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  • 1
    Publication Date: 2000-03-25
    Description: The fly Drosophila melanogaster is one of the most intensively studied organisms in biology and serves as a model system for the investigation of many developmental and cellular processes common to higher eukaryotes, including humans. We have determined the nucleotide sequence of nearly all of the approximately 120-megabase euchromatic portion of the Drosophila genome using a whole-genome shotgun sequencing strategy supported by extensive clone-based sequence and a high-quality bacterial artificial chromosome physical map. Efforts are under way to close the remaining gaps; however, the sequence is of sufficient accuracy and contiguity to be declared substantially complete and to support an initial analysis of genome structure and preliminary gene annotation and interpretation. The genome encodes approximately 13,600 genes, somewhat fewer than the smaller Caenorhabditis elegans genome, but with comparable functional diversity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Adams, M D -- Celniker, S E -- Holt, R A -- Evans, C A -- Gocayne, J D -- Amanatides, P G -- Scherer, S E -- Li, P W -- Hoskins, R A -- Galle, R F -- George, R A -- Lewis, S E -- Richards, S -- Ashburner, M -- Henderson, S N -- Sutton, G G -- Wortman, J R -- Yandell, M D -- Zhang, Q -- Chen, L X -- Brandon, R C -- Rogers, Y H -- Blazej, R G -- Champe, M -- Pfeiffer, B D -- Wan, K H -- Doyle, C -- Baxter, E G -- Helt, G -- Nelson, C R -- Gabor, G L -- Abril, J F -- Agbayani, A -- An, H J -- Andrews-Pfannkoch, C -- Baldwin, D -- Ballew, R M -- Basu, A -- Baxendale, J -- Bayraktaroglu, L -- Beasley, E M -- Beeson, K Y -- Benos, P V -- Berman, B P -- Bhandari, D -- Bolshakov, S -- Borkova, D -- Botchan, M R -- Bouck, J -- Brokstein, P -- Brottier, P -- Burtis, K C -- Busam, D A -- Butler, H -- Cadieu, E -- Center, A -- Chandra, I -- Cherry, J M -- Cawley, S -- Dahlke, C -- Davenport, L B -- Davies, P -- de Pablos, B -- Delcher, A -- Deng, Z -- Mays, A D -- Dew, I -- Dietz, S M -- Dodson, K -- Doup, L E -- Downes, M -- Dugan-Rocha, S -- Dunkov, B C -- Dunn, P -- Durbin, K J -- Evangelista, C C -- Ferraz, C -- Ferriera, S -- Fleischmann, W -- Fosler, C -- Gabrielian, A E -- Garg, N S -- Gelbart, W M -- Glasser, K -- Glodek, A -- Gong, F -- Gorrell, J H -- Gu, Z -- Guan, P -- Harris, M -- Harris, N L -- Harvey, D -- Heiman, T J -- Hernandez, J R -- Houck, J -- Hostin, D -- Houston, K A -- Howland, T J -- Wei, M H -- Ibegwam, C -- Jalali, M -- Kalush, F -- Karpen, G H -- Ke, Z -- Kennison, J A -- Ketchum, K A -- Kimmel, B E -- Kodira, C D -- Kraft, C -- Kravitz, S -- Kulp, D -- Lai, Z -- Lasko, P -- Lei, Y -- Levitsky, A A -- Li, J -- Li, Z -- Liang, Y -- Lin, X -- Liu, X -- Mattei, B -- McIntosh, T C -- McLeod, M P -- McPherson, D -- Merkulov, G -- Milshina, N V -- Mobarry, C -- Morris, J -- Moshrefi, A -- Mount, S M -- Moy, M -- Murphy, B -- Murphy, L -- Muzny, D M -- Nelson, D L -- Nelson, D R -- Nelson, K A -- Nixon, K -- Nusskern, D R -- Pacleb, J M -- Palazzolo, M -- Pittman, G S -- Pan, S -- Pollard, J -- Puri, V -- Reese, M G -- Reinert, K -- Remington, K -- Saunders, R D -- Scheeler, F -- Shen, H -- Shue, B C -- Siden-Kiamos, I -- Simpson, M -- Skupski, M P -- Smith, T -- Spier, E -- Spradling, A C -- Stapleton, M -- Strong, R -- Sun, E -- Svirskas, R -- Tector, C -- Turner, R -- Venter, E -- Wang, A H -- Wang, X -- Wang, Z Y -- Wassarman, D A -- Weinstock, G M -- Weissenbach, J -- Williams, S M -- WoodageT -- Worley, K C -- Wu, D -- Yang, S -- Yao, Q A -- Ye, J -- Yeh, R F -- Zaveri, J S -- Zhan, M -- Zhang, G -- Zhao, Q -- Zheng, L -- Zheng, X H -- Zhong, F N -- Zhong, W -- Zhou, X -- Zhu, S -- Zhu, X -- Smith, H O -- Gibbs, R A -- Myers, E W -- Rubin, G M -- Venter, J C -- P50-HG00750/HG/NHGRI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2000 Mar 24;287(5461):2185-95.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Celera Genomics, 45 West Gude Drive, Rockville, MD 20850, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10731132" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport/genetics ; Chromatin/genetics ; Cloning, Molecular ; Computational Biology ; Contig Mapping ; Cytochrome P-450 Enzyme System/genetics ; DNA Repair/genetics ; DNA Replication/genetics ; Drosophila melanogaster/*genetics/metabolism ; Euchromatin ; Gene Library ; Genes, Insect ; *Genome ; Heterochromatin/genetics ; Insect Proteins/chemistry/genetics/physiology ; Nuclear Proteins/genetics ; Protein Biosynthesis ; *Sequence Analysis, DNA ; Transcription, Genetic
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    Electronic ISSN: 1095-9203
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  • 2
    Publication Date: 2000-03-24
    Description: One of the rewards of having a Drosophila melanogaster whole-genome sequence will be the potential to understand the molecular bases for structural features of chromosomes that have been a long-standing puzzle. Analysis of 2.6 megabases of sequence from the tip of the X chromosome of Drosophila identifies 273 genes. Cloned DNAs from the characteristic bulbous structure at the tip of the X chromosome in the region of the broad complex display an unusual pattern of in situ hybridization. Sequence analysis revealed that this region comprises 154 kilobases of DNA flanked by 1.2-kilobases of inverted repeats, each composed of a 350-base pair satellite related element. Thus, some aspects of chromosome structure appear to be revealed directly within the DNA sequence itself.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benos, P V -- Gatt, M K -- Ashburner, M -- Murphy, L -- Harris, D -- Barrell, B -- Ferraz, C -- Vidal, S -- Brun, C -- Demailles, J -- Cadieu, E -- Dreano, S -- Gloux, S -- Lelaure, V -- Mottier, S -- Galibert, F -- Borkova, D -- Minana, B -- Kafatos, F C -- Louis, C -- Siden-Kiamos, I -- Bolshakov, S -- Papagiannakis, G -- Spanos, L -- Cox, S -- Madueno, E -- de Pablos, B -- Modolell, J -- Peter, A -- Schottler, P -- Werner, M -- Mourkioti, F -- Beinert, N -- Dowe, G -- Schafer, U -- Jackle, H -- Bucheton, A -- Callister, D M -- Campbell, L A -- Darlamitsou, A -- Henderson, N S -- McMillan, P J -- Salles, C -- Tait, E A -- Valenti, P -- Saunder, R D -- Glover, D M -- New York, N.Y. -- Science. 2000 Mar 24;287(5461):2220-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The European Bioinformatics Institute, Wellcome Trust Genome Campus, Hinxton Hall, Cambridge CB10 1SD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10731137" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Banding ; Computational Biology ; Cosmids ; DNA Transposable Elements ; DNA, Satellite ; Drosophila melanogaster/*genetics ; Genes, Insect ; In Situ Hybridization ; Repetitive Sequences, Nucleic Acid ; Sequence Analysis, DNA ; X Chromosome/*genetics/ultrastructure
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  • 3
    Publication Date: 2000-04-28
    Description: Severe combined immunodeficiency-X1 (SCID-X1) is an X-linked inherited disorder characterized by an early block in T and natural killer (NK) lymphocyte differentiation. This block is caused by mutations of the gene encoding the gammac cytokine receptor subunit of interleukin-2, -4, -7, -9, and -15 receptors, which participates in the delivery of growth, survival, and differentiation signals to early lymphoid progenitors. After preclinical studies, a gene therapy trial for SCID-X1 was initiated, based on the use of complementary DNA containing a defective gammac Moloney retrovirus-derived vector and ex vivo infection of CD34+ cells. After a 10-month follow-up period, gammac transgene-expressing T and NK cells were detected in two patients. T, B, and NK cell counts and function, including antigen-specific responses, were comparable to those of age-matched controls. Thus, gene therapy was able to provide full correction of disease phenotype and, hence, clinical benefit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cavazzana-Calvo, M -- Hacein-Bey, S -- de Saint Basile, G -- Gross, F -- Yvon, E -- Nusbaum, P -- Selz, F -- Hue, C -- Certain, S -- Casanova, J L -- Bousso, P -- Deist, F L -- Fischer, A -- New York, N.Y. -- Science. 2000 Apr 28;288(5466):669-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM Unit 429, Gene Therapy Laboratory, Cell Therapy Laboratory, Unite d'Immunologie et d'Hematologie Pediatriques, Hopital Necker, 75743 Paris Cedex 15, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10784449" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD34/analysis ; B-Lymphocytes/immunology ; Gene Transfer Techniques ; *Genetic Therapy ; Genetic Vectors ; Hematopoietic Stem Cell Transplantation ; *Hematopoietic Stem Cells/cytology ; Humans ; Immunoglobulins/blood ; Infant ; Killer Cells, Natural/immunology ; Lymphocyte Activation ; Lymphocyte Count ; Moloney murine leukemia virus/genetics ; Mutation ; Receptors, Antigen, T-Cell/analysis ; Receptors, Interleukin/biosynthesis/*genetics ; Severe Combined Immunodeficiency/genetics/*therapy ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes/immunology ; Transgenes
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  • 4
    Publication Date: 2000-06-17
    Description: The immune system recognizes invaders as foreign because they express determinants that are absent on host cells or because they lack "markers of self" that are normally present. Here we show that CD47 (integrin-associated protein) functions as a marker of self on murine red blood cells. Red blood cells that lacked CD47 were rapidly cleared from the bloodstream by splenic red pulp macrophages. CD47 on normal red blood cells prevented this elimination by binding to the inhibitory receptor signal regulatory protein alpha (SIRPalpha). Thus, macrophages may use a number of nonspecific activating receptors and rely on the presence or absence of CD47 to distinguish self from foreign. CD47-SIRPalpha may represent a potential pathway for the control of hemolytic anemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oldenborg, P A -- Zheleznyak, A -- Fang, Y F -- Lagenaur, C F -- Gresham, H D -- Lindberg, F P -- GM57573-01/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Jun 16;288(5473):2051-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Infectious Diseases, Department of Internal Medicine, Campus Box 8051, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10856220" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Hemolytic/immunology ; Animals ; Antigens, CD/blood/genetics/*metabolism ; Antigens, CD47 ; *Antigens, Differentiation ; Carrier Proteins/blood/genetics/*metabolism ; Clodronic Acid/pharmacology ; Erythrocyte Transfusion ; Erythrocytes/*immunology ; Female ; Humans ; Liposomes ; Macrophages/*immunology ; Male ; Membrane Glycoproteins/immunology/*metabolism ; Mice ; Mice, Inbred C57BL ; *Neural Cell Adhesion Molecule L1 ; Neural Cell Adhesion Molecules/immunology/*metabolism ; Phagocytosis ; Phosphorylation ; *Receptors, Immunologic ; *Self Tolerance ; Signal Transduction ; Spleen/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2000-08-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉White, S -- Meier, W -- Lovell, F -- McCoy, A -- Robinove, C J -- Creelan, T F -- Brun, R -- Gordon, I -- MacWest, R -- Collier, I E -- Gish, D T -- Hartmann, W K -- Behe, M J -- New York, N.Y. -- Science. 2000 Aug 11;289(5481):869-71.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10960317" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; Biology/education ; Religion and Science ; Science/*education
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  • 6
    Publication Date: 2000-11-04
    Description: We report on the discovery of two emission features observed in the x-ray spectrum of the afterglow of the gamma-ray burst (GRB) of 16 December 1999 by the Chandra X-ray Observatory. These features are identified with the Ly(alpha) line and the narrow recombination continuum by hydrogenic ions of iron at a redshift z = 1.00 +/- 0.02, providing an unambiguous measurement of the distance of a GRB. Line width and intensity imply that the progenitor of the GRB was a massive star system that ejected, before the GRB event, a quantity of iron approximately 0.01 of the mass of the sun at a velocity approximately 0.1 of the speed of light, probably by a supernova explosion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Piro, L -- Garmire, G -- Garcia, M -- Stratta, G -- Costa, E -- Feroci, M -- Meszaros, P -- Vietri, M -- Bradt, H -- Frail, D -- Frontera, F -- Halpern, J -- Heise, J -- Hurley, K -- Kawai, N -- Kippen, R M -- Marshall, F -- Murakami, T -- Sokolov, V V -- Takeshima, T -- Yoshida, A -- New York, N.Y. -- Science. 2000 Nov 3;290(5493):955-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Istituto Astrofisica Spaziale, Consiglio Nazionale delle Ricerche (CNR), Via Fosso del Cavaliere, 00133 Roma, Italy. piro@ias.rm.cnr.it〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11062121" target="_blank"〉PubMed〈/a〉
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  • 7
    Publication Date: 2000-01-05
    Description: The hCHK2 gene encodes the human homolog of the yeast Cds1 and Rad53 G2 checkpoint kinases, whose activation in response to DNA damage prevents cellular entry into mitosis. Here, it is shown that heterozygous germ line mutations in hCHK2 occur in Li-Fraumeni syndrome, a highly penetrant familial cancer phenotype usually associated with inherited mutations in the TP53 gene. These observations suggest that hCHK2 is a tumor suppressor gene conferring predisposition to sarcoma, breast cancer, and brain tumors, and they also provide a link between the central role of p53 inactivation in human cancer and the well-defined G2 checkpoint in yeast.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bell, D W -- Varley, J M -- Szydlo, T E -- Kang, D H -- Wahrer, D C -- Shannon, K E -- Lubratovich, M -- Verselis, S J -- Isselbacher, K J -- Fraumeni, J F -- Birch, J M -- Li, F P -- Garber, J E -- Haber, D A -- New York, N.Y. -- Science. 1999 Dec 24;286(5449):2528-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Center for Cancer Risk Analysis and Harvard Medical School, Building 149, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10617473" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Apoptosis ; Brain Neoplasms/genetics ; Breast Neoplasms/genetics ; Checkpoint Kinase 2 ; Female ; G1 Phase ; *G2 Phase ; *Genes, Tumor Suppressor ; Genes, p53 ; Genetic Predisposition to Disease ; *Germ-Line Mutation ; Heterozygote ; Humans ; Li-Fraumeni Syndrome/enzymology/*genetics/pathology ; Male ; Pedigree ; Polymorphism, Genetic ; Protein Kinases/genetics ; Protein-Serine-Threonine Kinases/*genetics/metabolism ; Sarcoma/genetics ; Signal Transduction ; Tumor Cells, Cultured
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  • 8
    Publication Date: 2000-10-29
    Description: The ejection of material from Mars is thought to be caused by large impacts that would heat much of the ejecta to high temperatures. Images of the magnetic field of martian meteorite ALH84001 reveal a spatially heterogeneous pattern of magnetization associated with fractures and rock fragments. Heating the meteorite to 40 degrees C reduces the intensity of some magnetic features, indicating that the interior of the rock has not been above this temperature since before its ejection from the surface of Mars. Because this temperature cannot sterilize most bacteria or eukarya, these data support the hypothesis that meteorites could transfer life between planets in the solar system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weiss, B P -- Kirschvink, J L -- Baudenbacher, F J -- Vali, H -- Peters, N T -- Macdonald, F A -- Wikswo, J P -- New York, N.Y. -- Science. 2000 Oct 27;290(5492):791-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Geological and Planetary Sciences, 170-25, California Institute of Technology, Pasadena, CA 91125, USA. bweiss@gps.caltech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11052940" target="_blank"〉PubMed〈/a〉
    Keywords: Crystallization ; *Exobiology ; Magnetics ; *Mars ; *Meteoroids ; Temperature
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  • 9
    Publication Date: 2000-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Robertson, D L -- Anderson, J P -- Bradac, J A -- Carr, J K -- Foley, B -- Funkhouser, R K -- Gao, F -- Hahn, B H -- Kalish, M L -- Kuiken, C -- Learn, G H -- Leitner, T -- McCutchan, F -- Osmanov, S -- Peeters, M -- Pieniazek, D -- Salminen, M -- Sharp, P M -- Wolinsky, S -- Korber, B -- New York, N.Y. -- Science. 2000 Apr 7;288(5463):55-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10766634" target="_blank"〉PubMed〈/a〉
    Keywords: Databases, Factual ; Genome, Viral ; HIV Infections/*virology ; HIV-1/*classification/genetics ; Humans ; Recombination, Genetic ; *Terminology as Topic
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  • 10
    Publication Date: 2000-05-20
    Description: In scrapie-infected mice, prions are found associated with splenic but not circulating B and T lymphocytes and in the stroma, which contains follicular dendritic cells (FDCs). Formation and maintenance of mature FDCs require the presence of B cells expressing membrane-bound lymphotoxin-alpha/beta. Treatment of mice with soluble lymphotoxin-beta receptor results in the disappearance of mature FDCs from the spleen. We show that this treatment abolishes splenic prion accumulation and retards neuroinvasion after intraperitoneal scrapie inoculation. These data provide evidence that FDCs are the principal sites for prion replication in the spleen.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Montrasio, F -- Frigg, R -- Glatzel, M -- Klein, M A -- Mackay, F -- Aguzzi, A -- Weissmann, C -- New York, N.Y. -- Science. 2000 May 19;288(5469):1257-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neuropathology, Department of Pathology, University of Zurich, Schmelzbergstrasse 12, CH-8091 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10818004" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/genetics/immunology ; Dendritic Cells, Follicular/metabolism/*pathology/*virology ; Immunoglobulins/genetics ; Lymphotoxin beta Receptor ; Lymphotoxin-alpha/antagonists & inhibitors/genetics/immunology ; Mice ; Mice, Inbred C57BL ; Mice, SCID ; PrPSc Proteins/administration & dosage/*biosynthesis ; Receptors, Tumor Necrosis Factor/antagonists & inhibitors/genetics/immunology ; Recombinant Fusion Proteins/administration & dosage ; Scrapie/immunology/metabolism ; Signal Transduction/genetics/immunology ; Spleen/immunology/metabolism/*pathology/*virology ; Virus Replication/genetics/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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