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  • Molecular Sequence Data  (6)
  • Signal Transduction  (5)
  • Lymphocyte Activation  (4)
  • American Association for the Advancement of Science (AAAS)  (13)
  • 2000-2004  (4)
  • 1995-1999  (9)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (13)
Years
Year
  • 1
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    Perforin gene defects in familial hemophagocytic lymphohistiocytosis (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-03
    Description: Familial hemophagocytic lymphohistiocytosis (FHL) is a rare, rapidly fatal, autosomal recessive immune disorder characterized by uncontrolled activation of T cells and macrophages and overproduction of inflammatory cytokines. Linkage analyses indicate that FHL is genetically heterogeneous and linked to 9q21.3-22, 10q21-22, or another as yet undefined locus. Sequencing of the coding regions of the perforin gene of eight unrelated 10q21-22-linked FHL patients revealed homozygous nonsense mutations in four patients and missense mutations in the other four patients. Cultured lymphocytes from patients had defective cytotoxic activity, and immunostaining revealed little or no perforin in the granules. Thus, defects in perforin are responsible for 10q21-22-linked FHL. Perforin-based effector systems are, therefore, involved not only in the lysis of abnormal cells but also in the down-regulation of cellular immune activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stepp, S E -- Dufourcq-Lagelouse, R -- Le Deist, F -- Bhawan, S -- Certain, S -- Mathew, P A -- Henter, J I -- Bennett, M -- Fischer, A -- de Saint Basile, G -- Kumar, V -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1957-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and the Graduate Program in Immunology, University of Texas Southwestern Medical School, Dallas, TX 75235, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10583959" target="_blank"〉PubMed〈/a〉
    Keywords: Antigen-Presenting Cells/immunology ; Cell Death ; Cell Line ; Cells, Cultured ; Chromosome Mapping ; Chromosomes, Human, Pair 10/*genetics ; Codon, Terminator ; Cytoplasmic Granules/chemistry ; Cytotoxicity, Immunologic ; Frameshift Mutation ; Genetic Linkage ; Granzymes ; Heterozygote ; Histiocytosis, Non-Langerhans-Cell/*genetics/immunology ; Humans ; Lymphocyte Activation ; Membrane Glycoproteins/analysis/*genetics/physiology ; Mutation, Missense ; Perforin ; Point Mutation ; Pore Forming Cytotoxic Proteins ; Serine Endopeptidases/analysis ; T-Lymphocytes, Cytotoxic/chemistry/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Molecular evidence for the early evolution of photosynthesis (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-08
    Description: The origin and evolution of photosynthesis have long remained enigmatic due to a lack of sequence information of photosynthesis genes across the entire photosynthetic domain. To probe early evolutionary history of photosynthesis, we obtained new sequence information of a number of photosynthesis genes from the green sulfur bacterium Chlorobium tepidum and the green nonsulfur bacterium Chloroflexus aurantiacus. A total of 31 open reading frames that encode enzymes involved in bacteriochlorophyll/porphyrin biosynthesis, carotenoid biosynthesis, and photosynthetic electron transfer were identified in about 100 kilobase pairs of genomic sequence. Phylogenetic analyses of multiple magnesium-tetrapyrrole biosynthesis genes using a combination of distance, maximum parsimony, and maximum likelihood methods indicate that heliobacteria are closest to the last common ancestor of all oxygenic photosynthetic lineages and that green sulfur bacteria and green nonsulfur bacteria are each other's closest relatives. Parsimony and distance analyses further identify purple bacteria as the earliest emerging photosynthetic lineage. These results challenge previous conclusions based on 16S ribosomal RNA and Hsp60/Hsp70 analyses that green nonsulfur bacteria or heliobacteria are the earliest phototrophs. The overall consensus of our phylogenetic analysis, that bacteriochlorophyll biosynthesis evolved before chlorophyll biosynthesis, also argues against the long-held Granick hypothesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xiong, J -- Fischer, W M -- Inoue, K -- Nakahara, M -- Bauer, C E -- GM53940/GM/NIGMS NIH HHS/ -- R01 GM053940/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Sep 8;289(5485):1724-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Indiana University, Bloomington, IN 47405, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10976061" target="_blank"〉PubMed〈/a〉
    Keywords: Bacteria/*genetics/metabolism ; Bacterial Proteins/genetics ; Bacteriochlorophylls/biosynthesis/genetics ; Chlorobi/*genetics/*metabolism ; Chlorophyll/biosynthesis ; Cyanobacteria/genetics/metabolism ; *Evolution, Molecular ; Genes, Bacterial ; Molecular Sequence Data ; Photosynthesis/*genetics ; Phylogeny ; Polymerase Chain Reaction ; Sequence Analysis, DNA
    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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  • 3
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    Impairment of mycobacterial immunity in human interleukin-12 receptor deficiency (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-20
    Description: In humans, interferon gamma (IFN-gamma) receptor deficiency leads to a predisposition to mycobacterial infections and impairs the formation of mature granulomas. Interleukin-12 (IL-12) receptor deficiency was found in otherwise healthy individuals with mycobacterial infections. Mature granulomas were seen, surrounded by T cells and centered with epithelioid and multinucleated giant cells, yet reduced IFN-gamma concentrations were found to be secreted by activated natural killer and T cells. Thus, IL-12-dependent IFN-gamma secretion in humans seems essential in the control of mycobacterial infections, despite the formation of mature granulomas due to IL-12-independent IFN-gamma secretion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Altare, F -- Durandy, A -- Lammas, D -- Emile, J F -- Lamhamedi, S -- Le Deist, F -- Drysdale, P -- Jouanguy, E -- Doffinger, R -- Bernaudin, F -- Jeppsson, O -- Gollob, J A -- Meinl, E -- Segal, A W -- Fischer, A -- Kumararatne, D -- Casanova, J L -- New York, N.Y. -- Science. 1998 May 29;280(5368):1432-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM U429, Hopital Necker-Enfants Malades, Paris 75015, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9603732" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytotoxicity, Immunologic ; Female ; Granuloma/immunology ; Humans ; Hypersensitivity, Delayed ; Interferon-gamma/biosynthesis/immunology/secretion ; Interleukin-12/*immunology ; Killer Cells, Natural/immunology ; Lymphocyte Activation ; Male ; Mice ; Mice, Knockout ; Mutation ; Mycobacterium avium-intracellulare Infection/*immunology ; *Mycobacterium bovis ; Pedigree ; Receptors, Interferon/genetics/immunology ; Receptors, Interleukin/deficiency/*genetics ; Receptors, Interleukin-12 ; T-Lymphocytes/immunology ; Tuberculosis/*immunology
    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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  • 4
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    Gene therapy of human severe combined immunodeficiency (SCID)-X1 disease (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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  • 5
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    Cleavage of the BMP-4 antagonist chordin by zebrafish tolloid (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-01-07
    Description: Dorsoventral patterning of vertebrate and Drosophila embryos requires bone morphogenetic proteins (BMPs) and antagonists of BMP activity. The Drosophila gene tolloid encodes a metalloprotease similar to BMP-1 that interacts genetically with decapentaplegic, the Drosophila homolog of vertebrate BMP-2/4. Zebrafish embryos overexpressing a zebrafish homolog of tolloid were shown to resemble loss-of-function mutations in chordino, the zebrafish homolog of the Xenopus BMP-4 antagonist Chordin. Furthermore, Chordin was degraded by COS cells expressing Tolloid. These data suggest that Tolloid antagonizes Chordin activity by proteolytically cleaving Chordin. A conserved function for zebrafish and Drosophila Tolloid during embryogenesis is proposed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blader, P -- Rastegar, S -- Fischer, N -- Strahle, U -- New York, N.Y. -- Science. 1997 Dec 12;278(5345):1937-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire (IGBMC), CNRS/INSERM/ULP, BP 163, 67404 Illkirch Cedex, C.U. de Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9395394" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Body Patterning ; Bone Morphogenetic Protein 4 ; Bone Morphogenetic Protein Receptors ; Bone Morphogenetic Proteins/antagonists & inhibitors/*metabolism ; COS Cells ; Cell Lineage ; *Drosophila Proteins ; Embryo, Nonmammalian/metabolism ; Gene Expression Regulation, Developmental ; Glycoproteins/*metabolism ; Insect Proteins/genetics/*metabolism ; *Intercellular Signaling Peptides and Proteins ; RNA, Messenger/genetics/metabolism ; Receptors, Cell Surface/metabolism ; *Receptors, Growth Factor ; Signal Transduction ; Tolloid-Like Metalloproteinases ; Transfection ; Xenopus Proteins ; Zebrafish/*embryology/genetics/metabolism ; Zebrafish 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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  • 6
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    Helicobacter pylori vacuolating cytotoxin inhibits T lymphocyte activation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-23
    Description: Helicobacter pylori (Hp) vacuolating cytotoxin VacA induces cellular vacuolation in epithelial cells. We found that VacA could efficiently block proliferation of T cells by inducing a G1/S cell cycle arrest. It interfered with the T cell receptor/interleukin-2 (IL-2) signaling pathway at the level of the Ca2+-calmodulin-dependent phosphatase calcineurin. Nuclear translocation of nuclear factor of activated T cells (NFAT), a transcription factor acting as a global regulator of immune response genes, was abrogated, resulting in down-regulation of IL-2 transcription. VacA partially mimicked the activity of the immunosuppressive drug FK506 by possibly inducing a local immune suppression, explaining the extraordinary chronicity of Hp infections.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gebert, Bettina -- Fischer, Wolfgang -- Weiss, Evelyn -- Hoffmann, Reinhard -- Haas, Rainer -- New York, N.Y. -- Science. 2003 Aug 22;301(5636):1099-102.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max von Pettenkofer-Institut fur Hygiene und Medizinische Mikrobiologie, LMU Munchen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12934009" target="_blank"〉PubMed〈/a〉
    Keywords: Apoptosis ; Bacterial Proteins/pharmacology/*physiology ; Bacterial Toxins/pharmacology ; Calcineurin/metabolism ; Calcineurin Inhibitors ; Cyclins/metabolism ; Cytotoxins/pharmacology ; DNA-Binding Proteins/genetics/metabolism ; G1 Phase ; Gene Expression Regulation ; HeLa Cells ; Helicobacter pylori/genetics/*pathogenicity ; Humans ; Interleukin-2/genetics/metabolism ; Jurkat Cells ; *Lymphocyte Activation ; NFATC Transcription Factors ; *Nuclear Proteins ; Oligonucleotide Array Sequence Analysis ; S Phase ; Signal Transduction ; T-Lymphocytes/*immunology/*microbiology/physiology ; Tacrolimus/pharmacology ; Transcription Factors/genetics/metabolism ; Transcription, Genetic ; Transfection
    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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  • 7
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    Axonal neuregulin-1 regulates myelin sheath thickness (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-03-27
    Description: In the nervous system of vertebrates, myelination is essential for rapid and accurate impulse conduction. Myelin thickness depends on axon fiber size. We use mutant and transgenic mouse lines to show that axonal Neuregulin-1 (Nrg1) signals information about axon size to Schwann cells. Reduced Nrg1 expression causes hypomyelination and reduced nerve conduction velocity. Neuronal overexpression of Nrg1 induces hypermyelination and demonstrates that Nrg1 type III is the responsible isoform. We suggest a model by which myelin-forming Schwann cells integrate axonal Nrg1 signals as a biochemical measure of axon size.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Michailov, Galin V -- Sereda, Michael W -- Brinkmann, Bastian G -- Fischer, Tobias M -- Haug, Bernhard -- Birchmeier, Carmen -- Role, Lorna -- Lai, Cary -- Schwab, Markus H -- Nave, Klaus-Armin -- New York, N.Y. -- Science. 2004 Apr 30;304(5671):700-3. Epub 2004 Mar 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurogenetics, Max Planck Institute of Experimental Medicine, 37075 Gottingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15044753" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology/*ultrastructure ; Ganglia, Spinal/chemistry ; Gene Targeting ; Genes, erbB ; Genes, erbB-2 ; Heterozygote ; Mice ; Mice, Knockout ; Mice, Transgenic ; Models, Neurological ; Myelin Sheath/*physiology/*ultrastructure ; Neural Conduction ; Neuregulin-1/genetics/*physiology ; Protein Isoforms/physiology ; Receptor, Epidermal Growth Factor/analysis/physiology ; Receptor, ErbB-2/analysis/physiology ; Receptor, ErbB-3/analysis/physiology ; Schwann Cells/physiology ; Sciatic Nerve/chemistry ; Signal Transduction
    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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  • 8
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    Dependence of germinal center B cells on expression of CD21/CD35 for survival (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-05-09
    Description: Affinity-driven selection of B lymphocytes within germinal centers is critical for the development of high-affinity memory cells and host protection. To investigate the role of the CD21/CD35 coreceptor in B cell competition for follicular retention and survival within the germinal center, either Cr2+ or Cr2null lysozyme-specific transgenic B cells were adoptively transferred into normal mice immunized with duck (DEL) or turkey (TEL) lysozyme, which bind with different affinities. In mice injected with high-affinity turkey lysozyme, Cr2null B cells responded by follicular retention; however, they could not survive within germinal centers. This suggests that CD21 provides a signal independent of antigen that is required for survival of B cells in the germinal center.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fischer, M B -- Goerg, S -- Shen, L -- Prodeus, A P -- Goodnow, C C -- Kelsoe, G -- Carroll, M C -- New York, N.Y. -- Science. 1998 Apr 24;280(5363):582-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9554848" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Amino Acid Sequence ; Animals ; B-Lymphocytes/cytology/*immunology ; Cell Division ; Cell Survival ; Female ; Gene Expression ; Germinal Center/cytology/*immunology ; Immunization ; Lymphocyte Activation ; Male ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Muramidase/immunology ; Receptors, Antigen, B-Cell/immunology ; Receptors, Complement 3b/genetics/*immunology ; Receptors, Complement 3d/genetics/*immunology ; Spleen/immunology
    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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  • 9
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    Natural and engineered disorders of lymphocyte development (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-05-02
    Description: Mammals have evolved complex developmental pathways to generate a large repertoire of B and T lymphocytes capable of mounting effective immune responses. Analysis of natural and engineered immunodeficiencies constitutes a powerful approach to delineating these pathways and identifying the molecular sensors that couple the survival of developing lymphocytes to the achievement of successful gene rearrangements at the loci coding for B and T cell antigen receptors. Besides identifying cytokines, growth factors, and transcription factors involved in lymphocyte development, genetic analysis also makes it possible to organize most of these protagonists into gene networks that control critical events in the life of developing lymphocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fischer, A -- Malissen, B -- New York, N.Y. -- Science. 1998 Apr 10;280(5361):237-43.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite INSERM U.429, Hopital Necker-Enfants Malades 149, Rue de Sevres, 75743, Paris Cedex 15, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9535646" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/cytology/*immunology ; Cytokines/physiology ; Gene Rearrangement, T-Lymphocyte ; Gene Transfer Techniques ; Humans ; Immunologic Deficiency Syndromes/genetics/*immunology ; Mice ; Mutagenesis ; *Mutation ; Receptors, Antigen, B-Cell/genetics/immunology/metabolism ; Receptors, Antigen, T-Cell, alpha-beta/genetics/immunology/metabolism ; Signal Transduction ; T-Lymphocytes/cytology/*immunology
    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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  • 10
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    Mutations in Fas associated with human lymphoproliferative syndrome and autoimmunity (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-06-02
    Description: Fas (also known as Apo1 and CD95) is a cell surface receptor involved in apoptotic cell death. Fas expression and function were analyzed in three children (including two siblings) with a lymphoproliferative syndrome, two of whom also had autoimmune disorders. A large deletion in the gene encoding Fas and no detectable cell surface expression characterized the most affected patient. Clinical manifestations in the two related patients were less severe: Fas-mediated apoptosis was impaired and a deletion within the intracytoplasmic domain was detected. These findings illustrate the crucial regulatory role of Fas and may provide a molecular basis for some autoimmune diseases in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rieux-Laucat, F -- Le Deist, F -- Hivroz, C -- Roberts, I A -- Debatin, K M -- Fischer, A -- de Villartay, J P -- New York, N.Y. -- Science. 1995 Jun 2;268(5215):1347-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut National de la Sante et de la Recherche Medicale (INSERM) U 429, Hopital Necker-Enfants Malades, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7539157" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antigens, CD95 ; Antigens, Surface/chemistry/*genetics/physiology ; Apoptosis ; Autoimmune Diseases/*genetics/immunology/pathology ; Base Sequence ; Child ; Female ; *Frameshift Mutation ; Humans ; Infant ; Lymphoproliferative Disorders/*genetics/immunology/pathology ; Male ; Molecular Sequence Data ; Sequence Deletion ; Syndrome ; Thrombocytopenia/genetics/immunology/pathology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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