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  • Mice  (503)
  • Transcription, Genetic  (151)
  • American Association for the Advancement of Science (AAAS)  (616)
  • Copernicus
  • 1985-1989  (616)
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  • American Association for the Advancement of Science (AAAS)  (616)
  • Copernicus
  • Springer  (28)
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  • 1
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    Amyloid protein precursor messenger RNAs: differential expression in Alzheimer's disease (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-08-26
    Description: In situ hybridization was used to assess total amyloid protein precursor (APP) messenger RNA and the subset of APP mRNA containing the Kunitz protease inhibitor (KPI) insert in 11 Alzheimer's disease (AD) and 7 control brains. In AD, a significant twofold increase was observed in total APP mRNA in nucleus basalis and locus ceruleus neurons but not in hippocampal subicular neurons, neurons of the basis pontis, or occipital cortical neurons. The increase in total APP mRNA in locus ceruleus and nucleus basalis neurons was due exclusively to an increase in APP mRNA lacking the KPI domain. These findings suggest that increased production of APP lacking the KPI domain in nucleus basalis and locus ceruleus neurons may play an important role in the deposition of cerebral amyloid that occurs in AD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palmert, M R -- Golde, T E -- Cohen, M L -- Kovacs, D M -- Tanzi, R E -- Gusella, J F -- Usiak, M F -- Younkin, L H -- Younkin, S G -- 5T32GM07250/GM/NIGMS NIH HHS/ -- AG06656/AG/NIA NIH HHS/ -- MH43444/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1988 Aug 26;241(4869):1080-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuropathology, Case Western Reserve University, School of Medicine, Cleveland, OH 44106.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2457949" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*genetics ; Amyloid/*genetics ; Bacteriophage lambda/genetics ; Brain/metabolism ; Cerebral Cortex/metabolism ; *Gene Expression Regulation ; Humans ; Locus Coeruleus/metabolism ; Neurons/metabolism ; Nucleic Acid Hybridization ; Operator Regions, Genetic ; Plasmids ; Protein Precursors/*genetics ; RNA/genetics ; RNA, Complementary ; RNA, Messenger/*genetics/metabolism ; Repressor Proteins/metabolism ; Transcription, Genetic ; Trypsin Inhibitors/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Site-directed mutagenesis of two trans-regulatory genes (tat-III,trs) of HIV-1 (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-02-19
    Description: Point mutations were introduced into the overlapping trans-regulatory genes (tat-III and trs) of human immunodeficiency virus type 1 (HIV-1), and the mutants were evaluated for virus expression. The results showed that tat-III has a positive transacting role and is required for transcriptional activation. A chain terminating mutation early in the trs gene resulted in an increase in transcription of viral messenger RNA as measured by nuclear transcription experiments, but only one major species of viral messenger RNA (1.8 kilobases) was detected, and little or no viral structural proteins were made. Thus, the trs gene product is essential for expression of virus structural proteins but, at the same time, may have a negative trans-regulatory role in transcription. Cotransfection of the point mutant proviruses defective in tat or trs with each other or with a complementary DNA clone containing tat and trs sequences restored the normal transcription pattern and subsequent virus production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sadaie, M R -- Benter, T -- Wong-Staal, F -- New York, N.Y. -- Science. 1988 Feb 19;239(4842):910-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Tumor Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3277284" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/genetics ; Acquired Immunodeficiency Syndrome/immunology ; Animals ; Cell Line ; Chloramphenicol O-Acetyltransferase ; Codon ; DNA/genetics ; *Genes, Regulator ; *Genes, Viral ; HIV/*genetics ; Humans ; Immunosorbent Techniques ; *Mutation ; Plasmids ; RNA, Messenger/genetics ; RNA, Viral/genetics ; Transcription, Genetic ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    The ras oncogenes increase the intrinsic resistance of NIH 3T3 cells to ionizing radiation (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-02-05
    Description: Identification of genes that function to protect cells from radiation damage is an essential step in understanding the molecular mechanisms by which mammalian cells cope with ionizing radiation. The intrinsic radiation resistance (D0) of NIH 3T3 cells was markedly and significantly increased by transformation with ras oncogenes activated by missense mutations. This radiobiologic activity appeared to be a specific consequence of the ras mutations rather than of transformation, since revertant cells that contained functional ras genes (but were no longer phenotypically transformed) retained their increased D0's.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sklar, M D -- CA 41166/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Feb 5;239(4840):645-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Radiation Oncology, University of Michigan Medical School, Ann Arbor 48109.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3277276" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Survival/*radiation effects ; Cell Transformation, Neoplastic ; Cells, Cultured ; Clone Cells ; Dose-Response Relationship, Radiation ; *Genes, ras ; Mice ; Mice, Inbred Strains
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Immunotherapy of the nonobese diabetic mouse: treatment with an antibody to T-helper lymphocytes (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-04-29
    Description: Spontaneous diabetes mellitus was blocked in nonobese diabetic mice by treatment with a monoclonal antibody against the L3T4 determinant present on the surface of T-helper lymphocytes. Sustained treatment with the monoclonal antibody led to cessation of the lymphocytic infiltration associated with the destruction of the insulin-producing beta cells. Moreover, the mice remained normoglycemic after the antibody therapy was stopped. These studies indicate that immunotherapy with monoclonal antibodies to the lymphocyte subset may not only halt the progression of diabetes, but may lead to long-term reversal of the disease after therapy has ended.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shizuru, J A -- Taylor-Edwards, C -- Banks, B A -- Gregory, A K -- Fathman, C G -- AI11313/AI/NIAID NIH HHS/ -- DK39959/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1988 Apr 29;240(4852):659-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Stanford University Medical Center, CA 94305-5111.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2966437" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/*therapeutic use ; Antigens, Differentiation, T-Lymphocyte/*immunology ; Cyclosporins/therapeutic use ; Diabetes Mellitus, Experimental/pathology/*therapy ; Female ; *Immunotherapy ; Islets of Langerhans/pathology ; Lymphocytes/pathology ; Mice ; Mice, Inbred ICR ; T-Lymphocytes, Helper-Inducer/*immunology/pathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Antisense RNA directed against the 3' noncoding region prevents dormant mRNA activation in mouse oocytes (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-08-05
    Description: Primary mouse oocytes contain untranslated stable messenger RNA for tissue plasminogen activator (t-PA). During meiotic maturation, this maternal mRNA undergoes a 3'-polyadenylation, is translated, and is degraded. Injections of maturing oocytes with different antisense RNA's complementary to both coding and noncoding portions of t-PA mRNA all selectively blocked t-PA synthesis. RNA blot analysis of t-PA mRNA in injected, matured oocytes suggested a cleavage of the RNA.RNA hybrid region, yielding a stable 5' portion, and an unstable 3' portion. In primary oocytes, the 3' noncoding region was susceptible to cleavage, while the other portions of the mRNA were blocked from hybrid formation until maturation occurred. Injection of antisense RNA complementary to 103 nucleotides of its extreme 3' untranslated region was sufficient to prevent the polyadenylation, translational activation, and destabilization of t-PA mRNA. These results demonstrate a critical role for the 3' noncoding region of a dormant mRNA in its translational recruitment during meiotic maturation of mouse oocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strickland, S -- Huarte, J -- Belin, D -- Vassalli, A -- Rickles, R J -- Vassalli, J D -- HD-17875/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1988 Aug 5;241(4866):680-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Histology and Embryology, University of Geneva Medical School, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2456615" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Mice ; Nucleic Acid Hybridization ; Oocytes/*metabolism ; Poly A/metabolism ; Protein Biosynthesis/drug effects ; RNA/*pharmacology ; RNA, Antisense ; RNA, Messenger/*antagonists & inhibitors/metabolism ; Tissue Plasminogen Activator/*genetics
    Print ISSN: 0036-8075
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  • 6
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    The effect of histone gene deletions on chromatin structure in Saccharomyces cerevisiae (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-11-04
    Description: As a way of studying nucleosome assembly and maintenance in Saccharomyces cerevisiae, mutants bearing deletions or duplications of the genes encoding histones H2A and H2B were analyzed. Previous genetic analysis had shown that only one of these mutants exhibited dramatic and pleiotropic phenotypes. This mutant was also the only one that contained disrupted chromatin, suggesting that the original phenotypes were attributable to alterations in chromosome structure. The chromatin disruption in the mutant, however, did not extend over the entire genome, but rather was localized to specific regions. Thus, while the arrangement of nucleosomes over the HIS4 and GAL1 genes, the telomeres, and the long terminal repeats (delta sequences) of Ty retrotransposons appeared essentially normal, nucleosomes over the CYH2 and UBI4 genes and the centromere of chromosome III were dramatically disrupted. The observation that the mutant exhibited localized chromatin disruptions implies that the assembly or maintenance of nucleosomes differs over different parts of the yeast genome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Norris, D -- Dunn, B -- Osley, M A -- GM40118/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Nov 4;242(4879):759-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2847314" target="_blank"〉PubMed〈/a〉
    Keywords: Centromere/ultrastructure ; Chromatin/physiology/*ultrastructure ; Chromosome Deletion ; DNA Transposable Elements ; Galactose ; Gene Expression Regulation ; Genes, Fungal ; Histidine ; Histones/*genetics ; Mutation ; Phenotype ; RNA, Messenger/genetics ; Repetitive Sequences, Nucleic Acid ; Saccharomyces cerevisiae/genetics/*ultrastructure ; Transcription, Genetic
    Print ISSN: 0036-8075
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  • 7
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    A transcriptional enhancer 3' of C beta 2 in the T cell receptor beta locus (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-08
    Description: Run-on transcription experiments were used to demonstrate that transcription of T cell receptor beta chain V genes is activated by DNA rearrangement, in a manner similar to immunoglobulin genes. A transcriptional enhancer likely to be involved in this activation has been identified. A 25-kilobase region from J beta 1 to V beta 14 was tested for enhancer activity by transient transfections, and an enhancer was found 7.5 kilobases 3' of C beta 2. The beta enhancer has low activity relative to the simian virus 40 viral enhancer, does not display a preference for V beta promoters, has a T cell-specific activity, and binds two purified immunoglobulin heavy chain enhancer factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDougall, S -- Peterson, C L -- Calame, K -- GM29361/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 8;241(4862):205-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, UCLA School of Medicine 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2968651" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; *Enhancer Elements, Genetic ; Gene Expression Regulation ; Genes, Immunoglobulin ; Immunoglobulin Heavy Chains/genetics ; In Vitro Techniques ; Mice ; Nuclear Proteins/physiology ; Receptors, Antigen, T-Cell/*genetics ; Receptors, Antigen, T-Cell, alpha-beta ; *Regulatory Sequences, Nucleic Acid ; Transcription Factors/physiology ; Transcription, Genetic
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Selection of variable-joining region combinations in the alpha chain of the T cell receptor (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-09-09
    Description: Most T lymphocytes express an antigen-specific receptor composed of two subunits, alpha and beta, each of which can exhibit structural variability. A complex selection process operates on T cells during development in the thymus such that cells expressing only particular alpha beta-receptors migrate to the periphery. The alpha-chain repertoire was dissected at different stages of the selection process by using the polymerase chain reaction (PCR) technique to amplify only those transcripts of a particular variable region gene (V58). Sequences from these V58 cDNAs reveal the predominant expression of four joining (J) segments by T cells in the adult thymus, suggesting that molecular or cellular processes select particular V alpha J alpha combinations during development. T cells expressing one of these V58J alpha chains appear to have been negatively selected at a later stage, since these transcripts were present in the spleen at approximately one-tenth the level in the thymus. Results also indicate that residues present at the V alpha J alpha junction may be important in an early selection process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roth, M E -- Lacy, M J -- McNeil, L K -- Kranz, D M -- AI24635/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 9;241(4871):1354-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Illinois, Urbana 61801.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2970673" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Genes ; *Major Histocompatibility Complex ; Mice ; Mice, Inbred Strains ; Molecular Sequence Data ; Receptors, Antigen, T-Cell/*genetics ; Receptors, Antigen, T-Cell, alpha-beta ; Recombination, Genetic ; Spleen/physiology ; T-Lymphocytes/*physiology ; Thymus Gland/physiology ; Tissue Distribution
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Alternative mechanisms for activation of human immunodeficiency virus enhancer in T cells (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-03-11
    Description: The expression of human immunodeficiency virus (HIV) after T cell activation is regulated by NF-kappa B, an inducible DNA-binding protein that stimulates transcription. Proteins encoded by a variety of DNA viruses are also able to activate expression from the HIV enhancer. To determine how this activation occurs, specific genes from herpes simplex virus type 1 and adenovirus that activate HIV in T lymphoma cells have been identified. The cis-acting regulatory sequences in the HIV enhancer that mediate their effect have also been characterized. The relevant genes are those for ICP0-an immediate-early product of herpes simplex virus type 1-and the form of E1A encoded by the 13S messenger RNA of adenovirus. Activation of HIV by adenovirus E1A was found to depend on the TATA box, whereas herpesvirus ICP0 did not work through a single defined cis-acting element. These findings suggest multiple pathways that can be used to bypass normal cellular activation of HIV, and they raise the possibility that infection by herpes simplex virus or adenovirus may directly contribute to the activation of HIV in acquired immunodeficiency syndrome by mechanisms independent of antigenic stimulation in T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nabel, G J -- Rice, S A -- Knipe, D M -- Baltimore, D -- AI20530/AI/NIAID NIH HHS/ -- F32GM11224/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 11;239(4845):1299-302.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2830675" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviruses, Human/genetics ; *Enhancer Elements, Genetic ; Genes, Regulator ; *Genes, Viral ; HIV/*genetics/growth & development ; Humans ; *Lymphocyte Activation ; Plasmids ; Simplexvirus/genetics ; T-Lymphocytes/*immunology ; Transcription, Genetic ; Virus Activation
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Salivary gland lysates from the sand fly Lutzomyia longipalpis enhance Leishmania infectivity (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-03-11
    Description: Leishmaniasis is a parasitic disease transmitted by phlebotomine sand flies. The role of sand fly saliva in transmission of the disease was investigated by injecting mice with Leishmania major parasites in the presence of homogenized salivary glands from Lutzomyia longipalpis. This procedure resulted in cutaneous lesions of Leishmania major that were routinely five to ten times as large and contained as much as 5000 times as many parasites as controls. With inocula consisting of low numbers of Leishmania major, parasites were detected at the site of injection only when the inoculum also contained salivary gland material. This enhancing effect of sand fly salivary glands on cutaneous leishmaniasis occurred with as little as 10 percent of the contents of one salivary gland of one fly. Material obtained from other bloodsucking arthropods could not mediate the phenomenon.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Titus, R G -- Ribeiro, J M -- 1 R29 AI24511/AI/NIAID NIH HHS/ -- 5 P01 AI22794/AI/NIAID NIH HHS/ -- AI18694 0481/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 11;239(4845):1306-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Rheumatology and Immunology, 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/3344436" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthropods ; *Diptera ; Leishmania tropica/*pathogenicity ; Leishmaniasis/*physiopathology ; Mice ; Mice, Inbred CBA ; Salivary Glands ; Species Specificity ; Tissue Extracts/*pharmacology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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