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  • Female  (163)
  • Mutation  (70)
  • American Association for the Advancement of Science (AAAS)  (228)
  • 1985-1989  (228)
  • 1950-1954
  • 1988  (112)
  • 1985  (116)
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  • American Association for the Advancement of Science (AAAS)  (228)
  • Springer  (7)
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  • 1985-1989  (228)
  • 1950-1954
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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-02-05
    Description: The acquired immunodeficiency syndrome (AIDS) and infection with the human immunodeficiency virus type 1 (HIV-1) constitute a worldwide public health problem. Whereas in Europe and in most of the Americas transmission of HIV-1 has occurred predominantly among homosexual men and intravenous drug abusers, in Africa a distinct epidemiologic pattern has emerged that indicates that HIV-1 infection is mainly heterosexually acquired. Heterosexual transmission appears to be increasing in some parts of Latin America and the Caribbean, and possibly in the United States. In addition to HIV-1, at least one other human retrovirus, namely HIV-2, has been implicated as a cause of AIDS in Africa and Europe. Factors that influence heterosexual transmission of HIV-1 include genital ulcerations, early or late stages of HIV-1 infection in the index case, and possibly oral contraception and immune activation. The rate of perinatal transmission is enhanced when the mother's illness is more advanced. AIDS and HIV-1 infection may have a significant impact not only on public health, but also on the demography and socioeconomic conditions of some developing countries. Programs for the prevention and control of AIDS should be an immediate priority in all countries.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Piot, P -- Plummer, F A -- Mhalu, F S -- Lamboray, J L -- Chin, J -- Mann, J M -- New York, N.Y. -- Science. 1988 Feb 5;239(4840):573-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Institute of Tropical Medicine, Antwerp, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3277271" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/epidemiology/prevention & ; control/*transmission ; Female ; HIV/classification/pathogenicity ; Humans ; Infant, Newborn ; Male ; Pregnancy ; Sexual Behavior
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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-11-25
    Description: The human immunodeficiency virus type 1 (HIV-1) shows extensive genetic variation and undergoes rapid evolution. The fidelity of purified HIV-1 reverse transcriptase was measured during DNA polymerization in vitro by means of three different assays. Reverse transcriptase from HIV-1 introduced base-substitution errors in DNA from the bacteriophage phi X174 amber3 at estimated frequencies of 1/2000 to 1/4000. Analyses of misincorporation rates opposite a single template adenine residue showed that HIV-1 reverse transcriptase catalyzed nucleotide mismatches with a specificity of A:C much greater than A:G greater than A:A. The high error rate of HIV-1 reverse transcriptase in vitro translates to approximately five to ten errors per HIV-1 genome per round of replication in vivo. This high error rate suggests that misincorporation by HIV-1 reverse transcriptase is, at least in part, responsible for the hypermutability of the AIDS virus. The specificity of misincorporation may provide a basis for the systematic construction of antiviral nucleosides.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Preston, B D -- Poiesz, B J -- Loeb, L A -- CA-07263-03/CA/NCI NIH HHS/ -- N01AI72654/AI/NIAID NIH HHS/ -- R35-CA-39903/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Nov 25;242(4882):1168-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2460924" target="_blank"〉PubMed〈/a〉
    Keywords: Avian Myeloblastosis Virus/enzymology ; Bacteriophage phi X 174/genetics ; DNA/*biosynthesis ; DNA Polymerase II/metabolism ; DNA, Viral/biosynthesis ; Electrophoresis, Polyacrylamide Gel ; HIV/*enzymology/genetics ; Kinetics ; Moloney murine leukemia virus/enzymology ; Mutation ; Nucleotides/metabolism ; RNA-Directed DNA Polymerase/*metabolism
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  • 3
    Publication Date: 1988-07-01
    Description: Expression of the interleukin-2 receptor (IL-2R alpha) gene is activated by the transcriptional activator protein, Tax (previously referred to as the tat gene product), encoded by the human T-cell leukemia virus (HTLV-I). Multiple protein binding sites for specific DNA-protein interactions were identified over the upstream IL-2R alpha transcriptional regulatory sequences. However, only one region, which includes the sequence motif GGGGAATCTCCC, was required for activation by both the tax gene product and mitogenic stimulation. Remarkably, this sequence also bound the nuclear factor NF kappa B, which is important for induction of kappa-immunoglobulin gene expression. A model is presented whereby regulation of cellular gene expression by the HTLV-I tax gene product occurs via an indirect mechanism that may involve a post-translational modification of preexistent cellular transcription factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ruben, S -- Poteat, H -- Tan, T H -- Kawakami, K -- Roeder, R -- Haseltine, W -- Rosen, C A -- New York, N.Y. -- Science. 1988 Jul 1;241(4861):89-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Oncology, Roche Institute of Molecular Biology, Nutley, NJ 07110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2838905" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Binding Sites ; Cell Line ; DNA/genetics/metabolism ; Deltaretrovirus/*genetics ; Gene Expression Regulation/*drug effects ; Gene Products, tat ; Immunoglobulin kappa-Chains/genetics ; Mutation ; Plasmids ; Promoter Regions, Genetic ; Receptors, Immunologic/*genetics ; Receptors, Interleukin-2 ; Regulatory Sequences, Nucleic Acid ; Transcription Factors/genetics/metabolism/*pharmacology
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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-02-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schekman, R -- Payne, G -- New York, N.Y. -- Science. 1988 Feb 19;239(4842):919.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3277285" target="_blank"〉PubMed〈/a〉
    Keywords: Clathrin/genetics/*physiology ; Mutation ; Saccharomyces cerevisiae/genetics/*physiology
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  • 5
    Publication Date: 1988-04-29
    Description: Spontaneous diabetes mellitus was blocked in nonobese diabetic mice by treatment with a monoclonal antibody against the L3T4 determinant present on the surface of T-helper lymphocytes. Sustained treatment with the monoclonal antibody led to cessation of the lymphocytic infiltration associated with the destruction of the insulin-producing beta cells. Moreover, the mice remained normoglycemic after the antibody therapy was stopped. These studies indicate that immunotherapy with monoclonal antibodies to the lymphocyte subset may not only halt the progression of diabetes, but may lead to long-term reversal of the disease after therapy has ended.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shizuru, J A -- Taylor-Edwards, C -- Banks, B A -- Gregory, A K -- Fathman, C G -- AI11313/AI/NIAID NIH HHS/ -- DK39959/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1988 Apr 29;240(4852):659-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Stanford University Medical Center, CA 94305-5111.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2966437" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/*therapeutic use ; Antigens, Differentiation, T-Lymphocyte/*immunology ; Cyclosporins/therapeutic use ; Diabetes Mellitus, Experimental/pathology/*therapy ; Female ; *Immunotherapy ; Islets of Langerhans/pathology ; Lymphocytes/pathology ; Mice ; Mice, Inbred ICR ; T-Lymphocytes, Helper-Inducer/*immunology/pathology
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  • 6
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-11-04
    Description: As a way of studying nucleosome assembly and maintenance in Saccharomyces cerevisiae, mutants bearing deletions or duplications of the genes encoding histones H2A and H2B were analyzed. Previous genetic analysis had shown that only one of these mutants exhibited dramatic and pleiotropic phenotypes. This mutant was also the only one that contained disrupted chromatin, suggesting that the original phenotypes were attributable to alterations in chromosome structure. The chromatin disruption in the mutant, however, did not extend over the entire genome, but rather was localized to specific regions. Thus, while the arrangement of nucleosomes over the HIS4 and GAL1 genes, the telomeres, and the long terminal repeats (delta sequences) of Ty retrotransposons appeared essentially normal, nucleosomes over the CYH2 and UBI4 genes and the centromere of chromosome III were dramatically disrupted. The observation that the mutant exhibited localized chromatin disruptions implies that the assembly or maintenance of nucleosomes differs over different parts of the yeast genome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Norris, D -- Dunn, B -- Osley, M A -- GM40118/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Nov 4;242(4879):759-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2847314" target="_blank"〉PubMed〈/a〉
    Keywords: Centromere/ultrastructure ; Chromatin/physiology/*ultrastructure ; Chromosome Deletion ; DNA Transposable Elements ; Galactose ; Gene Expression Regulation ; Genes, Fungal ; Histidine ; Histones/*genetics ; Mutation ; Phenotype ; RNA, Messenger/genetics ; Repetitive Sequences, Nucleic Acid ; Saccharomyces cerevisiae/genetics/*ultrastructure ; Transcription, Genetic
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  • 7
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-07-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McLaren, D S -- New York, N.Y. -- Science. 1988 Jul 22;241(4864):399-400.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3393905" target="_blank"〉PubMed〈/a〉
    Keywords: Energy Metabolism ; Female ; Humans ; *Longevity ; Male ; Sex Factors
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  • 8
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-01-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, M -- New York, N.Y. -- Science. 1988 Jan 15;239(4837):252.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3276002" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*etiology/prevention & control ; Clinical Trials as Topic/economics ; Dietary Fats/administration & dosage/*adverse effects ; Female ; Humans ; National Institutes of Health (U.S.) ; United States
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  • 9
    Publication Date: 1988-07-01
    Description: A method of combinatorial cassette mutagenesis was designed to readily determine the informational content of individual residues in protein sequences. The technique consists of simultaneously randomizing two or three positions by oligonucleotide cassette mutagenesis, selecting for functional protein, and then sequencing to determine the spectrum of allowable substitutions at each position. Repeated application of this method to the dimer interface of the DNA-binding domain of lambda repressor reveals that the number and type of substitutions allowed at each position are extremely variable. At some positions only one or two residues are functionally acceptable; at other positions a wide range of residues and residue types are tolerated. The number of substitutions allowed at each position roughly correlates with the solvent accessibility of the wild-type side chain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reidhaar-Olson, J F -- Sauer, R T -- AI-15706/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 1;241(4861):53-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3388019" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Binding Sites ; Codon ; DNA/genetics/metabolism ; *DNA-Binding Proteins ; Macromolecular Substances ; Molecular Sequence Data ; Mutation ; Plasmids ; Protein Conformation ; Repressor Proteins/*genetics ; Structure-Activity Relationship ; Transcription Factors/*genetics ; Viral Proteins ; Viral Regulatory and Accessory Proteins
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  • 10
    Publication Date: 1988-08-05
    Description: The human pS2 gene is specifically expressed under estrogen transcriptional control in a subclass of estrogen receptor-containing human breast cancer cells. The pS2 gene encodes an 84-amino acid protein that is secreted after signal peptide cleavage. The distribution of pS2 protein in normal human tissues was studied with antibodies to pS2; pS2 was specifically expressed and secreted by mucosa cells of the normal stomach antrum and body of both female and male individuals. Moreover, no estrogen receptor could be detected in these cells, indicating that pS2 gene expression is estrogen-independent in the stomach. The function of the pS2 protein in the gastrointestinal tract is unknown. However, the pS2 protein is similar in sequence to a porcine pancreatic protein that has been shown to inhibit gastrointestinal motility and gastric secretion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rio, M C -- Bellocq, J P -- Daniel, J Y -- Tomasetto, C -- Lathe, R -- Chenard, M P -- Batzenschlager, A -- Chambon, P -- New York, N.Y. -- Science. 1988 Aug 5;241(4866):705-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CNRS et U. 184 de l'INSERM, Institut de Chimie Biologique, Faculte de Medecine, Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3041593" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antibodies, Monoclonal ; Breast Neoplasms/*metabolism ; Estrogens/pharmacology ; Exons ; Female ; Gastric Mucosa/*metabolism ; *Gene Expression Regulation ; Histocytochemistry ; Humans ; Immunoenzyme Techniques ; Male ; Molecular Sequence Data ; Neoplasm Proteins/*biosynthesis/genetics/secretion ; *Proteins ; RNA, Messenger/metabolism ; Receptors, Estrogen/metabolism ; Sequence Homology, Nucleic Acid ; Tissue Distribution ; Tumor Cells, Cultured ; Tumor Suppressor Proteins
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  • 11
    Publication Date: 1988-10-14
    Description: Structural changes of the human retinoblastoma gene have been demonstrated previously in retinoblastoma and some clinically related tumors including osteosarcoma. Structural aberrations of the retinoblastoma locus (RB1) were observed in 25% of breast tumor cell lines studied and 7% of the primary tumors. These changes include homozygous internal deletions and total deletion of RB1; a duplication of an exon was observed in one of the cell lines. In all cases, structural changes either resulted in the absence or truncation of the RB1 transcript. No obvious defect in RB1 was detected by DNA blot analysis in primary tumors or cell lines from Wilms' tumor, cervical carcinoma, or hepatoma. These results further support the concept that the human RB1 gene has pleiotropic effects on specific types of cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉T'Ang, A -- Varley, J M -- Chakraborty, S -- Murphree, A L -- Fung, Y K -- CA44754/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Oct 14;242(4876):263-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology/Oncology, Childrens Hospital of Los Angeles, CA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175651" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*genetics ; Chromosome Aberrations ; Chromosomes, Human, Pair 13 ; DNA/genetics ; DNA Probes ; Exons ; Eye Neoplasms/*genetics ; Female ; *Gene Rearrangement ; Homozygote ; Humans ; Lymphatic Metastasis ; Menopause ; Mutation ; Nucleic Acid Hybridization ; Retinoblastoma/*genetics ; Risk Factors ; Tumor Cells, Cultured
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  • 12
    Publication Date: 1988-07-15
    Description: In 1979, a mass poisoning occurred in Taiwan from cooking oil contaminated by thermally degraded polychlorinated biphenyls. Because these chemicals persist in human tissue, children born to female patients after the outbreak were exposed in utero. In 1985, 117 children born to affected women and 108 unexposed controls were examined and evaluated. The exposed children were shorter and lighter than controls; they had abnormalities of gingiva, skin, nails, teeth, and lungs more frequently than did controls. The exposed children showed delay of developmental milestones, deficits on formal developmental testing, and abnormalities on behavioral assessment. These findings are most consistent with a generalized disorder of ectodermal tissue. This syndrome is one of very few documented to result from transplacental exposure to pollutant chemicals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rogan, W J -- Gladen, B C -- Hung, K L -- Koong, S L -- Shih, L Y -- Taylor, J S -- Wu, Y C -- Yang, D -- Ragan, N B -- Hsu, C C -- New York, N.Y. -- Science. 1988 Jul 15;241(4863):334-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3133768" target="_blank"〉PubMed〈/a〉
    Keywords: Conjunctivitis/chemically induced/congenital ; Female ; Growth Disorders/chemically induced ; Humans ; Lactation ; Maternal-Fetal Exchange ; Nails, Malformed ; Oils/*adverse effects ; Pigmentation Disorders/chemically induced/congenital ; Polychlorinated Biphenyls/*poisoning ; Pregnancy ; Taiwan
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  • 13
    Publication Date: 1988-01-29
    Description: Regulation of the synthesis of membrane-bound and secreted immunoglobulin mu heavy chains at the level of RNA processing is an important element for B cell development. The precursor mu RNA is either polyadenylated at the upstream poly(A) site (for the secreted form) or spliced (for the membrane-bound form) in a mutually exclusive manner. When the mouse mu gene linked to the SV40/HSV-TK hybrid promoter was microinjected into Xenopus oocytes, the mu messenger RNA (mRNA) was altered by coinjection of nuclei of mouse surface IgM-bearing B-lymphoma cells to include the synthesis of the membrane-bound form. An increase in the membrane-bound form was not observed when nuclei of IgM-secreting hybridoma cells or fibroblast cells were coinjected. Deletion of the upstream poly(A) site did not eliminate the effect of B-lymphoma nuclei suggesting that membrane-specific splicing is stimulated. Further, splicing of other mu gene introns was not affected by coinjection of B-lymphoma nuclei. These results suggest that mature B cells contain one or more transacting nuclear factors that stimulate splicing specific for membrane-bound mu mRNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsurushita, N -- Ho, L -- Korn, L J -- AI21298/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Jan 29;239(4839):494-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3124268" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology/ultrastructure ; Cell Membrane/metabolism ; Cell Nucleus/*physiology ; DNA, Recombinant ; Female ; Hybridomas/ultrastructure ; Immunoglobulin M/genetics ; Immunoglobulin mu-Chains/*genetics ; Introns ; Lymphoma/*immunology/ultrastructure ; Mice ; Microinjections ; Nuclear Transfer Techniques ; Oocytes/*metabolism ; Plasmids ; Promoter Regions, Genetic ; *RNA Splicing ; RNA, Messenger/*genetics ; Tumor Cells, Cultured ; Xenopus
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  • 14
    Publication Date: 1988-12-23
    Description: The ras p21 GTPase-activating protein (GAP) was purified from human placental tissue. Internal amino acid sequence was obtained from this 120,000-dalton protein and, by means of this sequence, two types of complementary DNA clones were isolated and characterized. One type encoded GAP with a predicted molecular mass of 116,000 daltons and 96% identity with bovine GAP. The messenger RNA of this GAP was detected in human lung, brain, liver, leukocytes, and placenta. The second type appeared to be generated by a differential splicing mechanism and encoded a novel form of GAP with a predicted molecular mass of 100,400 daltons. This protein lacks the hydrophobic amino terminus characteristic of the larger species, but retains GAP activity. The messenger RNA of this type was abundantly expressed in placenta and in several human cell lines, but not in adult tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trahey, M -- Wong, G -- Halenbeck, R -- Rubinfeld, B -- Martin, G A -- Ladner, M -- Long, C M -- Crosier, W J -- Watt, K -- Koths, K -- New York, N.Y. -- Science. 1988 Dec 23;242(4886):1697-700.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Cetus Corp., Emeryville, CA 94608.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3201259" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Brain Chemistry ; *Cloning, Molecular ; DNA/*genetics/isolation & purification ; Female ; GTPase-Activating Proteins ; Gene Expression Regulation ; Humans ; Leukocytes/analysis ; Liver/analysis ; Lung/analysis ; Molecular Sequence Data ; Molecular Weight ; Nucleic Acid Hybridization ; Oligonucleotide Probes ; Placenta/*analysis ; Pregnancy ; Proteins/*genetics/isolation & purification ; RNA, Messenger/analysis/genetics ; Sequence Homology, Nucleic Acid ; ras GTPase-Activating Proteins
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  • 15
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-06-17
    Description: Unequal crossing-over within a head-to-tail tandem array of the homologous red and green visual pigment genes has been proposed to explain the observed variation in green-pigment gene number among individuals and the prevalence of red-green fusion genes among color-blind subjects. This model was tested by probing the structure of the red and green pigment loci with long-range physical mapping techniques. The loci were found to constitute a gene array with an approximately 39-kilobase repeat length. The position of the red pigment gene at the 5' edge of the array explains its lack of variation in copy number. Restriction maps of the array in four individuals who differ in gene number are consistent with a head-to-tail configuration of the genes. These results provide physical evidence in support of the model and help to explain the high incidence of color blindness in the human population.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vollrath, D -- Nathans, J -- Davis, R W -- GM21891/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 17;240(4859):1669-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2837827" target="_blank"〉PubMed〈/a〉
    Keywords: Color Vision Defects/*genetics ; Crossing Over, Genetic ; DNA/genetics ; DNA Restriction Enzymes ; Electrophoresis, Agar Gel ; Exons ; Female ; Genetic Variation ; Humans ; Male ; Nucleic Acid Hybridization ; Recombination, Genetic ; Repetitive Sequences, Nucleic Acid ; Retinal Pigments/*genetics ; *X Chromosome
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  • 16
    Publication Date: 1988-04-15
    Description: A new type of agonist-binding subunit of rat neuronal nicotinic acetylcholine receptors (nAChRs) was identified. Rat genomic DNA and complementary DNA encoding this subunit (alpha 2) were cloned and analyzed. Complementary DNA expression studies in Xenopus oocytes revealed that the injection of messenger RNAs (mRNAs) for alpha 2 and beta 2 (a neuronal nAChR subunit) led to the generation of a functional nAChR. In contrast to the other known neuronal nAChRs, the receptor produced by the injection of alpha 2 and beta 2 mRNAs was resistant to the alpha-neurotoxin Bgt3.1. In situ hybridization histochemistry showed that alpha 2 mRNA was expressed in a small number of regions, in contrast to the wide distribution of the other known agonist-binding subunits (alpha 3 and alpha 4) mRNAs. These results demonstrate that the alpha 2 subunit differs from other known agonist-binding alpha-subunits of nAChRs in its distribution in the brain and in its pharmacology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wada, K -- Ballivet, M -- Boulter, J -- Connolly, J -- Wada, E -- Deneris, E S -- Swanson, L W -- Heinemann, S -- Patrick, J -- New York, N.Y. -- Science. 1988 Apr 15;240(4850):330-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salk Institute for Biological Studies, San Diego, CA 92138.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2832952" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain/*metabolism ; DNA Restriction Enzymes ; Female ; *Genes ; Molecular Sequence Data ; Neurons/metabolism ; Nucleotide Mapping ; Oocytes/metabolism ; Rats ; Receptors, Nicotinic/*genetics/metabolism ; Transcription, Genetic ; Xenopus laevis
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  • 17
    Publication Date: 1988-04-29
    Description: Zeins, the storage proteins of maize, are totally lacking in the essential amino acids lysine and tryptophan. Lysine codons and lysine- and tryptophan-encoding oligonucleotides were introduced at several positions into a 19-kilodalton zein complementary DNA by oligonucleotide-mediated mutagenesis. A 450-base pair open reading frame from a simian virus 40 (SV40) coat protein was also engineered into the zein coding region. Messenger RNAs for the modified zeins were synthesized in vitro with an SP6 RNA polymerase system and injected into Xenopus laevis oocytes. The modifications did not affect the translation, signal peptide cleavage, or stability of the zeins. The ability of the modified zeins to assemble into structures similar to maize protein bodies was assayed by two criteria: assembly into membrane-bound vesicles resistant to exogenously added protease, and ability to self-aggregate into dense structures. All of the modified zeins were membrane-bound; only the one containing a 17-kilodalton SV40 protein fragment was unable to aggregate. These findings suggest that it may be possible to create high-lysine corn by genetic engineering.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wallace, J C -- Galili, G -- Kawata, E E -- Cuellar, R E -- Shotwell, M A -- Larkins, B A -- New York, N.Y. -- Science. 1988 Apr 29;240(4852):662-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Botany and Plant Pathology, Purdue University, West Lafayette, IN 47907.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2834822" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Membrane/metabolism ; DNA/genetics ; DNA, Recombinant ; Female ; Genetic Engineering ; *Lysine/genetics ; Macromolecular Substances ; Molecular Sequence Data ; Mutation ; Oocytes/*metabolism ; Peptide Hydrolases/metabolism ; RNA, Messenger/genetics ; Simian virus 40/genetics ; Xenopus laevis ; Zea mays ; Zein/genetics/*metabolism
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  • 18
    Publication Date: 1988-12-09
    Description: Leber's hereditary optic neuropathy is a maternally inherited disease resulting in optic nerve degeneration and cardiac dysrhythmia. A mitochondrial DNA replacement mutation was identified that correlated with this disease in multiple families. This mutation converted a highly conserved arginine to a histidine at codon 340 in the NADH dehydrogenase subunit 4 gene and eliminated an Sfa NI site, thus providing a simple diagnostic test. This finding demonstrated that a nucleotide change in a mitochondrial DNA energy production gene can result in a neurological disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wallace, D C -- Singh, G -- Lott, M T -- Hodge, J A -- Schurr, T G -- Lezza, A M -- Elsas, L J 2nd -- Nikoskelainen, E K -- NS21328/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Dec 9;242(4884):1427-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3201231" target="_blank"〉PubMed〈/a〉
    Keywords: African Continental Ancestry Group ; Animals ; Arginine ; Cytochrome Reductases/*genetics ; DNA, Mitochondrial/*genetics ; European Continental Ancestry Group ; Female ; *Genes ; Georgia ; Hereditary Sensory and Motor Neuropathy/*genetics ; Histidine ; Humans ; Macromolecular Substances ; Male ; *Mutation ; NADH Dehydrogenase/*genetics ; Optic Atrophies, Hereditary/*genetics ; Pedigree ; Reference Values
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  • 19
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-10-21
    Description: The translational diffusion of wild-type and underglycosylated molecules of a membrane-integral glycoprotein the Ld class I major histocompatibility complex (MHC) antigen has been measured. The Ld mutant molecules, which lack one or more glycosylation sites, had larger translational diffusion coefficients, D, than did wild-type Ld molecules glycosylated at three sites. The increase in D is linear with loss of glycosylation. The highest value of D approaches that for translational diffusion of molecules constrained only by viscosity of the membrane lipid bilayer. These results indicate that the external portions of cell surface glycoproteins interact significantly with other nearby molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wier, M -- Edidin, M -- AI-14584/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Oct 21;242(4877):412-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, The Johns Hopkins University, Baltimore, MD 21218.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175663" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cell Membrane/immunology ; Diffusion ; Glycosylation ; *Histocompatibility Antigens Class I/genetics ; Humans ; Lipid Bilayers ; Major Histocompatibility Complex ; Membrane Glycoproteins/genetics/*metabolism ; Mutation
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  • 20
    Publication Date: 1988-04-29
    Description: Screening for human T-lymphotropic virus type I (HTLV-I) antibodies was performed on sera from 39,898 blood donors at eight blood centers in geographically distinct areas of the United States. Ten donors (0.025 percent) showed evidence of HTLV-I seropositivity by enzyme immunoassays; this was confirmed by protein immunoblot and radioimmunoprecipitation. Seroprevalence rates ranged from 0 to 0.10 percent at the locations sampled, with HTLV-I antibodies found predominantly in donors from the southeastern and southwestern United States. Matched case-control interviews and laboratory studies were performed on five seropositive women and two seropositive men who participated in an identity-linked collection of sera from a subset of 33,893 donors at six of the eight blood centers. Four of the women and both men are black; one woman is Caucasian. Four of the seven seropositive individuals admitted to prior intravenous drug abuse or sexual contact with an intravenous drug user. Sexual contact with native inhabitants of an HTLV-I endemic area was the only identified risk factor for one male. The distribution of HTLV-I antibodies in this U.S. blood donor sample corroborates the previously reported epidemiology of this agent and suggests that additional donor screening measures, including the testing of donated blood for HTLV-I markers, may be necessary to prevent the spread of HTLV-I to transfusion recipients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, A E -- Fang, C T -- Slamon, D J -- Poiesz, B J -- Sandler, S G -- Darr, W F 2nd -- Shulman, G -- McGowan, E I -- Douglas, D K -- Bowman, R J -- New York, N.Y. -- Science. 1988 Apr 29;240(4852):643-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉American Red Cross Jerome H. Holland Laboratory, Rockville, MD 20855.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2896386" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Antibodies, Viral/*analysis ; *Blood Donors ; Deltaretrovirus/*immunology/isolation & purification ; Deltaretrovirus Infections/diagnosis/*epidemiology/transmission ; Female ; Humans ; Immunoenzyme Techniques ; Immunosorbent Techniques ; Japan ; Male ; Middle Aged ; Risk Factors ; Sexual Partners ; Substance-Related Disorders ; United States
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  • 21
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-09-02
    Description: A 16-kilodalton protein expressed in cells producing the human immunodeficiency virus (HIV-1) was identified as the gene product of the vpu open reading frame. When expressed in vitro, the 81-amino acid vpu protein reacted with about one-third of the serum samples from AIDS patients that were tested, indicating that the vpu open reading frame is expressed in vivo as well. Introduction of a frame-shift mutation into the vpu open reading frame did not significantly interfere with expression of the major viral proteins in a transient expression system. However, a five- to tenfold reduction in progeny virions was observed after the infection of T lymphocytes with the mutant virus. These data suggest that the vpu gene product is required for efficient virus replication and may have a role in assembly or maturation of progeny virions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strebel, K -- Klimkait, T -- Martin, M A -- New York, N.Y. -- Science. 1988 Sep 2;241(4870):1221-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3261888" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology ; Base Sequence ; DNA, Viral/genetics ; Electrophoresis, Polyacrylamide Gel ; *Genes, Viral ; HIV/*genetics/physiology ; Humans ; Immune Sera/immunology ; Immunoassay ; Mutation ; Protein Biosynthesis ; RNA, Viral/genetics ; T-Lymphocytes/microbiology ; Transcription, Genetic ; Viral Proteins/*genetics/immunology/physiology ; Virus Replication
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  • 22
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-03-04
    Description: The heat-shock consensus element (HSE), CTNGAANNTTCNAG, is found in multiple copies upstream of all heat-shock genes. Here, the sequence requirements for heat-shock induction are tested by Drosophila germline transformation with an hsp70-lacZ gene fused to a pair of synthetic HSEs. Certain single-base substitutions in either HSE cause a dramatic reduction (forty-fold) in expression. Surprisingly, variations in sequences immediately flanking the HSEs also reduced levels of induction. One such variant that contains two perfect 14-base pair HSEs, which are correctly spaced relative to each other and the TATA box, retained only 7% of wild type-induced expression. These and additional analyses indicate that the heat-shock regulatory element includes sequences beyond the 14-base pair HSE and may be better described as a dimer of a 10-base pair sequence, NTTCNNGAAN.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xiao, H -- Lis, J T -- GM25232/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 4;239(4844):1139-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Biochemistry, Molecular and Cell Biology, Cornell University, Ithaca, NY 14853.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3125608" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Composition ; DNA, Recombinant ; Drosophila melanogaster/*genetics ; Gene Expression Regulation ; Heat-Shock Proteins/*genetics ; Hot Temperature ; Mutation ; Nucleic Acid Conformation ; Promoter Regions, Genetic ; *Regulatory Sequences, Nucleic Acid ; Repetitive Sequences, Nucleic Acid ; Transcription Factors/*metabolism ; *Transformation, Genetic
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  • 23
    Publication Date: 1988-02-19
    Description: In an in vitro system for the Drosophila melanogaster male accessory gland, it was found that 10(-9)M juvenile hormone III could accurately mimic the copulation-induced response of increased protein synthesis in glands from virgin flies. Stimulation by this hormone required calcium in the medium. Experiments with tumor-promoting phorbol esters indicated that activation of protein kinase C can also cause the glands to increase protein synthesis. Stimulation of protein synthesis by juvenile hormone did not occur in mutants deficient in kinase C activity. These results suggest a membrane-protein-mediated effect of juvenile hormone that involves calcium and kinase C.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamamoto, K -- Chadarevian, A -- Pellegrini, M -- New York, N.Y. -- Science. 1988 Feb 19;239(4842):916-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Section, University of Southern California, Los Angeles 90089.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3124270" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*physiology ; Drosophila melanogaster/*metabolism ; Enzyme Activation/drug effects ; Genitalia, Male/drug effects/metabolism ; Juvenile Hormones/genetics ; Male ; Membrane Proteins/metabolism ; Mutation ; Phorbol 12,13-Dibutyrate ; Phorbol Esters/pharmacology ; Protein Biosynthesis ; Protein Kinase C/*metabolism ; Sesquiterpenes/*pharmacology ; Tetradecanoylphorbol Acetate/pharmacology
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  • 24
    Publication Date: 1988-06-03
    Description: Inbred male mice typically prefer to mate with females of a different, non-self H-2 haplotype. To determine whether this natural preference is irrevocable or results from familial imprinting, a test system was used which relied on previous observations that B6 males (H-2b) mate preferentially with congenic B6-H-2k rather than B6 females, and B6-H-2k males with B6 females. This preference was reversed in B6 males fostered by B6-H-2k parents and in B6-H-2k males fostered by B6 parents, preference in these cases favoring the same H-2 type. Thus, H-2 selective mating preference is acquired by imprinting on familial H-2 types.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamazaki, K -- Beauchamp, G K -- Kupniewski, D -- Bard, J -- Thomas, L -- Boyse, E A -- CA-39827/CA/NCI NIH HHS/ -- GMCA-32096/GM/NIGMS NIH HHS/ -- NS-22623/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 3;240(4857):1331-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Monell Chemical Senses Center, Philadelphia, PA 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3375818" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; H-2 Antigens/*genetics ; *Imprinting (Psychology) ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Odors ; *Sexual Behavior, Animal ; Smell/physiology
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  • 25
    Publication Date: 1988-05-06
    Description: A point mutation in the human insulin receptor gene in a patient with type A insulin resistance alters the amino acid sequence within the tetrabasic processing site of the proreceptor molecule from Arg-Lys-Arg-Arg to Arg-Lys-Arg-Ser. Epstein-Barr virus-transformed lymphocytes from this patient synthesize an insulin receptor precursor that is normally glycosylated and inserted into the plasma membrane but is not cleaved to mature alpha and beta subunits. Insulin binding to these cells is severely reduced but can be increased about fivefold by gentle treatment with trypsin, accompanied by the appearance of normal alpha subunits. These results indicate that proteolysis of the proreceptor is necessary for its normal full insulin-binding sensitivity and signal-transducing activity and that a cellular protease that is more stringent in its specificity than trypsin is required to process the receptor precursor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoshimasa, Y -- Seino, S -- Whittaker, J -- Kakehi, T -- Kosaki, A -- Kuzuya, H -- Imura, H -- Bell, G I -- Steiner, D F -- AM 13914/AM/NIADDK NIH HHS/ -- AM 20595/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1988 May 6;240(4853):784-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, University of Chicago, IL 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3283938" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Amino Acid Sequence ; Cell Membrane/metabolism ; Cells, Cultured ; DNA/genetics ; Diabetes Mellitus/*genetics/metabolism ; Female ; Glycosylation ; Humans ; Insulin/metabolism ; Insulin Resistance/*genetics ; Lymphocytes/metabolism ; Molecular Sequence Data ; Mutation ; Nucleic Acid Hybridization ; Protein Precursors/*genetics/metabolism ; RNA, Messenger/metabolism ; Receptor, Insulin/*genetics/metabolism ; Trypsin/metabolism
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  • 26
    Publication Date: 1988-07-29
    Description: Familial hypobetalipoproteinemia is a syndrome in which the plasma levels of apolipoprotein B (apo-B) and cholesterol are abnormally low. A truncated species of apo-B was identified in the plasma lipoproteins of members of a kindred with familial hypobetalipoproteinemia. DNA sequencing studies on genomic clones and enzymatically amplified genomic DNA samples revealed a four-base pair deletion in the apo-B gene. This short deletion, which results in a frameshift and a premature stop codon, accounts for the truncated apo-B species and explains the low apo-B and low cholesterol levels in this family.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Young, S G -- Northey, S T -- McCarthy, B J -- HL-01672-03/HL/NHLBI NIH HHS/ -- HL-14197/HL/NHLBI NIH HHS/ -- HL-38781-01/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 29;241(4865):591-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gladstone Foundation Laboratories for Cardiovascular Disease, University of California, San Francisco 94140-0608.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3399894" target="_blank"〉PubMed〈/a〉
    Keywords: Apolipoproteins B/*genetics ; Cholesterol/*blood ; Chromosome Deletion ; Cloning, Molecular ; Heterozygote ; Humans ; Hypobetalipoproteinemias/*genetics ; Hypolipoproteinemias/*genetics ; Mutation ; Pedigree
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  • 27
    Publication Date: 1988-06-24
    Description: A 20-base pair region in the first intron of the human c-myc gene was identified as the binding site of a nuclear protein. This binding site is mutated in five out of seven Burkitt lymphomas sequenced to date. To investigate the protein-recognition region in greater detail, the abnormal c-myc allele from a Burkitt lymphoma line (PA682) that carries a t(8;22) chromosomal translocation was used. A point mutation in the binding region of the PA682 c-myc DNA abolished binding of this nuclear protein. This protein may be an important factor for control of c-myc expression, and mutations in its recognition sequence may be associated with c-myc activation in many cases of Burkitt lymphoma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zajac-Kaye, M -- Gelmann, E P -- Levens, D -- New York, N.Y. -- Science. 1988 Jun 24;240(4860):1776-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medicine Branch, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2454510" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Burkitt Lymphoma/*genetics ; DNA-Binding Proteins/*metabolism ; Gene Expression Regulation ; Humans ; Molecular Sequence Data ; Mutation ; Nuclear Proteins/*metabolism ; *Oncogenes ; Proto-Oncogene Proteins/*genetics ; RNA/genetics ; RNA, Antisense ; Transcription, Genetic
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  • 28
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-10-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1988 Oct 14;242(4876):183-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175643" target="_blank"〉PubMed〈/a〉
    Keywords: *Anabolic Agents/adverse effects ; *Doping in Sports/legislation & jurisprudence ; Female ; Humans ; Male ; Risk Factors ; Stanozolol ; Substance-Related Disorders/*economics
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  • 29
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-08-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1988 Aug 26;241(4869):1039-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2457946" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/congenital/immunology/*prevention & control ; Animals ; Antibodies, Viral/immunology ; Cats ; *Genes, Viral ; *Genetic Variation ; HIV/*genetics/immunology ; HIV Antibodies ; HIV Seropositivity ; Humans ; Leukemia Virus, Feline/genetics ; Mutation ; Pan troglodytes ; RNA-Directed DNA Polymerase ; Vaccines/*immunology ; Viral Envelope Proteins/genetics/immunology
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  • 30
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-03-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1988 Mar 25;239(4847):1493-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2832939" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Diseases/genetics ; Collagen/genetics ; *Genes ; *Growth ; Growth Substances/physiology ; Humans ; Intercellular Junctions ; Mutation ; Receptors, Cell Surface/genetics
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  • 31
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-01-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1988 Jan 22;239(4838):352-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3336789" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA/metabolism ; Female ; *Gene Expression Regulation ; Genes ; Humans ; Male ; Methylation ; Mice ; Mice, Transgenic ; *Sex Characteristics ; Tissue Distribution
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  • 32
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-08-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1988 Aug 19;241(4868):903-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3043664" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; Female ; Humans ; Male ; Menopause/*physiology ; Mice ; Pituitary Hormone-Releasing Hormones/*biosynthesis ; Puberty/*physiology ; Rats ; Sexual Maturation
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  • 33
    Publication Date: 1988-12-23
    Description: The aminoacylation specificity ("acceptor identity") of transfer RNAs (tRNAs) has previously been associated with the position of particular nucleotides, as opposed to distinctive elements of three-dimensional structure. The contribution of a G.U wobble pair in the acceptor helix of tRNA(Ala) to acceptor identity was examined with synthetic amber suppressor tRNAs in Escherichia coli. The acceptor identity was not affected by replacing the G.U wobble pair in tRNA(Ala) with a G.A, C.A, or U.U wobble pair. Furthermore, a tRNA(Ala) acceptor identity was conferred on tRNA(Lys) when the same site in the acceptor helix was replaced with any of several wobble pairs. Additional data with tRNA(Ala) show that a substantial acceptor identity was retained when the G.U wobble pair was translocated to another site in the acceptor helix. These results suggest that the G.U wobble pair induces an irregularity in the acceptor helix of tRNA(Ala) to match a complementary structure in the aminoacylating enzyme.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McClain, W H -- Chen, Y M -- Foss, K -- Schneider, J -- GM42123/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Dec 23;242(4886):1681-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bacteriology, University of Wisconsin, Madison 53706.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2462282" target="_blank"〉PubMed〈/a〉
    Keywords: Base Composition ; Escherichia coli/*genetics ; Mutation ; *Nucleic Acid Conformation ; RNA, Bacterial/*metabolism ; RNA, Transfer, Ala/*metabolism ; RNA, Transfer, Amino Acid-Specific/*metabolism ; Structure-Activity Relationship ; Suppression, Genetic
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  • 34
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-01-29
    Description: The nonobese diabetic (NOD) mouse is an animal model of type I diabetes and develops a characteristic autoimmune lesion in the islets of Langerhans with lymphocytic infiltration and destruction of pancreatic beta cells. The result is hypoinsulinemia, hyperglycemia, ketoacidosis, and death. Diabetes usually begins by the sixth month of age but can occur earlier when young NOD mice are infused with lymphocytes from older NOD donors. When newborn or adult NOD mice were infected with a lymphotropic virus they did not become diabetic. The interaction between viruses and lymphocytes is pivotal in aborting diabetes, as established by experiments in which lymphocytes from virus-infected donors failed to transfer diabetes. In contrast, lymphocytes from age- and sex-matched uninfected donors caused disease. Therefore, viruses and, presumably, their products can be developed to be beneficial and may have potential as a component for treatment of human diseases. Further, these results point to the utility of viruses as probes for dissecting the pathogenesis of a nonviral disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oldstone, M B -- AG-04342/AG/NIA NIH HHS/ -- AI-09484/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Jan 29;239(4839):500-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Research Institute of Scripps Clinic, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3277269" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmune Diseases/pathology ; Bone Marrow/pathology ; Diabetes Mellitus, Experimental/immunology/pathology/*prevention & control ; Diabetes Mellitus, Type 1/immunology/pathology/*prevention & control ; Female ; Islets of Langerhans/pathology ; Lymphocyte Transfusion ; Lymphocytes/immunology ; Lymphocytic Choriomeningitis/*immunology/pathology ; Mice ; Spleen/pathology ; T-Lymphocytes/immunology
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  • 35
    Publication Date: 1988-11-18
    Description: Human fetal globin genes are not expressed in hybrid cells produced by the fusion of normal human lymphocytes with mouse erythroleukemia cells. In contrast, when lymphocytes from persons with globin gene developmental mutations (hereditary persistence of fetal hemoglobin) are used for these fusions, fetal globin is expressed in the hybrid cells. Thus, mutations of developmental origin can be reconstituted in vitro by fusing mutant lymphoid cells with differentiated cell lines of the proper lineage. This system can readily be used for analyses, such as globin gene methylation, that normally require large numbers of pure nucleated erythroid cells, which are difficult to obtain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Papayannopoulou, T -- Enver, T -- Takegawa, S -- Anagnou, N P -- Stamatoyannopoulos, G -- DK30852/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1988 Nov 18;242(4881):1056-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2461587" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Fusion ; Chromosome Deletion ; Fetal Hemoglobin/*genetics ; Gene Expression Regulation ; Globins/*genetics ; Hemoglobinopathies/*genetics ; Humans ; Leukemia, Erythroblastic, Acute ; Mice ; Mutation ; Promoter Regions, Genetic ; RNA, Messenger/genetics
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  • 36
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-05-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, M -- New York, N.Y. -- Science. 1988 May 6;240(4853):714-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2966438" target="_blank"〉PubMed〈/a〉
    Keywords: *Abnormalities, Drug-Induced ; Acne Vulgaris/*drug therapy ; Female ; Humans ; Isotretinoin ; *Legislation, Drug ; Pregnancy ; Tretinoin/*adverse effects/therapeutic use ; United States ; United States Food and Drug Administration
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  • 37
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-01-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, M -- New York, N.Y. -- Science. 1988 Jan 1;239(4835):17-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3336770" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*etiology ; Dietary Fats/adverse effects ; Female ; Humans ; Research Support as Topic
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  • 38
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-04-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, L -- New York, N.Y. -- Science. 1988 Apr 1;240(4848):27.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3353707" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; China ; *Diet ; Diet Surveys ; Female ; *Health ; Humans ; Male ; Middle Aged ; Neoplasms/epidemiology
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  • 39
    Publication Date: 1988-06-17
    Description: The specificity of complex formation between cytochrome b5 (cyt b5) and cytochrome c (cyt c) is believed to involve the formation of salt linkages between specific carboxylic acid residues of cyt b5 with lysine residues on cyt c. Site-directed mutagenesis was used to alter the specified acidic residues of cyt b5 to the corresponding amide analogues, which resulted in a lower affinity for complex formation with cyt c. The dissociation of the complex under high pressure resulted in specific volume changes, the magnitude of which reflected the degree of solvation of the acidic residues in the proposed protein-protein interface.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rodgers, K K -- Pochapsky, T C -- Sligar, S G -- GM 31756/GM/NIGMS NIH HHS/ -- GM 33775/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 17;240(4859):1657-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Illinois, Urbana 61801.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2837825" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytochrome b Group/genetics/*metabolism ; Cytochrome c Group/*metabolism ; Cytochromes b5 ; Hydrogen Bonding ; Hydrogen-Ion Concentration ; Hydrostatic Pressure ; Macromolecular Substances ; Mutation ; Protein Conformation ; Rats ; Solubility ; Thermodynamics
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  • 40
    Publication Date: 1988-05-13
    Description: The human T-cell leukemia virus (HTLV) types I and II have two nonstructural genes that are encoded in overlapping reading frames. One of these genes, known as tax, has been shown to encode a protein responsible for enhanced transcription (transactivation) from the viral long terminal repeats (LTRs). Genetic evidence indicates that the second nonstructural gene of HTLV-II, here designated rex, acts in trans to modulate tax gene-mediated transactivation in a concentration-dependent fashion. The rex gene may regulate the process of transactivation during the viral life cycle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosenblatt, J D -- Cann, A J -- Slamon, D J -- Smalberg, I S -- Shah, N P -- Fujii, J -- Wachsman, W -- Chen, I S -- 1 R01 CA 43370/CA/NCI NIH HHS/ -- 1K11 CA 01314/CA/NCI NIH HHS/ -- CA 32737/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 May 13;240(4854):916-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, UCLA School of Medicine.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2834826" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; DNA, Recombinant ; DNA, Viral/genetics ; Deltaretrovirus/*genetics ; *Genes, Regulator ; *Genes, Viral ; Mutation ; Promoter Regions, Genetic ; RNA, Messenger/genetics/metabolism ; RNA, Viral/genetics/metabolism ; Simian virus 40/genetics ; *Transcription, Genetic ; Transfection
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  • 41
    Publication Date: 1988-10-14
    Description: A survey of rat tissues by RNA analysis, aimed at uncovering the physiological function of the parathyroid hormone-like peptide (PTH-LP) associated with hypercalcemia of malignancy, revealed the presence of a 1.5-kilobase messenger RNA encoding this peptide in lactating mammary glands. PTH-LP messenger RNA is expressed in mammary tissue only during lactation; it appears and disappears rapidly (2 to 4 hours) as a function of the sucking stimulus. The identity of this messenger RNA was confirmed by cloning the rat PTH-LP complementary DNA, which predicts a peptide with strong similarity to the human homolog. Moreover, extracts from lactating mammary tissue stimulated parathyroid hormone-dependent adenylate cyclase. These findings suggest that PTH-LP plays a physiological role in lactation, possibly as a hormone for the mobilization or transfer (or both) of calcium to the milk.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thiede, M A -- Rodan, G A -- New York, N.Y. -- Science. 1988 Oct 14;242(4876):278-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bone Biology and Osteoporosis Research, Merck Sharp & Dohme Research Laboratories, West Point, PA 19486.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175653" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/metabolism ; Amino Acid Sequence ; Animals ; Base Sequence ; Calcium/*metabolism ; Cloning, Molecular ; DNA/genetics ; Female ; *Gene Expression Regulation ; Humans ; Lactation/*metabolism ; Mammary Glands, Animal/*metabolism ; Molecular Sequence Data ; Neoplasm Proteins/*genetics/physiology ; Parathyroid Hormone-Related Protein ; Pregnancy ; RNA, Messenger/genetics/*metabolism ; Rats ; Sequence Homology, Nucleic Acid ; Tissue Distribution
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  • 42
    Publication Date: 1988-04-15
    Description: Immunization with radiation-attenuated malaria sporozoites induces potent cellular immune responses, but the target antigens are unknown and have not previously been elicited by subunit vaccines prepared from the circumsporozoite (CS) protein. A method is described here for inducing protective cell-mediated immunity to sporozoites by immunization with attenuated Salmonella typhimurium transformed with the Plasmodium berghei CS gene. These transformants constitutively express CS antigens and, when used to immunize mice orally, colonize the liver, induce antigen-specific cell-mediated immunity, and protect mice against sporozoite challenge in the absence of antisporozoite antibodies. These data indicate that the CS protein contains T cell epitopes capable of inducing protective cell-mediated immunity, and emphasize the importance of proper antigen presentation in generating this response. Analogous, orally administered vaccines against human malaria might be feasible.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sadoff, J C -- Ballou, W R -- Baron, L S -- Majarian, W R -- Brey, R N -- Hockmeyer, W T -- Young, J F -- Cryz, S J -- Ou, J -- Lowell, G H -- New York, N.Y. -- Science. 1988 Apr 15;240(4850):336-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bacterial Diseases, Walter Reed Army Institute of Research, Washington, DC 20307-5100.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3281260" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Surface/*immunology ; Bacterial Vaccines/*immunology ; Female ; Liver/microbiology ; Malaria/*immunology/prevention & control ; Mice ; Mice, Inbred BALB C ; Plasmids ; Plasmodium berghei/*immunology ; *Protozoan Proteins ; Salmonella typhimurium/genetics/*immunology
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  • 43
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-10-07
    Description: In the adult mammalian visual system, ganglion cell axons from the two eyes are segregated from each other into separate layers within their principal target, the lateral geniculate nucleus. The involvement of spontaneously generated action potential activity in the process of segregation was investigated during the fetal period in which segregation normally occurs in the cat, between embryonic day 45 (E45) and birth (E65). Tetrodotoxin, which blocks the voltage-sensitive sodium channel, was used to prevent action potentials. Fetuses received continuous intracranial infusions of tetrodotoxin from osmotic minipumps implanted in utero on E42. After a 2-week infusion, intraocular injections of anterograde tracers revealed that tetrodotoxin prevented segregation. The contralateral projection filled the lateral geniculate nucleus uniformly, and the ipsilateral projection expanded to occupy most of what would normally be contralaterally innervated layer A. Thus, in the fetus, long before the onset of vision, spontaneous action potential activity is likely to be present in the visual system and to contribute to the segregation of the retinogeniculate pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shatz, C J -- Stryker, M P -- EY 02874/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1988 Oct 7;242(4875):87-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175636" target="_blank"〉PubMed〈/a〉
    Keywords: Afferent Pathways/drug effects/*embryology ; Animals ; Cats ; Female ; Fetus ; Infusions, Parenteral ; Optic Chiasm/drug effects/*embryology ; Pregnancy ; Reference Values ; Tetrodotoxin/administration & dosage/*pharmacology ; Visual Pathways/drug effects/*embryology
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  • 44
    Publication Date: 1988-11-11
    Description: Despite its potential toxicity, H2O2 is used as an extracellular oxidant by Stronglylocentrotus purpuratus eggs to cross-link their fertilization envelopes. These eggs contain 5 mM 1-methyl-N alpha,N alpha-dimethyl-4-mercaptohistidine (ovothiol C), which reacts with H2O2. In consuming H2O2 and being reduced by glutathione, ovothiol acts as a glutathione peroxidase and replaces the function of the enzyme in eggs. The ovothiol system is more effective than egg catalase in destroying H2O2 at concentrations produced during fertilization and constitutes a principal mechanism for preventing oxidative damage at fertilization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Turner, E -- Hager, L J -- Shapiro, B M -- GM23910/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Nov 11;242(4880):939-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3187533" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids, Sulfur/*metabolism ; Animals ; Catalase/metabolism ; Disulfides/metabolism ; Female ; Fertilization ; Glutathione/metabolism ; Glutathione Peroxidase/*metabolism ; Kinetics ; *Methylhistidines ; NADP/metabolism ; Ovum/*metabolism ; Oxidation-Reduction ; Sea Urchins
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  • 45
    Publication Date: 1988-08-05
    Description: Qa-2, a cell-surface glycoprotein anchored by phosphatidylinositol (PI), is structurally related to the class I transplantation antigens H-2 K, D, and L, which are integral membrane glycoproteins. The predicted transmembrane segment of Qa-2 differs from those of H-2 K, D, and L by the presence of an aspartate in place of a valine at position 295. A single base change that replaced this aspartate with valine resulted in cell-surface Qa-2 molecules that were insensitive to hydrolysis by a PI-specific phospholipase C and more resistant to papain cleavage, properties shared by H-2D. Cells expressing Asp----Val mutant Qa-2 proteins were still able to attach a PI anchor to endogenous proteins such as Thy-1 and J11D. It therefore appears that this single amino acid change converts Qa-2 from a PI-linked form into an integral membrane protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Waneck, G L -- Stein, M E -- Flavell, R A -- AI24562/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Aug 5;241(4866):697-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biogen Research Corporation, Cambridge, MA 02142.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3399901" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Antigens, Surface/genetics ; *Aspartic Acid ; Cell Line ; DNA/genetics ; H-2 Antigens ; *Histocompatibility Antigens/genetics ; *Histocompatibility Antigens Class I ; Membrane Proteins/genetics/*metabolism ; Mutation ; Papain/metabolism ; Phosphatidylinositols/*metabolism ; Thymoma ; Thymus Neoplasms ; Transfection ; Tumor Cells, Cultured ; Type C Phospholipases/metabolism ; *Valine
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  • 46
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-06-17
    Description: A two-locus genetic model is studied in which one locus controls the tendency of individuals to act altruistically toward siblings and the other locus controls the mating habits of females. It is demonstrated that genetic variation at the altruism locus is often sufficient to induce an increase in the frequency of genes that cause females to produce all of their offspring with a single mate. This occurs because of nonrandom associations that develop between genes that cause altruism and those that affect female mating behavior. The results provide a new explanation for the evolution of monogamy, and they suggest a previously unexplored mechanism for the evolution of a variety of other behavioral traits as well.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peck, J R -- Feldman, M W -- GM 10452/GM/NIGMS NIH HHS/ -- GM 28016/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 17;240(4859):1672-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3381088" target="_blank"〉PubMed〈/a〉
    Keywords: *Altruism ; Animals ; *Biological Evolution ; Female ; Genotype ; Humans ; Male ; Mathematics ; Polymorphism, Genetic ; Recombination, Genetic ; *Sexual Behavior, Animal ; *Sibling Relations
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  • 47
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-10-21
    Description: Mutations caused by the insertion of members of the Ac or Spm family of transposable elements result in a great diversity of phenotypes. With the cloning of the mutant genes and the characterization of their products, the mechanisms underlying phenotypic diversity are being deciphered. These mechanisms include (i) imprecise excision of transposable elements, which can result in the addition of amino acids to proteins; (ii) DNA methylation, which has been correlated with the activity of the element; (iii) transposase-mediated deletions within elements, which can inactivate an element or lead to a new unstable phenotype; and (iv) removal of transcribed elements from RNA, which can facilitate gene expression despite the insertion of elements into exons. An understanding of the behavior of the maize elements has provided clues to the function of cryptic elements in all maize genomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wessler, S R -- GM32528/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Oct 21;242(4877):399-405.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Botany Department, University of Georgia, Athens 30602.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2845581" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; *DNA Transposable Elements ; Mutation ; Phenotype ; Plants/*genetics ; Zea mays/genetics
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  • 48
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-05-06
    Description: Although the genetic code for protein was established in the 1960's, the basis for amino acid identity of transfer RNA (tRNA) has remained unknown. To investigate the identity of a tRNA, the nucleotides at three computer-identified positions in tRNAPhe (phenylalanine tRNA) were replaced with the corresponding nucleotides from tRNAAla (alanine tRNA). The identity of the resulting tRNA, when examined as an amber suppressor in Escherichia coli, was that of tRNAAla.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McClain, W H -- Foss, K -- AI10257/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 May 6;240(4853):793-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bacteriology, University of Wisconsin, Madison 53706.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2452483" target="_blank"〉PubMed〈/a〉
    Keywords: Alanine/genetics ; Amino Acids/*genetics ; Base Composition ; Base Sequence ; Escherichia coli/*genetics ; Guanosine ; Mutation ; Phenylalanine/genetics ; RNA, Bacterial/*genetics ; RNA, Transfer/*genetics ; RNA, Transfer, Ala/genetics ; RNA, Transfer, Gly/genetics ; RNA, Transfer, Lys/genetics ; RNA, Transfer, Phe/genetics ; Suppression, Genetic ; Uridine
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  • 49
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-09-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, L -- New York, N.Y. -- Science. 1988 Sep 2;241(4870):1164.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3413481" target="_blank"〉PubMed〈/a〉
    Keywords: *Abortion, Induced ; *Ethics, Medical ; Female ; *Fetus ; Humans ; *Legislation, Medical ; National Institutes of Health (U.S.) ; Pregnancy ; United States
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  • 50
    Publication Date: 1988-02-19
    Description: A replication-defective variant of feline leukemia virus was molecularly cloned directly from infected tissue and found to induce a rapid and fatal immunodeficiency syndrome in cats. Studies with cloned viruses also showed that subtle mutational changes would convert a minimally pathogenic virus into one that would induce an acute form of immunodeficiency. The data suggest that acutely pathogenic viruses may be selected against by current methods for isolation of the human and simian immunodeficiency viruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Overbaugh, J -- Donahue, P R -- Quackenbush, S L -- Hoover, E A -- Mullins, J I -- CA01058/CA/NCI NIH HHS/ -- CA07966/CA/NCI NIH HHS/ -- CA43216/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Feb 19;239(4842):906-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Harvard School of Public Health, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2893454" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome ; Amino Acid Sequence ; Animals ; Base Sequence ; Bone Marrow/microbiology ; Cats ; *Cloning, Molecular ; DNA, Viral/genetics ; Humans ; Immunologic Deficiency Syndromes/*etiology/microbiology ; Leukemia Virus, Feline/*genetics/pathogenicity ; Molecular Sequence Data ; Mutation ; Polymorphism, Restriction Fragment Length ; Transfection ; Virus Replication
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  • 51
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-06-17
    Description: Angiotensin II (Ang II) is present in high concentrations in preovulatory follicular fluid, and ovarian follicular cells have specific Ang II receptors. To investigate the possible direct involvement of Ang II in ovulation the specific receptor antagonist of Ang II, saralasin, was administered by intraperitoneal injection to immature rats in which follide development and ovulation had been induced with pregnant mare serum gonadotrophin (PMSG) and human chorionic gonadotrophin (hCG), respectively. Saralasin halved the number of oocytes found in the fallopian tubes 17 to 20 hours after administration of hCG. The antiovulatory effect was observed when saralasin was given 1 hour before hCG or 1 or 3 hours after hCG but not when given 5 hours after hCG. Simultaneous administration of Ang II reversed the saralasin blockage of ovulation. These results indicate a direct, obligate role for Ang II in ovulation and raise the possibility of contraceptive and profertility applications for agonists or antagonists of the renin-angiotensin system that are aimed at the ovulatory process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pellicer, A -- Palumbo, A -- DeCherney, A H -- Naftolin, F -- HD22970/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 17;240(4859):1660-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, CT 06510.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3381087" target="_blank"〉PubMed〈/a〉
    Keywords: Angiotensin II/antagonists & inhibitors/*physiology ; Animals ; Cell Count ; Chorionic Gonadotropin/pharmacology ; Fallopian Tubes/cytology ; Female ; Gonadotropins, Equine/pharmacology ; Oocytes/cytology ; Ovulation/*drug effects ; Rats ; Rats, Inbred Strains ; Saralasin/*pharmacology
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  • 52
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-11-25
    Description: A study was conducted to determine the fidelity of DNA synthesis catalyzed in vitro by the reverse transcriptase from a human immunodeficiency virus type 1 (HIV-1). Like other retroviral reverse transcriptases, the HIV-1 enzyme does not correct errors by exonucleolytic proofreading. Measurements with M13mp2-based fidelity assays indicated that the HIV-1 enzyme, isolated either from virus particles or from Escherichia coli cells infected with a plasmid expressing the cloned gene, was exceptionally inaccurate, having an average error rate per detectable nucleotide incorporated of 1/1700. It was, in fact, the least accurate reverse transcriptase described to date, one-tenth as accurate as the polymerases isolated from avian myeloblastosis or murine leukemia viruses, which have average error rates of approximately 1/17,000 and approximately 1/30,000, respectively. DNA sequence analyses of mutations generated by HIV-1 polymerase showed that base substitution, addition, and deletion errors were all produced. Certain template positions were mutational hotspots where the error rate could be as high as 1 per 70 polymerized nucleotides. The data are consistent with the notion that the exceptional diversity of the HIV-1 genome results from error-prone reverse transcription.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, J D -- Bebenek, K -- Kunkel, T A -- New York, N.Y. -- Science. 1988 Nov 25;242(4882):1171-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2460925" target="_blank"〉PubMed〈/a〉
    Keywords: Avian Myeloblastosis Virus/enzymology ; DNA/*biosynthesis ; DNA-Directed DNA Polymerase/metabolism ; Electrophoresis, Polyacrylamide Gel ; Escherichia coli/enzymology ; Exonucleases/metabolism ; HIV/*enzymology ; Moloney murine leukemia virus/enzymology ; Mutation ; Nucleotides/metabolism ; RNA-Directed DNA Polymerase/genetics/*metabolism ; Recombinant Proteins/metabolism
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  • 53
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-01-29
    Description: A sequencing method called genomic amplification with transcript sequencing (GAWTS) is described that is based on amplification with the polymerase chain reaction (PCR). GAWTS bypasses cloning and increases the rate of sequence acquisition by at least fivefold. The method involves the attachment of a phage promoter onto at least one of the PCR primers. The segments amplified by PCR are transcribed to further increase the signal and to provide an abundance of single-stranded template for reverse transcriptase-mediated dideoxy sequencing. An end-labeled reverse transcriptase primer complementary to the desired sequence generates the additional specificity required to generate unambiguous sequence data. GAWTS can be performed on as little as a nanogram of genomic DNA. The rate of GAWTS can be increased by coamplification and cotranscription of multiple regions as illustrated by two regions of the factor IX gene. Since GAWTS lends itself well to automation, further increases in the rate of sequence acquisition can be expected.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stoflet, E S -- Koeberl, D D -- Sarkar, G -- Sommer, S S -- New York, N.Y. -- Science. 1988 Jan 29;239(4839):491-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Mayo Clinic/Foundation, Rochester, MN 55905.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3340835" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; DNA/genetics ; DNA-Directed DNA Polymerase/metabolism ; DNA-Directed RNA Polymerases ; Electrophoresis, Agar Gel ; Exons ; Factor IX/*genetics ; Hemophilia A/genetics ; Humans ; Molecular Sequence Data ; Mutation ; *Nucleic Acid Amplification Techniques ; T-Phages/enzymology ; *Transcription, Genetic
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  • 54
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-02-05
    Description: The epidemic of infection with the human immunodeficiency virus (HIV) and the acquired immunodeficiency syndrome (AIDS) poses a major ethical question: How can we control the epidemic and the harm that it causes without unjustly discriminating against particular social groups and without unnecessarily infringing on the freedom of individuals? This question pertains to three spheres of public policy in the United States: public health, the delivery of health care, and research. In the public health sphere, vigorous educational efforts will be required, as will modified approaches to intravenous drug use, prostitution, and homosexual and bisexual sexual activity. Carefully targeted, voluntary testing and screening programs should be coupled with counseling and with guarantees of confidentiality and nondiscrimination where these are appropriate. Both health care workers and the health care system have a moral obligation to provide care to people with HIV infection, but heroic self-sacrifice should not be required provided that infection control precautions are observed. Patients with neurological involvement and terminally ill patients will benefit from statutes allowing recognition of advance directives about preferred modes of care or nontreatment. There is a moral imperative to perform intensive research directed toward the understanding, treatment, and prevention of HIV infection and AIDS. The research process will raise challenging ethical questions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walters, L -- New York, N.Y. -- Science. 1988 Feb 5;239(4840):597-603.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Bioethics, Kennedy Institute of Ethics, Washington, DC 20057.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3340846" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*prevention & control/therapy ; Adult ; Beneficence ; Biomedical Research ; Bisexuality ; Brain Diseases ; Delivery of Health Care ; *Ethics, Medical ; Female ; Government Regulation ; Health Education ; Health Policy ; Homosexuality ; Humans ; Male ; Mandatory Programs ; *Moral Obligations ; Personal Autonomy ; Resource Allocation ; Risk Assessment ; Social Justice ; Substance-Related Disorders ; United States ; *Voluntary Programs
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  • 55
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-05-06
    Description: In many bird species, those pairs that breed earlier in the season have higher reproductive success than those that breed later. Since breeding date is known to be heritable, it is unclear why it does not evolve to an earlier time. Under assumptions outlined by Fisher, a model is developed that shows how breeding date may have considerable additive genetic variance, appear to be under directional selection, and yet not evolve. These results provide a general explanation for a persistent correlation of fitness with a variety of traits in natural populations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Price, T -- Kirkpatrick, M -- Arnold, S J -- 1R01GM3549201/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 May 6;240(4853):798-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California, San Diego, La Jolla 92093.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3363360" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Birds/*physiology ; Female ; Fertility ; Genetic Variation ; Nutritional Status ; *Reproduction ; *Seasons ; *Selection, Genetic ; Time Factors
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  • 56
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-09-02
    Description: A mutation has been found that dramatically shortens the period of the circadian locomotor rhythm of golden hamsters. The pattern of inheritance of this mutation suggests that it occurred at a single, autosomal locus (tau). Wild-type animals have rhythms with free-running periods averaging about 24 hours; animals heterozygous for the mutation have periods of about 22 hours, whereas homozygous animals have rhythms with periods close to 20 hours. Animals that carry the mutant alleles exhibit abnormal entrainment to 24-hour light:dark cycles or are unable to entrain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ralph, M R -- Menaker, M -- HD 13162/HD/NICHD NIH HHS/ -- MH 09483/MH/NIMH NIH HHS/ -- MH 17148/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 2;241(4870):1225-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neuroscience, University of Oregon, Eugene 97403.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3413487" target="_blank"〉PubMed〈/a〉
    Keywords: *Activity Cycles ; Animals ; *Circadian Rhythm ; Cricetinae/*genetics ; Heterozygote ; Homozygote ; Light ; Male ; Mesocricetus/*genetics/physiology ; Motor Activity/physiology ; Mutation ; Periodicity ; Phenotype
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  • 57
    Publication Date: 1988-09-30
    Description: Control of growth and differentiation during mammalian embryogenesis may be regulated by growth factors from embryonic or maternal sources. With the use of single-cell messenger RNA phenotyping, the simultaneous expression of growth factor transcripts in single or small numbers of preimplantation mouse embryos was examined. Transcripts for platelet-derived growth factor A chain (PDGF-A), transforming growth factor (TGF)-alpha, and TGF-beta 1, but not for four other growth factors, were found in whole blastocysts. TGF-alpha, TGF-beta 1, and PDGF antigens were detected in blastocysts by immunocytochemistry. Both PDGF-A and TGF-alpha were detected as maternal transcripts in the unfertilized ovulated oocyte, and again in blastocysts. TGF-beta 1 transcripts appeared only after fertilization. The expression of a subset of growth factors in mouse blastocysts suggests a role for these factors in the growth and differentiation of early mammalian embryos.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rappolee, D A -- Brenner, C A -- Schultz, R -- Mark, D -- Werb, Z -- 5T32 ES07106/ES/NIEHS NIH HHS/ -- HD22681/HD/NICHD NIH HHS/ -- HD23539/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 30;241(4874):1823-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Radiobiology and Environmental Health, University of California, San Francisco 94143-0750.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175624" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/*physiology ; Cleavage Stage, Ovum/physiology ; Embryonic Development ; Female ; Gene Expression Regulation ; Growth Substances/*genetics ; Mice ; Oocytes/physiology ; Platelet-Derived Growth Factor/*genetics ; Pregnancy ; RNA, Messenger/genetics ; Transcription, Genetic ; Transforming Growth Factors/*genetics
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  • 58
    Publication Date: 1988-03-11
    Description: The alterations in morphology and function of the ovarian follicle as it matures, ovulates, and becomes a corpus luteum are dramatic. A variety of steroid and polypeptide hormones influence these processes, and the ovary in turn produces specific hormonal signals for endocrine regulation. One such signal is inhibin, a heterodimeric protein that suppresses the secretion of follicle-stimulating hormone from pituitary gonadotrophs. Rat inhibin complementary DNA probes have been used to examine the levels and distribution of inhibin alpha-and beta A-subunit messenger RNAs in the ovaries of cycling animals. Striking, dynamic changes have been found in inhibin messenger RNA accumulation during the developmental maturation of the ovarian follicle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Woodruff, T K -- D'Agostino, J -- Schwartz, N B -- Mayo, K E -- HD07504/HD/NICHD NIH HHS/ -- HD21921/HD/NICHD NIH HHS/ -- P01 HD021921/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 11;239(4845):1296-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Molecular Biology and Cell Biology, Northwestern University, Evanston, IL 60208.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3125611" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Estrus ; Female ; Follicle Stimulating Hormone/blood ; Inhibins/*genetics ; Luteinizing Hormone/blood ; Macromolecular Substances ; Nucleic Acid Hybridization ; Ovarian Follicle/*physiology ; Ovary/physiology ; RNA, Messenger/*genetics/metabolism ; Rats
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  • 59
    Publication Date: 1988-02-05
    Description: To investigate the relation between protein stability and the predicted stabilities of individual secondary structural elements, residue Pro86 in an alpha-helix in phage T4 lysozyme was replaced by ten different amino acids. The x-ray crystal structures of seven of the mutant lysozymes were determined at high resolution. In each case, replacement of the proline resulted in the formation of an extended alpha-helix. This involves a large conformational change in residues 81 to 83 and smaller shifts that extend 20 angstroms across the protein surface. Unexpectedly, all ten amino acid substitutions marginally reduce protein thermostability. This insensitivity of stability to the amino acid at position 86 is not simply explained by statistical and thermodynamic criteria for helical propensity. The observed conformational changes illustrate a general mechanism by which proteins can tolerate mutations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alber, T -- Bell, J A -- Sun, D P -- Nicholson, H -- Wozniak, J A -- Cook, S -- Matthews, B W -- GM 20066/GM/NIGMS NIH HHS/ -- GM 21967/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Feb 5;239(4840):631-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physics, University of Oregon, Eugene 97403.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3277275" target="_blank"〉PubMed〈/a〉
    Keywords: Enzyme Stability ; Escherichia coli/enzymology ; Models, Molecular ; Muramidase/*genetics/metabolism ; Mutation ; *Proline ; Protein Conformation ; T-Phages/*enzymology/genetics ; X-Ray Diffraction
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  • 60
    Publication Date: 1988-01-22
    Description: Overexpression of the cellular src gene in NIH 3T3 cells causes reduction of cell-to-cell transmission of molecules in the 400- to 700-dalton range. This down-regulation of gap junctional communication correlates with the activity of the gene product, the protein tyrosine kinase pp60c-src. The down-regulation was enhanced by point mutation of Tyr527 (a site that is phosphorylated in pp60c-src and that inhibits kinase activity) or by substitution of the viral-src for the cellular-src carboxyl-terminal coding region. Mutation of Tyr416 (a site phosphorylated upon Tyr527 mutation) suppresses both the down-regulation of communication by Tyr527 mutation and that by gene overexpression. The regulation of communication by src may be important in the control of embryonic development and cellular growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Azarnia, R -- Reddy, S -- Kmiecik, T E -- Shalloway, D -- Loewenstein, W R -- CA-14464/CA/NCI NIH HHS/ -- CA-32317/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Jan 22;239(4838):398-401.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, University of Miami School of Medicine, FL 33136.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2447651" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Communication ; Cell Line ; Cell Membrane Permeability ; Gene Expression Regulation ; *Intercellular Junctions ; Mice ; Mutation ; Phosphorylation ; Plasmids ; Protein-Tyrosine Kinases/*genetics ; Proto-Oncogene Proteins/genetics/*physiology ; Proto-Oncogene Proteins pp60(c-src) ; Structure-Activity Relationship ; Transcription, Genetic ; Transfection ; Tyrosine/metabolism
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  • 61
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-12-23
    Description: Paralyzed motors of motA and motB point and deletion mutants of Escherichia coli were repaired by synthesis of wild-type protein. As found earlier with a point mutant of motB, torque was restored in a series of equally spaced steps. The size of the steps was the same for both MotA and MotB. Motors with one torque generator spent more time spinning counterclockwise than did motors with two or more generators. In deletion mutants, stepwise decreases in torque, rare in point mutants, were common. Several cells stopped accelerating after eight steps, suggesting that the maximum complement of torque generators is eight. Each generator appears to contain both MotA and MotB.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blair, D F -- Berg, H C -- AI07456/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Dec 23;242(4886):1678-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Developmental Biology, Harvard University, Cambridge, MA 02138.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2849208" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/genetics/*physiology ; Electrochemistry ; Escherichia coli/genetics/*physiology ; Flagella/*physiology ; Membrane Proteins/genetics/physiology ; Movement ; Mutation ; Plasmids ; Protons ; Transformation, Bacterial
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  • 62
    Publication Date: 1988-01-01
    Description: Follicle-stimulating hormone (FSH) is a glycoprotein essential for gonadal development and steroidogenesis. Recent studies suggest that deglycosylation of FSH results in the formation of antagonistic proteins that are capable of binding to gonadal receptors but that are devoid of bioactivity. Treatment of hypogonadal women with an antagonist of gonadotropin-releasing hormone substantially decreased serum FSH bioactivity with minimal changes in immunoreactivity. Chromatofocusing and size fractionation of the serum samples indicated the secretion of immunoreactive FSH isoforms that are devoid of bioactivity but that are capable of blocking FSH action in ovarian granulosa cells. These findings provide the first demonstration of naturally occurring circulating antihormones. These FSH antagonists may play an important role in the physiology and pathophysiology of the gonads.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dahl, K D -- Bicsak, T A -- Hsueh, A J -- HD-06875/HD/NICHD NIH HHS/ -- HD-06939/HD/NICHD NIH HHS/ -- HD-23273/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1988 Jan 1;239(4835):72-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Reproductive Medicine, University of California, San Diego, La Jolla 92093.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3122320" target="_blank"〉PubMed〈/a〉
    Keywords: Biological Assay ; Cross Reactions ; Female ; Follicle Stimulating Hormone/*antagonists & inhibitors/immunology/metabolism ; Glycoproteins/physiology ; Gonadotropin-Releasing Hormone/*antagonists & inhibitors ; Humans ; Isoelectric Point ; Radioligand Assay ; Structure-Activity Relationship
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  • 63
    Publication Date: 1988-09-30
    Description: Retinoblastoma (RB) is a malignant tumor of developing retina that arises when abnormalities resulting in loss of function affect both alleles of the gene at the retinoblastoma locus (RB1) on chromosome 13q. The majority of RB tumors do not show gross alterations in a 4.7-kb fragment (4.7R), which is a candidate RB1 gene. To search for more subtle mutations, the ribonuclease protection method was used to analyze 4.7R messenger RNA from RB tumors. Five of 11 RB tumors, which exhibit normal 4.7R DNA and normal-sized RNA transcripts, showed abnormal ribonuclease cleavage patterns. Three of the five mutations affected the same region of the messenger RNA, consistent with an effect on splicing involving an as yet unidentified 5' exon. The high frequency of mutations in 4.7R supports the identification of 4.7R as the RB1 gene. However, the unusual nature of some of the abnormalities of 4.7 R alleles indicates that the accepted sequence of genetic events involved in the genesis of RB may require reevaluation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dunn, J M -- Phillips, R A -- Becker, A J -- Gallie, B L -- New York, N.Y. -- Science. 1988 Sep 30;241(4874):1797-800.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hospital for Sick Children, Research Institute, Toronto, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175621" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cloning, Molecular ; DNA, Neoplasm/genetics ; Humans ; Mutation ; Retinoblastoma/*genetics
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  • 64
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-10-07
    Description: The mechanism by which the scanning ribosome recognizes the first AUG codon nearest the 5' end of eukaryotic messenger RNA has not been established. To investigate this an anticodon change (3'-UCC-5') was introduced into one of the four methionine initiator (tRNAi(met) genes of Saccharomyces cerevisiae. The ability of the mutant transfer RNA to restore growth properties to his4 initiator codon mutant yeast strains in the absence of histidine was then assayed. Only the complementary codon, AGG, at the his4 initiator region supported His+ growth. The mutant transfer RNA also directed the ribosome to initiate at an AGG placed in the upstream region of the his4 message. Initiation at this upstream AGG precluded initiation at a downstream AGG in accordance with the "scanning" model. Therefore, an anticodon: codon interaction between tRNAi(met) as part of the scanning ribosome and the first AUG must function in directing the ribosome to the eukaryotic initiator region.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cigan, A M -- Feng, L -- Donahue, T F -- GM32263/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Oct 7;242(4875):93-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Northwestern University Medical School, Chicago, IL 60611.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3051379" target="_blank"〉PubMed〈/a〉
    Keywords: Anticodon ; Base Sequence ; Codon ; *Genes, Fungal ; Molecular Sequence Data ; Mutation ; *Peptide Chain Initiation, Translational ; RNA, Transfer, Amino Acid-Specific/*genetics ; RNA, Transfer, Met/*genetics ; Ribosomes/*metabolism ; Saccharomyces cerevisiae/*genetics
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  • 65
    Publication Date: 1988-02-12
    Description: Four different regulatory sites required for transcriptional stimulation by the enhancers of two unrelated liver-specific genes alpha 1-antitrypsin and transthyretin appear to bind the same nuclear protein that is found mainly in the liver. Such proteins may provide a basis for a coordinated, hepatocyte-specific control of gene transcription.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grayson, D R -- Costa, R H -- Xanthopoulos, K G -- Darnell, J E -- CA 160006-14/CA/NCI NIH HHS/ -- CA 18213-11/CA/NCI NIH HHS/ -- GM 1066-02/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1988 Feb 12;239(4841 Pt 1):786-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3257586" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Enhancer Elements, Genetic ; Gene Expression Regulation ; *Genes ; Genes, Regulator ; Liver/*metabolism ; Mice ; Mutation ; Nuclear Proteins/*physiology ; Prealbumin/*genetics ; *Transcription, Genetic ; alpha 1-Antitrypsin/*genetics
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  • 66
    Publication Date: 1988-12-09
    Description: Cyclic AMP (cAMP) is an intracellular second messenger that activates transcription of many cellular genes. A palindromic consensus DNA sequence, TGACGTCA, functions as a cAMP-responsive transcriptional enhancer (CRE). The CRE binds a cellular protein of 38 kD in placental JEG-3 cells. A placental lambda gt11 library was screened for expression of specific CRE-binding proteins with the CRE sequence as a radioactive probe. A cDNA encoding a protein of 326 amino acids with the binding properties of a specific CRE-binding protein (CREB) was isolated. The protein contains a COOH-terminal basic region adjacent to a sequence similar to the "leucine zipper" sequence believed to be involved in DNA binding and in protein-protein contacts in several other DNA-associated transcriptional proteins including the products of the c-myc, c-fos, and c-jun oncogenes and GCN4. The CREB protein also contains an NH2-terminal acidic region proposed to be a potential transcriptional activation domain. The putative DNA-binding domain of CREB is structurally similar to the corresponding domains in the phorbol ester-responsive c-jun protein and the yeast transcription factor GCN4.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoeffler, J P -- Meyer, T E -- Yun, Y -- Jameson, J L -- Habener, J F -- DK 25532/DK/NIDDK NIH HHS/ -- DK 30457/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1988 Dec 9;242(4884):1430-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Endocrinology, Massachusetts General Hospital, Boston.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2974179" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; *Cloning, Molecular ; Cyclic AMP Response Element-Binding Protein ; DNA/*genetics ; DNA-Binding Proteins/*genetics/physiology ; Enhancer Elements, Genetic ; Female ; Humans ; Molecular Sequence Data ; Placenta/*metabolism ; Pregnancy ; Transcription, Genetic
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  • 67
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-08-12
    Description: Receptors for N-methyl-D-aspartate (NMDA) are involved in many plastic and pathological processes in the brain. Glycine has been reported to potentiate NMDA responses in neurons and in Xenopus oocytes injected with rat brain messenger RNA. Glycine is now shown to be absolutely required for activation of NMDA receptors in oocytes. In voltage-clamped oocytes, neither perfusion nor rapid pressure application of NMDA onto messenger RNA-injected oocytes caused a distinct ionic current without added glycine. When glycine was added, however, NMDA evoked large inward currents. The concentration of glycine required to produce a half-maximal response was 670 nanomolar, and the glycine dose-response curve extrapolated to zero in the absence of glycine. Several analogs of glycine could substitute for glycine, among which D-serine and D-alanine were the most effective. The observation that D-amino acids are effective will be important in developing drugs targeted at the glycine site.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kleckner, N W -- Dingledine, R -- NS17771/NS/NINDS NIH HHS/ -- NS22249/NS/NINDS NIH HHS/ -- NS23804/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Aug 12;241(4867):835-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of North Carolina, Chapel Hill 27599-7365.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2841759" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/pharmacology ; Animals ; Brain/metabolism ; Female ; Glycine/*analogs & derivatives/*pharmacology ; Kinetics ; Oocytes/drug effects/*metabolism ; RNA, Messenger/genetics ; Rats ; Receptors, N-Methyl-D-Aspartate ; Receptors, Neurotransmitter/drug effects/genetics/*metabolism ; Xenopus
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  • 68
    Publication Date: 1988-07-22
    Description: Fertilization initiates in the egg a dramatic increase in intracellular calcium that opens ion channels and causes exocytosis. To explore the possibility that these events might involve a receptor-mediated pathway, receptors for serotonin or acetylcholine (M1 muscarinic) were expressed in the Xenopus egg; serotonin or acetylcholine then could initiate a series of responses similar to those normally initiated by sperm. Thus, there may be an endogenous receptor in the egg membrane that is activated by sperm, and the serotonin or M1 muscarinic receptor may replace the sperm receptor in this pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kline, D -- Simoncini, L -- Mandel, G -- Maue, R A -- Kado, R T -- Jaffe, L A -- New York, N.Y. -- Science. 1988 Jul 22;241(4864):464-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Connecticut Health Center, Farmington 06032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3134693" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; Cytoplasmic Granules/physiology ; Endocytosis ; Exocytosis ; Female ; *Fertilization ; GTP-Binding Proteins/physiology ; Genetic Engineering ; Inositol Phosphates/physiology ; Male ; Membrane Potentials ; Receptors, Muscarinic/*physiology ; Receptors, Serotonin/*physiology ; Sperm-Ovum Interactions ; Xenopus laevis
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 69
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-06-03
    Description: Gonadotropin stimulates protein synthesis and growth in ovarian oocytes. The hormone is also known to modify transfollicular K+ fluxes and is now shown to cause increased intraoocytic K+ activity (aK). The hormone's effect on aK was duplicated by microinjecting K+ salts into oocytes which were incubated in paraffin oil. This treatment mimicked the influence of gonadotropin on both the rate of protein synthesis and the synthesis of specific polypeptides. These findings suggest that gonadotropin-stimulated oocyte growth is attributable largely to the hormone's influence on transfollicular K+ fluxes. They support the hypothesis that the K+ flux and aK changes observed during cell activation are critical in causing subsequent increases in protein synthesis and growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lau, Y T -- Yassin, R R -- Horowitz, S B -- New York, N.Y. -- Science. 1988 Jun 3;240(4857):1321-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, Michigan Cancer-Foundation, Detroit 48201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3375816" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chorionic Gonadotropin/*pharmacology ; Electrophoresis, Polyacrylamide Gel ; Female ; Leucine/metabolism ; Microinjections ; Oocytes/drug effects/growth & development/*metabolism ; Potassium/metabolism ; Potassium Chloride/*pharmacology ; Protein Biosynthesis ; Xenopus laevis
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  • 70
    Publication Date: 1988-12-16
    Description: Site-directed mutagenesis and expression in Xenopus oocytes were used to study acetylcholine receptors in which serine residues (i) were replaced by alanines (alpha, delta subunits) or (ii) replaced a phenylalanine (beta subunit) at a postulated polar site within the M2 transmembrane helix. As the number of serines decreased, there were decreases in the residence time and consequently the equilibrium binding affinity of QX-222, a quaternary ammonium anesthetic derivative thought to bind within the open channel. Receptors with three serine-to-alanine mutations also displayed a selective decrease in outward single-channel currents. Both the direction of this rectification and the voltage dependence of QX-222 blockade suggest that the residues mutated are within the aqueous pore of the receptor and near its cytoplasmic (inner) surface.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leonard, R J -- Labarca, C G -- Charnet, P -- Davidson, N -- Lester, H A -- NS-11756/NS/NINDS NIH HHS/ -- NS-8083/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Dec 16;242(4885):1578-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena 91125.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2462281" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/*physiology ; Cloning, Molecular ; Electric Conductivity ; Female ; Ion Channels/*physiology ; Kinetics ; Membrane Potentials ; Mutation ; Oocytes/physiology ; RNA, Messenger/genetics ; Receptors, Nicotinic/genetics/*physiology ; Transcription, Genetic ; Xenopus
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  • 71
    Publication Date: 1988-04-01
    Description: A mutant catalytic subunit of adenosine 3',5'-monophosphate (cAMP)-dependent protein kinase has been isolated from Saccharomyces cerevisiae that is no longer subject to regulation yet retains its catalytic activity. Biochemical analysis of the mutant subunit indicates a 100-fold decreased affinity for the regulatory subunit. The mutant catalytic subunit exhibits approximately a threefold increase in Michaelis constant for adenosine triphosphate and peptide cosubstrates, and is essentially unchanged in its catalytic rate. The nucleotide sequence of the mutant gene contains a single nucleotide change resulting in a threonine-to-alanine substitution at amino acid 241. This residue is conserved in other serine-threonine protein kinases. These results identify this threonine as an important contact between catalytic and regulatory subunits but only a minor contact in substrate recognition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levin, L R -- Kuret, J -- Johnson, K E -- Powers, S -- Cameron, S -- Michaeli, T -- Wigler, M -- Zoller, M J -- GM33986/GM/NIGMS NIH HHS/ -- R35 CA39829-02/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Apr 1;240(4848):68-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, NY 11724.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2832943" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Catalysis ; Cyclic AMP/*pharmacology ; Genes, Fungal ; Kinetics ; Macromolecular Substances ; Molecular Sequence Data ; Mutation ; Phosphorylation ; Protein Kinases/*genetics/metabolism ; Saccharomyces cerevisiae/enzymology/*genetics ; Structure-Activity Relationship ; Threonine
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  • 72
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-11-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1988 Nov 4;242(4879):668.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3187517" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Female ; Male ; Primates/*physiology ; Sexual Behavior, Animal/*physiology ; Spermatozoa/physiology ; Testis/anatomy & histology
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  • 73
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-06-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1988 Jun 3;240(4857):1277-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3375815" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Birds/physiology ; Female ; Male ; *Sex Characteristics ; *Sexual Behavior, Animal
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  • 74
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-05-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1988 May 13;240(4854):884.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3363371" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Body Constitution ; Body Height ; Body Weight ; Female ; *Fertility ; Male ; Models, Biological ; *Sex Characteristics
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  • 75
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-08-26
    Description: Centromeres are the structural elements of eukaryotic chromosomes that hold sister chromatids together and to which spindle tubules connect during cell division. Centromeres have been shown to suppress meiotic recombination in some systems. In this study yeast strains genetically marked within and flanking a centromere, were used to demonstrate that gene conversion (nonreciprocal recombination) tracts in mitosis can enter into and extend through the centromere.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liebman, S W -- Symington, L S -- Petes, T D -- GM24110/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Aug 26;241(4869):1074-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Cell Biology, University of Chicago, IL 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3137657" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Centromere/*metabolism ; Chromosomes/*metabolism ; Crossing Over, Genetic ; Gene Conversion ; Genes, Fungal ; Histidine/metabolism ; Leucine/metabolism ; *Mitosis ; Mutation ; *Recombination, Genetic ; Saccharomyces cerevisiae/*genetics/growth & development ; Threonine/metabolism ; Trichodermin/pharmacology ; Uracil/metabolism
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  • 76
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-04-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1988 Apr 22;240(4851):391.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3358126" target="_blank"〉PubMed〈/a〉
    Keywords: *Aborted Fetus ; Abortion, Spontaneous ; Advisory Committees ; Brain/embryology ; *Ethics ; Federal Government ; Female ; *Fetal Research ; Government Regulation ; Humans ; Nerve Tissue/transplantation ; Parkinson Disease/*therapy ; Pregnancy ; *Tissue and Organ Procurement
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  • 77
    Publication Date: 1988-03-04
    Description: Amino acid sequences deduced from rat complementary DNA clones encoding the insulin-like growth factor II (IGF-II) receptor closely resemble those of the bovine cation-independent mannose-6-phosphate receptor (Man-6-P receptorCI), suggesting they are identical structures. It is also shown that IGF-II receptors are adsorbed by immobilized pentamannosyl-6-phosphate and are specifically eluted with Man-6-P. Furthermore, Man-6-P specifically increases by about two times the apparent affinity of the purified rat placental receptor for 125I-labeled IGF-II. These results indicate that the type II IGF receptor contains cooperative, high-affinity binding sites for both IGF-II and Man-6-P-containing proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉MacDonald, R G -- Pfeffer, S R -- Coussens, L -- Tepper, M A -- Brocklebank, C M -- Mole, J E -- Anderson, J K -- Chen, E -- Czech, M P -- Ullrich, A -- CA 39240/CA/NCI NIH HHS/ -- DK 30648/DK/NIDDK NIH HHS/ -- DK 34063/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1988 Mar 4;239(4844):1134-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Massachusetts Medical Center, Worcester 01655.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2964083" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Carrier Proteins/genetics/*metabolism ; Cell Membrane/analysis/metabolism ; Chromatography, Affinity ; DNA/genetics ; Female ; Hexosephosphates/*metabolism ; Insulin-Like Growth Factor II/*metabolism ; Mannosephosphates/*metabolism ; Molecular Sequence Data ; Placenta/analysis ; Pregnancy ; Rats ; Receptor, IGF Type 2 ; Receptor, Insulin/genetics/*metabolism ; Receptors, Somatomedin ; Sequence Homology, Nucleic Acid ; Somatomedins/*metabolism
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  • 78
    Publication Date: 1988-11-04
    Description: Duchenne muscular dystrophy (DMD) and its less severe form Becker muscular dystrophy (BMD) are allelic disorders. It has been suggested that in the mutations involving BMD, the translational reading frame of messenger RNA is maintained and a smaller, though partially functional, protein is produced. In order to test this, the exon-intron boundaries of the first ten exons of the DMD gene were determined, and 29 patients were analyzed. In a number of BMD patients (mild and severe BMD), the reading frame of messenger RNA was not maintained. On the basis of these findings, a model for reinitiation from an internal start codon is suggested.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malhotra, S B -- Hart, K A -- Klamut, H J -- Thomas, N S -- Bodrug, S E -- Burghes, A H -- Bobrow, M -- Harper, P S -- Thompson, M W -- Ray, P N -- New York, N.Y. -- Science. 1988 Nov 4;242(4879):755-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genetics Department, Hospital for Sick Children, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3055295" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Blotting, Southern ; Chromosome Deletion ; DNA Probes ; Dystrophin ; Exons ; Genes ; Humans ; Muscle Proteins/*genetics ; Muscular Dystrophies/*genetics ; Mutation ; Phenotype ; *X Chromosome
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  • 79
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-03-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnes, D M -- New York, N.Y. -- Science. 1988 Mar 4;239(4844):1091-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2449731" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Egg Proteins ; Female ; Glycoproteins/genetics/physiology ; Humans ; *Interferon Type I ; Interferons ; Male ; *Membrane Glycoproteins ; Pregnancy Proteins/physiology ; *Receptors, Cell Surface ; *Sperm-Ovum Interactions ; Testicular Hormones/physiology
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  • 80
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-10-14
    Description: Oligonucleotide-directed mutagenesis of the codons for glutamine-68 (Gln68), lysine-72 (Lys72), isoleucine-79 (Ile79), alanine-80 (Ala80), and threonine-81 (Thr81) of the Escherichia coli trpR (tryptophan aporepressor) gene was used to make mutant repressors with each of 36 different amino acid changes. Mutant repressors were tested for binding to each member of a set of 28 different operators closely related to the consensus trp operator. Of the 36 mutant repressors, 11 bind a subset of the 28 operators; 5 of these have new binding specificities. These new specificities indicate that the hydroxyl group of Thr81 makes a specific contact with one of the four critical base pairs in a trp operator half-site, and the methyl group of Thr81 determines specificity at a second, critical base pair. The Trp repressor does not use the first two amino acids of its "recognition alpha-helix," Ile79 and Ala80, to make sequence-specific DNA contacts, and interacts with its operator in vivo in a way fundamentally different from the way that phage lambda repressor, lambda Cro protein, and coliphage 434 repressor contact their respective binding sites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bass, S -- Sorrells, V -- Youderian, P -- GM34150/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Oct 14;242(4876):240-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, University of Southern California, Los Angeles 90089-1481.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3140377" target="_blank"〉PubMed〈/a〉
    Keywords: Alanine/genetics ; Amino Acid Sequence ; Apoproteins/*genetics/metabolism ; Bacterial Proteins ; Base Sequence ; Binding Sites ; Codon ; DNA, Bacterial/*metabolism ; Escherichia coli/*genetics ; *Escherichia coli Proteins ; Glutamine/genetics ; Isoleucine/genetics ; Lysine/genetics ; Mutation ; Operator Regions, Genetic ; Protein Conformation ; Repressor Proteins/*genetics/metabolism ; Threonine/genetics ; Transcription Factors/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 81
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-03-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bloom, M -- New York, N.Y. -- Science. 1988 Mar 11;239(4845):1235-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3344431" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; American Medical Association ; *Editorial Policies ; Ethicists ; *Ethics, Medical ; *Euthanasia ; *Euthanasia, Active ; Euthanasia, Active, Voluntary ; Female ; Humans ; Morphine ; Ovarian Neoplasms/physiopathology ; Pain, Intractable/physiopathology ; *Periodicals as Topic ; United States
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  • 82
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-12-23
    Description: The position of selected chromosomes was assessed in samples of normal and epileptic human cortex with biotinylated probes specific for individual chromosome domains. Optical sectioning provided a rapid method for three-dimensional resolution of in situ hybridization signals in interphase cells, and solid models were reconstructed from digitized images for detailed rotational studies. There was a dramatic repositioning of the X chromosome in neurons of both males and females in electrophysiologically defined seizure foci. Other chromosomes (1, 9, and Y) showed more subtle positional changes. Specifically altered nuclear patterns involving the X chromosome may become established and create the genetic memory for intractable seizure activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Borden, J -- Manuelidis, L -- CA15044/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Dec 23;242(4886):1687-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Yale University School of Medicine, New Haven, CT 06510.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3201257" target="_blank"〉PubMed〈/a〉
    Keywords: Astrocytes/ultrastructure ; Cell Nucleolus/ultrastructure ; Cell Nucleus/ultrastructure ; Cerebral Cortex/ultrastructure ; DNA Probes ; Epilepsy/*genetics/physiopathology ; Female ; Humans ; Image Processing, Computer-Assisted ; Male ; Microscopy, Electron ; Neurons/ultrastructure ; Nuclear Envelope/ultrastructure ; Nucleic Acid Hybridization ; *X Chromosome
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 83
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-10-28
    Description: In some reptiles, egg incubation temperature determines whether the embryo hatches as male or female; in others, sex chromosomes determine sex. A cloned gene (ZFY) representing the putative testis-determining factor in mammals was hybridized to genomic DNA of reptiles with sex chromosomes and to DNA of reptiles with temperature-dependent sex determination. No sex differences in hybridization patterns were observed. Hybridization of ZFY to polyadenylated RNA indicates that reptilian versions of this gene are expressed in embryos of both sexes during the temperature-sensitive period. If these highly conserved sequences are important in reptilian sex determination, then temperature-dependent and genotypic sex determination may have a similar molecular basis. For reptiles with XX/XY or ZZ/ZW systems, the absence of sex differences in hybridization patterns raises the question of whether the ZFY sequences reside on their sex chromosomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bull, J J -- Hillis, D M -- O'Steen, S -- New York, N.Y. -- Science. 1988 Oct 28;242(4878):567-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, University of Texas, Austin 78712.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3140382" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Birds/*genetics ; Blotting, Southern ; DNA Probes ; DNA-Binding Proteins/*genetics ; Female ; Gonadal Steroid Hormones/*genetics ; Male ; Metalloproteins/*genetics ; Reptiles/*physiology ; *Sex Determination Analysis ; Temperature
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 84
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-08-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Byrne, G -- New York, N.Y. -- Science. 1988 Aug 19;241(4868):895.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3406745" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; Humans ; *Insemination, Artificial ; Male ; Sperm Banks/*legislation & jurisprudence/standards ; Tissue Banks/*legislation & jurisprudence ; United States
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  • 85
    Publication Date: 1988-03-18
    Description: Complementary DNA clones were isolated that represent the 5' terminal 2.5 kilobases of the murine Duchenne muscular dystrophy (Dmd) messenger RNA (mRNA). Mouse Dmd mRNA was detectable in skeletal and cardiac muscle and at a level approximately 90 percent lower in brain. Dmd mRNA is also present, but at much lower than normal levels, in both the muscle and brain of three different strains of dystrophic mdx mice. The identification of Dmd mRNA in brain raises the possibility of a relation between human Duchenne muscular dystrophy (DMD) gene expression and the mental retardation found in some DMD males. These results also provide evidence that the mdx mutations are allelic variants of mouse Dmd gene mutations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chamberlain, J S -- Pearlman, J A -- Muzny, D M -- Gibbs, R A -- Ranier, J E -- Caskey, C T -- Reeves, A A -- New York, N.Y. -- Science. 1988 Mar 18;239(4846):1416-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular Genetics, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3347839" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; DNA/genetics ; DNA, Recombinant ; *Gene Expression Regulation ; Intellectual Disability/genetics ; Mice ; Mice, Inbred ICR ; Mice, Mutant Strains ; Muscles/*metabolism ; Muscular Dystrophy, Animal/*genetics ; Mutation ; Nucleic Acid Hybridization ; RNA, Messenger/metabolism ; Ribonuclease, Pancreatic/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 86
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-05-20
    Description: The T lymphocyte antigen-receptor complex mediates antigen-specific cell activation, at least in part, through the production of inositolphospholipid-derived second messengers. Little is known about how second messenger events, typically measured within minutes of ligand binding, eventually lead to distal biologic responses such as expression of lymphokine genes. Several monoclonal antibodies directed against the receptor complex were tested for their ability to elicit transmembrane signaling in the parental Jurkat line and in a somatic mutant (J.CaM1) with a deficient receptor function. One antibody elicited substantial early Ca2+ mobilization responses in both cells but was unable to promote expression of the interleukin-2 gene in J.CaM1. In J.CaM1 there was a diminished production of phosphatidylinositol second messengers, and the elevation in intracellular free Ca2+ was transient. Thus, short-term Ca2+ mobilization does not always indicate complete signal transmission and lead to a full cellular response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldsmith, M A -- Weiss, A -- New York, N.Y. -- Science. 1988 May 20;240(4855):1029-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Francisco.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3259335" target="_blank"〉PubMed〈/a〉
    Keywords: Calcium/physiology ; Cell Line ; Cell Membrane/immunology ; Genes ; Humans ; Interleukin-2/biosynthesis/genetics ; Mutation ; Receptors, Antigen, T-Cell/*physiology ; T-Lymphocytes/*immunology
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  • 87
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-01-29
    Description: Dengue viruses occur as four antigenically related but distinct serotypes transmitted to humans by Aedes aegypti mosquitoes. These viruses generally cause a benign syndrome, dengue fever, in the American and African tropics, and a severe syndrome, dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS), in Southeast Asian children. This severe syndrome, which recently has also been identified in children infected with the virus in Puerto Rico, is characterized by increased vascular permeability and abnormal hemostasis. It occurs in infants less than 1 year of age born to dengue-immune mothers and in children 1 year and older who are immune to one serotype of dengue virus and are experiencing infection with a second serotype. Dengue viruses replicate in cells of mononuclear phagocyte lineage, and subneutralizing concentrations of dengue antibody enhance dengue virus infection in these cells. This antibody-dependent enhancement of infection regulates dengue disease in human beings, although disease severity may also be controlled genetically, possibly by permitting and restricting the growth of virus in monocytes. Monoclonal antibodies show heterogeneous distribution of antigenic epitopes on dengue viruses. These epitopes serve to regulate disease: when antibodies to shared antigens partially neutralize heterotypic virus, infection and disease are dampened; enhancing antibodies alone result in heightened disease response. Further knowledge of the structure of dengue genomes should permit rapid advances in understanding the pathogenetic mechanisms of dengue.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Halstead, S B -- New York, N.Y. -- Science. 1988 Jan 29;239(4839):476-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Health Sciences, Rockefeller Foundation, New York, NY 10036.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3277268" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Antibodies, Viral/physiology ; Antigens, Viral/immunology ; Asia, Southeastern ; Child ; Child, Preschool ; Cuba ; Dengue/epidemiology/ethnology/*etiology/immunology/microbiology/prevention & ; control ; *Dengue Virus/classification/genetics/immunology/physiology ; Female ; Humans ; Infant ; Male ; Puerto Rico ; Serotyping
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  • 88
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-10-07
    Description: The existence of spontaneous neural activity in mammalian retinal ganglion cells during prenatal life has long been suspected. This activity could play a key role in the refinement of retinal projections during development. Recordings in vivo from the retinas of rat fetuses between embryonic day 17 and 21 found action potentials in spontaneously active ganglion cells at all the ages studied.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Galli, L -- Maffei, L -- New York, N.Y. -- Science. 1988 Oct 7;242(4875):90-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Istituto di Neurofisiologia Consiglio Nazionale Delle Richerche via San Zeno, Pisa, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175637" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Electric Conductivity ; Female ; Fetus/physiology ; Pregnancy ; Rats ; Retina/*embryology/*physiology ; Retinal Ganglion Cells/*physiology
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  • 89
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-02-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1988 Feb 5;239(4840):545.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3340838" target="_blank"〉PubMed〈/a〉
    Keywords: Child ; *Child Care ; Female ; Humans ; *Science ; United States ; *Women ; *Women, Working
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  • 90
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-03-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arimura, A -- New York, N.Y. -- Science. 1988 Mar 11;239(4845):1313.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2830676" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenocorticotropic Hormone/*secretion ; Animals ; Female ; Interleukin-1/*pharmacology ; Male ; Pituitary Gland, Anterior/drug effects/*secretion ; Rats
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  • 91
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-08-19
    Description: The study of resistance marker rearrangement in Spiroplasma citri mutants provides evidence of transfer of chromosomal information followed by recombination. This is the first report of such a transfer in vivo in the mollicutes--that is, in the smallest self-replicating organisms. The double-resistant phenotypes obtained are stable even without selection pressure. The mechanism of gene transfer is insensitive to deoxyribonuclease, requires contact, and possibly, areas of fusion of the cell membranes; it shares properties with the transfer by protoplast fusion in Gram-positive bacteria. The extensive degenerative evolution of mollicutes has retained, in S. citri, bacterial functions of chromosomal transfer and recombination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barroso, G -- Labarere, J -- New York, N.Y. -- Science. 1988 Aug 19;241(4868):959-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Genetique Moleculaire, Universite de Bordeaux II-INRA, C.R.A. de Bordeaux, Pont-de-la-Maye, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3261453" target="_blank"〉PubMed〈/a〉
    Keywords: Arsenates/pharmacology ; *Chromosomes, Bacterial ; Cloning, Molecular ; Culture Media ; Drug Resistance, Microbial/genetics ; Herbicides/pharmacology ; Mutation ; Oxides/pharmacology ; Phenotype ; *Recombination, Genetic ; Spiroplasma/drug effects/*genetics ; Time Factors ; *Transfection ; Vanadates/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 92
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-01-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnes, D M -- New York, N.Y. -- Science. 1988 Jan 29;239(4839):457.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3277266" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*prevention & control ; Clinical Trials as Topic ; Female ; Humans ; Male ; United States ; *Viral Vaccines
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  • 93
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-12-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnes, D M -- New York, N.Y. -- Science. 1988 Dec 16;242(4885):1509.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3201238" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Estrogens/*physiology ; Female ; Humans ; Menstrual Cycle ; Progesterone/*physiology ; *Task Performance and Analysis
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  • 94
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-09-02
    Description: In the Research News article by Richard A. Kerr "In search of elusive little comets" (10 June, p. 1403), the position held by John Craven of the University of Iowa was incorrectly given. He is a senior research physicist.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ellett, W H -- New York, N.Y. -- Science. 1988 Sep 2;241(4870):1144.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3413478" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Female ; Humans ; Lung Neoplasms/*etiology ; Male ; Neoplasms, Radiation-Induced/*etiology ; Radon/*adverse effects ; Risk Factors ; Smoking/*adverse effects
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  • 95
    Publication Date: 1988-09-30
    Description: Patients who have received many transfusions become highly sensitized and develop antibodies against almost all HLA alloantigens, so that finding a cross-match negative kidney donor is difficult. A survey of those patients showed that 50 percent did not form antibodies against the noninherited maternal HLA antigens. Apart from the obvious clinical implications, the data indicate that a human equivalent of murine neonatal or actively acquired tolerance has now been identified.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Claas, F H -- Gijbels, Y -- van der Velden-de Munck, J -- van Rood, J J -- New York, N.Y. -- Science. 1988 Sep 30;241(4874):1815-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunohaematology, University Hospital, Leiden, the Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3051377" target="_blank"〉PubMed〈/a〉
    Keywords: B-Lymphocytes/*immunology ; Female ; Fetus/*immunology ; HLA-A Antigens/*immunology ; HLA-B Antigens/*immunology ; Humans ; *Immune Tolerance ; *Kidney Transplantation ; Maternal-Fetal Exchange ; Pregnancy
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  • 96
    Publication Date: 1988-03-04
    Description: One approach to analyzing the molecular mechanisms of gene expression in vivo is to reconstitute these events in cell-free systems in vitro. Although there is some evidence for tissue-specific transcription in vitro, transcriptionally active extracts that mimic a steroid hormone-dependent enhancement of transcription have not been described. In the study reported here, nuclear extracts of liver from the frog Xenopus laevis were capable of estrogen-dependent induction of a homologous vitellogenin promoter that contained the estrogen-responsive element.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Corthesy, B -- Hipskind, R -- Theulaz, I -- Wahli, W -- New York, N.Y. -- Science. 1988 Mar 4;239(4844):1137-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Biologie animale, Universite de Lausanne, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2830672" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/genetics ; Animals ; Cell Nucleus/*metabolism ; Chloramphenicol O-Acetyltransferase ; DNA, Recombinant ; Estradiol/*pharmacology ; Female ; HeLa Cells/metabolism ; Humans ; Liver/*ultrastructure ; Male ; *Promoter Regions, Genetic ; RNA Polymerase II/metabolism ; Simian virus 40/genetics ; Templates, Genetic ; Transcription, Genetic/*drug effects ; Vitellogenins/*genetics ; Xenopus laevis
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  • 97
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-10-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, C -- New York, N.Y. -- Science. 1988 Oct 21;242(4877):370-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175659" target="_blank"〉PubMed〈/a〉
    Keywords: Abortion, Spontaneous ; Contraception/*methods ; Contraceptive Agents ; Contraceptive Devices ; *Family Planning Services ; Female ; Humans ; Pregnancy ; Pregnancy, Unwanted ; Research Support as Topic ; United States
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  • 98
    Publication Date: 1988-03-11
    Description: A complementary DNA encoding the human low density lipoprotein (LDL) receptor under control of the mouse metallothionein-I promoter was injected into fertilized mouse eggs, and a strain of mice expressing high levels of LDL receptors was established. After administration of cadmium, these mice cleared intravenously injected 125I-labeled LDL from blood eight to ten times more rapidly than did normal mice. The plasma concentrations of apoproteins B-100 and E, the two ligands for the LDL receptor, declined by more than 90 percent after cadmium treatment, but the concentration of another apoprotein, A-I, was unaffected. Therefore, overexpression of an endocytotic receptor can dramatically lower the ambient concentration of its ligand in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hofmann, S L -- Russell, D W -- Brown, M S -- Goldstein, J L -- Hammer, R E -- HL 01287/HL/NHLBI NIH HHS/ -- HL 20948/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 11;239(4845):1277-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas 75235.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3344433" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; DNA/genetics ; Female ; *Genes ; Humans ; Kinetics ; Lipoproteins, LDL/*blood ; Mice ; Mice, Transgenic ; Plasmids ; Receptors, LDL/*genetics/metabolism ; Reference Values ; Transcription, Genetic
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  • 99
    Publication Date: 1988-12-23
    Description: Hypocalcemic vitamin D-resistant rickets is a human genetic disease resulting from target organ resistance to the action of 1,25-dihydroxyvitamin D3. Two families with affected children homozygous for this autosomal recessive disorder were studied for abnormalities in the intracellular vitamin D receptor (VDR) and its gene. Although the receptor displays normal binding of 1,25-dihydroxyvitamin D3 hormone, VDR from affected family members has a decreased affinity for DNA. Genomic DNA isolated from these families was subjected to oligonucleotide-primed DNA amplification, and each of the nine exons encoding the receptor protein was sequenced for a genetic mutation. In each family, a different single nucleotide mutation was found in the DNA binding domain of the protein; one family near the tip of the first zinc finger (Gly----Asp) and one at the tip of the second zinc finger (Arg----Gly). The mutant residues were created in vitro by oligonucleotide directed point mutagenesis of wild-type VDR complementary DNA and this cDNA was transfected into COS-1 cells. The produced protein is biochemically indistinguishable from the receptor isolated from patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hughes, M R -- Malloy, P J -- Kieback, D G -- Kesterson, R A -- Pike, J W -- Feldman, D -- O'Malley, B W -- New York, N.Y. -- Science. 1988 Dec 23;242(4886):1702-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2849209" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Calcitriol/metabolism ; Cell Line ; Cell Line, Transformed ; Codon ; DNA/genetics/metabolism ; Exons ; Female ; Gene Amplification ; Homozygote ; Humans ; Hypocalcemia/*genetics ; Immunoblotting ; Male ; Molecular Sequence Data ; *Mutation ; Receptors, Calcitriol ; Receptors, Steroid/*genetics/metabolism ; Rickets/*genetics ; 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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  • 100
    Publication Date: 1988-04-29
    Description: Pertussis toxin is produced by the causative agent of whooping cough, Bordetella pertussis, and is an adenosine diphosphate (ADP)-ribosyltransferase capable of covalently modifying and thereby inactivating many eukaryotic G proteins involved in cellular metabolism. The toxin is a principal determinant of virulence in whooping cough and is a primary candidate for an acellular pertussis vaccine, yet it is unclear whether the ADP-ribosyltransferase activity is required for both pathogenic and immunoprotective activities. A B. pertussis strain that produced an assembled pertussis holotoxin with only 1 percent of the ADP-ribosyltransferase activity of the native toxin was constructed and was found to be deficient in pathogenic activities associated with B. pertussis including induction of leukocytosis, potentiation of anaphylaxis, and stimulation of histamine sensitivity. Moreover, this mutant strain failed to function as an adjuvant and was less effective in protecting mice from intracerebral challenge infection. These data suggest that the ADP-ribosyltransferase activity is necessary for both pathogenicity and optimum immunoprotection. These findings bear directly on the design of a nontoxic pertussis vaccine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Black, W J -- Munoz, J J -- Peacock, M G -- Schad, P A -- Cowell, J L -- Burchall, J J -- Lim, M -- Kent, A -- Steinman, L -- Falkow, S -- AI-22462/AI/NIAID NIH HHS/ -- AI-23945/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Apr 29;240(4852):656-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Microbiology, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2896387" target="_blank"〉PubMed〈/a〉
    Keywords: ADP Ribose Transferases ; Adjuvants, Immunologic ; Anaphylaxis/etiology ; Animals ; Antigens/immunology ; Bordetella pertussis/enzymology/genetics/*immunology ; Codon ; Drug Tolerance ; Histamine/pharmacology ; Immunization ; Leukocytosis/etiology ; Macromolecular Substances ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mutation ; Ovalbumin/immunology ; Pentosyltransferases/*metabolism ; *Pertussis Toxin ; Virulence Factors, Bordetella/genetics/immunology/*metabolism
    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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