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  • 1
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    Lkb1 regulates quiescence and metabolic homeostasis of haematopoietic stem cells (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-12-03
    Description: The capacity to fine-tune cellular bioenergetics with the demands of stem-cell maintenance and regeneration is central to normal development and ageing, and to organismal survival during periods of acute stress. How energy metabolism and stem-cell homeostatic processes are coordinated is not well understood. Lkb1 acts as an evolutionarily conserved regulator of cellular energy metabolism in eukaryotic cells and functions as the major upstream kinase to phosphorylate AMP-activated protein kinase (AMPK) and 12 other AMPK-related kinases. Whether Lkb1 regulates stem-cell maintenance remains unknown. Here we show that Lkb1 has an essential role in haematopoietic stem cell (HSC) homeostasis. We demonstrate that ablation of Lkb1 in adult mice results in severe pancytopenia and subsequent lethality. Loss of Lkb1 leads to impaired survival and escape from quiescence of HSCs, resulting in exhaustion of the HSC pool and a marked reduction of HSC repopulating potential in vivo. Lkb1 deletion has an impact on cell proliferation in HSCs, but not on more committed compartments, pointing to context-specific functions for Lkb1 in haematopoiesis. The adverse impact of Lkb1 deletion on haematopoiesis was predominantly cell-autonomous and mTOR complex 1 (mTORC1)-independent, and involves multiple mechanisms converging on mitochondrial apoptosis and possibly downregulation of PGC-1 coactivators and their transcriptional network, which have critical roles in mitochondrial biogenesis and function. Thus, Lkb1 serves as an essential regulator of HSCs and haematopoiesis, and more generally, points to the critical importance of coupling energy metabolism and stem-cell homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058342/" 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/PMC3058342/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gan, Boyi -- Hu, Jian -- Jiang, Shan -- Liu, Yingchun -- Sahin, Ergun -- Zhuang, Li -- Fletcher-Sananikone, Eliot -- Colla, Simona -- Wang, Y Alan -- Chin, Lynda -- Depinho, Ronald A -- 01CA141508/CA/NCI NIH HHS/ -- R21 CA135057/CA/NCI NIH HHS/ -- R21 CA135057-01/CA/NCI NIH HHS/ -- R21CA135057/CA/NCI NIH HHS/ -- U01 CA141508/CA/NCI NIH HHS/ -- U01 CA141508-01/CA/NCI NIH HHS/ -- England -- Nature. 2010 Dec 2;468(7324):701-4. doi: 10.1038/nature09595.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21124456" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Cycle/*physiology ; Cell Proliferation ; Cell Survival ; *Energy Metabolism ; Female ; Gene Deletion ; Hematopoiesis ; Hematopoietic Stem Cells/*cytology/*metabolism/pathology ; *Homeostasis ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondria/metabolism/pathology ; Multiprotein Complexes ; Pancytopenia/genetics ; Phenotype ; Protein-Serine-Threonine Kinases/deficiency/genetics/*metabolism ; Proteins/metabolism ; Survival Analysis ; TOR Serine-Threonine Kinases ; Transcription Factors/metabolism
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  • 2
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    High-speed graphene transistors with a self-aligned nanowire gate (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-09-03
    Description: Graphene has attracted considerable interest as a potential new electronic material. With its high carrier mobility, graphene is of particular interest for ultrahigh-speed radio-frequency electronics. However, conventional device fabrication processes cannot readily be applied to produce high-speed graphene transistors because they often introduce significant defects into the monolayer of carbon lattices and severely degrade the device performance. Here we report an approach to the fabrication of high-speed graphene transistors with a self-aligned nanowire gate to prevent such degradation. A Co(2)Si-Al(2)O(3) core-shell nanowire is used as the gate, with the source and drain electrodes defined through a self-alignment process and the channel length defined by the nanowire diameter. The physical assembly of the nanowire gate preserves the high carrier mobility in graphene, and the self-alignment process ensures that the edges of the source, drain and gate electrodes are automatically and precisely positioned so that no overlapping or significant gaps exist between these electrodes, thus minimizing access resistance. It therefore allows for transistor performance not previously possible. Graphene transistors with a channel length as low as 140 nm have been fabricated with the highest scaled on-current (3.32 mA mum(-1)) and transconductance (1.27 mS mum(-1)) reported so far. Significantly, on-chip microwave measurements demonstrate that the self-aligned devices have a high intrinsic cut-off (transit) frequency of f(T) = 100-300 GHz, with the extrinsic f(T) (in the range of a few gigahertz) largely limited by parasitic pad capacitance. The reported intrinsic f(T) of the graphene transistors is comparable to that of the very best high-electron-mobility transistors with similar gate lengths.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2965636/" 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/PMC2965636/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liao, Lei -- Lin, Yung-Chen -- Bao, Mingqiang -- Cheng, Rui -- Bai, Jingwei -- Liu, Yuan -- Qu, Yongquan -- Wang, Kang L -- Huang, Yu -- Duan, Xiangfeng -- 1DP2OD004342-01/OD/NIH HHS/ -- DP2 OD004342-01/OD/NIH HHS/ -- England -- Nature. 2010 Sep 16;467(7313):305-8. doi: 10.1038/nature09405. Epub 2010 Sep 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, University of California, Los Angeles, California 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20811365" target="_blank"〉PubMed〈/a〉
    Keywords: Calibration ; Carbon/*chemistry ; Electric Capacitance ; Electrodes ; Electronics/*instrumentation ; Nanowires/*chemistry/ultrastructure ; Temperature ; *Transistors, Electronic
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  • 3
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    Lunar apatite with terrestrial volatile abundances (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-07-24
    Description: The Moon is thought to be depleted relative to the Earth in volatile elements such as H, Cl and the alkalis. Nevertheless, evidence for lunar explosive volcanism has been used to infer that some lunar magmas exsolved a CO-rich and CO(2)-rich vapour phase before or during eruption. Although there is also evidence for other volatile species on glass spherules, until recently there had been no unambiguous reports of indigenous H in lunar rocks. Here we report quantitative ion microprobe measurements of late-stage apatite from lunar basalt 14053 that document concentrations of H, Cl and S that are indistinguishable from apatites in common terrestrial igneous rocks. These volatile contents could reflect post-magmatic metamorphic volatile addition or growth from a late-stage, interstitial, sulphide-saturated melt that contained approximately 1,600 parts per million H(2)O and approximately 3,500 parts per million Cl. Both metamorphic and igneous models of apatite formation suggest a volatile inventory for at least some lunar materials that is similar to comparable terrestrial materials. One possible implication is that portions of the lunar mantle or crust are more volatile-rich than previously thought.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boyce, Jeremy W -- Liu, Yang -- Rossman, George R -- Guan, Yunbin -- Eiler, John M -- Stolper, Edward M -- Taylor, Lawrence A -- England -- Nature. 2010 Jul 22;466(7305):466-9. doi: 10.1038/nature09274.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Geological and Planetary Sciences, California Institute of Technology, Pasadena, California 91125-2500, USA. jwboyce@alum.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20651686" target="_blank"〉PubMed〈/a〉
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  • 4
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    The complete genome of an individual by massively parallel DNA sequencing (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-04-19
    Description: The association of genetic variation with disease and drug response, and improvements in nucleic acid technologies, have given great optimism for the impact of 'genomic medicine'. However, the formidable size of the diploid human genome, approximately 6 gigabases, has prevented the routine application of sequencing methods to deciphering complete individual human genomes. To realize the full potential of genomics for human health, this limitation must be overcome. Here we report the DNA sequence of a diploid genome of a single individual, James D. Watson, sequenced to 7.4-fold redundancy in two months using massively parallel sequencing in picolitre-size reaction vessels. This sequence was completed in two months at approximately one-hundredth of the cost of traditional capillary electrophoresis methods. Comparison of the sequence to the reference genome led to the identification of 3.3 million single nucleotide polymorphisms, of which 10,654 cause amino-acid substitution within the coding sequence. In addition, we accurately identified small-scale (2-40,000 base pair (bp)) insertion and deletion polymorphism as well as copy number variation resulting in the large-scale gain and loss of chromosomal segments ranging from 26,000 to 1.5 million base pairs. Overall, these results agree well with recent results of sequencing of a single individual by traditional methods. However, in addition to being faster and significantly less expensive, this sequencing technology avoids the arbitrary loss of genomic sequences inherent in random shotgun sequencing by bacterial cloning because it amplifies DNA in a cell-free system. As a result, we further demonstrate the acquisition of novel human sequence, including novel genes not previously identified by traditional genomic sequencing. This is the first genome sequenced by next-generation technologies. Therefore it is a pilot for the future challenges of 'personalized genome sequencing'.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wheeler, David A -- Srinivasan, Maithreyan -- Egholm, Michael -- Shen, Yufeng -- Chen, Lei -- McGuire, Amy -- He, Wen -- Chen, Yi-Ju -- Makhijani, Vinod -- Roth, G Thomas -- Gomes, Xavier -- Tartaro, Karrie -- Niazi, Faheem -- Turcotte, Cynthia L -- Irzyk, Gerard P -- Lupski, James R -- Chinault, Craig -- Song, Xing-zhi -- Liu, Yue -- Yuan, Ye -- Nazareth, Lynne -- Qin, Xiang -- Muzny, Donna M -- Margulies, Marcel -- Weinstock, George M -- Gibbs, Richard A -- Rothberg, Jonathan M -- U54 HG003273/HG/NHGRI NIH HHS/ -- England -- Nature. 2008 Apr 17;452(7189):872-6. doi: 10.1038/nature06884.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genome Sequencing Center, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18421352" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Computational Biology ; Genetic Predisposition to Disease/genetics ; Genetic Variation/*genetics ; Genome, Human/*genetics ; Genomics/economics/*methods/trends ; Genotype ; Humans ; Individuality ; Male ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Single Nucleotide/genetics ; Reproducibility of Results ; Sensitivity and Specificity ; Sequence Alignment ; Sequence Analysis, DNA/economics/*methods ; Software
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  • 5
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    The genome of the model beetle and pest Tribolium castaneum (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-03-26
    Description: Tribolium castaneum is a member of the most species-rich eukaryotic order, a powerful model organism for the study of generalized insect development, and an important pest of stored agricultural products. We describe its genome sequence here. This omnivorous beetle has evolved the ability to interact with a diverse chemical environment, as shown by large expansions in odorant and gustatory receptors, as well as P450 and other detoxification enzymes. Development in Tribolium is more representative of other insects than is Drosophila, a fact reflected in gene content and function. For example, Tribolium has retained more ancestral genes involved in cell-cell communication than Drosophila, some being expressed in the growth zone crucial for axial elongation in short-germ development. Systemic RNA interference in T. castaneum functions differently from that in Caenorhabditis elegans, but nevertheless offers similar power for the elucidation of gene function and identification of targets for selective insect control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tribolium Genome Sequencing Consortium -- Richards, Stephen -- Gibbs, Richard A -- Weinstock, George M -- Brown, Susan J -- Denell, Robin -- Beeman, Richard W -- Gibbs, Richard -- Bucher, Gregor -- Friedrich, Markus -- Grimmelikhuijzen, Cornelis J P -- Klingler, Martin -- Lorenzen, Marce -- Roth, Siegfried -- Schroder, Reinhard -- Tautz, Diethard -- Zdobnov, Evgeny M -- Muzny, Donna -- Attaway, Tony -- Bell, Stephanie -- Buhay, Christian J -- Chandrabose, Mimi N -- Chavez, Dean -- Clerk-Blankenburg, Kerstin P -- Cree, Andrew -- Dao, Marvin -- Davis, Clay -- Chacko, Joseph -- Dinh, Huyen -- Dugan-Rocha, Shannon -- Fowler, Gerald -- Garner, Toni T -- Garnes, Jeffrey -- Gnirke, Andreas -- Hawes, Alica -- Hernandez, Judith -- Hines, Sandra -- Holder, Michael -- Hume, Jennifer -- Jhangiani, Shalini N -- Joshi, Vandita -- Khan, Ziad Mohid -- Jackson, LaRonda -- Kovar, Christie -- Kowis, Andrea -- Lee, Sandra -- Lewis, Lora R -- Margolis, Jon -- Morgan, Margaret -- Nazareth, Lynne V -- Nguyen, Ngoc -- Okwuonu, Geoffrey -- Parker, David -- Ruiz, San-Juana -- Santibanez, Jireh -- Savard, Joel -- Scherer, Steven E -- Schneider, Brian -- Sodergren, Erica -- Vattahil, Selina -- Villasana, Donna -- White, Courtney S -- Wright, Rita -- Park, Yoonseong -- Lord, Jeff -- Oppert, Brenda -- Brown, Susan -- Wang, Liangjiang -- Weinstock, George -- Liu, Yue -- Worley, Kim -- Elsik, Christine G -- Reese, Justin T -- Elhaik, Eran -- Landan, Giddy -- Graur, Dan -- Arensburger, Peter -- Atkinson, Peter -- Beidler, Jim -- Demuth, Jeffery P -- Drury, Douglas W -- Du, Yu-Zhou -- Fujiwara, Haruhiko -- Maselli, Vincenza -- Osanai, Mizuko -- Robertson, Hugh M -- Tu, Zhijian -- Wang, Jian-jun -- Wang, Suzhi -- Song, Henry -- Zhang, Lan -- Werner, Doreen -- Stanke, Mario -- Morgenstern, Burkhard -- Solovyev, Victor -- Kosarev, Peter -- Brown, Garth -- Chen, Hsiu-Chuan -- Ermolaeva, Olga -- Hlavina, Wratko -- Kapustin, Yuri -- Kiryutin, Boris -- Kitts, Paul -- Maglott, Donna -- Pruitt, Kim -- Sapojnikov, Victor -- Souvorov, Alexandre -- Mackey, Aaron J -- Waterhouse, Robert M -- Wyder, Stefan -- Kriventseva, Evgenia V -- Kadowaki, Tatsuhiko -- Bork, Peer -- Aranda, Manuel -- Bao, Riyue -- Beermann, Anke -- Berns, Nicola -- Bolognesi, Renata -- Bonneton, Francois -- Bopp, Daniel -- Butts, Thomas -- Chaumot, Arnaud -- Denell, Robin E -- Ferrier, David E K -- Gordon, Cassondra M -- Jindra, Marek -- Lan, Que -- Lattorff, H Michael G -- Laudet, Vincent -- von Levetsow, Cornelia -- Liu, Zhenyi -- Lutz, Rebekka -- Lynch, Jeremy A -- da Fonseca, Rodrigo Nunes -- Posnien, Nico -- Reuter, Rolf -- Schinko, Johannes B -- Schmitt, Christian -- Schoppmeier, Michael -- Shippy, Teresa D -- Simonnet, Franck -- Marques-Souza, Henrique -- Tomoyasu, Yoshinori -- Trauner, Jochen -- Van der Zee, Maurijn -- Vervoort, Michel -- Wittkopp, Nadine -- Wimmer, Ernst A -- Yang, Xiaoyun -- Jones, Andrew K -- Sattelle, David B -- Ebert, Paul R -- Nelson, David -- Scott, Jeffrey G -- Muthukrishnan, Subbaratnam -- Kramer, Karl J -- Arakane, Yasuyuki -- Zhu, Qingsong -- Hogenkamp, David -- Dixit, Radhika -- Jiang, Haobo -- Zou, Zhen -- Marshall, Jeremy -- Elpidina, Elena -- Vinokurov, Konstantin -- Oppert, Cris -- Evans, Jay -- Lu, Zhiqiang -- Zhao, Picheng -- Sumathipala, Niranji -- Altincicek, Boran -- Vilcinskas, Andreas -- Williams, Michael -- Hultmark, Dan -- Hetru, Charles -- Hauser, Frank -- Cazzamali, Giuseppe -- Williamson, Michael -- Li, Bin -- Tanaka, Yoshiaki -- Predel, Reinhard -- Neupert, Susanne -- Schachtner, Joachim -- Verleyen, Peter -- Raible, Florian -- Walden, Kimberly K O -- Angeli, Sergio -- Foret, Sylvain -- Schuetz, Stefan -- Maleszka, Ryszard -- Miller, Sherry C -- Grossmann, Daniela -- BBS/B/12067/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBS/B/12067/2/Biotechnology and Biological Sciences Research Council/United Kingdom -- R01 GM058634/GM/NIGMS NIH HHS/ -- R01 HD029594/HD/NICHD NIH HHS/ -- R01 HD029594-16/HD/NICHD NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- Intramural NIH HHS/ -- England -- Nature. 2008 Apr 24;452(7190):949-55. doi: 10.1038/nature06784. Epub 2008 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genome Sequencing Center, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA. stephenr@bcm.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18362917" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Composition ; Body Patterning/genetics ; Cytochrome P-450 Enzyme System/genetics ; DNA Transposable Elements/genetics ; Genes, Insect/*genetics ; Genome, Insect/*genetics ; Growth and Development/genetics ; Humans ; Insecticides/pharmacology ; Neurotransmitter Agents/genetics ; Oogenesis/genetics ; Phylogeny ; Proteome/genetics ; RNA Interference ; Receptors, G-Protein-Coupled/genetics ; Receptors, Odorant/genetics ; Repetitive Sequences, Nucleic Acid/genetics ; Taste/genetics ; Telomere/genetics ; Tribolium/classification/embryology/*genetics/physiology ; Vision, Ocular/genetics
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  • 6
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    A key role for autophagy and the autophagy gene Atg16l1 in mouse and human intestinal Paneth cells (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-10-14
    Description: Susceptibility to Crohn's disease, a complex inflammatory disease involving the small intestine, is controlled by over 30 loci. One Crohn's disease risk allele is in ATG16L1, a gene homologous to the essential yeast autophagy gene ATG16 (ref. 2). It is not known how ATG16L1 or autophagy contributes to intestinal biology or Crohn's disease pathogenesis. To address these questions, we generated and characterized mice that are hypomorphic for ATG16L1 protein expression, and validated conclusions on the basis of studies in these mice by analysing intestinal tissues that we collected from Crohn's disease patients carrying the Crohn's disease risk allele of ATG16L1. Here we show that ATG16L1 is a bona fide autophagy protein. Within the ileal epithelium, both ATG16L1 and a second essential autophagy protein ATG5 are selectively important for the biology of the Paneth cell, a specialized epithelial cell that functions in part by secretion of granule contents containing antimicrobial peptides and other proteins that alter the intestinal environment. ATG16L1- and ATG5-deficient Paneth cells exhibited notable abnormalities in the granule exocytosis pathway. In addition, transcriptional analysis revealed an unexpected gain of function specific to ATG16L1-deficient Paneth cells including increased expression of genes involved in peroxisome proliferator-activated receptor (PPAR) signalling and lipid metabolism, of acute phase reactants and of two adipocytokines, leptin and adiponectin, known to directly influence intestinal injury responses. Importantly, Crohn's disease patients homozygous for the ATG16L1 Crohn's disease risk allele displayed Paneth cell granule abnormalities similar to those observed in autophagy-protein-deficient mice and expressed increased levels of leptin protein. Thus, ATG16L1, and probably the process of autophagy, have a role within the intestinal epithelium of mice and Crohn's disease patients by selective effects on the cell biology and specialized regulatory properties of Paneth cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2695978/" 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/PMC2695978/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cadwell, Ken -- Liu, John Y -- Brown, Sarah L -- Miyoshi, Hiroyuki -- Loh, Joy -- Lennerz, Jochen K -- Kishi, Chieko -- Kc, Wumesh -- Carrero, Javier A -- Hunt, Steven -- Stone, Christian D -- Brunt, Elizabeth M -- Xavier, Ramnik J -- Sleckman, Barry P -- Li, Ellen -- Mizushima, Noboru -- Stappenbeck, Thaddeus S -- Virgin, Herbert W 4th -- AI062773/AI/NIAID NIH HHS/ -- DK43351/DK/NIDDK NIH HHS/ -- P30 DK040561/DK/NIDDK NIH HHS/ -- P30 DK040561-13/DK/NIDDK NIH HHS/ -- P30 DK043351/DK/NIDDK NIH HHS/ -- P30 DK043351-18/DK/NIDDK NIH HHS/ -- P30 DK052574-09/DK/NIDDK NIH HHS/ -- P30 DK52574/DK/NIDDK NIH HHS/ -- R01 AI062773/AI/NIAID NIH HHS/ -- R01 AI062773-01A1/AI/NIAID NIH HHS/ -- R01 AI062832/AI/NIAID NIH HHS/ -- R01 AI062832-04/AI/NIAID NIH HHS/ -- T32 AR007279/AR/NIAMS NIH HHS/ -- T32 AR007279-30/AR/NIAMS NIH HHS/ -- T32 AR07279/AR/NIAMS NIH HHS/ -- U54 AI057160/AI/NIAID NIH HHS/ -- U54 AI057160-010005/AI/NIAID NIH HHS/ -- U54 AI057160-05S10018/AI/NIAID NIH HHS/ -- England -- Nature. 2008 Nov 13;456(7219):259-63. doi: 10.1038/nature07416. Epub 2008 Oct 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18849966" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Autophagy/*genetics ; Carrier Proteins/genetics/*metabolism ; Cell Line ; Crohn Disease/genetics/pathology ; Exocytosis/genetics ; Homozygote ; Humans ; Mice ; Mice, Inbred C57BL ; Mutation ; Paneth Cells/*metabolism/pathology
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  • 7
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    Crystal structure of the polymerase PA(C)-PB1(N) complex from an avian influenza H5N1 virus (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-07-11
    Description: The recent emergence of highly pathogenic avian influenza A virus strains with subtype H5N1 pose a global threat to human health. Elucidation of the underlying mechanisms of viral replication is critical for development of anti-influenza virus drugs. The influenza RNA-dependent RNA polymerase (RdRp) heterotrimer has crucial roles in viral RNA replication and transcription. It contains three proteins: PA, PB1 and PB2. PB1 harbours polymerase and endonuclease activities and PB2 is responsible for cap binding; PA is implicated in RNA replication and proteolytic activity, although its function is less clearly defined. Here we report the 2.9 angstrom structure of avian H5N1 influenza A virus PA (PA(C), residues 257-716) in complex with the PA-binding region of PB1 (PB1(N), residues 1-25). PA(C) has a fold resembling a dragon's head with PB1(N) clamped into its open 'jaws'. PB1(N) is a known inhibitor that blocks assembly of the polymerase heterotrimer and abolishes viral replication. Our structure provides details for the binding of PB1(N) to PA(C) at the atomic level, demonstrating a potential target for novel anti-influenza therapeutics. We also discuss a potential nucleotide binding site and the roles of some known residues involved in polymerase activity. Furthermore, to explore the role of PA in viral replication and transcription, we propose a model for the influenza RdRp heterotrimer by comparing PA(C) with the lambda3 reovirus polymerase structure, and docking the PA(C) structure into an available low resolution electron microscopy map.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, Xiaojing -- Zhou, Jie -- Bartlam, Mark -- Zhang, Rongguang -- Ma, Jianyuan -- Lou, Zhiyong -- Li, Xuemei -- Li, Jingjing -- Joachimiak, Andrzej -- Zeng, Zonghao -- Ge, Ruowen -- Rao, Zihe -- Liu, Yingfang -- England -- Nature. 2008 Aug 28;454(7208):1123-6. doi: 10.1038/nature07120. Epub 2008 Jul 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18615018" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Birds/*virology ; Crystallography, X-Ray ; Influenza A Virus, H5N1 Subtype/*enzymology ; Models, Molecular ; Multienzyme Complexes/chemistry/metabolism ; Nucleotides/metabolism ; Peptide Fragments/chemistry/metabolism ; Protein Binding ; Protein Structure, Quaternary ; RNA Replicase/*chemistry/metabolism ; Viral Proteins/*chemistry/*metabolism ; Virus Replication
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  • 8
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    The zinc-finger protein Zelda is a key activator of the early zygotic genome in Drosophila (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-10-22
    Description: In all animals, the initial events of embryogenesis are controlled by maternal gene products that are deposited into the developing oocyte. At some point after fertilization, control of embryogenesis is transferred to the zygotic genome in a process called the maternal-to-zygotic transition. During this time, many maternal RNAs are degraded and transcription of zygotic RNAs ensues. There is a long-standing question as to which factors regulate these events. The recent findings that microRNAs and Smaug mediate maternal transcript degradation have shed new light on this aspect of the problem. However, the transcription factor(s) that activate the zygotic genome remain elusive. The discovery that many of the early transcribed genes in Drosophila share a cis-regulatory heptamer motif, CAGGTAG and related sequences, collectively referred to as TAGteam sites raised the possibility that a dedicated transcription factor could interact with these sites to activate transcription. Here we report that the zinc-finger protein Zelda (Zld; Zinc-finger early Drosophila activator) binds specifically to these sites and is capable of activating transcription in transient transfection assays. Mutant embryos lacking zld are defective in cellular blastoderm formation, and fail to activate many genes essential for cellularization, sex determination and pattern formation. Global expression profiling confirmed that Zld has an important role in the activation of the early zygotic genome and suggests that Zld may also regulate maternal RNA degradation during the maternal-to-zygotic transition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597674/" 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/PMC2597674/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liang, Hsiao-Lan -- Nien, Chung-Yi -- Liu, Hsiao-Yun -- Metzstein, Mark M -- Kirov, Nikolai -- Rushlow, Christine -- GM63024/GM/NIGMS NIH HHS/ -- R01 GM063024/GM/NIGMS NIH HHS/ -- R01 GM063024-01A1/GM/NIGMS NIH HHS/ -- R01 GM063024-02/GM/NIGMS NIH HHS/ -- R01 GM063024-03/GM/NIGMS NIH HHS/ -- R01 GM063024-04/GM/NIGMS NIH HHS/ -- R01 GM063024-05/GM/NIGMS NIH HHS/ -- England -- Nature. 2008 Nov 20;456(7220):400-3. doi: 10.1038/nature07388. Epub 2008 Oct 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, New York University, 100 Washington Square East, New York, New York 10003, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18931655" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastoderm/cytology/embryology/metabolism ; Body Patterning/genetics ; Drosophila Proteins/deficiency/genetics/*metabolism ; Drosophila melanogaster/cytology/*embryology/*genetics ; Female ; Gene Deletion ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Genome, Insect/*genetics ; Male ; RNA Stability ; RNA, Messenger, Stored/genetics/metabolism ; Sex Determination Processes ; Transcription Factors/deficiency/genetics/*metabolism ; Transcriptional Activation ; *Zinc Fingers ; Zygote/cytology/growth & development/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Difference in direct charge-parity violation between charged and neutral B meson decays (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-03-21
    Description: Equal amounts of matter and antimatter are predicted to have been produced in the Big Bang, but our observable Universe is clearly matter-dominated. One of the prerequisites for understanding this elimination of antimatter is the nonconservation of charge-parity (CP) symmetry. So far, two types of CP violation have been observed in the neutral K meson (K(0)) and B meson (B(0)) systems: CP violation involving the mixing between K(0) and its antiparticle (and likewise for B(0) and ), and direct CP violation in the decay of each meson. The observed effects for both types of CP violation are substantially larger for the B(0) meson system. However, they are still consistent with the standard model of particle physics, which has a unique source of CP violation that is known to be too small to account for the matter-dominated Universe. Here we report that the direct CP violation in charged B(+/-)--〉K(+/-)pi(0) decay is different from that in the neutral B(0) counterpart. The direct CP-violating decay rate asymmetry, (that is, the difference between the number of observed B(-)--〉K(-)pi(0) event versus B(+)--〉K(+) pi(0) events, normalized to the sum of these events) is measured to be about +7%, with an uncertainty that is reduced by a factor of 1.7 from a previous measurement. However, the asymmetry for versus B(0)--〉K(+)pi(-) is at the -10% level. Although it is susceptible to strong interaction effects that need further clarification, this large deviation in direct CP violation between charged and neutral B meson decays could be an indication of new sources of CP violation-which would help to explain the dominance of matter in the Universe.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Belle Collaboration -- Lin, S-W -- Unno, Y -- Hou, W-S -- Chang, P -- Adachi, I -- Aihara, H -- Akai, K -- Arinstein, K -- Aulchenko, V -- Aushev, T -- Aziz, T -- Bakich, A M -- Balagura, V -- Barberio, E -- Bay, A -- Bedny, I -- Bitenc, U -- Bondar, A -- Bozek, A -- Bracko, M -- Browder, T E -- Chang, M-C -- Chao, Y -- Chen, A -- Chen, K-F -- Chen, W T -- Cheon, B G -- Chiang, C-C -- Chistov, R -- Cho, I-S -- Choi, S-K -- Choi, Y -- Choi, Y K -- Cole, S -- Dalseno, J -- Danilov, M -- Dash, M -- Drutskoy, A -- Eidelman, S -- Epifanov, D -- Fratina, S -- Fujikawa, M -- Furukawa, K -- Gabyshev, N -- Goldenzweig, P -- Golob, B -- Ha, H -- Haba, J -- Hara, T -- Hayasaka, K -- Hayashii, H -- Hazumi, M -- Heffernan, D -- Hokuue, T -- Hoshi, Y -- Hsiung, Y B -- Hyun, H J -- Iijima, T -- Ikado, K -- Inami, K -- Ishikawa, A -- Ishino, H -- Itoh, R -- Iwabuchi, M -- Iwasaki, M -- Iwasaki, Y -- Kah, D H -- Kaji, H -- Kataoka, S U -- Kawai, H -- Kawasaki, T -- Kibayashi, A -- Kichimi, H -- Kikutani, E -- Kim, H J -- Kim, S K -- Kim, Y J -- Kinoshita, K -- Korpar, S -- Kozakai, Y -- Krizan, P -- Krokovny, P -- Kumar, R -- Kuo, C C -- Kuzmin, A -- Kwon, Y-J -- Lee, M J -- Lee, S E -- Lesiak, T -- Li, J -- Liu, Y -- Liventsev, D -- Mandl, F -- Marlow, D -- McOnie, S -- Medvedeva, T -- Mimashi, T -- Mitaroff, W -- Miyabayashi, K -- Miyake, H -- Miyazaki, Y -- Mizuk, R -- Mori, T -- Nakamura, T T -- Nakano, E -- Nakao, M -- Nakazawa, H -- Nishida, S -- Nitoh, O -- Noguchi, S -- Nozaki, T -- Ogawa, S -- Ogawa, Y -- Ohshima, T -- Okuno, S -- Olsen, S L -- Ozaki, H -- Pakhlova, G -- Park, C W -- Park, H -- Peak, L S -- Pestotnik, R -- Peters, M -- Piilonen, L E -- Poluektov, A -- Sahoo, H -- Sakai, Y -- Schneider, O -- Schumann, J -- Schwartz, A J -- Seidl, R -- Senyo, K -- Sevior, M E -- Shapkin, M -- Shen, C P -- Shibuya, H -- Shidara, T -- Shinomiya, S -- Shiu, J-G -- Shwartz, B -- Singh, J B -- Sokolov, A -- Somov, A -- Stanic, S -- Staric, M -- Sumisawa, K -- Sumiyoshi, T -- Suzuki, S -- Tajima, O -- Takasaki, F -- Tamura, N -- Tanaka, M -- Tawada, M -- Taylor, G N -- Teramoto, Y -- Tikhomirov, I -- Trabelsi, K -- Uehara, S -- Ueno, K -- Uglov, T -- Uno, S -- Urquijo, P -- Ushiroda, Y -- Usov, Y -- Varner, G -- Varvell, K E -- Vervink, K -- Villa, S -- Wang, C C -- Wang, C H -- Wang, M-Z -- Watanabe, Y -- Wedd, R -- Wicht, J -- Won, E -- Yabsley, B D -- Yamaguchi, A -- Yamashita, Y -- Yamauchi, M -- Yoshida, M -- Yuan, C Z -- Yusa, Y -- Zhang, C C -- Zhang, Z P -- Zhilich, V -- Zhulanov, V -- Zupanc, A -- England -- Nature. 2008 Mar 20;452(7185):332-5. doi: 10.1038/nature06827.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physics, National Taiwan University, Taipei, 106, Taiwan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18354478" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
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    A fasting inducible switch modulates gluconeogenesis via activator/coactivator exchange (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-10-14
    Description: During early fasting, increases in skeletal muscle proteolysis liberate free amino acids for hepatic gluconeogenesis in response to pancreatic glucagon. Hepatic glucose output diminishes during the late protein-sparing phase of fasting, when ketone body production by the liver supplies compensatory fuel for glucose-dependent tissues. Glucagon stimulates the gluconeogenic program by triggering the dephosphorylation and nuclear translocation of the CREB regulated transcription coactivator 2 (CRTC2; also known as TORC2), while parallel decreases in insulin signalling augment gluconeogenic gene expression through the dephosphorylation and nuclear shuttling of forkhead box O1 (FOXO1). Here we show that a fasting-inducible switch, consisting of the histone acetyltransferase p300 and the nutrient-sensing deacetylase sirtuin 1 (SIRT1), maintains energy balance in mice through the sequential induction of CRTC2 and FOXO1. After glucagon induction, CRTC2 stimulated gluconeogenic gene expression by an association with p300, which we show here is also activated by dephosphorylation at Ser 89 during fasting. In turn, p300 increased hepatic CRTC2 activity by acetylating it at Lys 628, a site that also targets CRTC2 for degradation after its ubiquitination by the E3 ligase constitutive photomorphogenic protein (COP1). Glucagon effects were attenuated during late fasting, when CRTC2 was downregulated owing to SIRT1-mediated deacetylation and when FOXO1 supported expression of the gluconeogenic program. Disrupting SIRT1 activity, by liver-specific knockout of the Sirt1 gene or by administration of a SIRT1 antagonist, increased CRTC2 activity and glucose output, whereas exposure to SIRT1 agonists reduced them. In view of the reciprocal activation of FOXO1 and its coactivator peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha, encoded by Ppargc1a) by SIRT1 activators, our results illustrate how the exchange of two gluconeogenic regulators during fasting maintains energy balance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597669/" 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/PMC2597669/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Yi -- Dentin, Renaud -- Chen, Danica -- Hedrick, Susan -- Ravnskjaer, Kim -- Schenk, Simon -- Milne, Jill -- Meyers, David J -- Cole, Phil -- Yates, John 3rd -- Olefsky, Jerrold -- Guarente, Leonard -- Montminy, Marc -- R37 GM037828/GM/NIGMS NIH HHS/ -- R37 GM037828-24/GM/NIGMS NIH HHS/ -- England -- Nature. 2008 Nov 13;456(7219):269-73. doi: 10.1038/nature07349. Epub 2008 Oct 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Salk Institute for Biological Studies, 10010 North Torrey Pines Rd, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18849969" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; CREB-Binding Protein/metabolism ; Cell Line, Transformed ; Cyclic AMP Response Element-Binding Protein/metabolism ; Enzyme Inhibitors/pharmacology ; Fasting/*physiology ; Forkhead Transcription Factors/metabolism ; Gene Expression Regulation/drug effects ; Gluconeogenesis/*physiology ; Heterocyclic Compounds with 4 or More Rings/pharmacology ; Humans ; Liver/metabolism ; Male ; Mice ; Mice, Knockout ; Nuclear Proteins/metabolism ; Sirtuin 1 ; Sirtuins/genetics/metabolism ; Stilbenes/pharmacology ; Trans-Activators/metabolism ; Transcription Factors ; Ubiquitin-Protein Ligases/metabolism ; p300-CBP Transcription Factors/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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