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  • Mutation  (45)
  • American Association for the Advancement of Science (AAAS)  (45)
  • Annual Reviews
  • 1985-1989  (45)
  • 1980-1984
  • 1960-1964
  • 1935-1939
  • 1988  (45)
  • 1960
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (45)
  • Annual Reviews
  • Springer  (4)
Years
  • 1985-1989  (45)
  • 1980-1984
  • 1960-1964
  • 1935-1939
Year
  • 1
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    Fidelity of HIV-1 reverse transcriptase (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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  • 2
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    Cellular transcription factors and regulation of IL-2 receptor gene expression by HTLV-I tax gene product (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 3
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    Clathrin: a matter of life or death? (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 4
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    The effect of histone gene deletions on chromatin structure in Saccharomyces cerevisiae (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 5
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    Combinatorial cassette mutagenesis as a probe of the informational content of protein sequences (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 6
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    Structural rearrangement of the retinoblastoma gene in human breast carcinoma (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 7
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    Aggregation of lysine-containing zeins into protein bodies in Xenopus oocytes (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 8
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    Constraint of the translational diffusion of a membrane glycoprotein by its external domains (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 9
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    A novel gene of HIV-1, vpu, and its 16-kilodalton product (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 10
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    Germline transformation used to define key features of heat-shock response elements (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 11
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    Juvenile hormone action mediated in male accessory glands of Drosophila by calcium and kinase C (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 12
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    Insulin-resistant diabetes due to a point mutation that prevents insulin proreceptor processing (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 13
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    Low plasma cholesterol levels caused by a short deletion in the apolipoprotein B gene (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 14
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    A point mutation in the c-myc locus of a Burkitt lymphoma abolishes binding of a nuclear protein (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 15
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    The AIDS virus can take on many guises (1988)
    American Association for the Advancement of Science (AAAS)
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    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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  • 16
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    Symposium focuses on genes in development (1988)
    American Association for the Advancement of Science (AAAS)
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    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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  • 17
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    Association of transfer RNA acceptor identity with a helical irregularity (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 18
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    Activation of developmentally mutated human globin genes by cell fusion (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 19
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    Probing the mechanisms of macromolecular recognition: the cytochrome b5-cytochrome c complex (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 20
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    HTLV-II transactivation is regulated by the overlapping tax/rex nonstructural genes (1988)
    American Association for the Advancement of Science (AAAS)
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    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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  • 21
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    Conversion of a PI-anchored protein to an integral membrane protein by a single amino acid mutation (1988)
    American Association for the Advancement of Science (AAAS)
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    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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  • 22
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    Phenotypic diversity mediated by the maize transposable elements Ac and Spm (1988)
    American Association for the Advancement of Science (AAAS)
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    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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  • 23
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    Changing the identity of a tRNA by introducing a G-U wobble pair near the 3' acceptor end (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 24
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    Molecular cloning of a feline leukemia virus that induces fatal immunodeficiency disease in cats (1988)
    American Association for the Advancement of Science (AAAS)
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    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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  • 25
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    The accuracy of reverse transcriptase from HIV-1 (1988)
    American Association for the Advancement of Science (AAAS)
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    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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  • 26
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    Genomic amplification with transcript sequencing (1988)
    American Association for the Advancement of Science (AAAS)
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    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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  • 27
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    A mutation of the circadian system in golden hamsters (1988)
    American Association for the Advancement of Science (AAAS)
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    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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  • 28
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    Replacements of Pro86 in phage T4 lysozyme extend an alpha-helix but do not alter protein stability (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    The cellular src gene product regulates junctional cell-to-cell communication (1988)
    American Association for the Advancement of Science (AAAS)
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    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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    Restoration of torque in defective flagellar motors (1988)
    American Association for the Advancement of Science (AAAS)
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    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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    Identification of germline and somatic mutations affecting the retinoblastoma gene (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    tRNAi(met) functions in directing the scanning ribosome to the start site of translation (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    One factor recognizes the liver-specific enhancers in alpha 1-antitrypsin and transthyretin genes (1988)
    American Association for the Advancement of Science (AAAS)
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    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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    Evidence that the M2 membrane-spanning region lines the ion channel pore of the nicotinic receptor (1988)
    American Association for the Advancement of Science (AAAS)
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    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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    A mutation in the catalytic subunit of cAMP-dependent protein kinase that disrupts regulation (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Mitotic recombination within the centromere of a yeast chromosome (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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    Frame-shift deletions in patients with Duchenne and Becker muscular dystrophy (1988)
    American Association for the Advancement of Science (AAAS)
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    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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    Mutant Trp repressors with new DNA-binding specificities (1988)
    American Association for the Advancement of Science (AAAS)
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    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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  • 39
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    Expression of the murine Duchenne muscular dystrophy gene in muscle and brain (1988)
    American Association for the Advancement of Science (AAAS)
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    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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  • 40
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    Early signal transduction by the antigen receptor without commitment to T cell activation (1988)
    American Association for the Advancement of Science (AAAS)
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    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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    Chromosomal gene transfer in Spiroplasma citri (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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  • 42
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    ADP-ribosyltransferase activity of pertussis toxin and immunomodulation by Bordetella pertussis (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Tumor formation dependent on proteoglycan biosynthesis (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-08-26
    Description: The role proteoglycans play in tumor formation was examined by measuring the tumorigenicity of proteoglycan-deficient Chinese hamster ovary cell mutants in nude mice. When 10(7) cells were injected subcutaneously, mutants with less than about 15% of the wild-type level of proteoglycan synthesis did not produce tumors. Mutants defective in the synthesis of heparan sulfate proteoglycans also did not form tumors, whereas mutants with altered chondroitin sulfate proteoglycans were tumorigenic. Tumors arose from mixtures of wild-type and nontumorigenic mutant cells and contained both cell types, suggesting that wild-type cell proteoglycans enabled mutant cells to survive. The failure of heparan sulfate-deficient mutants to form tumors depended on the ability of the host to mount a B cell-mediated immune reaction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Esko, J D -- Rostand, K S -- Weinke, J L -- GM33063/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Aug 26;241(4869):1092-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, School of Medicine, University of Alabama, Birmingham 35294.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3137658" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology ; Cell Line ; Chondroitin Sulfate Proteoglycans/genetics/physiology ; Chondroitin Sulfates/genetics/physiology ; Cricetinae ; Heparan Sulfate Proteoglycans ; Heparitin Sulfate/genetics/physiology ; Immunologic Deficiency Syndromes/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Mutation ; Neoplasm Transplantation ; Neoplasms, Experimental/*etiology ; Pentosyltransferases/genetics/metabolism ; Proteoglycans/*physiology
    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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  • 44
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    Two mutant alleles of the insulin receptor gene in a patient with extreme insulin resistance (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-05-06
    Description: Insulin receptor complementary DNA has been cloned from an insulin-resistant patient with leprechaunism whose receptors exhibited multiple abnormalities in insulin binding. The patient is a compound heterozygote, having inherited two different mutant alleles of the insulin receptor gene. One allele contains a missense mutation encoding the substitution of glutamic acid for lysine at position 460 in the alpha subunit of the receptor. The second allele has a nonsense mutation causing premature chain termination after amino acid 671 in the alpha subunit, thereby deleting both the transmembrane and tyrosine kinase domains of the receptor. Interestingly, the father is heterozygous for this nonsense mutation and exhibits a moderate degree of insulin resistance. This raises the possibility that mutations in the insulin receptor gene may account for the insulin resistance in some patients with non-insulin-dependent diabetes mellitus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kadowaki, T -- Bevins, C L -- Cama, A -- Ojamaa, K -- Marcus-Samuels, B -- Kadowaki, H -- Beitz, L -- McKeon, C -- Taylor, S I -- New York, N.Y. -- Science. 1988 May 6;240(4853):787-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biochemistry and Molecular Pathophysiology Section, National Institute of Diabetes, Digestive, and Kidney Disease, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2834824" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Base Sequence ; Cell Line ; Cell Membrane/metabolism ; Cell Transformation, Viral ; DNA/genetics ; Diabetes Mellitus, Type 2/*genetics ; Endocrine System Diseases/genetics ; Female ; Gene Amplification ; Growth Disorders/genetics ; Herpesvirus 4, Human ; Heterozygote ; Humans ; Hydrogen-Ion Concentration ; Insulin/blood ; Insulin Resistance/*genetics ; Lymphocytes/metabolism ; Monocytes/metabolism ; Mutation ; Receptor, Insulin/*genetics ; Syndrome ; Transfection
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Distinct regions of Sp1 modulate DNA binding and transcriptional activation (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-12-16
    Description: Sp1 is a sequence-specific DNA binding protein that activates RNA polymerase II transcription from promoters that contain properly positioned GC boxes. A series of deletion mutants of Sp1 were expressed in Escherichia coli and used to identify separate regions of the protein that are important for three different biochemical activities. The sequence-specificity of DNA binding was conferred by Zn(II) fingers, whereas a different region of Sp1 appeared to regulate the affinity of DNA binding. The E. coli-synthesized Sp1 was able to stimulate initiation of RNA synthesis in vitro, and at least two distinct segments of the protein contributed to its transcriptional activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kadonaga, J T -- Courey, A J -- Ladika, J -- Tjian, R -- New York, N.Y. -- Science. 1988 Dec 16;242(4885):1566-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biochemistry, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3059495" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosome Deletion ; Cloning, Molecular ; DNA, Neoplasm/genetics ; DNA-Binding Proteins/*genetics/metabolism ; *Gene Expression Regulation ; *Genes ; HeLa Cells/metabolism ; Humans ; Mutation ; Sp1 Transcription Factor ; Transcription Factors/*genetics/metabolism ; *Transcription, Genetic
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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