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  • Humans  (7)
  • 2000-2004  (7)
  • 2003  (7)
  • 1
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    Lamin a truncation in Hutchinson-Gilford progeria (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2003-04-19
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉De Sandre-Giovannoli, Annachiara -- Bernard, Rafaelle -- Cau, Pierre -- Navarro, Claire -- Amiel, Jeanne -- Boccaccio, Irene -- Lyonnet, Stanislas -- Stewart, Colin L -- Munnich, Arnold -- Le Merrer, Martine -- Levy, Nicolas -- New York, N.Y. -- Science. 2003 Jun 27;300(5628):2055. Epub 2003 Apr 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Inserm U491: Genetique Medicale et Developpement, Faculte de Medecine Timone, Marseille, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12702809" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alleles ; Cell Nucleus/ultrastructure ; Child ; Exons ; Female ; Humans ; Lamin Type A/analysis/*chemistry/*genetics ; Lymphocytes/chemistry/ultrastructure ; Mutation ; Polymorphism, Genetic ; Progeria/blood/*genetics ; RNA Splicing ; RNA, Messenger/genetics ; Sequence Deletion ; 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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  • 2
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    Public health. Toward evidence-based health claims for foods (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2003-01-11
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Katan, Martijn B -- de Roos, Nicole M -- New York, N.Y. -- Science. 2003 Jan 10;299(5604):206-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Human Nutrition and Epidemiology, Wageningen University, the Netherlands. wcfs1@wur.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12522235" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Advertising as Topic ; Biomedical Research ; Clinical Trials as Topic ; *Dietary Supplements ; European Union ; Food Labeling ; *Food, Fortified ; *Food, Organic ; Humans ; *Legislation, Food ; Nutritional Physiological Phenomena ; *Public Health/legislation & jurisprudence ; United States ; United States Food and Drug Administration
    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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    Brazilian science at a crossroads (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2003-07-12
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Castro Moreira, Ildeu -- New York, N.Y. -- Science. 2003 Jul 11;301(5630):141.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12855773" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Brazil ; Educational Status ; Humans ; Research ; Research Support as Topic ; *Science/education ; Technology
    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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    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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  • 6
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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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  • 7
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    LMO2-associated clonal T cell proliferation in two patients after gene therapy for SCID-X1 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2003-10-18
    Beschreibung: We have previously shown correction of X-linked severe combined immunodeficiency [SCID-X1, also known as gamma chain (gamma(c)) deficiency] in 9 out of 10 patients by retrovirus-mediated gamma(c) gene transfer into autologous CD34 bone marrow cells. However, almost 3 years after gene therapy, uncontrolled exponential clonal proliferation of mature T cells (with gammadelta+ or alphabeta+ T cell receptors) has occurred in the two youngest patients. Both patients' clones showed retrovirus vector integration in proximity to the LMO2 proto-oncogene promoter, leading to aberrant transcription and expression of LMO2. Thus, retrovirus vector insertion can trigger deregulated premalignant cell proliferation with unexpected frequency, most likely driven by retrovirus enhancer activity on the LMO2 gene promoter.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hacein-Bey-Abina, S -- Von Kalle, C -- Schmidt, M -- McCormack, M P -- Wulffraat, N -- Leboulch, P -- Lim, A -- Osborne, C S -- Pawliuk, R -- Morillon, E -- Sorensen, R -- Forster, A -- Fraser, P -- Cohen, J I -- de Saint Basile, G -- Alexander, I -- Wintergerst, U -- Frebourg, T -- Aurias, A -- Stoppa-Lyonnet, D -- Romana, S -- Radford-Weiss, I -- Gross, F -- Valensi, F -- Delabesse, E -- Macintyre, E -- Sigaux, F -- Soulier, J -- Leiva, L E -- Wissler, M -- Prinz, C -- Rabbitts, T H -- Le Deist, F -- Fischer, A -- Cavazzana-Calvo, M -- New York, N.Y. -- Science. 2003 Oct 17;302(5644):415-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM Unit 429, Cedex 15, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14564000" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adaptor Proteins, Signal Transducing ; Clinical Trials as Topic ; Clone Cells/physiology ; DNA-Binding Proteins/*genetics ; Gene Expression Regulation ; Gene Transfer Techniques ; Genetic Therapy/*adverse effects ; *Genetic Vectors ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/physiology ; Humans ; Infant ; LIM Domain Proteins ; Leukemia-Lymphoma, Adult T-Cell/*etiology ; Metalloproteins/*genetics ; Mutagenesis, Insertional ; Promoter Regions, Genetic ; Proto-Oncogene Proteins ; Proto-Oncogenes ; Receptors, Interleukin-2/genetics ; Retroviridae/*genetics/physiology ; Severe Combined Immunodeficiency/*therapy ; T-Lymphocytes/*physiology ; Transcription, Genetic ; Virus Integration ; Virus Replication
    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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