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  • 2000  (225)
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  • 2000-2004  (225)
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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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  • 2
    Publication Date: 2000-03-10
    Description: The 2,272,351-base pair genome of Neisseria meningitidis strain MC58 (serogroup B), a causative agent of meningitis and septicemia, contains 2158 predicted coding regions, 1158 (53.7%) of which were assigned a biological role. Three major islands of horizontal DNA transfer were identified; two of these contain genes encoding proteins involved in pathogenicity, and the third island contains coding sequences only for hypothetical proteins. Insights into the commensal and virulence behavior of N. meningitidis can be gleaned from the genome, in which sequences for structural proteins of the pilus are clustered and several coding regions unique to serogroup B capsular polysaccharide synthesis can be identified. Finally, N. meningitidis contains more genes that undergo phase variation than any pathogen studied to date, a mechanism that controls their expression and contributes to the evasion of the host immune system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tettelin, H -- Saunders, N J -- Heidelberg, J -- Jeffries, A C -- Nelson, K E -- Eisen, J A -- Ketchum, K A -- Hood, D W -- Peden, J F -- Dodson, R J -- Nelson, W C -- Gwinn, M L -- DeBoy, R -- Peterson, J D -- Hickey, E K -- Haft, D H -- Salzberg, S L -- White, O -- Fleischmann, R D -- Dougherty, B A -- Mason, T -- Ciecko, A -- Parksey, D S -- Blair, E -- Cittone, H -- Clark, E B -- Cotton, M D -- Utterback, T R -- Khouri, H -- Qin, H -- Vamathevan, J -- Gill, J -- Scarlato, V -- Masignani, V -- Pizza, M -- Grandi, G -- Sun, L -- Smith, H O -- Fraser, C M -- Moxon, E R -- Rappuoli, R -- Venter, J C -- New York, N.Y. -- Science. 2000 Mar 10;287(5459):1809-15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Institute for Genomic Research (TIGR), 9712 Medical Center Drive, Rockville, MD 20850, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10710307" target="_blank"〉PubMed〈/a〉
    Keywords: Antigenic Variation ; Antigens, Bacterial/immunology ; Bacteremia/microbiology ; Bacterial Capsules/genetics ; Bacterial Proteins/genetics/physiology ; DNA Transposable Elements ; Evolution, Molecular ; Fimbriae, Bacterial/genetics ; *Genome, Bacterial ; Humans ; Meningitis, Meningococcal/microbiology ; Meningococcal Infections/microbiology ; Molecular Sequence Data ; Mutation ; Neisseria meningitidis/classification/*genetics/*pathogenicity/physiology ; Open Reading Frames ; Operon ; Phylogeny ; Recombination, Genetic ; *Sequence Analysis, DNA ; Serotyping ; Transformation, Bacterial ; Virulence/genetics
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  • 3
    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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  • 4
    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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  • 5
    Publication Date: 2000-10-20
    Description: With accumulating evidence indicating the importance of cytotoxic T lymphocytes (CTLs) in containing human immunodeficiency virus-1 (HIV-1) replication in infected individuals, strategies are being pursued to elicit virus-specific CTLs with prototype HIV-1 vaccines. Here, we report the protective efficacy of vaccine-elicited immune responses against a pathogenic SHIV-89.6P challenge in rhesus monkeys. Immune responses were elicited by DNA vaccines expressing SIVmac239 Gag and HIV-1 89.6P Env, augmented by the administration of the purified fusion protein IL-2/Ig, consisting of interleukin-2 (IL-2) and the Fc portion of immunoglobulin G (IgG), or a plasmid encoding IL-2/Ig. After SHIV-89.6P infection, sham-vaccinated monkeys developed weak CTL responses, rapid loss of CD4+ T cells, no virus-specific CD4+ T cell responses, high setpoint viral loads, significant clinical disease progression, and death in half of the animals by day 140 after challenge. In contrast, all monkeys that received the DNA vaccines augmented with IL-2/Ig were infected, but demonstrated potent secondary CTL responses, stable CD4+ T cell counts, preserved virus-specific CD4+ T cell responses, low to undetectable setpoint viral loads, and no evidence of clinical disease or mortality by day 140 after challenge.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barouch, D H -- Santra, S -- Schmitz, J E -- Kuroda, M J -- Fu, T M -- Wagner, W -- Bilska, M -- Craiu, A -- Zheng, X X -- Krivulka, G R -- Beaudry, K -- Lifton, M A -- Nickerson, C E -- Trigona, W L -- Punt, K -- Freed, D C -- Guan, L -- Dubey, S -- Casimiro, D -- Simon, A -- Davies, M E -- Chastain, M -- Strom, T B -- Gelman, R S -- Montefiori, D C -- Lewis, M G -- Emini, E A -- Shiver, J W -- Letvin, N L -- AI-65301/AI/NIAID NIH HHS/ -- AI-85343/AI/NIAID NIH HHS/ -- CA-50139/CA/NCI NIH HHS/ -- P01 AI041521/AI/NIAID NIH HHS/ -- R01 CA050139/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 2000 Oct 20;290(5491):486-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA. dan_barouch@hotmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11039923" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/*therapeutic use ; Acquired Immunodeficiency Syndrome/*prevention & control ; Animals ; Antibodies, Viral/blood/immunology ; CD4 Lymphocyte Count ; CD4-Positive T-Lymphocytes/immunology ; Disease Progression ; HIV Antibodies/blood/immunology ; HIV Infections/immunology/*therapy/virology ; *HIV-1/genetics/immunology/physiology ; Humans ; Interleukin-2/genetics/immunology/*therapeutic use ; Lymphocyte Activation ; Macaca mulatta ; Neutralization Tests ; Recombinant Fusion Proteins/therapeutic use ; Simian Acquired Immunodeficiency Syndrome/immunology/prevention & ; control/therapy/virology ; Simian Immunodeficiency Virus/genetics/immunology/physiology ; T-Lymphocytes, Cytotoxic/immunology ; Vaccination ; Vaccines, DNA/*therapeutic use ; Viral Load ; Viremia ; Virus Replication
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  • 6
    Publication Date: 2000-05-08
    Description: The c-Jun NH2-terminal kinase (JNK) is activated when cells are exposed to ultraviolet (UV) radiation. However, the functional consequence of JNK activation in UV-irradiated cells has not been established. It is shown here that JNK is required for UV-induced apoptosis in primary murine embryonic fibroblasts. Fibroblasts with simultaneous targeted disruptions of all the functional Jnk genes were protected against UV-stimulated apoptosis. The absence of JNK caused a defect in the mitochondrial death signaling pathway, including the failure to release cytochrome c. These data indicate that mitochondria are influenced by proapoptotic signal transduction through the JNK pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tournier, C -- Hess, P -- Yang, D D -- Xu, J -- Turner, T K -- Nimnual, A -- Bar-Sagi, D -- Jones, S N -- Flavell, R A -- Davis, R J -- New York, N.Y. -- Science. 2000 May 5;288(5467):870-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Program in Molecular Medicine, Department of Biochemistry & Molecular Biology, 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/10797012" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptotic Protease-Activating Factor 1 ; Caspase 3 ; Caspase 9 ; Caspases/metabolism ; Cell Count ; Cell Division ; Cells, Cultured ; Cytochrome c Group/*metabolism ; DNA Fragmentation ; Enzyme Activation ; Fibroblasts ; Gene Targeting ; JNK Mitogen-Activated Protein Kinases ; MAP Kinase Signaling System ; Methyl Methanesulfonate/pharmacology ; Mice ; Mitochondria/metabolism ; Mitogen-Activated Protein Kinases/genetics/*metabolism ; NF-kappa B/metabolism ; *Protein-Serine-Threonine Kinases ; Proteins/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Tumor Suppressor Protein p53/metabolism ; Ultraviolet Rays
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  • 7
    Publication Date: 2000-12-23
    Description: Recent studies suggest that insulin-degrading enzyme (IDE) in neurons and microglia degrades Abeta, the principal component of beta-amyloid and one of the neuropathological hallmarks of Alzheimer's disease (AD). We performed parametric and nonparametric linkage analyses of seven genetic markers on chromosome 10q, six of which map near the IDE gene, in 435 multiplex AD families. These analyses revealed significant evidence of linkage for adjacent markers (D10S1671, D10S583, D10S1710, and D10S566), which was most pronounced in late-onset families. Furthermore, we found evidence for allele-specific association between the putative disease locus and marker D10S583, which has recently been located within 195 kilobases of the IDE gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bertram, L -- Blacker, D -- Mullin, K -- Keeney, D -- Jones, J -- Basu, S -- Yhu, S -- McInnis, M G -- Go, R C -- Vekrellis, K -- Selkoe, D J -- Saunders, A J -- Tanzi, R E -- New York, N.Y. -- Science. 2000 Dec 22;290(5500):2302-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genetics and Aging Unit, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11125142" target="_blank"〉PubMed〈/a〉
    Keywords: Age of Onset ; Aged ; Aged, 80 and over ; Alleles ; Alzheimer Disease/*genetics ; Apolipoproteins E/genetics ; Chromosome Mapping ; Chromosomes, Human, Pair 10/*genetics ; *Genetic Linkage ; Genetic Markers ; Humans ; Insulysin/*genetics ; Linkage Disequilibrium ; Middle Aged
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  • 8
    Publication Date: 2000-03-24
    Description: We report on the quality of a whole-genome assembly of Drosophila melanogaster and the nature of the computer algorithms that accomplished it. Three independent external data sources essentially agree with and support the assembly's sequence and ordering of contigs across the euchromatic portion of the genome. In addition, there are isolated contigs that we believe represent nonrepetitive pockets within the heterochromatin of the centromeres. Comparison with a previously sequenced 2.9- megabase region indicates that sequencing accuracy within nonrepetitive segments is greater than 99. 99% without manual curation. As such, this initial reconstruction of the Drosophila sequence should be of substantial value to the scientific community.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Myers, E W -- Sutton, G G -- Delcher, A L -- Dew, I M -- Fasulo, D P -- Flanigan, M J -- Kravitz, S A -- Mobarry, C M -- Reinert, K H -- Remington, K A -- Anson, E L -- Bolanos, R A -- Chou, H H -- Jordan, C M -- Halpern, A L -- Lonardi, S -- Beasley, E M -- Brandon, R C -- Chen, L -- Dunn, P J -- Lai, Z -- Liang, Y -- Nusskern, D R -- Zhan, M -- Zhang, Q -- Zheng, X -- Rubin, G M -- Adams, M D -- Venter, J C -- New York, N.Y. -- Science. 2000 Mar 24;287(5461):2196-204.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Celera Genomics, Inc., 45 West Gude Drive, Rockville, MD 20850, USA. Gene.Myers@celera.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10731133" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Chromatin/genetics ; *Computational Biology ; Contig Mapping ; Drosophila melanogaster/*genetics ; Euchromatin ; Genes, Insect ; *Genome ; Heterochromatin/genetics ; Molecular Sequence Data ; Physical Chromosome Mapping ; Repetitive Sequences, Nucleic Acid ; *Sequence Analysis, DNA ; Sequence Tagged Sites
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  • 9
    Publication Date: 2000-10-29
    Description: Lentiviral delivery of glial cell line-derived neurotrophic factor (lenti-GDNF) was tested for its trophic effects upon degenerating nigrostriatal neurons in nonhuman primate models of Parkinson's disease (PD). We injected lenti-GDNF into the striatum and substantia nigra of nonlesioned aged rhesus monkeys or young adult rhesus monkeys treated 1 week prior with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Extensive GDNF expression with anterograde and retrograde transport was seen in all animals. In aged monkeys, lenti-GDNF augmented dopaminergic function. In MPTP-treated monkeys, lenti-GDNF reversed functional deficits and completely prevented nigrostriatal degeneration. Additionally, lenti-GDNF injections to intact rhesus monkeys revealed long-term gene expression (8 months). In MPTP-treated monkeys, lenti-GDNF treatment reversed motor deficits in a hand-reach task. These data indicate that GDNF delivery using a lentiviral vector system can prevent nigrostriatal degeneration and induce regeneration in primate models of PD and might be a viable therapeutic strategy for PD patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kordower, J H -- Emborg, M E -- Bloch, J -- Ma, S Y -- Chu, Y -- Leventhal, L -- McBride, J -- Chen, E Y -- Palfi, S -- Roitberg, B Z -- Brown, W D -- Holden, J E -- Pyzalski, R -- Taylor, M D -- Carvey, P -- Ling, Z -- Trono, D -- Hantraye, P -- Deglon, N -- Aebischer, P -- NS40578/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2000 Oct 27;290(5492):767-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurological Sciences, Rush Presbyterian-St. Luke's Medical Center, Chicago, IL 60612, USA. jkordowe@rush.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11052933" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine ; Aging ; Animals ; Antigens, CD/analysis ; Dihydroxyphenylalanine/*analogs & derivatives/metabolism ; Disease Models, Animal ; Dopamine/*metabolism ; Female ; Gene Expression ; *Genetic Therapy ; Genetic Vectors ; Glial Cell Line-Derived Neurotrophic Factor ; Lentivirus/genetics ; Macaca mulatta ; Neostriatum/metabolism/pathology ; Nerve Degeneration/*prevention & control ; *Nerve Growth Factors ; Nerve Tissue Proteins/*genetics/metabolism/therapeutic use ; Neurons/enzymology ; Parkinson Disease/metabolism/pathology/physiopathology/*therapy ; Parkinsonian Disorders/metabolism/pathology/physiopathology/therapy ; Psychomotor Performance ; Substantia Nigra/metabolism/pathology ; Tyrosine 3-Monooxygenase/metabolism
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  • 10
    Publication Date: 2000-07-15
    Description: p53 plays an essential pro-apoptotic role, a function thought to be shared with its family members p73 and p63. Here, we show that p73 is primarily present in developing neurons as a truncated isoform whose levels are dramatically decreased when sympathetic neurons apoptose after nerve growth factor (NGF) withdrawal. Increased expression of truncated p73 rescues these neurons from apoptosis induced by NGF withdrawal or p53 overexpression. In p73-/- mice, all isoforms of p73 are deleted and the apoptosis of developing sympathetic neurons is greatly enhanced. Thus, truncated p73 is an essential anti-apoptotic protein in neurons, serving to counteract the pro-apoptotic function of p53.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pozniak, C D -- Radinovic, S -- Yang, A -- McKeon, F -- Kaplan, D R -- Miller, F D -- New York, N.Y. -- Science. 2000 Jul 14;289(5477):304-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neuronal Survival, Brain Tumor Research Center, Montreal Neurological Institute, McGill University, Montreal, Canada H3A 2B4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10894779" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Animals ; Apoptosis/*physiology ; Cells, Cultured ; DNA-Binding Proteins/biosynthesis/chemistry/*physiology ; Escherichia coli ; Genes, Tumor Suppressor ; Humans ; Mice ; Mice, Inbred BALB C ; Nerve Growth Factor/pharmacology ; Neurons/*physiology ; Nuclear Proteins/biosynthesis/chemistry/*physiology ; Protein Isoforms/biosynthesis/chemistry/physiology ; Recombinant Proteins ; Sympathetic Nervous System/cytology/*physiology ; Tumor Suppressor Protein p53/antagonists & inhibitors/*physiology ; Tumor Suppressor Proteins
    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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