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  • Cell Line  (75)
  • Kinetics  (53)
  • American Association for the Advancement of Science (AAAS)  (123)
  • Uppsala
  • 2010-2014  (69)
  • 1980-1984  (54)
  • 2010  (69)
  • 1981  (54)
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  • 2010-2014  (69)
  • 1980-1984  (54)
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  • 1
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    Differential arginylation of actin isoforms is regulated by coding sequence-dependent degradation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-18
    Description: The mammalian cytoskeletal proteins beta- and gamma-actin are highly homologous, but only beta-actin is amino-terminally arginylated in vivo, which regulates its function. We examined the metabolic fate of exogenously expressed arginylated and nonarginylated actin isoforms. Arginylated gamma-actin, unlike beta-, was highly unstable and was selectively ubiquitinated and degraded in vivo. This instability was regulated by the differences in the nucleotide coding sequence between the two actin isoforms, which conferred different translation rates. gamma-actin was translated more slowly than beta-actin, and this slower processing resulted in the exposure of a normally hidden lysine residue for ubiquitination, leading to the preferential degradation of gamma-actin upon arginylation. This degradation mechanism, coupled to nucleotide coding sequence, may regulate protein arginylation in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2941909/" 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/PMC2941909/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Fangliang -- Saha, Sougata -- Shabalina, Svetlana A -- Kashina, Anna -- 5R01HL084419/HL/NHLBI NIH HHS/ -- R01 HL084419/HL/NHLBI NIH HHS/ -- R01 HL084419-03/HL/NHLBI NIH HHS/ -- R01 HL084419-03S1/HL/NHLBI NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 17;329(5998):1534-7. doi: 10.1126/science.1191701.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20847274" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/chemistry/genetics/*metabolism ; Amino Acid Sequence ; Animals ; Arginine/*metabolism ; Cell Line ; Cell Line, Tumor ; *Codon ; Humans ; Lysine/metabolism ; Mice ; Nucleic Acid Conformation ; Proteasome Endopeptidase Complex/metabolism ; Protein Biosynthesis ; Protein Folding ; Protein Isoforms/chemistry/genetics/metabolism ; *Protein Modification, Translational ; Protein Stability ; RNA, Messenger/chemistry/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Ubiquitination
    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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    Arsenic trioxide controls the fate of the PML-RARalpha oncoprotein by directly binding PML (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-04-10
    Description: Arsenic, an ancient drug used in traditional Chinese medicine, has attracted worldwide interest because it shows substantial anticancer activity in patients with acute promyelocytic leukemia (APL). Arsenic trioxide (As2O3) exerts its therapeutic effect by promoting degradation of an oncogenic protein that drives the growth of APL cells, PML-RARalpha (a fusion protein containing sequences from the PML zinc finger protein and retinoic acid receptor alpha). PML and PML-RARalpha degradation is triggered by their SUMOylation, but the mechanism by which As2O3 induces this posttranslational modification is unclear. Here we show that arsenic binds directly to cysteine residues in zinc fingers located within the RBCC domain of PML-RARalpha and PML. Arsenic binding induces PML oligomerization, which increases its interaction with the small ubiquitin-like protein modifier (SUMO)-conjugating enzyme UBC9, resulting in enhanced SUMOylation and degradation. The identification of PML as a direct target of As2O3 provides new insights into the drug's mechanism of action and its specificity for APL.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Xiao-Wei -- Yan, Xiao-Jing -- Zhou, Zi-Ren -- Yang, Fei-Fei -- Wu, Zi-Yu -- Sun, Hong-Bin -- Liang, Wen-Xue -- Song, Ai-Xin -- Lallemand-Breitenbach, Valerie -- Jeanne, Marion -- Zhang, Qun-Ye -- Yang, Huai-Yu -- Huang, Qiu-Hua -- Zhou, Guang-Biao -- Tong, Jian-Hua -- Zhang, Yan -- Wu, Ji-Hui -- Hu, Hong-Yu -- de The, Hugues -- Chen, Sai-Juan -- Chen, Zhu -- New York, N.Y. -- Science. 2010 Apr 9;328(5975):240-3. doi: 10.1126/science.1183424.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Rui Jin Hospital affiliated to Shanghai Jiao Tong University School of Medicine, 197 Rui Jin Road II, Shanghai 200025, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20378816" target="_blank"〉PubMed〈/a〉
    Keywords: Arsenic/*metabolism ; Arsenicals/*metabolism/*pharmacology ; Cell Line ; Humans ; Leukemia, Promyelocytic, Acute/drug therapy/genetics ; Mutant Proteins/chemistry/metabolism ; Mutation ; Nuclear Proteins/chemistry/genetics/*metabolism ; Oncogene Proteins, Fusion/chemistry/genetics/*metabolism ; Oxazines/metabolism ; Oxides/*metabolism/*pharmacology ; Protein Conformation ; Protein Multimerization ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Receptors, Retinoic Acid/metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Small Ubiquitin-Related Modifier Proteins/metabolism ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; Transcription Factors/chemistry/genetics/*metabolism ; Tumor Suppressor Proteins/chemistry/genetics/*metabolism ; Ubiquitination ; 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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  • 3
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    Covering a broad dynamic range: information processing at the erythropoietin receptor (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-22
    Description: Cell surface receptors convert extracellular cues into receptor activation, thereby triggering intracellular signaling networks and controlling cellular decisions. A major unresolved issue is the identification of receptor properties that critically determine processing of ligand-encoded information. We show by mathematical modeling of quantitative data and experimental validation that rapid ligand depletion and replenishment of the cell surface receptor are characteristic features of the erythropoietin (Epo) receptor (EpoR). The amount of Epo-EpoR complexes and EpoR activation integrated over time corresponds linearly to ligand input; this process is carried out over a broad range of ligand concentrations. This relation depends solely on EpoR turnover independent of ligand binding, which suggests an essential role of large intracellular receptor pools. These receptor properties enable the system to cope with basal and acute demand in the hematopoietic system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Becker, Verena -- Schilling, Marcel -- Bachmann, Julie -- Baumann, Ute -- Raue, Andreas -- Maiwald, Thomas -- Timmer, Jens -- Klingmuller, Ursula -- New York, N.Y. -- Science. 2010 Jun 11;328(5984):1404-8. doi: 10.1126/science.1184913. Epub 2010 May 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division Systems Biology of Signal Transduction, DKFZ-ZMBH Alliance, German Cancer Research Center, 69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20488988" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Membrane/*metabolism ; Computer Simulation ; Endocytosis ; Epoetin Alfa ; Erythropoietin/metabolism/pharmacology ; Kinetics ; Ligands ; Mice ; Models, Biological ; Protein Binding ; Receptors, Erythropoietin/*metabolism ; Recombinant Proteins ; 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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  • 4
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    Cellodextrin transport in yeast for improved biofuel production (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-11
    Description: Fungal degradation of plant biomass may provide insights for improving cellulosic biofuel production. We show that the model cellulolytic fungus Neurospora crassa relies on a high-affinity cellodextrin transport system for rapid growth on cellulose. Reconstitution of the N. crassa cellodextrin transport system in Saccharomyces cerevisiae promotes efficient growth of this yeast on cellodextrins. In simultaneous saccharification and fermentation experiments, the engineered yeast strains more rapidly convert cellulose to ethanol when compared with yeast lacking this system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Galazka, Jonathan M -- Tian, Chaoguang -- Beeson, William T -- Martinez, Bruno -- Glass, N Louise -- Cate, Jamie H D -- New York, N.Y. -- Science. 2010 Oct 1;330(6000):84-6. doi: 10.1126/science.1192838. Epub 2010 Sep 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20829451" target="_blank"〉PubMed〈/a〉
    Keywords: *Biofuels ; Biological Transport ; Biomass ; Cellobiose/metabolism ; Cellulase/metabolism ; Cellulose/*analogs & derivatives/*metabolism ; Dextrins/*metabolism ; Ethanol/metabolism ; Fermentation ; Fungal Proteins/genetics/*metabolism ; Genetic Engineering ; Kinetics ; Membrane Transport Proteins/genetics/*metabolism ; Neurospora crassa/genetics/growth & development/*metabolism ; Saccharomyces cerevisiae/genetics/growth & development/*metabolism ; Saccharomyces cerevisiae Proteins/metabolism ; beta-Glucosidase/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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    Regulation of cellular metabolism by protein lysine acetylation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-02-20
    Description: Protein lysine acetylation has emerged as a key posttranslational modification in cellular regulation, in particular through the modification of histones and nuclear transcription regulators. We show that lysine acetylation is a prevalent modification in enzymes that catalyze intermediate metabolism. Virtually every enzyme in glycolysis, gluconeogenesis, the tricarboxylic acid (TCA) cycle, the urea cycle, fatty acid metabolism, and glycogen metabolism was found to be acetylated in human liver tissue. The concentration of metabolic fuels, such as glucose, amino acids, and fatty acids, influenced the acetylation status of metabolic enzymes. Acetylation activated enoyl-coenzyme A hydratase/3-hydroxyacyl-coenzyme A dehydrogenase in fatty acid oxidation and malate dehydrogenase in the TCA cycle, inhibited argininosuccinate lyase in the urea cycle, and destabilized phosphoenolpyruvate carboxykinase in gluconeogenesis. Our study reveals that acetylation plays a major role in metabolic regulation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3232675/" 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/PMC3232675/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhao, Shimin -- Xu, Wei -- Jiang, Wenqing -- Yu, Wei -- Lin, Yan -- Zhang, Tengfei -- Yao, Jun -- Zhou, Li -- Zeng, Yaxue -- Li, Hong -- Li, Yixue -- Shi, Jiong -- An, Wenlin -- Hancock, Susan M -- He, Fuchu -- Qin, Lunxiu -- Chin, Jason -- Yang, Pengyuan -- Chen, Xian -- Lei, Qunying -- Xiong, Yue -- Guan, Kun-Liang -- MC_U105181009/Medical Research Council/United Kingdom -- MC_UP_A024_1008/Medical Research Council/United Kingdom -- R01 CA065572/CA/NCI NIH HHS/ -- R01 CA065572-13/CA/NCI NIH HHS/ -- R01 CA065572-14/CA/NCI NIH HHS/ -- R01 CA065572-15/CA/NCI NIH HHS/ -- R01CA108941/CA/NCI NIH HHS/ -- R01CA65572/CA/NCI NIH HHS/ -- R01GM51586/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Feb 19;327(5968):1000-4. doi: 10.1126/science.1179689.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Life Sciences, Fudan University, Shanghai 20032, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20167786" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Hydroxyacyl CoA Dehydrogenases/metabolism ; Acetylation ; Argininosuccinate Lyase/genetics/metabolism ; Cell Line ; Citric Acid Cycle ; Enoyl-CoA Hydratase/metabolism ; Enzymes/*metabolism ; Fatty Acids/metabolism ; Gluconeogenesis ; Glycogen/metabolism ; Glycolysis ; Hepatocytes/enzymology/*metabolism ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Isomerases/metabolism ; Liver/enzymology/*metabolism ; Lysine/*metabolism ; Malate Dehydrogenase/metabolism ; Multienzyme Complexes/metabolism ; Oxidation-Reduction ; Peroxisomal Bifunctional Enzyme ; Phosphoenolpyruvate Carboxykinase (GTP)/metabolism ; *Protein Processing, Post-Translational ; Proteins/*metabolism ; Proteome ; Urea/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 6
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    Step-growth polymerization of inorganic nanoparticles (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-10
    Description: Self-organization of nanoparticles is an efficient strategy for producing nanostructures with complex, hierarchical architectures. The past decade has witnessed great progress in nanoparticle self-assembly, yet the quantitative prediction of the architecture of nanoparticle ensembles and of the kinetics of their formation remains a challenge. We report on the marked similarity between the self-assembly of metal nanoparticles and reaction-controlled step-growth polymerization. The nanoparticles act as multifunctional monomer units, which form reversible, noncovalent bonds at specific bond angles and organize themselves into a colloidal polymer. We show that the kinetics and statistics of step-growth polymerization enable a quantitative prediction of the architecture of linear, branched, and cyclic self-assembled nanostructures; their aggregation numbers and size distribution; and the formation of structural isomers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Kun -- Nie, Zhihong -- Zhao, Nana -- Li, Wei -- Rubinstein, Michael -- Kumacheva, Eugenia -- 1-R01-HL077546-03A2/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2010 Jul 9;329(5988):197-200. doi: 10.1126/science.1189457.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of Toronto, 80 Saint George Street, Toronto, Ontario M5S 3H6, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20616274" target="_blank"〉PubMed〈/a〉
    Keywords: Cetrimonium Compounds/chemistry ; Colloids ; Cyclization ; Gold ; Isomerism ; Kinetics ; Metal Nanoparticles/*chemistry ; Microscopy, Electron, Transmission ; Nanotechnology/methods ; Physicochemical Processes ; Polymers ; Polystyrenes/chemistry
    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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    FAN1 acts with FANCI-FANCD2 to promote DNA interstrand cross-link repair (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-31
    Description: Fanconi anemia (FA) is caused by mutations in 13 Fanc genes and renders cells hypersensitive to DNA interstrand cross-linking (ICL) agents. A central event in the FA pathway is mono-ubiquitylation of the FANCI-FANCD2 (ID) protein complex. Here, we characterize a previously unrecognized nuclease, Fanconi anemia-associated nuclease 1 (FAN1), that promotes ICL repair in a manner strictly dependent on its ability to accumulate at or near sites of DNA damage and that relies on mono-ubiquitylation of the ID complex. Thus, the mono-ubiquitylated ID complex recruits the downstream repair protein FAN1 and facilitates the repair of DNA interstrand cross-links.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Ting -- Ghosal, Gargi -- Yuan, Jingsong -- Chen, Junjie -- Huang, Jun -- New York, N.Y. -- Science. 2010 Aug 6;329(5992):693-6. doi: 10.1126/science.1192656. Epub 2010 Jul 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang 310058, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20671156" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cell Line ; Cell Nucleus/metabolism ; DNA/*metabolism ; DNA Damage ; *DNA Repair ; Exodeoxyribonucleases/chemistry/genetics/*metabolism ; Fanconi Anemia Complementation Group D2 Protein/*metabolism ; Fanconi Anemia Complementation Group Proteins/*metabolism ; Gene Knockdown Techniques ; HeLa Cells ; Humans ; Mitomycin/pharmacology ; Molecular Sequence Data ; Mutant Proteins/metabolism ; Protein Binding ; Ubiquitinated Proteins/metabolism ; Ubiquitination ; 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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  • 8
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    Darwinian evolution of prions in cell culture (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-02
    Description: Prions are infectious proteins consisting mainly of PrP(Sc), a beta sheet-rich conformer of the normal host protein PrP(C), and occur in different strains. Strain identity is thought to be encoded by PrP(Sc) conformation. We found that biologically cloned prion populations gradually became heterogeneous by accumulating "mutants," and selective pressures resulted in the emergence of different mutants as major constituents of the evolving population. Thus, when transferred from brain to cultured cells, "cell-adapted" prions outcompeted their "brain-adapted" counterparts, and the opposite occurred when prions were returned from cells to brain. Similarly, the inhibitor swainsonine selected for a resistant substrain, whereas, in its absence, the susceptible substrain outgrew its resistant counterpart. Prions, albeit devoid of a nucleic acid genome, are thus subject to mutation and selective amplification.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2848070/" 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/PMC2848070/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Jiali -- Browning, Shawn -- Mahal, Sukhvir P -- Oelschlegel, Anja M -- Weissmann, Charles -- NS059543/NS/NINDS NIH HHS/ -- R01 NS059543/NS/NINDS NIH HHS/ -- R01 NS059543-01/NS/NINDS NIH HHS/ -- R01 NS059543-02/NS/NINDS NIH HHS/ -- R01 NS067214/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2010 Feb 12;327(5967):869-72. doi: 10.1126/science.1183218. Epub 2009 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Infectology, Scripps Florida, 130 Scripps Way, Jupiter, FL 33458, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20044542" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain Chemistry ; Cell Line ; Cell Line, Tumor ; Culture Media ; Culture Media, Conditioned ; *Evolution, Molecular ; Mice ; Mice, Inbred C57BL ; Mutation ; *PrPSc Proteins/chemistry/classification/pathogenicity ; Prion Diseases ; Prions/chemistry/classification/*pathogenicity/*physiology ; Protein Conformation ; Swainsonine/pharmacology
    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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    Ku70 corrupts DNA repair in the absence of the Fanconi anemia pathway (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-12
    Description: A conserved DNA repair response is defective in the human genetic illness Fanconi anemia (FA). Mutation of some FA genes impairs homologous recombination and error-prone DNA repair, rendering FA cells sensitive to DNA cross-linking agents. We found a genetic interaction between the FA gene FANCC and the nonhomologous end joining (NHEJ) factor Ku70. Disruption of both FANCC and Ku70 suppresses sensitivity to cross-linking agents, diminishes chromosome breaks, and reverses defective homologous recombination. Ku70 binds directly to free DNA ends, committing them to NHEJ repair. We show that purified FANCD2, a downstream effector of the FA pathway, might antagonize Ku70 activity by modifying such DNA substrates. These results reveal a function for the FA pathway in processing DNA ends, thereby diverting double-strand break repair away from abortive NHEJ and toward homologous recombination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pace, Paul -- Mosedale, Georgina -- Hodskinson, Michael R -- Rosado, Ivan V -- Sivasubramaniam, Meera -- Patel, Ketan J -- MC_U105178811/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Jul 9;329(5988):219-23. doi: 10.1126/science.1192277. Epub 2010 Jun 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20538911" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Nuclear/*genetics/metabolism ; Cell Line ; Chickens ; Chromosome Breakage ; Cross-Linking Reagents/pharmacology ; *DNA Breaks, Double-Stranded ; *DNA Repair ; DNA-Binding Proteins/*genetics/metabolism ; Fanconi Anemia Complementation Group C Protein/*genetics/metabolism ; Fanconi Anemia Complementation Group D2 Protein/chemistry/genetics/*metabolism ; Gene Conversion ; Genes, Immunoglobulin ; Humans ; Immunoglobulin M/genetics ; Point Mutation ; Recombinant Proteins/metabolism ; *Recombination, Genetic
    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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  • 10
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    Variation in transcription factor binding among humans (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-20
    Description: Differences in gene expression may play a major role in speciation and phenotypic diversity. We examined genome-wide differences in transcription factor (TF) binding in several humans and a single chimpanzee by using chromatin immunoprecipitation followed by sequencing. The binding sites of RNA polymerase II (PolII) and a key regulator of immune responses, nuclear factor kappaB (p65), were mapped in 10 lymphoblastoid cell lines, and 25 and 7.5% of the respective binding regions were found to differ between individuals. Binding differences were frequently associated with single-nucleotide polymorphisms and genomic structural variants, and these differences were often correlated with differences in gene expression, suggesting functional consequences of binding variation. Furthermore, comparing PolII binding between humans and chimpanzee suggests extensive divergence in TF binding. Our results indicate that many differences in individuals and species occur at the level of TF binding, and they provide insight into the genetic events responsible for these differences.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2938768/" 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/PMC2938768/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kasowski, Maya -- Grubert, Fabian -- Heffelfinger, Christopher -- Hariharan, Manoj -- Asabere, Akwasi -- Waszak, Sebastian M -- Habegger, Lukas -- Rozowsky, Joel -- Shi, Minyi -- Urban, Alexander E -- Hong, Mi-Young -- Karczewski, Konrad J -- Huber, Wolfgang -- Weissman, Sherman M -- Gerstein, Mark B -- Korbel, Jan O -- Snyder, Michael -- R01 CA077808/CA/NCI NIH HHS/ -- R01 CA077808-09/CA/NCI NIH HHS/ -- T32 GM007205/GM/NIGMS NIH HHS/ -- T32 GM007205-34/GM/NIGMS NIH HHS/ -- T32GM07205/GM/NIGMS NIH HHS/ -- U54 HG004558/HG/NHGRI NIH HHS/ -- U54 HG004558-04/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Apr 9;328(5975):232-5. doi: 10.1126/science.1183621. Epub 2010 Mar 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20299548" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Cell Line ; Chromatin Immunoprecipitation ; DNA Copy Number Variations ; DNA, Intergenic ; Female ; *Gene Expression Regulation ; Humans ; Male ; Pan troglodytes/genetics ; *Polymorphism, Single Nucleotide ; Protein Binding ; RNA Polymerase II/genetics/*metabolism ; Sequence Analysis, DNA ; Species Specificity ; Transcription Factor RelA/genetics/*metabolism ; Transcription Initiation Site
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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    Evidence for an alternative glycolytic pathway in rapidly proliferating cells (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-18
    Description: Proliferating cells, including cancer cells, require altered metabolism to efficiently incorporate nutrients such as glucose into biomass. The M2 isoform of pyruvate kinase (PKM2) promotes the metabolism of glucose by aerobic glycolysis and contributes to anabolic metabolism. Paradoxically, decreased pyruvate kinase enzyme activity accompanies the expression of PKM2 in rapidly dividing cancer cells and tissues. We demonstrate that phosphoenolpyruvate (PEP), the substrate for pyruvate kinase in cells, can act as a phosphate donor in mammalian cells because PEP participates in the phosphorylation of the glycolytic enzyme phosphoglycerate mutase (PGAM1) in PKM2-expressing cells. We used mass spectrometry to show that the phosphate from PEP is transferred to the catalytic histidine (His11) on human PGAM1. This reaction occurred at physiological concentrations of PEP and produced pyruvate in the absence of PKM2 activity. The presence of histidine-phosphorylated PGAM1 correlated with the expression of PKM2 in cancer cell lines and tumor tissues. Thus, decreased pyruvate kinase activity in PKM2-expressing cells allows PEP-dependent histidine phosphorylation of PGAM1 and may provide an alternate glycolytic pathway that decouples adenosine triphosphate production from PEP-mediated phosphotransfer, allowing for the high rate of glycolysis to support the anabolic metabolism observed in many proliferating cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3030121/" 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/PMC3030121/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vander Heiden, Matthew G -- Locasale, Jason W -- Swanson, Kenneth D -- Sharfi, Hadar -- Heffron, Greg J -- Amador-Noguez, Daniel -- Christofk, Heather R -- Wagner, Gerhard -- Rabinowitz, Joshua D -- Asara, John M -- Cantley, Lewis C -- 1K08CA136983/CA/NCI NIH HHS/ -- 1P01CA120964-01A/CA/NCI NIH HHS/ -- 5 T32 CA009361-28/CA/NCI NIH HHS/ -- 5P30CA006516-43/CA/NCI NIH HHS/ -- K08 CA136983/CA/NCI NIH HHS/ -- K08 CA136983-02/CA/NCI NIH HHS/ -- P01 CA089021/CA/NCI NIH HHS/ -- P01 CA089021-10/CA/NCI NIH HHS/ -- P01 CA120964/CA/NCI NIH HHS/ -- P01 CA120964-01A1/CA/NCI NIH HHS/ -- P01 GM047467/GM/NIGMS NIH HHS/ -- P01 GM047467-20/GM/NIGMS NIH HHS/ -- P01CA089021/CA/NCI NIH HHS/ -- P01GM047467/GM/NIGMS NIH HHS/ -- P30 CA006516/CA/NCI NIH HHS/ -- P30 CA006516-43S1/CA/NCI NIH HHS/ -- R01 AI078063/AI/NIAID NIH HHS/ -- R01 GM056203/GM/NIGMS NIH HHS/ -- R01-GM56302/GM/NIGMS NIH HHS/ -- R21 CA128620/CA/NCI NIH HHS/ -- R21/R33 DK070299/DK/NIDDK NIH HHS/ -- R33 DK070299/DK/NIDDK NIH HHS/ -- R33 DK070299-03/DK/NIDDK NIH HHS/ -- T32 CA009172/CA/NCI NIH HHS/ -- T32 CA009361/CA/NCI NIH HHS/ -- T32 CA009361-28/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 17;329(5998):1492-9. doi: 10.1126/science.1188015.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20847263" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Cell Line ; Cell Line, Tumor ; *Cell Proliferation ; Female ; Glucose/*metabolism ; Glyceric Acids/metabolism ; *Glycolysis ; Histidine/metabolism ; Humans ; Isoenzymes/metabolism ; Kinetics ; Male ; Mammary Neoplasms, Animal/metabolism ; Mice ; Neoplasms/*metabolism/pathology ; Phosphoenolpyruvate/metabolism ; Phosphoglycerate Mutase/*metabolism ; Phosphopyruvate Hydratase/metabolism ; Phosphorylation ; Prostatic Neoplasms/metabolism ; Pyruvate Kinase/*metabolism ; Pyruvic Acid/metabolism ; Recombinant Proteins/metabolism
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  • 12
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    Btbd7 regulates epithelial cell dynamics and branching morphogenesis (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-31
    Description: During embryonic development, many organs form by extensive branching of epithelia through the formation of clefts and buds. In cleft formation, buds are delineated by the conversion of epithelial cell-cell adhesions to cell-matrix adhesions, but the mechanisms of cleft formation are not clear. We have identified Btbd7 as a dynamic regulator of branching morphogenesis. Btbd7 provides a mechanistic link between the extracellular matrix and cleft propagation through its highly focal expression leading to local regulation of Snail2 (Slug), E-cadherin, and epithelial cell motility. Inhibition experiments show that Btbd7 is required for branching of embryonic mammalian salivary glands and lungs. Hence, Btbd7 is a regulatory gene that promotes epithelial tissue remodeling and formation of branched organs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3412157/" 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/PMC3412157/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Onodera, Tomohiro -- Sakai, Takayoshi -- Hsu, Jeff Chi-feng -- Matsumoto, Kazue -- Chiorini, John A -- Yamada, Kenneth M -- ZIA DE000525-20/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Jul 30;329(5991):562-5. doi: 10.1126/science.1191880.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell and Developmental Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892-4370, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20671187" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cadherins/metabolism ; Cell Adhesion ; Cell Line ; Cell Movement ; Dogs ; Epithelial Cells/*physiology ; Fibronectins/genetics/metabolism ; Genes, Regulator ; Lung/*embryology/metabolism ; Mice ; Mice, Inbred ICR ; Models, Biological ; Molecular Sequence Data ; *Morphogenesis ; Nuclear Proteins ; Organ Culture Techniques ; Proteins/chemistry/*genetics/*physiology ; RNA, Small Interfering ; Salivary Glands/*embryology/metabolism ; Submandibular Gland/embryology ; Transcription Factors/genetics/metabolism ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Stem cells. Diseases in a dish take off (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-11-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2010 Nov 26;330(6008):1172-3. doi: 10.1126/science.330.6008.1172.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21109645" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Drug Discovery/*methods ; Drug Evaluation, Preclinical/methods ; *Genetic Diseases, Inborn/drug therapy/genetics/pathology/physiopathology ; *Heredodegenerative Disorders, Nervous System/drug ; therapy/genetics/pathology/physiopathology ; Humans ; *Induced Pluripotent Stem Cells/cytology/physiology
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  • 14
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    Requirement of prorenin receptor and vacuolar H+-ATPase-mediated acidification for Wnt signaling (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-01-23
    Description: Wnt/beta-catenin signaling is important in stem cell biology, embryonic development, and disease, including cancer. However, the mechanism of Wnt signal transmission, notably how the receptors are activated, remains incompletely understood. We found that the prorenin receptor (PRR) is a component of the Wnt receptor complex. PRR functions in a renin-independent manner as an adaptor between Wnt receptors and the vacuolar H+-adenosine triphosphatase (V-ATPase) complex. Moreover, PRR and V-ATPase were required to mediate Wnt signaling during antero-posterior patterning of Xenopus early central nervous system development. The results reveal an unsuspected role for the prorenin receptor, V-ATPase activity, and acidification during Wnt/beta-catenin signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cruciat, Cristina-Maria -- Ohkawara, Bisei -- Acebron, Sergio P -- Karaulanov, Emil -- Reinhard, Carmen -- Ingelfinger, Dierk -- Boutros, Michael -- Niehrs, Christof -- New York, N.Y. -- Science. 2010 Jan 22;327(5964):459-63. doi: 10.1126/science.1179802.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Embryology, DKFZ-ZMBH Alliance, Deutsches Krebsforschungszentrum, Im Neuenheimer Feld 280, D-69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20093472" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Patterning ; Cell Line ; Cell Line, Tumor ; Central Nervous System/cytology/embryology ; Embryo, Nonmammalian/metabolism ; Frizzled Receptors/metabolism ; Gene Expression Regulation, Developmental ; Homeodomain Proteins/genetics/metabolism ; Humans ; Hydrogen-Ion Concentration ; LDL-Receptor Related Proteins/metabolism ; Low Density Lipoprotein Receptor-Related Protein-6 ; Mice ; Nerve Tissue Proteins/genetics/metabolism ; Phosphorylation ; RNA, Small Interfering ; Receptors, Cell Surface/genetics/*metabolism ; *Signal Transduction ; Vacuolar Proton-Translocating ATPases/antagonists & inhibitors/*metabolism ; Wnt Proteins/*metabolism ; Wnt3 Protein ; Xenopus/embryology/metabolism ; Xenopus Proteins/genetics/*metabolism ; beta Catenin/metabolism
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  • 15
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    Stem cells. Reprogrammed cells come up short, for now (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-03-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2010 Mar 5;327(5970):1191. doi: 10.1126/science.327.5970.1191.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20203025" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Cell Line ; *Cellular Reprogramming ; Embryonic Stem Cells/cytology/*physiology ; Humans ; Induced Pluripotent Stem Cells/cytology/*physiology ; Mice ; Neurogenesis ; Neuroglia/cytology ; Neurons/cytology
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  • 16
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    Glutamine deamidation and dysfunction of ubiquitin/NEDD8 induced by a bacterial effector family (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-08-07
    Description: A family of bacterial effectors including Cif homolog from Burkholderia pseudomallei (CHBP) and Cif from Enteropathogenic Escherichia coli (EPEC) adopt a functionally important papain-like hydrolytic fold. We show here that CHBP was a potent inhibitor of the eukaryotic ubiquitination pathway. CHBP acted as a deamidase that specifically and efficiently deamidated Gln40 in ubiquitin and ubiquitin-like protein NEDD8 both in vitro and during Burkholderia infection. Deamidated ubiquitin was impaired in supporting ubiquitin-chain synthesis. Cif selectively deamidated NEDD8, which abolished the activity of neddylated Cullin-RING ubiquitin ligases (CRLs). Ubiquitination and ubiquitin-dependent degradation of multiple CRL substrates were impaired by Cif in EPEC-infected cells. Mutations of substrate-contacting residues in Cif abolished or attenuated EPEC-induced cytopathic phenotypes of cell cycle arrest and actin stress fiber formation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3031172/" 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/PMC3031172/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cui, Jixin -- Yao, Qing -- Li, Shan -- Ding, Xiaojun -- Lu, Qiuhe -- Mao, Haibin -- Liu, Liping -- Zheng, Ning -- Chen, She -- Shao, Feng -- R01 CA107134/CA/NCI NIH HHS/ -- R01 CA107134-08/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Sep 3;329(5996):1215-8. doi: 10.1126/science.1193844. Epub 2010 Aug 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Program in Chinese Academy of Medical Sciences and Beijing Union Medical College, Beijing 100730, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20688984" target="_blank"〉PubMed〈/a〉
    Keywords: Amidohydrolases/*metabolism ; Bacterial Proteins/*metabolism ; Burkholderia/pathogenicity ; Burkholderia pseudomallei/*metabolism/pathogenicity ; Cell Cycle ; Cell Line ; Cullin Proteins/metabolism ; Enteropathogenic Escherichia coli/*metabolism/pathogenicity ; Escherichia coli Proteins/genetics/*metabolism ; Glutamine/*metabolism ; HeLa Cells ; Humans ; Point Mutation ; Stress Fibers/metabolism ; Transfection ; Ubiquitin/*metabolism ; Ubiquitin C/metabolism ; Ubiquitin-Conjugating Enzymes/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitination ; Ubiquitins/*metabolism
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    Permissive secondary mutations enable the evolution of influenza oseltamivir resistance (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-06-05
    Description: The His274--〉Tyr274 (H274Y) mutation confers oseltamivir resistance on N1 influenza neuraminidase but had long been thought to compromise viral fitness. However, beginning in 2007-2008, viruses containing H274Y rapidly became predominant among human seasonal H1N1 isolates. We show that H274Y decreases the amount of neuraminidase that reaches the cell surface and that this defect can be counteracted by secondary mutations that also restore viral fitness. Two such mutations occurred in seasonal H1N1 shortly before the widespread appearance of H274Y. The evolution of oseltamivir resistance was therefore enabled by "permissive" mutations that allowed the virus to tolerate subsequent occurrences of H274Y. An understanding of this process may provide a basis for predicting the evolution of oseltamivir resistance in other influenza strains.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2913718/" 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/PMC2913718/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bloom, Jesse D -- Gong, Lizhi Ian -- Baltimore, David -- P01 CA132681/CA/NCI NIH HHS/ -- P01 CA132681-01A27259/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Jun 4;328(5983):1272-5. doi: 10.1126/science.1187816.〈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/20522774" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; Antiviral Agents/*pharmacology ; Cell Line ; Cell Line, Tumor ; Cell Membrane/metabolism ; Drug Resistance, Viral/*genetics ; *Evolution, Molecular ; Genes, Viral ; Genetic Fitness ; Humans ; Influenza A Virus, H1N1 Subtype/*drug effects/*genetics/growth & development ; Influenza, Human/drug therapy/*virology ; Mutation ; Neuraminidase/antagonists & inhibitors/chemistry/genetics/metabolism ; Oseltamivir/*pharmacology ; Phylogeny ; Selection, Genetic
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  • 18
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    Decreased clearance of CNS beta-amyloid in Alzheimer's disease (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-12-15
    Description: Alzheimer's disease is hypothesized to be caused by an imbalance between beta-amyloid (Abeta) production and clearance that leads to Abeta accumulation in the central nervous system (CNS). Abeta production and clearance are key targets in the development of disease-modifying therapeutic agents for Alzheimer's disease. However, there has not been direct evidence of altered Abeta production or clearance in Alzheimer's disease. By using metabolic labeling, we measured Abeta42 and Abeta40 production and clearance rates in the CNS of participants with Alzheimer's disease and cognitively normal controls. Clearance rates for both Abeta42 and Abeta40 were impaired in Alzheimer's disease compared with controls. On average, there were no differences in Abeta40 or Abeta42 production rates. Thus, the common late-onset form of Alzheimer's disease is characterized by an overall impairment in Abeta clearance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3073454/" 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/PMC3073454/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mawuenyega, Kwasi G -- Sigurdson, Wendy -- Ovod, Vitaliy -- Munsell, Ling -- Kasten, Tom -- Morris, John C -- Yarasheski, Kevin E -- Bateman, Randall J -- K08 AG027091/AG/NIA NIH HHS/ -- K08 AG027091-03/AG/NIA NIH HHS/ -- K23 AG030946/AG/NIA NIH HHS/ -- K23 AG030946-04/AG/NIA NIH HHS/ -- P01 AG003991/AG/NIA NIH HHS/ -- P01 AG003991-28/AG/NIA NIH HHS/ -- P01 AG03991/AG/NIA NIH HHS/ -- P30 DK056341/DK/NIDDK NIH HHS/ -- P30 DK056341-10/DK/NIDDK NIH HHS/ -- P41 GM103422/GM/NIGMS NIH HHS/ -- P41 RR000954/RR/NCRR NIH HHS/ -- P41 RR000954-34/RR/NCRR NIH HHS/ -- P50 AG005681/AG/NIA NIH HHS/ -- P50 AG005681-28/AG/NIA NIH HHS/ -- P50 AG05681/AG/NIA NIH HHS/ -- P60 DK020579/DK/NIDDK NIH HHS/ -- P60 DK020579-31/DK/NIDDK NIH HHS/ -- R01 NS065667/NS/NINDS NIH HHS/ -- R01 NS065667-03/NS/NINDS NIH HHS/ -- UL1 RR024992/RR/NCRR NIH HHS/ -- UL1 RR024992-05/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2010 Dec 24;330(6012):1774. doi: 10.1126/science.1197623. Epub 2010 Dec 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21148344" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Aged, 80 and over ; Alzheimer Disease/cerebrospinal fluid/*metabolism ; Amyloid beta-Peptides/cerebrospinal fluid/*metabolism ; Brain/*metabolism ; Female ; Humans ; Kinetics ; Male ; Middle Aged ; Peptide Fragments/cerebrospinal fluid/*metabolism
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    Alpha-synuclein promotes SNARE-complex assembly in vivo and in vitro (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-28
    Description: Presynaptic nerve terminals release neurotransmitters repeatedly, often at high frequency, and in relative isolation from neuronal cell bodies. Repeated release requires cycles of soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE)-complex assembly and disassembly, with continuous generation of reactive SNARE-protein intermediates. Although many forms of neurodegeneration initiate presynaptically, only few pathogenic mechanisms are known, and the functions of presynaptic proteins linked to neurodegeneration, such as alpha-synuclein, remain unclear. Here, we show that maintenance of continuous presynaptic SNARE-complex assembly required a nonclassical chaperone activity mediated by synucleins. Specifically, alpha-synuclein directly bound to the SNARE-protein synaptobrevin-2/vesicle-associated membrane protein 2 (VAMP2) and promoted SNARE-complex assembly. Moreover, triple-knockout mice lacking synucleins developed age-dependent neurological impairments, exhibited decreased SNARE-complex assembly, and died prematurely. Thus, synucleins may function to sustain normal SNARE-complex assembly in a presynaptic terminal during aging.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3235365/" 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/PMC3235365/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burre, Jacqueline -- Sharma, Manu -- Tsetsenis, Theodoros -- Buchman, Vladimir -- Etherton, Mark R -- Sudhof, Thomas C -- 075615/Wellcome Trust/United Kingdom -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Sep 24;329(5999):1663-7. doi: 10.1126/science.1195227. Epub 2010 Aug 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Physiology, and Howard Hughes Medical Institute, Stanford University, 1050 Arastradero Road, Palo Alto, CA 94304-5543, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20798282" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Animals ; Cell Line ; Cells, Cultured ; HSP40 Heat-Shock Proteins/metabolism ; Humans ; Membrane Fusion ; Membrane Proteins/metabolism ; Mice ; Mice, Knockout ; Mice, Transgenic ; Nerve Degeneration/*metabolism ; Neurons/*metabolism ; Presynaptic Terminals/*metabolism ; Protein Binding ; Rats ; Recombinant Fusion Proteins/metabolism ; SNARE Proteins/*metabolism ; Vesicle-Associated Membrane Protein 2/metabolism ; alpha-Synuclein/chemistry/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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  • 20
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    Dynamic kinetic resolution of biaryl atropisomers via peptide-catalyzed asymmetric bromination (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-05
    Description: Despite the widespread use of axially chiral, or atropisomeric, biaryl ligands in modern synthesis and the occurrence of numerous natural products exhibiting axial chirality, few catalytic methods have emerged for the direct asymmetric preparation of this compound class. Here, we present a tripeptide-derived small-molecule catalyst for the dynamic kinetic resolution of racemic biaryl substrates. The reaction proceeds via an atropisomer-selective electrophilic aromatic substitution reaction using simple bromination reagents. The result is an enantioselective synthesis that delivers chiral nonracemic biaryl compounds with excellent optical purity and good isolated chemical yields (in most cases a 〉95:5 enantiomer ratio and isolated yields of 65 to 87%). A mechanistic model is advanced that accounts for the basis of selectivity observed.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3066098/" 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/PMC3066098/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gustafson, Jeffrey L -- Lim, Daniel -- Miller, Scott J -- GM068649/GM/NIGMS NIH HHS/ -- R01 GM068649/GM/NIGMS NIH HHS/ -- R01 GM068649-10/GM/NIGMS NIH HHS/ -- R37 GM068649/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Jun 4;328(5983):1251-5. doi: 10.1126/science.1188403.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Yale University, 225 Prospect Street, Post Office Box 208107, New Haven, CT 06520-8107, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20522769" target="_blank"〉PubMed〈/a〉
    Keywords: Biphenyl Compounds/*chemical synthesis/chemistry ; Bromine/chemistry ; Catalysis ; *Halogenation ; Kinetics ; Ligands ; Molecular Structure ; Oligopeptides/*chemistry ; Physicochemical Processes ; *Stereoisomerism ; Temperature
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  • 21
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    FCHo proteins are nucleators of clathrin-mediated endocytosis (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-08
    Description: Clathrin-mediated endocytosis, the major pathway for ligand internalization into eukaryotic cells, is thought to be initiated by the clustering of clathrin and adaptors around receptors destined for internalization. However, here we report that the membrane-sculpting F-BAR domain-containing Fer/Cip4 homology domain-only proteins 1 and 2 (FCHo1/2) were required for plasma membrane clathrin-coated vesicle (CCV) budding and marked sites of CCV formation. Changes in FCHo1/2 expression levels correlated directly with numbers of CCV budding events, ligand endocytosis, and synaptic vesicle marker recycling. FCHo1/2 proteins bound specifically to the plasma membrane and recruited the scaffold proteins eps15 and intersectin, which in turn engaged the adaptor complex AP2. The FCHo F-BAR membrane-bending activity was required, leading to the proposal that FCHo1/2 sculpt the initial bud site and recruit the clathrin machinery for CCV formation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2883440/" 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/PMC2883440/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Henne, William Mike -- Boucrot, Emmanuel -- Meinecke, Michael -- Evergren, Emma -- Vallis, Yvonne -- Mittal, Rohit -- McMahon, Harvey T -- MC_U105178795/Medical Research Council/United Kingdom -- U.1051.02.007(78795)/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Jun 4;328(5983):1281-4. doi: 10.1126/science.1188462. Epub 2010 May 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council, Laboratory of Molecular Biology (MRC-LMB), Hills Road, Cambridge CB2 0QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20448150" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Protein Complex 2/metabolism ; Adaptor Proteins, Signal Transducing ; Adaptor Proteins, Vesicular Transport/metabolism ; Animals ; Calcium-Binding Proteins/metabolism ; Cell Line ; Cell Membrane/metabolism ; Cells, Cultured ; Clathrin/*metabolism ; Clathrin-Coated Vesicles/*metabolism ; *Endocytosis ; HeLa Cells ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Membrane Proteins ; Mice ; Models, Molecular ; Neurons/cytology/metabolism ; Phosphoproteins/metabolism ; Protein Multimerization ; Protein Structure, Tertiary ; Proteins/chemistry/*metabolism ; RNA Interference ; Rats ; Rats, Sprague-Dawley ; Recombinant Fusion Proteins/metabolism ; Synaptic Vesicles/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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  • 22
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    Intravascular danger signals guide neutrophils to sites of sterile inflammation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-16
    Description: Neutrophils are recruited from the blood to sites of sterile inflammation, where they contribute to wound healing but may also cause tissue damage. By using spinning disk confocal intravital microscopy, we examined the kinetics and molecular mechanisms of neutrophil recruitment to sites of focal hepatic necrosis in vivo. Adenosine triphosphate released from necrotic cells activated the Nlrp3 inflammasome to generate an inflammatory microenvironment that alerted circulating neutrophils to adhere within liver sinusoids. Subsequently, generation of an intravascular chemokine gradient directed neutrophil migration through healthy tissue toward foci of damage. Lastly, formyl-peptide signals released from necrotic cells guided neutrophils through nonperfused sinusoids into the injury. Thus, dynamic in vivo imaging revealed a multistep hierarchy of directional cues that guide neutrophil localization to sites of sterile inflammation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDonald, Braedon -- Pittman, Keir -- Menezes, Gustavo B -- Hirota, Simon A -- Slaba, Ingrid -- Waterhouse, Christopher C M -- Beck, Paul L -- Muruve, Daniel A -- Kubes, Paul -- Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2010 Oct 15;330(6002):362-6. doi: 10.1126/science.1195491.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology Research Group, University of Calgary, Alberta T2N 4N1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20947763" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Carrier Proteins/metabolism ; Cell Adhesion ; Chemokine CXCL2/metabolism ; Chemokines/metabolism ; Chemotaxis, Leukocyte ; Cues ; Endothelium, Vascular/physiology ; Inflammation/*immunology/metabolism/*pathology ; Kinetics ; Liver/blood supply/*immunology/metabolism/*pathology ; Liver Diseases/*immunology/metabolism/*pathology ; Macrophage-1 Antigen/physiology ; Mice ; Microscopy/methods ; Microscopy, Confocal ; Microvessels/physiology ; Necrosis ; *Neutrophil Infiltration ; Neutrophils/physiology ; Peptides/metabolism ; Receptors, Formyl Peptide/metabolism ; Receptors, Interleukin-8B/metabolism ; Receptors, Purinergic P2/metabolism ; Receptors, Purinergic P2X7 ; Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 23
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    An autophagy-enhancing drug promotes degradation of mutant alpha1-antitrypsin Z and reduces hepatic fibrosis (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-05
    Description: In the classical form of alpha1-antitrypsin (AT) deficiency, a point mutation in AT alters the folding of a liver-derived secretory glycoprotein and renders it aggregation-prone. In addition to decreased serum concentrations of AT, the disorder is characterized by accumulation of the mutant alpha1-antitrypsin Z (ATZ) variant inside cells, causing hepatic fibrosis and/or carcinogenesis by a gain-of-toxic function mechanism. The proteasomal and autophagic pathways are known to mediate degradation of ATZ. Here we show that the autophagy-enhancing drug carbamazepine (CBZ) decreased the hepatic load of ATZ and hepatic fibrosis in a mouse model of AT deficiency-associated liver disease. These results provide a basis for testing CBZ, which has an extensive clinical safety profile, in patients with AT deficiency and also provide a proof of principle for therapeutic use of autophagy enhancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hidvegi, Tunda -- Ewing, Michael -- Hale, Pamela -- Dippold, Christine -- Beckett, Caroline -- Kemp, Carolyn -- Maurice, Nicholas -- Mukherjee, Amitava -- Goldbach, Christina -- Watkins, Simon -- Michalopoulos, George -- Perlmutter, David H -- DK076918/DK/NIDDK NIH HHS/ -- HL037784/HL/NHLBI NIH HHS/ -- R01 DK076918/DK/NIDDK NIH HHS/ -- R01 DK084512/DK/NIDDK NIH HHS/ -- RR022241/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2010 Jul 9;329(5988):229-32. doi: 10.1126/science.1190354. Epub 2010 Jun 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20522742" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autophagy/*drug effects ; Carbamazepine/administration & dosage/*pharmacology/therapeutic use ; Cell Line ; Disease Models, Animal ; Endoplasmic Reticulum/metabolism ; HeLa Cells ; Humans ; Liver/drug effects/*metabolism/pathology ; Liver Cirrhosis/*drug therapy/etiology/metabolism/pathology ; Mice ; Mice, Transgenic ; Mutant Proteins/chemistry/metabolism ; Phagosomes/drug effects/ultrastructure ; Phenotype ; Proteasome Endopeptidase Complex/metabolism ; Protein Folding ; Solubility ; alpha 1-Antitrypsin/chemistry/genetics/*metabolism ; alpha 1-Antitrypsin Deficiency/complications/*metabolism/pathology
    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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  • 24
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    mTORC1-mediated cell proliferation, but not cell growth, controlled by the 4E-BPs (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-29
    Description: The mammalian target of rapamycin complex 1 (mTORC1) integrates mitogen and nutrient signals to control cell proliferation and cell size. Hence, mTORC1 is implicated in a large number of human diseases--including diabetes, obesity, heart disease, and cancer--that are characterized by aberrant cell growth and proliferation. Although eukaryotic translation initiation factor 4E-binding proteins (4E-BPs) are critical mediators of mTORC1 function, their precise contribution to mTORC1 signaling and the mechanisms by which they mediate mTORC1 function have remained unclear. We inhibited the mTORC1 pathway in cells lacking 4E-BPs and analyzed the effects on cell size, cell proliferation, and cell cycle progression. Although the 4E-BPs had no effect on cell size, they inhibited cell proliferation by selectively inhibiting the translation of messenger RNAs that encode proliferation-promoting proteins and proteins involved in cell cycle progression. Thus, control of cell size and cell cycle progression appear to be independent in mammalian cells, whereas in lower eukaryotes, 4E-BPs influence both cell growth and proliferation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2893390/" 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/PMC2893390/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dowling, Ryan J O -- Topisirovic, Ivan -- Alain, Tommy -- Bidinosti, Michael -- Fonseca, Bruno D -- Petroulakis, Emmanuel -- Wang, Xiaoshan -- Larsson, Ola -- Selvaraj, Anand -- Liu, Yi -- Kozma, Sara C -- Thomas, George -- Sonenberg, Nahum -- P50 NS057531/NS/NINDS NIH HHS/ -- P50 NS057531-01A2/NS/NINDS NIH HHS/ -- R01 DK078019/DK/NIDDK NIH HHS/ -- R01 DK73802/DK/NIDDK NIH HHS/ -- U01 CA84292-06/CA/NCI NIH HHS/ -- Canadian Institutes of Health Research/Canada -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 May 28;328(5982):1172-6. doi: 10.1126/science.1187532.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Goodman Cancer Research Centre, McGill University, Montreal, Quebec H3A 1A3, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20508131" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/genetics/*metabolism ; Cell Cycle ; *Cell Enlargement ; Cell Line ; *Cell Proliferation ; Cell Size ; Cell Survival ; Eukaryotic Initiation Factors/genetics/*metabolism ; Humans ; Mice ; Mice, Knockout ; Multiprotein Complexes ; Phosphoproteins/genetics/*metabolism ; Phosphorylation ; Protein Biosynthesis ; Proteins ; RNA, Messenger/genetics/metabolism ; Ribosomal Protein S6 Kinases/metabolism ; Signal Transduction ; Sirolimus/pharmacology ; TOR Serine-Threonine Kinases ; Transcription Factors/*metabolism
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    Computational design of an enzyme catalyst for a stereoselective bimolecular Diels-Alder reaction (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-07-22
    Description: The Diels-Alder reaction is a cornerstone in organic synthesis, forming two carbon-carbon bonds and up to four new stereogenic centers in one step. No naturally occurring enzymes have been shown to catalyze bimolecular Diels-Alder reactions. We describe the de novo computational design and experimental characterization of enzymes catalyzing a bimolecular Diels-Alder reaction with high stereoselectivity and substrate specificity. X-ray crystallography confirms that the structure matches the design for the most active of the enzymes, and binding site substitutions reprogram the substrate specificity. Designed stereoselective catalysts for carbon-carbon bond-forming reactions should be broadly useful in synthetic chemistry.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3241958/" 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/PMC3241958/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Siegel, Justin B -- Zanghellini, Alexandre -- Lovick, Helena M -- Kiss, Gert -- Lambert, Abigail R -- St Clair, Jennifer L -- Gallaher, Jasmine L -- Hilvert, Donald -- Gelb, Michael H -- Stoddard, Barry L -- Houk, Kendall N -- Michael, Forrest E -- Baker, David -- R01 GM075962/GM/NIGMS NIH HHS/ -- T32 GM008268/GM/NIGMS NIH HHS/ -- T32 GM008268-24/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jul 16;329(5989):309-13. doi: 10.1126/science.1190239.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20647463" target="_blank"〉PubMed〈/a〉
    Keywords: Acrylamides/chemistry ; Algorithms ; Butadienes/chemistry ; Carbon/*chemistry ; Catalysis ; Catalytic Domain ; Computer Simulation ; *Computer-Aided Design ; Crystallography, X-Ray ; Enzymes/*chemistry/genetics ; Hydrogen Bonding ; Hydrophobic and Hydrophilic Interactions ; Kinetics ; Models, Molecular ; Mutagenesis ; Physicochemical Processes ; Protein Conformation ; *Protein Engineering ; Proteins/*chemistry/genetics ; Software ; Stereoisomerism ; Substrate Specificity
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    Generating a prion with bacterially expressed recombinant prion protein (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-30
    Description: The prion hypothesis posits that a misfolded form of prion protein (PrP) is responsible for the infectivity of prion disease. Using recombinant murine PrP purified from Escherichia coli, we created a recombinant prion with the attributes of the pathogenic PrP isoform: aggregated, protease-resistant, and self-perpetuating. After intracerebral injection of the recombinant prion, wild-type mice developed neurological signs in approximately 130 days and reached the terminal stage of disease in approximately 150 days. Characterization of diseased mice revealed classic neuropathology of prion disease, the presence of protease-resistant PrP, and the capability of serially transmitting the disease; these findings confirmed that the mice succumbed to prion disease. Thus, as postulated by the prion hypothesis, the infectivity in mammalian prion disease results from an altered conformation of PrP.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2893558/" 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/PMC2893558/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Fei -- Wang, Xinhe -- Yuan, Chong-Gang -- Ma, Jiyan -- R01 NS060729/NS/NINDS NIH HHS/ -- R01 NS060729-01A1/NS/NINDS NIH HHS/ -- R01NS060729/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2010 Feb 26;327(5969):1132-5. doi: 10.1126/science.1183748. Epub 2010 Jan 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biochemistry, Ohio State University, Columbus, OH 43210, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20110469" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/pathology ; Brain Chemistry ; Cell Line ; Endopeptidase K/metabolism ; Escherichia coli/genetics ; Female ; Glycosylation ; Liver/chemistry ; Mice ; Neurons/chemistry ; Phosphatidylglycerols/*chemistry ; PrPC Proteins/chemistry/pathogenicity ; PrPSc Proteins/analysis/*chemistry/*pathogenicity ; Prion Diseases/*etiology/pathology ; Prions/*chemistry/*pathogenicity ; Protein Folding ; RNA/*chemistry ; Recombinant Proteins/chemistry
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  • 27
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    Signaling kinase AMPK activates stress-promoted transcription via histone H2B phosphorylation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-22
    Description: The mammalian adenosine monophosphate-activated protein kinase (AMPK) is a serine-threonine kinase protein complex that is a central regulator of cellular energy homeostasis. However, the mechanisms by which AMPK mediates cellular responses to metabolic stress remain unclear. We found that AMPK activates transcription through direct association with chromatin and phosphorylation of histone H2B at serine 36. AMPK recruitment and H2B Ser36 phosphorylation colocalized within genes activated by AMPK-dependent pathways, both in promoters and in transcribed regions. Ectopic expression of H2B in which Ser36 was substituted by alanine reduced transcription and RNA polymerase II association to AMPK-dependent genes, and lowered cell survival in response to stress. Our results place AMPK-dependent H2B Ser36 phosphorylation in a direct transcriptional and chromatin regulatory pathway leading to cellular adaptation to stress.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3922052/" 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/PMC3922052/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bungard, David -- Fuerth, Benjamin J -- Zeng, Ping-Yao -- Faubert, Brandon -- Maas, Nancy L -- Viollet, Benoit -- Carling, David -- Thompson, Craig B -- Jones, Russell G -- Berger, Shelley L -- CA078831/CA/NCI NIH HHS/ -- CA09171/CA/NCI NIH HHS/ -- CA105463/CA/NCI NIH HHS/ -- MC_U120027537/Medical Research Council/United Kingdom -- MOP-93799/Canadian Institutes of Health Research/Canada -- P01 AG031862/AG/NIA NIH HHS/ -- P01 CA104838/CA/NCI NIH HHS/ -- R01 CA078831/CA/NCI NIH HHS/ -- R01 CA105463/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 3;329(5996):1201-5. doi: 10.1126/science.1191241. Epub 2010 Jul 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Developmental Biology, University of Pennsylvania Medical School, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20647423" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/chemistry/*metabolism ; Adaptation, Physiological ; Amino Acid Motifs ; Amino Acid Substitution ; Animals ; Cell Line ; Cell Line, Tumor ; Cell Survival ; Cells, Cultured ; Chromatin/*metabolism ; Chromatin Immunoprecipitation ; Enzyme Activation ; Gene Expression Regulation ; Histones/chemistry/*metabolism ; Humans ; Mice ; Phosphorylation ; Promoter Regions, Genetic ; Protein-Serine-Threonine Kinases/genetics/metabolism ; Serine/metabolism ; Signal Transduction ; *Stress, Physiological ; *Transcription, Genetic ; Tumor Suppressor Protein p53/metabolism
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    Photorhabdus luminescens toxins ADP-ribosylate actin and RhoA to force actin clustering (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-02-27
    Description: The bacterium Photorhabdus luminescens is mutualistically associated with entomopathogenetic nematodes. These nematodes invade insect larvae and release the bacteria from their intestine, which kills the insects through the action of toxin complexes. We elucidated the mode of action of two of these insecticidal toxins from P. luminescens. We identified the biologically active components TccC3 and TccC5 as adenosine diphosphate (ADP)-ribosyltransferases, which modify unusual amino acids. TccC3 ADP-ribosylated threonine-148 of actin, resulting in actin polymerization. TccC5 ADP-ribosylated Rho guanosine triphosphatase proteins at glutamine-61 and glutamine-63, inducing their activation. The concerted action of both toxins inhibited phagocytosis of target insect cells and induced extensive intracellular polymerization and clustering of actin. Several human pathogenic bacteria produce related toxins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lang, Alexander E -- Schmidt, Gudula -- Schlosser, Andreas -- Hey, Timothy D -- Larrinua, Ignacio M -- Sheets, Joel J -- Mannherz, Hans G -- Aktories, Klaus -- New York, N.Y. -- Science. 2010 Feb 26;327(5969):1139-42. doi: 10.1126/science.1184557.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Experimentelle und Klinische Pharmakologie und Toxikologie, Albert-Ludwigs-Universitat Freiburg, 79104 Freiburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20185726" target="_blank"〉PubMed〈/a〉
    Keywords: ADP Ribose Transferases/chemistry/*metabolism ; Actins/chemistry/*metabolism ; Adenosine Diphosphate Ribose/*metabolism ; Animals ; Bacterial Toxins/chemistry/*metabolism/pharmacology ; Cell Line ; Glutamine/metabolism ; HeLa Cells ; Hemocytes/immunology ; Humans ; Moths ; Phagocytosis/drug effects ; *Photorhabdus ; Signal Transduction ; Stress Fibers/metabolism ; Threonine/metabolism ; Thymosin/metabolism/pharmacology ; rhoA GTP-Binding Protein/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Target RNA-directed trimming and tailing of small silencing RNAs (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-19
    Description: In Drosophila, microRNAs (miRNAs) typically guide Argonaute1 to repress messenger RNA (mRNA), whereas small interfering RNAs (siRNAs) guide Argonaute2 to destroy viral and transposon RNA. Unlike siRNAs, miRNAs rarely form extensive numbers of base pairs to the mRNAs they regulate. We find that extensive complementarity between a target RNA and an Argonaute1-bound miRNA triggers miRNA tailing and 3'-to-5' trimming. In flies, Argonaute2-bound small RNAs--but not those bound to Argonaute1--bear a 2'-O-methyl group at their 3' ends. This modification blocks target-directed small RNA remodeling: In flies lacking Hen1, the enzyme that adds the 2'-O-methyl group, Argonaute2-associated siRNAs are tailed and trimmed. Target complementarity also affects small RNA stability in human cells. These results provide an explanation for the partial complementarity between animal miRNAs and their targets.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2902985/" 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/PMC2902985/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ameres, Stefan L -- Horwich, Michael D -- Hung, Jui-Hung -- Xu, Jia -- Ghildiyal, Megha -- Weng, Zhiping -- Zamore, Phillip D -- F30AG030283/AG/NIA NIH HHS/ -- GM62862/GM/NIGMS NIH HHS/ -- GM65236/GM/NIGMS NIH HHS/ -- J 2832/Austrian Science Fund FWF/Austria -- R01 GM065236/GM/NIGMS NIH HHS/ -- R01 GM065236-08/GM/NIGMS NIH HHS/ -- R37 GM062862/GM/NIGMS NIH HHS/ -- R37 GM062862-10/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jun 18;328(5985):1534-9. doi: 10.1126/science.1187058.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20558712" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Argonaute Proteins ; *Base Pairing ; Cell Line ; Drosophila Proteins/genetics/metabolism ; Drosophila melanogaster/embryology/genetics ; Eukaryotic Initiation Factors/metabolism ; Green Fluorescent Proteins/genetics ; Humans ; Methylation ; Methyltransferases/genetics/metabolism ; MicroRNAs/chemistry/genetics/*metabolism ; Models, Biological ; RNA Caps ; *RNA Stability ; RNA, Complementary ; RNA, Messenger/chemistry/genetics/*metabolism ; RNA, Small Interfering/chemistry/genetics/*metabolism ; RNA-Induced Silencing Complex/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Structures of the CXCR4 chemokine GPCR with small-molecule and cyclic peptide antagonists (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-12
    Description: Chemokine receptors are critical regulators of cell migration in the context of immune surveillance, inflammation, and development. The G protein-coupled chemokine receptor CXCR4 is specifically implicated in cancer metastasis and HIV-1 infection. Here we report five independent crystal structures of CXCR4 bound to an antagonist small molecule IT1t and a cyclic peptide CVX15 at 2.5 to 3.2 angstrom resolution. All structures reveal a consistent homodimer with an interface including helices V and VI that may be involved in regulating signaling. The location and shape of the ligand-binding sites differ from other G protein-coupled receptors and are closer to the extracellular surface. These structures provide new clues about the interactions between CXCR4 and its natural ligand CXCL12, and with the HIV-1 glycoprotein gp120.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3074590/" 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/PMC3074590/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Beili -- Chien, Ellen Y T -- Mol, Clifford D -- Fenalti, Gustavo -- Liu, Wei -- Katritch, Vsevolod -- Abagyan, Ruben -- Brooun, Alexei -- Wells, Peter -- Bi, F Christopher -- Hamel, Damon J -- Kuhn, Peter -- Handel, Tracy M -- Cherezov, Vadim -- Stevens, Raymond C -- F32 GM083463/GM/NIGMS NIH HHS/ -- F32 GM083463-03/GM/NIGMS NIH HHS/ -- GM075915/GM/NIGMS NIH HHS/ -- P50 GM073197/GM/NIGMS NIH HHS/ -- P50 GM073197-07/GM/NIGMS NIH HHS/ -- R01 AI037113/AI/NIAID NIH HHS/ -- R01 AI037113-13/AI/NIAID NIH HHS/ -- R01 GM071872/GM/NIGMS NIH HHS/ -- R01 GM081763/GM/NIGMS NIH HHS/ -- R01 GM081763-03/GM/NIGMS NIH HHS/ -- R01 GM089857/GM/NIGMS NIH HHS/ -- R21 AI087189/AI/NIAID NIH HHS/ -- R21 AI087189-02/AI/NIAID NIH HHS/ -- R21 RR025336/RR/NCRR NIH HHS/ -- R21 RR025336-01A1/RR/NCRR NIH HHS/ -- U54 GM074961/GM/NIGMS NIH HHS/ -- U54 GM074961-050001/GM/NIGMS NIH HHS/ -- U54 GM094618/GM/NIGMS NIH HHS/ -- Y1-CO-1020/CO/NCI NIH HHS/ -- Y1-GM-1104/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Nov 19;330(6007):1066-71. doi: 10.1126/science.1194396. Epub 2010 Oct 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, The 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/20929726" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chemokine CXCL12 ; Crystallography, X-Ray ; HIV Envelope Protein gp120/metabolism ; Humans ; Membrane Proteins ; Models, Molecular ; Protein Binding ; Protein Conformation ; Protein Multimerization ; Receptors, CXCR4/antagonists & inhibitors/*chemistry/metabolism ; Recombinant Proteins/chemistry ; Spodoptera ; Thiourea/analogs & derivatives/chemistry
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    Siah regulation of Pard3A controls neuronal cell adhesion during germinal zone exit (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-11-27
    Description: The brain's circuitry is established by directed migration and synaptogenesis of neurons during development. Although neurons mature and migrate in specific patterns, little is known about how neurons exit their germinal zone niche. We found that cerebellar granule neuron germinal zone exit is regulated by proteasomal degradation of Pard3A by the Seven in Absentia homolog (Siah) E3 ubiquitin ligase. Pard3A gain of function and Siah loss of function induce precocious radial migration. Time-lapse imaging using a probe to measure neuronal cell contact reveals that Pard3A promotes adhesive interactions needed for germinal zone exit by recruiting the epithelial tight junction adhesion molecule C to the neuronal cell surface. Our findings define a Siah-Pard3A signaling pathway that controls adhesion-dependent exit of neuronal progenitors or immature neurons from a germinal zone niche.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3065828/" 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/PMC3065828/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Famulski, Jakub K -- Trivedi, Niraj -- Howell, Danielle -- Yang, Yuan -- Tong, Yiai -- Gilbertson, Richard -- Solecki, David J -- P01 CA096832/CA/NCI NIH HHS/ -- P01 CA096832-07/CA/NCI NIH HHS/ -- P30 CA021765/CA/NCI NIH HHS/ -- P30 CA021765-33/CA/NCI NIH HHS/ -- R01 CA129541/CA/NCI NIH HHS/ -- R01 CA129541-04/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Dec 24;330(6012):1834-8. doi: 10.1126/science.1198480. Epub 2010 Nov 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Neurobiology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21109632" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Adhesion ; Cell Adhesion Molecules/chemistry/*metabolism ; Cell Line ; *Cell Movement ; Cell Polarity ; Cerebellum/*cytology/embryology/*metabolism ; Dogs ; Humans ; Immunoglobulins/chemistry/metabolism ; Mice ; Morphogenesis ; Neurons/cytology/*physiology ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Structure, Tertiary ; RNA Interference ; Signal Transduction ; Stem Cells/physiology ; Transfection ; Ubiquitin-Protein Ligases/genetics/*metabolism ; Ubiquitination
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    Self-assembly of filopodia-like structures on supported lipid bilayers (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-11
    Description: Filopodia are finger-like protrusive structures, containing actin bundles. By incubating frog egg extracts with supported lipid bilayers containing phosphatidylinositol 4,5 bisphosphate, we have reconstituted the assembly of filopodia-like structures (FLSs). The actin assembles into parallel bundles, and known filopodial components localize to the tip and shaft. The filopodia tip complexes self-organize--they are not templated by preexisting membrane microdomains. The F-BAR domain protein toca-1 recruits N-WASP, followed by the Arp2/3 complex and actin. Elongation proteins, Diaphanous-related formin, VASP, and fascin are recruited subsequently. Although the Arp2/3 complex is required for FLS initiation, it is not essential for elongation, which involves formins. We propose that filopodia form via clustering of Arp2/3 complex activators, self-assembly of filopodial tip complexes on the membrane, and outgrowth of actin bundles.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2982780/" 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/PMC2982780/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Kwonmoo -- Gallop, Jennifer L -- Rambani, Komal -- Kirschner, Marc W -- GM26875/GM/NIGMS NIH HHS/ -- R01 GM026875/GM/NIGMS NIH HHS/ -- R01 GM026875-34/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 10;329(5997):1341-5. doi: 10.1126/science.1191710.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Systems 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/20829485" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/ultrastructure ; Actin-Related Protein 2-3 Complex/metabolism ; Actins/*metabolism ; Animals ; Carrier Proteins/metabolism ; Cell Adhesion Molecules/metabolism ; Cell Membrane/metabolism ; Humans ; Kinetics ; *Lipid Bilayers ; Membrane Microdomains ; Mice ; Microfilament Proteins/metabolism ; Microtubule-Associated Proteins/metabolism ; NADPH Dehydrogenase/metabolism ; Phosphatidylinositol Phosphates/metabolism ; Phosphoproteins/metabolism ; Pseudopodia/*metabolism/*ultrastructure ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Wiskott-Aldrich Syndrome Protein, Neuronal/metabolism ; Xenopus ; Xenopus Proteins/metabolism
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    O-mannosyl phosphorylation of alpha-dystroglycan is required for laminin binding (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-02
    Description: Alpha-dystroglycan (alpha-DG) is a cell-surface glycoprotein that acts as a receptor for both extracellular matrix proteins containing laminin-G domains and certain arenaviruses. Receptor binding is thought to be mediated by a posttranslational modification, and defective binding with laminin underlies a subclass of congenital muscular dystrophy. Using mass spectrometry- and nuclear magnetic resonance (NMR)-based structural analyses, we identified a phosphorylated O-mannosyl glycan on the mucin-like domain of recombinant alpha-DG, which was required for laminin binding. We demonstrated that patients with muscle-eye-brain disease and Fukuyama congenital muscular dystrophy, as well as mice with myodystrophy, commonly have defects in a postphosphoryl modification of this phosphorylated O-linked mannose, and that this modification is mediated by the like-acetylglucosaminyltransferase (LARGE) protein. These findings expand our understanding of the mechanisms that underlie congenital muscular dystrophy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2978000/" 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/PMC2978000/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoshida-Moriguchi, Takako -- Yu, Liping -- Stalnaker, Stephanie H -- Davis, Sarah -- Kunz, Stefan -- Madson, Michael -- Oldstone, Michael B A -- Schachter, Harry -- Wells, Lance -- Campbell, Kevin P -- 1U54NS053672/NS/NINDS NIH HHS/ -- AI55540/AI/NIAID NIH HHS/ -- P30 DK 54759/DK/NIDDK NIH HHS/ -- P30 DK054759/DK/NIDDK NIH HHS/ -- P41 RR018502/RR/NCRR NIH HHS/ -- R01 AI009484/AI/NIAID NIH HHS/ -- R01 AI009484-40/AI/NIAID NIH HHS/ -- R01 AI009484-41/AI/NIAID NIH HHS/ -- R01 AI045927/AI/NIAID NIH HHS/ -- R01 AI045927-08/AI/NIAID NIH HHS/ -- R01 AI045927-09/AI/NIAID NIH HHS/ -- R01 AI045927-10/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jan 1;327(5961):88-92. doi: 10.1126/science.1180512.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Iowa Roy J. and Lucille A. Carver College of Medicine, 4283 Carver Biomedical Research Building, 285 Newton Road, Iowa City, IA 52242-1101, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20044576" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbohydrate Conformation ; Cell Line ; Dystroglycans/chemistry/*metabolism ; Glycosylation ; Humans ; Laminin/*metabolism ; Magnetic Resonance Spectroscopy ; Mannose/*metabolism ; Mass Spectrometry ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal/metabolism ; Muscular Dystrophies/metabolism ; Muscular Dystrophy, Animal/metabolism ; N-Acetylglucosaminyltransferases/genetics/metabolism ; Phosphorylation ; Protein Binding ; Recombinant Proteins/chemistry/metabolism
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    Structure of a eukaryotic CLC transporter defines an intermediate state in the transport cycle (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-12
    Description: CLC proteins transport chloride (Cl(-)) ions across cell membranes to control the electrical potential of muscle cells, transfer electrolytes across epithelia, and control the pH and electrolyte composition of intracellular organelles. Some members of this protein family are Cl(-) ion channels, whereas others are secondary active transporters that exchange Cl(-) ions and protons (H(+)) with a 2:1 stoichiometry. We have determined the structure of a eukaryotic CLC transporter at 3.5 angstrom resolution. Cytoplasmic cystathionine beta-synthase (CBS) domains are strategically positioned to regulate the ion-transport pathway, and many disease-causing mutations in human CLCs reside on the CBS-transmembrane interface. Comparison with prokaryotic CLC shows that a gating glutamate residue changes conformation and suggests a basis for 2:1 Cl(-)/H(+) exchange and a simple mechanistic connection between CLC channels and transporters.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3079386/" 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/PMC3079386/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feng, Liang -- Campbell, Ernest B -- Hsiung, Yichun -- MacKinnon, Roderick -- P30 EB009998/EB/NIBIB NIH HHS/ -- R01 GM043949/GM/NIGMS NIH HHS/ -- R01 GM043949-20/GM/NIGMS NIH HHS/ -- R01 GM043949-21/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Oct 29;330(6004):635-41. doi: 10.1126/science.1195230. Epub 2010 Sep 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Neurobiology and Biophysics, Rockefeller University, Howard Hughes Medical Institute, 1230 York Avenue, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929736" target="_blank"〉PubMed〈/a〉
    Keywords: Algal Proteins/chemistry/metabolism ; Animals ; Antiporters/*chemistry/metabolism ; Binding Sites ; Cell Line ; Cell Membrane/chemistry ; Chloride Channels/*chemistry/metabolism ; Chlorides/*metabolism ; Crystallization ; Crystallography, X-Ray ; Cystathionine beta-Synthase/chemistry ; Cytoplasm/chemistry ; Glutamic Acid/metabolism ; Ion Channel Gating ; Ion Transport ; Models, Biological ; Models, Molecular ; Protein Conformation ; Protein Multimerization ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Protein Subunits/chemistry ; Protons ; Rhodophyta/*chemistry/metabolism
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    Human SIRT6 promotes DNA end resection through CtIP deacetylation (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-09-11
    Description: SIRT6 belongs to the sirtuin family of protein lysine deacetylases, which regulate aging and genome stability. We found that human SIRT6 has a role in promoting DNA end resection, a crucial step in DNA double-strand break (DSB) repair by homologous recombination. SIRT6 depletion impaired the accumulation of replication protein A and single-stranded DNA at DNA damage sites, reduced rates of homologous recombination, and sensitized cells to DSB-inducing agents. We identified the DSB resection protein CtIP [C-terminal binding protein (CtBP) interacting protein] as a SIRT6 interaction partner and showed that SIRT6-dependent CtIP deacetylation promotes resection. A nonacetylatable CtIP mutant alleviated the effect of SIRT6 depletion on resection, thus identifying CtIP as a key substrate by which SIRT6 facilitates DSB processing and homologous recombination. These findings further clarify how SIRT6 promotes genome stability.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3276839/" 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/PMC3276839/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaidi, Abderrahmane -- Weinert, Brian T -- Choudhary, Chunaram -- Jackson, Stephen P -- 11224/Cancer Research UK/United Kingdom -- A5290/Cancer Research UK/United Kingdom -- Cancer Research UK/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2010 Sep 10;329(5997):1348-53. doi: 10.1126/science.1192049.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gurdon Institute and Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20829486" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Camptothecin/pharmacology ; Carrier Proteins/genetics/*metabolism ; Cell Cycle ; Cell Line ; Cell Line, Tumor ; Cell Proliferation ; DNA/*metabolism ; *DNA Breaks, Double-Stranded ; *DNA Repair ; DNA, Single-Stranded/metabolism ; Genomic Instability ; Humans ; Mice ; Mutant Proteins/metabolism ; Niacinamide/pharmacology ; Nuclear Proteins/genetics/*metabolism ; Protein Binding ; Recombination, Genetic/drug effects ; Sirtuins/genetics/*metabolism
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    Breakthrough of the year. Whiplash for stem cell researchers (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2010 Dec 17;330(6011):1609. doi: 10.1126/science.330.6011.1609.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21163983" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Embryonic Stem Cells ; Financing, Government/legislation & jurisprudence ; Humans ; Research Support as Topic/legislation & jurisprudence ; Stem Cell Research/economics/*legislation & jurisprudence ; United States
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    Spiroindolones, a potent compound class for the treatment of malaria (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-04
    Description: Recent reports of increased tolerance to artemisinin derivatives--the most recently adopted class of antimalarials--have prompted a need for new treatments. The spirotetrahydro-beta-carbolines, or spiroindolones, are potent drugs that kill the blood stages of Plasmodium falciparum and Plasmodium vivax clinical isolates at low nanomolar concentration. Spiroindolones rapidly inhibit protein synthesis in P. falciparum, an effect that is ablated in parasites bearing nonsynonymous mutations in the gene encoding the P-type cation-transporter ATPase4 (PfATP4). The optimized spiroindolone NITD609 shows pharmacokinetic properties compatible with once-daily oral dosing and has single-dose efficacy in a rodent malaria model.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3050001/" 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/PMC3050001/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rottmann, Matthias -- McNamara, Case -- Yeung, Bryan K S -- Lee, Marcus C S -- Zou, Bin -- Russell, Bruce -- Seitz, Patrick -- Plouffe, David M -- Dharia, Neekesh V -- Tan, Jocelyn -- Cohen, Steven B -- Spencer, Kathryn R -- Gonzalez-Paez, Gonzalo E -- Lakshminarayana, Suresh B -- Goh, Anne -- Suwanarusk, Rossarin -- Jegla, Timothy -- Schmitt, Esther K -- Beck, Hans-Peter -- Brun, Reto -- Nosten, Francois -- Renia, Laurent -- Dartois, Veronique -- Keller, Thomas H -- Fidock, David A -- Winzeler, Elizabeth A -- Diagana, Thierry T -- R01 AI059472/AI/NIAID NIH HHS/ -- R01 AI059472-04/AI/NIAID NIH HHS/ -- R01 AI059472-05/AI/NIAID NIH HHS/ -- R01AI059472/AI/NIAID NIH HHS/ -- WT078285/Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2010 Sep 3;329(5996):1175-80. doi: 10.1126/science.1193225.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Swiss Tropical and Public Health Institute, Parasite Chemotherapy, CH-4002 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20813948" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/antagonists & inhibitors/chemistry/genetics/metabolism ; Animals ; Antimalarials/administration & dosage/chemistry/pharmacokinetics/*pharmacology ; Cell Line ; Drug Discovery ; Drug Resistance ; Erythrocytes/parasitology ; Female ; Genes, Protozoan ; Humans ; Indoles/administration & dosage/chemistry/pharmacokinetics/*pharmacology ; Malaria/*drug therapy/parasitology ; Male ; Mice ; Models, Molecular ; Mutant Proteins/antagonists & inhibitors/chemistry/metabolism ; Mutation ; Parasitic Sensitivity Tests ; Plasmodium berghei/*drug effects ; Plasmodium falciparum/*drug effects/genetics/growth & development ; Plasmodium vivax/*drug effects/growth & development ; Protein Synthesis Inhibitors/administration & ; dosage/chemistry/pharmacokinetics/pharmacology ; Protozoan Proteins/biosynthesis/chemistry/genetics/metabolism ; Rats ; Rats, Wistar ; Spiro Compounds/administration & dosage/chemistry/pharmacokinetics/*pharmacology
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    miR-16 targets the serotonin transporter: a new facet for adaptive responses to antidepressants (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-18
    Description: The serotonin transporter (SERT) ensures the recapture of serotonin and is the pharmacological target of selective serotonin reuptake inhibitor (SSRI) antidepressants. We show that SERT is a target of microRNA-16 (miR-16). miR-16 is expressed at higher levels in noradrenergic than in serotonergic cells; its reduction in noradrenergic neurons causes de novo SERT expression. In mice, chronic treatment with the SSRI fluoxetine (Prozac) increases miR-16 levels in serotonergic raphe nuclei, which reduces SERT expression. Further, raphe exposed to fluoxetine release the neurotrophic factor S100beta, which acts on noradrenergic cells of the locus coeruleus. By decreasing miR-16, S100beta turns on the expression of serotonergic functions in noradrenergic neurons. Based on pharmacological and behavioral data, we propose that miR-16 contributes to the therapeutic action of SSRI antidepressants in monoaminergic neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baudry, Anne -- Mouillet-Richard, Sophie -- Schneider, Benoit -- Launay, Jean-Marie -- Kellermann, Odile -- New York, N.Y. -- Science. 2010 Sep 17;329(5998):1537-41. doi: 10.1126/science.1193692.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cellules Souches, Signalisation et Prions, INSERM U747, Universite Paris Descartes, 75006 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20847275" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Animals ; Antidepressive Agents, Second-Generation/administration & ; dosage/metabolism/*pharmacology ; Cell Line ; Depression ; Fluoxetine/administration & dosage/metabolism/*pharmacology ; HeLa Cells ; Humans ; Locus Coeruleus/metabolism ; Mice ; MicroRNAs/administration & dosage/genetics/*metabolism ; Nerve Growth Factors/metabolism ; Neurons/drug effects/*metabolism ; Norepinephrine/metabolism ; Protein Biosynthesis ; Raphe Nuclei/drug effects/*metabolism ; S100 Calcium Binding Protein beta Subunit ; S100 Proteins/metabolism ; Serotonin/metabolism ; Serotonin Plasma Membrane Transport Proteins/*genetics/metabolism ; Serotonin Uptake Inhibitors/administration & dosage/metabolism/*pharmacology ; Up-Regulation
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    MicroRNA-33 and the SREBP host genes cooperate to control cholesterol homeostasis (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-05-15
    Description: Proper coordination of cholesterol biosynthesis and trafficking is essential to human health. The sterol regulatory element-binding proteins (SREBPs) are key transcription regulators of genes involved in cholesterol biosynthesis and uptake. We show here that microRNAs (miR-33a/b) embedded within introns of the SREBP genes target the adenosine triphosphate-binding cassette transporter A1 (ABCA1), an important regulator of high-density lipoprotein (HDL) synthesis and reverse cholesterol transport, for posttranscriptional repression. Antisense inhibition of miR-33 in mouse and human cell lines causes up-regulation of ABCA1 expression and increased cholesterol efflux, and injection of mice on a western-type diet with locked nucleic acid-antisense oligonucleotides results in elevated plasma HDL. Our findings indicate that miR-33 acts in concert with the SREBP host genes to control cholesterol homeostasis and suggest that miR-33 may represent a therapeutic target for ameliorating cardiometabolic diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3840500/" 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/PMC3840500/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Najafi-Shoushtari, S Hani -- Kristo, Fjoralba -- Li, Yingxia -- Shioda, Toshi -- Cohen, David E -- Gerszten, Robert E -- Naar, Anders M -- P30 DK034854/DK/NIDDK NIH HHS/ -- P30 DK34854/DK/NIDDK NIH HHS/ -- R01 DK048873/DK/NIDDK NIH HHS/ -- R01 DK056626/DK/NIDDK NIH HHS/ -- R01 GM071449/GM/NIGMS NIH HHS/ -- R01DK48873/DK/NIDDK NIH HHS/ -- R01DK56626/DK/NIDDK NIH HHS/ -- R01GM071449/GM/NIGMS NIH HHS/ -- R21 DK084459/DK/NIDDK NIH HHS/ -- R21DK084459/DK/NIDDK NIH HHS/ -- R37 DK048873/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2010 Jun 18;328(5985):1566-9. doi: 10.1126/science.1189123. Epub 2010 May 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Cancer Center, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20466882" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters/genetics/*metabolism ; Animals ; Cell Line ; Cholesterol/*metabolism ; Cholesterol, HDL/*blood ; Diet ; Gene Expression Regulation ; Homeostasis ; Humans ; Introns ; Liver/metabolism ; Macrophages/metabolism ; Mice ; Mice, Inbred C57BL ; MicroRNAs/genetics/*metabolism ; Oligonucleotides, Antisense/pharmacology ; RNA Interference ; Sterol Regulatory Element Binding Protein 1/genetics/metabolism ; Sterol Regulatory Element Binding Protein 2/genetics/metabolism ; Sterol Regulatory Element Binding Proteins/*genetics/metabolism ; Up-Regulation
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    Sequential checkpoints govern substrate selection during cotranslational protein targeting (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-05-08
    Description: Proper protein localization is essential for all cells. However, the precise mechanism by which high fidelity is achieved is not well understood for any protein-targeting pathway. To address this fundamental question, we investigated the signal recognition particle (SRP) pathway in Escherichia coli, which delivers proteins to the bacterial inner membrane through recognition of signal sequences on cargo proteins. Fidelity was thought to arise from the inability of SRP to bind strongly to incorrect cargos. Using biophysical assays, we found that incorrect cargos were also rejected through a series of checkpoints during subsequent steps of targeting. Thus, high fidelity of substrate selection is achieved through the cumulative effect of multiple checkpoints; this principle may be generally applicable to other pathways involving selective signal recognition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3760334/" 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/PMC3760334/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Xin -- Rashid, Rumana -- Wang, Kai -- Shan, Shu-ou -- GM078024/GM/NIGMS NIH HHS/ -- R01 GM078024/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 May 7;328(5979):757-60. doi: 10.1126/science.1186743.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Chemistry and Chemical Engineering, California Institute of Technology, 1200 East California Boulevard, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20448185" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Membrane/metabolism ; Escherichia coli/*metabolism ; Escherichia coli Proteins/chemistry/*metabolism ; Fluorescence Resonance Energy Transfer ; Guanosine Triphosphate/metabolism ; Hydrophobic and Hydrophilic Interactions ; Kinetics ; Models, Biological ; Protein Binding ; Protein Biosynthesis ; *Protein Sorting Signals ; *Protein Transport ; Ribosomes/metabolism ; Signal Recognition Particle/*metabolism ; Thermodynamics
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    Embryonic stem cells. Controversial ruling throws U.S. research into a tailspin (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- Vogel, Gretchen -- New York, N.Y. -- Science. 2010 Sep 3;329(5996):1132-3. doi: 10.1126/science.329.5996.1132.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20813924" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Embryo Research/economics/*legislation & jurisprudence ; *Embryonic Stem Cells ; Financing, Government/legislation & jurisprudence ; Humans ; *National Institutes of Health (U.S.)/economics/legislation & jurisprudence ; Research Support as Topic/*legislation & jurisprudence ; United States
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    Research ethics. NIH guidelines for stem cell research and gamete donors (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-02-20
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2892655/" 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/PMC2892655/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lo, Bernard -- Parham, Lindsay -- Cedars, Marcelle -- Fisher, Susan -- Gates, Elena -- Giudice, Linda -- Halme, Dina Gould -- Hershon, William -- Kriegstein, Arnold -- Rao, Radhika -- Roberts, Clifford -- Wagner, Richard -- UL1 RR024131/RR/NCRR NIH HHS/ -- UL1 RR024131-04/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2010 Feb 19;327(5968):962-3. doi: 10.1126/science.1180725.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Medical Ethics, University of California, San Francisco (UCSF), San Francisco, CA 94143, USA. bernie@medicine.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20167773" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Disclosure ; Embryo Disposition/*ethics/standards ; Embryo Research/*ethics ; *Embryonic Stem Cells ; Female ; Fertilization in Vitro ; *Guidelines as Topic ; Humans ; Informed Consent ; *National Institutes of Health (U.S.) ; *Oocyte Donation ; *Tissue Donors ; United States
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    Three-dimensional, flexible nanoscale field-effect transistors as localized bioprobes (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-14
    Description: Nanoelectronic devices offer substantial potential for interrogating biological systems, although nearly all work has focused on planar device designs. We have overcome this limitation through synthetic integration of a nanoscale field-effect transistor (nanoFET) device at the tip of an acute-angle kinked silicon nanowire, where nanoscale connections are made by the arms of the kinked nanostructure, and remote multilayer interconnects allow three-dimensional (3D) probe presentation. The acute-angle probe geometry was designed and synthesized by controlling cis versus trans crystal conformations between adjacent kinks, and the nanoFET was localized through modulation doping. 3D nanoFET probes exhibited conductance and sensitivity in aqueous solution, independent of large mechanical deflections, and demonstrated high pH sensitivity. Additionally, 3D nanoprobes modified with phospholipid bilayers can enter single cells to allow robust recording of intracellular potentials.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3149824/" 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/PMC3149824/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tian, Bozhi -- Cohen-Karni, Tzahi -- Qing, Quan -- Duan, Xiaojie -- Xie, Ping -- Lieber, Charles M -- 5DP1OD003900/OD/NIH HHS/ -- DP1 OD003900/OD/NIH HHS/ -- DP1 OD003900-04/OD/NIH HHS/ -- New York, N.Y. -- Science. 2010 Aug 13;329(5993):830-4. doi: 10.1126/science.1192033.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20705858" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biosensing Techniques/instrumentation/methods ; Cell Line ; Cells, Cultured ; Chick Embryo ; Electric Conductivity ; Electrophysiological Phenomena ; Equipment Design ; Hydrogen-Ion Concentration ; Lipid Bilayers ; Membrane Potentials ; Mice ; Microfluidics ; Myocytes, Cardiac/*physiology ; *Nanowires ; Sensitivity and Specificity ; Sodium Chloride ; *Transistors, Electronic
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    Regulation of alternative splicing by histone modifications (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-02-06
    Description: Alternative splicing of pre-mRNA is a prominent mechanism to generate protein diversity, yet its regulation is poorly understood. We demonstrated a direct role for histone modifications in alternative splicing. We found distinctive histone modification signatures that correlate with the splicing outcome in a set of human genes, and modulation of histone modifications causes splice site switching. Histone marks affect splicing outcome by influencing the recruitment of splicing regulators via a chromatin-binding protein. These results outline an adaptor system for the reading of histone marks by the pre-mRNA splicing machinery.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2913848/" 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/PMC2913848/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luco, Reini F -- Pan, Qun -- Tominaga, Kaoru -- Blencowe, Benjamin J -- Pereira-Smith, Olivia M -- Misteli, Tom -- MOP-67011/Canadian Institutes of Health Research/Canada -- R01 AG032134/AG/NIA NIH HHS/ -- R01 AG032134-01/AG/NIA NIH HHS/ -- R01 AG032134-02/AG/NIA NIH HHS/ -- R01 AG032134-03/AG/NIA NIH HHS/ -- R01 AG032134-04/AG/NIA NIH HHS/ -- ZIA BC010309-11/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Feb 19;327(5968):996-1000. doi: 10.1126/science.1184208. Epub 2010 Feb 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20133523" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Cell Line ; Chromatin/metabolism ; Epithelial Cells/metabolism ; Exons ; Histone-Lysine N-Methyltransferase/genetics/metabolism ; Histones/*metabolism ; Humans ; Male ; Mesenchymal Stromal Cells/metabolism ; Polypyrimidine Tract-Binding Protein/metabolism ; Prostate/cytology ; Protein Binding ; RNA Precursors/*metabolism ; Receptor, Fibroblast Growth Factor, Type 2/genetics ; Transcription Factors/genetics/metabolism
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    The CRAC channel activator STIM1 binds and inhibits L-type voltage-gated calcium channels (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-12
    Description: Voltage- and store-operated calcium (Ca(2+)) channels are the major routes of Ca(2+) entry in mammalian cells, but little is known about how cells coordinate the activity of these channels to generate coherent calcium signals. We found that STIM1 (stromal interaction molecule 1), the main activator of store-operated Ca(2+) channels, directly suppresses depolarization-induced opening of the voltage-gated Ca(2+) channel Ca(V)1.2. STIM1 binds to the C terminus of Ca(V)1.2 through its Ca(2+) release-activated Ca(2+) activation domain, acutely inhibits gating, and causes long-term internalization of the channel from the membrane. This establishes a previously unknown function for STIM1 and provides a molecular mechanism to explain the reciprocal regulation of these two channels in cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Park, Chan Young -- Shcheglovitov, Aleksandr -- Dolmetsch, Ricardo -- DP1 OD003889/OD/NIH HHS/ -- DP1OD003889/OD/NIH HHS/ -- R01 NS048564/NS/NINDS NIH HHS/ -- R21MH087898/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2010 Oct 1;330(6000):101-5. doi: 10.1126/science.1191027.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929812" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Calcium Channels, L-Type/chemistry/genetics/*metabolism ; Calcium Signaling ; Cell Line ; Cell Membrane/*metabolism ; Humans ; Ion Channel Gating ; Jurkat Cells ; Membrane Proteins/chemistry/genetics/*metabolism ; Models, Biological ; Neoplasm Proteins/chemistry/genetics/*metabolism ; Neurons/*metabolism ; Patch-Clamp Techniques ; Protein Binding ; Protein Structure, Tertiary ; Rats ; Rats, Sprague-Dawley ; T-Lymphocytes/*metabolism
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    Long noncoding RNA as modular scaffold of histone modification complexes (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-10
    Description: Long intergenic noncoding RNAs (lincRNAs) regulate chromatin states and epigenetic inheritance. Here, we show that the lincRNA HOTAIR serves as a scaffold for at least two distinct histone modification complexes. A 5' domain of HOTAIR binds polycomb repressive complex 2 (PRC2), whereas a 3' domain of HOTAIR binds the LSD1/CoREST/REST complex. The ability to tether two distinct complexes enables RNA-mediated assembly of PRC2 and LSD1 and coordinates targeting of PRC2 and LSD1 to chromatin for coupled histone H3 lysine 27 methylation and lysine 4 demethylation. Our results suggest that lincRNAs may serve as scaffolds by providing binding surfaces to assemble select histone modification enzymes, thereby specifying the pattern of histone modifications on target genes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2967777/" 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/PMC2967777/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsai, Miao-Chih -- Manor, Ohad -- Wan, Yue -- Mosammaparast, Nima -- Wang, Jordon K -- Lan, Fei -- Shi, Yang -- Segal, Eran -- Chang, Howard Y -- R01 CA118750/CA/NCI NIH HHS/ -- R01 CA119176/CA/NCI NIH HHS/ -- R01 CA119176-05/CA/NCI NIH HHS/ -- R01-CA118487/CA/NCI NIH HHS/ -- R01-HG004361/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Aug 6;329(5992):689-93. doi: 10.1126/science.1192002. Epub 2010 Jul 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Program in Epithelial Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20616235" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Carrier Proteins/metabolism ; Cell Line ; Cells, Cultured ; Chromatin/*metabolism ; Chromatin Immunoprecipitation ; Co-Repressor Proteins ; DNA-Binding Proteins/*metabolism ; HeLa Cells ; Histone Demethylases/*metabolism ; Histones/*metabolism ; Humans ; Methylation ; Mutation ; Nerve Tissue Proteins/metabolism ; Nuclear Proteins/metabolism ; Nucleic Acid Conformation ; Polycomb Repressive Complex 2 ; Polycomb-Group Proteins ; Promoter Regions, Genetic ; Protein Binding ; RNA Interference ; RNA, Untranslated/chemistry/*metabolism ; Repressor Proteins/*metabolism ; Transcription Factors/*metabolism ; Transcription, Genetic
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    Cells rewrite their own destiny (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2010 Dec 17;330(6011):1618. doi: 10.1126/science.330.6011.1618.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21163990" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Dedifferentiation ; Cell Line ; *Cellular Reprogramming ; Gene Expression ; Humans ; *Induced Pluripotent Stem Cells/cytology/physiology ; Mice
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    Cbln1 is a ligand for an orphan glutamate receptor delta2, a bidirectional synapse organizer (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-04-17
    Description: Cbln1, secreted from cerebellar granule cells, and the orphan glutamate receptor delta2 (GluD2), expressed by Purkinje cells, are essential for synapse integrity between these neurons in adult mice. Nevertheless, no endogenous binding partners for these molecules have been identified. We found that Cbln1 binds directly to the N-terminal domain of GluD2. GluD2 expression by postsynaptic cells, combined with exogenously applied Cbln1, was necessary and sufficient to induce new synapses in vitro and in the adult cerebellum in vivo. Further, beads coated with recombinant Cbln1 directly induced presynaptic differentiation and indirectly caused clustering of postsynaptic molecules via GluD2. These results indicate that the Cbln1-GluD2 complex is a unique synapse organizer that acts bidirectionally on both pre- and postsynaptic components.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsuda, Keiko -- Miura, Eriko -- Miyazaki, Taisuke -- Kakegawa, Wataru -- Emi, Kyoichi -- Narumi, Sakae -- Fukazawa, Yugo -- Ito-Ishida, Aya -- Kondo, Tetsuro -- Shigemoto, Ryuichi -- Watanabe, Masahiko -- Yuzaki, Michisuke -- New York, N.Y. -- Science. 2010 Apr 16;328(5976):363-8. doi: 10.1126/science.1185152.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, School of Medicine, Keio University, Tokyo 160-8582, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20395510" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Cell Line ; Cells, Cultured ; Cerebellum/cytology/*physiology ; Coculture Techniques ; Excitatory Postsynaptic Potentials ; Humans ; Ligands ; Mice ; Nerve Tissue Proteins/*metabolism ; Presynaptic Terminals/physiology ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Precursors/*metabolism ; Purkinje Cells/metabolism/*physiology ; Rats ; Receptors, Glutamate/chemistry/*metabolism ; Recombinant Fusion Proteins/metabolism ; Synapses/*physiology ; Synaptic Membranes/metabolism
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    PML regulates apoptosis at endoplasmic reticulum by modulating calcium release (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-30
    Description: The promyelocytic leukemia (PML) tumor suppressor is a pleiotropic modulator of apoptosis. However, the molecular basis for such a diverse proapoptotic role is currently unknown. We show that extranuclear Pml was specifically enriched at the endoplasmic reticulum (ER) and at the mitochondria-associated membranes, signaling domains involved in ER-to-mitochondria calcium ion (Ca(2+)) transport and in induction of apoptosis. We found Pml in complexes of large molecular size with the inositol 1,4,5-trisphosphate receptor (IP(3)R), protein kinase Akt, and protein phosphatase 2a (PP2a). Pml was essential for Akt- and PP2a-dependent modulation of IP(3)R phosphorylation and in turn for IP(3)R-mediated Ca(2+) release from ER. Our findings provide a mechanistic explanation for the pleiotropic role of Pml in apoptosis and identify a pharmacological target for the modulation of Ca(2+) signals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3017677/" 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/PMC3017677/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giorgi, Carlotta -- Ito, Keisuke -- Lin, Hui-Kuan -- Santangelo, Clara -- Wieckowski, Mariusz R -- Lebiedzinska, Magdalena -- Bononi, Angela -- Bonora, Massimo -- Duszynski, Jerzy -- Bernardi, Rosa -- Rizzuto, Rosario -- Tacchetti, Carlo -- Pinton, Paolo -- Pandolfi, Pier Paolo -- GGP05284/Telethon/Italy -- K99 CA139009/CA/NCI NIH HHS/ -- K99 CA139009-01A1/CA/NCI NIH HHS/ -- K99 CA139009-02/CA/NCI NIH HHS/ -- R01 CA071692/CA/NCI NIH HHS/ -- R01 CA071692-04S1/CA/NCI NIH HHS/ -- R01 CA102142/CA/NCI NIH HHS/ -- R01 CA102142-07/CA/NCI NIH HHS/ -- R01 CA142874/CA/NCI NIH HHS/ -- R01 CA142874-01/CA/NCI NIH HHS/ -- R01 CA142874-02/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Nov 26;330(6008):1247-51. doi: 10.1126/science.1189157. Epub 2010 Oct 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Experimental and Diagnostic Medicine, Section of General Pathology, Interdisciplinary Center for the Study of Inflammation (ICSI), Emilia Romagna Laboratory BioPharmaNet, and Laboratory for Technologies of Advanced Therapies (LTTA) University of Ferrara, Ferrara, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21030605" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; *Apoptosis ; Calcium/*metabolism ; *Calcium Signaling ; Cell Line ; Cell Nucleus/metabolism ; Cells, Cultured ; Cytosol/metabolism ; Endoplasmic Reticulum/*metabolism ; Homeostasis ; Humans ; Inositol 1,4,5-Trisphosphate/metabolism ; Inositol 1,4,5-Trisphosphate Receptors/metabolism ; Intracellular Membranes/metabolism ; Mice ; Mitochondria/metabolism ; Nuclear Proteins/genetics/*metabolism ; Phosphorylation ; Protein Phosphatase 2/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Recombinant Fusion Proteins/metabolism ; Stress, Physiological ; Transcription Factors/genetics/*metabolism ; Tumor Suppressor Proteins/genetics/*metabolism
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    Reprogramming cellular behavior with RNA controllers responsive to endogenous proteins (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-11-27
    Description: Synthetic genetic devices that interface with native cellular pathways can be used to change natural networks to implement new forms of control and behavior. The engineering of gene networks has been limited by an inability to interface with native components. We describe a class of RNA control devices that overcome these limitations by coupling increased abundance of particular proteins to targeted gene expression events through the regulation of alternative RNA splicing. We engineered RNA devices that detect signaling through the nuclear factor kappaB and Wnt signaling pathways in human cells and rewire these pathways to produce new behaviors, thereby linking disease markers to noninvasive sensing and reprogrammed cellular fates. Our work provides a genetic platform that can build programmable sensing-actuation devices enabling autonomous control over cellular behavior.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3171693/" 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/PMC3171693/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Culler, Stephanie J -- Hoff, Kevin G -- Smolke, Christina D -- RC1 GM091298/GM/NIGMS NIH HHS/ -- RC1 GM091298-01/GM/NIGMS NIH HHS/ -- RC1 GM091298-02/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Nov 26;330(6008):1251-5. doi: 10.1126/science.1192128.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Chemistry and Chemical Engineering, 1200 East California Boulevard, MC 210-41, 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/21109673" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Apoptosis ; Aptamers, Nucleotide/chemistry/genetics/*metabolism ; Capsid Proteins/metabolism ; Cell Line ; Cell Nucleus/metabolism ; Exons ; Ganciclovir/pharmacology ; *Gene Expression Regulation ; Gene Regulatory Networks ; *Genetic Engineering ; Green Fluorescent Proteins/genetics ; Humans ; Introns ; Ligands ; Mutation ; NF-kappa B p50 Subunit/genetics/metabolism ; Protein Binding ; Signal Transduction ; Survival of Motor Neuron 1 Protein/genetics ; Transcription Factor RelA/genetics/metabolism ; Transfection ; Wnt Proteins/metabolism ; beta Catenin/genetics/metabolism
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    Atomic-level characterization of the structural dynamics of proteins (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-10-16
    Description: Molecular dynamics (MD) simulations are widely used to study protein motions at an atomic level of detail, but they have been limited to time scales shorter than those of many biologically critical conformational changes. We examined two fundamental processes in protein dynamics--protein folding and conformational change within the folded state--by means of extremely long all-atom MD simulations conducted on a special-purpose machine. Equilibrium simulations of a WW protein domain captured multiple folding and unfolding events that consistently follow a well-defined folding pathway; separate simulations of the protein's constituent substructures shed light on possible determinants of this pathway. A 1-millisecond simulation of the folded protein BPTI reveals a small number of structurally distinct conformational states whose reversible interconversion is slower than local relaxations within those states by a factor of more than 1000.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shaw, David E -- Maragakis, Paul -- Lindorff-Larsen, Kresten -- Piana, Stefano -- Dror, Ron O -- Eastwood, Michael P -- Bank, Joseph A -- Jumper, John M -- Salmon, John K -- Shan, Yibing -- Wriggers, Willy -- New York, N.Y. -- Science. 2010 Oct 15;330(6002):341-6. doi: 10.1126/science.1187409.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉D. E. Shaw Research, 120 West 45th Street, New York, NY 10036, USA. David.Shaw@DEShawResearch.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20947758" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Aprotinin/*chemistry ; Computational Biology ; Computers ; Kinetics ; Microfilament Proteins/chemistry ; Models, Molecular ; *Molecular Dynamics Simulation ; Mutant Proteins/chemistry ; *Protein Conformation ; *Protein Folding ; Protein Structure, Tertiary ; Proteins/*chemistry ; Solvents ; Thermodynamics
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    Repulsion of superinfecting virions: a mechanism for rapid virus spread (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-01-23
    Description: Viruses are thought to spread across susceptible cells through an iterative process of infection, replication, and release, so that the rate of spread is limited by replication kinetics. Here, we show that vaccinia virus spreads across one cell every 75 minutes, fourfold faster than its replication cycle would permit. To explain this phenomenon, we found that newly infected cells express two surface proteins that mark cells as infected and, via exploitation of cellular machinery, induce the repulsion of superinfecting virions away toward uninfected cells. Mechanistically, early expression of proteins A33 and A36 was critical for virion repulsion and rapid spread, and cells expressing these proteins repelled exogenous virions rapidly. Additional spreading mechanisms may exist for other viruses that also spread faster than predicted by replication kinetics.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4202693/" 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/PMC4202693/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Doceul, Virginie -- Hollinshead, Michael -- van der Linden, Lonneke -- Smith, Geoffrey L -- 061484/Wellcome Trust/United Kingdom -- 090315/Wellcome Trust/United Kingdom -- G0501257/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Feb 12;327(5967):873-6. doi: 10.1126/science.1183173. Epub 2010 Jan 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Virology, Faculty of Medicine, Imperial College London, St Mary's Campus, Norfolk Place, London W2 1PG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20093437" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Cell Membrane/metabolism ; Genes, Viral ; HeLa Cells ; Humans ; Kinetics ; Membrane Glycoproteins/genetics/*metabolism ; Vaccinia virus/genetics/pathogenicity/*physiology ; Viral Envelope Proteins/genetics/*metabolism ; Viral Plaque Assay ; Viral Structural Proteins/genetics/*metabolism ; Virion/physiology ; Virus Release ; Virus Replication
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    Local and long-range reciprocal regulation of cAMP and cGMP in axon/dendrite formation (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-01-30
    Description: Cytosolic cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) often mediate antagonistic cellular actions of extracellular factors, from the regulation of ion channels to cell volume control and axon guidance. We found that localized cAMP and cGMP activities in undifferentiated neurites of cultured hippocampal neurons promote and suppress axon formation, respectively, and exert opposite effects on dendrite formation. Fluorescence resonance energy transfer imaging showed that alterations of the amount of cAMP resulted in opposite changes in the amount of cGMP, and vice versa, through the activation of specific phosphodiesterases and protein kinases. Local elevation of cAMP in one neurite resulted in cAMP reduction in all other neurites of the same neuron. Thus, local and long-range reciprocal regulation of cAMP and cGMP together ensures coordinated development of one axon and multiple dendrites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shelly, Maya -- Lim, Byung Kook -- Cancedda, Laura -- Heilshorn, Sarah C -- Gao, Hongfeng -- Poo, Mu-ming -- NS-22764/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2010 Jan 29;327(5965):547-52. doi: 10.1126/science.1179735.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neurobiology, Department of Molecular and Cell Biology, Helen Wills Neuroscience Institute, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20110498" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclase Inhibitors ; Adenylyl Cyclases/metabolism ; Animals ; Axons/metabolism/*physiology ; Cell Differentiation ; Cell Line ; Cell Polarity ; Cells, Cultured ; Cyclic AMP/*metabolism ; Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors/metabolism ; Cyclic GMP/*metabolism ; Dendrites/metabolism/*physiology ; Enzyme Inhibitors/pharmacology ; Fluorescence Resonance Energy Transfer ; Guanylate Cyclase/antagonists & inhibitors/metabolism ; Hippocampus/*cytology ; Humans ; Neurites/metabolism/physiology ; Neurons/cytology/*physiology ; Phosphodiesterase Inhibitors/pharmacology ; Phosphoric Diester Hydrolases/metabolism ; Phosphorylation ; Rats ; Signal Transduction ; Transfection
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    A transient and low-populated protein-folding intermediate at atomic resolution (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-09-11
    Description: Proteins can sample conformational states that are critical for function but are seldom detected directly because of their low occupancies and short lifetimes. In this work, we used chemical shifts and bond-vector orientation constraints obtained from nuclear magnetic resonance relaxation dispersion spectroscopy, in concert with a chemical shift-based method for structure elucidation, to determine an atomic-resolution structure of an "invisible" folding intermediate of a small protein module: the FF domain. The structure reveals non-native elements preventing formation of the native conformation in the carboxyl-terminal part of the protein. This is consistent with the kinetics of folding in which a well-structured intermediate forms rapidly and then rearranges slowly to the native state. The approach introduces a general strategy for structure determination of low-populated and transiently formed protein states.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Korzhnev, Dmitry M -- Religa, Tomasz L -- Banachewicz, Wiktor -- Fersht, Alan R -- Kay, Lewis E -- MC_U105484373/Medical Research Council/United Kingdom -- Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2010 Sep 10;329(5997):1312-6. doi: 10.1126/science.1191723.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, the University of Toronto, Toronto, Ontario M5S 1A8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20829478" target="_blank"〉PubMed〈/a〉
    Keywords: Carrier Proteins/*chemistry ; Computational Biology ; Kinetics ; Models, Molecular ; Nuclear Magnetic Resonance, Biomolecular ; Protein Conformation ; *Protein Folding ; Protein Structure, Secondary ; *Protein Structure, Tertiary ; Software ; Thermodynamics
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    Heritable individual-specific and allele-specific chromatin signatures in humans (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-03-20
    Description: The extent to which variation in chromatin structure and transcription factor binding may influence gene expression, and thus underlie or contribute to variation in phenotype, is unknown. To address this question, we cataloged both individual-to-individual variation and differences between homologous chromosomes within the same individual (allele-specific variation) in chromatin structure and transcription factor binding in lymphoblastoid cells derived from individuals of geographically diverse ancestry. Ten percent of active chromatin sites were individual-specific; a similar proportion were allele-specific. Both individual-specific and allele-specific sites were commonly transmitted from parent to child, which suggests that they are heritable features of the human genome. Our study shows that heritable chromatin status and transcription factor binding differ as a result of genetic variation and may underlie phenotypic variation in humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2929018/" 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/PMC2929018/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDaniell, Ryan -- Lee, Bum-Kyu -- Song, Lingyun -- Liu, Zheng -- Boyle, Alan P -- Erdos, Michael R -- Scott, Laura J -- Morken, Mario A -- Kucera, Katerina S -- Battenhouse, Anna -- Keefe, Damian -- Collins, Francis S -- Willard, Huntington F -- Lieb, Jason D -- Furey, Terrence S -- Crawford, Gregory E -- Iyer, Vishwanath R -- Birney, Ewan -- U54 HG004563/HG/NHGRI NIH HHS/ -- U54 HG004563-03/HG/NHGRI NIH HHS/ -- Z01 HG000024/HG/NHGRI NIH HHS/ -- Z01 HG000024-13/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Apr 9;328(5975):235-9. doi: 10.1126/science.1184655. Epub 2010 Mar 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Systems and Synthetic Biology, Institute for Cellular and Molecular Biology, Section of Molecular Genetics and Microbiology, University of Texas, Austin, TX 78712, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20299549" target="_blank"〉PubMed〈/a〉
    Keywords: African Continental Ancestry Group ; *Alleles ; Binding Sites ; Cell Line ; Chromatin/chemistry/*genetics/*metabolism ; Chromatin Immunoprecipitation ; Chromosomes, Human/genetics/metabolism ; Chromosomes, Human, X/genetics/metabolism ; Deoxyribonuclease I/metabolism ; European Continental Ancestry Group ; Female ; *Gene Expression Regulation ; *Genetic Variation ; Humans ; Male ; Nuclear Family ; Polymorphism, Single Nucleotide ; Protein Binding ; Regulatory Elements, Transcriptional ; Repressor Proteins/*metabolism ; Sequence Analysis, DNA ; Transcription Factors/*metabolism ; X Chromosome Inactivation
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    Kinetic scaffolding mediated by a phospholipase C-beta and Gq signaling complex (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-23
    Description: Transmembrane signals initiated by a broad range of extracellular stimuli converge on nodes that regulate phospholipase C (PLC)-dependent inositol lipid hydrolysis for signal propagation. We describe how heterotrimeric guanine nucleotide-binding proteins (G proteins) activate PLC-betas and in turn are deactivated by these downstream effectors. The 2.7-angstrom structure of PLC-beta3 bound to activated Galpha(q) reveals a conserved module found within PLC-betas and other effectors optimized for rapid engagement of activated G proteins. The active site of PLC-beta3 in the complex is occluded by an intramolecular plug that is likely removed upon G protein-dependent anchoring and orientation of the lipase at membrane surfaces. A second domain of PLC-beta3 subsequently accelerates guanosine triphosphate hydrolysis by Galpha(q), causing the complex to dissociate and terminate signal propagation. Mutations within this domain dramatically delay signal termination in vitro and in vivo. Consequently, this work suggests a dynamic catch-and-release mechanism used to sharpen spatiotemporal signals mediated by diverse sensory inputs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3046049/" 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/PMC3046049/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Waldo, Gary L -- Ricks, Tiffany K -- Hicks, Stephanie N -- Cheever, Matthew L -- Kawano, Takeharu -- Tsuboi, Kazuhito -- Wang, Xiaoyue -- Montell, Craig -- Kozasa, Tohru -- Sondek, John -- Harden, T Kendall -- EY010852/EY/NEI NIH HHS/ -- GM074001/GM/NIGMS NIH HHS/ -- GM38213/GM/NIGMS NIH HHS/ -- GM57391/GM/NIGMS NIH HHS/ -- GM61454/GM/NIGMS NIH HHS/ -- R01 GM057391/GM/NIGMS NIH HHS/ -- R01 GM057391-13/GM/NIGMS NIH HHS/ -- R01 GM062299/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Nov 12;330(6006):974-80. doi: 10.1126/science.1193438. Epub 2010 Oct 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20966218" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Catalytic Domain ; Crystallography, X-Ray ; Enzyme Activation ; GTP-Binding Protein alpha Subunits, Gq-G11/*chemistry/*metabolism ; Guanosine Triphosphate/metabolism ; Humans ; Hydrogen Bonding ; Hydrolysis ; Isoenzymes/chemistry/metabolism ; Kinetics ; Mice ; Models, Molecular ; Molecular Sequence Data ; Mutagenesis ; Phospholipase C beta/*chemistry/metabolism ; Protein Binding ; Protein Structure, Tertiary ; Recombinant Fusion Proteins/chemistry/metabolism ; Signal Transduction
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    Genome-wide kinetics of nucleosome turnover determined by metabolic labeling of histones (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-29
    Description: Nucleosome disruption and replacement are crucial activities that maintain epigenomes, but these highly dynamic processes have been difficult to study. Here, we describe a direct method for measuring nucleosome turnover dynamics genome-wide. We found that nucleosome turnover is most rapid over active gene bodies, epigenetic regulatory elements, and replication origins in Drosophila cells. Nucleosomes turn over faster at sites for trithorax-group than polycomb-group protein binding, suggesting that nucleosome turnover differences underlie their opposing activities and challenging models for epigenetic inheritance that rely on stability of histone marks. Our results establish a general strategy for studying nucleosome dynamics and uncover nucleosome turnover differences across the genome that are likely to have functional importance for epigenome maintenance, gene regulation, and control of DNA replication.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2879085/" 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/PMC2879085/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deal, Roger B -- Henikoff, Jorja G -- Henikoff, Steven -- 1F32GM083449/GM/NIGMS NIH HHS/ -- 1R21DA025758/DA/NIDA NIH HHS/ -- F32 GM083449-03/GM/NIGMS NIH HHS/ -- R21 DA025758/DA/NIDA NIH HHS/ -- R21 DA025758-02/DA/NIDA NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 May 28;328(5982):1161-4. doi: 10.1126/science.1186777.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basic Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20508129" target="_blank"〉PubMed〈/a〉
    Keywords: Alanine/analogs & derivatives/metabolism ; Animals ; Cell Line ; Drosophila Proteins/*metabolism ; Drosophila melanogaster ; *Genome, Insect ; Histones/*metabolism ; Kinetics ; Methionine/metabolism ; *Molecular Probe Techniques ; Nucleosomes/*metabolism ; Oligonucleotide Array Sequence Analysis
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    Cross-reacting antibodies enhance dengue virus infection in humans (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-08
    Description: Dengue virus co-circulates as four serotypes, and sequential infections with more than one serotype are common. One hypothesis for the increased severity seen in secondary infections is antibody-dependent enhancement (ADE) leading to increased replication in Fc receptor-bearing cells. In this study, we have generated a panel of human monoclonal antibodies to dengue virus. Antibodies to the structural precursor-membrane protein (prM) form a major component of the response. These antibodies are highly cross-reactive among the dengue virus serotypes and, even at high concentrations, do not neutralize infection but potently promote ADE. We propose that the partial cleavage of prM from the viral surface reduces the density of antigen available for viral neutralization, leaving dengue viruses susceptible to ADE by antibody to prM, a finding that has implications for future vaccine design.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3837288/" 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/PMC3837288/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dejnirattisai, Wanwisa -- Jumnainsong, Amonrat -- Onsirisakul, Naruthai -- Fitton, Patricia -- Vasanawathana, Sirijitt -- Limpitikul, Wannee -- Puttikhunt, Chunya -- Edwards, Carolyn -- Duangchinda, Thaneeya -- Supasa, Sunpetchuda -- Chawansuntati, Kriangkrai -- Malasit, Prida -- Mongkolsapaya, Juthathip -- Screaton, Gavin -- 078121/Wellcome Trust/United Kingdom -- G0400720/Medical Research Council/United Kingdom -- G0600000/Medical Research Council/United Kingdom -- G0600000(77433)/Medical Research Council/United Kingdom -- G0801508/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2010 May 7;328(5979):745-8. doi: 10.1126/science.1185181.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Imperial College London, London W12 0NN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20448183" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes ; Animals ; Antibodies, Monoclonal/immunology ; Antibodies, Neutralizing/immunology ; Antibodies, Viral/*immunology ; *Antibody-Dependent Enhancement ; Antigens, Viral/*immunology ; Cell Line ; Cross Reactions ; Dengue/*immunology ; Dengue Vaccines/immunology ; Dengue Virus/classification/*immunology/physiology ; Encephalitis Virus, Japanese/immunology ; Humans ; Immune Evasion ; Monocytes/immunology/virology ; Receptors, Fc/immunology ; Serotyping ; U937 Cells ; Viral Envelope Proteins/immunology ; Viral Matrix Proteins/*immunology/metabolism ; Virus Replication
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    Dom34:Hbs1 promotes subunit dissociation and peptidyl-tRNA drop-off to initiate no-go decay (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-16
    Description: No-go decay (NGD) is one of several messenger RNA (mRNA) surveillance systems dedicated to the removal of defective mRNAs from the available pool. Two interacting factors, Dom34 and Hbs1, are genetically implicated in NGD in yeast. Using a reconstituted yeast translation system, we show that Dom34:Hbs1 interacts with the ribosome to promote subunit dissociation and peptidyl-tRNA drop-off. Our data further indicate that these recycling activities are shared by the homologous translation termination factor complex eRF1:eRF3, suggesting a common ancestral function. Because Dom34:Hbs1 activity exhibits no dependence on either peptide length or A-site codon identity, we propose that this quality-control system functions broadly to recycle ribosomes throughout the translation cycle whenever stalls occur.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4022135/" 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/PMC4022135/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shoemaker, Christopher J -- Eyler, Daniel E -- Green, Rachel -- R01 GM059425/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Oct 15;330(6002):369-72. doi: 10.1126/science.1192430.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and 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/20947765" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Cycle Proteins/genetics/*metabolism ; Codon ; Codon, Terminator ; Endoribonucleases/genetics/*metabolism ; GTP-Binding Proteins/genetics/*metabolism ; Guanosine Triphosphate/metabolism ; HSP70 Heat-Shock Proteins/genetics/*metabolism ; Kinetics ; Peptide Chain Termination, Translational ; Peptide Elongation Factors/genetics/*metabolism ; Peptide Termination Factors/metabolism ; Protein Biosynthesis ; *RNA Stability ; RNA, Fungal/genetics/*metabolism ; RNA, Messenger/genetics/*metabolism ; RNA, Transfer, Amino Acyl/genetics/*metabolism ; Recombinant Proteins/metabolism ; Ribosome Subunits/*metabolism ; Saccharomyces cerevisiae/*genetics/metabolism ; Saccharomyces cerevisiae Proteins/genetics/*metabolism
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    Histone H3 Thr-3 phosphorylation by Haspin positions Aurora B at centromeres in mitosis (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-14
    Description: Aurora B is a component of the chromosomal passenger complex (CPC) required for correct spindle-kinetochore attachments during chromosome segregation and for cytokinesis. The chromatin factors that recruit the CPC to centromeres are unknown, however. Here we show that phosphorylation of histone H3 threonine 3 (H3T3ph) by Haspin is necessary for CPC accumulation at centromeres and that the CPC subunit Survivin binds directly to H3T3ph. A nonbinding Survivin-D70A/D71A mutant does not support centromeric CPC concentration, and both Haspin depletion and Survivin-D70A/D71A mutation diminish centromere localization of the kinesin MCAK and the mitotic checkpoint response to taxol. Survivin-D70A/D71A mutation and microinjection of H3T3ph-specific antibody both compromise centromeric Aurora B functions but do not prevent cytokinesis. Therefore, H3T3ph generated by Haspin positions the CPC at centromeres to regulate selected targets of Aurora B during mitosis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2967368/" 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/PMC2967368/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Fangwei -- Dai, Jun -- Daum, John R -- Niedzialkowska, Ewa -- Banerjee, Budhaditya -- Stukenberg, P Todd -- Gorbsky, Gary J -- Higgins, Jonathan M G -- R01 GM050412/GM/NIGMS NIH HHS/ -- R01 GM050412-16/GM/NIGMS NIH HHS/ -- R01 GM063045/GM/NIGMS NIH HHS/ -- R01 GM063045-10/GM/NIGMS NIH HHS/ -- R01 GM074210/GM/NIGMS NIH HHS/ -- R01 GM074210-04/GM/NIGMS NIH HHS/ -- R01-GM050412/GM/NIGMS NIH HHS/ -- R01-GM063045/GM/NIGMS NIH HHS/ -- R01-GM074210/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Oct 8;330(6001):231-5. doi: 10.1126/science.1189435. Epub 2010 Aug 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Harvard Medical School, Smith Building, 1 Jimmy Fund Way, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20705812" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aurora Kinase B ; Aurora Kinases ; Cell Cycle Proteins/metabolism ; Cell Line ; Cell Line, Tumor ; Centromere/*metabolism ; Chromatin/*metabolism ; HeLa Cells ; Histones/*metabolism ; Humans ; Inhibitor of Apoptosis Proteins ; Intracellular Signaling Peptides and Proteins/genetics/*metabolism ; Kinesin/metabolism ; Kinetochores/metabolism ; Microtubule-Associated Proteins/chemistry/genetics/*metabolism ; *Mitosis ; Mutation ; Phosphorylation ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; RNA Interference ; Recombinant Proteins/metabolism ; Spindle Apparatus/metabolism ; Swine ; Threonine/metabolism ; Xenopus
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    Mechanosensitive self-replication driven by self-organization (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-20
    Description: Self-replicating molecules are likely to have played an important role in the origin of life, and a small number of fully synthetic self-replicators have already been described. Yet it remains an open question which factors most effectively bias the replication toward the far-from-equilibrium distributions characterizing even simple organisms. We report here two self-replicating peptide-derived macrocycles that emerge from a small dynamic combinatorial library and compete for a common feedstock. Replication is driven by nanostructure formation, resulting from the assembly of the peptides into fibers held together by beta sheets. Which of the two replicators becomes dominant is influenced by whether the sample is shaken or stirred. These results establish that mechanical forces can act as a selection pressure in the competition between replicators and can determine the outcome of a covalent synthesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carnall, Jacqui M A -- Waudby, Christopher A -- Belenguer, Ana M -- Stuart, Marc C A -- Peyralans, Jerome J-P -- Otto, Sijbren -- New York, N.Y. -- Science. 2010 Mar 19;327(5972):1502-6. doi: 10.1126/science.1182767.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Cambridge, Department of Chemistry, Lensfield Road, Cambridge CB2 1EW, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20299594" target="_blank"〉PubMed〈/a〉
    Keywords: Circular Dichroism ; Combinatorial Chemistry Techniques ; Cryoelectron Microscopy ; Evolution, Chemical ; Hydrogen-Ion Concentration ; Kinetics ; Leucine/chemistry ; Lysine/chemistry ; Macrocyclic Compounds/*chemistry ; Mechanical Phenomena ; Models, Chemical ; Molecular Conformation ; Origin of Life ; Peptide Library ; Peptides/*chemistry ; Physicochemical Processes ; Spectrum Analysis ; Stress, Mechanical ; Sulfhydryl Compounds/chemistry ; Thermodynamics
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    The calcium store sensor, STIM1, reciprocally controls Orai and CaV1.2 channels (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-10-12
    Description: Calcium signals, pivotal in controlling cell function, can be generated by calcium entry channels activated by plasma membrane depolarization or depletion of internal calcium stores. We reveal a regulatory link between these two channel subtypes mediated by the ubiquitous calcium-sensing STIM proteins. STIM1 activation by store depletion or mutational modification strongly suppresses voltage-operated calcium (Ca(V)1.2) channels while activating store-operated Orai channels. Both actions are mediated by the short STIM-Orai activating region (SOAR) of STIM1. STIM1 interacts with Ca(V)1.2 channels and localizes within discrete endoplasmic reticulum/plasma membrane junctions containing both Ca(V)1.2 and Orai1 channels. Hence, STIM1 interacts with and reciprocally controls two major calcium channels hitherto thought to operate independently. Such coordinated control of the widely expressed Ca(V)1.2 and Orai channels has major implications for Ca(2+) signal generation in excitable and nonexcitable cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3601900/" 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/PMC3601900/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Youjun -- Deng, Xiaoxiang -- Mancarella, Salvatore -- Hendron, Eunan -- Eguchi, Satoru -- Soboloff, Jonathan -- Tang, Xiang D -- Gill, Donald L -- AI058173/AI/NIAID NIH HHS/ -- HL55426/HL/NHLBI NIH HHS/ -- R01 AI058173/AI/NIAID NIH HHS/ -- R01 HL055426/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2010 Oct 1;330(6000):105-9. doi: 10.1126/science.1191086.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Cardiovascular Research Center, Temple University School of Medicine, 3400 North Broad Street, Philadelphia, PA 19140, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929813" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Calcium Channels/genetics/*metabolism ; Calcium Channels, L-Type/*metabolism ; Calcium Signaling ; Cell Line ; Cell Membrane/metabolism ; Endoplasmic Reticulum/metabolism ; Humans ; Membrane Glycoproteins/chemistry/genetics/*metabolism ; Muscle, Smooth, Vascular/cytology ; Mutant Proteins/metabolism ; Myocytes, Smooth Muscle/*metabolism ; Patch-Clamp Techniques ; RNA Interference ; Rats ; Transfection
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    The junctional adhesion molecule JAML is a costimulatory receptor for epithelial gammadelta T cell activation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-04
    Description: Gammadelta T cells present in epithelial tissues provide a crucial first line of defense against environmental insults, including infection, trauma, and malignancy, yet the molecular events surrounding their activation remain poorly defined. Here we identify an epithelial gammadelta T cell-specific costimulatory molecule, junctional adhesion molecule-like protein (JAML). Binding of JAML to its ligand Coxsackie and adenovirus receptor (CAR) provides costimulation leading to cellular proliferation and cytokine and growth factor production. Inhibition of JAML costimulation leads to diminished gammadelta T cell activation and delayed wound closure akin to that seen in the absence of gammadelta T cells. Our results identify JAML as a crucial component of epithelial gammadelta T cell biology and have broader implications for CAR and JAML in tissue homeostasis and repair.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943937/" 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/PMC2943937/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Witherden, Deborah A -- Verdino, Petra -- Rieder, Stephanie E -- Garijo, Olivia -- Mills, Robyn E -- Teyton, Luc -- Fischer, Wolfgang H -- Wilson, Ian A -- Havran, Wendy L -- AI064811/AI/NIAID NIH HHS/ -- AI42266/AI/NIAID NIH HHS/ -- AI52257/AI/NIAID NIH HHS/ -- CA58896/CA/NCI NIH HHS/ -- NS057096/NS/NINDS NIH HHS/ -- R01 AI036964/AI/NIAID NIH HHS/ -- R01 AI052257/AI/NIAID NIH HHS/ -- R01 AI052257-05/AI/NIAID NIH HHS/ -- R01 AI064811/AI/NIAID NIH HHS/ -- R01 AI064811-05/AI/NIAID NIH HHS/ -- R01 GM080301/GM/NIGMS NIH HHS/ -- R37 AI042266/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 3;329(5996):1205-10. doi: 10.1126/science.1192698.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20813954" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Cell Adhesion Molecules/*metabolism ; Cell Line ; Cell Proliferation ; Coxsackie and Adenovirus Receptor-Like Membrane Protein ; Cytokines/metabolism ; Epidermis/cytology/*immunology/injuries ; Epithelial Cells ; Epithelium/immunology/metabolism ; Intercellular Signaling Peptides and Proteins/metabolism ; Keratinocytes/metabolism ; Ligands ; *Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Phosphatidylinositol 3-Kinases/metabolism ; Protein Binding ; Receptors, Antigen, T-Cell, gamma-delta/*immunology/metabolism ; Receptors, Virus/*metabolism ; T-Lymphocyte Subsets/*immunology/*metabolism ; Wound Healing
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    Structure of the human dopamine D3 receptor in complex with a D2/D3 selective antagonist (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-26
    Description: Dopamine modulates movement, cognition, and emotion through activation of dopamine G protein-coupled receptors in the brain. The crystal structure of the human dopamine D3 receptor (D3R) in complex with the small molecule D2R/D3R-specific antagonist eticlopride reveals important features of the ligand binding pocket and extracellular loops. On the intracellular side of the receptor, a locked conformation of the ionic lock and two distinctly different conformations of intracellular loop 2 are observed. Docking of R-22, a D3R-selective antagonist, reveals an extracellular extension of the eticlopride binding site that comprises a second binding pocket for the aryl amide of R-22, which differs between the highly homologous D2R and D3R. This difference provides direction to the design of D3R-selective agents for treating drug abuse and other neuropsychiatric indications.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058422/" 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/PMC3058422/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chien, Ellen Y T -- Liu, Wei -- Zhao, Qiang -- Katritch, Vsevolod -- Han, Gye Won -- Hanson, Michael A -- Shi, Lei -- Newman, Amy Hauck -- Javitch, Jonathan A -- Cherezov, Vadim -- Stevens, Raymond C -- DA022413/DA/NIDA NIH HHS/ -- DA023694/DA/NIDA NIH HHS/ -- GM075915/GM/NIGMS NIH HHS/ -- K05 DA022413/DA/NIDA NIH HHS/ -- K05 DA022413-05/DA/NIDA NIH HHS/ -- MH54137/MH/NIMH NIH HHS/ -- P50 GM073197/GM/NIGMS NIH HHS/ -- P50 GM073197-07/GM/NIGMS NIH HHS/ -- R00 DA023694/DA/NIDA NIH HHS/ -- R00 DA023694-04/DA/NIDA NIH HHS/ -- R01 GM089857/GM/NIGMS NIH HHS/ -- R01 MH054137/MH/NIMH NIH HHS/ -- R01 MH054137-16/MH/NIMH NIH HHS/ -- R21 RR025336/RR/NCRR NIH HHS/ -- R21 RR025336-01A1/RR/NCRR NIH HHS/ -- U54 GM074961/GM/NIGMS NIH HHS/ -- U54 GM074961-050001/GM/NIGMS NIH HHS/ -- U54 GM094618/GM/NIGMS NIH HHS/ -- U54 GM094618-01/GM/NIGMS NIH HHS/ -- Y1-CO-1020/CO/NCI NIH HHS/ -- Y1-GM-1104/GM/NIGMS NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Nov 19;330(6007):1091-5. doi: 10.1126/science.1197410.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, The 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/21097933" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arginine/chemistry ; Binding Sites ; Cell Line ; Crystallography, X-Ray ; Dopamine Antagonists/*chemistry ; Dopamine D2 Receptor Antagonists ; Humans ; Models, Molecular ; Protein Conformation ; Receptors, Dopamine D3/antagonists & inhibitors/*chemistry ; Recombinant Proteins/chemistry ; Salicylamides/*chemistry ; Spodoptera
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    A septin diffusion barrier at the base of the primary cilium maintains ciliary membrane protein distribution (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-06-19
    Description: In animal cells, the primary cilium transduces extracellular signals through signaling receptors localized in the ciliary membrane, but how these ciliary membrane proteins are retained in the cilium is unknown. We found that ciliary membrane proteins were highly mobile, but their diffusion was impeded at the base of the cilium by a diffusion barrier. Septin 2 (SEPT2), a member of the septin family of guanosine triphosphatases that form a diffusion barrier in budding yeast, localized at the base of the ciliary membrane. SEPT2 depletion resulted in loss of ciliary membrane protein localization and Sonic hedgehog signal transduction, and inhibited ciliogenesis. Thus, SEPT2 is part of a diffusion barrier at the base of the ciliary membrane and is essential for retaining receptor-signaling pathways in the primary cilium.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3092790/" 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/PMC3092790/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, Qicong -- Milenkovic, Ljiljana -- Jin, Hua -- Scott, Matthew P -- Nachury, Maxence V -- Spiliotis, Elias T -- Nelson, W James -- GM089933/GM/NIGMS NIH HHS/ -- GM35527/GM/NIGMS NIH HHS/ -- R01 GM089933/GM/NIGMS NIH HHS/ -- R37 GM035527/GM/NIGMS NIH HHS/ -- R37 GM035527-27/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jul 23;329(5990):436-9. doi: 10.1126/science.1191054. Epub 2010 Jun 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20558667" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axoneme/metabolism ; Cell Line ; Cells, Cultured ; Cilia/*metabolism/ultrastructure ; Cytoskeletal Proteins/*metabolism ; Diffusion ; Fluorescence Recovery After Photobleaching ; GTP-Binding Proteins/*metabolism ; Hedgehog Proteins/metabolism ; Membrane Proteins/*metabolism ; Mice ; RNA, Small Interfering ; Receptors, Cell Surface/metabolism ; Receptors, G-Protein-Coupled/metabolism ; Receptors, Serotonin/metabolism ; Receptors, Somatostatin/metabolism ; Septins ; *Signal Transduction ; Transfection
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    MiR-33 contributes to the regulation of cholesterol homeostasis (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-15
    Description: Cholesterol metabolism is tightly regulated at the cellular level. Here we show that miR-33, an intronic microRNA (miRNA) located within the gene encoding sterol-regulatory element-binding factor-2 (SREBF-2), a transcriptional regulator of cholesterol synthesis, modulates the expression of genes involved in cellular cholesterol transport. In mouse and human cells, miR-33 inhibits the expression of the adenosine triphosphate-binding cassette (ABC) transporter, ABCA1, thereby attenuating cholesterol efflux to apolipoprotein A1. In mouse macrophages, miR-33 also targets ABCG1, reducing cholesterol efflux to nascent high-density lipoprotein (HDL). Lentiviral delivery of miR-33 to mice represses ABCA1 expression in the liver, reducing circulating HDL levels. Conversely, silencing of miR-33 in vivo increases hepatic expression of ABCA1 and plasma HDL levels. Thus, miR-33 appears to regulate both HDL biogenesis in the liver and cellular cholesterol efflux.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3114628/" 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/PMC3114628/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rayner, Katey J -- Suarez, Yajaira -- Davalos, Alberto -- Parathath, Saj -- Fitzgerald, Michael L -- Tamehiro, Norimasa -- Fisher, Edward A -- Moore, Kathryn J -- Fernandez-Hernando, Carlos -- 1P30HL101270-01/HL/NHLBI NIH HHS/ -- P30 HL101270/HL/NHLBI NIH HHS/ -- R01 AG020255/AG/NIA NIH HHS/ -- R01 AG020255-09/AG/NIA NIH HHS/ -- R01AG02055/AG/NIA NIH HHS/ -- R01HL074136/HL/NHLBI NIH HHS/ -- R01HL084312/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2010 Jun 18;328(5985):1570-3. doi: 10.1126/science.1189862. Epub 2010 May 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Leon H. Charney Division of Cardiology and the Marc and Ruti Bell Vascular Biology and Disease Program, New York University School of Medicine, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20466885" target="_blank"〉PubMed〈/a〉
    Keywords: ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters/genetics/metabolism ; Animals ; Apolipoprotein A-I/metabolism ; Carrier Proteins/genetics/metabolism ; Cell Line ; Cholesterol/*metabolism ; Cholesterol, Dietary/administration & dosage ; Dietary Fats/administration & dosage ; Gene Expression Regulation ; Homeostasis ; Humans ; Hypercholesterolemia/genetics/metabolism ; Introns ; Lipoproteins/genetics/metabolism ; Lipoproteins, HDL/blood/*metabolism ; Liver/*metabolism ; Macrophages/metabolism ; Macrophages, Peritoneal/metabolism ; Membrane Glycoproteins/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; MicroRNAs/genetics/*metabolism ; Proteins/genetics/metabolism ; Sterol Regulatory Element Binding Protein 2/genetics/metabolism ; Transfection
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    Visualizing ribosome biogenesis: parallel assembly pathways for the 30S subunit (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-30
    Description: Ribosomes are self-assembling macromolecular machines that translate DNA into proteins, and an understanding of ribosome biogenesis is central to cellular physiology. Previous studies on the Escherichia coli 30S subunit suggest that ribosome assembly occurs via multiple parallel pathways rather than through a single rate-limiting step, but little mechanistic information is known about this process. Discovery single-particle profiling (DSP), an application of time-resolved electron microscopy, was used to obtain more than 1 million snapshots of assembling 30S subunits, identify and visualize the structures of 14 assembly intermediates, and monitor the population flux of these intermediates over time. DSP results were integrated with mass spectrometry data to construct the first ribosome-assembly mechanism that incorporates binding dependencies, rate constants, and structural characterization of populated intermediates.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2990404/" 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/PMC2990404/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mulder, Anke M -- Yoshioka, Craig -- Beck, Andrea H -- Bunner, Anne E -- Milligan, Ronald A -- Potter, Clinton S -- Carragher, Bridget -- Williamson, James R -- GM-52468/GM/NIGMS NIH HHS/ -- P41 RR017573/RR/NCRR NIH HHS/ -- P41 RR017573-10/RR/NCRR NIH HHS/ -- R01 GM052468/GM/NIGMS NIH HHS/ -- R01 GM052468-16/GM/NIGMS NIH HHS/ -- R01 RR023093/RR/NCRR NIH HHS/ -- R01 RR023093-09/RR/NCRR NIH HHS/ -- R37 GM053757/GM/NIGMS NIH HHS/ -- R37 GM053757-16/GM/NIGMS NIH HHS/ -- R37-GM-53757/GM/NIGMS NIH HHS/ -- RR023093/RR/NCRR NIH HHS/ -- RR175173/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2010 Oct 29;330(6004):673-7. doi: 10.1126/science.1193220.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, The Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21030658" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/chemistry/metabolism ; Image Processing, Computer-Assisted ; Kinetics ; Mass Spectrometry ; Microscopy, Electron/methods ; Models, Molecular ; Nucleic Acid Conformation ; Protein Binding ; Protein Conformation ; RNA, Bacterial/chemistry ; RNA, Ribosomal/chemistry ; Ribosomal Proteins/chemistry/*metabolism ; Ribosome Subunits, Small, Bacterial/chemistry/*metabolism/*ultrastructure
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    Cytochrome P450 compound I: capture, characterization, and C-H bond activation kinetics (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-13
    Description: Cytochrome P450 enzymes are responsible for the phase I metabolism of approximately 75% of known pharmaceuticals. P450s perform this and other important biological functions through the controlled activation of C-H bonds. Here, we report the spectroscopic and kinetic characterization of the long-sought principal intermediate involved in this process, P450 compound I (P450-I), which we prepared in approximately 75% yield by reacting ferric CYP119 with m-chloroperbenzoic acid. The Mossbauer spectrum of CYP119-I is similar to that of chloroperoxidase compound I, although its electron paramagnetic resonance spectrum reflects an increase in |J|/D, the ratio of the exchange coupling to the zero-field splitting. CYP119-I hydroxylates the unactivated C-H bonds of lauric acid [D(C-H) ~ 100 kilocalories per mole], with an apparent second-order rate constant of k(app) = 1.1 x 10(7) per molar per second at 4 degrees C. Direct measurements put a lower limit of k 〉/= 210 per second on the rate constant for bound substrate oxidation, whereas analyses involving kinetic isotope effects predict a value in excess of 1400 per second.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rittle, Jonathan -- Green, Michael T -- New York, N.Y. -- Science. 2010 Nov 12;330(6006):933-7. doi: 10.1126/science.1193478.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Pennsylvania State University, University Park, PA 16802, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21071661" target="_blank"〉PubMed〈/a〉
    Keywords: Biocatalysis ; Catalytic Domain ; Chlorobenzoates/chemistry ; Cytochrome P-450 Enzyme System/*chemistry/*isolation & purification/*metabolism ; Electron Spin Resonance Spectroscopy ; Fatty Acids/chemistry/metabolism ; Freezing ; Hydroxylation ; Kinetics ; Lauric Acids/chemistry/metabolism ; Ligands ; Oxidation-Reduction ; Oxygen/chemistry/metabolism ; Physicochemical Processes ; Spectroscopy, Mossbauer ; Sulfolobus acidocaldarius/enzymology
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    Integrative modeling defines the Nova splicing-regulatory network and its combinatorial controls (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-06-19
    Description: The control of RNA alternative splicing is critical for generating biological diversity. Despite emerging genome-wide technologies to study RNA complexity, reliable and comprehensive RNA-regulatory networks have not been defined. Here, we used Bayesian networks to probabilistically model diverse data sets and predict the target networks of specific regulators. We applied this strategy to identify approximately 700 alternative splicing events directly regulated by the neuron-specific factor Nova in the mouse brain, integrating RNA-binding data, splicing microarray data, Nova-binding motifs, and evolutionary signatures. The resulting integrative network revealed combinatorial regulation by Nova and the neuronal splicing factor Fox, interplay between phosphorylation and splicing, and potential links to neurologic disease. Thus, we have developed a general approach to understanding mammalian RNA regulation at the systems level.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3412410/" 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/PMC3412410/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Chaolin -- Frias, Maria A -- Mele, Aldo -- Ruggiu, Matteo -- Eom, Taesun -- Marney, Christina B -- Wang, Huidong -- Licatalosi, Donny D -- Fak, John J -- Darnell, Robert B -- K99 GM095713/GM/NIGMS NIH HHS/ -- NS34389/NS/NINDS NIH HHS/ -- UL1 RR024143/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jul 23;329(5990):439-43. doi: 10.1126/science.1191150. Epub 2010 Jun 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Neuro-Oncology, Howard Hughes Medical Institute, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA. czhang@rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20558669" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Animals ; Antigens, Neoplasm/*metabolism ; Artificial Intelligence ; Bayes Theorem ; Binding Sites ; Brain/*metabolism ; Cell Line ; Computational Biology ; Evolution, Molecular ; Exons ; *Gene Regulatory Networks ; Humans ; Introns ; Mice ; Models, Genetic ; Models, Statistical ; Nerve Tissue Proteins/*metabolism ; Nervous System Diseases/genetics ; Oligonucleotide Array Sequence Analysis ; Phosphorylation ; Protein Binding ; Proteins/genetics/metabolism ; RNA/metabolism ; RNA-Binding Proteins/*metabolism
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    Benzodiazepine inhibition of the calcium-calmodulin protein kinase system in brain membrane (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-07-31
    Description: Benzodiazepines inhibit Ca2+-calmodulin-stimulated membrane protein phosphorylation. The effects of the benzodiazepines on protein phosphorylation are stereospecific and produced by membrane-bound benzodiazepine. The potency of benzodiazepine kinase inhibition is correlated with the ability of the benzodiazepines to inhibit electric shock-induced convulsions. These findings provide evidence that some of the anticonvulsant and neuronal stabilizing effects of benzodiazepines may be modulated by the Ca2+-calmodulin protein kinase system and indicate that this calmodulin-kinase system represents an identifiable benzodiazepine receptor in brain that is distinquishable by several criteria from the previously described high affinity benzodiazepine receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉DeLorenzo, R J -- Burdette, S -- Holderness, J -- NS 1352/NS/NINDS NIH HHS/ -- NSI-EA-1-K04-NS245/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1981 Jul 31;213(4507):546-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6264605" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzodiazepines/metabolism ; Brain/*enzymology ; Calcium/*pharmacology ; Calcium-Binding Proteins/*pharmacology ; Calmodulin/*pharmacology ; Cell Membrane/enzymology ; Chlordiazepoxide/*pharmacology ; Diazepam/*pharmacology ; Enzyme Activation ; Kinetics ; Molecular Weight ; Phosphorylation ; Protein Kinases/*metabolism ; Rats ; Receptors, Drug/metabolism ; Receptors, GABA-A
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Renin and angiotensin: the complete system within the neuroblastoma x glioma cell (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-11-20
    Description: Cells of the homogeneous hybrid line neuroblastoma x glioma (NG108-15) have many neuronal properties. Immunocytochemical tests show that they contain both immunoreactive renin and angiotensin; direct radioimmunoassays show that they are positive for renin, angiotensin I, and angiotensin II; enzymatic assays show that they contain angiotensinogen and converting enzyme as well. The renin appears to be present in an enzymatically inactive form that can be activated by trypsin and then blocked by antiserum to purified mouse submaxillary renin. Renin concentration and activity are increased by enhancing cellular differentiation with dibutyryl cyclic adenosine monophosphate or by serum withdrawal. These findings demonstrate a complete renin-angiotensin system within these neuron-like cells, and suggest that activation of intracellular renin could generate angiotensin II.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fishman, M C -- Zimmerman, E A -- Slater, E E -- HL-21247/HL/NHLBI NIH HHS/ -- HL-24105/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1981 Nov 20;214(4523):921-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6272392" target="_blank"〉PubMed〈/a〉
    Keywords: Angiotensin I/*analysis ; Angiotensin II/*analysis ; Angiotensins/*analysis ; Animals ; Cell Line ; Cricetinae ; Glioma/*metabolism ; Hybrid Cells/*metabolism ; Mice ; Neuroblastoma/*metabolism ; Peptidyl-Dipeptidase A/metabolism ; Radioimmunoassay ; Rats ; Renin/*metabolism
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    Isolation of biological materials by use of erbium (III)--induced magnetic susceptibilities (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-08-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Evans, C H -- Tew, W P -- New York, N.Y. -- Science. 1981 Aug 7;213(4508):653-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7256262" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Cations ; *Erbium ; Kinetics ; *Magnetics
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    Malignant potential of murine stromal cells after transplantation of human tumors into nude mice (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-04-03
    Description: Human malignant cancer tumors grafted into nude mice produce tumors containing both human cancer cells and the host's stromal cells. After short-term propagation of these tumors in vitro, the murine mesenchymal cells appear transformed and are tumorigenic in nude mice. However, established human cancer cell lines fail to similarly after adjacent murine stromal cells when used to produce tumors in nude mice. These experiments suggest that cancer cells may recruit normal cells to become malignant, qualifying the view of the clonal (unicellular) origin of cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldenberg, D M -- Pavia, R A -- 1R01 CA17198/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1981 Apr 3;212(4490):65-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7209521" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/pathology ; Animals ; Cell Line ; Cells, Cultured ; Colonic Neoplasms/pathology ; Fibrosarcoma/*etiology ; Humans ; Karyotyping ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Middle Aged ; Neoplasm Transplantation ; Neoplasms, Experimental/*etiology ; Transplantation, Heterologous
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    Vagotomy abolishes cues of satiety produced by gastric distension (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-06-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gonzalez, M F -- Deutsch, J A -- New York, N.Y. -- Science. 1981 Jun 12;212(4500):1283-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7233218" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Feeding Behavior ; Kinetics ; Male ; Rats ; *Satiation ; *Satiety Response ; Stomach/*physiology ; *Vagotomy
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  • 75
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    Plasmid-assisted molecular breeding: new technique for enhanced biodegradation of persistent toxic chemicals (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-12-04
    Description: The persistence of synthetic herbicides such as 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) and its release in massive amounts as a herbicide (Agent Orange) have created toxicological problems in many countries. In nature, 2,4,5-T is slowly degraded by cooxidation and is not utilized as a sole source of carbon and energy. The technique of plasmid-assisted molecular breeding has led to the development of bacterial strains capable of totally degrading 2,4,5-T by using it as their sole source of carbon at high concentrations (greater than 1 mg/ml). Spectrophotometry and gas chromatography reveal various intermediates during growth of the culture with 2,4,5-T.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kellogg, S T -- Chatterjee, D K -- Chakrabarty, A M -- New York, N.Y. -- Science. 1981 Dec 4;214(4525):1133-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7302584" target="_blank"〉PubMed〈/a〉
    Keywords: 2,4,5-Trichlorophenoxyacetic Acid/*metabolism ; Bacteria/*genetics/metabolism ; Biotransformation ; Cell Division ; Kinetics ; Nucleic Acid Hybridization ; *Plasmids
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  • 76
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    Insulin as a potent, specific growth factor in a rat hepatoma cell line (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-02-27
    Description: A line or rat hepatoma cells in culture which, in response to serum starvation, become arrested in the early G1 phase of growth, can be stimulated by insulin alone to enter the cell cycle and traverse S phase. A half-maximum response is observed at 30 to 70 picomolar concentrations and the maximum response is essentially identical to that found with optimum serum concentrations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koontz, J W -- Iwahashi, M -- AM 24047/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1981 Feb 27;211(4485):947-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7008195" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle/drug effects ; Cell Division/drug effects ; Cell Line ; *Growth Substances ; Insulin/*pharmacology ; Liver Neoplasms, Experimental/*pathology ; Mitosis/drug effects ; Proinsulin/pharmacology ; Rats ; Structure-Activity Relationship
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  • 77
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    Divalent cation ionophores stimulate resorption and inhibit DNA synthesis in cultured fetal rat bone (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-06-05
    Description: Two divalent cation ionophores, A23187 and Ionomycin, which are selective for calcium, stimulated the resorption of fetal rat long bones in organ culture at 0.1 to 1 micromolar but not at higher concentrations. Both agents inhibited DNA synthesis at concentrations that stimulated resorption. These results might explain the differences in ionophore effects on bone previously reported, and they imply that cell replication is not required for osteoclast formation in fetal rat long bone cultures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lorenzo, J A -- Raisz, L G -- AM 07290/AM/NIADDK NIH HHS/ -- AM 18063/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1981 Jun 5;212(4499):1157-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6785885" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/*pharmacology ; Bone Resorption/*drug effects ; Bone and Bones/drug effects/*metabolism ; Calcimycin/*pharmacology ; Calcium/metabolism ; Calcium Radioisotopes ; Cells, Cultured ; DNA/*biosynthesis ; DNA Replication/*drug effects ; Ethers/pharmacology ; Fetus ; Ionomycin ; Ionophores/pharmacology ; Kinetics ; Mice ; Parathyroid Hormone/pharmacology
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  • 78
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    The AF64a-treated mouse: possible model for central cholinergic hypofunction (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-07-31
    Description: A loss in the number of functional, sodium ion-dependent, high-affinity choline transport sites was observed in the cortex and hippocampus of mice given an intracerebroventricular injection of 65 nanomoles of AF64A (ethylcholine mustard aziridinium ion) 3 days earlier. Such an effect was not observed in the striatum. This effect of AF64A represents a long-term neurochemical deficit at cholinergic nerve terminals in some brain regions which can lead to a persistent deficiency in central cholinergic transmission. The AF64A-treated animal may thus be a model for certain psychiatric or neurological disorders that appear to involve central cholinergic hypofunction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mantione, C R -- Fisher, A -- Hanin, I -- MH 26320/MH/NIMH NIH HHS/ -- MH/AG 34893/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1981 Jul 31;213(4507):579-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6894649" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aziridines/*pharmacology ; Azirines/*pharmacology ; Biological Transport/drug effects ; Brain/drug effects/*metabolism ; Cerebral Cortex/metabolism ; Choline/*analogs & derivatives/*metabolism/pharmacology ; Corpus Striatum/metabolism ; Hippocampus/metabolism ; Kinetics ; Mice ; Sodium/pharmacology ; Synaptosomes/drug effects/*metabolism
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  • 79
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    A monosialoganglioside is a monoclonal antibody-defined antigen of colon carcinoma (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-04-03
    Description: The antigen of a monoclonal antibody that is specific for cells of human carcinoma of the colon is a monosialoganglioside as determined by the direct binding of antibody to thin-layer chromatograms of total lipid extracts of tissues. Binding of antibody to chromatograms is detected by autoradiography after the application of iodine-125-labeled F(ab')2 of rabbit immunoglobulin G antibodies to mouse immunoglobulins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Magnani, J L -- Brockhaus, M -- Smith, D F -- Ginsburg, V -- Blaszczyk, M -- Mitchell, K F -- Steplewski, Z -- Koprowski, H -- CA-10815/CA/NCI NIH HHS/ -- CA-21124/CA/NCI NIH HHS/ -- RR-05540/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1981 Apr 3;212(4490):55-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7209516" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/*immunology ; Antibodies, Neoplasm/*immunology ; Antibody Specificity ; Antigens, Neoplasm/*immunology/isolation & purification ; Cell Line ; Chromatography, Thin Layer ; Colonic Neoplasms/*immunology ; Gangliosides/*immunology/isolation & purification ; Humans ; Melanoma/immunology ; Neuraminidase/pharmacology
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  • 80
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    Growth inhibition by adenosine 3',5-monophosphate derivatives does not require 3',5' phosphodiester linkage (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-09-04
    Description: Analogs of adenosine 3',5'-monophosphate (cyclic AMP) inhibit the growth of cultured cell lines. The effects of 8-bromo- and N6-butyryl-substituted analogs of cyclic and noncyclic AMP on six cell lines were examined and were equally inhibitory. Variant cell lines with altered cyclic AMP-dependent protein kinase were more resistant to both cyclic and noncyclic nucleotides. We conclude that growth inhibition by analogs of cyclic AMP (i) does not require a 3',5' phosphodiester bond and (ii) may be mediated by a pathway involving endogenous cyclic AMP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martin, T F -- Kowalchyk, J A -- AM 25861/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1981 Sep 4;213(4512):1120-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6267695" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division/*drug effects ; Cell Line ; Cricetinae ; Cyclic AMP/*pharmacology ; DNA/biosynthesis ; Growth Inhibitors/*pharmacology ; Mice ; Phosphodiesterase Inhibitors/pharmacology ; Structure-Activity Relationship
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  • 81
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    Human lupus inclusions and interferon (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-08-14
    Description: Raji cells, a human B lymphoblastoid cell line of Burkitt lymphoma origin, formed lupus inclusions when grown in a medium conditioned by the growth of Raji cells whose DNA thymidine residues had been unifilarly (single-strandedly) substituted with bromodeoxyuridine. Ultracentrifugation of this medium in excess of that required to remove Epstein-Barr virus and all other known mammalian viruses did not prevent the formation of the inclusions, and treatment of the conditioned medium with pronase destroyed the activity. These results demonstrate the presence of a protein that is secreted from bromodeoxyuridine-substituted Raji cells and is capable of inducing nonbromodeoxyuridine-substituted cells to form lupus inclusions. Interferon (100 units per milliliter) was found in the conditioned medium. Inclusions also formed in Raji cells grown in fresh medium supplemented with human leukocyte or fibroblast interferon (100 units per milliliter).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rich, S A -- New York, N.Y. -- Science. 1981 Aug 14;213(4509):772-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6166984" target="_blank"〉PubMed〈/a〉
    Keywords: Bromodeoxyuridine/*metabolism ; Burkitt Lymphoma ; Cell Line ; Culture Media ; Cytoplasmic Granules/ultrastructure ; DNA Replication ; Humans ; Interferons/*biosynthesis ; Lupus Erythematosus, Systemic/*pathology
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  • 82
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    Diameter of the cell-to-cell junctional membrane channels as probed with neutral molecules (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-07-31
    Description: The cell-to-cell channels in the junctions of an insect salivary gland and of insect and mammalian cells in culture were probed with fluorescent molecules-neutral linear oligosaccharides, neutral branched glycopeptides, and charged linear peptides. From the molecular dimensions of the largest permeants and smallest impermeants the permeation-limiting channel diameter was obtained: 16 to 20 angstroms for the mammalian cells and 20 to 30 angstroms for the insect cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwarzmann, G -- Wiegandt, H -- Rose, B -- Zimmerman, A -- Ben-Haim, D -- Loewenstein, W R -- CA 14464/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1981 Jul 31;213(4507):551-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7244653" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chironomidae ; Fluorescent Dyes ; Glycopeptides/*metabolism ; Intercellular Junctions/*ultrastructure ; Mice ; Mice, Inbred BALB C ; Models, Molecular ; Oligosaccharides/*metabolism ; Protein Conformation ; Salivary Glands/*ultrastructure ; Species Specificity
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  • 83
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    Early removal of one eye reduces normally occurring cell death in the remaining eye (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-07-31
    Description: During normal development of the hamster eye, there is a substantial loss of cells from the retinal ganglion cell layer in the first two postnatal weeks. If one eye is lost at birth, this cell death is reduced in the remaining eye. This may account for the increased ipsilateral projection from this eye to the thalamus and midbrain observed in these animals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sengelaub, D R -- Finlay, B L -- New York, N.Y. -- Science. 1981 Jul 31;213(4507):573-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7244655" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Cell Survival ; Cricetinae ; Kinetics ; Neurons/*physiology ; Rats ; Retina/cytology/*physiology
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  • 84
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    Bee venom enhances guanylate cyclase activity (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-07-17
    Description: Bee venom and phospholipase A2 extracted from bee venom enhanced guanylate cyclase (E.C. 4.6.1.2) activity two- to threefold in rat liver, lung, heart, kidney, ileum, and cerebellum. Dose-response relationships revealed that bee venom at concentrations as low as 1 microgram per milliliter and phospholipase A2 at 1 microunit per milliliter caused a maximal enhancement of guanylate cyclase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vesely, D L -- New York, N.Y. -- Science. 1981 Jul 17;213(4505):359-60.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6113689" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bee Venoms/*pharmacology ; Dose-Response Relationship, Drug ; Enzyme Activation ; Guanylate Cyclase/*metabolism ; Kinetics ; Organ Specificity ; Phospholipases/*pharmacology ; Phospholipases A/*pharmacology ; Phospholipases A2 ; Rats
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  • 85
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    Biopterin cofactor biosynthesis: independent regulation of GTP cyclohydrolase in adrenal medulla and cortex (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-07-17
    Description: Guanosine triphosphate cyclohydrolase, the enzyme that is apparently rate-limiting in biopterin biosynthesis, is increased in adrenal cortex and medulla of rats treated with insulin or reserpine. Denervation and hypophysectomy block the increase in medullary and cortical enzyme activity, respectively, whereas cycloheximide presents the increase in both tissues. These results provide evidence for induction and regulation of guanosine triphosphate cyclohydrolase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Viveros, O H -- Lee, C L -- Abou-Donia, M M -- Nixon, J C -- Nichol, C A -- New York, N.Y. -- Science. 1981 Jul 17;213(4505):349-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7017928" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Cortex/drug effects/*enzymology ; Adrenal Glands/innervation ; Adrenal Medulla/drug effects/*enzymology ; Aminohydrolases/*metabolism ; Animals ; Biopterin/*biosynthesis ; Cycloheximide/pharmacology ; Denervation ; GTP Cyclohydrolase/*metabolism ; Hypophysectomy ; Insulin/pharmacology ; Kinetics ; Male ; Organ Specificity ; Pteridines/*biosynthesis ; Rats ; Reserpine/pharmacology
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  • 86
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    Receptor for albumin on the liver cell surface may mediate uptake of fatty acids and other albumin-bound substances (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-03-06
    Description: Kinetic analysis of the uptake of carbon-14-labeled oleate in a single-pass perfusion of rat liver and saturable and specific binding of iodine-125-labeled albumin to hepatocytes in suspension suggest the existence of a receptor for albumin on the liver cell surface. The putative receptor appears to mediate uptake of albumin-bound fatty acids by the cell and may account for the efficient hepatic extraction of many other substances tightly bound to albumin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weisiger, R -- Gollan, J -- Ockner, R -- AM-07007/AM/NIADDK NIH HHS/ -- AM-13328/AM/NIADDK NIH HHS/ -- AM-21899/AM/NIADDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1981 Mar 6;211(4486):1048-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6258226" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport ; Fatty Acids/*metabolism ; Female ; Kinetics ; Liver/*metabolism ; Oleic Acids/metabolism ; Protein Binding ; Rats ; Receptors, Albumin ; Receptors, Cell Surface/*metabolism ; Serum Albumin/*metabolism
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  • 87
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    Tumor cell killing by phorbol ester--differentiated human leukemia cells (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-08-07
    Description: The tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate causes differentiation of cells of the human leukemia cell line HL60 to nondividing macrophage-like cells. These differentiated cells are cytotoxic for tumor cells (including parent, untreated HL60 cells) in vitro. Agents that induce this desirable differentiation to nondividing, antitumor effector cells may be useful in the experimental treatment of leukemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weinberg, J B -- 27070-02/PHS HHS/ -- New York, N.Y. -- Science. 1981 Aug 7;213(4508):655-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7196085" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/drug effects ; Cell Line ; *Cytotoxicity, Immunologic ; Humans ; Immunity, Cellular ; Leukemia, Experimental/immunology/*pathology ; Macrophages/cytology/*immunology ; Phorbols/*pharmacology ; Tetradecanoylphorbol Acetate/*pharmacology
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  • 88
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    Nalidixic acid, oxolinic acid, and novobiocin inhibit yeast glycyl- and leucyl-transfer RNA synthetases (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-07-24
    Description: Nalidixic acid and novobiocin inhibit the aminoacylation and pyrophosphate exchange activities of glycyl- and leucyl-transfer RNA synthetases from bakers' yeast. Similar types of inhibition are observed for both enzymes, suggesting similar mechanisms. The potency of these inhibitors is comparable to that observed for their inhibition of in vivo DNA synthesis in eukaryotic cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wright, H T -- Nurse, K C -- Goldstein, D J -- GM 07654/GM/NIGMS NIH HHS/ -- GM 23598/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1981 Jul 24;213(4506):455-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7017932" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acyl-tRNA Synthetases/*antagonists & inhibitors ; Glycine-tRNA Ligase/*antagonists & inhibitors ; Kinetics ; Leucine-tRNA Ligase/*antagonists & inhibitors ; Nalidixic Acid/*pharmacology ; Novobiocin/*pharmacology ; Oxolinic Acid/*pharmacology ; Saccharomyces cerevisiae/*enzymology
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  • 89
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    Mesenchymal cells from the human embryonic palate are highly responsive to epidermal growth factor (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-07-31
    Description: An established line of mesenchymal cells from the human embryonic palate is highly sensitive to the stimulatory effect of epidermal growth factor on growth, labeled thymidine incorporation, and ornithine decarboxylase activity. The results suggest that epidermal growth factor may play a key role in development of various human embryonic and fetal tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoneda, T -- Pratt, R M -- New York, N.Y. -- Science. 1981 Jul 31;213(4507):563-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7017936" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Division/drug effects ; Cell Line ; DNA Replication/drug effects ; Embryo, Mammalian ; Epidermal Growth Factor/*pharmacology ; Female ; Humans ; Insulin/pharmacology ; Kinetics ; Organ Specificity ; Ornithine Decarboxylase/metabolism ; Palate/drug effects/*physiology ; Peptides/*pharmacology ; Pregnancy
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  • 90
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    Metastatic potential is positively correlated with cell surface sialylation of cultured murine tumor cell lines (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-06-26
    Description: The ability of murine tumor cells to metastasize spontaneously from subcutaneous sites is positively correlated with the total sialic acid content of the cells in culture, the degree to which the sialic acid is exposed on the tumor cell surface, and, most strongly, with the degree of sialylation of galactosyl and N-acetylgalactosaminyl residues in cell surface glycoconjugates. These findings suggest that sialic acid on the cell surface may play a role in tumor cell metastasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yogeeswaran, G -- Salk, P L -- CA19312-01/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1981 Jun 26;212(4502):1514-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7233237" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Membrane/*physiology ; Cell Transformation, Neoplastic ; Cell Transformation, Viral ; Mice ; *Neoplasm Metastasis ; Neoplasms, Experimental/*physiopathology ; Sialic Acids/*analysis
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  • 91
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    Adenosine 3',5'-monophosphate modulates thyrotropin receptor clustering and thyrotropin activity in culture (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-12-11
    Description: A biologically active rhodamine conjugate of thyrotropin binds at 4 degrees C to diffusely distributed membrane thyrotropin receptors which patch and become endocytosed into thyroid cells in a temperature-sensitive process. When the cells are first incubated with 8-bromo-cyclic adenosine monophosphate at 37 degrees C, the conjugate also binds to clustered receptors at 4 degrees C. Furthermore, 8-bromo-cyclic adenosine monophosphate reduces the amount of adenosine 3',5'-monophosphate (cyclic AMP) induced by thyrotropin. Hence, increased intracellular cyclic AMP induces receptor patching and reduces the concentration of cyclic AMP normally induced by thyrotropin. This suggests that cyclic AMP acts both as the second messenger of thyrotropin and also as the regulator of the level of thyrotropin receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Avivi, A -- Tramontano, D -- Ambesi-Impiombato, F S -- Schlessinger, J -- CA-25820/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1981 Dec 11;214(4526):1237-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6272396" target="_blank"〉PubMed〈/a〉
    Keywords: 8-Bromo Cyclic Adenosine Monophosphate ; Animals ; Cell Line ; Cell Membrane/drug effects/metabolism ; Cyclic AMP/*analogs & derivatives/*metabolism/pharmacology ; Rats ; Receptors, Cell Surface/drug effects/*metabolism ; Receptors, Thyrotropin ; Thyroid Gland/metabolism ; Thyrotropin/*metabolism/pharmacology
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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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    Transport of energy in muscle: the phosphorylcreatine shuttle (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-01-30
    Description: In order to explain the insulin-like effect of exercise, it was proposed in 1951 that contracting muscle fibers liberate creatine, which acts to produce an acceptor effect--later called respiratory control--on the muscle mitochondria. The development of this notion paralleled the controversy between biochemists and physiologists over the delivery of energy for muscle contraction. With the demonstration of functional compartmentation of creatine kinase on the mitochondrion, it became clear that the actual form of energy transport in the muscle fiber is phosphorylcreatine. The finding of an isoenzyme of creatine phosphokinase attached to the M-line region of the myofibril revealed the peripheral receptor for the mitochondrially generated phosphorylcreatine. This established a molecular basis for a phosphorylcreatine-creatine shuttle for energy transport in heart and skeletal muscle and provided an explanation for the inability to demonstrate experimentally a direct relation between muscle activity and the concentrations of adenosine triphosphate and adenosine diphosphate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bessman, S P -- Geiger, P J -- New York, N.Y. -- Science. 1981 Jan 30;211(4481):448-52.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6450446" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/metabolism ; Adenosine Triphosphate/*metabolism ; Animals ; Creatine/metabolism ; Creatine Kinase/metabolism ; *Energy Metabolism ; Kinetics ; Mitochondria, Heart/metabolism ; *Muscle Contraction ; Muscles/*metabolism ; Myosins/metabolism ; Phosphocreatine/*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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    Delta9-tetrahydrocannabinol increase plasma testosterone concentrations in mice (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-07-31
    Description: Oral administration of delta 9-tetrahydrocannabinol had a biphasic effect on plasma testosterone concentrations in male mice, causing rapid sustained increases at low doses and subsequent decreases at higher doses. In hypophysectomized and intact mice receiving gonadotropins (human chorionic gonadotropin), treatment with delta 9-tetrahydrocannabinol maintained higher plasma testosterone concentrations. Thus, this cannabinoid may interact with gonadotropin and directly influence testicular steroidogenesis in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dalterio, S -- Bartke, A -- Mayfield, D -- 1R01 DA 02/DA/NIDA NIH HHS/ -- P 30 HD 10202/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1981 Jul 31;213(4507):581-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6264607" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chorionic Gonadotropin/pharmacology ; Dronabinol/*analogs & derivatives/pharmacology ; Hypophysectomy ; Kinetics ; Luteinizing Hormone/*blood ; Male ; Mice ; Testosterone/*blood
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 94
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    Blood-brain glucose transfer: repression in chronic hyperglycemia (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-10-23
    Description: Diabetic patients with increased plasma glucose concentrations may develop cerebral symptoms of hypoglycemia when their plasma glucose is rapidly lowered to normal concentrations. The symptoms may indicate insufficient transport of glucose from blood to brain. In rats with chronic hyperglycemia the maximum glucose transport capacity of the blood-brain barrier decreased from 400 to 290 micromoles per 100 grams per minute. When plasma glucose was lowered to normal values, the glucose transport rate into brain was 20 percent below normal. This suggests that repressive changes of the glucose transport mechanism occur in brain endothelial cells in response to increased plasma glucose.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gjedde, A -- Crone, C -- New York, N.Y. -- Science. 1981 Oct 23;214(4519):456-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7027439" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport ; *Blood-Brain Barrier ; Brain/blood supply ; Diabetes Mellitus, Experimental/metabolism ; Glucose/*metabolism ; Hyperglycemia/*metabolism ; Insulin/physiology ; Kinetics ; Rats ; Regional Blood Flow
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 95
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    Korean hemorrhagic fever: propagation of the etiologic agent in a cell line of human origin (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-03-06
    Description: The etiologic agent of Korean hemorrhagic fever has been propagated in a human cultured cell line derived from a carcinoma of the lung. The cells, described as type II, alveolar epithelial, support replication of the agent and successive passages. Antigen of the Korean hemorrhagic fever agent is readily detected in infected cells by means of direct or indirect fluorescent antibody techniques. Previous attempts to propagate this agent in vitro had been unsuccessful.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉French, G R -- Foulke, R S -- Brand, O A -- Eddy, G A -- Lee, H W -- Lee, P W -- New York, N.Y. -- Science. 1981 Mar 6;211(4486):1046-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6110243" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Viral/analysis ; Cell Line ; Hantavirus/*growth & development/immunology ; Hemorrhagic Fever with Renal Syndrome/*microbiology ; Humans ; Pulmonary Alveoli/microbiology ; RNA Viruses/*growth & development
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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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    Retinal chromophore of rhodopsin photoisomerizes within picoseconds (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-02-27
    Description: A new picosecond resonance Raman technique shows that resonance Raman lines characteristic of a distorted all-trans retinal appear within 30 picoseconds after photolysis of rhodopsin or isorhodopsin. This finding suggests that isomerization is nearly complete within picoseconds of the absorption of a photon.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hayward, G -- Carlsen, W -- Siegman, A -- Stryer, L -- EY-02387/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1981 Feb 27;211(4485):942-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7466366" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; In Vitro Techniques ; Isomerism ; Kinetics ; Light ; Retinal Pigments/*radiation effects ; *Retinaldehyde/radiation effects ; Rhodopsin/*radiation effects ; Spectrum Analysis, Raman ; *Vision, Ocular ; *Vitamin A/analogs & derivatives
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  • 97
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    Somatic cell hybrids from frog lymphocytes and mouse myeloma cells (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-05-29
    Description: Stable somatic cell hybrids were obtained by fusing Xenopus lymphocytes with mouse myeloma cells. These hybrids contained one to four Xenopus chromosomes and expressed Xenopus gene products, one of which was a lymphocyte membrane protein of 85,000 daltons precipitated by a monoclonal antibody.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hengartner, H -- Du Pasquier, L -- New York, N.Y. -- Science. 1981 May 29;212(4498):1034-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6785884" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies ; Antibodies, Monoclonal ; Cell Line ; Clone Cells ; Genes ; Hybrid Cells/*physiology ; Lymphocytes/*physiology ; Membrane Proteins/biosynthesis ; Mice ; Molecular Weight ; Neoplasms, Experimental/physiopathology ; Plasmacytoma/*physiopathology ; Xenopus
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 98
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    Purified reduced nicotinamide adenine dinucleotide: responses to lactate dehydrogenase isozymes from three cell sources (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-05-01
    Description: Lactate dehydrogenase (LDH, E.C. 1.1.1.27) isozymes from three single-cell sources reacted differently with reduced nicotinamide adenine dinucleotide (NADH) purified to published chromatographic and spectrophotometric specifications and free of inhibitors of LDH, when compared with a commercial preparation of NADH. The activity of LDH-1, purified from rabbit erythrocytes, increased the most with inhibitor-free NADH; the next most stimulated were the LDH isozymes from a control hepatocyte line; but hardly responsive at all were the same isozymes from chemically transformed cells. Thus isozyme composition alone did not account for the range of responses to purified NADH. The commercial preparation of NADH used in these studies contains the Strandjord-Clayson inhibitors, the most potent group identified in NADH preparations relative to LDH activity. The results suggest that specific molecular differences in individual isozymes contribute to the differential response to the Strandjord-Clayson inhibitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaplan, A E -- Weiss, E R -- Byrne, S T -- El-Torkey, N M -- Margolis, S A -- New York, N.Y. -- Science. 1981 May 1;212(4494):553-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7209551" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Transformation, Neoplastic/metabolism ; Erythrocytes/enzymology ; Isoenzymes ; L-Lactate Dehydrogenase/antagonists & inhibitors/*metabolism ; Liver Neoplasms, Experimental/enzymology ; NAD/analysis/*metabolism ; Rabbits ; Rats
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  • 99
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    Serum albumin beads: an injectable, biodegradable system for the sustained release of drugs (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-07-10
    Description: Biologically active compounds were entrapped in cross-linked serum albumin microbeads. Injection of these drug-impregnated beads into rabbits produced no adverse immunological reactions. Sustained release (20 days) of progesterone was demonstrated in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, T K -- Sokoloski, T D -- Royer, G P -- New York, N.Y. -- Science. 1981 Jul 10;213(4504):233-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6787705" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Delayed-Action Preparations ; Glutaral ; Injections, Intramuscular ; Injections, Subcutaneous ; Kinetics ; Male ; Microscopy, Electron, Scanning ; Norgestrel/administration & dosage ; Progesterone/*administration & dosage/blood ; Rabbits ; Serum Albumin, Bovine/*administration & dosage
    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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  • 100
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    Pancreatic islet-acinar cell interaction: amylase messenger RNA levels ar determined by insulin (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-07-17
    Description: Pancreatic amylase messenger RNA progressively decreases in rats rendered diabetic with streptozotocin. Insulin reverses this effect, inducing a selective decrease in amylase messenger RNA in the pancreas. Parotid amylase messenger RNA is not significantly affected by either diabetes or insulin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Korc, M -- Owerbach, D -- Quinto, C -- Rutter, W J -- AM 21344/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1981 Jul 17;213(4505):351-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6166044" target="_blank"〉PubMed〈/a〉
    Keywords: Amylases/*genetics ; Animals ; Diabetes Mellitus, Experimental/*enzymology ; Insulin/pharmacology/*physiology ; Islets of Langerhans/*physiology ; Kinetics ; Male ; Pancreas/drug effects/*enzymology ; Pancreatic Elastase/genetics ; Protein Biosynthesis/drug effects ; RNA, Messenger/*genetics ; Rats ; Transcription, Genetic/drug effects ; Trypsinogen/genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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