ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Mutation  (312)
  • American Association for the Advancement of Science (AAAS)  (312)
  • Annual Reviews
  • 1990-1994  (260)
  • 1980-1984  (52)
Collection
Keywords
Publisher
Years
Year
  • 1
    facet.materialart.
    Unknown
    GT-1 binding site confers light responsive expression in transgenic tobacco (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-04-27
    Description: Light-dependent expression of rbcS, the gene encoding the small subunit of ribulose-1,5-bisphosphate carboxylase, which is the key enzyme involved in carbon fixation in higher plants, is regulated at the transcriptional level. Sequence analysis of the gene has uncovered a conserved GT motif in the -150 to -100 region of many rbcS promoters. This motif serves as the binding site of a nuclear factor, designated GT-1. Analysis of site-specific mutants of pea rbcS-3A promoter demonstrated that GT-1 binding in vitro is correlated with light-responsive expression of the rbcS promoter in transgenic plants. However, it is not known whether factors other than GT-1 might also be required for activation of transcription by light. A synthetic tetramer of box II (TGTGTGGTTAATATG), the GT-1 binding site located between -152 to -138 of the rbcS-3A promoter, inserted upstream of a truncated cauliflower mosaic virus 35S promoter is sufficient to confer expression in leaves of transgenic tobacco. This expression occurs principally in chloroplast-containing cells, is induced by light, and is correlated with the ability of box II to bind GT-1 in vitro. The data show that the binding site for GT-1 is likely to be a part of the molecular light switch for rbcS activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lam, E -- Chua, N H -- New York, N.Y. -- Science. 1990 Apr 27;248(4954):471-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Plant Molecular Biology, Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2330508" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Binding Sites ; Chloramphenicol O-Acetyltransferase/genetics ; Cloning, Molecular ; DNA-Binding Proteins/*metabolism ; Gene Expression Regulation/*physiology ; Genetic Vectors ; *Light ; Molecular Sequence Data ; Mutation ; Nuclear Proteins/*metabolism ; Plant Proteins/*metabolism ; *Plants, Toxic ; Promoter Regions, Genetic/genetics ; Ribulose-Bisphosphate Carboxylase/*genetics ; Tobacco/enzymology/*genetics ; Transcription, Genetic/radiation effects ; Transformation, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    Common modifications of trimeric G proteins and ras protein: involvement of polyisoprenylation (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-13
    Description: The heterotrimeric guanine nucleotide-binding regulatory proteins act at the inner surface of the plasma membrane to relay information from cell surface receptors to effectors inside the cell. These G proteins are not integral membrane proteins, yet are membrane associated. The processing and function of the gamma subunit of the yeast G protein involved in mating-pheromone signal transduction was found to be affected by the same mutations that block ras processing. The nature of these mutations implied that the gamma subunit was polyisoprenylated and that this modification was necessary for membrane association and biological activity. A microbial screen was developed for pharmacological agents that inhibit polyisoprenylation and that have potential application in cancer therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finegold, A A -- Schafer, W R -- Rine, J -- Whiteway, M -- Tamanoi, F -- CA 41996/CA/NCI NIH HHS/ -- GM 07183/GM/NIGMS NIH HHS/ -- GM 35827/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jul 13;249(4965):165-9.〈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/1695391" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cell Membrane/metabolism ; Cloning, Molecular ; Epitopes/genetics ; GTP-Binding Proteins/genetics/*metabolism ; Hemagglutinins, Viral/immunology ; Lovastatin/pharmacology ; Mevalonic Acid/pharmacology ; Molecular Sequence Data ; Mutation ; Oncogene Protein p21(ras)/genetics/*metabolism ; Orthomyxoviridae/immunology ; Protein Processing, Post-Translational ; Saccharomyces cerevisiae/*genetics/metabolism ; Signal Transduction ; Suppression, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    GTP-GDP exchange proteins (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-05-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levitzki, A -- New York, N.Y. -- Science. 1990 May 18;248(4957):794.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, Hebrew University of Jerusalem, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2188357" target="_blank"〉PubMed〈/a〉
    Keywords: Guanine Nucleotides/*metabolism ; Guanosine Diphosphate/*metabolism ; Guanosine Triphosphate/*metabolism ; Mutation ; Oncogene Protein p21(ras)/genetics/*metabolism ; Proto-Oncogene Proteins/genetics/*metabolism ; Proto-Oncogene Proteins p21(ras) ; Saccharomyces cerevisiae/genetics/metabolism ; Schizosaccharomyces/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    DNA looping and unlooping by AraC protein (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-10-26
    Description: Expression of the L-arabinose BAD operon in Escherichia coli is regulated by AraC protein which acts both positively in the presence of arabinose to induce transcription and negatively in the absence of arabinose to repress transcription. The repression of the araBAD promoter is mediated by DNA looping between AraC protein bound at two sites near the promoter separated by 210 base pairs, araI and araO2. In vivo and in vitro experiments presented here show that an AraC dimer, with binding to half of araI and to araO2, maintains the repressed state of the operon. The addition of arabinose, which induces the operon, breaks the loop, and shifts the interactions from the distal araO2 site to the previously unoccupied half of the araI site. The conversion between the two states does not require additional binding of AraC protein and appears to be driven largely by properties of the protein rather than being specified by the slightly different DNA sequences of the binding sites. Slight reorientation of the subunits of AraC could specify looping or unlooping by the protein. Such a mechanism could account for regulation of DNA looping in other systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lobell, R B -- Schleif, R F -- GM18277/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Oct 26;250(4980):528-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Department of Biochemistry, Brandeis University, Waltham, MA 02254.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2237403" target="_blank"〉PubMed〈/a〉
    Keywords: AraC Transcription Factor ; Arabinose/genetics/pharmacology ; *Bacterial Proteins ; Binding Sites ; *DNA, Bacterial/genetics/metabolism ; DNA, Superhelical/metabolism ; Escherichia coli/*genetics ; Escherichia coli Proteins ; Fucose/pharmacology ; Gene Expression Regulation, Bacterial/*drug effects ; Guanine/metabolism ; Macromolecular Substances ; Methylation ; Mutation ; Nucleic Acid Conformation/*drug effects ; Operon ; Protein Conformation/drug effects ; Repressor Proteins/metabolism/*pharmacology ; *Transcription Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unknown
    An insertion in the human thyrotropin receptor critical for high affinity hormone binding (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-21
    Description: Thyrotropin (TSH), luteinizing hormone (LH), and chorionic gonadotropin (CG) are structurally related glycoprotein hormones, which bind to receptors that share a high degree of sequence similarity. However, comparison of the primary amino acid sequences of the TSH and LH-CG receptors reveals two unique insertions of 8 and 50 amino acids in the extracellular domain of the TSH receptor. The functional significance of these insertions were determined by site-directed mutagenesis. Deletion of the 50-amino acid tract (residues 317 to 366) had no effect on TSH binding or on TSH and thyroid-stimulating immunoglobulin (TSI) biological activities. In contrast, either deletion or substitution of the eight-amino acid region (residues 38 to 45) abolished these activities. This eight-amino acid tract near the amino terminus of the TSH receptor appears to be an important site of interaction for both TSH and TSI.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wadsworth, H L -- Chazenbalk, G D -- Nagayama, Y -- Russo, D -- Rapoport, B -- DK-19289/DK/NIDDK NIH HHS/ -- DK-36182/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Sep 21;249(4975):1423-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Veterans Administration Medical Center, San Francisco, CA 94121.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2169649" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Binding Sites ; Cell Line ; Chromosome Deletion ; Clone Cells ; Cyclic AMP/metabolism ; Humans ; Molecular Sequence Data ; Mutation ; Oligonucleotide Probes ; Receptors, Thyrotropin/*genetics/metabolism ; Thyrotropin/*metabolism/pharmacology ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 6
    facet.materialart.
    Unknown
    Testing for carcinogens with rodents (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abelson, P H -- New York, N.Y. -- Science. 1990 Sep 21;249(4975):1357.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2402628" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogenicity Tests/*methods ; *Carcinogens ; Mutation ; *Rodentia
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 7
    facet.materialart.
    Unknown
    Defective presentation of endogenous antigen by a cell line expressing class I molecules (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-04-20
    Description: Cytotoxic T lymphocytes (CTLs) recognize class I major histocompatibility complex (MHC) molecules associated with antigenic peptides derived from endogenously synthesized proteins. Binding to such peptides is a requirement for class I assembly in the endoplasmic reticulum (ER). A mutant human cell line, T2, assembles and transports to its surface some, but not all, class I MHC molecules. The class I molecules expressed on the surface of T2 do not present peptides derived from cytosolic antigens, although they can present exogenously added peptides to CTL. The transported class I molecules may interact weakly with an unknown retaining factor in the ER such that they can assemble despite the relative shortage of peptides.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hosken, N A -- Bevan, M J -- AI-19335/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1990 Apr 20;248(4953):367-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Research Institute of Scripps Clinic, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2326647" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/*immunology ; Antigens/immunology ; Antigens, Viral/immunology ; B-Lymphocytes/immunology ; Capsid/immunology ; Cell Line ; Endoplasmic Reticulum/immunology ; Gene Expression ; H-2 Antigens/genetics/immunology ; HLA Antigens/genetics ; Histocompatibility Antigens Class I/*immunology ; Histocompatibility Antigens Class II/genetics ; Humans ; Mice ; Mutation ; Ovalbumin/immunology ; Peptides/immunology ; T-Lymphocytes, Cytotoxic/immunology ; Transfection ; Tumor Cells, Cultured ; Viral Core Proteins/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 8
    facet.materialart.
    Unknown
    Involvement of the silencer and UAS binding protein RAP1 in regulation of telomere length (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-10-26
    Description: The yeast protein RAP1, initially described as a transcriptional regulator, binds in vitro to sequences found in a number of seemingly unrelated genomic loci. These include the silencers at the transcriptionally repressed mating-type genes, the promoters of many genes important for cell growth, and the poly[(cytosine)1-3 adenine] [poly(C1-3A)] repeats of telomeres. Because RAP1 binds in vitro to the poly(C1-3A) repeats of telomeres, it has been suggested that RAP1 may be involved in telomere function in vivo. In order to test this hypothesis, the telomere tract lengths of yeast strains that contained conditionally lethal (ts) rap1 mutations were analyzed. Several rap1ts alleles reduced telomere length in a temperature-dependent manner. In addition, plasmids that contain small, synthetic telomeres with intact or mutant RAP1 binding sites were tested for their ability to function as substrates for poly(C1-3A) addition in vivo. Mutations in the RAP1 binding sites reduced the efficiency of the addition reaction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lustig, A J -- Kurtz, S -- Shore, D -- GM 40094/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Oct 26;250(4980):549-53.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Memorial Sloan-Kettering Cancer Center, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2237406" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Binding Sites ; Chromosomes, Fungal/metabolism/*ultrastructure ; DNA-Binding Proteins/metabolism ; Fungal Proteins/genetics/*metabolism ; *Genes, Fungal ; *Genes, Mating Type, Fungal ; Molecular Sequence Data ; Mutation ; Plasmids ; Poly A/metabolism ; Poly C/metabolism ; Repetitive Sequences, Nucleic Acid ; Saccharomyces cerevisiae/*genetics ; Temperature ; *Transcription Factors ; Transformation, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 9
    facet.materialart.
    Unknown
    Translation initiation and ribosomal biogenesis: involvement of a putative rRNA helicase and RPL46 (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-03-02
    Description: Cold-sensitive mutations in the SPB genes (spb1-spb7) of Saccharomyces cerevisiae suppress the inhibition of translation initiation resulting from deletion of the poly(A)-binding protein gene (PAB1). The SPB4 protein belongs to a family of adenosine triphosphate (ATP)-dependent RNA helicases. The aberrant production of 25S ribosomal RNA (rRNA) occurring in spb4-1 mutants or the deletion of SPB2 (RPL46) permits the deletion of PAB1. These data suggest that mutations affecting different steps of 60S subunit formation can allow PAB-independent translation, and they indicate that further characterization of the spb mutations could lend insight into the biogenesis of the ribosome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sachs, A B -- Davis, R W -- R37 GM 21891/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Mar 2;247(4946):1077-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Stanford Medical Center, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2408148" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Carrier Proteins/genetics/metabolism ; DEAD-box RNA Helicases ; Molecular Sequence Data ; Mutation ; Poly(A)-Binding Proteins ; *Protein Biosynthesis ; RNA Nucleotidyltransferases/genetics/*metabolism ; RNA Processing, Post-Transcriptional ; RNA, Fungal/genetics/metabolism ; RNA, Ribosomal/genetics/*metabolism ; Ribosomal Proteins/genetics/*metabolism ; Ribosomes/*metabolism ; Saccharomyces cerevisiae/enzymology/*genetics ; *Saccharomyces cerevisiae Proteins ; Sequence Homology, Nucleic Acid
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 10
    facet.materialart.
    Unknown
    T cells responsive to myelin basic protein in patients with multiple sclerosis (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-09
    Description: Gene mutation in vivo in human T lymphocytes appears to occur preferentially in dividing cells. Individuals with multiple sclerosis (MS) are assumed to have one or more populations of diving T cells that are being stimulated by autoantigens. Mutant T cell clones from MS patients were isolated and tested for reactivity to myelin basic protein, an antigen that is thought to participate in the induction of the disease. The hypoxanthine guanine phosphoribosyltransferase (hprt) clonal assay was used to determine mutant frequency values in MS patients with chronic progressive disease. Eleven of 258 thioguanine-resistant (hprt-) T cell clones from five of the six MS patients who were tested proliferated in response to human myelin basic protein without prior in vitro exposure to this antigen. No wild-type clones from these patients, nor any hprt- or wild-type clones from three healthy individuals responded to myelin basic protein. Thus, T cell clones that react with myelin basic protein can be isolated from the peripheral blood of MS patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allegretta, M -- Nicklas, J A -- Sriram, S -- Albertini, R J -- CA30688-07/CA/NCI NIH HHS/ -- NS00849/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 9;247(4943):718-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genetics Laboratory, University of Vermont, Burlington 05401.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1689076" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Autoantigens/immunology ; Cell Division ; Clone Cells/immunology ; Female ; Humans ; Hypoxanthine Phosphoribosyltransferase/genetics ; Male ; Middle Aged ; Multiple Sclerosis/genetics/*immunology ; Mutation ; Myelin Basic Protein/*immunology ; T-Lymphocytes/drug effects/*immunology ; Thioguanine/pharmacology ; X Chromosome
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 11
    facet.materialart.
    Unknown
    A mouse model of the aniridia-Wilms tumor deletion syndrome (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-09
    Description: Deletion of chromosome 11p13 in humans produces the WAGR syndrome, consisting of aniridia (an absence or malformation of the iris), Wilms tumor (nephroblastoma), genitourinary malformations, and mental retardation. An interspecies backcross between Mus musculus/domesticus and Mus spretus was made in order to map the homologous chromosomal region in the mouse genome and to define an animal model of this syndrome. Nine evolutionarily conserved DNA clones from proximal human 11p were localized on mouse chromosome 2 near Small-eyes (Sey), a semidominant mutation that is phenotypically similar to aniridia. Analysis of Dickie's Small-eye (SeyDey), a poorly viable allele that has pleiotropic effects, revealed the deletion of three clones, f3, f8, and k13, which encompass the aniridia (AN2) and Wilms tumor susceptibility genes in man. Unlike their human counterparts, SeyDey/+ mice do not develop nephroblastomas. These findings suggest that the Small-eye defect is genetically equivalent to human aniridia, but that loss of the murine homolog of the Wilms tumor gene is not sufficient for tumor initiation. A comparison among Sey alleles suggests that the AN2 gene product is required for induction of the lens and nasal placodes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Glaser, T -- Lane, J -- Housman, D -- 2 T32 GMO7753-11/GM/NIGMS NIH HHS/ -- GM27882/GM/NIGMS NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 9;250(4982):823-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cancer Research, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2173141" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aniridia/*genetics ; Blotting, Southern ; Chromosome Deletion ; Chromosome Mapping ; DNA/analysis ; *Disease Models, Animal ; Eye/embryology/pathology ; Female ; Genes, Wilms Tumor/*genetics ; Genetic Markers ; Kidney Neoplasms/*genetics ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Muridae ; Mutation ; Phenotype ; Polymorphism, Genetic ; Syndrome ; Wilms Tumor/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 12
    facet.materialart.
    Unknown
    HSP104 required for induced thermotolerance (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-01
    Description: A heat shock protein gene, HSP104, was isolated from Saccharomyces cerevisiae and a deletion mutation was introduced into yeast cells. Mutant cells grew at the same rate as wild-type cells and died at the same rate when exposed directly to high temperatures. However, when given a mild pre-heat treatment, the mutant cells did not acquire tolerance to heat, as did wild-type cells. Transformation with the wild-type gene rescued the defect of mutant cells. The results demonstrate that a particular heat shock protein plays a critical role in cell survival at extreme temperatures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanchez, Y -- Lindquist, S L -- GM 35483/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 1;248(4959):1112-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular Genetics and Cell Biology, University of Chicago, Illinois 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2188365" target="_blank"〉PubMed〈/a〉
    Keywords: Cloning, Molecular ; Fungal Proteins/biosynthesis/*genetics ; Genes, Fungal ; Heat-Shock Proteins/biosynthesis/genetics/*physiology ; *Hot Temperature ; Mutation ; Restriction Mapping ; Saccharomyces cerevisiae/genetics/growth & development/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 13
    facet.materialart.
    Unknown
    Transmembrane protein structure: spin labeling of bacteriorhodopsin mutants (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-01
    Description: Transmembrane proteins serve important biological functions, yet precise information on their secondary and tertiary structure is very limited. The boundaries and structures of membrane-embedded domains in integral membrane proteins can be determined by a method based on a combination of site-specific mutagenesis and nitroxide spin labeling. The application to one polypeptide segment in bacteriorhodopsin, a transmembrane chromoprotein that functions as a light-driven proton pump is described. Single cysteine residues were introduced at 18 consecutive positions (residues 125 to 142). Each mutant was reacted with a specific spin label and reconstituted into vesicles that were shown to be functional. The relative collision frequency of each spin label with freely diffusing oxygen and membrane-impermeant chromium oxalate was estimated with power saturation EPR (electron paramagnetic resonance) spectroscopy. The results indicate that residues 129 to 131 form a short water-exposed loop, while residues 132 to 142 are membrane-embedded. The oxygen accessibility for positions 131 to 138 varies with a periodicity of 3.6 residues, thereby providing a striking demonstration of an alpha helix. The orientation of this helical segment with respect to the remainder of the protein was determined.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Altenbach, C -- Marti, T -- Khorana, H G -- Hubbell, W L -- AI 11479/AI/NIAID NIH HHS/ -- EY05216/EY/NEI NIH HHS/ -- GM28289/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 1;248(4959):1088-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Jules Stein Eye Institute, University of California, Los Angeles 90024-7008.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2160734" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Bacteriorhodopsins/genetics ; Cysteine/genetics ; Electron Spin Resonance Spectroscopy ; *Membrane Proteins/genetics ; Molecular Sequence Data ; Mutation ; Oxalates ; Oxalic Acid ; Oxygen ; Protein Conformation ; Spin Labels
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 14
    facet.materialart.
    Unknown
    Paleoanthropology gets physical (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1990 Feb 16;247(4944):798-801.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2369435" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Anthropology ; Carbon Radioisotopes ; DNA, Mitochondrial/genetics ; Hominidae/*genetics ; Humans ; Israel ; Mutation ; *Paleontology ; South Africa
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 15
    facet.materialart.
    Unknown
    Ligand-induced transformation by a noninternalizing epidermal growth factor receptor (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-23
    Description: Identification of a mutant epidermal growth factor (EGF) receptor that does not undergo downregulation has provided a genetic probe to investigate the role of internalization in ligand-induced mitogenesis. Contact-inhibited cells expressing this internalization-defective receptor exhibited a normal mitogenic response at significantly lower ligand concentrations than did cells expressing wild-type receptors. A transformed phenotype and anchorage-independent growth were observed at ligand concentrations that failed to elicit these responses in cells expressing wild-type receptors. These findings imply that activation of the protein tyrosine kinase activity at the cell membrane is sufficient for the growth-enhancing effects of EGF. Thus, downregulation can serve as an attenuation mechanism, without which transformation ensues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wells, A -- Welsh, J B -- Lazar, C S -- Wiley, H S -- Gill, G N -- Rosenfeld, M G -- DDK 13149/DK/NIDDK NIH HHS/ -- DDK 18477/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 23;247(4945):962-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of California-San Diego, La Jolla 92093.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2305263" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Division ; Cell Line ; Down-Regulation ; *Endocytosis ; Enzyme Activation ; Epidermal Growth Factor/pharmacology ; Genetic Vectors ; Moloney murine leukemia virus/genetics ; Mutation ; Phenotype ; Protein-Tyrosine Kinases/metabolism ; Receptor, Epidermal Growth Factor/genetics/*metabolism ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 16
    facet.materialart.
    Unknown
    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
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 17
    facet.materialart.
    Unknown
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 18
    facet.materialart.
    Unknown
    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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 19
    facet.materialart.
    Unknown
    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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 20
    facet.materialart.
    Unknown
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 21
    facet.materialart.
    Unknown
    Actin constitution: guaranteeing the right to assemble (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wertman, K F -- Drubin, D G -- GM42759/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Oct 30;258(5083):759-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1439782" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*chemistry/genetics/metabolism ; Adenosine Diphosphate/metabolism ; Adenosine Triphosphate/metabolism ; Amino Acid Sequence ; Animals ; Binding Sites ; Models, Molecular ; Molecular Structure ; Mutation ; Rabbits ; Tetrahymena/chemistry
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 22
    facet.materialart.
    Unknown
    Emerging viruses, emerging threat (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-01-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Culliton, B J -- New York, N.Y. -- Science. 1990 Jan 19;247(4940):279-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2153314" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/transmission ; Agriculture ; Animals ; Arenaviruses, New World ; Ebolavirus ; Hiv ; Hemorrhagic Fevers, Viral/transmission ; Herpesvirus 6, Human ; Humans ; Influenza A virus/genetics ; Influenza, Human/mortality/transmission ; Mutation ; Virus Diseases/epidemiology/etiology/*transmission ; Viruses/genetics/pathogenicity
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 23
    facet.materialart.
    Unknown
    Transplanted suprachiasmatic nucleus determines circadian period (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-23
    Description: The pacemaker role of the suprachiasmatic nucleus in a mammalian circadian system was tested by neural transplantation by using a mutant strain of hamster that shows a short circadian period. Small neural grafts from the suprachiasmatic region restored circadian rhythms to arrhythmic animals whose own nucleus had been ablated. The restored rhythms always exhibited the period of the donor genotype regardless of the direction of the transplant or genotype of the host. The basic period of the overt circadian rhythm therefore is determined by cells of the suprachiasmatic region.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ralph, M R -- Foster, R G -- Davis, F C -- Menaker, M -- HD13162/HD/NICHD NIH HHS/ -- HD18686/HD/NICHD NIH HHS/ -- MH09483/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 23;247(4945):975-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Virginia, Charlottesville 22903.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2305266" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Circadian Rhythm/genetics/*physiology ; Cricetinae ; Immunohistochemistry ; Male ; Mutation ; Nerve Tissue/*transplantation ; Neuropeptide Y/analysis ; Suprachiasmatic Nucleus/embryology/*physiology ; Vasopressins/analysis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 24
    facet.materialart.
    Unknown
    The MerR metalloregulatory protein binds mercuric ion as a tricoordinate, metal-bridged dimer (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-23
    Description: Bacterial MerR proteins are dimeric DNA-binding proteins that mediate the Hg(II)-dependent induction of mercury resistance operons. Site-directed mutagenesis of the Bacillus sp. RC607 MerR protein reveals that three of four Cys residues per monomer are required for Hg(II) binding at the single high-affinity binding site. Inactive mutant homodimers can exchange subunits to form heterodimers active for Hg(II) binding. Studies of a heterodimer retaining only three of eight cysteine residues per dimer reveal that Cys79 in one subunit and Cys114 and Cys123 in the second subunit are necessary and sufficient for high-affinity Hg(II) binding in an asymmetric, subunit bridging coordination complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Helmann, J D -- Ballard, B T -- Walsh, C T -- GM20011/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 23;247(4945):946-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2305262" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Bacillus/*analysis/genetics ; Bacterial Proteins/genetics/*metabolism ; Base Sequence ; Binding Sites ; Cations ; DNA-Binding Proteins/genetics/*metabolism ; Macromolecular Substances ; Mercury/*metabolism ; Molecular Sequence Data ; Mutation ; Structure-Activity Relationship
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 25
    facet.materialart.
    Unknown
    Down to the wire for the NF gene (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, L -- New York, N.Y. -- Science. 1990 Jul 20;249(4966):236-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2115688" target="_blank"〉PubMed〈/a〉
    Keywords: DNA/genetics ; *Genes ; Humans ; Mutation ; Neurofibromatosis 1/*genetics ; Suppression, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 26
    facet.materialart.
    Unknown
    Structural mutations of the T cell receptor zeta chain and its role in T cell activation (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-13
    Description: T cell hybridomas that express zeta zeta, but not zeta eta, dimers in their T cell receptors (TCRs) produce interleukin-2 (IL-2) and undergo an inhibition of spontaneous growth when activated by antigen, antibodies to the receptor, or antibodies to Thy-1. Hybridomas without zeta and eta were reconstituted with mutated zeta chains. Cytoplasmic truncations of up to 40% of the zeta molecule reconstituted normal surface assembly of TCRs, but antigen-induced IL-2 secretion and growth inhibition were lost. In contrast, cross-linking antibodies to the TCR activated these cells. A point mutation conferred the same signaling phenotype as did the truncations and caused defective antigen-induced tyrosine kinase activation. Thus zeta allows the binding of antigen/major histocompatibility complex (MHC) to alpha beta to effect TCR signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frank, S J -- Niklinska, B B -- Orloff, D G -- Mercep, M -- Ashwell, J D -- Klausner, R D -- New York, N.Y. -- Science. 1990 Jul 13;249(4965):174-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2371564" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cross-Linking Reagents ; Dose-Response Relationship, Immunologic ; Hybridomas ; Immunity, Cellular ; Immunoblotting ; Interleukin-2/*biosynthesis ; Ligands ; *Lymphocyte Activation ; Major Histocompatibility Complex ; Mice ; Molecular Sequence Data ; Mutation ; Peptide Fragments/genetics/*immunology ; Precipitin Tests ; Receptors, Antigen, T-Cell/genetics/*immunology ; Signal Transduction ; T-Lymphocytes/*immunology ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 27
    facet.materialart.
    Unknown
    Genetic mechanisms of tumor suppression by the human p53 gene (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-14
    Description: Mutations of the gene encoding p53, a 53-kilodalton cellular protein, are found frequently in human tumor cells, suggesting a crucial role for this gene in human oncogenesis. To model the stepwise mutation or loss of both p53 alleles during tumorigenesis, a human osteosarcoma cell line, Saos-2, was used that completely lacked endogenous p53. Single copies of exogenous p53 genes were then introduced by infecting cells with recombinant retroviruses containing either point-mutated or wild-type versions of the p53 cDNA sequence. Expression of wild-type p53 suppressed the neoplastic phenotype of Saos-2 cells, whereas expression of mutated p53 conferred a limited growth advantage to cells in the absence of wild-type p53. Wild-type p53 was phenotypically dominant to mutated p53 in a two-allele configuration. These results suggest that, as with the retinoblastoma gene, mutation of both alleles of the p53 gene is essential for its role in oncogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, P L -- Chen, Y M -- Bookstein, R -- Lee, W H -- CA51495/CA/NCI NIH HHS/ -- EY00278/EY/NEI NIH HHS/ -- EY05758/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1990 Dec 14;250(4987):1576-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, School of Medicine, University of California, San Diego, La Jolla 92093-0612.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2274789" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Base Sequence ; *Cinnamates ; Cloning, Molecular ; DNA/genetics ; Drug Resistance/genetics ; Genes, p53/*genetics ; Genetic Vectors ; Humans ; Hygromycin B/analogs & derivatives ; Molecular Sequence Data ; Moloney murine leukemia virus/genetics ; Mutation ; Neomycin ; Osteosarcoma/*genetics ; Plasmids ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 28
    facet.materialart.
    Unknown
    Secondary structure is the major determinant for interaction of HIV rev protein with RNA (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-16
    Description: A region in the human immunodeficiency virus (HIV) env message, with the potential to form a complex secondary structure (designated RRE), interacts with the rev protein (Rev). This interaction is believed to mediate export of HIV structural messenger RNAs from the nucleus to the cytoplasm. In this report the regions essential for Rev interaction with the RRE are further characterized and the functional significance of Rev-RRE interaction in vivo is examined. A single hairpin loop structure within the RRE was found to be a primary determinant for Rev binding in vitro and Rev response in vivo. Maintenance of secondary structure, rather than primary nucleotide sequence alone, appeared to be necessary for Rev-RNA interaction, which distinguishes it from the mechanism for cis-acting elements in DNA. Limited changes within the 200 nucleotides, which preserved the proper RRE conformational structure, were well tolerated for Rev binding and function. Thus, variation among the RRE elements present in the diverse HIV isolates would have little, if any, effect on Rev responsiveness.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olsen, H S -- Nelbock, P -- Cochrane, A W -- Rosen, C A -- New York, N.Y. -- Science. 1990 Feb 16;247(4944):845-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Oncology and Virology, 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/2406903" target="_blank"〉PubMed〈/a〉
    Keywords: Base Composition ; Base Sequence ; Chromosome Deletion ; Gene Products, rev/genetics/*metabolism ; Genes, rev ; HIV/*genetics/metabolism ; Molecular Sequence Data ; Mutation ; Nucleic Acid Conformation ; Plasmids ; Protein Conformation ; RNA, Messenger/*genetics/metabolism ; RNA, Viral/genetics/metabolism ; Trans-Activators/*metabolism ; rev Gene Products, Human Immunodeficiency Virus
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 29
    facet.materialart.
    Unknown
    Poliovirus mutants resistant to neutralization with soluble cell receptors (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-14
    Description: Poliovirus mutants resistant to neutralization with soluble cellular receptor were isolated. Replication of soluble receptor-resistant (srr) mutants was blocked by a monoclonal antibody directed against the HeLa cell receptor for poliovirus, indicating that the mutants use this receptor to enter cells. The srr mutants showed reduced binding to HeLa cells and cell membranes. However, the reduced binding phenotype did not have a major impact on viral replication, as judged by plaque size and one-step growth curves. These results suggest that the use of soluble receptors as antiviral agents could lead to the selection of neutralization-resistant mutants that are able to bind cell surface receptors, replicate, and cause disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaplan, G -- Peters, D -- Racaniello, V R -- AI20017/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1990 Dec 14;250(4987):1596-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, College of Physicians and Surgeons of Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2177226" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Antiviral Agents ; Baculoviridae/genetics ; Cell Line ; Cell Membrane/metabolism ; Centrifugation, Density Gradient ; DNA/genetics ; Genetic Vectors ; HeLa Cells ; Humans ; Insects ; Mutation ; Neutralization Tests ; Poliovirus/genetics/*physiology ; Receptors, Virus/genetics/*physiology ; Recombinant Proteins/physiology ; Transfection ; Virus Replication
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 30
    facet.materialart.
    Unknown
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 31
    facet.materialart.
    Unknown
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 32
    facet.materialart.
    Unknown
    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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 33
    facet.materialart.
    Unknown
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 34
    facet.materialart.
    Unknown
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 35
    facet.materialart.
    Unknown
    Genome analysis and the human X chromosome (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-02
    Description: A unified genetic, physical, and functional map of the human X chromosome is being built through a concerted, international effort. About 40 percent of the 160 million base pairs of the X chromosome DNA have been cloned in overlapping, ordered contigs derived from yeast artificial chromosomes. This rapid progress toward a physical map is accelerating the identification of inherited disease genes, 26 of which are already cloned and more than 50 others regionally localized by linkage analysis. This article summarizes the mapping strategies now used and the impact of genome research on the understanding of X chromosome inactivation and X-linked diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mandel, J L -- Monaco, A P -- Nelson, D L -- Schlessinger, D -- Willard, H -- New York, N.Y. -- Science. 1992 Oct 2;258(5079):103-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Genetique Moleculaire des Eucaryotes du CNRS, INSERM, Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1439756" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chromosome Mapping ; Dosage Compensation, Genetic ; Female ; *Genome, Human ; Humans ; Macropodidae ; Male ; Mice ; Mutation ; Sex Chromosome Aberrations ; *X Chromosome
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 36
    facet.materialart.
    Unknown
    Human growth hormone and extracellular domain of its receptor: crystal structure of the complex (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-17
    Description: Binding of human growth hormone (hGH) to its receptor is required for regulation of normal human growth and development. Examination of the 2.8 angstrom crystal structure of the complex between the hormone and the extracellular domain of its receptor (hGHbp) showed that the complex consists of one molecule of growth hormone per two molecules of receptor. The hormone is a four-helix bundle with an unusual topology. The binding protein contains two distinct domains, similar in some respects to immunoglobulin domains. The relative orientation of these domains differs from that found between constant and variable domains in immunoglobulin Fab fragments. Both hGHbp domains contribute residues that participate in hGH binding. In the complex both receptors donate essentially the same residues to interact with the hormone, even though the two binding sites on hGH have no structural similarity. Generally, the hormone-receptor interfaces match those identified by previous mutational analyses. In addition to the hormone-receptor interfaces, there is also a substantial contact surface between the carboxyl-terminal domains of the receptors. The relative extents of the contact areas support a sequential mechanism for dimerization that may be crucial for signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Vos, A M -- Ultsch, M -- Kossiakoff, A A -- New York, N.Y. -- Science. 1992 Jan 17;255(5042):306-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Protein Engineering, Genentech, Inc., South San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1549776" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Crystallography ; Growth Hormone/*chemistry/metabolism ; Humans ; Hydrogen Bonding ; Models, Molecular ; Molecular Structure ; Mutation ; Receptors, Somatotropin/*chemistry/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 37
    facet.materialart.
    Unknown
    Comparative genomic hybridization for molecular cytogenetic analysis of solid tumors (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-30
    Description: Comparative genomic hybridization produces a map of DNA sequence copy number as a function of chromosomal location throughout the entire genome. Differentially labeled test DNA and normal reference DNA are hybridized simultaneously to normal chromosome spreads. The hybridization is detected with two different fluorochromes. Regions of gain or loss of DNA sequences, such as deletions, duplications, or amplifications, are seen as changes in the ratio of the intensities of the two fluorochromes along the target chromosomes. Analysis of tumor cell lines and primary bladder tumors identified 16 different regions of amplification, many in loci not previously known to be amplified.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kallioniemi, A -- Kallioniemi, O P -- Sudar, D -- Rutovitz, D -- Gray, J W -- Waldman, F -- Pinkel, D -- CA 44768/CA/NCI NIH HHS/ -- CA 45919/CA/NCI NIH HHS/ -- CA 47537/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 Oct 30;258(5083):818-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Laboratory Medicine, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1359641" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosome Mapping ; DNA Probes ; DNA, Neoplasm/*genetics ; Female ; Fluorescein-5-isothiocyanate ; Fluorescent Dyes ; Gene Amplification ; Gene Deletion ; Humans ; In Situ Hybridization, Fluorescence ; Male ; Mutation ; Neoplasms/*genetics ; *Nucleic Acid Hybridization ; Oncogenes ; Polymorphism, Restriction Fragment Length ; Rhodamines ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 38
    facet.materialart.
    Unknown
    Mechanism of DNA strand transfer reactions catalyzed by HIV-1 reverse transcriptase (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-13
    Description: Two DNA strand transfer reactions occur during retroviral reverse transcription. The mechanism of the first, minus strand strong-stop DNA, transfer has been studied in vitro with human immunodeficiency virus 1 reverse transcriptase (HIV-1 RT) and a model template-primer system derived from the HIV-1 genome. The results reveal that HIV-1 RT alone can catalyze DNA strand transfer reactions. Two kinetically distinct ribonuclease (RNase) H activities associated with HIV-1 RT are required for removal of RNA fragments annealed to the nascent DNA strand. Examination of the binding of DNA.RNA duplex and single-stranded RNA to HIV-1 RT during strand transfer supports a model where the enzyme accommodates both the acceptor RNA template and the nascent DNA strand before the transfer event is completed. The polymerase activity incorporated additional bases beyond the 5' end of the RNA template, resulting in a base misincorporation upon DNA strand transfer. Such a process occurring in vivo during retroviral homologous recombination could contribute to the hypermutability of the HIV-1 genome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peliska, J A -- Benkovic, S J -- AI08275/AI/NIAID NIH HHS/ -- GM13306/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Nov 13;258(5085):1112-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Pennsylvania State University, University Park 16802.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1279806" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Catalysis ; DNA, Viral/biosynthesis/chemistry/*metabolism ; Deoxyribonucleotides ; HIV Reverse Transcriptase ; HIV-1/*enzymology/genetics ; Kinetics ; Molecular Sequence Data ; Mutation ; Nucleic Acid Hybridization ; RNA, Transfer/metabolism ; RNA, Viral/chemistry/metabolism ; RNA-Directed DNA Polymerase/genetics/*metabolism ; Ribonuclease H/metabolism ; Templates, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 39
    facet.materialart.
    Unknown
    A surface protease and the invasive character of plague (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-06
    Description: A 9.5-kilobase plasmid of Yersinia pestis, the causative agent of plague, is required for high virulence when mice are inoculated with the bacterium by subcutaneous injection. Inactivation of the plasmid gene pla, which encodes a surface protease, increased the median lethal dose of the bacteria for mice by a millionfold. Moreover, cloned pla was sufficient to restore segregants lacking the entire pla-bearing plasmid to full virulence. Both pla+ strains injected subcutaneously and pla- mutants injected intravenously reached high titers in liver and spleen of infected mice, whereas pla- mutants injected subcutaneously failed to do so even though they establish a sustained local infection at the injection site. More inflammatory cells accumulated in lesions caused by the pla- mutants than in lesions produced by the pla+ parent. The Pla protease was shown to be a plasminogen activator with unusual kinetic properties. It can also cleave complement C3 at a specific site.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sodeinde, O A -- Subrahmanyam, Y V -- Stark, K -- Quan, T -- Bao, Y -- Goguen, J D -- AI22176/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1992 Nov 6;258(5084):1004-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester 01655.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1439793" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Bacterial Proteins ; Colony Count, Microbial ; Escherichia coli/enzymology ; Fibrinolysin/chemistry/metabolism ; Injections, Intravenous ; Kinetics ; Liver/microbiology ; Mice ; Molecular Sequence Data ; Mutation ; Plague/microbiology ; Plasmids ; Plasminogen Activators/genetics/*physiology ; Recombinant Proteins/metabolism ; Spleen/microbiology ; Tissue Plasminogen Activator/metabolism ; Urokinase-Type Plasminogen Activator/metabolism ; Yersinia pestis/*enzymology/isolation & purification/*pathogenicity
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 40
    facet.materialart.
    Unknown
    Defective epithelial chloride transport in a gene-targeted mouse model of cystic fibrosis (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-21
    Description: The cystic fibrosis transmembrane conductance regulator (CFTR) gene encodes an adenosine 3',5'-monophosphate (cyclic AMP)-activated chloride channel. In cystic fibrosis (CF) patients, loss of CFTR function because of a genetic mutation results in defective cyclic AMP-mediated chloride secretion across epithelia. Because of their potential role as an animal model for CF, mice with targeted disruption of the murine CFTR gene [CFTR(-/-)] were tested for abnormalities in epithelial chloride transport. In both freshly excised tissue from the intestine and in cultured epithelia from the proximal airways, the cyclic AMP-activated chloride secretory response was absent in CFTR(-/-) mice as compared to littermate controls. Thus, disruption of the murine CFTR gene results in the chloride transport abnormalities predicted from studies of human CF epithelia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clarke, L L -- Grubb, B R -- Gabriel, S E -- Smithies, O -- Koller, B H -- Boucher, R C -- GM20069/GM/NIGMS NIH HHS/ -- HL 42384/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1992 Aug 21;257(5073):1125-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of North Carolina, Chapel Hill 27514.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1380724" target="_blank"〉PubMed〈/a〉
    Keywords: Amiloride/pharmacology ; Animals ; Biological Transport ; Cells, Cultured ; Chlorides/*metabolism ; Colforsin/pharmacology ; Cyclic AMP/pharmacology ; Cystic Fibrosis/genetics/*metabolism ; Cystic Fibrosis Transmembrane Conductance Regulator ; *Disease Models, Animal ; Epithelium/metabolism ; Intestines/metabolism ; Membrane Proteins/genetics/*physiology ; Mice ; Mutation ; Nose/metabolism ; Trachea/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 41
    facet.materialart.
    Unknown
    Identification of small clusters of divergent amino acids that mediate the opposing effects of ras and Krev-1 (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-13
    Description: Krev-1 is an anti-oncogene that was originally identified by its ability to induce morphologic reversion of ras-transformed cells that continue to express the ras gene. The Krev-1-encoded protein is structurally related to Ras proteins. The biological activities of a series of ras-Krev-1 chimeras were studied to test the hypothesis that Krev-1 may directly interfere with a ras function. The ras-specific and Krev-1-specific amino acids immediately surrounding residues 32 to 44, which are identical between the two proteins, determined whether the protein induced cellular transformation or suppressed ras transformation. Because this region in Ras proteins has been implicated in effector function, the results suggest that Krev-1 suppresses ras-induced transformation by interfering with interaction of Ras with its effector.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, K -- Noda, M -- Vass, W C -- Papageorge, A G -- Lowy, D R -- New York, N.Y. -- Science. 1990 Jul 13;249(4965):162-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular Oncology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2115210" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acids/*physiology ; Animals ; Cell Transformation, Neoplastic/*genetics ; Chimera ; GTP-Binding Proteins/*genetics ; *Gene Expression Regulation, Neoplastic ; *Genes, ras ; Harvey murine sarcoma virus/genetics ; Molecular Sequence Data ; Mutation ; Restriction Mapping ; *Suppression, Genetic ; rap GTP-Binding Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 42
    facet.materialart.
    Unknown
    A T cell-specific transcriptional enhancer within the human T cell receptor delta locus (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-03-09
    Description: The T cell antigen receptor (TCR) delta gene is located within the TCR alpha locus. A T cell-specific transcriptional enhancer, distinct from the TCR alpha enhancer, has been identified within the J delta 3-C delta intron of the human T cell receptor delta gene. This enhancer activates transcription from the V delta 1 and V delta 3 promoters as well as from heterologous promoters. Enhancer activity has been localized to a 250-bp region that contains multiple binding sites for nuclear proteins. Thus, transcriptional control of the TCR delta and TCR alpha genes is mediated by distinct regulatory elements.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Redondo, J M -- Hata, S -- Brocklehurst, C -- Krangel, M S -- R01-GM41052/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Mar 9;247(4947):1225-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Tumor Virology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2156339" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Binding Sites ; Cell Line ; Chloramphenicol O-Acetyltransferase/genetics ; DNA Restriction Enzymes ; Deoxyribonuclease I ; Enhancer Elements, Genetic/*genetics ; Gene Rearrangement ; Gene Rearrangement, alpha-Chain T-Cell Antigen Receptor ; Humans ; Molecular Sequence Data ; Mutation ; Nuclear Proteins/metabolism ; Plasmids ; Promoter Regions, Genetic/genetics ; Receptors, Antigen, T-Cell/*genetics ; Repetitive Sequences, Nucleic Acid ; *Transcription, Genetic ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 43
    facet.materialart.
    Unknown
    Suppression of tumorigenicity of human prostate carcinoma cells by replacing a mutated RB gene (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-09
    Description: Introduction of a normal retinoblastoma gene (RB) into retinoblastoma cells was previously shown to suppress several aspects of their neoplastic phenotype, including tumorigenicity in nude mice, thereby directly demonstrating a cancer suppression function of RB. To explore the possibility of a similar activity in a common adult tumor, RB expression was examined in three human prostate carcinoma cell lines. One of these, DU145, contained an abnormally small protein translated from an RB messenger RNA transcript that lacked 105 nucleotides encoded by exon 21. To assess the functional consequences of this mutation, normal RB expression was restored in DU145 cells by retrovirus-mediated gene transfer. Cells that maintained stable exogenous RB expression lost their ability to form tumors in nude mice, although their growth rate in culture was apparently unaltered. These results suggest that RB inactivation can play a significant role in the genesis of a common adult neoplasm and that restoration of normal RB-encoded protein in tumors could have clinical utility.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bookstein, R -- Shew, J Y -- Chen, P L -- Scully, P -- Lee, W H -- 5758/PHS HHS/ -- New York, N.Y. -- Science. 1990 Feb 9;247(4943):712-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, School of Medicine, University of California, San Diego, La Jolla 92093.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2300823" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; DNA/genetics ; Gene Amplification ; Gene Expression ; Humans ; Male ; Mice ; Mice, Nude ; Molecular Sequence Data ; Mutation ; Nucleic Acid Hybridization ; Prostatic Neoplasms/*genetics/pathology ; RNA, Messenger/genetics ; Retinoblastoma/*genetics ; *Suppression, Genetic ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 44
    facet.materialart.
    Unknown
    An essential signaling role for the m3G cap in the transport of U1 snRNP to the nucleus (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-17
    Description: The major small nuclear ribonucleoprotein particles (snRNPs) U1, U2, U4 + U6, and U5 have to be transported from the cytoplasm, where they are synthesized, to the nucleus, where they splice pre-messenger RNAs. Since the free core snRNP proteins in the cytoplasm do not enter the nucleus on their own, the nuclear location signal must either reside on the snRNA or be created as a result of snRNA-protein interaction. Here the involvement by the 5'-terminal cap of snRNA molecules in the nucleo-cytoplasmic transport of UsnRNPs has been studied by microinjection of synthetic U1 RNA molecules into frog oocytes; the U1 RNA bore either the normal cap (m3G) or a chemical derivative. Antibodies in the cytoplasm against the m3G cap inhibited the nuclear uptake of U1 snRNP. U1 RNA that was uncapped or contained an unnatural ApppG cap did not enter the nucleus, even though it carried a normal complement of protein molecules. When the ribose ring of the m3G cap was oxidized with periodate, nuclear transport of U1 snRNPs was severely inhibited. Finally, microinjection of m3G cap alone (but not m7G cap) into oocytes severely inhibited the transport of U1 snRNPs to the nucleus. These data suggest that one step in the nuclear uptake of U1 snRNPs involves the m3G cap structure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fischer, U -- Luhrmann, R -- New York, N.Y. -- Science. 1990 Aug 17;249(4970):786-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Molekularbiologie und Tumorforschung, Phillipps-Universitat Marburg, Federal Republic of Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2143847" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport ; Cell Nucleus/*metabolism ; Cytoplasm/metabolism ; Female ; Guanosine/*analogs & derivatives/physiology ; Kinetics ; Mutation ; Oocytes/*ultrastructure ; RNA Caps/*physiology ; Ribonucleoproteins/genetics/*metabolism ; Ribonucleoproteins, Small Nuclear ; Signal Transduction/*physiology ; Xenopus laevis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 45
    facet.materialart.
    Unknown
    Cystic fibrosis pilot projects go begging (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, L -- New York, N.Y. -- Science. 1990 Nov 23;250(4984):1076-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2251497" target="_blank"〉PubMed〈/a〉
    Keywords: Cystic Fibrosis/*genetics/prevention & control ; Financing, Government ; *Genetic Testing/standards ; Humans ; Mutation ; National Institutes of Health (U.S.) ; Research Support as Topic ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 46
    facet.materialart.
    Unknown
    Phosphorylation of the polymeric immunoglobulin receptor required for its efficient transcytosis (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-05-11
    Description: The endosomal compartment of polarized epithelial cells is a major crossroads for membrane traffic. Proteins entering this compartment from the cell surface are sorted for transport to one of several destinations: recycling to the original cell surface, targeting to lysosomes for degradation, or transcytosis to the opposite surface. The polymeric immunoglobulin receptor (pIgR), which is normally transcytosed from the basolateral to the apical surface, was used as a model to dissect the signals that mediate this sorting event. When exogenous receptor was expressed in Madin-Darby Canine Kidney (MDCK) cells, it was shown that phosphorylation of pIgR at the serine residue at position 664 is required for efficient transcytosis. Replacement of this serine with alanine generated a receptor that is transcytosed only slowly, and appears to be recycled. Conversely, substitution with aspartic acid (which mimics the negative charge of the phosphate group) results in rapid transcytosis. It was concluded that phosphorylation is the signal that directs the pIgR from the endosome into the transcytotic pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Casanova, J E -- Breitfeld, P P -- Ross, S A -- Mostov, K E -- R01-AI-25144/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1990 May 11;248(4956):742-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2110383" target="_blank"〉PubMed〈/a〉
    Keywords: Alanine ; Animals ; Aspartic Acid ; Cell Line ; Cell Membrane/immunology/metabolism ; Endocytosis ; Immunoglobulin A/metabolism ; Kinetics ; Ligands ; Membrane Glycoproteins/metabolism ; Molecular Weight ; Mutation ; Phosphorylation ; Rats ; Receptors, Immunologic ; Secretory Component/genetics/*metabolism ; Serine
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 47
    facet.materialart.
    Unknown
    Regulation of the timing of transposable element excision during maize development (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-22
    Description: The ability of transposable elements (TEs) to insert into or excise out of a genetic locus can be regulated by genetic, environmental, and developmental factors. Tissue- or organ-specific activity of TEs is a frequent and well-characterized example of spatial, developmental regulation. Regulation of the timing of TE activity during ontogeny is less well understood. To analyze timing, TE-induced variegation was quantified in the aleurone of maize kernels, a tissue composed of only a single layer of cells, and sector sizes were assigned to specific cell divisions in aleurone development. Three TE families, Mu, Spm, and Ac/Ds, were studied at two genetic loci. It was found that the frequency of transposon excision changes drastically (up to 30-fold increase or equivalent decrease) during the proliferation of the aleurone. Moreover, these changes occur at the same cell divisions in all three TE families. These results suggest that the timing of TE excision during maize development can be controlled by the host.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levy, A A -- Walbot, V -- GM 32422/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 22;248(4962):1534-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Stanford University, CA 94305-5020.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2163107" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Anthocyanins/biosynthesis/genetics ; Cell Division ; DNA Transposable Elements/*genetics ; Mutation ; Zea mays/*genetics/growth & development
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 48
    facet.materialart.
    Unknown
    CF screening delayed for awhile, perhaps forever (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-03-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, L -- New York, N.Y. -- Science. 1990 Mar 16;247(4948):1296-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2315698" target="_blank"〉PubMed〈/a〉
    Keywords: Cystic Fibrosis/*diagnosis/genetics ; Ethics, Medical ; Humans ; Mutation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 49
    facet.materialart.
    Unknown
    Type 1 neurofibromatosis gene: identification of a large transcript disrupted in three NF1 patients (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-13
    Description: Von Recklinghausen neurofibromatosis (NF1) is a common autosomal dominant disorder characterized by abnormalities in multiple tissues derived from the neural crest. No reliable cellular phenotypic marker has been identified, which has hampered direct efforts to identify the gene. The chromosome location of the NF1 gene has been previously mapped genetically to 17q11.2, and data from two NF1 patients with balanced translocations in this region have further narrowed the candidate interval. The use of chromosome jumping and yeast artificial chromosome technology has now led to the identification of a large (approximately 13 kilobases) ubiquitously expressed transcript (denoted NF1LT) from this region that is definitely interrupted by one and most likely by both translocations. Previously identified candidate genes, which failed to show abnormalities in NF1 patients, are apparently located within introns of NF1LT, on the antisense strand. A new mutation patient with NF1 has been identified with a de novo 0.5-kilobase insertion in the NF1LT gene. These observations, together with the high spontaneous mutation rate of NF1 (which is consistent with a large locus), suggest that NF1LT represents the elusive NF1 gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wallace, M R -- Marchuk, D A -- Andersen, L B -- Letcher, R -- Odeh, H M -- Saulino, A M -- Fountain, J W -- Brereton, A -- Nicholson, J -- Mitchell, A L -- NS23410/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jul 13;249(4965):181-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Ann Arbor, MI.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2134734" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Amino Acid Sequence ; Animals ; Base Sequence ; Blotting, Northern ; Blotting, Southern ; Cell Line ; Cloning, Molecular ; DNA, Neoplasm/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Hybrid Cells ; Male ; Mice ; Molecular Sequence Data ; Mutation ; Neurofibromatosis 1/*genetics ; Protein Biosynthesis ; RNA, Neoplasm/*genetics ; Transcription, Genetic ; *Translocation, Genetic ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 50
    facet.materialart.
    Unknown
    The other human genome (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palca, J -- New York, N.Y. -- Science. 1990 Sep 7;249(4973):1104-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2204113" target="_blank"〉PubMed〈/a〉
    Keywords: DNA, Mitochondrial/*genetics ; Genetic Diseases, Inborn/*genetics ; History, 20th Century ; Humans ; Mutation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 51
    facet.materialart.
    Unknown
    Complementation of the mitotic activator, p80cdc25, by a human protein-tyrosine phosphatase (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-14
    Description: The onset of M phase requires the activation of the pp34 protein kinase in all eukaryotes thus far examined. In Schizosaccharomyces pombe, pp34 is phosphorylated on Tyr15, and dephosphorylation of this residue regulates the initiation of mitosis. In this study, it is shown that dephosphorylation of Tyr15 triggered activation of the pp34-cyclin complex from fission yeast, that a human protein-tyrosine phosphatase can catalyze this event both in vitro and in vivo, and that activation of fission yeast pp34 does not require threonine dephosphorylation. The complementary DNA that encoded the tyrosine phosphatase replaced the mitotic activator p80cdc25, closely associating the cdc25(+)-activating pathway with tyrosine dephosphorylation of pp34.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gould, K L -- Moreno, S -- Tonks, N K -- Nurse, P -- New York, N.Y. -- Science. 1990 Dec 14;250(4987):1573-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Oxford, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1703321" target="_blank"〉PubMed〈/a〉
    Keywords: *Cell Cycle Proteins ; Cyclins/metabolism ; Enzyme Activation ; Fungal Proteins/*metabolism ; Humans ; *Mitosis ; Mutation ; Phosphoprotein Phosphatases/genetics/*metabolism ; Phosphorylation ; Phosphotyrosine ; Protein Kinases/*metabolism ; Protein Tyrosine Phosphatases ; Schizosaccharomyces/genetics/*metabolism ; Transformation, Genetic ; Tyrosine/analogs & derivatives/metabolism ; *ras-GRF1
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 52
    facet.materialart.
    Unknown
    Deciphering Alzheimer's disease: the amyloid precursor protein yields new clues (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Selkoe, D J -- New York, N.Y. -- Science. 1990 Jun 1;248(4959):1058-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurologic Diseases, Harvard Medical School, Brigham and Women's Hospital, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2111582" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*metabolism ; Amyloid/genetics/*metabolism/physiology ; Amyloid beta-Protein Precursor ; Animals ; Brain/metabolism ; Humans ; Molecular Structure ; Mutation ; Nerve Tissue Proteins/metabolism ; Protein Precursors/genetics/*metabolism/physiology ; Protein Processing, Post-Translational
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 53
    facet.materialart.
    Unknown
    Association of human papillomavirus types 16 and 18 E6 proteins with p53 (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-04-06
    Description: Human papillomavirus type 16 (HPV-16) is a DNA tumor virus that is associated with human anogenital cancers and encodes two transforming proteins, E6 and E7. The E7 protein has been shown to bind to the retinoblastoma tumor suppressor gene product, pRB. This study shows that the E6 protein of HPV-16 is capable of binding to the cellular p53 protein. The ability of the E6 proteins from different human papillomaviruses to form complexes with p53 was assayed and found to correlate with the in vivo clinical behavior and the in vitro transforming activity of these different papillomaviruses. The wild-type p53 protein has tumor suppressor properties and has also been found in association with large T antigen and the E1B 55-kilodalton protein in cells transformed by SV40 and by adenovirus type 5, respectively, providing further evidence that the human papillomaviruses, the adenoviruses, and SV40 may effect similar cellular pathways in transformation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Werness, B A -- Levine, A J -- Howley, P M -- New York, N.Y. -- Science. 1990 Apr 6;248(4951):76-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Tumor Virus Biology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2157286" target="_blank"〉PubMed〈/a〉
    Keywords: Adenovirus Early Proteins ; Amino Acid Sequence ; Antigens, Polyomavirus Transforming/metabolism ; Base Sequence ; Cell Transformation, Neoplastic ; Cell Transformation, Viral ; Cloning, Molecular ; *DNA-Binding Proteins ; Humans ; Immunosorbent Techniques ; Molecular Sequence Data ; Mutation ; Oncogene Proteins/genetics/*metabolism ; Oncogene Proteins, Viral/genetics/*metabolism ; Papillomaviridae/*analysis ; Phosphoproteins/genetics/*metabolism ; Polymerase Chain Reaction ; Protein Binding ; Simian virus 40/immunology ; Tumor Suppressor Protein p53
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 54
    facet.materialart.
    Unknown
    Human brain disease recreated in mice (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1990 Dec 14;250(4987):1509-10.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2274781" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Diseases/*genetics/microbiology ; Creutzfeldt-Jakob Syndrome/*genetics/microbiology ; Gerstmann-Straussler-Scheinker Disease/*genetics/*microbiology ; Humans ; Mice ; Mice, Transgenic ; Mutation ; Prions/*genetics ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 55
    facet.materialart.
    Unknown
    Alzheimer's pathology explored (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1990 Aug 31;249(4972):984-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2118681" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/metabolism/*pathology ; Amyloid/metabolism ; Amyloid beta-Protein Precursor ; Animals ; Disease Models, Animal ; Humans ; Mutation ; Nematoda/genetics ; Protease Inhibitors/metabolism ; Protein Precursors/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 56
    facet.materialart.
    Unknown
    Altered synaptic plasticity in Drosophila memory mutants with a defective cyclic AMP cascade (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 57
    facet.materialart.
    Unknown
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 58
    facet.materialart.
    Unknown
    Antigenic diversity thresholds and the development of AIDS (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 59
    facet.materialart.
    Unknown
    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
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 60
    facet.materialart.
    Unknown
    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
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 61
    facet.materialart.
    Unknown
    Transactivation by AP-1 is a molecular target of T cell clonal anergy (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-21
    Description: Anergy is a mechanism of T lymphocyte tolerance induced by antigen receptor stimulation in the absence of co-stimulation. Anergic T cells were shown to have a defect in antigen-induced transcription of the interleukin-2 gene. Analysis of the promoter indicated that the transcription factor AP-1 and its corresponding cis element were specifically down-regulated. Exposure of anergic T cells to interleukin-2 restored both antigen responsiveness and activity of the AP-1 element.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, S M -- Beverly, B -- Tran, A C -- Brorson, K -- Schwartz, R H -- Lenardo, M J -- New York, N.Y. -- Science. 1992 Aug 21;257(5073):1134-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1509265" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; Antigens/*immunology ; Base Sequence ; Binding Sites ; Blotting, Northern ; Cell Line ; Concanavalin A/pharmacology ; *Gene Expression Regulation ; *Immune Tolerance ; Interleukin-2/*genetics/pharmacology ; Mice ; Molecular Sequence Data ; Mutation ; Promoter Regions, Genetic/genetics ; Proto-Oncogene Proteins c-jun/*physiology ; RNA, Messenger/metabolism ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/*immunology ; Transcription, Genetic ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 62
    facet.materialart.
    Unknown
    Molecular code for cooperativity in hemoglobin (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-03
    Description: Although tetrameric hemoglobin has been studied extensively as a prototype for understanding mechanisms of allosteric regulation, the functional and structural properties of its eight intermediate ligation forms have remained elusive. Recent experiments on the energetics of cooperativity of these intermediates, along with assignments of their quaternary structures, have revealed that the allosteric mechanism is controlled by a previously unrecognized symmetry feature: quaternary switching from form T to form R occurs whenever heme-site binding creates a tetramer with at least one ligated subunit on each dimeric half-molecule. This "symmetry rule" translates the configurational isomers of heme-site ligation into six observed switchpoints of quaternary transition. Cooperativity arises from both "concerted" quaternary switching and "sequential" modulation of binding within each quaternary form, T and R. Binding affinity is regulated through a hierarchical code of tertiary-quaternary coupling that includes the classical allosteric models as limiting cases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ackers, G K -- Doyle, M L -- Myers, D -- Daugherty, M A -- P01-HL40453/HL/NHLBI NIH HHS/ -- R37-GM24486/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Jan 3;255(5040):54-63.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1553532" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Regulation ; Calorimetry ; Circular Dichroism ; Hemoglobins/*chemistry/genetics/metabolism ; Kinetics ; Ligands ; Macromolecular Substances ; Models, Molecular ; Mutation ; Oxyhemoglobins/chemistry/metabolism ; Protein Conformation ; Thermodynamics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 63
    facet.materialart.
    Unknown
    Functional complementation of yeast ste6 by a mammalian multidrug resistance mdr gene (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-04-10
    Description: Multidrug resistance in mammalian tumor cells is associated with the overexpression of mdr genes encoding P-glycoproteins, which function as drug efflux pumps. A yeast homolog of mdr, STE6, mediates export of a-factor mating peptide. Yeast MATa cells carrying a ste6 deletion produce no extracellular a-factor and therefore are defective in mating. Expression of a complementary DNA for the mouse mdr3 gene in a yeast ste6 deletion strain restored ability to export a-factor and to mate. A mutation (a serine to phenylalanine substitution at amino acid 939) known to affect the activity of the mdr3 gene product abolished its ability to complement the yeast ste6 deletion. Thus, functions of P-glycoproteins in normal mammalian cells may include the transmembrane export of endogenous peptides.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raymond, M -- Gros, P -- Whiteway, M -- Thomas, D Y -- New York, N.Y. -- Science. 1992 Apr 10;256(5054):232-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Research Council of Canada, Biotechnology Research Institute, Montreal, Quebec.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1348873" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Chromosome Deletion ; Crosses, Genetic ; Drug Resistance/*genetics ; *Genes, Fungal ; Genetic Complementation Test ; Membrane Glycoproteins/*genetics ; Mice ; Mutation ; P-Glycoprotein ; Peptides/*genetics ; Phenylalanine ; Pheromones/genetics ; Plasmids ; Saccharomyces cerevisiae/*genetics ; Serine ; Transformation, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 64
    facet.materialart.
    Unknown
    Nuclear localization of Agrobacterium VirE2 protein in plant cells (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-06-26
    Description: The Agrobacterium single-stranded DNA (ssDNA) intermediate T-strand is likely transferred to the plant cell nucleus as a complex with a single VirD2 molecule at its 5' end and multiple VirE2 molecules along its length. VirD2 contains a nuclear localization signal (NLS); however, because the T-strand is principally coated with VirE2 molecules, VirE2 also might assist in nuclear uptake. Indeed, VirE2 fused to a reporter protein localizes to plant cell nuclei, a process mediated by two amino acid sequences with homology to the bipartite NLS of Xenopus nucleoplasmin. Moreover, tumorigenicity of an avirulent virE2 mutant is restored when inoculated on transgenic plants expressing VirE2, supporting in planta function of VirE2.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Citovsky, V -- Zupan, J -- Warnick, D -- Zambryski, P -- GM-45244-01/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Jun 26;256(5065):1802-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1615325" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Bacterial Proteins/genetics/*pharmacokinetics ; Biological Transport/physiology ; Cell Nucleus/*microbiology ; DNA Probes ; DNA, Single-Stranded/metabolism ; *DNA-Binding Proteins ; *Ion Channels ; Molecular Sequence Data ; Mutation ; Nuclear Localization Signals ; Nuclear Proteins/physiology ; Plants/*microbiology ; Rhizobium/*pathogenicity ; Sequence Homology, Nucleic Acid
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 65
    facet.materialart.
    Unknown
    HLA-A2.1-associated peptides from a mutant cell line: a second pathway of antigen presentation (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-03-06
    Description: Peptides extracted from HLA-A2.1 class I major histocompatibility complex (MHC) molecules expressed on the antigen processing mutant CEMx721.174.T2 were characterized by electrospray ionization-tandem mass spectrometry. Only seven dominant peptides were found, in contrast to over 200 associated with HLA-A2.1 on normal cells. These peptides were derived from the signal peptide domains of normal cellular proteins, were usually larger than nine residues, and were also associated with HLA-A2.1 in normal cells. These results suggest that proteolysis of signal peptide domains in the endoplasmic reticulum is a second mechanism for processing and presentation of peptides for association with class I molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Henderson, R A -- Michel, H -- Sakaguchi, K -- Shabanowitz, J -- Appella, E -- Hunt, D F -- Engelhard, V H -- AI20963/AI/NIAID NIH HHS/ -- GM37537/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Mar 6;255(5049):1264-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of Virginia School of Medicine, Charlottesville 22908.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1546329" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antigen-Presenting Cells/*immunology ; Antigens/chemistry/immunology/*metabolism ; Cell Line ; Chromatography, High Pressure Liquid ; HLA-A2 Antigen/chemistry/*metabolism ; Humans ; Mass Spectrometry ; Molecular Sequence Data ; Mutation ; Peptides/chemistry/immunology/*metabolism ; Protein Sorting Signals/chemistry ; T-Lymphocytes/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 66
    facet.materialart.
    Unknown
    Genetic analysis of histone H4: essential role of lysines subject to reversible acetylation (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-16
    Description: The nucleosome is the fundamental unit of assembly of the chromosome and reversible modifications of the histones have been suggested to be important in many aspects of nucleosome function. The structure-function relations of the amino-terminal domain of yeast histone H4 were examined by the creation of directed point mutations. The four lysines subject to reversible acetylation were essential for histone function as the substitution of arginine or asparagine at these four positions was lethal. No single lysine residue was completely essential since arginine substitutions at each position were viable, although several of these mutants were slower in completing DNA replication. The simultaneous substitution of glutamine for the four lysine residues was viable but conferred several phenotypes including mating sterility, slow progression through the G2/M period of the division cycle, and temperature-sensitive growth, as well as a prolonged period of DNA replication. These results provide genetic proof for the roles of the H4 amino-terminal domain lysines in gene expression, replication, and nuclear division.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Megee, P C -- Morgan, B A -- Mittman, B A -- Smith, M M -- GM28920/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 16;247(4944):841-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, School of Medicine, University of Virginia, Charlottesville 22908.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2106160" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Alleles ; Cell Cycle ; Chromosome Deletion ; Codon/genetics ; Glutamine ; Histones/*genetics/metabolism ; *Lysine ; Mutation ; Plasmids ; Protein Processing, Post-Translational ; Saccharomyces cerevisiae/cytology/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 67
    facet.materialart.
    Unknown
    Engineering human prolactin to bind to the human growth hormone receptor (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-03-23
    Description: A strategy of iterative site-directed mutagenesis and binding analysis was used to incorporate the receptor-binding determinants from human growth hormone (hGH) into the nonbinding homolog, human prolactin (hPRL). The complementary DNA for hPRL was cloned, expressed in Escherichia coli, and mutated to introduce sequentially those substitutions from hGH that were predicted by alanine-scanning mutagenesis and other studies to be most critical for binding to the hGH receptor from human liver. After seven rounds of site-specific mutagenesis, a variant of hPRL was obtained containing eight mutations with an association constant for the hGH receptor that was increased more than 10,000-fold. This hPRL variant binds one-sixth as strongly as wild-type hGH, but shares only 26 percent overall sequence identity with hGH. These studies show the feasibility of recruiting receptor-binding properties from distantly related and functionally divergent hormones and show that a detailed functional database can be used to guide the design of a protein-protein interface in the absence of direct structural information.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cunningham, B C -- Henner, D J -- Wells, J A -- New York, N.Y. -- Science. 1990 Mar 23;247(4949 Pt 1):1461-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Protein Engineering, Genentech, Inc. South San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2321008" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cloning, Molecular ; Growth Hormone/genetics ; Humans ; Molecular Sequence Data ; Mutation ; Plasmids ; Prolactin/genetics/*metabolism ; Protein Conformation ; Receptors, Somatotropin/*metabolism ; Recombinant Proteins/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 68
    facet.materialart.
    Unknown
    Murine developmental control genes (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-27
    Description: Various strategies have been used to isolate genes that participate in the regulation of mouse development. Gene families that have been identified on the basis of their homology to motifs within Drosophila control genes or human transcription factor genes, namely homeobox (Hox), paired-box (Pax), and POU genes, can be compared with respect to gene organization, structure, and expression patterns. The functions of these genes can be analyzed molecularly in vitro and in vivo with the use of available mouse mutants or transgenic mice. In addition, it has been possible to generate gain- or loss-of-function mutations by random or targeted introduction of transgenes. Models derived from these studies can reveal the successive steps of developmental control on a genetic level.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kessel, M -- Gruss, P -- New York, N.Y. -- Science. 1990 Jul 27;249(4967):374-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck-Institute of Biophysical Chemistry, Department of Molecular Cell Biology, Gottingen, FRG.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1974085" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drosophila/genetics ; *Embryonic and Fetal Development ; Gene Expression ; *Genes ; Genes, Homeobox ; Mice ; Mice, Transgenic ; Mutation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 69
    facet.materialart.
    Unknown
    Mini-mouse: disruption of the pygmy locus in a transgenic insertional mutant (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-23
    Description: A founder transgenic mouse harbored two different integration patterns of a transgene at the same locus, each of which gave rise to a similar autosomal recessive mutation. Mice of the mutant phenotype were of small stature but had normal levels of growth hormone. The disrupted locus was cloned, and a genetic and molecular analysis showed that the insertional mutants were allelic to a spontaneous mutant, pygmy. The mice should be a useful model for the growth hormone-resistant human dwarf syndromes and could lead to a greater understanding of the pathways involved in growth and development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xiang, X -- Benson, K F -- Chada, K -- GM38731/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 23;247(4945):967-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, Piscataway 08854.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2305264" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; DNA/genetics ; Disease Models, Animal ; Dwarfism/*genetics ; Female ; Growth Hormone/blood ; Male ; Mice ; Mice, Mutant Strains ; Mice, Transgenic ; Mutation ; Nucleic Acid Hybridization ; Pedigree ; Restriction Mapping
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 70
    facet.materialart.
    Unknown
    A 49-kilodalton phosphoprotein in the Drosophila photoreceptor is an arrestin homolog (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-04-27
    Description: The gene encoding the 49-kilodalton protein that undergoes light-induced phosphorylation in the Drosophila photoreceptor has been isolated and characterized. The encoded protein has 401 amino acid residues and a molecular mass of 44,972 daltons, and it shares approximately 42 percent amino acid sequence identity with arrestin (S-antigen), which has been proposed to quench the light-induced cascade of guanosine 3',5'-monophosphate hydrolysis in vertebrate photoreceptors. Unlike the 49-kilodalton protein, however, arrestin, which appears to bind to phosphorylated rhodopsin, has not itself been reported to undergo phosphorylation. In vitro, Ca2+ was the only agent found that would stimulate the phosphorylation of the 49-kilodalton protein. The phosphorylation of this arrestin-like protein in vivo may therefore be triggered by a Ca2+ signal that is likely to be regulated by light-activated phosphoinositide-specific phospholipase C.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamada, T -- Takeuchi, Y -- Komori, N -- Kobayashi, H -- Sakai, Y -- Hotta, Y -- Matsumoto, H -- EY06595/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1990 Apr 27;248(4954):483-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City 73190.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2158671" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Antigens ; Arrestin ; Binding Sites ; Calcium/pharmacology ; Cloning, Molecular ; Cyclic GMP/metabolism ; DNA/genetics ; Drosophila melanogaster/*genetics ; Enzyme Activation/drug effects ; *Eye Proteins ; Isoelectric Point ; Molecular Sequence Data ; Molecular Weight ; Mutation ; Phosphatidylinositol Diacylglycerol-Lyase ; *Phosphoproteins/genetics/metabolism ; Phosphoric Diester Hydrolases/metabolism ; Phosphorylation ; Photoreceptor Cells/*analysis ; Protein Biosynthesis ; Restriction Mapping ; Sequence Homology, Nucleic Acid
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 71
    facet.materialart.
    Unknown
    Electrostatic and steric contributions to regulation at the active site of isocitrate dehydrogenase (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-31
    Description: The isocitrate dehydrogenase of Escherichia coli is regulated by covalent modification at the active site rather than, as expected, at an allosteric site. As a means of evaluating the mechanism of regulation, the kinetics of the substrate, 2R,3S-isocitrate, and a substrate analog, 2R-malate, were compared for the native, phosphorylated, and mutant enzymes. Phosphorylation decreases activity by more than a factor of 10(6) for the true substrate, but causes minor changes in the activity of the substrate analog. The kinetic results indicate that electrostatic repulsion and steric hindrance between the phosphoryl moiety and the gamma carboxyl group of 2R,3S-isocitrate are the major causes of the inactivation, with a lesser contribution from the loss of a hydrogen bond.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dean, A M -- Koshland, D E Jr -- New York, N.Y. -- Science. 1990 Aug 31;249(4972):1044-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2204110" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Site ; Amino Acid Sequence ; Binding Sites ; Escherichia coli/*enzymology/genetics ; Isocitrate Dehydrogenase/genetics/*metabolism ; Models, Molecular ; Mutation ; Protein Conformation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 72
    facet.materialart.
    Unknown
    An E. coli ribonucleoprotein containing 4.5S RNA resembles mammalian signal recognition particle (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-23
    Description: The signal recognition particle (SRP) plays a central role in directing the export of nascent proteins from the cytoplasm of mammalian cells. An SRP-dependent translocation machinery in bacteria has not been demonstrated in previous genetic and biochemical studies. Sequence comparisons, however, have identified (i) a gene in Escherichia coli (ffh) whose product is homologous to the 54-kilodalton subunit (SRP54) of SRP, and (ii) an RNA encoded by the ffs gene (4.5S RNA) that shares a conserved domain with the 7SL RNA of SRP. An antiserum to Ffh precipitated 4.5S RNA from E. coli extracts, implying that the two molecules reside in a complex. The 4.5S RNA can also bind to SRP54 and can replace 7SL RNA in an enzymatic assay. The product of a dominant mutation in the ffs gene (4.5S RNAdl1) is also coprecipitated by the antiserum to Ffh protein and is lethal when expressed from an inducible promoter. After induction of 4.5S RNAdl1, the earliest observed phenotype was a permanent induction of the heat shock response, suggesting that there was an accumulation of aberrant proteins in the cytoplasm. Late after induction, translocation of beta-lactamase was impaired; this may be an indirect effect of heat shock, however, because translocation of ribose binding protein or of the porin, OmpA, was unaffected. An unusual separation of the inner and outer membranes, suggestive of a defect in cell envelope, was also observed. Protein synthesis did not cease until very late, an indication that 4.5S RNA probably does not have a direct role in this process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Poritz, M A -- Bernstein, H D -- Strub, K -- Zopf, D -- Wilhelm, H -- Walter, P -- New York, N.Y. -- Science. 1990 Nov 23;250(4984):1111-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of California Medical School, San Francisco 94143-0448.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1701272" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/metabolism ; Base Sequence ; Enzyme Activation ; Escherichia coli/*genetics ; GTP Phosphohydrolases/metabolism ; Genes, Bacterial ; Heat-Shock Proteins/biosynthesis ; Hot Temperature ; Immunosorbent Techniques ; Isopropyl Thiogalactoside/pharmacology ; Molecular Sequence Data ; Mutation ; Protein Sorting Signals/metabolism ; RNA, Bacterial/*genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Ribonucleoproteins/*genetics/metabolism ; Sequence Homology, Nucleic Acid ; Signal Recognition Particle
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 73
    facet.materialart.
    Unknown
    MHC-linked protection from diabetes dissociated from clonal deletion of T cells (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-20
    Description: The I-E molecule of the major histocompatibility complex (MHC) can prevent the spontaneous development of diabetes in nonobese diabetic (NOD) mice. The mechanism of this protection has been investigated by breeding wild-type and promoter-mutated E kappa alpha transgenes onto the NOD genetic background. Animals carrying the various mutated transgenes expressed I-E on different subsets of immunocompetent cells, and thus cells important for the I-E protective effect could be identified. Although the wild-type transgene prevented the infiltration of lymphocytes into pancreatic islets, none of the mutants did. However, all of the transgenes could mediate the intrathymic elimination of T cells bearing antigen receptors with variable regions that recognize I-E. Thus, the I-E molecule does not protect NOD mice from diabetes simply by inducing the deletion of self-reactive T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bohme, J -- Schuhbaur, B -- Kanagawa, O -- Benoist, C -- Mathis, D -- New York, N.Y. -- Science. 1990 Jul 20;249(4966):293-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Genetique Moleculaire des Eucaryotes du CNRS, Faculte de Medecine, Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2115690" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Clone Cells ; Crosses, Genetic ; Diabetes Mellitus, Experimental/*immunology/prevention & control ; Genes, MHC Class II ; Histocompatibility Antigens Class II/genetics/*immunology ; Islets of Langerhans/immunology ; *Major Histocompatibility Complex ; Mice ; Mice, Mutant Strains ; Mice, Transgenic ; Mutation ; Promoter Regions, Genetic ; Receptors, Antigen, T-Cell/genetics ; T-Lymphocytes/*immunology ; Thymus Gland/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 74
    facet.materialart.
    Unknown
    Activation of ras oncogenes preceding the onset of neoplasia (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-01
    Description: The identification of ras oncogenes in human and animal cancers including precancerous lesions indicates that these genes participate in the early stages of neoplastic development. Yet, these observations do not define the timing of ras oncogene activation in the multistep process of carcinogenesis. To ascertain the timing of ras oncogene activation, an animal model system was devised that involves the induction of mammary carcinomas in rats exposed at birth to the carcinogen nitrosomethylurea. High-resolution restriction fragment length polymorphism analysis of polymerase chain reaction-amplified ras sequences revealed the presence of both H-ras and K-ras oncogenes in normal mammary glands 2 weeks after carcinogen treatment and at least 2 months before the onset of neoplasia. These ras oncogenes can remain latent within the mammary gland until exposure to estrogens, demonstrating that activation of ras oncogenes can precede the onset of neoplasia and suggesting that normal physiological proliferative processes such as estrogen-induced mammary gland development may lead to neoplasia if the targeted cells harbor latent ras oncogenes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kumar, R -- Sukumar, S -- Barbacid, M -- 1-RO1-CA48943/CA/NCI NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 1;248(4959):1101-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Squibb Institute for Medical Research, Princeton, NJ 08543.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2188364" target="_blank"〉PubMed〈/a〉
    Keywords: Adenofibroma/genetics ; Animals ; Animals, Newborn ; Base Sequence ; Carcinoma/genetics ; Cell Transformation, Neoplastic/*genetics ; Estrogens/physiology ; Female ; Gene Expression Regulation, Neoplastic/*physiology ; Genes, ras/*physiology ; Mammary Glands, Animal/growth & development ; Mammary Neoplasms, Experimental/chemically induced/*genetics ; Methylnitrosourea ; Molecular Sequence Data ; Mutation ; Polymerase Chain Reaction ; Rats ; Rats, Inbred Strains ; Sexual Maturation ; Time Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 75
    facet.materialart.
    Unknown
    Binding of the Wilms' tumor locus zinc finger protein to the EGR-1 consensus sequence (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-30
    Description: The Wilms' tumor locus (WTL) at 11p13 contains a gene that encodes a zinc finger-containing protein that has characteristics of a DNA-binding protein. However, binding of this protein to DNA in a sequence-specific manner has not been demonstrated. A synthetic gene was constructed that contained the zinc finger region, and the protein was expressed in Escherichia coli. The recombinant protein was used to identify a specific DNA binding site from a pool of degenerate oligonucleotides. The binding sites obtained were similar to the sequence recognized by the early growth response-1 (EGR-1) gene product, a zinc finger-containing protein that is induced by mitogenic stimuli. A mutation in the zinc finger region of the protein originally identified in a Wilms' tumor patient abolished its DNA-binding activity. These results suggest that the WTL protein may act at the DNA binding site of a growth factor-inducible gene and that loss of DNA-binding activity contributes to the tumorigenic process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rauscher, F J 3rd -- Morris, J F -- Tournay, O E -- Cook, D M -- Curran, T -- CA0917-15/CA/NCI NIH HHS/ -- CA10817/CA/NCI NIH HHS/ -- CA23413/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 30;250(4985):1259-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wistar Institute, Philadelphia, PA 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2244209" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Binding Sites ; Binding, Competitive ; Chromosomes, Human, Pair 11 ; Consensus Sequence ; DNA/genetics/*metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Early Growth Response Protein 1 ; Escherichia coli/genetics ; *Genes, Wilms Tumor ; Humans ; *Immediate-Early Proteins ; Molecular Sequence Data ; Mutation ; Oligonucleotides/metabolism ; Polymerase Chain Reaction ; Recombinant Proteins/metabolism ; Restriction Mapping ; Transcription Factors/genetics/*metabolism ; *Zinc Fingers/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 76
    facet.materialart.
    Unknown
    Two domains of yeast U6 small nuclear RNA required for both steps of nuclear precursor messenger RNA splicing (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-10-19
    Description: U6 is one of the five small nuclear RNA's (snRNA's) that are required for splicing of nuclear precursor messenger RNA (pre-mRNA). The size and sequence of U6 RNA are conserved among organisms as diverse as yeast and man, and so it has been proposed that U6 RNA functions as a catalytic element in splicing. A procedure for in vitro reconstitution of functional yeast U6 small nuclear ribonucleoproteins (snRNP's) with synthetic U6 RNA was applied in an attempt to elucidate the function of yeast U6 RNA. Two domains in U6 RNA were identified, each of which is required for in vitro splicing. Single nucleotide substitutions in these two domains block splicing either at the first or the second step. Invariably, U6 RNA mutants that block the first step of splicing do not enter the spliceosome. On the other hand, those that block the second step of splicing form a spliceosome but block cleavage at the 3' splice site of the intron. In both domains, the positions of base changes that block the second step of splicing correspond exactly to the site of insertion of pre-mRNA-type introns into the U6 gene of two yeast species, providing a possible explanation for the mechanism of how these introns originated and adding further evidence for the proposed catalytic role of U6 RNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fabrizio, P -- Abelson, J -- GM 32637/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Oct 19;250(4979):404-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉California Institute of Technology, Division of Biology, Pasadena 91125.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2145630" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cell Nucleus/*metabolism ; Introns ; Models, Molecular ; Molecular Sequence Data ; Mutation ; Nucleic Acid Conformation ; RNA Precursors/*genetics ; *RNA Splicing ; RNA, Small Nuclear/*genetics/metabolism ; Ribonucleoproteins/metabolism ; Ribonucleoproteins, Small Nuclear ; Saccharomyces cerevisiae/genetics ; Schizosaccharomyces/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 77
    facet.materialart.
    Unknown
    Organization of the human and mouse low-affinity Fc gamma R genes: duplication and recombination (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-05-11
    Description: Receptors for immunoglobulin G immune complexes (Fc gamma RII and Fc gamma RIII) are expressed on most hematopoietic cells and show much structural and functional diversity. In order to determine the genetic basis for this diversity, a family of genes encoding the human and mouse receptors was isolated and characterized. Humans have five distinct genes for low-affinity Fc gamma Rs, in contrast to two in the mouse. With the use of yeast artificial chromosomes, the genes encoding the human receptors were oriented and linked, which established the structure of this complex locus. Comparison of the human and mouse genes generated a model for the evolutionary amplification of this locus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Qiu, W Q -- de Bruin, D -- Brownstein, B H -- Pearse, R -- Ravetch, J V -- GM 36306/GM/NIGMS NIH HHS/ -- GM 39256/GM/NIGMS NIH HHS/ -- K23 AG022476/AG/NIA NIH HHS/ -- R01 AG031171/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1990 May 11;248(4956):732-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Biology, Sloan-Kettering Institute, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2139735" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Differentiation/*genetics/metabolism ; Base Sequence ; Blotting, Southern ; Exons ; Genome, Human ; Humans ; Immunoglobulin G/metabolism ; Introns ; Mice ; Molecular Sequence Data ; *Multigene Family ; Mutation ; Receptors, Fc/*genetics/metabolism ; Receptors, IgG ; Recombination, Genetic ; Restriction Mapping ; Spleen/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 78
    facet.materialart.
    Unknown
    Partial symmetrization of the photosynthetic reaction center (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-15
    Description: The bacterial photosynthetic reaction center (RC) is a pigmented intrinsic membrane protein that performs the primary charge separation event of photosynthesis, thereby converting light to chemical energy. The RC pigments are bound primarily by two homologous peptides, the L and M subunits, each containing five transmembrane helices. These alpha helices and pigments are arranged in an approximate C2 symmetry and form two possible electron transfer pathways. Only one of these pathways is actually used. In an attempt to identify nonhomologous residues that are responsible for functional differences between the two branches, homologous helical regions that interact extensively with the pigments were genetically symmetrized (that is, exchanged). For example, replacement of the fourth transmembrane helix (D helix) in the M subunit with the homologous helix from the L subunit yields photosynthetically inactive RCs lacking a critical photoactive pigment. Photosynthetic revertants have been isolated in which single amino acid substitutions (intragenic suppressors) compensate for this partial symmetrization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Robles, S J -- Breton, J -- Youvan, D C -- RIGM42645A/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1402-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Program in Applied Biological Sciences, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2192455" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Bacterial Proteins/genetics ; Cloning, Molecular ; Electron Transport ; Macromolecular Substances ; Molecular Sequence Data ; Molecular Structure ; Mutation ; Photosynthesis ; Photosynthetic Reaction Center Complex Proteins ; Protein Conformation ; Rhodopseudomonas/analysis/genetics/growth & development ; Spectrophotometry
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 79
    facet.materialart.
    Unknown
    A new member of the leucine zipper class of proteins that binds to the HLA DR alpha promoter (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-03-30
    Description: Several mutants derived from transformed human B cell lines are defective in expressing major histocompatibility complex (MHC) class II genes. The failure to express a class II gene in at least one such mutant line has been mapped to the MHC class II X box, a conserved transcriptional element in the promoter region. A complementary DNA encoding a DNA-binding protein (human X box binding protein, hXBP-1) whose target is the human DR alpha X box and the 3' flanking region has now been cloned. This complementary DNA encoded a protein with structural similarities to the c-jun proto-oncogene product, and its target sequence was closely related to the palindromic target sequence of c-jun. Mutation of the hXBP-1 DNA target sequence decreased DR alpha promoter activity in vivo. These studies suggest that the hXBP-1 protein acts as a transcription factor in B cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liou, H C -- Boothby, M R -- Finn, P W -- Davidon, R -- Nabavi, N -- Zeleznik-Le, N J -- Ting, J P -- Glimcher, L H -- CA42771-01/CA/NCI NIH HHS/ -- GM36864/GM/NIGMS NIH HHS/ -- R01-CA48185/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Mar 30;247(4950):1581-4.〈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/2321018" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; B-Lymphocytes ; Base Sequence ; Binding Sites ; Cell Line, Transformed ; DNA/*genetics ; DNA-Binding Proteins/*genetics/metabolism ; HLA-DR Antigens/*genetics/metabolism ; Humans ; Leucine ; Molecular Sequence Data ; Mutation ; *Promoter Regions, Genetic ; Transcription Factors/*genetics/metabolism ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 80
    facet.materialart.
    Unknown
    Two gap genes mediate maternal terminal pattern information in Drosophila (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-04-27
    Description: In Drosophila three maternal pattern organizing activities, the anterior, the posterior, and the terminal, establish the anterior-posterior body pattern of the embryo by initiating the spatially restricted activities of the gap class of zygotic segmentation genes. The activities of tailless (tll) and the newly identified gap gene huckebein (hkb) are specifically involved in mediating the maternal terminal information at the posterior end of the blastoderm embryo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weigel, D -- Jurgens, G -- Klingler, M -- Jackle, H -- New York, N.Y. -- Science. 1990 Apr 27;248(4954):495-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Universitat Munchen, Institut fur Genetik und Mikrobiologie, Federal Republic of Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2158673" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastoderm/*physiology ; Cell Differentiation ; Drosophila/embryology/*genetics ; Female ; Gene Expression ; Genes/*physiology ; Genotype ; Mutation ; Phenotype ; Protein-Tyrosine Kinases/genetics ; Receptors, Cell Surface/genetics ; Suppression, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 81
    facet.materialart.
    Unknown
    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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 82
    facet.materialart.
    Unknown
    Recent advances in the polymerase chain reaction (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 83
    facet.materialart.
    Unknown
    Zeroing in on individual cancer risk (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 84
    facet.materialart.
    Unknown
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 85
    facet.materialart.
    Unknown
    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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 86
    facet.materialart.
    Unknown
    Mitochondrial genetics: a paradigm for aging and degenerative diseases? (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-01
    Description: Studies of diseases caused by mitochondrial DNA mutations suggest that a variety of degenerative processes may be associated with defects in oxidative phosphorylation (OXPHOS). Application of this hypothesis has provided new insights into such diverse clinical problems as ischemic heart disease, late-onset diabetes, Parkinson's disease, Alzheimer's disease, and aging.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wallace, D C -- GM46915/GM/NIGMS NIH HHS/ -- HL45572/HL/NHLBI NIH HHS/ -- NS21328/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 May 1;256(5057):628-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Molecular Medicine, Emory University School of Medicine, Atlanta, GA 30322.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1533953" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*genetics ; Alzheimer Disease/genetics ; Base Sequence ; Coronary Disease/genetics ; DNA, Mitochondrial/chemistry/*genetics ; Humans ; Huntington Disease/genetics ; Molecular Sequence Data ; Muscular Diseases/genetics ; Mutation ; Nervous System Diseases/genetics ; *Oxidative Phosphorylation ; Parkinson Disease/genetics ; RNA, Transfer/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 87
    facet.materialart.
    Unknown
    A yeast chromosomal origin of DNA replication defined by multiple functional elements (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-02-14
    Description: Although it has been demonstrated that discrete origins of DNA replication exist in eukaryotic cellular chromosomes, the detailed organization of a eukaryotic cellular origin remains to be determined. Linker substitution mutations were constructed across the entire Saccharomyces cerevisiae chromosomal origin, ARS1. Functional studies of these mutants revealed one essential element (A), which includes a match to the ARS consensus sequence, and three additional elements (B1, B2, and B3), which collectively are also essential for origin function. These four elements arranged exactly as in ARS1, but surrounded by completely unrelated sequence, functioned as an efficient origin. Element B3 is the binding site for the transcription factor-origin binding protein ABF1. Other transcription factor binding sites substitute for the B3 element and a trans-acting transcriptional activation domain is required. The multipartite nature of a chromosomal replication origin and the role of transcriptional activators in its function present a striking similarity to the organization of eukaryotic promoters.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marahrens, Y -- Stillman, B -- AI20460/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1992 Feb 14;255(5046):817-23.〈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/1536007" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Chromosome Mapping ; Chromosomes, Fungal/chemistry ; *DNA Replication ; DNA, Fungal/*physiology ; *DNA-Binding Proteins ; Fungal Proteins/genetics ; Gene Expression Regulation, Fungal ; Genetic Linkage ; Molecular Sequence Data ; Mutation ; Plasmids ; Replicon/physiology ; Saccharomyces cerevisiae/*genetics ; *Saccharomyces cerevisiae Proteins ; Trans-Activators/physiology ; *Transcription Factors ; Transformation, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 88
    facet.materialart.
    Unknown
    Abnormal chromosome behavior in Neurospora mutants defective in DNA methylation (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-10
    Description: The function and regulation of DNA methylation in eukaryotes remain unclear. Genes affecting methylation were identified in the fungus Neurospora crassa. A mutation in one gene, dim-2, resulted in the loss of all detectable DNA methylation. Abnormal segregation of the methylation defects in crosses led to the discovery that the methylation mutants frequently generate strains with extra chromosomes or chromosomal parts. Starvation for S-adenosylmethionine, the presumed methyl group donor for DNA methylation, also produced aneuploidy. These results suggest that DNA methylation plays a role in the normal control of chromosome behavior.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Foss, H M -- Roberts, C J -- Claeys, K M -- Selker, E U -- GM-35690/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Dec 10;262(5140):1737-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Biology, University of Oregon, Eugene 97403.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7505062" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine ; Aneuploidy ; Azacitidine/pharmacology ; Blotting, Southern ; Chromosomes, Fungal/*metabolism ; Crosses, Genetic ; Cytosine/*analogs & derivatives/analysis ; DNA, Fungal/chemistry/*metabolism ; Genes, Fungal ; Genetic Complementation Test ; Methionine/metabolism ; Methylation ; Mutation ; Neurospora crassa/*genetics/growth & development ; Phenotype ; S-Adenosylmethionine/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 89
    facet.materialart.
    Unknown
    Transcription factor TFIIB sites important for interaction with promoter-bound TFIID (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-23
    Description: Transcription initiation factor TFIIB recruits RNA polymerase II to the promoter subsequent to interaction with a preformed TFIID-promoter complex. The domains of TFIIB required for binding to the TFIID-promoter complex and for transcription initiation have been determined. The carboxyl-terminal two-thirds of TFIIB, which contains two direct repeats and two basic residue repeats, is sufficient for interaction with the TFIID-promoter complex. An extra 84-residue amino-terminal region, with no obvious known structural motifs, is required for basal transcription activity. Basic residues within the second basic repeat of TFIIB are necessary for stable interaction with the TFIID-promoter complex, whereas the basic character of the first basic repeat is not. Functional roles of other potential structural motifs are discussed in light of the present study.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamashita, S -- Hisatake, K -- Kokubo, T -- Doi, K -- Roeder, R G -- Horikoshi, M -- Nakatani, Y -- AI27397/AI/NIAID NIH HHS/ -- CA42567/CA/NCI NIH HHS/ -- GM45258/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Jul 23;261(5120):463-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8332911" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; DNA-Binding Proteins/*metabolism ; Drosophila ; Molecular Sequence Data ; Mutation ; *Promoter Regions, Genetic ; Protein Binding ; Transcription Factor TFIIB ; Transcription Factor TFIID ; Transcription Factors/*chemistry/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 90
    facet.materialart.
    Unknown
    Origin recognition complex (ORC) in transcriptional silencing and DNA replication in S. cerevisiae (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-17
    Description: In Saccharomyces cerevisiae, the HMR-E silencer blocks site-specific interactions between proteins and their recognition sequences in the vicinity of the silencer. Silencer function is correlated with the firing of an origin of replication at HMR-E. An essential gene with a role in transcriptional silencing was identified by means of a screen for mutations affecting expression of HMR. This gene, known as ORC2, was shown to encode a component of the origin recognition complex that binds yeast origins of replication. A temperature-sensitive mutation in ORC2 disrupted silencing in cells grown at the permissive temperature. At the restrictive temperature, the orc2-1 mutation caused cell cycle arrest at a point in the cell cycle indicative of blocks in DNA replication. The orc2-1 mutation also resulted in the enhanced mitotic loss of a plasmid, suggestive of a defect in replication. These results provide strong evidence for an in vivo role of ORC in both chromosomal replication and silencing, and provide a link between the mechanism of silencing and DNA replication.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Foss, M -- McNally, F J -- Laurenson, P -- Rine, J -- GM31105/GM/NIGMS NIH HHS/ -- P30ES01896-12/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1993 Dec 17;262(5141):1838-44.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8266071" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Cell Cycle ; Cloning, Molecular ; *DNA Replication ; DNA, Fungal/genetics/metabolism ; *DNA-Binding Proteins ; Fungal Proteins/chemistry/*genetics/metabolism ; *Gene Expression Regulation, Fungal ; *Genes, Fungal ; Molecular Sequence Data ; Mutation ; Origin Recognition Complex ; Phenotype ; Plasmids ; *Replicon ; Repressor Proteins/chemistry/*genetics/metabolism ; Saccharomyces cerevisiae/cytology/*genetics/metabolism ; Saccharomyces cerevisiae Proteins ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 91
    facet.materialart.
    Unknown
    An unstable triplet repeat in a gene related to myotonic muscular dystrophy (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-03-16
    Description: Synthetic oligonucleotides containing GC-rich triplet sequences were used in a scanning strategy to identify unstable genetic sequences at the myotonic dystrophy (DM) locus. A highly polymorphic GCT repeat was identified and found to be unstable, with an increased number of repeats occurring in DM patients. In the case of severe congenital DM, the paternal triplet allele was inherited unaltered while the maternal, DM-associated allele was unstable. These studies suggest that the mutational mechanism leading to DM is triplet amplification, similar to that occurring in the fragile X syndrome. The triplet repeat sequence is within a gene (to be referred to as myotonin-protein kinase), which has a sequence similar to protein kinases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fu, Y H -- Pizzuti, A -- Fenwick, R G Jr -- King, J -- Rajnarayan, S -- Dunne, P W -- Dubel, J -- Nasser, G A -- Ashizawa, T -- de Jong, P -- 5-M01-RR00350/RR/NCRR NIH HHS/ -- P30-HG00210/HG/NHGRI NIH HHS/ -- P50HL42267-01/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1992 Mar 6;255(5049):1256-8.〈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/1546326" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Chromosomes, Human, Pair 19 ; Cloning, Molecular ; DNA/chemistry ; Humans ; Molecular Sequence Data ; Mutation ; Myotonic Dystrophy/*genetics ; Nucleic Acid Hybridization ; Polymerase Chain Reaction ; Polymorphism, Genetic ; *Repetitive Sequences, Nucleic Acid
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 92
    facet.materialart.
    Unknown
    Debate on AIDS origin: Rolling Stone weighs in (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-03-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1992 Mar 20;255(5051):1505.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1549779" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*etiology ; Africa ; Animals ; HIV/genetics ; Haplorhini ; Humans ; Mutation ; Poliovirus Vaccine, Inactivated/*adverse effects ; Simian Immunodeficiency Virus/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 93
    facet.materialart.
    Unknown
    Participation of the intron in the reaction catalyzed by the Xenopus tRNA splicing endonuclease (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-03-13
    Description: Introns have generally been assumed to be passive in the transfer RNA splicing reaction. Experiments have now been done showing that the endonuclease is able to cut a precursor provided that a base in the single-stranded loop of the intron can pair with the base of the 5' exon situated at the position that immediately follows the anticodon stem (position 33 in the yeast tRNA isoacceptor pre-tRNA(Leu)3, position 32 in yeast pre-tRNA(Phe)). The elucidation of the role of the intron reveals that in addition to the conserved bases, there are positions in the mature domain which, although not necessarily occupied by the same base in all pre-tRNA's, nevertheless have a fundamental role in the splicing reaction. These positions are termed cardinal positions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baldi, M I -- Mattoccia, E -- Bufardeci, E -- Fabbri, S -- Tocchini-Valentini, G P -- New York, N.Y. -- Science. 1992 Mar 13;255(5050):1404-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Cell Biology, Consiglio Nazionale delle Ricerche, Roma, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1542788" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Binding Sites ; Endoribonucleases/*metabolism ; Exons/physiology ; Introns/*physiology ; Molecular Sequence Data ; Mutation ; Nucleic Acid Conformation ; RNA Precursors/chemistry/*metabolism ; RNA Splicing/*physiology ; RNA, Transfer/chemistry/*metabolism ; RNA, Transfer, Leu/metabolism ; RNA, Transfer, Phe/metabolism ; Xenopus laevis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 94
    facet.materialart.
    Unknown
    Deletion of the paired alpha 5(IV) and alpha 6(IV) collagen genes in inherited smooth muscle tumors (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-27
    Description: The gene encoding alpha 6(IV) collagen, COL4A6, was identified on the human X chromosome in a head-to-head arrangement and within 452 base pairs of the alpha 5(IV) collagen gene, COL4A5. In earlier studies, intragenic deletions of COL4A5 were detected in a subset of patients with Alport syndrome (AS), a hereditary defect of basement membranes. In some families, AS cosegregates with diffuse leiomyomatosis (DL), a benign smooth muscle tumor diathesis. Here it is shown that patients with AS-DL harbor deletions that disrupt both COL4A5 and COL4A6. Thus, type IV collagen may regulate smooth muscle differentiation and morphogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, J -- Mochizuki, T -- Smeets, H -- Antignac, C -- Laurila, P -- de Paepe, A -- Tryggvason, K -- Reeders, S T -- New York, N.Y. -- Science. 1993 Aug 27;261(5125):1167-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06536-0812.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8356449" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Differentiation ; Collagen/chemistry/*genetics ; Exons ; Female ; Fetus/metabolism ; *Gene Deletion ; Genetic Linkage ; Humans ; Leiomyoma/*genetics ; Male ; Molecular Sequence Data ; Morphogenesis ; Muscle, Smooth/cytology ; Mutation ; Nephritis, Hereditary/*genetics ; RNA, Messenger/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 95
    facet.materialart.
    Unknown
    Elements of the yeast pheromone response pathway required for filamentous growth of diploids (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-10
    Description: Transmission of an external signal from receptors to downstream targets is often mediated by a conserved set of protein kinases that act in sequence (a kinase cascade). In haploid strains of Saccharomyces cerevisiae, a signal initiated by peptide pheromones is transmitted through this kinase cascade to a transcription factor STE12, which is required for the expression of many mating-specific genes. Here it was shown that in diploids some of the same kinases and STE12 are required for filamentous growth, but the pheromone receptors and guanosine triphosphate-binding protein are not required for filament formation. Thus, a similar kinase cascade is activated by different signals in haploids and diploids and mediates different developmental outcomes in the two cell types.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, H -- Styles, C A -- Fink, G R -- GM 35010/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Dec 10;262(5140):1741-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Cambridge 02142.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8259520" target="_blank"〉PubMed〈/a〉
    Keywords: Fungal Proteins/*metabolism ; GTP-Binding Proteins/metabolism ; Genes, Fungal ; Mutation ; Peptides/*metabolism/pharmacology ; Phenotype ; Protein Kinases/*metabolism ; Receptors, Mating Factor ; Receptors, Peptide/metabolism ; Saccharomyces cerevisiae/genetics/*growth & development/metabolism ; *Saccharomyces cerevisiae Proteins ; *Signal Transduction ; Transcription Factors/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 96
    facet.materialart.
    Unknown
    A genetic linkage map of the mouse: current applications and future prospects (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-10-01
    Description: Technological advances have made possible the development of high-resolution genetic linkage maps for the mouse. These maps in turn offer exciting prospects for understanding mammalian genome evolution through comparative mapping, for developing mouse models of human disease, and for identifying the function of all genes in the organism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Copeland, N G -- Jenkins, N A -- Gilbert, D J -- Eppig, J T -- Maltais, L J -- Miller, J C -- Dietrich, W F -- Weaver, A -- Lincoln, S E -- Steen, R G -- HG00198/HG/NHGRI NIH HHS/ -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Oct 1;262(5130):57-66.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ABL-Basic Research Program, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8211130" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; *Chromosome Mapping ; Cloning, Molecular ; Crosses, Genetic ; Female ; Genetic Markers ; *Genome ; Human Genome Project ; Humans ; Male ; Mice/*genetics ; Multigene Family ; Muridae/*genetics ; Mutation ; Neoplasms/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 97
    facet.materialart.
    Unknown
    Uncovering of functional alternative CTLA-4 counter-receptor in B7-deficient mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-11-05
    Description: B7 delivers a costimulatory signal through CD28, resulting in interleukin-2 secretion and T cell proliferation. Blockade of this pathway results in T cell anergy. The in vivo role of B7 was evaluated with B7-deficient mice. These mice had a 70 percent decrease in costimulation of the response to alloantigen. Despite lacking B7 expression, activated B cells from these mice bound CTLA-4 and GL1 monoclonal antibody, demonstrating that alternative CTLA-4 ligand or ligands exist. These receptors are functionally important because the residual allogenic mixed lymphocyte responses were blocked by CTLA4Ig. Characterization of these CTLA-4 ligands should lead to strategies for manipulating the immune response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freeman, G J -- Borriello, F -- Hodes, R J -- Reiser, H -- Hathcock, K S -- Laszlo, G -- McKnight, A J -- Kim, J -- Du, L -- Lombard, D B -- CA 40216/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Nov 5;262(5135):907-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematologic Malignancies, Dana-Farber Cancer Institute, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7694362" target="_blank"〉PubMed〈/a〉
    Keywords: Abatacept ; Animals ; Antigens, CD ; Antigens, CD80/genetics/*immunology/metabolism ; Antigens, Differentiation/immunology/*metabolism ; B-Lymphocytes/*immunology ; Base Sequence ; CTLA-4 Antigen ; Cell Line ; *Immunoconjugates ; Interleukin-2/secretion ; Isoantigens/immunology ; Lymphocyte Activation ; Lymphocyte Culture Test, Mixed ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; Mutation ; T-Lymphocytes/*immunology ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 98
    facet.materialart.
    Unknown
    Isolation of new ribozymes from a large pool of random sequences [see comment] (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-10
    Description: An iterative in vitro selection procedure was used to isolate a new class of catalytic RNAs (ribozymes) from a large pool of random-sequence RNA molecules. These ribozymes ligate two RNA molecules that are aligned on a template by catalyzing the attack of a 3'-hydroxyl on an adjacent 5'-triphosphate--a reaction similar to that employed by the familiar protein enzymes that synthesize RNA. The corresponding uncatalyzed reaction also yields a 3',5'-phosphodiester bond. In vitro evolution of the population of new ribozymes led to improvement of the average ligation activity and the emergence of ribozymes with reaction rates 7 million times faster than the uncatalyzed reaction rate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bartel, D P -- Szostak, J W -- New York, N.Y. -- Science. 1993 Sep 10;261(5127):1411-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Massachusetts General Hospital, Boston 02114.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7690155" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Biological Evolution ; Catalysis ; Kinetics ; Magnesium/metabolism ; Molecular Sequence Data ; Mutation ; Oligoribonucleotides/metabolism ; RNA/*metabolism ; RNA Ligase (ATP)/chemistry/isolation & purification/metabolism ; RNA, Catalytic/chemistry/*isolation & purification/metabolism ; Temperature ; Templates, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 99
    facet.materialart.
    Unknown
    AI helps researchers find meaning in molecules (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-08-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freedman, D -- New York, N.Y. -- Science. 1993 Aug 13;261(5123):844-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8346437" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Artificial Intelligence ; Base Sequence ; Collagen/chemistry/genetics/physiology ; DNA/chemistry/genetics ; Humans ; Molecular Sequence Data ; Mutation ; *Protein Structure, Secondary ; *Protein Structure, Tertiary ; *Sequence Analysis, DNA ; Software
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 100
    facet.materialart.
    Unknown
    A detailed genetic map for the X chromosome of the malaria vector, Anopheles gambiae (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-30
    Description: Anopheles gambiae, the primary vector of human malaria in Africa, is responsible for approximately a million deaths per year, mostly of children. Despite its significance in disease transmission, this mosquito has not been studied extensively by genetic or molecular techniques. To facilitate studies on this vector, a genetic map has been developed that covers the X chromosome at an average resolution of 2 centimorgans. This map has been integrated with the chromosome banding pattern and used to localize a recessive, sex-linked mutation (white eye) to within 1 centimorgan of flanking markers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zheng, L -- Collins, F H -- Kumar, V -- Kafatos, F C -- New York, N.Y. -- Science. 1993 Jul 30;261(5121):605-8.〈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/8342025" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Anopheles/*genetics ; Base Sequence ; Chromosome Banding ; *Chromosome Mapping ; Crosses, Genetic ; DNA, Satellite/genetics ; Female ; *Genes, Insect ; Genes, Recessive ; Genetic Markers ; Insect Vectors/*genetics ; Malaria/transmission ; Male ; Molecular Sequence Data ; Mutation ; Recombination, Genetic ; *X Chromosome
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...