CDN) synthesis. Stereocontrolled installation of this chiral motif has long been hampered by the systemic use of phosphorus(III) [P(III)]–based reagent systems as the sole practical means of oligonucleotide assembly. A fundamentally different approach is described herein: the invention of a P(V)-based reagent platform for programmable, traceless, diastereoselective phosphorus-sulfur incorporation. The power of this reagent system is demonstrated through the robust and stereocontrolled synthesis of various nucleotidic architectures, including ASOs and CDNs, via an efficient, inexpensive, and operationally simple protocol.
    Keywords: Chemistry
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
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    Superconductivity and the quantization of energy (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-01-12
    Description: Ideas about quantized energy levels originated in atomic physics, but research in superconductivity has led to unparalleled precision in the measurement of energy levels. A comparison of levels produced by two Josephson junctions shows that they differ by no more than 3 parts in 10(19) at an energy of 0.0003 electron volt. The fact that the myriad of interactions of 10(12) particles in a macroscopic body, a Josephson junction, can produce sharply defined energy levels suggests a dynamical state effectively divorced from the complexities of its environment. The existence of this state, the macroscopic quantum state of superconductors, is well established, but its isolation from intrinsic perturbations has recently been shown to be extraordinary. These new results, with an improved precision of about ten orders of magnitude, are discussed in the context of highly accurate results from quantum electrodynamics, atomic spectroscopy, and the standards of metrology. Further refinements in precision may be achievable at higher energy levels, about 12 electron volts, as they become available from a new series array of 18,992 Josephson junctions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDonald, D G -- New York, N.Y. -- Science. 1990 Jan 12;247(4939):177-82.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17813283" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
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  • 19
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    Energetic charged particles in the magnetosphere of neptune (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-12-15
    Description: The Voyager 2 cosmic ray system (CRS) measured significant fluxes of energetic [〉/=1 megaelectron volt (MeV)] trapped electrons and protons in the magnetosphere of Neptune. The intensities are maximum near a magnetic L shell of 7, decreasing closer to the planet because of absorption by satellites and rings. In the region of the inner satellites of Neptune, the radiation belts have a complicated structure, which provides some constraints on the magnetic field geometry of the inner magnetosphere. Electron phase-space densities have a positive radial gradient, indicating that they diffuse inward from a source in the outer magnetosphere. Electron spectra from 1 to 5 MeV are generally well represented by power laws with indices near 6, which harden in the region of peak flux to power law indices of 4 to 5. Protons have significantly lower fluxes than electrons throughout the magnetosphere, with large anisotropies due to radial intensity gradients. The radiation belts resemble those of Uranus to the extent allowed by the different locations of the satellites, which limit the flux at each planet.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stone, E C -- Cummings, A C -- Loooper, M D -- Selesnick, R S -- Lal, N -- McDonald, F B -- Trainor, J H -- Chenette, D L -- New York, N.Y. -- Science. 1989 Dec 15;246(4936):1489-94.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17756005" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
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  • 20
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    The gene for enhancer binding proteins E12/E47 lies at the t(1;19) breakpoint in acute leukemias (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-10-20
    Description: The gene (E2A) that codes for proteins with the properties of immunoglobulin enhancer binding factors E12/E47 was mapped to chromosome region 19p13.2-p13.3, a site associated with nonrandom translocations in acute lymphoblastic leukemias. The majority of t(1;19)(q23;p13)-carrying leukemias and cell lines studied contained rearrangements of E2A as determined by DNA blot analyses. The rearrangements altered the E2A transcriptional unit, resulting in the synthesis of a transcript larger than the normal-sized E2A mRNAs in one of the cell lines with this translocation. These observations indicate that the gene for a transcription factor is located at the breakpoint of a consistently recurring chromosomal translocation in many acute leukemias and suggest a direct role for alteration of such factors in the pathogenesis of some malignancies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mellentin, J D -- Murre, C -- Donlon, T A -- McCaw, P S -- Smith, S D -- Carroll, A J -- McDonald, M E -- Baltimore, D -- Cleary, M L -- CA30969/CA/NCI NIH HHS/ -- CA42106/CA/NCI NIH HHS/ -- CA42971/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 Oct 20;246(4928):379-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Stanford University School of Medicine, CA 94025.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2799390" target="_blank"〉PubMed〈/a〉
    Keywords: Child ; Chromosome Mapping ; *Chromosomes, Human, Pair 1 ; *Chromosomes, Human, Pair 19 ; DNA-Binding Proteins/*genetics ; Humans ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*genetics ; Transcription Factors/*genetics ; Translocation, Genetic/*physiology ; Tumor Cells, Cultured
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