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  • Molecular Sequence Data  (17)
  • American Association for the Advancement of Science (AAAS)  (17)
  • American Physical Society (APS)
  • 1990-1994  (17)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (17)
  • American Physical Society (APS)
Years
Year
  • 11
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    Deletion of the paired alpha 5(IV) and alpha 6(IV) collagen genes in inherited smooth muscle tumors (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-27
    Description: The gene encoding alpha 6(IV) collagen, COL4A6, was identified on the human X chromosome in a head-to-head arrangement and within 452 base pairs of the alpha 5(IV) collagen gene, COL4A5. In earlier studies, intragenic deletions of COL4A5 were detected in a subset of patients with Alport syndrome (AS), a hereditary defect of basement membranes. In some families, AS cosegregates with diffuse leiomyomatosis (DL), a benign smooth muscle tumor diathesis. Here it is shown that patients with AS-DL harbor deletions that disrupt both COL4A5 and COL4A6. Thus, type IV collagen may regulate smooth muscle differentiation and morphogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, J -- Mochizuki, T -- Smeets, H -- Antignac, C -- Laurila, P -- de Paepe, A -- Tryggvason, K -- Reeders, S T -- New York, N.Y. -- Science. 1993 Aug 27;261(5125):1167-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06536-0812.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8356449" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Differentiation ; Collagen/chemistry/*genetics ; Exons ; Female ; Fetus/metabolism ; *Gene Deletion ; Genetic Linkage ; Humans ; Leiomyoma/*genetics ; Male ; Molecular Sequence Data ; Morphogenesis ; Muscle, Smooth/cytology ; Mutation ; Nephritis, Hereditary/*genetics ; RNA, Messenger/genetics/metabolism
    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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  • 12
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    Surface expression of two distinct functional antigen receptors on human gamma delta T cells (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-18
    Description: Lymphocytes recognize antigens with highly variable heterodimeric surface receptors. Although four distinct antigen receptors could in principle be produced by any lymphocyte, only one functional combination of receptor chains has thus far been found expressed on their surface. Examination of human gamma delta T cells revealed a population that violated this rule by expressing on their surface two distinct functional gamma delta T cell receptors (TCRs) that used different TCR gamma gene alleles. Thus, current models for T cell clonal selection may need modification, and a possible escape mechanism for autoreactive TCRs is suggested.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davodeau, F -- Peyrat, M A -- Houde, I -- Hallet, M M -- De Libero, G -- Vie, H -- Bonneville, M -- New York, N.Y. -- Science. 1993 Jun 18;260(5115):1800-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM U211, Institut de Biologie, Nantes, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8390096" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Base Sequence ; Cell Line ; Cytotoxicity, Immunologic ; *Gene Expression ; Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor ; Humans ; Molecular Sequence Data ; Receptors, Antigen, T-Cell, gamma-delta/analysis/*genetics/immunology ; T-Lymphocytes/*immunology ; T-Lymphocytes, Cytotoxic/*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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  • 13
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    Mesodermal patterning by a gradient of the vertebrate homeobox gene goosecoid (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-11
    Description: Amphibian mesoderm arises from the marginal zone of the early gastrula and generates various tissues such as notochord, muscle, kidney, and blood. Small changes (twofold) in the amount of microinjected messenger RNA encoding the goosecoid (gsc) homeodomain protein resulted in marked changes in the differentiation of mesoderm in Xenopus laevis. At least three thresholds were observed, which were sufficient to specify four mesodermal cell states. Endogenous gsc messenger RNA was expressed in the marginal zone in a graded fashion that is congruent with a role for this gene in dorso-ventral patterning of mesoderm at the early gastrula stage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Niehrs, C -- Steinbeisser, H -- De Robertis, E M -- HD21502-08/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):817-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Institute, University of California, Los Angeles 90024-1737.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7905664" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Differentiation ; Culture Techniques ; DNA-Binding Proteins/*genetics ; Gastrula/*cytology/metabolism ; Gene Expression ; *Genes, Homeobox ; Goosecoid Protein ; *Homeodomain Proteins ; Mesoderm/*cytology ; Microinjections ; Molecular Sequence Data ; RNA, Messenger/genetics/metabolism ; *Repressor Proteins ; *Transcription Factors ; Xenopus laevis
    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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  • 14
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    An osmosensing signal transduction pathway in yeast (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-19
    Description: Yeast genes were isolated that are required for restoring the osmotic gradient across the cell membrane in response to increased external osmolarity. Two of these genes, HOG1 and PBS2, encode members of the mitogen-activated protein kinase (MAP kinase) and MAP kinase kinase gene families, respectively. MAP kinases are activated by extracellular ligands such as growth factors and function as intermediate kinases in protein phosphorylation cascades. A rapid, PBS2-dependent tyrosine phosphorylation of HOG1 protein occurred in response to increases in extracellular osmolarity. These data define a signal transduction pathway that is activated by changes in the osmolarity of the extracellular environment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brewster, J L -- de Valoir, T -- Dwyer, N D -- Winter, E -- Gustin, M C -- GM45772/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Mar 19;259(5102):1760-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Cell Biology, Rice University, Houston, TX 77251.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7681220" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Blotting, Northern ; Calcium-Calmodulin-Dependent Protein Kinases ; *Genes, Fungal ; Molecular Sequence Data ; Osmolar Concentration ; Phosphorylation ; Phosphothreonine/metabolism ; Phosphotyrosine ; Protein Kinases/chemistry/*genetics ; Restriction Mapping ; Saccharomyces cerevisiae/*genetics ; Signal Transduction/*genetics ; Tyrosine/analogs & derivatives/metabolism ; Water-Electrolyte Balance/*genetics
    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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  • 15
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    inhA, a gene encoding a target for isoniazid and ethionamide in Mycobacterium tuberculosis (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-14
    Description: Isoniazid (isonicotinic acid hydrazide, INH) is one of the most widely used antituberculosis drugs, yet its precise target of action on Mycobacterium tuberculosis is unknown. A missense mutation within the mycobacterial inhA gene was shown to confer resistance to both INH and ethionamide (ETH) in M. smegmatis and in M. bovis. The wild-type inhA gene also conferred INH and ETH resistance when transferred on a multicopy plasmid vector to M. smegmatis and M. bovis BCG. The InhA protein shows significant sequence conservation with the Escherichia coli enzyme EnvM, and cell-free assays indicate that it may be involved in mycolic acid biosynthesis. These results suggest that InhA is likely a primary target of action for INH and ETH.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Banerjee, A -- Dubnau, E -- Quemard, A -- Balasubramanian, V -- Um, K S -- Wilson, T -- Collins, D -- de Lisle, G -- Jacobs, W R Jr -- AI27160/AI/NIAID NIH HHS/ -- UO1AI30189/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1994 Jan 14;263(5144):227-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Albert Einstein College of Medicine, Bronx, NY 10461.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8284673" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Bacterial Proteins/chemistry/*genetics ; Base Sequence ; Cloning, Molecular ; Drug Resistance, Microbial/*genetics ; Ethionamide/metabolism/*pharmacology ; *Genes, Bacterial ; Isoniazid/metabolism/*pharmacology ; Molecular Sequence Data ; Mutation ; Mycobacterium/drug effects/genetics ; Mycobacterium bovis/drug effects/genetics ; Mycobacterium tuberculosis/chemistry/drug effects/*genetics/metabolism ; Mycolic Acids/metabolism ; Open Reading Frames ; *Oxidoreductases ; Sequence Alignment
    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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  • 16
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    Homozygous human TAP peptide transporter mutation in HLA class I deficiency (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-08
    Description: Human lymphocyte antigen (HLA) class I proteins of the major histocompatibility complex are largely dependent for expression on small peptides supplied to them by transporter associated with antigen processing (TAP) protein. An inherited human deficiency in the TAP transporter was identified in two siblings suffering from recurrent respiratory bacterial infections. The expression on the cell surface of class I proteins was very low, whereas that of CD1a was normal, and the cytotoxicity of natural killer cells was affected. In addition, CD8+ alpha beta T cells were present in low but significant numbers and were cytotoxic in the most severely affected sibling, who also showed an increase in CD4+CD8+ T cells and gamma delta T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de la Salle, H -- Hanau, D -- Fricker, D -- Urlacher, A -- Kelly, A -- Salamero, J -- Powis, S H -- Donato, L -- Bausinger, H -- Laforet, M -- New York, N.Y. -- Science. 1994 Jul 8;265(5169):237-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire d'Histocompatibilite, Centre Regional de Transfusion Sanguine, Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7517574" target="_blank"〉PubMed〈/a〉
    Keywords: *ATP-Binding Cassette Transporters ; Adolescent ; Amino Acid Sequence ; Antigens, CD/analysis ; Antigens, CD1 ; Base Sequence ; Carrier Proteins/analysis/*genetics ; Child ; Female ; Histocompatibility Antigens Class I/*analysis/metabolism ; Homozygote ; Humans ; Immunologic Deficiency Syndromes/*genetics/immunology ; Killer Cells, Natural/immunology ; Langerhans Cells/immunology ; Leukocyte Count ; Lymphocytes/*immunology ; Male ; Molecular Sequence Data ; Mutation ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes, Cytotoxic/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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  • 17
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    Recovery from hemophilia B Leyden: an androgen-responsive element in the factor IX promoter (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-17
    Description: One form of the inherited, X-linked, bleeding disorder, hemophilia B, resolves after puberty. Mutations at -20 and -26 in the clotting factor IX promoter impair transcription by disrupting the binding site for the liver-enriched transcription factor LF-A1/HNF4. The -26 but not the -20 mutation also disrupts an androgen-responsive element, which overlaps the LF-A1/HNF4 site. This explains the improvement seen in patients with the -20 mutation and the failure of the -26 patient to recover.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Crossley, M -- Ludwig, M -- Stowell, K M -- De Vos, P -- Olek, K -- Brownlee, G G -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1992 Jul 17;257(5068):377-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Chemical Pathology Unit, Sir William Dunn School of Pathology, University of Oxford, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1631558" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Binding Sites/genetics ; Binding, Competitive ; Cloning, Molecular ; Electrophoresis, Polyacrylamide Gel ; Factor IX/*physiology ; Hemophilia B/*genetics ; Humans ; Molecular Sequence Data ; Mutation ; Promoter Regions, Genetic/*physiology ; Receptors, Androgen/metabolism ; Sequence Homology, Nucleic Acid ; 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
    Published by American Association for the Advancement of Science (AAAS)
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