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  • Animals  (10)
  • 2000-2004  (10)
  • 1995-1999
  • 2003  (10)
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  • 2000-2004  (10)
  • 1995-1999
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  • 1
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    Mutations in dynein link motor neuron degeneration to defects in retrograde transport (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2003-05-06
    Beschreibung: Degenerative disorders of motor neurons include a range of progressive fatal diseases such as amyotrophic lateral sclerosis (ALS), spinal-bulbar muscular atrophy (SBMA), and spinal muscular atrophy (SMA). Although the causative genetic alterations are known for some cases, the molecular basis of many SMA and SBMA-like syndromes and most ALS cases is unknown. Here we show that missense point mutations in the cytoplasmic dynein heavy chain result in progressive motor neuron degeneration in heterozygous mice, and in homozygotes this is accompanied by the formation of Lewy-like inclusion bodies, thus resembling key features of human pathology. These mutations exclusively perturb neuron-specific functions of dynein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hafezparast, Majid -- Klocke, Rainer -- Ruhrberg, Christiana -- Marquardt, Andreas -- Ahmad-Annuar, Azlina -- Bowen, Samantha -- Lalli, Giovanna -- Witherden, Abi S -- Hummerich, Holger -- Nicholson, Sharon -- Morgan, P Jeffrey -- Oozageer, Ravi -- Priestley, John V -- Averill, Sharon -- King, Von R -- Ball, Simon -- Peters, Jo -- Toda, Takashi -- Yamamoto, Ayumu -- Hiraoka, Yasushi -- Augustin, Martin -- Korthaus, Dirk -- Wattler, Sigrid -- Wabnitz, Philipp -- Dickneite, Carmen -- Lampel, Stefan -- Boehme, Florian -- Peraus, Gisela -- Popp, Andreas -- Rudelius, Martina -- Schlegel, Juergen -- Fuchs, Helmut -- Hrabe de Angelis, Martin -- Schiavo, Giampietro -- Shima, David T -- Russ, Andreas P -- Stumm, Gabriele -- Martin, Joanne E -- Fisher, Elizabeth M C -- New York, N.Y. -- Science. 2003 May 2;300(5620):808-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurodegenerative Disease, Institute of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730604" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Anterior Horn Cells/pathology ; Apoptosis ; *Axonal Transport ; Cell Differentiation ; Cell Movement ; Central Nervous System/embryology ; Chromosome Mapping ; Dimerization ; Dyneins/chemistry/*genetics/*physiology ; Female ; Ganglia, Spinal/pathology ; Golgi Apparatus/metabolism/ultrastructure ; Heterozygote ; Homozygote ; Lewy Bodies/pathology ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Motor Neuron Disease/*genetics/pathology/physiopathology ; Motor Neurons/*physiology/ultrastructure ; Mutation ; Mutation, Missense ; *Nerve Degeneration ; Peptide Fragments/metabolism ; Phenotype ; Point Mutation ; Spinal Nerves/growth & development ; Tetanus Toxin/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Requirement of Cks2 for the first metaphase/anaphase transition of mammalian meiosis (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2003-04-26
    Beschreibung: We generated mice lacking Cks2, one of two mammalian homologs of the yeast Cdk1-binding proteins, Suc1 and Cks1, and found them to be viable but sterile in both sexes. Sterility is due to failure of both male and female germ cells to progress past the first meiotic metaphase. The chromosomal events up through the end of prophase I are normal in both CKS2-/- males and females, suggesting that the phenotype is due directly to failure to enter anaphase and not a consequence of a checkpoint-mediated metaphase I arrest.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Spruck, Charles H -- de Miguel, Maria P -- Smith, Adrian P L -- Ryan, Aimee -- Stein, Paula -- Schultz, Richard M -- Lincoln, A Jeannine -- Donovan, Peter J -- Reed, Steven I -- CA74224/CA/NCI NIH HHS/ -- HD22681/HD/NICHD NIH HHS/ -- HD38252/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2003 Apr 25;300(5619):647-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, MB-7, 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/12714746" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Anaphase ; Animals ; Apoptosis ; *CDC2-CDC28 Kinases ; CDC28 Protein Kinase, S cerevisiae/genetics/*physiology ; Chromosome Segregation ; Cyclin A/metabolism ; Cyclin B/metabolism ; Epididymis/cytology/physiology ; Female ; Gene Targeting ; In Situ Hybridization ; Infertility, Female/physiopathology ; Infertility, Male/physiopathology ; Male ; *Meiosis ; *Metaphase ; Mice ; Mutation ; Oocytes/*physiology ; Ovary/cytology/physiology ; RNA, Messenger/genetics/metabolism ; Recombination, Genetic ; Spermatocytes/*physiology ; Spermatogenesis ; Testis/cytology/physiology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Cell therapy of alpha-sarcoglycan null dystrophic mice through intra-arterial delivery of mesoangioblasts (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2003-07-12
    Beschreibung: Preclinical or clinical trials for muscular dystrophies have met with modest success, mainly because of inefficient delivery of viral vectors or donor cells to dystrophic muscles. We report here that intra-arterial delivery of wild-type mesoangioblasts, a class of vessel-associated stem cells, corrects morphologically and functionally the dystrophic phenotype of virtually all downstream muscles in adult immunocompetent alpha-sarcoglycan (alpha-SG) null mice, a model organism for limb-girdle muscular dystrophy. When mesoangioblasts isolated from juvenile dystrophic mice and transduced with a lentiviral vector expressing alpha-SG were injected into the femoral artery of dystrophic mice, they reconstituted skeletal muscle in a manner similar to that seen in wild-type cells. The success of this protocol was mainly due to widespread distribution of donor stem cells through the capillary network, a distinct advantage of this strategy over previous approaches.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sampaolesi, Maurilio -- Torrente, Yvan -- Innocenzi, Anna -- Tonlorenzi, Rossana -- D'Antona, Giuseppe -- Pellegrino, M Antonietta -- Barresi, Rita -- Bresolin, Nereo -- De Angelis, M Gabriella Cusella -- Campbell, Kevin P -- Bottinelli, Roberto -- Cossu, Giulio -- 1322/Telethon/Italy -- 463/BI/Telethon/Italy -- New York, N.Y. -- Science. 2003 Jul 25;301(5632):487-92. Epub 2003 Jul 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cell Research Institute, H. S. Raffaele, Via Olgettina 58, 20132 Milan, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12855815" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Blood Vessels/cytology/embryology ; Cell Differentiation ; Cell Line ; Cell Movement ; Cytoskeletal Proteins/*genetics/*metabolism ; Dystrophin/metabolism ; Endothelium, Vascular/physiology ; Female ; Femoral Artery ; Genetic Vectors ; Lentivirus/genetics ; Locomotion ; Male ; Membrane Glycoproteins/*genetics/*metabolism ; Mesoderm/cytology ; Mice ; Mice, Knockout ; Mice, Transgenic ; Muscle Contraction ; Muscle Fibers, Skeletal/cytology/physiology ; Muscle, Skeletal/cytology/metabolism/pathology/*physiology ; Muscular Dystrophy, Animal/metabolism/pathology/*therapy ; Regeneration ; Sarcoglycans ; *Stem Cell Transplantation ; Stem Cells/*physiology ; Transfection
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    Talin binding to integrin beta tails: a final common step in integrin activation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2003-10-04
    Beschreibung: Control of integrin affinity for ligands (integrin activation) is essential for normal cell adhesion, migration, and assembly of an extracellular matrix. Integrin activation is usually mediated through the integrin beta subunit cytoplasmic tail and can be regulated by many different biochemical signaling pathways. We report that specific binding of the cytoskeletal protein talin to integrin beta subunit cytoplasmic tails leads to the conformational rearrangements of integrin extracellular domains that increase their affinity. Thus, regulated binding of talin to integrin beta tails is a final common element of cellular signaling cascades that control integrin activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tadokoro, Seiji -- Shattil, Sanford J -- Eto, Koji -- Tai, Vera -- Liddington, Robert C -- de Pereda, Jose M -- Ginsberg, Mark H -- Calderwood, David A -- New York, N.Y. -- Science. 2003 Oct 3;302(5642):103-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, The Scripps Research Institute, The Burnham Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14526080" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Antibodies, Monoclonal/immunology ; Antigens, CD29/chemistry/metabolism ; Cell Line ; Fibronectins/metabolism ; Humans ; Integrin beta Chains/chemistry/*metabolism ; Integrin beta3/chemistry/metabolism ; Molecular Sequence Data ; Mutation ; Platelet Glycoprotein GPIIb-IIIa Complex/chemistry/immunology/metabolism ; Protein Binding ; Protein Conformation ; Protein Structure, Tertiary ; RNA, Small Interfering ; Recombinant Proteins/metabolism ; *Signal Transduction ; Talin/*metabolism ; Transfection
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    Derivation of oocytes from mouse embryonic stem cells (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2003-05-06
    Beschreibung: Continuation of mammalian species requires the formation and development of the sexually dimorphic germ cells. Cultured embryonic stem cells are generally considered pluripotent rather than totipotent because of the failure to detect germline cells under differentiating conditions. Here we show that mouse embryonic stem cells in culture can develop into oogonia that enter meiosis, recruit adjacent cells to form follicle-like structures, and later develop into blastocysts. Oogenesis in culture should contribute to various areas, including nuclear transfer and manipulation of the germ line, and advance studies on fertility treatment and germ and somatic cell interaction and differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hubner, Karin -- Fuhrmann, Guy -- Christenson, Lane K -- Kehler, James -- Reinbold, Rolland -- De La Fuente, Rabindranath -- Wood, Jennifer -- Strauss, Jerome F 3rd -- Boiani, Michele -- Scholer, Hans R -- 1RO1HD42011-01/HD/NICHD NIH HHS/ -- HD06274/HD/NICHD NIH HHS/ -- T32 HD07305/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2003 May 23;300(5623):1251-6. Epub 2003 May 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Germline Development Group, Center for Animal Transgenesis and Germ Cell Research, School of Veterinary Medicine, University of Pennsylvania, New Bolton Center, 382 West Street Road, Kennett Square, PA 19348, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730498" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Biomarkers/analysis ; Blastocyst/cytology/*physiology ; Cell Adhesion ; Cell Aggregation ; *Cell Differentiation ; Cell Lineage ; Cell Separation ; Cells, Cultured ; DNA-Binding Proteins/genetics ; Embryo, Mammalian/*cytology ; Estradiol/metabolism ; Female ; Gene Expression ; Genes, Reporter ; Meiosis ; Mice ; Mice, Transgenic ; Octamer Transcription Factor-3 ; Oocytes/cytology/*physiology ; *Oogenesis ; Ovarian Follicle/cytology/physiology ; Recombinant Fusion Proteins ; Totipotent Stem Cells/*physiology ; *Transcription Factors ; Transfection
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
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    A giant virus in amoebae (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2003-03-29
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉La Scola, Bernard -- Audic, Stephane -- Robert, Catherine -- Jungang, Liang -- de Lamballerie, Xavier -- Drancourt, Michel -- Birtles, Richard -- Claverie, Jean-Michel -- Raoult, Didier -- New York, N.Y. -- Science. 2003 Mar 28;299(5615):2033.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite des Rickettsies, Universite de la Mediterranee, CNRS UMR 6020, 13385 Marseille, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12663918" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acanthamoeba/*virology ; Animals ; DNA Viruses/*classification/isolation & purification/physiology/*ultrastructure ; DNA, Circular/genetics ; DNA, Viral/genetics ; Genome, Viral ; Open Reading Frames ; Phylogeny ; Viral Proteins/analysis/genetics
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
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    Cerebellar LTD and learning-dependent timing of conditioned eyelid responses (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2003-09-23
    Beschreibung: Mammals can be trained to make a conditioned movement at a precise time, which is correlated to the interval between the conditioned stimulus and unconditioned stimulus during the learning. This learning-dependent timing has been shown to depend on an intact cerebellar cortex, but which cellular process is responsible for this form of learning remains to be demonstrated. Here, we show that protein kinase C-dependent long-term depression in Purkinje cells is necessary for learning-dependent timing of Pavlovian-conditioned eyeblink responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koekkoek, S K E -- Hulscher, H C -- Dortland, B R -- Hensbroek, R A -- Elgersma, Y -- Ruigrok, T J H -- De Zeeuw, C I -- New York, N.Y. -- Science. 2003 Sep 19;301(5640):1736-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Erasmus MC, 3000 DR Rotterdam, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14500987" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Blinking ; Cerebellum/*physiology ; *Conditioning, Eyelid ; Electroshock ; *Learning ; *Long-Term Synaptic Depression ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation ; N-Methylaspartate/pharmacology ; Protein Kinase C/genetics/metabolism ; Purkinje Cells/*physiology ; Time Factors
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
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    Role of histone H3 lysine 27 methylation in X inactivation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2003-03-22
    Beschreibung: The Polycomb group (PcG) protein Eed is implicated in regulation of imprinted X-chromosome inactivation in extraembryonic cells but not of random X inactivation in embryonic cells. The Drosophila homolog of the Eed-Ezh2 PcG protein complex achieves gene silencing through methylation of histone H3 on lysine 27 (H3-K27), which suggests a role for H3-K27 methylation in imprinted X inactivation. Here we demonstrate that transient recruitment of the Eed-Ezh2 complex to the inactive X chromosome (Xi) occurs during initiation of X inactivation in both extraembryonic and embryonic cells and is accompanied by H3-K27 methylation. Recruitment of the complex and methylation on the Xi depend on Xist RNA but are independent of its silencing function. Together, our results suggest a role for Eed-Ezh2-mediated H3-K27 methylation during initiation of both imprinted and random X inactivation and demonstrate that H3-K27 methylation is not sufficient for silencing of the Xi.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Plath, Kathrin -- Fang, Jia -- Mlynarczyk-Evans, Susanna K -- Cao, Ru -- Worringer, Kathleen A -- Wang, Hengbin -- de la Cruz, Cecile C -- Otte, Arie P -- Panning, Barbara -- Zhang, Yi -- New York, N.Y. -- Science. 2003 Apr 4;300(5616):131-5. Epub 2003 Mar 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of California San Francisco, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12649488" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Blastocyst/metabolism/*physiology ; Cell Differentiation ; Cell Nucleus/metabolism ; Cells, Cultured ; *Dosage Compensation, Genetic ; Female ; Fluorescent Antibody Technique ; Genomic Imprinting ; HeLa Cells ; Histones/*metabolism ; Humans ; In Situ Hybridization, Fluorescence ; Lysine/metabolism ; Male ; Methylation ; Mice ; Mutation ; Polycomb Repressive Complex 2 ; RNA, Long Noncoding ; RNA, Untranslated/genetics/metabolism ; Repressor Proteins/metabolism ; Stem Cells/metabolism/*physiology ; Transgenes ; Trophoblasts/*physiology ; X Chromosome/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 9
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    Mass mortality of krill caused by parasitoid ciliates (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2003-07-19
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gomez-Gutierrez, Jaime -- Peterson, William T -- De Robertis, Alex -- Brodeur, Richard D -- New York, N.Y. -- Science. 2003 Jul 18;301(5631):339.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centro Interdisciplinario de Ciencias Marinas, La Paz, B.C.S., 23096, Mexico. jgomezgu@coas.oregonstate.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12869754" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Ciliophora/growth & development/*pathogenicity ; Euphausiacea/*parasitology/physiology ; Host-Parasite Interactions ; Pacific Ocean ; Population Density
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 10
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    Discovery of gene function by expression profiling of the malaria parasite life cycle (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2003-08-02
    Beschreibung: The completion of the genome sequence for Plasmodium falciparum, the species responsible for most malaria human deaths, has the potential to reveal hundreds of new drug targets and proteins involved in pathogenesis. However, only approximately 35% of the genes code for proteins with an identifiable function. The absence of routine genetic tools for studying Plasmodium parasites suggests that this number is unlikely to change quickly if conventional serial methods are used to characterize encoded proteins. Here, we use a high-density oligonucleotide array to generate expression profiles of human and mosquito stages of the malaria parasite's life cycle. Genes with highly correlated levels and temporal patterns of expression were often involved in similar functions or cellular processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Le Roch, Karine G -- Zhou, Yingyao -- Blair, Peter L -- Grainger, Muni -- Moch, J Kathleen -- Haynes, J David -- De La Vega, Patricia -- Holder, Anthony A -- Batalov, Serge -- Carucci, Daniel J -- Winzeler, Elizabeth A -- MC_U117532067/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2003 Sep 12;301(5639):1503-8. Epub 2003 Jul 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology ICND202, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. leroch@scripps.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12893887" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Anopheles/parasitology ; Cell Cycle ; Chromosomes/genetics ; Cluster Analysis ; Erythrocytes/parasitology ; *Gene Expression ; *Gene Expression Profiling ; Gene Expression Regulation, Developmental ; *Genes, Protozoan ; Humans ; Life Cycle Stages ; Liver/parasitology ; Malaria, Falciparum/parasitology ; Oligonucleotide Array Sequence Analysis ; Plasmodium falciparum/*genetics/*growth & development/metabolism ; Proteome ; Protozoan Proteins/genetics/metabolism/physiology ; RNA, Messenger/genetics/metabolism ; RNA, Protozoan/genetics/metabolism ; Salivary Glands/parasitology ; Sporozoites/genetics/growth & development ; Transcription, Genetic
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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