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  • Mutation
  • American Association for the Advancement of Science (AAAS)  (22)
  • American Geophysical Union
  • American Geophysical Union (AGU)
  • American Institute of Physics
  • Annual Reviews
  • 1985-1989  (22)
  • 1980-1984
  • 1970-1974
  • 1935-1939
  • 1986  (22)
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  • American Association for the Advancement of Science (AAAS)  (22)
  • American Geophysical Union
  • American Geophysical Union (AGU)
  • American Institute of Physics
  • Annual Reviews
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Erscheinungszeitraum
  • 1985-1989  (22)
  • 1980-1984
  • 1970-1974
  • 1935-1939
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  • 1
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    Lipoprotein mutations in pigs are associated with elevated plasma cholesterol and atherosclerosis (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1986-12-19
    Beschreibung: A strain of pigs bearing three immunogenetically defined lipoprotein-associated markers (allotypes), designated Lpb5, Lpr1, and Lpu1, has marked hypercholesterolemia on a low fat, cholesterol-free diet. Unlike individuals with familial hypercholesterolemia or WHHL rabbits, the affected pigs have normal low density lipoprotein receptor activity. The animals, by 7 months of age, have extensive atherosclerotic lesions in all three coronary arteries. This strain of pig represents an animal model for atherosclerosis and hypercholesterolemia associated with mutations affecting the structures of plasma lipoproteins. One of the variant apolipoproteins, Lpb5, is apolipoprotein-B. A second variant apolipoprotein (Lpr1), termed apo-R, is a 23-kilodalton protein present in both the very low density (d less than 1.006 g/ml) and the very high density (d greater than 1.21 g/ml) fractions of pig plasma. Isoforms of this protein correlate with two Lpr alleles, Lpr1 and Lpr2. The Lpr genes segregate independently of the Lpb5 and Lpu1 alleles. The Lpu1 allotype is a component of low density lipoprotein and is genetically linked to Lpb5.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rapacz, J -- Hasler-Rapacz, J -- Taylor, K M -- Checovich, W J -- Attie, A D -- AG05-856/AG/NIA NIH HHS/ -- HL30594/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1986 Dec 19;234(4783):1573-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3787263" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alleles ; Animals ; Apolipoproteins B/genetics ; Arteriosclerosis/blood/*genetics ; Cholesterol/blood ; *Disease Models, Animal ; Female ; Genotype ; Hypercholesterolemia/blood/*genetics ; Immunologic Tests ; Lipoproteins/blood/*genetics ; Lipoproteins, LDL/blood/genetics ; Lipoproteins, VLDL/blood/genetics ; Male ; Mutation ; Receptors, LDL/metabolism ; Swine
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 2
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    A genetic approach to analyzing membrane protein topology (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1986-09-26
    Beschreibung: Fusions of the secreted protein alkaline phosphatase to an integral cytoplasmic membrane protein of Escherichia coli showed different activities depending on where in the membrane protein the alkaline phosphatase was fused. Fusions to positions in or near the periplasmic domain led to high alkaline phosphatase activity, whereas those to positions in the cytoplasmic domain gave low activity. Analysis of alkaline phosphatase fusions to membrane proteins of unknown structure may thus be generally useful in determining their membrane topologies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Manoil, C -- Beckwith, J -- New York, N.Y. -- Science. 1986 Sep 26;233(4771):1403-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3529391" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alkaline Phosphatase/genetics ; Cell Membrane/ultrastructure ; Chromosome Deletion ; Escherichia coli/genetics ; Membrane Proteins/*genetics ; Mutation ; Plasmids ; Protein Conformation ; Recombinant Proteins/analysis
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 3
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    Deletion in cysteine-rich region of LDL receptor impedes transport to cell surface in WHHL rabbit (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1986-06-06
    Beschreibung: The Watanabe heritable hyperlipidemic (WHHL) rabbit, an animal with familial hypercholesterolemia, produces a mutant receptor for plasma low-density lipoprotein (LDL) that is not transported to the cell surface at a normal rate. Cloning and sequencing of complementary DNA's from normal and WHHL rabbits, shows that this defect arises from an in-frame deletion of 12 nucleotides that eliminates four amino acids from the cysteine-rich ligand binding domain of the LDL receptor. A similar mutation, detected by S1 nuclease mapping of LDL receptor messenger RNA, occurred in a patient with familial hypercholesterolemia whose receptor also fails to be transported to the cell surface. These findings suggest that animal cells may have fail-safe mechanisms that prevent the surface expression of improperly folded proteins with unpaired or improperly bonded cysteine residues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4451858/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4451858/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamamoto, T -- Bishop, R W -- Brown, M S -- Goldstein, J L -- Russell, D W -- HL 01287/HL/NHLBI NIH HHS/ -- HL 20948/HL/NHLBI NIH HHS/ -- HL 31346/HL/NHLBI NIH HHS/ -- P01 HL020948/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1986 Jun 6;232(4755):1230-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3010466" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Base Sequence ; Biological Transport ; *Chromosome Deletion ; Cloning, Molecular ; Cysteine/genetics ; Dna ; DNA Restriction Enzymes ; Genes ; Humans ; Hyperlipoproteinemia Type II/*genetics ; Mutation ; RNA, Messenger ; Rabbits ; Receptors, LDL/*genetics
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 4
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    Derivation and diversification of monoclonal antibodies (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1986-09-19
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kohler, G -- New York, N.Y. -- Science. 1986 Sep 19;233(4770):1281-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3092353" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antibodies, Monoclonal/*biosynthesis/genetics/immunology ; *Antibody Diversity ; Antibody Specificity ; Cell Fusion ; Hybridomas ; Immunoglobulin Heavy Chains/immunology ; Immunoglobulin Light Chains/immunology ; Immunoglobulin Variable Region/immunology ; Immunoglobulin kappa-Chains/immunology ; Immunoglobulin mu-Chains/immunology ; Mice ; Mice, Inbred BALB C ; Mutation
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 5
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    The hypogonadal mouse: reproductive functions restored by gene therapy (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1986-12-12
    Beschreibung: The hypogonadal (hpg) mouse lacks a complete gonadotropin-releasing hormone (GnRH) gene and consequently cannot reproduce. Introduction of an intact GnRH gene into the genome of these mutant mice resulted in complete reversal of the hypogonadal phenotype. Transgenic hpg/hpg homozygotes of both sexes were capable of mating and producing offspring. Pituitary and serum concentrations of luteinizing hormone, follicle-stimulating hormone, and prolactin were restored to those of normal animals. Immunocytochemistry and in situ hybridization showed that GnRH expression was restored in the appropriate hypothalamic neurons of the transgenic hpg animals, an indication of neural-specific expression of the introduced gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mason, A J -- Pitts, S L -- Nikolics, K -- Szonyi, E -- Wilcox, J N -- Seeburg, P H -- Stewart, T A -- New York, N.Y. -- Science. 1986 Dec 12;234(4782):1372-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3097822" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Female ; Follicle Stimulating Hormone/blood ; Gene Expression Regulation ; *Genetic Engineering ; Gonadotropin-Releasing Hormone/genetics ; Histocytochemistry ; Hypogonadism/*genetics ; Hypothalamus/analysis/cytology ; Infertility/genetics/*therapy ; Luteinizing Hormone/blood ; Male ; Mice ; Mutation ; Neurons/analysis ; Phenotype ; Prolactin/blood ; Tissue Distribution
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 6
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    Different mutations in Ashkenazi Jewish and non-Jewish French Canadians with Tay-Sachs disease (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1986-06-27
    Beschreibung: Tay-Sachs disease patients of Ashkenazi Jewish and non-Jewish French Canadian origin are affected with a clinically identical form of this inherited disease. Both have a similar gene frequency for the disorder, which is tenfold higher than that found in the general population. Unlike other patients with the disease, who often display variation at the clinical or biochemical level, the absence of such differences between these two groups has prompted the idea that they may harbor the same mutation. In this report, a complementary DNA clone coding for the alpha chain of human beta-hexosaminidase has been used to analyze the genetic lesions in the alpha-chain locus of two patients with Tay-Sachs disease from each of these groups. On the basis of DNA hybridization analyses, the alpha-chain gene of the Ashkenazi patients appears intact while the alpha-chain gene of French Canadian patients has a 5' deletion of approximately 5 to 8 kilobases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Myerowitz, R -- Hogikyan, N D -- New York, N.Y. -- Science. 1986 Jun 27;232(4758):1646-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3754980" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Canada ; DNA/genetics ; France/ethnology ; Heterozygote ; Humans ; *Jews ; Mutation ; Nucleic Acid Hybridization ; Tay-Sachs Disease/*genetics
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 7
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    A mouse homeo box gene is expressed in spermatocytes and embryos (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1986-08-08
    Beschreibung: The MH-3 gene, which contains a homeo box that is expressed specifically in the adult testis, was identified and mapped to mouse chromosome 6. By means of in situ hybridization with adult testis sections and Northern blot hybridization with testis RNA from prepuberal mice and from Sl/Sld mutant mice, it was demonstrated that this gene is expressed in male germ cells during late meiosis. In the embryo, MH-3 transcripts were present at day 11.5 post coitum, a stage in mouse development when gonadal differentiation has not yet occurred. The MH-3 gene may have functions in spermatogenesis and embryogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rubin, M R -- Toth, L E -- Patel, M D -- D'Eustachio, P -- Nguyen-Huu, M C -- New York, N.Y. -- Science. 1986 Aug 8;233(4764):663-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3726554" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; DNA/genetics ; Drosophila ; Embryo, Mammalian/*metabolism ; *Embryo, Nonmammalian ; *Genes ; Male ; Mice ; Morphogenesis ; Mutation ; Nucleic Acid Hybridization ; Sequence Homology, Nucleic Acid ; Spermatocytes/*metabolism ; Spermatogenesis
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 8
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    Biochemical and genetic evidence for the hepatitis B virus replication strategy (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1986-04-25
    Beschreibung: Hepatitis B viruses synthesize their open circular DNA genomes by reverse transcription of an RNA intermediate. The details of this process have been examined with the use of mammalian hepatitis B viruses to map the sites for initiation and termination of DNA synthesis and to explore the consequences of mutations introduced at short, separated direct repeats (DR1 and DR2) implicated in the mechanisms of initiation. The first DNA strand to be synthesized is initiated within DR1, apparently by a protein primer, and the completed strand has a short terminal redundancy. In contrast, the second DNA strand begins with the sequence adjacent to DR2, but its 5' end is joined to an oligoribonucleotide that contains DR1; thus the putative RNA primer has been transposed to the position of DR2. It is now possible to propose a detailed strategy for reverse transcription by hepatitis B viruses that can be instructively compared with that used by retroviruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seeger, C -- Ganem, D -- Varmus, H E -- New York, N.Y. -- Science. 1986 Apr 25;232(4749):477-84.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3961490" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Base Sequence ; DNA, Viral/metabolism ; Hepatitis B virus/genetics/*physiology ; Mutation ; RNA, Viral/metabolism ; Sciuridae ; Templates, Genetic ; *Virus Replication
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 9
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    Fine structure genetic analysis of a beta-globin promoter (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1986-05-02
    Beschreibung: A novel procedure for saturation mutagenesis of cloned DNA was used to obtain more than 100 single base substitutions within the promoter of the mouse beta-major globin gene. The effects of these promoter substitutions on transcription were determined by transfecting the cloned mutant genes into HeLa cells on plasmids containing an SV40 transcription enhancer, and measuring the levels of correctly initiated beta-globin transcripts after 2 days. Mutations in three regions of the promoter resulted in a significant decrease in the level of transcription: (i) the CACCC box, located between -87 and -95, (ii) the CCAAT box, located between -72 and -77, and (iii) the TATA box, located between -26 and -30 relative to the start site of transcription. In contrast, two different mutations in nucleotides immediately upstream from the CCAAT box resulted in a 3- to 3.5-fold increase in transcription. With two minor exceptions, single base substitutions in all other regions of the promoter had no effect on transcription. These results precisely delineate the cis-acting sequences required for accurate and efficient initiation of beta-globin transcription, and they establish a general approach for the fine structure genetic analysis of eukaryotic regulatory sequences.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Myers, R M -- Tilly, K -- Maniatis, T -- New York, N.Y. -- Science. 1986 May 2;232(4750):613-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3457470" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Base Sequence ; Cloning, Molecular ; DNA/genetics ; Genes ; Genetic Engineering ; Globins/biosynthesis/*genetics ; HeLa Cells ; Humans ; Mice ; Mutation ; *Promoter Regions, Genetic ; Transcription, Genetic
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 10
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    The 1985 Nobel Prize in physiology or medicine (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1986-01-10
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Motulsky, A G -- New York, N.Y. -- Science. 1986 Jan 10;231(4734):126-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3510453" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adult ; Arteriosclerosis/therapy ; Cholesterol/blood/metabolism ; Endocytosis ; History, 20th Century ; Humans ; Hyperlipoproteinemia Type II/genetics/therapy ; Lipoproteins/metabolism ; Male ; Middle Aged ; Mutation ; *Nobel Prize ; Receptors, LDL/genetics ; United States
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 11
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    From antibody structure to immunological diversification of immune response (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1986-03-14
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Milstein, C -- New York, N.Y. -- Science. 1986 Mar 14;231(4743):1261-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3080810" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antibodies/immunology/*physiology ; Antibodies, Monoclonal/genetics ; *Antibody Diversity ; *Antibody Formation ; DNA, Recombinant/metabolism ; Genes, MHC Class II ; Genetic Engineering ; Humans ; Hybridomas/metabolism ; Immunoglobulin Heavy Chains/genetics ; Immunoglobulin Light Chains/genetics ; Immunoglobulins/physiology ; Mice ; Multiple Myeloma/genetics ; Mutation ; Myeloma Proteins/genetics ; RNA, Messenger/genetics
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 12
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    Occult Drosophila calcium channels and twinning of calcium and voltage-activated potassium channels (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1986-08-15
    Beschreibung: In the membrane of the flight muscle cells of developing Drosophila a large calcium-sensitive potassium current, IKc, was found. It was present before the development of voltage-activated potassium channels and seems to be the first potassium current to develop in the membrane. Also present in these early cells were large numbers of occult (hidden) calcium channels, which remained inactive until the end of pupal development. These inactive calcium channels could be made to function by injecting adenosine triphosphate or ethyleneglycol tetraacetic acid into the early cells. IKc has kinetic properties resembling the later developing voltage-sensitive current IKv, and is distinct from the fast, transient calcium-dependent outward current IAc, which appears much later in development. IAc closely resembles the voltage-sensitive current IAv, also present in these cells. Thus, both of the voltage-sensitive potassium channel types, IAv and IKv, have similar calcium-sensitive counterparts, IAc and IKc, that are present in the same cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wei, A -- Salkoff, L -- 5-T32-NS07057-08/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1986 Aug 15;233(4765):780-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2426780" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Action Potentials/drug effects ; Adenosine Triphosphate/pharmacology ; Alleles ; Animals ; Calcium/*metabolism/pharmacology ; Drosophila/genetics/*growth & development/physiology ; Egtazic Acid/pharmacology ; Ion Channels/drug effects/*physiology ; Mutation ; Potassium/*metabolism ; Pupa
    Print ISSN: 0036-8075
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 13
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    Infectious mutants of HTLV-III with changes in the 3' region and markedly reduced cytopathic effects (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1986-08-08
    Beschreibung: A variant of human T-lymphotropic virus type III (HTLV-III) is described that replicates but does not kill normal human T cells in vitro. This variant, designated X10-1, was derived from the genome of a cytopathic HTLV-III clone (pHXB2D) by excision of a 200-base pair segment in the 3' region of the virus, spanning the env and 3'-orf genes. Comparable variants with 55 to 109 base pairs deleted exclusively in 3'-orf produced, in contrast, virus that was extremely cytopathic. On the basis of these findings it is concluded that the 3'-orf gene is not required for cytopathogenicity or replication of HTLV-III. In addition, the results suggest that virus replication and cytotoxicity are not intrinsically coupled. Furthermore, since clone X10-1 retains the ability to trans-activate genes linked to the viral long terminal repeats, trans-activation per se is not responsible for T-cell killing by HTLV-III. These results also raise the possibility that the carboxyl terminus of the envelope gene of HTLV-III has a direct role in T-cell killing by this virus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fisher, A G -- Ratner, L -- Mitsuya, H -- Marselle, L M -- Harper, M E -- Broder, S -- Gallo, R C -- Wong-Staal, F -- New York, N.Y. -- Science. 1986 Aug 8;233(4764):655-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3014663" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acquired Immunodeficiency Syndrome/*microbiology ; Cloning, Molecular ; Deltaretrovirus/*genetics/pathogenicity ; Humans ; Mutation ; Nucleic Acid Hybridization ; RNA, Viral/genetics ; T-Lymphocytes/microbiology
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 14
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    Modification of the active site of alkaline phosphatase by site-directed mutagenesis (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1986-01-10
    Beschreibung: The catalytically essential amino acid in the active site of bacterial alkaline phosphatase (Ser-102) has been replaced with a cysteine by site-directed mutagenesis. The resulting thiol enzyme catalyzes the hydrolysis of a variety of phosphate monoesters. The rate-determining step of hydrolysis, however, is no longer the same for catalysis when the active protein nucleophile is changed from the hydroxyl of serine to the thiol of cysteine. Unlike the steady-state kinetics of native alkaline phosphatase, those of the mutant show sensitivity to the leaving group of the phosphate ester.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ghosh, S S -- Bock, S C -- Rokita, S E -- Kaiser, E T -- AM 07122-02/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1986 Jan 10;231(4734):145-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3510454" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *2,4-Dinitrophenol/*analogs & derivatives ; Alkaline Phosphatase/*genetics/metabolism ; Amino Acid Sequence ; Binding Sites ; DNA/genetics ; Dinitrophenols/metabolism ; Escherichia coli/enzymology/genetics ; Kinetics ; Mutation ; Nitrophenols/metabolism ; Organophosphates/metabolism ; Organophosphorus Compounds/metabolism ; Plasmids
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 15
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    Saturation mutagenesis of the yeast his3 regulatory site: requirements for transcriptional induction and for binding by GCN4 activator protein (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1986-10-24
    Beschreibung: Expression of the yeast his3 and other amino acid biosynthetic genes is induced during conditions of amino acid starvation. The coordination of this response is mediated by a positive regulatory protein called GCN4, which binds specifically to regulatory sites upstream of all coregulated genes and stimulates their transcription. The nucleotide sequence requirements of the his3 regulatory site were determined by analysis of numerous point mutations obtained by a novel method of cloning oligonucleotides. Almost all single base pair mutations within the nine base pair sequence ATGACTCTT significantly reduce his3 induction in vivo and GCN4 binding in vitro, whereas changes outside this region have minimal effects. One mutation, which generates a sequence that most closely resembles the consensus for 15 coregulated genes, increases both the level of induction and the affinity for GCN4 protein. The palindromic nature of the optimal sequence, ATGACTCAT, suggest that GCN4 protein binds as a dimer to adjacent half-sites that possibly overlap.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hill, D E -- Hope, I A -- Macke, J P -- Struhl, K -- GM 30186/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 Oct 24;234(4775):451-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3532321" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Base Sequence ; DNA, Fungal/genetics ; *DNA-Binding Proteins ; Enzyme Induction ; Fungal Proteins/*physiology ; Genes, Regulator ; Histidine/*genetics ; Mutation ; *Protein Kinases ; Saccharomyces cerevisiae/*genetics ; *Saccharomyces cerevisiae Proteins ; Sequence Homology, Nucleic Acid ; Transcription Factors/*physiology ; Transcription, Genetic
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 16
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    Restoration by calmodulin of a Ca2+-dependent K+ current missing in a mutant of Paramecium (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1986-04-25
    Beschreibung: A combination of genetics, biochemistry, and biophysics was used to show that calmodulin is involved in the regulation of an ion channel. Calmodulin restored the Ca2+-dependent K+ current in pantophobiac, a mutant in Paramecium that lacks this current. The restoration of the current occurred within 2 hours after the injection of 1 picogram of wild-type calmodulin into the mutant. The current remained for approximately 30 hours before the mutant phenotype returned. The injection of calmodulin isolated from pantophobiac had no effect. These results imply that calmodulin is required for the function or regulation of the Ca2+-dependent K+ current in Paramecium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hinrichsen, R D -- Burgess-Cassler, A -- Soltvedt, B C -- Hennessey, T -- Kung, C -- 1 F 32 NS 07502-01/NS/NINDS NIH HHS/ -- GM 22714/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 25;232(4749):503-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2421410" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Calcium/physiology ; Calmodulin/*pharmacology ; Dictyostelium/metabolism ; Ion Channels/*drug effects/physiology ; Mutation ; Paramecium/drug effects/genetics/*metabolism ; Potassium/*metabolism
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 17
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    A receptor-mediated pathway for cholesterol homeostasis (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1986-04-04
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, M S -- Goldstein, J L -- New York, N.Y. -- Science. 1986 Apr 4;232(4746):34-47.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3513311" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Biological Transport ; Cholesterol/*metabolism ; Endocytosis ; *Homeostasis ; Humans ; Hyperlipoproteinemia Type II/*metabolism ; Kinetics ; Lipid Metabolism, Inborn Errors/metabolism ; Lipoproteins, HDL/blood ; Lipoproteins, LDL/blood/*metabolism ; Models, Biological ; Mutation ; Receptors, LDL/genetics/*metabolism
    Print ISSN: 0036-8075
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 18
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    Uroporphyrinogen decarboxylase structural mutant (Gly281----Glu) in a case of porphyria (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1986-11-07
    Beschreibung: Uroporphyrinogen decarboxylase deficiency in man is responsible for familial porphyria cutanea tarda and hepatoerythropoietic porphyria. A recent study of a family with hepatoerythropoietic porphyria showed that the enzyme defect resulted from rapid degradation of the protein in vivo. Cloning and sequencing of a complementary DNA for the mutated gene revealed that the mutation was due to the replacement of a glycine residue by a glutamic acid residue at position 281. This base change leads to a protein that is very rapidly degraded in the presence of cell lysate. Characterization of the mutation will allow comparison of this defect in a homozygous patient with defects in other patients with familial porphyria cutanea tarda.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Verneuil, H -- Grandchamp, B -- Beaumont, C -- Picat, C -- Nordmann, Y -- New York, N.Y. -- Science. 1986 Nov 7;234(4777):732-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3775362" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Carboxy-Lyases/*genetics ; Cloning, Molecular ; DNA/genetics ; Humans ; Liver Diseases/genetics ; Mutation ; Porphyrias/*genetics ; Skin Diseases/genetics ; Structure-Activity Relationship ; Uroporphyrinogen Decarboxylase/deficiency/*genetics/metabolism
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    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 19
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    Genetic variation in HTLV-III/LAV over time in patients with AIDS or at risk for AIDS (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1986-06-20
    Beschreibung: In a study of genetic variation in the AIDS virus, HTLV-III/LAV, sequential virus isolates from persistently infected individuals were examined by Southern blot genomic analysis, molecular cloning, and nucleotide sequencing. Four to six virus isolates were obtained from each of three individuals over a 1-year or 2-year period. Changes were detected throughout the viral genomes and consisted of isolated and clustered nucleotide point mutations as well as short deletions or insertions. Results from genomic restriction mapping and nucleotide sequence comparisons indicated that viruses isolated sequentially had evolved in parallel from a common progenitor virus. The rate of evolution of HTLV-III/LAV was estimated to be at least 10(-3) nucleotide substitutions per site per year for the env gene and 10(-4) for the gag gene, values a millionfold greater than for most DNA genomes. Despite this relatively rapid rate of sequence divergence, virus isolates from any one patient were all much more related to each other than to viruses from other individuals. In view of the substantial heterogeneity among most independent HTLV-III/LAV isolates, the repeated isolation from a given individual of only highly related viruses raises the possibility that some type of interference mechanism may prevent simultaneous infection by more than one major genotypic form of the virus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hahn, B H -- Shaw, G M -- Taylor, M E -- Redfield, R R -- Markham, P D -- Salahuddin, S Z -- Wong-Staal, F -- Gallo, R C -- Parks, E S -- Parks, W P -- AI 23616-01/AI/NIAID NIH HHS/ -- AI 23854-01/AI/NIAID NIH HHS/ -- P30 CA 13148/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Jun 20;232(4757):1548-53.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3012778" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acquired Immunodeficiency Syndrome/*microbiology ; Amino Acid Sequence ; Base Sequence ; Chromosome Deletion ; DNA Restriction Enzymes ; DNA Transposable Elements ; Deltaretrovirus/*genetics/isolation & purification ; *Genetic Variation ; Humans ; Mutation ; Nucleic Acid Hybridization ; Risk
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    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 20
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    Identification of a missense mutation in the factor VIII gene of a mild hemophiliac (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1986-06-13
    Beschreibung: DNA probes derived from the cloned factor VIII gene can be used to detect mutations in the factor VIII gene of hemophiliacs. DNA hybridization analysis led to the identification of two contrasting point mutations in the same codon. In a severe hemophiliac with no detectable factor VIII activity, the normal arginine codon (number 2307) is converted to a stop codon, while in a mild hemophiliac with 10 percent of normal activity, this same codon is converted to glutamine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gitschier, J -- Wood, W I -- Shuman, M A -- Lawn, R M -- New York, N.Y. -- Science. 1986 Jun 13;232(4756):1415-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3012775" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Base Sequence ; DNA Restriction Enzymes ; Factor VIII/*genetics/metabolism ; Hemophilia A/*genetics ; Humans ; Metabolic Clearance Rate ; Mutation
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    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 21
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    A genetic approach to promoter recognition during trans induction of viral gene expression (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1986-10-03
    Beschreibung: Viral infection of mammalian cells entails the regulated induction of viral gene expression. The induction of many viral genes, including the herpes simplex virus gene encoding thymidine kinase (tk), depends on viral regulatory proteins that act in trans. Because recognition of the tk promoter by cellular transcription factors is well understood, its trans induction by viral regulatory proteins may serve as a useful model for the regulation of eukaryotic gene expression. A comprehensive set of mutations was therefore introduced into the chromosome of herpes simplex virus at the tk promoter to directly analyze the effects of promoter mutations on tk transcription. The promoter domains required for efficient tk expression under conditions of trans induction corresponded to those important for recognition by cellular transcription factors. Thus, trans induction of tk expression may be catalyzed initially by the interaction of viral regulatory proteins with cellular transcription factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coen, D M -- Weinheimer, S P -- McKnight, S L -- New York, N.Y. -- Science. 1986 Oct 3;234(4772):53-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3018926" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Gene Expression Regulation ; Genes, Viral ; Mutation ; *Promoter Regions, Genetic ; RNA, Messenger/genetics ; Simplexvirus/genetics/growth & development ; Transcription, Genetic ; *Virus Activation ; Xenopus
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    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 22
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    Functional role of aspartic acid-27 in dihydrofolate reductase revealed by mutagenesis (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1986-03-07
    Beschreibung: The crystal structures and enzymic properties of two mutant dihydrofolate reductases (Escherichia coli) were studied in order to clarify the functional role of an invariant carboxylic acid (aspartic acid at position 27) at the substrate binding site. One mutation, constructed by oligonucleotide-directed mutagenesis, replaces Asp27 with asparagine; the other is a primary-site revertant to Ser27. The only structural perturbations involve two internally bound water molecules. Both mutants have low but readily measurable activity, which increases rapidly with decreasing pH. The mutant enzymes were also characterized with respect to relative folate: dihydrofolate activities and kinetic deuterium isotope effects. It is concluded that Asp27 participates in protonation of the substrate but not in electrostatic stabilization of a positively charged, protonated transition state.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Howell, E E -- Villafranca, J E -- Warren, M S -- Oatley, S J -- Kraut, J -- F32 GM09375/GM/NIGMS NIH HHS/ -- GM10928/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 Mar 7;231(4742):1123-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3511529" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Aspartic Acid ; Crystallography ; Deuterium ; Escherichia coli ; Kinetics ; Methotrexate/metabolism ; Mutation ; Protein Binding ; Structure-Activity Relationship ; *Tetrahydrofolate Dehydrogenase
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    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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