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  • Mutation
  • American Association for the Advancement of Science (AAAS)  (20)
  • American Institute of Physics
  • 1990-1994  (20)
  • 1991  (20)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (20)
  • American Institute of Physics
  • Springer  (5)
Years
  • 1990-1994  (20)
Year
  • 1
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    Linkage of a cardiac arrhythmia, the long QT syndrome, and the Harvey ras-1 gene (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-05-03
    Description: Genetic factors contribute to heart disease. In this study, linkage analyses have been performed in a family that is predisposed to sudden death from cardiac arrhythmias, the long QT syndrome (LQT). A DNA marker at the Harvey ras-1 locus (H-ras-1) was linked to LQT with a logarithm of the likelihood ratio for linkage (lod score) of 16.44 at theta = 0, which confirms the genetic basis of this trait and localizes this gene to the short arm of chromosome 11. As no recombination was observed between LQT and H-ras-1, and there is a physiological rationale for its involvement in this disease, ras becomes a candidate for the disease locus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keating, M -- Atkinson, D -- Dunn, C -- Timothy, K -- Vincent, G M -- Leppert, M -- New York, N.Y. -- Science. 1991 May 3;252(5006):704-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics, University of Utah Health Sciences Center, Salt Lake City 84132.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1673802" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosome Mapping ; Chromosomes, Human, Pair 11 ; Electrocardiography ; *Genes, ras ; Humans ; *Lod Score ; Long QT Syndrome/*genetics/physiopathology ; Mutation ; Pedigree ; Polymorphism, Restriction Fragment Length
    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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  • 2
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    Generation of cAMP-activated chloride currents by expression of CFTR (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-02-08
    Description: Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) cause cystic fibrosis. In order to evaluate its function, CFTR was expressed in HeLa, Chinese hamster ovary (CHO), and NIH 3T3 fibroblast cells, and anion permeability was assessed with a fluorescence microscopic assay and the whole-cell patch-clamp technique. Adenosine 3',5'-monophosphate (cAMP) increased anion permeability and chloride currents in cells expressing CFTR, but not in cells expressing a mutant CFTR (delta F508) or in nontransfected cells. The simplest interpretation of these observations is that CFTR is itself a cAMP-activated chloride channel. The alternative interpretation, that CFTR directly or indirectly regulates chloride channels, requires that these cells have endogenous cryptic, chloride channels that are stimulated by cAMP only in the presence of CFTR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, M P -- Rich, D P -- Gregory, R J -- Smith, A E -- Welsh, M J -- New York, N.Y. -- Science. 1991 Feb 8;251(4994):679-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1704151" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chloride Channels ; Chlorides/*metabolism ; Cricetinae ; Cyclic AMP/*physiology ; Cystic Fibrosis Transmembrane Conductance Regulator ; Humans ; Membrane Proteins/*metabolism/*physiology ; Mice ; Mutation ; Recombinant Proteins ; Structure-Activity Relationship
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  • 3
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    Global suppression of protein folding defects and inclusion body formation (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-07-05
    Description: Amino acid substitutions at a site in the center of the bacteriophage protein P22 tailspike polypeptide chain suppress temperature-sensitive folding mutations at many sites throughout the chain. Characterization of the intracellular folding and chain assembly process reveals that the suppressors act in the folding pathway, inhibiting the aggregation of an early folding intermediate into the kinetically trapped inclusion body state. The suppressors alone increase the folding efficiency of the otherwise wild-type polypeptide chain without altering the stability or activity of the native state. These amino acid substitutions identify an unexpected aspect of the protein folding grammar--sequences within the chain that carry information inhibiting unproductive off-pathway conformations. Such mutations may serve to increase the recovery of protein products of cloned genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mitraki, A -- Fane, B -- Haase-Pettingell, C -- Sturtevant, J -- King, J -- GMS17,980/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Jul 5;253(5015):54-8.〈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/1648264" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Coliphages ; DNA Mutational Analysis ; Electrophoresis, Polyacrylamide Gel ; Gene Expression Regulation ; Inclusion Bodies/*chemistry ; Molecular Sequence Data ; Mutation ; *Protein Conformation ; Viral Proteins/*chemistry ; Viral Tail Proteins
    Print ISSN: 0036-8075
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  • 4
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    Laser ablation studies of the role of the Drosophila oocyte nucleus in pattern formation (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-11
    Description: Somatic and germline cells interact during oogenesis to establish the pattern axes of the Drosophila eggshell and embryo. The role of the oocyte nucleus in pattern formation was tested with the use of laser ablation. Ablation in stage 6 to 9 egg chambers caused partial or complete ventralization of the eggshell, phenotypes similar to those of eggs produced by gurken or torpedo females. Accumulation of vasa protein at the posterior pole of treated oocytes was also disrupted. Thus the oocyte nucleus is required as late as stage 9 for dorsoventral patterning within the follicle cells and for polar plasm assembly in the oocyte.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Montell, D J -- Keshishian, H -- Spradling, A C -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 1991 Oct 11;254(5029):290-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Carnegie Institution of Washington, Baltimore, MD 21210.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1925585" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Nucleus/*physiology ; Cell Polarity/physiology ; Drosophila/*embryology ; Egg Shell ; Genes ; Laser Therapy ; Microsurgery ; Morphogenesis ; Mutation ; Oocytes/*physiology ; Oogenesis
    Print ISSN: 0036-8075
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  • 5
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    Critical structural elements of the VP16 transcriptional activation domain (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-01-04
    Description: Virion protein 16 (VP16) of herpes simplex virus type 1 contains an acidic transcriptional activation domain. Missense mutations within this domain have provided insights into the structural elements critical for its function. Net negative charge contributed to, but was not sufficient for, transcriptional activation by VP16. A putative amphipathic alpha helix did not appear to be an important structural component of the activation domain. A phenylalanine residue at position 442 was exquisitely sensitive to mutation. Transcriptional activators of several classes contain hydrophobic amino acids arranged in patterns resembling that of VP16. Therefore, the mechanism of transcriptional activation by VP16 and other proteins may involve both ionic and specific hydrophobic interactions with target molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cress, W D -- Triezenberg, S J -- AI 27323/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1991 Jan 4;251(4989):87-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Michigan State University, East Lansing 48824-1319.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1846049" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Immediate-Early Proteins ; Molecular Sequence Data ; Mutation ; Protein Conformation ; *Simplexvirus ; Structure-Activity Relationship ; Transcription Factors/*chemistry/genetics/pharmacology ; Transcription, Genetic/*drug effects ; Transfection ; Viral Proteins/*genetics ; Virion
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  • 6
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    Atomic structure of adenosine deaminase complexed with a transition-state analog: understanding catalysis and immunodeficiency mutations (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-05-31
    Description: The crystal structure of a murine adenosine deaminase complexed with 6-hydroxyl-1,6-dihydropurine ribonucleoside, a nearly ideal transition-state analog, has been determined and refined at 2.4 angstrom resolution. The structure is folded as an eight-stranded parallel alpha/beta barrel with a deep pocket at the beta-barrel COOH-terminal end wherein the inhibitor and a zinc are bound and completely sequestered. The presence of the zinc cofactor and the precise structure of the bound analog were not previously known. The 6R isomer of the analog is very tightly held in place by the coordination of the 6-hydroxyl to the zinc and the formation of nine hydrogen bonds. On the basis of the structure of the complex a stereoselective addition-elimination or SN2 mechanism of the enzyme is proposed with the zinc atom and the Glu and Asp residues playing key roles. A molecular explanation of a hereditary disease caused by several point mutations of an enzyme is also presented.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, D K -- Rudolph, F B -- Quiocho, F A -- CA14030/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 May 31;252(5010):1278-84.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1925539" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Deaminase/*chemistry/deficiency/metabolism ; Amino Acid Sequence ; Animals ; Binding Sites ; Catalysis ; Crystallization ; Immunologic Deficiency Syndromes/*enzymology/genetics ; Mice ; Models, Molecular ; Molecular Structure ; Mutation ; Protein Conformation ; Purine Nucleosides/chemistry/*metabolism ; Ribonucleosides/chemistry/*metabolism ; Zinc/metabolism
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  • 7
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    Identification of a gene located at chromosome 5q21 that is mutated in colorectal cancers (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-15
    Description: Recent studies have suggested the existence of a tumor suppressor gene located at chromosome region 5q21. DNA probes from this region were used to study a panel of sporadic colorectal carcinomas. One of these probes, cosmid 5.71, detected a somatically rearranged restriction fragment in the DNA from a single tumor. Further analysis of the 5.71 cosmid revealed two regions that were highly conserved in rodent DNA. These sequences were used to identify a gene, MCC (mutated in colorectal cancer), which encodes an 829-amino acid protein with a short region of similarity to the G protein-coupled m3 muscarinic acetylcholine receptor. The rearrangement in the tumor disrupted the coding region of the MCC gene. Moreover, two colorectal tumors were found with somatically acquired point mutations in MCC that resulted in amino acid substitutions. MCC is thus a candidate for the putative colorectal tumor suppressor gene located at 5q21. Further studies will be required to determine whether the gene is mutated in other sporadic tumors or in the germ line of patients with an inherited predisposition to colonic tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kinzler, K W -- Nilbert, M C -- Vogelstein, B -- Bryan, T M -- Levy, D B -- Smith, K J -- Preisinger, A C -- Hamilton, S R -- Hedge, P -- Markham, A -- 6M 07184/PHS HHS/ -- CA 06973/CA/NCI NIH HHS/ -- CA 09243/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Mar 15;251(4999):1366-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Genetics Laboratory, Johns Hopkins Oncology Center, Baltimore, MD 21231.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1848370" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli/*genetics ; Amino Acid Sequence ; Animals ; Base Sequence ; *Chromosomes, Human, Pair 5 ; Colorectal Neoplasms/*genetics ; Exons ; GTP-Binding Proteins/metabolism ; Gene Expression ; *Genes, Tumor Suppressor ; Humans ; Molecular Sequence Data ; Mutation ; Oligonucleotides/chemistry ; Polymerase Chain Reaction ; Proteins/*genetics/metabolism ; Rats ; Sequence Homology, Nucleic Acid ; *Tumor Suppressor Proteins
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  • 8
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    Toward cloning and mapping the genome of Drosophila (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-11
    Description: An ultimate goal of Drosophila genetics is to identify and define the functions of all the genes in the organism. Traditional approaches based on the isolation of mutant genes have been extraordinary fruitful. Recent advances in the manipulation and analysis of large DNA fragments have made it possible to develop detailed molecular maps of the Drosophila genome as the initial steps in determining the complete DNA sequence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Merriam, J -- Ashburner, M -- Hartl, D L -- Kafatos, F C -- New York, N.Y. -- Science. 1991 Oct 11;254(5029):221-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California, Los Angeles 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1925579" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Biological Evolution ; *Chromosome Mapping ; Chromosomes ; *Cloning, Molecular ; Drosophila melanogaster/*genetics ; Gene Rearrangement ; Genes ; *Genome ; Mutation
    Print ISSN: 0036-8075
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  • 9
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    Targets for cell cycle arrest by the immunosuppressant rapamycin in yeast (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-08-23
    Description: FK506 and rapamycin are related immunosuppressive compounds that block helper T cell activation by interfering with signal transduction. In vitro, both drugs bind and inhibit the FK506-binding protein (FKBP) proline rotamase. Saccharomyces cerevisiae cells treated with rapamycin irreversibly arrested in the G1 phase of the cell cycle. An FKBP-rapamycin complex is concluded to be the toxic agent because (i) strains that lack FKBP proline rotamase, encoded by FPR1, were viable and fully resistant to rapamycin and (ii) FK506 antagonized rapamycin toxicity in vivo. Mutations that conferred rapamycin resistance altered conserved residues in FKBP that are critical for drug binding. Two genes other than FPR1, named TOR1 and TOR2, that participate in rapamycin toxicity were identified. Nonallelic noncomplementation between FPR1, TOR1, and TOR2 alleles suggests that the products of these genes may interact as subunits of a protein complex. Such a complex may mediate nuclear entry of signals required for progression through the cell cycle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heitman, J -- Movva, N R -- Hall, M N -- New York, N.Y. -- Science. 1991 Aug 23;253(5022):905-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1715094" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Anti-Bacterial Agents/metabolism/pharmacology ; Base Sequence ; Binding Sites ; Carrier Proteins/antagonists & inhibitors/chemistry/genetics/metabolism ; Cell Cycle/*drug effects ; Cyclosporins/pharmacology ; Drug Resistance, Microbial/genetics ; G1 Phase/drug effects ; Humans ; Immunosuppressive Agents/pharmacology ; Molecular Sequence Data ; Molecular Structure ; Mutation ; Polyenes/metabolism/*pharmacology ; Saccharomyces cerevisiae/*cytology/drug effects ; Sequence Homology, Nucleic Acid ; Signal Transduction ; Sirolimus ; Tacrolimus ; Tacrolimus Binding Proteins
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  • 10
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    Isolation of sequences that span the fragile X and identification of a fragile X-related CpG island (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-08
    Description: Yeast artificial chromosomes (YACs) were obtained from a 550-kilobase region that contains three probes previously mapped as very close to the locus of the fragile X syndrome. These YACs spanned the fragile site in Xq27.3 as shown by fluorescent in situ hybridization. An internal 200-kilobase segment contained four chromosomal breakpoints generated by induction of fragile X expression. A single CpG island was identified in the cloned region between markers DXS463 and DXS465 that appears methylated in mentally retarded fragile X males, but not in nonexpressing male carriers of the mutation nor in normal males. This CpG island may indicate the presence of a gene involved in the clinical phenotype of the syndrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heitz, D -- Rousseau, F -- Devys, D -- Saccone, S -- Abderrahim, H -- Le Paslier, D -- Cohen, D -- Vincent, A -- Toniolo, D -- Della Valle, G -- New York, N.Y. -- Science. 1991 Mar 8;251(4998):1236-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Genetique Moleculaire des Eucaryotes du CNRS, Institut de Chimie Biologique, Faculte de Medecine, Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2006411" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Chromosomes, Fungal ; Cloning, Molecular ; DNA Probes ; *Dinucleoside Phosphates ; Fragile X Syndrome/*genetics ; Humans ; Male ; Molecular Sequence Data ; Mutation ; Nucleic Acid Hybridization ; Oligonucleotide Probes ; Polymerase Chain Reaction ; Reference Values ; Restriction Mapping ; Saccharomyces cerevisiae/genetics ; *X Chromosome
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  • 11
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    Altered synaptic plasticity in Drosophila memory mutants with a defective cyclic AMP cascade (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-01-11
    Description: Synaptic transmission was examined in Drosophila mutants deficient in memory function. These mutants, dunce and rutabaga, are defective in different steps of the cyclic adenosine 3',5'-monophosphate (cAMP) cascade. In both dunce and rutabaga larvae, voltage-clamp analysis of neuromuscular transmission revealed impaired synaptic facilitation and post-tetanic potentiation as well as abnormal responses to direct application of dibutyryl cAMP. In addition, the calcium dependence of transmitter release was shifted in dunce. The results suggest that the cAMP cascade plays a role in synaptic facilitation and potentiation and indicate that synaptic plasticity is altered in Drosophila memory mutants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhong, Y -- Wu, C F -- New York, N.Y. -- Science. 1991 Jan 11;251(4990):198-201.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Iowa, Iowa City 52242.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1670967" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Animals ; Bucladesine/pharmacology ; Calcium/pharmacology ; Cyclic AMP/*physiology ; Drosophila/*genetics ; Electric Stimulation ; Larva/physiology ; Memory/physiology ; Muscle Contraction/physiology ; Mutation ; Neuromuscular Junction/physiology ; Neuronal Plasticity/*physiology ; Neurotransmitter Agents/secretion ; Synapses/*physiology
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  • 12
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    Dual role of the Drosophila pattern gene tailless in embryonic termini (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-18
    Description: One of the first zygotically active genes required for formation of the terminal domains of the Drosophila embryo is tailless (tll). Expression of the tll gene is activated ectopically in gain-of-function mutants of the maternal terminal gene torso (tor); this suggests that tor normally activates the tll gene in the termini. Ectopic expression of tll under the control of an inducible promoter results in differentiation of ectopic terminal-specific structures, the Filzkorper, and leads to the activation of at least one gene, hunchback, that is required to form these structures. Ectopic expression of the tll gene also represses segmentation by repressing the gap genes Kruppel and knirps and probably also pair rule genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steingrimsson, E -- Pignoni, F -- Liaw, G J -- Lengyel, J A -- 09948/PHS HHS/ -- New York, N.Y. -- Science. 1991 Oct 18;254(5030):418-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California, Los Angeles 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1925599" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drosophila/embryology/*genetics ; Embryonic Development ; Female ; Genes, Regulator ; Heat-Shock Proteins/genetics ; Hot Temperature ; Male ; Mutation ; Phenotype ; Promoter Regions, Genetic
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  • 13
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    Antigenic diversity thresholds and the development of AIDS (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-11-15
    Description: Longitudinal studies of patients infected with HIV-1 reveal a long and variable incubation period between infection and the development of AIDS. Data from a small number of infected patients show temporal changes in the number of genetically distinct strains of the virus throughout the incubation period, with a slow but steady rise in diversity during the progression to disease. A mathematical model of the dynamic interaction between viral diversity and the human immune system suggests the existence of an antigen diversity threshold, below which the immune system is able to regulate viral population growth but above which the virus population induces the collapse of the CD4+ lymphocyte population. The model suggests that antigenic diversity is the cause, not a consequence, of immunodeficiency disease. The model is compared with available data, and is used to assess how the timing of the application of chemotherapy or immunotherapy influences the rate of progress to disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nowak, M A -- Anderson, R M -- McLean, A R -- Wolfs, T F -- Goudsmit, J -- May, R M -- New York, N.Y. -- Science. 1991 Nov 15;254(5034):963-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, University of Oxford, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1683006" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*immunology/prevention & control/therapy ; Base Sequence ; CD4-Positive T-Lymphocytes ; Computer Simulation ; DNA, Viral/genetics ; HIV Antigens/genetics ; HIV Core Protein p24/metabolism ; HIV-1/genetics/*immunology ; Humans ; Immunotherapy ; Leukocyte Count ; Molecular Sequence Data ; Mutation ; Oligonucleotides/chemistry ; Time Factors ; Vaccination
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  • 14
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    A virus-encoded "superantigen" in a retrovirus-induced immunodeficiency syndrome of mice (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-04-19
    Description: The development of an immunodeficiency syndrome of mice caused by a replication-defective murine leukemia virus (MuLV) is paradoxically associated with a rapid activation and proliferation of CD4+ T cells that are dependent on the presence of B cells. The responses of normal spleen cells to B cell lines that express the defective virus indicated that these lines express a cell surface determinant that shares "superantigenic" properties with some microbial antigens and Mls-like self antigens. This antigen elicited a potent proliferative response that was dependent on the presence of CD4+ T cells and was associated with selective expansion of cells bearing V beta 5. This response was markedly inhibited by a monoclonal antibody specific for the MuLV gag-encoded p30 antigen.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hugin, A W -- Vacchio, M S -- Morse, H C 3rd -- N01-AI-72622/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1991 Apr 19;252(5004):424-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1850169" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Viral/genetics/*immunology ; B-Lymphocytes/immunology ; Gene Products, gag/genetics ; HIV-1/immunology ; Histocompatibility Antigens Class II/immunology ; Leukemia Virus, Murine/genetics/*immunology ; Lymphocyte Activation ; Mice ; Mice, Inbred CBA ; Murine Acquired Immunodeficiency Syndrome/immunology/*microbiology ; Mutation ; Receptors, Antigen, T-Cell/genetics/immunology ; T-Lymphocytes/immunology ; T-Lymphocytes, Helper-Inducer/immunology ; Virus Replication/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    Identification of the envelope V3 loop as the primary determinant of cell tropism in HIV-1 (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-07-05
    Description: Cells of the monocyte-macrophage lineage are targets for human immunodeficiency virus-1 (HIV-1) infection in vivo. However, many laboratory strains of HIV-1 that efficiently infect transformed T cell lines replicate poorly in macrophages. A 20-amino acid sequence from the macrophage-tropic BaL isolate of HIV-1 was sufficient to confer macrophage tropism on HTLV-IIIB, a T cell line--tropic isolate. This small sequence element is in the V3 loop, the envelope domain that is the principal neutralizing determinant of HIV-1. Thus, the V3 loop not only serves as a target of the host immune response but is also pivotal in determining HIV-1 tissue tropism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hwang, S S -- Boyle, T J -- Lyerly, H K -- Cullen, B R -- New York, N.Y. -- Science. 1991 Jul 5;253(5015):71-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1905842" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Movement/*genetics ; Chimera ; Genes, env/physiology ; HIV-1/genetics/*physiology ; Haplorhini ; Molecular Sequence Data ; Mutation ; Proviruses ; Restriction Mapping ; Sequence Homology, Nucleic Acid ; Viral Envelope Proteins/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    Modular organization of genes required for complex polyketide biosynthesis (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-05-03
    Description: In Saccharopolyspora erythraea, the genes that govern synthesis of the polyketide portion of the macrolide antibiotic erythromycin are organized in six repeated units that encode fatty acid synthase (FAS)-like activities. Each repeated unit is designated a module, and two modules are contained in a single open reading frame. A model for the synthesis of this complex polyketide is proposed, where each module encodes a functional synthase unit and each synthase unit participates specifically in one of the six FAS-like elongation steps required for formation of the polyketide. In addition, genetic organization and biochemical order of events appear to be colinear. Evidence for the model is provided by construction of a selected mutant and by isolation of a polyketide of predicted structure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Donadio, S -- Staver, M J -- McAlpine, J B -- Swanson, S J -- Katz, L -- New York, N.Y. -- Science. 1991 May 3;252(5006):675-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Corporate Molecular Biology, Abbott Laboratories, Abbott Park, IL 60064.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2024119" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Binding Sites ; Cloning, Molecular ; DNA, Bacterial/genetics ; Erythromycin/analogs & derivatives/biosynthesis/chemistry ; Genes, Bacterial ; Gram-Positive Bacteria/enzymology/genetics ; Hydroxylation ; Models, Molecular ; Molecular Sequence Data ; Molecular Structure ; Multienzyme Complexes/*genetics ; Mutation ; Nucleic Acid Hybridization ; Repetitive Sequences, Nucleic Acid
    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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  • 17
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    Recent advances in the polymerase chain reaction (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-06-21
    Description: The polymerase chain reaction (PCR) has dramatically altered how molecular studies are conducted as well as what questions can be asked. In addition to simplifying molecular tasks typically carried out with the use of recombinant DNA technology, PCR has allowed a spectrum of advances ranging from the identification of novel genes and pathogens to the quantitation of characterized nucleotide sequences. PCR can provide insights into the intricacies of single cells as well as the evolution of species. Some recent developments in instrumentation, methodology, and applications of the PCR are presented in this review.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Erlich, H A -- Gelfand, D -- Sninsky, J J -- New York, N.Y. -- Science. 1991 Jun 21;252(5013):1643-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics, Core Technology, Cetus Corporation, Emeryville, CA 94608.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2047872" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Biological Evolution ; DNA/genetics ; DNA Fingerprinting ; Forensic Medicine/methods ; Gene Expression ; Genetic Diseases, Inborn/genetics ; Human Genome Project ; Humans ; Multigene Family ; Mutation ; Oligonucleotides/chemistry ; *Polymerase Chain Reaction
    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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  • 18
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    Zeroing in on individual cancer risk (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-08-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1991 Aug 9;253(5020):612-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1651561" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli/genetics ; Antineoplastic Agents ; Biomarkers, Tumor/analysis ; Carcinogens ; Genetic Predisposition to Disease ; Humans ; Mutation ; Neoplasms/diagnosis/*etiology/genetics/prevention & control ; Risk Factors
    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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  • 19
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    Control of larval development by chemosensory neurons in Caenorhabditis elegans (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-08
    Description: Larval development of the nematode Caenorhabditis elegans is controlled by the activities of four classes of chemosensory neurons. The choice between normal development and development into a specialized larval form called a dauer larva is regulated by competing environmental stimuli: food and a dauer pheromone. When the neuron classes ADF, ASG, ASI, and ASJ are killed, animals develop as dauer larvae regardless of environmental conditions. These neurons might sense food or dauer pheromone, or both, to initiate the specialized differentiation of many cell types that occurs during dauer formation. Entry into and exit from the dauer stage are primarily controlled by different chemosensory neurons. The analysis of mutants defective in dauer formation indicates that the chemosensory neurons are active in the absence of sensory inputs and that dauer pheromone inhibits the ability of these neurons to generate a signal necessary for normal development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bargmann, C I -- Horvitz, H R -- GM24663/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Mar 8;251(4998):1243-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, 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/2006412" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis/*growth & development ; Cell Survival ; Larva ; Models, Neurological ; Mutation ; Neurons, Afferent/cytology/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 20
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    Coordinate regulation of beta-lactamase induction and peptidoglycan composition by the amp operon (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-01-11
    Description: The amp operon, which is located on the Escherichia coli chromosome, modulates the induction of plasmid-borne beta-lactamase genes by extracellular beta-lactam antibiotics. This suggests that the gene products AmpD and AmpE may function in the transduction of external signals. beta-Lactam antibiotics are analogs of cell wall components that can be released during cell wall morphogenesis of enterobacteria. The amp operon was studied to determine its importance in signal transduction during cell wall morphogenesis. The peptidoglycan compositions of amp mutants were determined by high-performance liquid chromatography and fast atom bombardment mass spectrometry. When a chromosomal or plasmid-borne copy of ampD was present, the amount of pentapeptide-containing muropeptides in the cell wall increased upon addition of the cell wall constituent diaminopimelic acid to the growth medium. These results suggest that beta-lactamase induction and modulation of the composition of the cell wall share elements of a regulatory circuit that involves AmpD. Escherichia coli requires AmpD to respond to extracellular signaling amino acids, such as diaminopimelic acid, and this signal transduction system may regulate peptidoglycan composition in response to cell wall turnover products.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tuomanen, E -- Lindquist, S -- Sande, S -- Galleni, M -- Light, K -- Gage, D -- Normark, S -- AI23459/AI/NIAID NIH HHS/ -- AI27913/AI/NIAID NIH HHS/ -- DRR00480/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1991 Jan 11;251(4990):201-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Microbiology, Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1987637" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Bacterial Proteins/*genetics/metabolism ; Carboxypeptidases/metabolism ; Cell Wall/metabolism ; Diaminopimelic Acid/pharmacology ; Enzyme Induction ; Escherichia coli/*genetics/metabolism ; *Gene Expression Regulation/drug effects ; Genotype ; Membrane Proteins/*genetics/metabolism ; Molecular Sequence Data ; Mutation ; *N-Acetylmuramoyl-L-alanine Amidase ; Oligopeptides/metabolism ; *Operon ; Peptidoglycan/metabolism ; Plasmids ; Signal Transduction ; Spectrometry, Mass, Fast Atom Bombardment ; beta-Lactamases/*biosynthesis/genetics
    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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