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  • Articles  (153)
  • Gene Expression Regulation  (83)
  • Nucleic Acid Hybridization  (77)
  • American Association for the Advancement of Science (AAAS)  (153)
  • American Association for the Advancement of Science
  • Elsevier
  • 1985-1989  (153)
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  • 1988  (73)
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  • Chemistry and Pharmacology  (153)
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  • Articles  (153)
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  • American Association for the Advancement of Science (AAAS)  (153)
  • American Association for the Advancement of Science
  • Elsevier
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  • 1985-1989  (153)
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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
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  • 2
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    DNA amplification for direct detection of HIV-1 in DNA of peripheral blood mononuclear cells (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-01-15
    Description: By means of a selective DNA amplification technique called polymerase chain reaction, proviral sequences of the human immunodeficiency virus (HIV-1) were identified directly in DNA isolated from peripheral blood mononuclear cells (PBMCs) of persons seropositive but not in DNA isolated from PBMCs of persons seronegative for the virus. Primer pairs from multiple regions of the HIV-1 genome were used to achieve maximum sensitivity of provirus detection. HIV-1 sequences were detected in 100% of DNA specimens from seropositive, homosexual men from whom the virus was isolated by coculture, but in none of the DNA specimens from a control group of seronegative, virus culture-negative persons. However, HIV-1 sequences were detected in 64% of DNA specimens from seropositive, virus culture-negative homosexual men. This method of DNA amplification made it possible to obtain results within 3 days, whereas virus isolation takes up to 3 to 4 weeks. The method may therefore be used to complement or replace virus isolation as a routine means of determining HIV-1 infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ou, C Y -- Kwok, S -- Mitchell, S W -- Mack, D H -- Sninsky, J J -- Krebs, J W -- Feorino, P -- Warfield, D -- Schochetman, G -- New York, N.Y. -- Science. 1988 Jan 15;239(4837):295-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Infectious Diseases, Centers for Disease Control, Atlanta, GA 30333.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3336784" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*microbiology ; Base Sequence ; DNA, Viral/*blood ; DNA-Directed DNA Polymerase ; *Gene Amplification ; HIV/*genetics/isolation & purification ; HIV Seropositivity ; Homosexuality ; Humans ; Leukocytes, Mononuclear/*analysis ; Male ; Nucleic Acid Amplification Techniques ; Nucleic Acid Hybridization ; Virus Cultivation
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  • 3
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    Mammalian glucocorticoid receptor derivatives enhance transcription in yeast (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-08-19
    Description: In mammalian cells, the glucocorticoid receptor binds specifically to glucocorticoid response element (GRE) DNA sequences and enhances transcription from linked promoters. It is shown here that derivatives of the glucocorticoid receptor also enhance transcription when expressed in yeast. Receptor-mediated enhancement in yeast was observed in fusions of GRE sequences to the yeast cytochrome c1 (CYC1) promoter; the CYC1 upstream activator sequences were not essential, since enhancement was observed in fusions of GREs to mutant CYC1 promoters retaining only the TATA region and transcription startpoints. It is concluded that the receptor operates by a common, highly conserved mechanism in yeast and mammalian cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schena, M -- Yamamoto, K R -- CA20535-12/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Aug 19;241(4868):965-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3043665" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA/metabolism ; *Enhancer Elements, Genetic ; Gene Expression Regulation ; Immunoassay ; Plasmids ; Promoter Regions, Genetic ; Rats ; Receptors, Glucocorticoid/*genetics ; Saccharomyces cerevisiae/*genetics ; *Transcription, Genetic
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  • 4
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    DNA looping (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-04-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schleif, R -- New York, N.Y. -- Science. 1988 Apr 8;240(4849):127-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Brandeis University, Waltham, Massachusetts 02254.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3353710" target="_blank"〉PubMed〈/a〉
    Keywords: DNA/*genetics ; DNA-Binding Proteins/physiology ; Eukaryotic Cells/physiology ; Gene Expression Regulation ; Nucleic Acid Conformation ; Prokaryotic Cells/physiology ; Regulatory Sequences, Nucleic Acid
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  • 5
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    A newly characterized HLA DQ beta allele associated with pemphigus vulgaris (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-02-26
    Description: The inheritance of particular alleles of major histocompatibility complex class II genes increases the risk for various human autoimmune diseases; however, only a small percentage of individuals having an allele associated with susceptibility develop disease. The identification of allelic variants more precisely correlated with disease susceptibility would greatly facilitate clinical screening and diagnosis. Oligonucleotide-primed gene amplification in vitro was used to determine the nucleotide sequence of a class II variant found almost exclusively in patients with the autoimmune skin disease pemphigus vulgaris. In addition to clinical implications, the disease-restricted distribution of this variant should provide insight into the molecular mechanisms underlying associations between diseases and HLA-class II genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sinha, A A -- Brautbar, C -- Szafer, F -- Friedmann, A -- Tzfoni, E -- Todd, J A -- Steinman, L -- McDevitt, H O -- New York, N.Y. -- Science. 1988 Feb 26;239(4843):1026-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Microbiology, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2894075" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Autoimmune Diseases/*genetics/immunology ; Base Sequence ; DNA/genetics ; Gene Amplification ; Genetic Variation ; HLA-D Antigens/*genetics ; HLA-DQ Antigens/*genetics/immunology ; HLA-DR Antigens/immunology ; Humans ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Pemphigus/*genetics/immunology ; Polymorphism, Restriction Fragment Length
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  • 6
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    Cloning of a lymphoid-specific cDNA encoding a protein binding the regulatory octamer DNA motif (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-29
    Description: An octamer DNA sequence plays a critical role in directing transcription of immunoglobulin genes in B lymphocytes. A new technique of direct binding of radioactive DNA was used to screen a complementary DNA expression library from the BJAB cell line in lambda gt11 phage to derive molecular cDNA clones representing a putative B lymphocyte-specific octamer binding protein. The plaques were screened with DNA containing four copies of the octamer sequence and positive phage recombinants were identified. The fusion protein produced on inducing a lysogen of one phage bound to a monomeric octamer probe. The cDNA insert from this phage hybridized to messenger RNA found in B lymphocytes, but not in most other cells. Thus, this cDNA derives from a gene (oct-2) that specifies an octamer binding protein expressed preferentially in B lymphocytes, proving that, for at least one gene, a cell-specific transcription factor exists and its amount is controlled through messenger RNA availability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Staudt, L M -- Clerc, R G -- Singh, H -- LeBowitz, J H -- Sharp, P A -- Baltimore, D -- P01-CA42063/CA/NCI NIH HHS/ -- P30-CAL4051/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 29;241(4865):577-80.〈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/3399892" target="_blank"〉PubMed〈/a〉
    Keywords: Cloning, Molecular ; DNA/genetics ; DNA-Binding Proteins/*physiology ; Gene Expression Regulation ; *Genes ; Humans ; Lymphocytes/*physiology ; *Regulatory Sequences, Nucleic Acid ; Transcription Factors/*physiology
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  • 7
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    Astrocytes synthesize angiotensinogen in brain (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-12-09
    Description: Cell types associated with angiotensinogen mRNA in rat brain were identified in individual brain sections by in situ hybridization with tritiated RNA probes or with a sulfur-35--labeled oligonucleotide combined with immunocytochemical detection of either glial fibrillary acidic protein (GFAP) for astrocytes or microtubule-associated protein (MAP-2) for neurons. Autoradiography revealed silver grains clustered primarily over GFAP-reactive soma and processes; most grain clusters were not associated with MAP-2--reactive cells. These results demonstrate that, in contrast to other known neuropeptide precursors, angiotensinogen is synthesized by glia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stornetta, R L -- Hawelu-Johnson, C L -- Guyenet, P G -- Lynch, K R -- R01 HL33513/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Dec 9;242(4884):1444-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, 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/3201232" target="_blank"〉PubMed〈/a〉
    Keywords: Angiotensinogen/*biosynthesis/genetics ; Animals ; Astrocytes/*metabolism ; Brain/*metabolism ; Glial Fibrillary Acidic Protein/analysis ; Histocytochemistry ; Microtubule-Associated Proteins/analysis ; Nucleic Acid Hybridization ; RNA, Messenger/analysis/genetics ; Rats
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  • 8
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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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  • 9
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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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  • 10
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    Ordered interstrand and intrastrand DNA transfer during reverse transcription (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-08-26
    Description: Retroviruses contain two copies of the plus stranded viral RNA genome. As a means of determining whether both of these RNA's are used in the reverse transcription reaction, cells were infected with heterozygous virus particles that varied in nucleotide sequence at two separate locations at the RNA termini. The DNA proviruses formed from a single cycle of reverse transcription were then examined. Of the 12 proviruses that were characterized, all exhibited long terminal repeats (LTR's) that would be expected to arise only if both RNA templates were used for the generation of minus strand DNA. In contrast, only a single minus strand DNA appeared to be used as template for the plus strand DNA in the generation of fully double-stranded viral DNA. These results indicate that the first strand transfer step in reverse transcription is an intermolecular event while that of the second transfer is intramolecular. Thus, retroviruses contain two functionally active RNA's, and both may be required for the generation of a single linear DNA molecule. Formation of heterozygotes during retrovirus infection would be expected to result in the efficient generation of LTR recombinants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Panganiban, A T -- Fiore, D -- New York, N.Y. -- Science. 1988 Aug 26;241(4869):1064-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉McArdle Laboratory for Cancer Research, University of Wisconsin, Madison 53706.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2457948" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; DNA Restriction Enzymes ; DNA, Viral/*genetics/metabolism ; Deoxyribonuclease HindIII ; Genes, Viral ; Nucleic Acid Hybridization ; Polymorphism, Restriction Fragment Length ; RNA, Viral/*genetics/metabolism ; RNA-Directed DNA Polymerase/*metabolism ; Repetitive Sequences, Nucleic Acid ; Retroviridae/*genetics ; Templates, Genetic ; *Transcription, Genetic ; Transfection ; Virion/genetics ; Virus Replication
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  • 11
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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
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  • 12
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    Structural rearrangement of the retinoblastoma gene in human breast carcinoma (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-10-14
    Description: Structural changes of the human retinoblastoma gene have been demonstrated previously in retinoblastoma and some clinically related tumors including osteosarcoma. Structural aberrations of the retinoblastoma locus (RB1) were observed in 25% of breast tumor cell lines studied and 7% of the primary tumors. These changes include homozygous internal deletions and total deletion of RB1; a duplication of an exon was observed in one of the cell lines. In all cases, structural changes either resulted in the absence or truncation of the RB1 transcript. No obvious defect in RB1 was detected by DNA blot analysis in primary tumors or cell lines from Wilms' tumor, cervical carcinoma, or hepatoma. These results further support the concept that the human RB1 gene has pleiotropic effects on specific types of cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉T'Ang, A -- Varley, J M -- Chakraborty, S -- Murphree, A L -- Fung, Y K -- CA44754/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Oct 14;242(4876):263-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology/Oncology, Childrens Hospital of Los Angeles, CA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175651" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*genetics ; Chromosome Aberrations ; Chromosomes, Human, Pair 13 ; DNA/genetics ; DNA Probes ; Exons ; Eye Neoplasms/*genetics ; Female ; *Gene Rearrangement ; Homozygote ; Humans ; Lymphatic Metastasis ; Menopause ; Mutation ; Nucleic Acid Hybridization ; Retinoblastoma/*genetics ; Risk Factors ; Tumor Cells, Cultured
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  • 13
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    Vasopressin mRNA in the suprachiasmatic nuclei: daily regulation of polyadenylate tail length (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-15
    Description: Daily variation has been found in the length of the polyadenylate tail attached to vasopressin messenger RNA in the suprachiasmatic nuclei, which is the location of an endogenous circadian pacemaker in mammals. No such variation was found in the supraoptic or paraventricular nuclei. This variation in the length of the polyadenylate tail may underlie the circadian rhythm of vasopressin peptide levels in cerebrospinal fluid and is a unique example of a daily rhythm in messenger RNA structure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Robinson, B G -- Frim, D M -- Schwartz, W J -- Majzoub, J A -- 1P50HL36568/HL/NHLBI NIH HHS/ -- R01NS24542/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 15;241(4863):342-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3388044" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arginine Vasopressin/*physiology ; Biological Clocks ; Circadian Rhythm ; Gene Expression Regulation ; Poly A/*physiology ; RNA, Messenger/*physiology ; Rats ; Suprachiasmatic Nucleus/*physiology
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  • 14
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    In situ transcription: specific synthesis of complementary DNA in fixed tissue sections (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-06-17
    Description: A technique, in situ transcription, is described, in which reverse transcription of mRNAs is achieved within fixed tissue sections. An oligonucleotide complementary to proopiomelanocortin (POMC) mRNA was used as a primer for the specific synthesis of radiolabeled POMC cDNA in fixed sections of rat pituitary, thus permitting the rapid anatomical localization of POMC mRNA by autoradiography. Intermediate lobe signal intensities were sensitive to dopaminergic drugs, demonstrating that the method can be used for studies of mRNA regulation. The transcripts may also be eluted from tissue sections for a variety of uses, including the identification and cloning of autoradiographically localized cDNAs from small amounts of tissue.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tecott, L H -- Barchas, J D -- Eberwine, J H -- DA-05010/DA/NIDA NIH HHS/ -- MH-23861/MH/NIMH NIH HHS/ -- MH09099/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 17;240(4859):1661-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nancy Pritzker Laboratory of Behavioral Neurochemistry, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2454508" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; DNA/*biosynthesis ; Deoxycytidine/metabolism ; Electrophoresis, Polyacrylamide Gel ; Nucleic Acid Denaturation ; Nucleic Acid Hybridization ; Oligonucleotides/genetics ; Pituitary Gland/*metabolism ; Pro-Opiomelanocortin/*genetics ; RNA, Messenger/*metabolism ; RNA-Directed DNA Polymerase/metabolism ; Rats ; *Transcription, Genetic
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  • 15
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    Molecular cloning of two types of GAP complementary DNA from human placenta (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-12-23
    Description: The ras p21 GTPase-activating protein (GAP) was purified from human placental tissue. Internal amino acid sequence was obtained from this 120,000-dalton protein and, by means of this sequence, two types of complementary DNA clones were isolated and characterized. One type encoded GAP with a predicted molecular mass of 116,000 daltons and 96% identity with bovine GAP. The messenger RNA of this GAP was detected in human lung, brain, liver, leukocytes, and placenta. The second type appeared to be generated by a differential splicing mechanism and encoded a novel form of GAP with a predicted molecular mass of 100,400 daltons. This protein lacks the hydrophobic amino terminus characteristic of the larger species, but retains GAP activity. The messenger RNA of this type was abundantly expressed in placenta and in several human cell lines, but not in adult tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trahey, M -- Wong, G -- Halenbeck, R -- Rubinfeld, B -- Martin, G A -- Ladner, M -- Long, C M -- Crosier, W J -- Watt, K -- Koths, K -- New York, N.Y. -- Science. 1988 Dec 23;242(4886):1697-700.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Cetus Corp., Emeryville, CA 94608.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3201259" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Brain Chemistry ; *Cloning, Molecular ; DNA/*genetics/isolation & purification ; Female ; GTPase-Activating Proteins ; Gene Expression Regulation ; Humans ; Leukocytes/analysis ; Liver/analysis ; Lung/analysis ; Molecular Sequence Data ; Molecular Weight ; Nucleic Acid Hybridization ; Oligonucleotide Probes ; Placenta/*analysis ; Pregnancy ; Proteins/*genetics/isolation & purification ; RNA, Messenger/analysis/genetics ; Sequence Homology, Nucleic Acid ; ras GTPase-Activating Proteins
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  • 16
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    Tandem array of human visual pigment genes at Xq28 (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-06-17
    Description: Unequal crossing-over within a head-to-tail tandem array of the homologous red and green visual pigment genes has been proposed to explain the observed variation in green-pigment gene number among individuals and the prevalence of red-green fusion genes among color-blind subjects. This model was tested by probing the structure of the red and green pigment loci with long-range physical mapping techniques. The loci were found to constitute a gene array with an approximately 39-kilobase repeat length. The position of the red pigment gene at the 5' edge of the array explains its lack of variation in copy number. Restriction maps of the array in four individuals who differ in gene number are consistent with a head-to-tail configuration of the genes. These results provide physical evidence in support of the model and help to explain the high incidence of color blindness in the human population.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vollrath, D -- Nathans, J -- Davis, R W -- GM21891/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 17;240(4859):1669-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2837827" target="_blank"〉PubMed〈/a〉
    Keywords: Color Vision Defects/*genetics ; Crossing Over, Genetic ; DNA/genetics ; DNA Restriction Enzymes ; Electrophoresis, Agar Gel ; Exons ; Female ; Genetic Variation ; Humans ; Male ; Nucleic Acid Hybridization ; Recombination, Genetic ; Repetitive Sequences, Nucleic Acid ; Retinal Pigments/*genetics ; *X Chromosome
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  • 17
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    Translocation and rearrangement of myeloperoxidase gene in acute promyelocytic leukemia (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-05-06
    Description: Acute promyelocytic leukemia (subtype M3) is characterized by malignant promyelocytes exhibiting an abundance of abnormally large or aberrant primary granules. Myeloperoxidase (MPO) activity of these azurophilic granules, as assessed by cytochemical staining, is unusually intense. In addition, M3 is universally associated with a chromosomal translocation, t(15;17)(q22;q11.2). In this report, the MPO gene was localized to human chromosome 17 (q12-q21), the region of the breakpoint on chromosome 17 in the t(15;17), by somatic cell hybrid analysis and in situ chromosomal hybridization. By means of MPO complementary DNA clones for in situ hybridization and Southern blot analysis, the effect of this specific translocation on the MPO gene was examined. In all cases of M3 examined, MPO is translocated to chromosome 15. Genomic blot analyses indicate rearrangement of MPO in leukemia cells of two of four cases examined. These findings suggest that MPO may be pivotal in the pathogenesis of acute promyelocytic leukemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weil, S C -- Rosner, G L -- Reid, M S -- Chisholm, R L -- Lemons, R S -- Swanson, M S -- Carrino, J J -- Diaz, M O -- Le Beau, M M -- 1R01 CA44475/CA/NCI NIH HHS/ -- CA09273/CA/NCI NIH HHS/ -- CA16910/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 May 6;240(4853):790-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Northwestern University Medical Center, Chicago, IL 60611.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2896388" target="_blank"〉PubMed〈/a〉
    Keywords: Bone Marrow/analysis ; Chromosome Mapping ; Chromosomes, Human, Pair 15 ; Chromosomes, Human, Pair 17 ; DNA/genetics ; DNA Restriction Enzymes ; DNA, Recombinant ; Humans ; Leukemia, Myeloid, Acute/*enzymology/genetics ; Nucleic Acid Hybridization ; Peroxidase/*genetics ; Plasmids ; Polymorphism, Restriction Fragment Length ; *Translocation, Genetic
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  • 18
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    Duchenne muscular dystrophy gene expression in normal and diseased human muscle (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-03-18
    Description: A probe for the 5' end of the Duchenne muscular dystrophy (DMD) gene was used to study expression of the gene in normal human muscle, myogenic cell cultures, and muscle from patients with DMD. Expression was found in RNA from normal fetal muscle, adult cardiac and skeletal muscle, and cultured muscle after myoblast fusion. In DMD muscle, expression of this portion of the gene was also revealed by in situ RNA hybridization, particularly in regenerating muscle fibers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scott, M O -- Sylvester, J E -- Heiman-Patterson, T -- Shi, Y J -- Fieles, W -- Stedman, H -- Burghes, A -- Ray, P -- Worton, R -- Fischbeck, K H -- GM32592/GM/NIGMS NIH HHS/ -- NS08075/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 18;239(4846):1418-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurology Department, Hospital of the University of Pennsylvania, Philadelphia, 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2450401" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; DNA/genetics ; DNA, Recombinant ; *Gene Expression Regulation ; Humans ; Muscles/embryology/*metabolism ; Muscular Dystrophies/*genetics ; Myocardium/metabolism ; Nucleic Acid Hybridization ; RNA/metabolism ; RNA, Messenger/metabolism ; Regeneration ; Transcription, Genetic
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  • 19
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    Germline transformation used to define key features of heat-shock response elements (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-03-04
    Description: The heat-shock consensus element (HSE), CTNGAANNTTCNAG, is found in multiple copies upstream of all heat-shock genes. Here, the sequence requirements for heat-shock induction are tested by Drosophila germline transformation with an hsp70-lacZ gene fused to a pair of synthetic HSEs. Certain single-base substitutions in either HSE cause a dramatic reduction (forty-fold) in expression. Surprisingly, variations in sequences immediately flanking the HSEs also reduced levels of induction. One such variant that contains two perfect 14-base pair HSEs, which are correctly spaced relative to each other and the TATA box, retained only 7% of wild type-induced expression. These and additional analyses indicate that the heat-shock regulatory element includes sequences beyond the 14-base pair HSE and may be better described as a dimer of a 10-base pair sequence, NTTCNNGAAN.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xiao, H -- Lis, J T -- GM25232/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 4;239(4844):1139-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Biochemistry, Molecular and Cell Biology, Cornell University, Ithaca, NY 14853.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3125608" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Composition ; DNA, Recombinant ; Drosophila melanogaster/*genetics ; Gene Expression Regulation ; Heat-Shock Proteins/*genetics ; Hot Temperature ; Mutation ; Nucleic Acid Conformation ; Promoter Regions, Genetic ; *Regulatory Sequences, Nucleic Acid ; Repetitive Sequences, Nucleic Acid ; Transcription Factors/*metabolism ; *Transformation, Genetic
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  • 20
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    Insulin-resistant diabetes due to a point mutation that prevents insulin proreceptor processing (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-05-06
    Description: A point mutation in the human insulin receptor gene in a patient with type A insulin resistance alters the amino acid sequence within the tetrabasic processing site of the proreceptor molecule from Arg-Lys-Arg-Arg to Arg-Lys-Arg-Ser. Epstein-Barr virus-transformed lymphocytes from this patient synthesize an insulin receptor precursor that is normally glycosylated and inserted into the plasma membrane but is not cleaved to mature alpha and beta subunits. Insulin binding to these cells is severely reduced but can be increased about fivefold by gentle treatment with trypsin, accompanied by the appearance of normal alpha subunits. These results indicate that proteolysis of the proreceptor is necessary for its normal full insulin-binding sensitivity and signal-transducing activity and that a cellular protease that is more stringent in its specificity than trypsin is required to process the receptor precursor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoshimasa, Y -- Seino, S -- Whittaker, J -- Kakehi, T -- Kosaki, A -- Kuzuya, H -- Imura, H -- Bell, G I -- Steiner, D F -- AM 13914/AM/NIADDK NIH HHS/ -- AM 20595/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1988 May 6;240(4853):784-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, University of Chicago, IL 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3283938" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Amino Acid Sequence ; Cell Membrane/metabolism ; Cells, Cultured ; DNA/genetics ; Diabetes Mellitus/*genetics/metabolism ; Female ; Glycosylation ; Humans ; Insulin/metabolism ; Insulin Resistance/*genetics ; Lymphocytes/metabolism ; Molecular Sequence Data ; Mutation ; Nucleic Acid Hybridization ; Protein Precursors/*genetics/metabolism ; RNA, Messenger/metabolism ; Receptor, Insulin/*genetics/metabolism ; Trypsin/metabolism
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  • 21
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    A point mutation in the c-myc locus of a Burkitt lymphoma abolishes binding of a nuclear protein (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-06-24
    Description: A 20-base pair region in the first intron of the human c-myc gene was identified as the binding site of a nuclear protein. This binding site is mutated in five out of seven Burkitt lymphomas sequenced to date. To investigate the protein-recognition region in greater detail, the abnormal c-myc allele from a Burkitt lymphoma line (PA682) that carries a t(8;22) chromosomal translocation was used. A point mutation in the binding region of the PA682 c-myc DNA abolished binding of this nuclear protein. This protein may be an important factor for control of c-myc expression, and mutations in its recognition sequence may be associated with c-myc activation in many cases of Burkitt lymphoma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zajac-Kaye, M -- Gelmann, E P -- Levens, D -- New York, N.Y. -- Science. 1988 Jun 24;240(4860):1776-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medicine Branch, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2454510" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Burkitt Lymphoma/*genetics ; DNA-Binding Proteins/*metabolism ; Gene Expression Regulation ; Humans ; Molecular Sequence Data ; Mutation ; Nuclear Proteins/*metabolism ; *Oncogenes ; Proto-Oncogene Proteins/*genetics ; RNA/genetics ; RNA, Antisense ; Transcription, Genetic
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  • 22
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    Independent molecular pathways in initiation and loss of hormone responsiveness of breast carcinomas (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-04-22
    Description: These studies were set up to determine whether those oncogenes participating in the initiation of mammary carcinogenesis (for example, ras oncogenes) play a direct role in the outcome of events associated with the late stages of tumor development such as loss of hormone dependency. Mammary carcinomas induced by a single carcinogenic insult in pubescent rats was selected as an in vivo model system with direct relevance to human breast cancer. Acquisition of hormone-independent growth in these carcinogen-induced tumors was found to be independent of the activation of ras oncogenes during the early stages of carcinogenesis. In agreement with these observations, introduction of a human ras oncogene into human MCF-7 breast carcinoma cells did not abrogate their hormonal dependency for growth in vivo. These findings suggest that those events responsible for the critical stages of breast cancer development occur independently and in an uncoordinated manner.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sukumar, S -- Carney, W P -- Barbacid, M -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Apr 22;240(4851):524-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Oncology Section, Basic Research Program, Frederick Cancer Research Facility, MD 21701.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3282307" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/*physiopathology ; Cell Line ; Estrogens/*physiology ; Gene Expression Regulation ; *Genes, ras ; Humans ; Mammary Neoplasms, Experimental/*physiopathology ; Methylnitrosourea ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Rats ; Receptors, Estrogen/*physiology
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  • 23
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    jun Is bustin' out all over (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-12-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1988 Dec 9;242(4884):1377-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3201229" target="_blank"〉PubMed〈/a〉
    Keywords: DNA-Binding Proteins/genetics/metabolism ; Gene Expression Regulation ; *Oncogenes ; Retroviridae Proteins/*genetics
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  • 24
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    Evolution's link to development explored (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-05-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1988 May 13;240(4854):880-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3363370" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Gene Expression Regulation ; *Genes ; *Growth ; Plant Development ; Plants/genetics
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  • 25
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    Activation of developmentally mutated human globin genes by cell fusion (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-11-18
    Description: Human fetal globin genes are not expressed in hybrid cells produced by the fusion of normal human lymphocytes with mouse erythroleukemia cells. In contrast, when lymphocytes from persons with globin gene developmental mutations (hereditary persistence of fetal hemoglobin) are used for these fusions, fetal globin is expressed in the hybrid cells. Thus, mutations of developmental origin can be reconstituted in vitro by fusing mutant lymphoid cells with differentiated cell lines of the proper lineage. This system can readily be used for analyses, such as globin gene methylation, that normally require large numbers of pure nucleated erythroid cells, which are difficult to obtain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Papayannopoulou, T -- Enver, T -- Takegawa, S -- Anagnou, N P -- Stamatoyannopoulos, G -- DK30852/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1988 Nov 18;242(4881):1056-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2461587" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Fusion ; Chromosome Deletion ; Fetal Hemoglobin/*genetics ; Gene Expression Regulation ; Globins/*genetics ; Hemoglobinopathies/*genetics ; Humans ; Leukemia, Erythroblastic, Acute ; Mice ; Mutation ; Promoter Regions, Genetic ; RNA, Messenger/genetics
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  • 26
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    Platelet-derived growth factor A chain is maternally encoded in Xenopus embryos (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-09-02
    Description: Transcription of zygotic genes does not occur in early Xenopus embryos until the mid-blastula transition, 6 to 7 hours after fertilization. Before this time, development is directed by maternal proteins and messenger RNAs stored within the egg. Two different forms of the A chain of platelet-derived growth factor (PDGF) are shown here to be encoded by maternal messenger RNAs. The two forms closely resemble human PDGF; however, the long form contains a hydrophobic region near the carboxyl terminus. The presence of PDGF messenger RNA in the embryo supports the idea that endogenous growth factors act at the earliest stages of embryogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mercola, M -- Melton, D A -- Stiles, C D -- New York, N.Y. -- Science. 1988 Sep 2;241(4870):1223-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3413486" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Blastocyst/metabolism ; DNA/genetics/isolation & purification ; Gastrula/analysis ; Humans ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Oocytes/analysis ; Platelet-Derived Growth Factor/*genetics ; RNA, Messenger/analysis/genetics ; Xenopus laevis/*embryology/genetics
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  • 27
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    The DNA-binding properties of the major regulatory protein alpha 4 of herpes simplex viruses (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-03-25
    Description: The transition from the expression of alpha, the first set of five herpes simplex virus genes expressed after infection, to beta and gamma genes, expressed later in infection, requires the participation of infected cell protein 4 (alpha 4), the major viral regulatory protein. The alpha 4 protein is present in complexes formed by proteins extracted from infected cells and viral DNA fragments derived from promoter domains. This report shows that the alpha 4 protein forms specific complexes with DNA fragments derived from 5' transcribed noncoding domains of late (gamma 2) genes whose expression requires viral DNA synthesis as well as functional alpha 4 protein. Some of the DNA fragments to which alpha 4 binds do not contain homologs of the previously reported DNA binding site consensus sequence, suggesting that alpha 4 may recognize and interact with more than one type of DNA binding site. The alpha 4 proteins can bind to DNA directly. A posttranslationally modified form of the alpha 4 protein designated alpha 4c differs from the alpha 4a and alpha 4b forms with respect to its affinity for DNA fragments differing in the nucleotide sequences of the binding sites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Michael, N -- Spector, D -- Mavromara-Nazos, P -- Kristie, T M -- Roizman, B -- AI124009/AI/NIAID NIH HHS/ -- CA08494/CA/NCI NIH HHS/ -- CA19264/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1988 Mar 25;239(4847):1531-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Marjorie B. Kovler Viral Oncology Laboratories, University of Chicago, IL 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2832940" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Binding Sites ; DNA, Viral/*metabolism ; DNA-Binding Proteins ; Electrophoresis, Polyacrylamide Gel ; Gene Expression Regulation ; Genes, Viral ; *Immediate-Early Proteins ; Immunoassay ; Molecular Sequence Data ; Sequence Homology, Nucleic Acid ; Simplexvirus/*analysis/genetics ; Transcription Factors ; Viral Proteins/*metabolism
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    Primer-directed enzymatic amplification of DNA with a thermostable DNA polymerase (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-01-29
    Description: A thermostable DNA polymerase was used in an in vitro DNA amplification procedure, the polymerase chain reaction. The enzyme, isolated from Thermus aquaticus, greatly simplifies the procedure and, by enabling the amplification reaction to be performed at higher temperatures, significantly improves the specificity, yield, sensitivity, and length of products that can be amplified. Single-copy genomic sequences were amplified by a factor of more than 10 million with very high specificity, and DNA segments up to 2000 base pairs were readily amplified. In addition, the method was used to amplify and detect a target DNA molecule present only once in a sample of 10(5) cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saiki, R K -- Gelfand, D H -- Stoffel, S -- Scharf, S J -- Higuchi, R -- Horn, G T -- Mullis, K B -- Erlich, H A -- New York, N.Y. -- Science. 1988 Jan 29;239(4839):487-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cetus Corporation, Department of Human Genetics, Emeryville, CA 94608.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2448875" target="_blank"〉PubMed〈/a〉
    Keywords: Cloning, Molecular ; DNA/*genetics ; DNA, Recombinant ; DNA-Directed DNA Polymerase/*metabolism ; Electrophoresis, Agar Gel ; Globins/genetics ; *Hot Temperature ; Humans ; *Nucleic Acid Amplification Techniques ; Nucleic Acid Denaturation ; Nucleic Acid Hybridization ; RNA/genetics ; Thermus/enzymology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Infection of the SCID-hu mouse by HIV-1 (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-12-23
    Description: SCID-hu mice with human fetal thymic or lymph node implants were inoculated with the cloned human immunodeficiency virus-1 isolate, HIV-1JR-CSF. In a time- and dose-dependent fashion, viral replication spread within the human lymphoid organs. Combination immunohistochemistry and in situ hybridization revealed only viral RNA transcripts in most infected cells, but some cells had both detectable viral transcripts and viral protein. Infected cells were always more apparent in the medulla than in the cortex of the thymus. These studies demonstrate that an acute infection of human lymphoid organs with HIV-1 can be followed in the SCID-hu mouse.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Namikawa, R -- Kaneshima, H -- Lieberman, M -- Weissman, I L -- McCune, J M -- AR5P40RR03624-029/AR/NIAMS NIH HHS/ -- CA03352/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Dec 23;242(4886):1684-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3201256" target="_blank"〉PubMed〈/a〉
    Keywords: *Acquired Immunodeficiency Syndrome ; Animals ; Chimera ; *Disease Models, Animal ; HIV/genetics/*physiology ; Humans ; Immunohistochemistry ; Lymph Nodes/microbiology/transplantation ; Mice ; Mice, Mutant Strains ; Nucleic Acid Hybridization ; RNA, Viral/genetics ; Thymus Gland/microbiology/transplantation ; Transcription, Genetic ; Viral Proteins/biosynthesis ; Virus Replication
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 30
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    cDNA expression cloning of the IL-1 receptor, a member of the immunoglobulin superfamily (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-29
    Description: Interleukin-1 alpha and -1 beta (IL-1 alpha and IL-1 beta) are cytokines that participate in the regulation of immune responses, inflammatory reactions, and hematopoiesis. A direct expression strategy was used to clone the receptor for IL-1 from mouse T cells. The product of the cloned complementary DNA binds both IL-1 alpha and IL-1 beta in a manner indistinguishable from that of the native T cell IL-1 receptor. The extracellular, IL-1 binding portion of the receptor is 319 amino acids in length and is composed of three immunoglobulin-like domains. The cytoplasmic portion of the receptor is 217 amino acids long.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sims, J E -- March, C J -- Cosman, D -- Widmer, M B -- MacDonald, H R -- McMahan, C J -- Grubin, C E -- Wignall, J M -- Jackson, J L -- Call, S M -- New York, N.Y. -- Science. 1988 Jul 29;241(4865):585-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunex Corporation, Seattle, WA 98101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2969618" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cloning, Molecular ; DNA/genetics ; Gene Expression Regulation ; Genes, Immunoglobulin ; Interleukin-1/*physiology ; Mice ; Molecular Sequence Data ; *Multigene Family ; Receptors, Immunologic/*genetics ; Receptors, Interleukin-1
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Unusual immunoglobulin gene rearrangement leads to replacement of recombinational signal sequences (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-10-14
    Description: An unexpected immunoglobulin gene rearrangement, signal sequence replacement, was observed in which the recombinational signal sequences of a VH gene segment are fused intact to the 5' end of a DJH element. Nucleotides are not lost from the signal sequences, but they may be lost from the DJH coding sequence. Signal sequence replacement may result from the alternative resolution of an intermediate in VH-to-DJH recombination. This type of rearrangement provides a means to alter the targeting of immunoglobulin gene segments and suggests a mechanism for the occurrence of VH-JH junctions in vivo. Signal sequence replacement may represent an additional pathway for the generation of antibody diversity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morzycka-Wroblewska, E -- Lee, F E -- Desiderio, S V -- New York, N.Y. -- Science. 1988 Oct 14;242(4876):261-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute Laboratory of Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3140378" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; DNA, Recombinant ; *Gene Rearrangement ; *Genes, Immunoglobulin ; Immunoglobulin Heavy Chains/genetics ; Immunoglobulin Variable Region/genetics ; Mice ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Protein Sorting Signals/*genetics ; Recombination, Genetic ; Retroviridae/genetics
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    Multiple principal sigma factor homologs in eubacteria: identification of the "rpoD box" (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-11-18
    Description: Genes for the principal sigma factor (rpoD genes) of various eubacteria were identified with a synthetic oligonucleotide probe corresponding to a conserved sequence in rpoD gene products of Escherichia coli and Bacillus subtilis. Multiple rpoD homologs were found in the strains of Micrococcus, Pseudomonas, and Streptomyces, whereas single genes were detected in E. coli, B. subtilis, and Staphylococcus aureus. The four rpoD homologs of Streptomyces coelicolor A3(2) were cloned and sequenced. A homologous portion with 13 amino acids was found in the rpoD genes of S. coelicolor A3(2), E. coli, and B. subtilis and was named the "rpoD box."〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tanaka, K -- Shiina, T -- Takahashi, H -- New York, N.Y. -- Science. 1988 Nov 18;242(4881):1040-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Applied Microbiology, University of Tokyo, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3194753" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Bacteria/*genetics ; DNA Probes ; DNA, Bacterial/genetics ; DNA-Binding Proteins/*genetics ; *Genes, Bacterial ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Sequence Homology, Nucleic Acid ; Sigma Factor/*genetics ; Transcription Factors/*genetics
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    Wound macrophages express TGF-alpha and other growth factors in vivo: analysis by mRNA phenotyping (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-08-05
    Description: The presence of macrophages is required for the regeneration of many cell types during wound healing. Macrophages have been reported to express a wide range of mitogenic factors and cytokines, but none of these factors has been shown in vivo to sustain all the wound-healing processes. It has been suggested that transforming growth factor-alpha (TGF-alpha) may mediate angiogenesis, epidermal regrowth, and formation of granulation tissue in vivo. Macrophages isolated from a wound site, and not exposed to cell culture conditions, expressed messenger RNA transcripts for TGF-alpha, TGF-beta, platelet-derived growth factor A-chain, and insulin-like growth factor-1. The expression of these transcripts was determined by a novel method for RNA analysis in which low numbers of mouse macrophages were isolated from wound cylinders, their RNA was purified and reverse-transcribed, and the complementary DNA was amplified in a polymerase chain reaction primed with growth factor sequence-specific primers. This single-cell RNA phenotyping procedure is rapid and has the potential for quantification, and mRNA transcripts from a single cell or a few cells can be unambiguously demonstrated, with the simultaneous analysis of several mRNA species. Macrophages from wounds expressed TGF-alpha antigen, and wound fluids contained TGF-alpha. Elicited macrophages in culture also expressed TGF-alpha transcripts and polypeptide in a time-dependent manner after stimulation with modified low-density lipoproteins and lipopolysaccharide endotoxin, which are characteristic of the activators found in injured tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rappolee, D A -- Mark, D -- Banda, M J -- Werb, Z -- AR 32746/AR/NIAMS NIH HHS/ -- GM 27345/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Aug 5;241(4866):708-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Radiobiology and Environmental Health, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3041594" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; DNA/genetics ; Enzyme-Linked Immunosorbent Assay ; Epidermal Growth Factor/biosynthesis/genetics ; Fibroblast Growth Factors/biosynthesis/genetics ; Fibroblasts/metabolism ; Fluorescent Antibody Technique ; Growth Substances/*biosynthesis/genetics ; Insulin-Like Growth Factor I/biosynthesis/genetics ; Macrophages/*metabolism ; Male ; Mice ; Nucleic Acid Hybridization ; *Peptide Biosynthesis ; Peptides/genetics ; Platelet-Derived Growth Factor/biosynthesis/genetics ; Protein Biosynthesis ; RNA, Messenger/*biosynthesis ; Rabbits ; Transcription, Genetic ; Transforming Growth Factors ; *Wound Healing ; Wounds and Injuries/*pathology
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    Coding of two sphingolipid activator proteins (SAP-1 and SAP-2) by same genetic locus (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-08-26
    Description: Several complementary DNAs (cDNAs) coding for sphingolipid activator protein-2 (SAP-2) were isolated from a lambda gt-11 human hepatoma library by means of polyclonal antibodies. The nucleotide sequence of the largest cDNA was colinear with the derived amino acid sequence of SAP-2 and with the nucleotide sequence of the cDNA coding for the 70-kilodalton precursor of SAP-1 (SAP precursor cDNA). The coding sequence for mature SAP-2 was located 3' to that coding for SAP-1 in the SAP precursor cDNA. Both SAP-1 and SAP-2 appeared to be derived by proteolytic processing from a common precursor that is coded by a genetic locus on human chromosome 10. Two other domains similar to SAP-1 and SAP-2 were also identified in SAP precursor protein. Each of the four domains was approximately 80 amino acid residues long, had nearly identical placement of cysteine residues, potential glycosylation sites, and proline residues. Each domain also contained internal amino acid sequences capable of forming amphipathic helices separated by helix breakers to give a cylindrical hydrophobic domain that is probably stabilized by disulfide bridges. Protein immunoblotting experiments indicated that SAP precursor protein (70 kilodaltons) as well as immunoreactive SAP-like proteins of intermediate sizes (65, 50, and 31 kilodaltons) are present in most human tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Brien, J S -- Kretz, K A -- Dewji, N -- Wenger, D A -- Esch, F -- Fluharty, A L -- DK 38795/DK/NIDDK NIH HHS/ -- HD 18983/HD/NICHD NIH HHS/ -- NS 08682/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1988 Aug 26;241(4869):1098-101.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosciences, 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/2842863" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Carcinoma, Hepatocellular/analysis ; Chromosome Mapping ; Chromosomes, Human, Pair 10 ; DNA/genetics/isolation & purification ; Glycoproteins/analysis/*genetics ; Humans ; Liver Neoplasms/analysis ; Male ; Mice ; Mice, Nude ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Protein Conformation ; Protein Precursors/analysis/genetics ; Protein Processing, Post-Translational ; Rats ; Saposins ; Sphingolipid Activator Proteins ; Tissue Distribution
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    Molecular cloning of the zeta chain of the T cell antigen receptor (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-02-26
    Description: The T cell antigen receptor is a multi-subunit receptor complex present on the surface of all mature and many developing T cells. It consists of clonotypic heterodimers noncovalently linked to five invariant chains that are encoded by four genes and referred to as the CD3 complex. The CD3 gamma, delta, and epsilon chains have been molecularly characterized. In this report the molecular cloning of a complementary DNA encoding the zeta chain of the murine T cell antigen receptor is described. The predicted protein sequence of the zeta chain suggests a structure distinct from those of any of the previously described receptor subunits.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weissman, A M -- Baniyash, M -- Hou, D -- Samelson, L E -- Burgess, W H -- Klausner, R D -- New York, N.Y. -- Science. 1988 Feb 26;239(4843):1018-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3278377" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Membrane/metabolism ; Chromatography, High Pressure Liquid ; *Cloning, Molecular ; Cyanogen Bromide ; DNA/genetics ; Electrophoresis, Polyacrylamide Gel ; Immunosorbent Techniques ; Macromolecular Substances ; *Membrane Proteins ; Mice ; Molecular Sequence Data ; Molecular Weight ; Nucleic Acid Hybridization ; Peptide Fragments ; Protein Biosynthesis ; RNA, Messenger/genetics ; Receptors, Antigen, T-Cell/*genetics ; T-Lymphocytes/analysis ; Transcription, Genetic ; Tumor Cells, Cultured
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    Developmental expression of PDGF, TGF-alpha, and TGF-beta genes in preimplantation mouse embryos (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-09-30
    Description: Control of growth and differentiation during mammalian embryogenesis may be regulated by growth factors from embryonic or maternal sources. With the use of single-cell messenger RNA phenotyping, the simultaneous expression of growth factor transcripts in single or small numbers of preimplantation mouse embryos was examined. Transcripts for platelet-derived growth factor A chain (PDGF-A), transforming growth factor (TGF)-alpha, and TGF-beta 1, but not for four other growth factors, were found in whole blastocysts. TGF-alpha, TGF-beta 1, and PDGF antigens were detected in blastocysts by immunocytochemistry. Both PDGF-A and TGF-alpha were detected as maternal transcripts in the unfertilized ovulated oocyte, and again in blastocysts. TGF-beta 1 transcripts appeared only after fertilization. The expression of a subset of growth factors in mouse blastocysts suggests a role for these factors in the growth and differentiation of early mammalian embryos.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rappolee, D A -- Brenner, C A -- Schultz, R -- Mark, D -- Werb, Z -- 5T32 ES07106/ES/NIEHS NIH HHS/ -- HD22681/HD/NICHD NIH HHS/ -- HD23539/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 30;241(4874):1823-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Radiobiology and Environmental Health, University of California, San Francisco 94143-0750.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175624" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/*physiology ; Cleavage Stage, Ovum/physiology ; Embryonic Development ; Female ; Gene Expression Regulation ; Growth Substances/*genetics ; Mice ; Oocytes/physiology ; Platelet-Derived Growth Factor/*genetics ; Pregnancy ; RNA, Messenger/genetics ; Transcription, Genetic ; Transforming Growth Factors/*genetics
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    Dynamic changes in inhibin messenger RNAs in rat ovarian follicles during the reproductive cycle (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-03-11
    Description: The alterations in morphology and function of the ovarian follicle as it matures, ovulates, and becomes a corpus luteum are dramatic. A variety of steroid and polypeptide hormones influence these processes, and the ovary in turn produces specific hormonal signals for endocrine regulation. One such signal is inhibin, a heterodimeric protein that suppresses the secretion of follicle-stimulating hormone from pituitary gonadotrophs. Rat inhibin complementary DNA probes have been used to examine the levels and distribution of inhibin alpha-and beta A-subunit messenger RNAs in the ovaries of cycling animals. Striking, dynamic changes have been found in inhibin messenger RNA accumulation during the developmental maturation of the ovarian follicle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Woodruff, T K -- D'Agostino, J -- Schwartz, N B -- Mayo, K E -- HD07504/HD/NICHD NIH HHS/ -- HD21921/HD/NICHD NIH HHS/ -- P01 HD021921/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 11;239(4845):1296-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Molecular Biology and Cell Biology, Northwestern University, Evanston, IL 60208.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3125611" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Estrus ; Female ; Follicle Stimulating Hormone/blood ; Inhibins/*genetics ; Luteinizing Hormone/blood ; Macromolecular Substances ; Nucleic Acid Hybridization ; Ovarian Follicle/*physiology ; Ovary/physiology ; RNA, Messenger/*genetics/metabolism ; Rats
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    Gene encoding the beta subunit of S100 protein is on chromosome 21: implications for Down syndrome (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-03-11
    Description: S100 protein is a calcium-binding protein found predominantly in the vertebrate nervous system. Genomic and complementary DNA probes were used in conjunction with a panel of rodent-human somatic cell hybrids to assign the gene for the beta subunit of S100 protein to the distal half of the long arm of human chromosome 21. This gene was identified as a candidate sequence which, when expressed in the trisomic state, may underlie the neurologic disturbances in Down syndrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allore, R -- O'Hanlon, D -- Price, R -- Neilson, K -- Willard, H F -- Cox, D R -- Marks, A -- Dunn, R J -- 140-17001/PHS HHS/ -- New York, N.Y. -- Science. 1988 Mar 11;239(4845):1311-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Genetics, University of Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2964086" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosome Mapping ; *Chromosomes, Human, Pair 21 ; Cloning, Molecular ; Down Syndrome/*genetics ; Humans ; Macromolecular Substances ; Nucleic Acid Hybridization ; S100 Proteins/*genetics
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    The cellular src gene product regulates junctional cell-to-cell communication (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-01-22
    Description: Overexpression of the cellular src gene in NIH 3T3 cells causes reduction of cell-to-cell transmission of molecules in the 400- to 700-dalton range. This down-regulation of gap junctional communication correlates with the activity of the gene product, the protein tyrosine kinase pp60c-src. The down-regulation was enhanced by point mutation of Tyr527 (a site that is phosphorylated in pp60c-src and that inhibits kinase activity) or by substitution of the viral-src for the cellular-src carboxyl-terminal coding region. Mutation of Tyr416 (a site phosphorylated upon Tyr527 mutation) suppresses both the down-regulation of communication by Tyr527 mutation and that by gene overexpression. The regulation of communication by src may be important in the control of embryonic development and cellular growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Azarnia, R -- Reddy, S -- Kmiecik, T E -- Shalloway, D -- Loewenstein, W R -- CA-14464/CA/NCI NIH HHS/ -- CA-32317/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Jan 22;239(4838):398-401.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, University of Miami School of Medicine, FL 33136.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2447651" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Communication ; Cell Line ; Cell Membrane Permeability ; Gene Expression Regulation ; *Intercellular Junctions ; Mice ; Mutation ; Phosphorylation ; Plasmids ; Protein-Tyrosine Kinases/*genetics ; Proto-Oncogene Proteins/genetics/*physiology ; Proto-Oncogene Proteins pp60(c-src) ; Structure-Activity Relationship ; Transcription, Genetic ; Transfection ; Tyrosine/metabolism
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    Cone cell-specific genes expressed in retinoblastoma (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-04-01
    Description: Retinoblastoma, an intraocular tumor that occurs in children, has long been regarded, on the basis of morphological criteria, as a malignancy of the photoreceptor cell lineage. Here it is shown that when this tumor is grown in vitro, the cells express highly specialized photoreceptor cell genes. Transcripts for the transducin alpha subunit, TC alpha, which is specific to the cone cell, as well as transcripts for the red or green cone cell photopigment, were found in seven out of seven low-passage retinoblastoma cell lines. No marker genes specific to rod cell were expressed, suggesting that retinoblastoma has a cone cell lineage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bogenmann, E -- Lochrie, M A -- Simon, M I -- EY04950/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1988 Apr 1;240(4848):76-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology Oncology, Childrens Hospital of Los Angeles, CA 90027.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2451289" target="_blank"〉PubMed〈/a〉
    Keywords: DNA/genetics ; Gene Expression Regulation ; Humans ; Membrane Proteins/*genetics ; Nucleic Acid Hybridization ; Photoreceptor Cells/*metabolism ; RNA/genetics ; Retinoblastoma/*genetics ; Transcription, Genetic ; Transducin ; Tumor Cells, Cultured
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    A general method for the chromosomal amplification of genes in yeast (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-01-15
    Description: The yeast retrotransposon Ty can be used to insert multiple copies of a gene at new sites in the genome. The gene of interest is inserted into a GALI-Ty fusion construct; the entire "amplification cassette" is then introduced into yeast on a high copy number plasmid vector. Transposition of the Ty element carrying the gene occurs at multiple sites in the genome. Two genes, a bacterial neomycin phosphotransferase gene and the yeast TRPl gene, were amplified in this way. Although the amplified genes were about 1 kilobase in length, they were amplified to about the same extent as a 40-base pair segment. The benefit of this "shotgun" approach is that amplification can be achieved in one set of manipulations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boeke, J D -- Xu, H -- Fink, G R -- GM35010/GM/NIGMS NIH HHS/ -- GM36481/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jan 15;239(4837):280-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2827308" target="_blank"〉PubMed〈/a〉
    Keywords: DNA Transposable Elements ; DNA, Bacterial/genetics ; DNA, Fungal/genetics ; DNA, Recombinant ; *Genes, Fungal ; Kanamycin Kinase ; *Nucleic Acid Amplification Techniques ; Nucleic Acid Hybridization ; Phosphotransferases/genetics ; Plasmids ; Promoter Regions, Genetic ; Saccharomyces cerevisiae/*genetics ; Transcription, Genetic ; Transformation, Genetic
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    One factor recognizes the liver-specific enhancers in alpha 1-antitrypsin and transthyretin genes (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-02-12
    Description: Four different regulatory sites required for transcriptional stimulation by the enhancers of two unrelated liver-specific genes alpha 1-antitrypsin and transthyretin appear to bind the same nuclear protein that is found mainly in the liver. Such proteins may provide a basis for a coordinated, hepatocyte-specific control of gene transcription.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grayson, D R -- Costa, R H -- Xanthopoulos, K G -- Darnell, J E -- CA 160006-14/CA/NCI NIH HHS/ -- CA 18213-11/CA/NCI NIH HHS/ -- GM 1066-02/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1988 Feb 12;239(4841 Pt 1):786-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3257586" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Enhancer Elements, Genetic ; Gene Expression Regulation ; *Genes ; Genes, Regulator ; Liver/*metabolism ; Mice ; Mutation ; Nuclear Proteins/*physiology ; Prealbumin/*genetics ; *Transcription, Genetic ; alpha 1-Antitrypsin/*genetics
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    Virus-specific splicing inhibitor in extracts from cells infected with HIV-1 (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-09-16
    Description: Human immunodeficiency virus type 1 (HIV-1), in contrast with most other retroviruses, encodes trans-regulatory proteins for virus gene expression. It is shown in this study, by means of an in vitro splicing system, that nuclear extracts obtained from cells infected with HIV-1 contain a factor (or factors) that specifically inhibits splicing of a synthetic SP6/HIV pre-messenger RNA (pre-mRNA)-containing donor and acceptor splice sites in the coding region for the envelope protein. It is also shown that the SP6/HIV pre-mRNA is not capable of assembly in a ribonucleoprotein complex, spliceosome, in extracts from infected cells. These findings raise the possibility that specific inhibition of pre-mRNA splicing in the envelope protein coding region by HIV-1 trans-regulatory factors might be one control mechanism for efficient production of structural viral proteins and virion assembly.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gutman, D -- Goldenberg, C J -- AI-24479/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 16;241(4872):1492-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of Miami School of Medicine, FL 33101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3047873" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Nucleus/physiology ; Cloning, Molecular ; DNA Mutational Analysis ; Gene Expression Regulation ; HIV/*genetics ; HeLa Cells ; Humans ; RNA Processing, Post-Transcriptional ; *RNA Splicing ; RNA, Viral/*genetics ; Ribonucleoproteins/physiology
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    Hormone-sensitive lipase: sequence, expression, and chromosomal localization to 19 cent-q13.3 (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-09-16
    Description: Hormone-sensitive lipase, a key enzyme in fatty acid mobilization, overall energy homeostasis, and possibly steroidogenesis, is acutely controlled through reversible phosphorylation by catecholamines and insulin. The 757-amino acid sequence predicted from a cloned rat adipocyte complementary DNA showed no homology with any other known lipase or protein. The activity-controlling phosphorylation site was localized to Ser563 in a markedly hydrophilic domain, and a lipid-binding consensus site was tentatively identified. One or several messenger RNA species (3.3, 3.5, or 3.9 kilobases) were expressed in adipose and steroidogenic tissues and heart and skeletal muscle. The human hormone-sensitive lipase gene mapped to chromosome 19 cent-q13.3.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holm, C -- Kirchgessner, T G -- Svenson, K L -- Fredrikson, G -- Nilsson, S -- Miller, C G -- Shively, J E -- Heinzmann, C -- Sparkes, R S -- Mohandas, T -- New York, N.Y. -- Science. 1988 Sep 16;241(4872):1503-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical and Physiological Chemistry, University of Lund, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3420405" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Chromosome Mapping ; *Chromosomes, Human, Pair 19 ; Cloning, Molecular ; DNA/genetics ; Gene Expression Regulation ; Humans ; Molecular Sequence Data ; Rats ; Sterol Esterase/*genetics
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  • 45
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    Molecular characterization of a functional cDNA encoding the serotonin 1c receptor (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-29
    Description: Neurons that release serotonin as a neurotransmitter project to most regions of the central and peripheral nervous system and mediate diverse neural functions. The physiological effects of serotonin are initiated by the activation of multiple, distinct receptor subtypes. Cloning in RNA expression vectors was combined with a sensitive electrophysiological assay in Xenopus oocytes in order to isolate a functional cDNA clone encoding the 5HTlc serotonin receptor. Injection of RNA transcribed in vitro from this clone into Xenopus oocytes elicits serotonin sensitivity. Mouse fibroblasts transformed with this clone bind serotonin agonists and antagonists and exhibit an increase in intracellular Ca2+ concentrations in response to serotonin. The sequence of the 5HTlc receptor reveals that it belongs to the family of G protein-coupled receptors, which are thought to traverse the cytoplasmic membrane seven times. Moreover, in situ hybridization and RNA blot analysis indicate that the 5HTlc receptor is expressed in neurons in many regions of the central nervous system and suggest that this subclass of receptor may mediate many of the central actions of serotonin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Julius, D -- MacDermott, A B -- Axel, R -- Jessell, T M -- New York, N.Y. -- Science. 1988 Jul 29;241(4865):558-64.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biophysics, College of Physicians and Surgeons, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3399891" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cloning, Molecular ; DNA/genetics ; Fibroblasts/physiology ; Gene Expression Regulation ; Membrane Glycoproteins/genetics ; Molecular Sequence Data ; Oocytes/physiology ; Phosphoproteins/physiology ; Rats ; Receptors, Serotonin/*genetics ; Serotonin/*physiology ; Xenopus laevis
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    A ligase-mediated gene detection technique (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-08-26
    Description: An assay for the presence of given DNA sequences has been developed, based on the ability of two oligonucleotides to anneal immediately adjacent to each other on a complementary target DNA molecule. The two oligonucleotides are then joined covalently by the action of a DNA ligase, provided that the nucleotides at the junction are correctly base-paired. Thus single nucleotide substitutions can be distinguished. This strategy permits the rapid and standardized identification of single-copy gene sequences in genomic DNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Landegren, U -- Kaiser, R -- Sanders, J -- Hood, L -- New York, N.Y. -- Science. 1988 Aug 26;241(4869):1077-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena 91125.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3413476" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Line ; DNA/*analysis/genetics/metabolism ; DNA Ligases/*metabolism ; DNA, Recombinant/metabolism ; Fluorescent Dyes ; Globins/genetics ; Humans ; Molecular Sequence Data ; Nucleic Acid Denaturation ; Nucleic Acid Hybridization ; Polymorphism, Genetic ; Polynucleotide Ligases/*metabolism
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    Generation of cDNA probes directed by amino acid sequence: cloning of urate oxidase (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-03-11
    Description: Urate oxidase (E.C. 1.7.3.3) catalyzes the oxidation of uric acid to allantoin in most mammals except humans and certain primates. The amino-terminal amino acid sequence for porcine urate oxidase was determined and used in a novel procedure for generating complementary DNA (cDNA) probes to this amino acid sequence. The procedure is based on the polymerase chain reaction and utilizes mixed oligonucleotide primers complementary to the reverse translation products of an amino acid sequence. This rapid and simple cDNA cloning procedure is generally applicable and requires only a partial amino acid sequence. A cDNA probe developed by this procedure was used to isolate a full-length porcine urate oxidase cDNA and to demonstrate the presence of homologous genomic sequences in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, C C -- Wu, X W -- Gibbs, R A -- Cook, R G -- Muzny, D M -- Caskey, C T -- DK31428/DK/NIDDK NIH HHS/ -- GM34428/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Mar 11;239(4845):1288-91.〈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/3344434" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; *Cloning, Molecular ; DNA/*genetics ; Gene Amplification ; Liver/enzymology ; Mice ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Swine ; Urate Oxidase/*genetics
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    Inactivation of the retinoblastoma susceptibility gene in human breast cancers (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-08
    Description: Mutational inactivation of the retinoblastoma susceptibility (RB) gene, a recessive cancer gene, has been implicated in the genesis of retinoblastoma and certain other human neoplasms. This gene is now shown to be inactivated in two of nine human breast cancer cell lines examined. The RB gene of one cell line had a homozygous internal duplication of a 5-kilobase region containing exons 5 and 6. The RB messenger RNA transcript was correspondingly lengthened, and its translation was probably terminated prematurely due to a shifted reading frame. The other cell line had a homozygous deletion of the RB gene that removed the entire gene beyond exon 2. The RB gene product, pp110RB, was not detectable in either cell line by immuno-precipitation with specific antibodies. These findings are significant in relation to proposed genetic mechanisms of breast cancer formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, E Y -- To, H -- Shew, J Y -- Bookstein, R -- Scully, P -- Lee, W H -- CA39537/CA/NCI NIH HHS/ -- EY00278/EY/NEI NIH HHS/ -- EY05758/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 8;241(4862):218-21.〈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/3388033" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*genetics ; Chromosomes, Human, Pair 13 ; DNA, Neoplasm/*genetics ; Gene Expression Regulation ; Genes ; Humans ; Retinoblastoma/*genetics ; Tumor Cells, Cultured
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    Induction of gene amplification by arsenic (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-07-01
    Description: Arsenic is a well-established carcinogen in humans, but there is little evidence for its carcinogenicity in animals and it is inactive as an initiator or tumor promoter in two-stage models of carcinogenicity in mice. Two arsenic salts (sodium arsenite and sodium arsenate) induced a high frequency of methotrexate-resistant 3T6 cells, which were shown to have amplified copies of the dihydrofolate reductase gene. The ability of arsenic to induce gene amplification may relate to its carcinogenic effects in humans since amplification of oncogenes is observed in many human tumors. The inability of arsenic to induce gene mutations may relate to the negative results of arsenic in long-term animal studies and suggests that these experiments may not detect some environmental agents that act late in the carcinogenic process in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, T C -- Tanaka, N -- Lamb, P W -- Gilmer, T M -- Barrett, J C -- New York, N.Y. -- Science. 1988 Jul 1;241(4861):79-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3388020" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arsenates/*pharmacology ; Arsenic/*pharmacology ; *Arsenites ; Cell Line ; DNA/genetics ; Drug Resistance ; Gene Amplification/*drug effects ; Humans ; Methotrexate ; Mice ; Neoplasms, Experimental/chemically induced/genetics ; Nucleic Acid Hybridization ; Oncogenes ; *Sodium Compounds ; Tetrahydrofolate Dehydrogenase/*genetics
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    Development of disease and virus recovery in transgenic mice containing HIV proviral DNA (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-12-23
    Description: Transgenic mice containing intact copies of the human immunodeficiency virus (HIV) proviral DNA were constructed. Founder animals were not viremic for HIV and remained healthy during a 9-month observation period. After being mated with nontransgenic animals, one founder mouse (No. 13) gave rise to F1 progeny that developed a disease syndrome characterized by marked epidermal hyperplasia, lymphadenopathy, splenomegaly, pulmonary lymphoid infiltrates, growth retardation, and death by day 25 of life. Infectious HIV, indistinguishable from parental virus by immunoblot analysis, was recovered from the spleen, lymph nodes, and skin of five of five affected animals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leonard, J M -- Abramczuk, J W -- Pezen, D S -- Rutledge, R -- Belcher, J H -- Hakim, F -- Shearer, G -- Lamperth, L -- Travis, W -- Fredrickson, T -- New York, N.Y. -- Science. 1988 Dec 23;242(4886):1665-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3201255" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology/*microbiology/pathology ; Animals ; DNA Probes ; *DNA, Viral/analysis ; *Disease Models, Animal ; Epidermis/pathology ; HIV/*genetics/immunology/isolation & purification ; HIV Antibodies/analysis ; Lung/pathology ; Lymph Nodes/microbiology/pathology ; Mice ; Mice, Transgenic ; Nucleic Acid Hybridization ; Skin/microbiology/pathology ; Spleen/microbiology/pathology
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    Heterologous expression of excitability proteins: route to more specific drugs? (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-08-26
    Description: Many clinically important drugs act on the intrinsic membrane proteins (ion channels, receptors, and ion pumps) that control cell excitability. A major goal of pharmacology has been to develop drugs that are more specific for a particular subtype of excitability molecule. DNA cloning has revealed that many excitability proteins are encoded by multigene families and that the diversity of previously recognized pharmacological subtypes is matched, and probably surpassed, by the diversity of messenger RNAs that encode excitability molecules. In general, the diverse subtypes retain their properties when the excitability proteins are expressed in foreign cells such as oocytes and mammalian cell lines. Such heterologous expression may therefore become a tool for testing drugs against specific subtypes. In a systematic research program to exploit this possibility, major considerations include alternative processing of messenger RNA for excitability proteins, coupling to second-messenger systems, and expression of enough protein to provide material for structural studies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lester, H A -- New York, N.Y. -- Science. 1988 Aug 26;241(4869):1057-63.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena 91125.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2457947" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Physiological Phenomena ; Cloning, Molecular ; Drug-Related Side Effects and Adverse Reactions ; GTP-Binding Proteins/genetics/physiology ; Gene Expression Regulation ; *Genetic Variation ; Humans ; Ion Channels/drug effects/physiology ; Membrane Proteins/*genetics/physiology ; *Pharmacology ; Receptors, Cell Surface/drug effects/genetics/physiology
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    DNA clock conflict continues (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-09-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1988 Sep 30;241(4874):1756-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175618" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Base Sequence ; *Biological Evolution ; DNA/*genetics ; Hominidae/*genetics ; Humans ; Nucleic Acid Hybridization ; *Sequence Homology, Nucleic Acid
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    Distinct cloned class II MHC DNA binding proteins recognize the X box transcription element (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-10-07
    Description: The class II (Ia) major histocompatibility complex (MHC) antigens are a family of integral membrane proteins whose expression is limited to certain cell types. A pair of consensus sequences, X and Y, is found upstream of all class II genes, and deletion of each of these sequences eliminates expression of transfected genes. Furthermore, the absence of a specific X box binding protein in patients with severe combined immunodeficiency disease whose cells lack class II suggests an important role for these proteins in class II regulation. Here, the cloning of two lambda gt11 complementary DNAs encoding DNA binding proteins (murine X box binding proteins lambda mXBP and lambda mXBP-2) is reported. Both phage-encoded fusion proteins bind specifically to the X box of the A alpha, but not to E alpha or E beta class II genes. These two independent isolates do not cross-hybridize. The lambda mXBP complementary DNA hybridizes to two RNA species, 6.2 and 3.0 kilobases in mouse, that are expressed in both Ia positive and Ia negative cells. By means of DNA blot analysis with the lambda mXBP complementary DNA insert and probes generated from each end of this complementary DNA insert, lambda mXBP was found to arise from a multigene family. These data illustrate the high degree of complexity in the transcriptional control of this coordinately regulated gene family.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liou, H C -- Boothby, M R -- Glimcher, L H -- New York, N.Y. -- Science. 1988 Oct 7;242(4875):69-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Harvard School of Public Health, Boston, Massachusetts 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3140376" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; *Cloning, Molecular ; DNA-Binding Proteins/*genetics ; Gene Expression Regulation ; *Genes ; *Genes, MHC Class II ; Humans ; Mice ; Molecular Sequence Data ; *Transcription, Genetic ; Transfection
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    Apolipoprotein E: cholesterol transport protein with expanding role in cell biology (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-04-29
    Description: Apolipoprotein E is a plasma protein that serves as a ligand for low density lipoprotein receptors and, through its interaction with these receptors, participates in the transport of cholesterol and other lipids among various cells of the body. A mutant form of apolipoprotein E that is defective in binding to low density lipoprotein receptors is associated with familial type III hyperlipoproteinemia, a genetic disorder characterized by elevated plasma cholesterol levels and accelerated coronary artery disease. Apolipoprotein E is synthesized in various organs, including liver, brain, spleen, and kidney, and is present in high concentrations in interstitial fluid, where it appears to participate in cholesterol redistribution from cells with excess cholesterol to those requiring cholesterol. Apolipo-protein E also appears to be involved in the repair response to tissue injury; for example, markedly increased amounts of apolipoprotein E are found at sites of peripheral nerve injury and regeneration. Other functions of apolipoprotein E, unrelated to lipid transport, are becoming known, including immunoregulation and modulation of cell growth and differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mahley, R W -- New York, N.Y. -- Science. 1988 Apr 29;240(4852):622-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gladstone Foundation Laboratories for Cardiovascular Disease, University of California, San Francisco 94140-0608.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3283935" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Apolipoproteins E/genetics/*physiology ; Biological Transport ; Cholesterol/*metabolism ; Gene Expression Regulation ; Humans ; Hyperlipoproteinemia Type III/genetics/metabolism ; Immunity ; Lipid Metabolism ; Molecular Sequence Data ; Polymorphism, Genetic ; Protein Conformation ; Receptors, LDL/metabolism
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    Research on bacteria in the mainstream of biology (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-06-10
    Description: The study of the genetics, biochemistry, and physiology of bacteria during the last 40 years has provided the concepts and methods for the study of cells of all types at the molecular level. Although much is already known about the mechanisms bacteria use to regulate the expression of their genes, a great deal more remains to be discovered that will have relevance to both prokaryotic and eukaryotic cells. Similarly, the study in bacteria of the transactions of DNA, of the synthesis and function of the cell membrane, of differentiation, and of the interaction with eukaryotic cells will undoubtedly produce results of general importance. The advantages of using bacteria for these studies include their simple noncompartmented structure, the accessibility of their genetic material, and the possibility of correlating the expression of a gene in the intact cell with its expression in a system composed of highly purified components. Finally, the comparative study of a wide variety of microorganisms may result in a better understanding of the evolution of prokaryotes and eukaryotes and lead to a comprehensive theory of cell biology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Magasanik, B -- AM-13894/AM/NIADDK NIH HHS/ -- GM-07446/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 10;240(4858):1435-9.〈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/3287618" target="_blank"〉PubMed〈/a〉
    Keywords: *Bacteria/genetics ; Escherichia coli/genetics ; Gene Expression Regulation ; Models, Biological ; Models, Genetic ; *Research Design
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    Movement of the X chromosome in epilepsy (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-12-23
    Description: The position of selected chromosomes was assessed in samples of normal and epileptic human cortex with biotinylated probes specific for individual chromosome domains. Optical sectioning provided a rapid method for three-dimensional resolution of in situ hybridization signals in interphase cells, and solid models were reconstructed from digitized images for detailed rotational studies. There was a dramatic repositioning of the X chromosome in neurons of both males and females in electrophysiologically defined seizure foci. Other chromosomes (1, 9, and Y) showed more subtle positional changes. Specifically altered nuclear patterns involving the X chromosome may become established and create the genetic memory for intractable seizure activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Borden, J -- Manuelidis, L -- CA15044/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Dec 23;242(4886):1687-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Yale University School of Medicine, New Haven, CT 06510.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3201257" target="_blank"〉PubMed〈/a〉
    Keywords: Astrocytes/ultrastructure ; Cell Nucleolus/ultrastructure ; Cell Nucleus/ultrastructure ; Cerebral Cortex/ultrastructure ; DNA Probes ; Epilepsy/*genetics/physiopathology ; Female ; Humans ; Image Processing, Computer-Assisted ; Male ; Microscopy, Electron ; Neurons/ultrastructure ; Nuclear Envelope/ultrastructure ; Nucleic Acid Hybridization ; *X Chromosome
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    Expression of the murine Duchenne muscular dystrophy gene in muscle and brain (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-03-18
    Description: Complementary DNA clones were isolated that represent the 5' terminal 2.5 kilobases of the murine Duchenne muscular dystrophy (Dmd) messenger RNA (mRNA). Mouse Dmd mRNA was detectable in skeletal and cardiac muscle and at a level approximately 90 percent lower in brain. Dmd mRNA is also present, but at much lower than normal levels, in both the muscle and brain of three different strains of dystrophic mdx mice. The identification of Dmd mRNA in brain raises the possibility of a relation between human Duchenne muscular dystrophy (DMD) gene expression and the mental retardation found in some DMD males. These results also provide evidence that the mdx mutations are allelic variants of mouse Dmd gene mutations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chamberlain, J S -- Pearlman, J A -- Muzny, D M -- Gibbs, R A -- Ranier, J E -- Caskey, C T -- Reeves, A A -- New York, N.Y. -- Science. 1988 Mar 18;239(4846):1416-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular Genetics, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3347839" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; DNA/genetics ; DNA, Recombinant ; *Gene Expression Regulation ; Intellectual Disability/genetics ; Mice ; Mice, Inbred ICR ; Mice, Mutant Strains ; Muscles/*metabolism ; Muscular Dystrophy, Animal/*genetics ; Mutation ; Nucleic Acid Hybridization ; RNA, Messenger/metabolism ; Ribonuclease, Pancreatic/metabolism
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    Expression and function of the segmentation gene fushi tarazu during Drosophila neurogenesis (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-01-08
    Description: Segmentation genes control cell identities during early pattern formation in Drosophila. One of these genes, fushi tarazu (ftz), is now shown also to control cell fate during neurogenesis. Early in development, ftz is expressed in a striped pattern at the blastoderm stage. Later, it is transiently expressed in a specific subset of neuronal precursor cells, neurons (such as aCC, pCC, RP1, and RP2), and glia in the developing central nervous system (CNS). The function of ftz in the CNS was determined by creating ftz mutant embryos that express ftz in the blastoderm stripes but not in the CNS. In the absence of ftz CNS expression, some neurons appear normal (for example, the aCC, pCC, and RP1), whereas the RP2 neuron extends its growth cone along an abnormal pathway, mimicking its sibling (RP1), suggesting a transformation in neuronal identity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Doe, C Q -- Hiromi, Y -- Gehring, W J -- Goodman, C S -- New York, N.Y. -- Science. 1988 Jan 8;239(4836):170-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2892267" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Drosophila melanogaster/*embryology/genetics ; Gene Expression Regulation ; Genes, Homeobox ; Morphogenesis ; Nervous System/*embryology ; Neuroglia/cytology/physiology ; Neurons/cytology/physiology
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    Coordinate hormonal and synaptic regulation of vasopressin messenger RNA (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-08-19
    Description: Previous studies have shown that adrenalectomy augments arginine vasopressin (AVP) messenger RNA levels in the adult paraventricular nucleus. It is now demonstrated that unilateral lesions in the lateral septal nucleus enhance the adrenalectomy-induced expression of AVP mRNA. This effect was entirely ipsilateral to the lesion and most prominent in the rostral paraventricular nucleus and related nuclei. Moreover, AVP and AVP mRNA were found to be colocalized with oxytocin in a few neurons. These results indicate that mRNA expression is modulated by synaptic influences and raise the possibility that synaptically mediated selection of neuronal phenotypes is a dynamic feature of the mature central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baldino, F Jr -- O'Kane, T M -- Fitzpatrick-McElligott, S -- Wolfson, B -- New York, N.Y. -- Science. 1988 Aug 19;241(4868):978-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Products Department, E. I. du Pont de Nemours & Company, Wilmington, DE 19898.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3406747" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenalectomy ; Animals ; Gene Expression Regulation ; Male ; Neurons/analysis/*physiology ; Oxytocin/analysis ; Paraventricular Hypothalamic Nucleus/*physiology ; Phenotype ; RNA, Messenger/analysis/*biosynthesis ; Rats ; Rats, Inbred Strains ; Synapses/*physiology ; Vasopressins/analysis/*genetics
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    Comparison of biological properties and transforming potential of human PDGF-A and PDGF-B chains (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-09-09
    Description: Human platelet-derived growth factor (PDGF) consists of two distinct but related polypeptide chains designated PDGF-A and PDGF-B. The gene encoding PDGF-B has given rise to the v-sis oncogene. In the present study the transforming activities of PDGF-A and PDGF-B genes are compared. The PDGF-A chain gene is markedly less efficient in inducing transformation than the PDGF-B gene under the influence of the same promoter. There are significant differences in the secretory and growth stimulating properties of the two chains. These properties appear to account for the much more potent transforming ability of the PDGF-B gene. These findings provide insights into biologic properties of a growth factor responsible for potent autocrine stimulation of abnormal cell proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beckmann, M P -- Betsholtz, C -- Heldin, C H -- Westermark, B -- Di Marco, E -- Di Fiore, P P -- Robbins, K C -- Aaronson, S A -- New York, N.Y. -- Science. 1988 Sep 9;241(4871):1346-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2842868" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Compartmentation ; Cell Line ; *Cell Transformation, Neoplastic ; Gene Expression Regulation ; Immunologic Techniques ; Mice ; Molecular Weight ; Platelet-Derived Growth Factor/*physiology ; Proto-Oncogene Proteins/*physiology ; Receptors, Cell Surface/*physiology ; Receptors, Platelet-Derived Growth Factor ; Solubility
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    Site-specific oligonucleotide binding represses transcription of the human c-myc gene in vitro (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-22
    Description: A 27-base-long DNA oligonucleotide was designed that binds to duplex DNA at a single site within the 5' end of the human c-myc gene, 115 base pairs upstream from the transcription origin P1. On the basis of the physical properties of its bound complex, it was concluded that the oligonucleotide forms a colinear triplex with the duplex binding site. By means of an in vitro assay system, it was possible to show a correlation between triplex formation at -115 base pairs and repression of c-myc transcription. The possibility is discussed that triplex formation (site-specific RNA binding to a DNA duplex) could serve as the basis for an alternative program of gene control in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cooney, M -- Czernuszewicz, G -- Postel, E H -- Flint, S J -- Hogan, M E -- New York, N.Y. -- Science. 1988 Jul 22;241(4864):456-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Princeton University, NJ 08544.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3293213" target="_blank"〉PubMed〈/a〉
    Keywords: Electrophoresis ; Gene Expression Regulation ; Humans ; In Vitro Techniques ; Nucleic Acid Hybridization ; Oligodeoxyribonucleotides/*pharmacology ; Proto-Oncogene Proteins/*genetics ; *Proto-Oncogenes ; *Transcription, Genetic/drug effects
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    Evidence of estrogen receptors in normal human osteoblast-like cells (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-01
    Description: In seven strains of cultured normal human osteoblast-like cells, a mean of 1615 molecules of tritium-labeled 17 beta-estradiol per cell nucleus could be bound to specific nuclear sites. The nuclear binding of the labeled steroid was temperature-dependent, steroid-specific, saturable, and cell type-specific. These are characteristics of biologically active estrogen receptors. Pretreatment with 10 nanomolar estradiol in vitro increased the specific nuclear binding of progesterone in four of six cell strains, indicating an induction of functional progesterone receptors. RNA blot analysis demonstrated the presence of messenger RNA for the human estrogen receptor. The data suggest that estrogen acts directly on human bone cells through a classical estrogen receptor-mediated mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eriksen, E F -- Colvard, D S -- Berg, N J -- Graham, M L -- Mann, K G -- Spelsberg, T C -- Riggs, B L -- AG-04875/AG/NIA NIH HHS/ -- CA-90441/CA/NCI NIH HHS/ -- HD-9140/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 1;241(4861):84-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Endocrine Research Unit, Mayo Clinic, Rochester, MN 55905.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3388021" target="_blank"〉PubMed〈/a〉
    Keywords: Binding, Competitive ; Cell Nucleus/metabolism ; Cells, Cultured ; DNA/genetics ; Dexamethasone/metabolism ; Diethylstilbestrol/metabolism ; Estradiol/metabolism/pharmacology ; Humans ; Nucleic Acid Hybridization ; Osteoblasts/drug effects/*metabolism ; Progesterone/metabolism ; Promegestone/metabolism ; RNA, Messenger/metabolism ; Receptors, Estrogen/drug effects/genetics/*metabolism ; Receptors, Progesterone/drug effects/metabolism ; Tritium
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    Isotypic exclusion of gamma delta T cell receptors in transgenic mice bearing a rearranged beta-chain gene (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-08-26
    Description: The rearrangement of T cell antigen receptor beta- and gamma-chain gene segments was studied in transgenic mice that bear a functional beta-chain gene. Virtually all CD3-positive T cells derived from transgenic mice express beta chains containing the transgene-encoded V beta 8.2 variable region on their surfaces and do not express endogenous beta-chain variable regions. Expression of endogenous V beta genes is inhibited at the level of somatic recombination during thymic ontogeny. Furthermore, rearrangements of the TCR gamma-chain genes are also markedly inhibited in these transgenic animals. Hence expression of the TCR beta transgene has led to allelic exclusion of alpha beta receptors and isotypic exclusion of gamma delta T cell receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fenton, R G -- Marrack, P -- Kappler, J W -- Kanagawa, O -- Seidman, J G -- New York, N.Y. -- Science. 1988 Aug 26;241(4869):1089-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2970670" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Antibodies, Monoclonal ; Bacteriophage lambda/genetics ; Cloning, Molecular ; DNA, Recombinant ; Enhancer Elements, Genetic ; Gene Expression Regulation ; Genes, Immunoglobulin ; Immunoassay ; Immunoglobulin Heavy Chains/genetics ; Liver/analysis ; Mice ; Mice, Transgenic ; Ovalbumin/immunology ; Receptors, Antigen, T-Cell/*genetics ; Recombination, Genetic ; T-Lymphocytes/metabolism ; Thymus Gland/analysis
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    Estrogen binding, receptor mRNA, and biologic response in osteoblast-like osteosarcoma cells (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-01
    Description: High specific activity estradiol labeled with iodine-125 was used to detect approximately 200 saturable, high-affinity (dissociation constant approximately equal to 1.0 nM) nuclear binding sites in rat (ROS 17/2.8) and human (HOS TE85) clonal osteoblast-like osteosarcoma cells. Of the steroids tested, only testosterone exhibited significant cross-reactivity with estrogen binding. RNA blot analysis with a complementary DNA probe to the human estrogen receptor revealed putative receptor transcripts of 6 to 6.2 kilobases in both rat and human osteosarcoma cells. Type I procollagen and transforming growth factor-beta messenger RNA levels were enhanced in cultured human osteoblast-like cells treated with 1 nM estradiol. Thus, estrogen can act directly on osteoblasts by a receptor-mediated mechanism and thereby modulate the extracellular matrix and other proteins involved in the maintenance of skeletal mineralization and remodeling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Komm, B S -- Terpening, C M -- Benz, D J -- Graeme, K A -- Gallegos, A -- Korc, M -- Greene, G L -- O'Malley, B W -- Haussler, M R -- New York, N.Y. -- Science. 1988 Jul 1;241(4861):81-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Arizona College of Medicine, Tucson 85724.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3164526" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding, Competitive ; Cell Nucleus/metabolism ; DNA/genetics ; Estradiol/*metabolism/pharmacology ; Humans ; Iodine Radioisotopes ; Nucleic Acid Hybridization ; Osteoblasts/drug effects/*metabolism ; Osteosarcoma/*metabolism ; Peptides/genetics ; Procollagen/genetics ; RNA, Messenger/*metabolism ; Rats ; Receptors, Estrogen/genetics/*metabolism ; Transcription, Genetic ; Transforming Growth Factors ; Tumor Cells, Cultured
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    Mitogen-induced replication of woodchuck hepatitis virus in cultured peripheral blood lymphocytes (1988)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1988-09-02
    Description: Peripheral blood lymphocytes (PBLs) isolated from woodchucks chronically infected with the woodchuck hepatitis virus (WHV) carry low levels of nonreplicating WHV DNA. When PBLs from chronic carrier woodchucks were activated in culture with the generalized mitogen lipopolysaccharide (LPS), WHV DNA replication was initiated in cells obtained from one of three animals examined. Intracellular WHV core particles, containing WHV DNA replication intermediates, RNA/DNA hybrid molecules, and an active endogenous DNA polymerase, appeared 3 days after the start of LPS stimulation. After 5 to 7 days of LPS stimulation, WHV DNA-containing particles, which displayed the properties of intact, mature virions, were released into the culture medium. These studies provide evidence for reactivation of a latent WHV infection of circulating lymphoid cells and indicate that the presence of nonreplicating hepadnaviral DNA in lymphoid cells represents a potentially active infection following cellular activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Korba, B E -- Cote, P J -- Gerin, J L -- N01-AI-02651/AI/NIAID NIH HHS/ -- N01-AI-72623/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 2;241(4870):1213-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Virology and Immunology, Georgetown University Medical Center, Rockville, MD 20852.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3261887" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Centrifugation, Density Gradient ; Concanavalin A/pharmacology ; *DNA Replication ; Ducks/microbiology ; Hepatitis B virus/physiology ; Hepatitis Viruses/*physiology ; Hepatitis, Viral, Animal/*microbiology ; Interleukin-2/pharmacology ; Lipopolysaccharides/pharmacology ; Lymphocyte Activation ; Lymphocytes/*microbiology ; Marmota/*microbiology ; Mitogens/*pharmacology ; Nucleic Acid Hybridization ; Phytohemagglutinins/pharmacology ; Sciuridae/*microbiology ; *Virus Replication/*drug effects
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    Heterogeneity of glycine receptors and their messenger RNAs in rat brain and spinal cord (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-10-14
    Description: Messenger RNAs isolated from adult or newborn rat spinal cord were fractionated in a sucrose gradient. The fractions were injected into Xenopus oocytes to determine their potencies for expression of glycine receptors (GlyRs), which were then examined electrophysiologically. The sedimentation profiles disclosed two classes of GlyR mRNAs, one heavy and the other light. The adult spinal cord was rich in heavy GlyR mRNA, whereas the light GlyR mRNA was more abundant in neonatal spinal cord and in adult cerebral cortex. Glycine receptors encoded by heavy and light mRNAs of adult spinal cord showed some electrophysiological differences. Thus there are two types of GlyRs encoded by mRNAs of different sizes, and the expression of these mRNAs is developmentally regulated. A tissue- and age-dependent distribution of heterogeneous GlyR mRNAs may imply diverse roles of the GlyRs in neuronal function in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akagi, H -- Miledi, R -- R01-NS23284/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Oct 14;242(4876):270-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychobiology, University of California, Irvine 92717.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2845580" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Cell Membrane/physiology ; Centrifugation, Density Gradient ; Cerebral Cortex/*analysis ; DNA/genetics ; Electric Conductivity ; Glycine/pharmacology ; Nucleic Acid Hybridization ; Oocytes/drug effects/physiology ; RNA, Messenger/*genetics/isolation & purification ; Rats ; Receptors, Glycine ; Receptors, Neurotransmitter/*genetics/physiology ; Spinal Cord/*analysis ; Transcription, Genetic ; Xenopus laevis
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    Nef protein of HIV-1 is a transcriptional repressor of HIV-1 LTR (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-09-16
    Description: In studies of the genetics of human immunodeficiency virus type 1 (HIV-1), the product of the nef gene, formerly known as F, 3'-orf, or B-ORF, was a negative regulator of HIV-1 replication. Proviruses with mutations in the nef gene replicated better than their standard counterparts during transient expression, and the mutant virus maintained its enhanced replication even after serial passages in T lymphocytes. The nef protein trans-suppressed, in a dose-dependent manner, the replication of wild-type and nef mutant proviruses and the expression of reporter genes linked to the HIV-1 long terminal repeat (LTR). The repression induced by the nef protein was mediated by inhibition of transcription from the HIV-1 LTR, which contains a far upstream cis element (previously recognized to be a negative regulatory element) between 340 and 156 nucleotides upstream of the RNA initiation site.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ahmad, N -- Venkatesan, S -- New York, N.Y. -- Science. 1988 Sep 16;241(4872):1481-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3262235" target="_blank"〉PubMed〈/a〉
    Keywords: Gene Expression Regulation ; Gene Products, nef ; HIV/*genetics ; Regulatory Sequences, Nucleic Acid ; Repetitive Sequences, Nucleic Acid ; Repressor Proteins/*physiology ; Retroviridae Proteins/*physiology ; Transcription Factors/*physiology ; Transcription, Genetic ; Virus Replication ; nef Gene Products, Human Immunodeficiency Virus
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    Expression of the beta-nerve growth factor gene in hippocampal neurons (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-06-03
    Description: In situ hybridization with complementary DNA probes for nerve growth factor (NGF) was used to identify cells containing NGF messenger RNA in rat and mouse brain. The most intense labeling occurred in hippocampus, where hybridizing neurons were found in the dentate gyrus and the pyramidal cell layer. The neuronal identity of NGF mRNA-containing cells was further assessed by a loss of NGF-hybridizing mRNA in hippocampal areas where neurons had been destroyed by kainic acid or colchicine. RNA blot analysis also revealed a considerable decrease in the level of NGF mRNA in rat dentate gyrus after a lesion was produced by colchicine. This lesion also caused a decrease in the level of Thy-1 mRNA and an increase in the level of glial fibrillary acidic protein mRNA. Neuronal death was thus associated with the disappearance of NGF mRNA. These results suggest a synthesis of NGF by neurons in the brain and imply that, in hippocampus, NGF influences NGF-sensitive neurons through neuron-to-neuron interactions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ayer-LeLievre, C -- Olson, L -- Ebendal, T -- Seiger, A -- Persson, H -- New York, N.Y. -- Science. 1988 Jun 3;240(4857):1339-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Chemistry, Karolinska Institutet, Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2897715" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Surface/genetics ; Antigens, Thy-1 ; Colchicine/pharmacology ; Dna ; *Gene Expression Regulation ; Glial Fibrillary Acidic Protein/genetics ; Hippocampus/drug effects/*metabolism ; Kainic Acid/pharmacology ; Nerve Growth Factors/*genetics ; Neurons/*metabolism ; Nucleic Acid Hybridization ; RNA, Messenger/*metabolism ; Rats
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    The steroid and thyroid hormone receptor superfamily (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-05-13
    Description: Analyses of steroid receptors are important for understanding molecular details of transcriptional control, as well as providing insight as to how an individual transacting factor contributes to cell identity and function. These studies have led to the identification of a superfamily of regulatory proteins that include receptors for thyroid hormone and the vertebrate morphogen retinoic acid. Although animals employ complex and often distinct ways to control their physiology and development, the discovery of receptor-related molecules in a wide range of species suggests that mechanisms underlying morphogenesis and homeostasis may be more ubiquitous than previously expected.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Evans, R M -- New York, N.Y. -- Science. 1988 May 13;240(4854):889-95.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Salk Institute for Biological Studies, La Jolla, CA 92138-9216.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3283939" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Binding Sites ; DNA/metabolism ; Gene Expression Regulation ; Humans ; Receptors, Steroid/genetics/*physiology ; Receptors, Thyroid Hormone/genetics/*physiology
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    A quantitative bioassay for HIV-1 based on trans-activation (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-01-08
    Description: A bioassay that is based on trans-activation has been developed for the detection and quantitation of the human immunodeficiency virus type 1 (HIV-1). Indicator cell lines were constructed that contain the HIV-1 long terminal repeat ligated to the chloramphenicol acetyltransferase (CAT) gene. Infection of these cells by HIV activates the expression of CAT protein. Isolates of HIV-1 with divergent nucleotide sequences activated the indicator cell lines to a similar extent, approximately 500- to 1000-fold. Human T cell lymphotropic viruses types 1 and 2, equine infectious anemia virus, and herpes simplex virus 1 did not activate the indicator cell lines. Isolates of simian immunodeficiency virus and human T cell lymphotropic virus type 4 activated these cells to a much lesser extent, which suggests that these viruses contain similar, but distinct, trans-activators. This assay can be used for the detection, quantitation, and typing of HIV and for studying the effect of drugs on the replication of HIV in different cellular backgrounds.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Felber, B K -- Pavlakis, G N -- N01-CO-74101/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1988 Jan 8;239(4836):184-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Cancer Institute, Frederick Cancer Research Facility, Bionetics Research, Inc., MD 21701.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3422113" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/genetics ; Antiviral Agents/pharmacology ; Cell Line ; Chloramphenicol O-Acetyltransferase ; DNA, Recombinant ; Gene Expression Regulation ; Genes, Viral ; HIV/analysis/drug effects/*genetics ; Humans ; Promoter Regions, Genetic ; Repetitive Sequences, Nucleic Acid ; Virus Replication/drug effects
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    The CD14 monocyte differentiation antigen maps to a region encoding growth factors and receptors (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-01-29
    Description: CD14 is a myelomonocytic differentiation antigen expressed by monocytes, macrophages, and activated granulocytes and is detectable with the monoclonal antibodies MO2, MY4, and LeuM3. Analyses of complementary DNA and genomic clones of CD14 show that it has a novel structure and that it maps to chromosome 5 within a region containing other genes encoding growth factors and receptors; it may therefore represent a new receptor important for myeloid differentiation. In addition, the CD14 gene is included in the "critical" region that is frequently deleted in certain myeloid leukemias.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goyert, S M -- Ferrero, E -- Rettig, W J -- Yenamandra, A K -- Obata, F -- Le Beau, M M -- R01-AI23859/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 Jan 29;239(4839):497-500.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Rheumatic Diseases, Hospital for Joint Diseases Orthopaedic Institute, New York, NY 10003.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2448876" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Antigens, CD14 ; Antigens, Differentiation/*genetics/immunology ; Cell Differentiation ; Chromosome Mapping ; Chromosomes, Human, Pair 5 ; DNA/genetics ; Electrophoresis, Polyacrylamide Gel ; Granulocytes/immunology ; Growth Substances/*genetics ; Humans ; Immunosorbent Techniques ; Leukemia/genetics ; Macrophages/immunology ; Mice ; Monocytes/*immunology ; Myelodysplastic Syndromes/genetics ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; Receptors, Cell Surface/*genetics
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    Conversion of normal behavior to shiverer by myelin basic protein antisense cDNA in transgenic mice (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-29
    Description: Myelin basic proteins (MBPs) are coded by the single gene necessary for myelin formation in the central nervous system of the mouse. An antisense MBP mini-gene was constructed and used to determine the function of antisense DNA in transgenic mice. Several transgenic offspring of a founder transgenic mouse, AS100, were converted from the normal to mutant shiverer phenotype. Antisense MBP messenger RNA was expressed in these mice, and the endogenous MBP messenger RNA, the MBP, and the myelination in the central nervous system were reduced.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Katsuki, M -- Sato, M -- Kimura, M -- Yokoyama, M -- Kobayashi, K -- Nomura, T -- New York, N.Y. -- Science. 1988 Jul 29;241(4865):593-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of DNA Biology, School of Medicine, Tokai University, Isehara, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2456614" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Brain/physiology ; DNA/genetics ; Gene Expression Regulation ; Mice ; Mice, Neurologic Mutants/*physiology ; Mice, Transgenic ; Molecular Sequence Data ; Myelin Basic Protein/genetics/*physiology ; Myelin Sheath/physiology ; Phenotype ; RNA/*genetics ; RNA, Antisense
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    The presence of fibroblast growth factor in the frog egg: its role as a natural mesoderm inducer (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-11-18
    Description: A complementary DNA clone corresponding to a 4.2-kilobase transcript that is present in the Xenopus oocyte and newly transcribed in the neurula stages of development has been isolated. This messenger RNA encodes a 155-amino acid protein that is 84% identical to the human basic fibroblast growth factor (bFGF). When expressed in Escherichia coli and purified, the Xenopus FGF induced mesoderm in animal cell blastomeres as measured by muscle actin expression. Immunoblots with an antibody to a Xenopus FGF peptide show that the oocyte and early embryo contain a store of the FGF polypeptide at high enough concentrations to induce mesoderm. The presence of FGF in the oocyte, together with the apparent lack of a secretory signal sequence in the protein, suggest that the regulation of mesoderm induction may involve novel mechanisms that occur after the translation of FGF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kimelman, D -- Abraham, J A -- Haaparanta, T -- Palisi, T M -- Kirschner, M W -- New York, N.Y. -- Science. 1988 Nov 18;242(4881):1053-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3194757" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/genetics ; Amino Acid Sequence ; Animals ; Blotting, Northern ; Blotting, Western ; Cloning, Molecular ; DNA/genetics ; DNA Probes ; Fibroblast Growth Factors/*physiology ; Gene Expression Regulation ; Mesoderm/*cytology ; Molecular Sequence Data ; Oocytes/physiology ; Xenopus laevis/*embryology
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    Relationship between the c-myb locus and the 6q-chromosomal aberration in leukemias and lymphomas (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-02-27
    Description: Deletions of the long arm of chromosome 6 (6q-) are frequently found in hematopoietic neoplasms, including acute lymphoblastic leukemias, non-Hodgkin lymphomas and (less frequently) myeloid leukemias. The c-myb proto-oncogene has been mapped to region 6q21-24, which suggests that it could be involved in the 6q- aberrations. By means of in situ chromosomal hybridization on cells from six hematopoietic malignancies, it was demonstrated that the c-myb locus is not deleted, but is retained on band q22, which is consistently bordered by the chromosomal breakpoints in both interstitial and terminal 6q- deletions. The deletion breakpoints were located at some distance from the myb locus since no rearrangement of c-myb sequences was found. In one case, however, amplification of the entire c-myb locus was detectable. Furthermore, in all cases tested that carry 6q- deletions, myb messenger RNA levels were significantly higher than in normal cells or in malignant cells matched for lineage and stage of differentiation but lacking the 6q- marker. These results indicate that 6q- deletions are accompanied by structural and functional alterations of the c-myb locus and that these alterations may be involved in the pathogenesis of leukemias and lymphomas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barletta, C -- Pelicci, P G -- Kenyon, L C -- Smith, S D -- Dalla-Favera, R -- CA16239/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Feb 27;235(4792):1064-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3469751" target="_blank"〉PubMed〈/a〉
    Keywords: *Chromosome Deletion ; *Chromosomes, Human, Pair 6 ; DNA/genetics ; Gene Amplification ; Humans ; Leukemia/*genetics ; Leukemia, Lymphoid/genetics ; Leukemia, Myeloid/genetics ; Lymphoma, Non-Hodgkin/*genetics ; Nucleic Acid Hybridization ; RNA, Messenger/genetics
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    Differential expression of c-myb mRNA in murine B lymphomas by a block to transcription elongation (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-09-18
    Description: Expression of c-myb proto-oncogene messenger RNA (mRNA) and protein has been detected principally in tumors and in normal tissue of hematopoietic origin. In each hematopoietic lineage examined, expression of the c-myb gene is markedly downregulated during hematopoietic maturation. However, the mechanism by which differential expression of the c-myb gene is regulated is not known. In murine B-lymphoid tumor cell lines, the amount of steady-state c-myb mRNA is 10 to more than 100 times greater in pre-B cell lymphomas than in B cell lymphomas and plasmacytomas. The downregulation of c-myb mRNA correlates with events at the pre-B cell-B cell junction. Differential expression of c-myb mRNA levels detected between a pre-B cell lymphoma and a mature B cell lymphoma is now shown to be mediated by a block to transcription elongation in the first intron of the c-myb locus. In addition, this developmentally regulated difference in transcriptional activity is correlated with alterations in higher order chromatin structure as reflected by changes in the patterns of hypersensitivity to deoxyribonuclease I at the 5' end of the c-myb transcription unit. Regulation of transcription elongation may provide a more sensitive mechanism for rapidly increasing and decreasing mRNA levels in response to external stimuli than regulation of the initiation of transcription.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bender, T P -- Thompson, C B -- Kuehl, W M -- New York, N.Y. -- Science. 1987 Sep 18;237(4821):1473-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3498214" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes ; Chromosome Mapping ; *Gene Expression Regulation ; Introns ; Lymphoma/*genetics ; Mice ; Nucleic Acid Hybridization ; *Peptide Chain Elongation, Translational ; *Proto-Oncogenes ; RNA, Messenger/*metabolism ; *Transcription, Genetic
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    Transformation of rat fibroblasts by FSV rapidly increases glucose transporter gene transcription (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-03-20
    Description: Elevation of glucose transport is an alteration common to most virally induced tumors. Rat fibroblasts transformed with wild-type or a temperature-sensitive Fujinami sarcoma virus (FSV) were studied in order to determine the mechanisms underlying the increased transport. Five- to tenfold increases in total cellular glucose transporter protein in response to transformation were accompanied by similar increases in transporter messenger RNA levels. This, in turn, was preceded by an absolute increase in the rate of glucose transporter gene transcription within 30 minutes after shift of the temperature-sensitive FSV-transformed cells to the permissive temperature. The transporter messenger RNA levels in transformed fibroblasts were higher than those found in proliferating cells maintained at the nonpermissive temperature. The activation of transporter gene transcription by transformation represents one of the earliest known effects of oncogenesis on the expression of a gene encoding a protein of well-defined function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Birnbaum, M J -- Haspel, H C -- Rosen, O M -- AM35430-01/AM/NIADDK NIH HHS/ -- DK 35158/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Mar 20;235(4795):1495-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3029870" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avian Sarcoma Viruses ; Cell Division ; Cell Line ; *Cell Transformation, Viral ; Fibroblasts ; Gene Expression Regulation ; Kinetics ; Monosaccharide Transport Proteins/*genetics ; RNA, Messenger/genetics ; Rats ; Transcription, Genetic
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    erbB-2 is a potent oncogene when overexpressed in NIH/3T3 cells (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-07-10
    Description: A wide variety of human tumors contain an amplified or overexpressed erbB-2 gene, which encodes a growth factor receptor-like protein. When erbB-2 complementary DNA was expressed in NIH/3T3 cells under the control of the SV40 promoter, the gene lacked transforming activity despite expression of detectable levels of the erbB-2 protein. A further five- to tenfold increase in its expression under influence of the long terminal repeat of Moloney murine leukemia virus was associated with activation of erbB-2 as a potent oncogene. The high levels of the erbB-2 product associated with malignant transformation of NIH/3T3 cells were observed in human mammary tumor cells that overexpressed this gene. These findings demonstrate a new mechanism for acquisition of oncogenic properties by genes encoding growth factor receptor-like proteins and provide a functional basis for the role of their overexpression in the development of human malignancies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Di Fiore, P P -- Pierce, J H -- Kraus, M H -- Segatto, O -- King, C R -- Aaronson, S A -- New York, N.Y. -- Science. 1987 Jul 10;237(4811):178-82.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2885917" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/genetics ; Cell Line ; *Cell Transformation, Neoplastic/genetics ; DNA/genetics ; Fibroblasts/*metabolism ; Gene Expression Regulation ; Genes, Viral ; Humans ; Mice ; Moloney murine leukemia virus/genetics ; Promoter Regions, Genetic ; Proto-Oncogene Proteins/biosynthesis/genetics/*physiology ; Rats ; Receptor, Epidermal Growth Factor ; Receptor, ErbB-2 ; Receptors, Cell Surface/genetics ; Recombinant Fusion Proteins/biosynthesis/genetics/physiology ; Simian virus 40/genetics ; Tumor Stem Cell Assay
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    Identification and localization of mutations at the Lesch-Nyhan locus by ribonuclease A cleavage (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-04-17
    Description: Many mutations leading to human disease are the result of single DNA base pair changes that cannot be identified by Southern analysis. This has prompted the development of alternative assays for point mutation detection. The recently described ribonuclease A cleavage procedure, with a polyuridylic acid-paper affinity chromatography step, has been used to identify the mutational lesions in the hypoxanthine phosphoribosyltransferase (HPRT) messenger RNAs of patients with Lesch-Nyhan syndrome. Distinctive ribonuclease A cleavage patterns were identified in messenger RNA from 5 of 14 Lesch-Nyhan patients who were chosen because no HPRT Southern or Northern blotting pattern changes had been found. This approach now allows HPRT mutation detection in 50 percent of the cases of Lesch-Nyhan syndrome. The polyuridylic acid-paper affinity procedure provides a general method for analysis of low abundance messenger RNAs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbs, R A -- Caskey, C T -- New York, N.Y. -- Science. 1987 Apr 17;236(4799):303-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3563511" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Chromosome Deletion ; HeLa Cells/enzymology ; Humans ; Hypoxanthine Phosphoribosyltransferase/*genetics ; Lesch-Nyhan Syndrome/*genetics ; *Mutation ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; Ribonuclease, Pancreatic
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    A small viral RNA is required for in vitro packaging of bacteriophage phi 29 DNA (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-08
    Description: A small RNA of Bacillus subtilis bacteriophage phi 29 is shown to have a novel and essential role in viral DNA packaging in vitro. This requirement for RNA in the encapsidation of viral DNA provides a new dimension of complexity to the attendant protein-DNA interactions. The RNA is a constituent of the viral precursor shell of the DNA-packaging machine but is not a component of the mature virion. Studies of the sequential interactions involving this RNA molecule are likely to provide new insight into the structural and possible catalytic roles of small RNA molecules. The phi 29 assembly in extracts and phi 29 DNA packaging in the defined in vitro system were strongly inhibited by treatment with the ribonucleases A or T1. However, phage assembly occurred normally in the presence of ribonuclease A that had been treated with a ribonuclease inhibitor. An RNA of approximately 120 nucleotides co-purified with the phi 29 precursor protein shell (prohead), and this particle was the target of ribonuclease action. Removal of RNA from the prohead by ribonuclease rendered it inactive for DNA packaging. By RNA-DNA hybridization analysis, the RNA was shown to originate from a viral DNA segment very near the left end of the genome, the end packaged first during in vitro assembly.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guo, P X -- Erickson, S -- Anderson, D -- DE-3606/DE/NIDCR NIH HHS/ -- New York, N.Y. -- Science. 1987 May 8;236(4802):690-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3107124" target="_blank"〉PubMed〈/a〉
    Keywords: Bacillus subtilis ; Bacteriophages/*genetics ; DNA, Viral/*metabolism ; Genes, Viral ; Nucleic Acid Hybridization ; RNA, Viral/isolation & purification/*physiology ; Ribonuclease T1/metabolism ; Ribonuclease, Pancreatic/metabolism ; Viral Proteins/metabolism
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  • 80
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    Conservation of the Duchenne muscular dystrophy gene in mice and humans (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-16
    Description: A portion of the Duchenne muscular dystrophy (DMD) gene transcript from human fetal skeletal muscle and mouse adult heart was sequenced, representing approximately 25 percent of the total, 14-kb DMD transcript. The nucleic acid and predicted amino acid sequences from the two species are nearly 90 percent homologous. The amino acid sequence that is predicted from this portion of the DMD gene indicates that the protein product might serve a structural role in muscle, but the abundance and tissue distribution of the messenger RNA suggests that the DMD protein is not nebulin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffman, E P -- Monaco, A P -- Feener, C C -- Kunkel, L M -- 2T 32 GM07753-07/GM/NIGMS NIH HHS/ -- HD18658/HD/NICHD NIH HHS/ -- R01 NS23740/NS/NINDS NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 16;238(4825):347-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Genetics, Children's Hospital, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3659917" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; DNA/*genetics ; DNA, Recombinant ; Exons ; Humans ; Male ; Mice ; Molecular Sequence Data ; Muscle Proteins/genetics ; Muscles/analysis/embryology ; Muscular Dystrophies/*genetics ; Muscular Dystrophy, Animal/*genetics ; Myocardium/analysis ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; X Chromosome
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  • 81
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    Identification of an amplified, highly expressed gene in a human glioma (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-04-03
    Description: A gene, termed gli, was identified that is amplified more than 50-fold in a malignant glioma. The gene is expressed at high levels in the original tumor and its derived cell line and is located at chromosome 12 position (q13 to q14.3). The gli gene is a member of a select group of cellular genes that are genetically altered in primary human tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kinzler, K W -- Bigner, S H -- Bigner, D D -- Trent, J M -- Law, M L -- O'Brien, S J -- Wong, A J -- Vogelstein, B -- CA-09243/CA/NCI NIH HHS/ -- CA-43722/CA/NCI NIH HHS/ -- NS-20023/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Apr 3;236(4797):70-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3563490" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; *Chromosomes, Human, Pair 12 ; Cloning, Molecular ; DNA, Neoplasm/*genetics ; *Gene Amplification ; Gene Expression Regulation ; Glioma/*genetics ; Humans ; RNA, Messenger/genetics ; RNA, Neoplasm/genetics
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  • 82
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    The raf oncogene is associated with a radiation-resistant human laryngeal cancer (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-08-28
    Description: In order to identify the genetic factors associated with the radiation-resistant human laryngeal carcinoma cell line (SQ-20B), tumor cell DNA was transfected into NIH/3T3 cells. A high incidence (six out of six) of raf sequences was found in transfected NIH/3T3 clones and the tumorigenic potential of SQ-20B DNA could be linked to genomic fragments that represent most of the kinase domain of human c-raf-1. An apparently unaltered 3.5-kilobase pair (kb) human c-raf transcript was identified in SQ-20B cells but was not observed in the transfected NIH/3T3 cell clones. Two new transcripts (4.2 kb and 2.6 kb) were found in tumorigenic clones; the large transcript was missing in a very poorly tumorigenic clone. Cytogenetic analysis indicated that the normal autosomes of chromosome 3 were absent in SQ-20B karyotypes and had formed apparently stable marker chromosomes. Unlike the recipient NIH/3T3 cell line, 30 percent of the transformed clone-1 metaphases had minute and double-minute chromosomes representative of amplified DNA sequences. The frequency of the c-raf-1 identification by NIH/3T3 transfection of SQ-20B DNA suggests the presence of some genetic abnormality within this locus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kasid, U -- Pfeifer, A -- Weichselbaum, R R -- Dritschilo, A -- Mark, G E -- CA425969/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 28;237(4818):1039-41.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3616625" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; DNA, Neoplasm/genetics ; Humans ; Karyotyping ; Laryngeal Neoplasms/*genetics/radiotherapy ; Mice ; Mice, Nude ; Nucleic Acid Hybridization ; Oncogenes/*radiation effects ; Proto-Oncogenes/radiation effects ; *Radiation Tolerance
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  • 83
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    Ouabain resistance conferred by expression of the cDNA for a murine Na+, K+-ATPase alpha subunit (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-08-21
    Description: The molecular basis for the marked difference between primate and rodent cells in sensitivity to the cardiac glycoside ouabain has been established by genetic techniques. A complementary DNA encoding the entire alpha 1 subunit of the mouse Na+- and K+-dependent adenosine triphosphatase (ATPase) was inserted into the expression vector pSV2. This engineered DNA molecule confers resistance against 10(-4) M ouabain to monkey CV-1 cells. Deletion of sequences encoding the carboxyl terminus of the alpha 1 subunit abolish the activity of the complementary DNA. The ability to assay the biological activity of this ATPase in a transfection protocol permits the application of molecular genetic techniques to the analysis of structure-function relationships for the enzyme that establishes the internal Na+/K+ environment of most animal cells. The full-length alpha 1 subunit complementary DNA will also be useful as a dominant selectable marker for somatic cell genetic studies utilizing ouabain-sensitive cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kent, R B -- Emanuel, J R -- Ben Neriah, Y -- Levenson, R -- Housman, D E -- CA-07919/CA/NCI NIH HHS/ -- CA-26712/CA/NCI NIH HHS/ -- CA-38992/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 21;237(4817):901-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3039660" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Cercopithecus aethiops ; DNA/genetics ; Drug Resistance ; Gene Expression Regulation ; Macromolecular Substances ; Mice ; Ouabain/*pharmacology ; Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors/*genetics ; Species Specificity ; Structure-Activity Relationship ; Transfection
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  • 84
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    My close cousin the chimpanzee (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1987 Oct 16;238(4825):273-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3116670" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; *Biological Evolution ; DNA/genetics ; Dental Enamel/anatomy & histology ; Gait ; Haplorhini/anatomy & histology/*genetics ; Humans ; Metacarpophalangeal Joint/anatomy & histology ; Molar ; Nucleic Acid Hybridization ; Pan troglodytes/anatomy & histology/*genetics ; Sequence Homology, Nucleic Acid
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  • 85
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    The fos gene as "master switch" (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-08-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1987 Aug 21;237(4817):854-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3039659" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Gene Expression Regulation ; Growth Substances/pharmacology ; Proto-Oncogene Proteins/*physiology ; *Proto-Oncogenes ; Receptors, GABA-A/physiology
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  • 86
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    Control protein for AIDS virus identified (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-04-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1987 Apr 24;236(4800):393.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3494309" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*microbiology ; Gene Expression Regulation ; HIV/*genetics ; Humans ; Lymphocyte Activation ; T-Lymphocytes/cytology/*microbiology
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  • 87
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    Mapping patterns of c-fos expression in the central nervous system after seizure (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-10
    Description: A dramatic and specific induction of c-fos was observed in identifiable neuronal populations in vivo after administration of the convulsant Metrazole. This effect was time- and dose-dependent and was abolished by prior treatment with the anticonvulsant drugs diazepam or pentobarbital. About 60 minutes after administration of Metrazole, c-fos messenger RNA reached a maximum and declined to basal levels after 180 minutes. A further decrease below that in normal brain was observed before a return to basal levels after 16 hours. While Metrazole still elicited seizures during this period, reinduction of c-fos was largely refractory. At 90 minutes, c-fos protein was observed in the nuclei of neurons in the dentate gyrus, and in the pyriform and cingulate cortices. Subsequently, c-fos protein appeared throughout the cortex, hippocampus, and limbic system. Thus, seizure activity results in increased c-fos gene expression in particular subsets of neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morgan, J I -- Cohen, D R -- Hempstead, J L -- Curran, T -- New York, N.Y. -- Science. 1987 Jul 10;237(4811):192-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3037702" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain Chemistry/drug effects ; DNA-Binding Proteins/biosynthesis/genetics ; Diazepam/pharmacology ; Fluorescent Antibody Technique ; Gene Expression Regulation ; Mice ; Mice, Inbred BALB C ; Neurons/metabolism ; Pentobarbital/pharmacology ; Pentylenetetrazole/antagonists & inhibitors/toxicity ; Proto-Oncogene Proteins/*biosynthesis/genetics ; Proto-Oncogene Proteins c-fos ; Receptors, GABA-A/drug effects ; Seizures/chemically induced/*metabolism
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  • 88
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    Allelic exclusion in transgenic mice that express the membrane form of immunoglobulin mu (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-15
    Description: Antibody-producing cells display a special form of regulation whereby each cell produces immunoglobulin from only one of its two sets of antibody genes. This phenomenon, called allelic exclusion, is thought to be mediated by the product of one heavy chain allele restricting the expression of the other. Heavy chains are synthesized in two molecular forms, secreted and membrane bound. In order to determine whether it is specifically the membrane-bound form of the immunoglobulin M (IgM) heavy chain (mu) that mediates this regulation, transgenic mice were created that carry a human mu chain gene altered so that it can only direct the synthesis of the membrane-bound protein. The membrane-bound form of the human mu chain was made by most of the B cells in these animals as measured by assays of messenger RNA and surface immunoglobulins. Further, the many B cells that express the human gene do not express endogenous mouse IgM, and the few B cells that express endogenous mouse mu do not express the transgene. Thus, the membrane-bound form of the mu chain is sufficient to mediate allelic exclusion. In addition, the molecular structures recognized for this purpose are conserved between human and mouse systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nussenzweig, M C -- Shaw, A C -- Sinn, E -- Danner, D B -- Holmes, K L -- Morse, H C 3rd -- Leder, P -- New York, N.Y. -- Science. 1987 May 15;236(4803):816-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3107126" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Animals ; Antibody-Producing Cells/*immunology ; Gene Expression Regulation ; *Genes ; Humans ; Immunoglobulin M/genetics ; Immunoglobulin mu-Chains/*genetics ; Mice ; Mice, Inbred Strains ; RNA, Messenger/genetics ; Transcription, Genetic
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  • 89
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    Expression and properties of two types of protein kinase C: alternative splicing from a single gene (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-29
    Description: Two complementary DNA's, encoding the complete sequences of 671 and 673 amino acids for subspecies of rat brain protein kinase C, were expressed in COS 7 cells. The complementary DNA sequence analysis predicted that the two enzymes are derived from different ways of splicing and differ from each other only in the short ranges of their carboxyl-terminal regions. Both enzymes showed typical characteristics of protein kinase C that responded to Ca2+, phospholipid, and diacylglycerol. The enzymes showed practically identical physical and kinetic properties and were indistinguishable from one of the several subspecies of protein kinase C that occurs in rat brain but not in untransfected COS 7 cells. Partial analysis of the genomic structure confirmed that these two subspecies of protein kinase C resulted indeed from alternative splicing of a single gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ono, Y -- Kikkawa, U -- Ogita, K -- Fujii, T -- Kurokawa, T -- Asaoka, Y -- Sekiguchi, K -- Ase, K -- Igarashi, K -- Nishizuka, Y -- New York, N.Y. -- Science. 1987 May 29;236(4805):1116-20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3576226" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Brain/enzymology ; Chromatography, High Pressure Liquid ; DNA/genetics ; Nucleic Acid Hybridization ; Protein Kinase C/*genetics/metabolism ; RNA Splicing ; Rabbits ; Rats
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  • 90
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    Cloning of genomic and complementary DNA from Shaker, a putative potassium channel gene from Drosophila (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-08-14
    Description: On the basis of electrophysiological analysis of Shaker mutants, the Shaker locus of Drosophila melanogaster has been proposed to encode a structural component of a voltage-dependent potassium channel, the A channel. Unlike sodium channels, acetylcholine receptors, and calcium channels, K+ channels have not been purified biochemically. To facilitate biochemical studies of a K+ channel, genomic DNA from the Shaker locus has been cloned. Rearrangements in five Shaker mutants have been mapped to a 60-kilobase segment of the genome. Four complementary DNA clones have been analyzed. These clones indicate that the Shaker gene contains multiple exons distributed over at least 65 kilobases of genomic DNA in the region where the mutations mapped. Furthermore, the gene may produce several classes of alternatively spliced transcripts. Two of the complementary DNA clones have been sequenced and their sequences support the hypothesis that Shaker encodes a component of a K+ channel.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Papazian, D M -- Schwarz, T L -- Tempel, B L -- Jan, Y N -- Jan, L Y -- NS15963/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 14;237(4816):749-53.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2441470" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cloning, Molecular ; DNA/*genetics/isolation & purification ; Drosophila melanogaster/*genetics ; Exons ; *Ion Channels ; Membrane Proteins/*genetics ; Mutation ; Nucleic Acid Hybridization ; Potassium/*metabolism ; RNA Splicing ; Transcription, Genetic ; Translocation, Genetic
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  • 91
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    The mitochondrial genotype can influence nuclear gene expression in yeast (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-01-30
    Description: Isochromosomal, respiratory-deficient yeast strains, such as a mit-, a hypersuppressive petite, and a petite lacking mitochondrial DNA, are phenotypically identical in spite of differences in their mitochondrial genomes. Subtractive hybridizations of complementary DNA's to polyadenylated RNA isolated from derepressed cultures of these strains reveal the presence of nuclear-encoded transcripts whose abundance varies not only between them and their respiratory-competent parent, but among the respiratory-deficient strains themselves. Transcripts of some nuclear-encoded mitochondrial proteins, like cytochrome c and the alpha and beta subunits of the mitochondrial adenosine triphosphatase, whose abundance is affected by glucose or heme, do not vary. In the absence of major metabolic variables, yeast cells seem to respond to the quality and quantity of mitochondrial DNA and modulate the levels of nuclear-encoded RNA's, perhaps as a means of intergenomic regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parikh, V S -- Morgan, M M -- Scott, R -- Clements, L S -- Butow, R A -- New York, N.Y. -- Science. 1987 Jan 30;235(4788):576-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3027892" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cell Nucleus/physiology ; Cytochrome c Group/genetics ; DNA, Fungal/genetics ; DNA, Mitochondrial/genetics ; Electron Transport Complex IV/genetics ; Gene Expression Regulation ; Genes, Fungal ; Genotype ; Mitochondria/*physiology ; Mutation ; RNA, Fungal/genetics ; RNA, Messenger/genetics ; RNA, Ribosomal/genetics ; Saccharomyces cerevisiae/*genetics
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  • 92
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    Protein-DNA interactions in vivo upstream of a cell cycle-regulated human H4 histone gene (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-06-05
    Description: Cell cycle-dependent histone genes are transcribed at a basal level throughout the cell cycle, with a three- to fivefold increase during early S phase. Protein-DNA interactions in the 5' promoter region of a cell cycle-regulated human H4 histone gene have been analyzed at single-nucleotide resolution in vivo. This region contains two sites, with four potential protein-binding domains, at which the DNA is protected from reaction with dimethyl sulfate in cells and from digestion with deoxyribonuclease I in nuclei. These protein-DNA interactions persist during all phases of the cell cycle and dissociate with 0.16 to 0.2M sodium chloride.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pauli, U -- Chrysogelos, S -- Stein, G -- Stein, J -- Nick, H -- GM32010/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jun 5;236(4806):1308-11.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3035717" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cell Cycle ; Cell Line ; Dna ; DNA Restriction Enzymes ; Deoxyribonuclease I ; Gene Expression Regulation ; Histones/*genetics ; Humans ; Nucleic Acid Hybridization ; *Promoter Regions, Genetic ; Protein Binding ; Sulfuric Acid Esters
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  • 93
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    Primary structure and biochemical properties of an M2 muscarinic receptor (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-01
    Description: A partial amino acid sequence obtained for porcine atrial muscarinic acetylcholine receptor was used to isolate complementary DNA clones containing the complete receptor coding region. The deduced 466-amino acid polypeptide exhibits extensive structural and sequence homology with other receptors coupled to guanine nucleotide binding (G) proteins (for example, the beta-adrenergic receptor and rhodopsins); this similarity predicts a structure of seven membrane-spanning regions distinguished by the disposition of a large cytoplasmic domain. Stable transfection of the Chinese hamster ovary cell line with the atrial receptor complementary DNA leads to the binding of muscarinic antagonists in these cells with affinities characteristic of the M2 receptor subtype. The atrial muscarinic receptor is encoded by a unique gene consisting of a single coding exon and multiple, alternatively spliced 5' noncoding regions. The atrial receptor is distinct from the cerebral muscarinic receptor gene product, sharing only 38% overall amino acid homology and possessing a completely nonhomologous large cytoplasmic domain, suggesting a role for the latter region in differential effector coupling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peralta, E G -- Winslow, J W -- Peterson, G L -- Smith, D H -- Ashkenazi, A -- Ramachandran, J -- Schimerlik, M I -- Capon, D J -- CA16417/CA/NCI NIH HHS/ -- HL23632/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1987 May 1;236(4801):600-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3107123" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; DNA/genetics ; Exons ; GTP-Binding Proteins/metabolism ; Heart Atria/analysis ; Immunosorbent Techniques ; Membrane Proteins ; Molecular Weight ; Nucleic Acid Hybridization ; Peptide Fragments/metabolism ; Quinuclidinyl Benzilate/metabolism ; Receptors, Muscarinic/*genetics/metabolism ; Sequence Homology, Nucleic Acid ; Swine ; 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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  • 94
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    Identification of human uromodulin as the Tamm-Horsfall urinary glycoprotein (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-04-03
    Description: The primary structure of human uromodulin, a 616-amino acid, 85-kilodalton glycoprotein with in vitro immunosuppressive properties, was determined through isolation and characterization of complementary DNA and genomic clones. The amino acid sequence encoded by one of the exons of the uromodulin gene has homology to the low-density-lipoprotein receptor and the epidermal growth factor precursor. Northern hybridization analyses demonstrate that uromodulin is synthesized by the kidney. Evidence is provided that uromodulin is identical to the previously characterized Tamm-Horsfall glycoprotein, the most abundant protein in normal human urine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennica, D -- Kohr, W J -- Kuang, W J -- Glaister, D -- Aggarwal, B B -- Chen, E Y -- Goeddel, D V -- New York, N.Y. -- Science. 1987 Apr 3;236(4797):83-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3453112" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acids/analysis ; Base Sequence ; Chemistry, Physical ; Cloning, Molecular ; Cysteine ; DNA/genetics ; Gene Expression Regulation ; Genes ; Glycoproteins/*genetics ; Humans ; Mucoproteins/*analysis/*genetics ; Peptide Fragments/analysis ; Physicochemical Phenomena ; RNA, Messenger/genetics ; Uromodulin
    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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  • 95
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    Malaria diagnosis (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-04-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pettersson, U -- Wigzell, H -- Perlman, P -- New York, N.Y. -- Science. 1987 Apr 3;236(4797):11-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3551070" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; Malaria/*diagnosis ; Nucleic Acid Hybridization ; Plasmodium falciparum/genetics ; 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
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  • 96
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    Avian v-myc replaces chromosomal translocation in murine plasmacytomagenesis (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-02-13
    Description: Deregulation of c-myc expression in association with chromosomal translocations occurs in over 95% of murine plasmacytomas, rat immunocytomas, and human Burkitt lymphomas. Infection with a murine retrovirus (J-3) containing an avian v-myc rapidly induced plasmacytomas in pristane-primed BALB/cAn mice. Only 17% of the induced plasmacytomas that were karyotyped showed the characteristic chromosomal translocations involving the c-myc locus. Instead, all of the translocation-negative tumors demonstrated characteristic J-3 virus integration sites that were actively transcribed. Thus, the high levels of v-myc expression have replaced the requirement for chromosomal translocation in plasmacytomagenesis and accelerated the process of transformation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Potter, M -- Mushinski, J F -- Mushinski, E B -- Brust, S -- Wax, J S -- Wiener, F -- Babonits, M -- Rapp, U R -- Morse, H C 3rd -- New York, N.Y. -- Science. 1987 Feb 13;235(4790):787-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3810165" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Birds ; *Cell Transformation, Neoplastic ; *Genes, Viral ; Mice ; Mice, Inbred BALB C ; Mice, Inbred Strains ; Moloney murine leukemia virus/*genetics ; Nucleic Acid Hybridization ; *Oncogenes ; Plasmacytoma/genetics/*microbiology ; Retroviridae/*genetics ; Transcription, Genetic ; *Translocation, 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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  • 97
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    Redesigning metabolic routes: manipulation of TOL plasmid pathway for catabolism of alkylbenzoates (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-01-30
    Description: Increasing quantities of man-made organic chemicals are released each year into the biosphere. Some of these compounds are both toxic and relatively resistant to physical, chemical, or biological degradation, and they thus constitute an environmental burden of considerable magnitude. Genetic manipulation of microbial catabolic pathways offers a powerful means by which to accelerate evolution of biodegradative routes through which such compounds might be eliminated from the environment. In the experiments described here, a catabolic pathway for alkylbenzoates specified by the TOL plasmid of Pseudomonas was restructured to produce a pathway capable of processing a new substrate, 4-ethylbenzoate. Analysis of critical steps in the TOL pathway that prevent metabolism of 4-ethylbenzoate revealed that this compound fails to induce synthesis of the catabolic enzymes and that one of its metabolic intermediates inactivates catechol 2,3-dioxygenase (C23O), the enzyme that cleaves the aromatic ring. Consequently, the pathway was sequentially modified by recruitment of genes from mutant bacteria selected for their production of either an altered pathway operon regulator that is activated by 4-ethylbenzoate or an altered C23O that is less sensitive to metabolite inactivation. The redesigned pathway was stably expressed and enabled host bacteria to degrade 4-ethylbenzoate in addition to the normal substrates of the TOL pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramos, J L -- Wasserfallen, A -- Rose, K -- Timmis, K N -- New York, N.Y. -- Science. 1987 Jan 30;235(4788):593-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3468623" target="_blank"〉PubMed〈/a〉
    Keywords: *Benzoates/*metabolism ; Biotransformation ; Catechol 2,3-Dioxygenase ; *Dioxygenases ; Gene Expression Regulation ; Genetic Engineering ; Oxygenases/metabolism ; *Plasmids ; Pseudomonas/enzymology/*genetics/growth & development ; Substrate Specificity
    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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  • 98
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    Activated oncogenes in B6C3F1 mouse liver tumors: implications for risk assessment (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-09-11
    Description: The validity of mouse liver tumor end points in assessing the potential hazards of chemical exposure to humans is a controversial but important issue, since liver neoplasia in mice is the most frequent tumor target tissue end point in 2-year carcinogenicity studies. The ability to distinguish between promotion of background tumors versus a genotoxic mechanism of tumor initiation by chemical treatment would aid in the interpretation of rodent carcinogenesis data. Activated oncogenes in chemically induced and spontaneously occurring mouse liver tumors were examined and compared as one approach to determine the mechanism by which chemical treatment caused an increased incidence of mouse liver tumors. Data suggest that furan and furfural caused an increased incidence in mouse liver tumors at least in part by induction of novel weakly activating point mutations in ras genes even though both chemicals did not induce mutations in Salmonella assays. In addition to ras oncogenes, two activated raf genes and four non-ras transforming genes were detected. The B6C3F1 mouse liver may thus provide a sensitive assay system to detect various classes of proto-oncogenes that are susceptible to activation by carcinogenic insult. As illustrated with mouse liver tumors, analysis of activated oncogenes in spontaneously occurring and chemically induced rodent tumors will provide information at a molecular level to aid in the use of rodent carcinogenesis data for risk assessment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reynolds, S H -- Stowers, S J -- Patterson, R M -- Maronpot, R R -- Aaronson, S A -- Anderson, M W -- New York, N.Y. -- Science. 1987 Sep 11;237(4820):1309-16.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3629242" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Liver Neoplasms/*genetics ; Mice ; Mutation ; Nucleic Acid Hybridization ; *Oncogenes ; *Proto-Oncogenes ; Risk
    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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  • 99
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    Identification of a novel thyroid hormone receptor expressed in the mammalian central nervous system (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-09-25
    Description: A complementary DNA clone derived from rat brain messenger RNA has been isolated on the basis of homology to the human thyroid hormone receptor gene. Expression of this complementary DNA produces a high-affinity binding protein for thyroid hormones. Sequence analysis and the mapping of this gene to a distinct human genetic locus indicate the existence of multiple human thyroid hormone receptors. Messenger RNA from this gene is expressed in a tissue-specific fashion with highest levels in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, C C -- Weinberger, C -- Lebo, R -- Evans, R M -- GM-266444-09/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Sep 25;237(4822):1610-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3629259" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain/*physiology ; DNA/genetics ; DNA-Binding Proteins/*genetics ; Gene Expression Regulation ; Genes ; Humans ; RNA, Messenger/genetics ; Rats ; Receptors, Thyroid Hormone/*genetics/metabolism ; Tissue Distribution ; Triiodothyronine/metabolism
    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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  • 100
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    Assemblage of ortho cleavage route for simultaneous degradation of chloro- and methylaromatics (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-12-04
    Description: Genetic engineering is a powerful means of accelerating the evolution of new biological activities and has considerable potential for constructing microorganisms that can degrade environmental pollutants. Critical enzymes from five different catabolic pathways of three distinct soil bacteria have been combined in patchwork fashion into a functional ortho cleavage route for the degradation of methylphenols and methylbenzoates. The new bacterium thereby evolved was able to degrade and grow on mixtures of chloro- and methylaromatics that were toxic even for the bacteria that could degrade the individual components of the mixtures. Except for one enzymatic step, the pathway was fully regulated and its component enzymes were only synthesized in response to the presence of pathway substrates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rojo, F -- Pieper, D H -- Engesser, K H -- Knackmuss, H J -- Timmis, K N -- New York, N.Y. -- Science. 1987 Dec 4;238(4832):1395-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Biochemistry, University of Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3479842" target="_blank"〉PubMed〈/a〉
    Keywords: Alcaligenes/enzymology/genetics ; Bacterial Proteins/genetics/*metabolism ; Benzoates/*metabolism ; *Biodegradation, Environmental ; Chlorobenzoates/*metabolism ; Gene Expression Regulation ; *Genes, Bacterial ; Genetic Engineering ; *Intramolecular Transferases ; Isomerases/genetics/metabolism ; Mixed Function Oxygenases/genetics/metabolism ; Oxidoreductases/genetics/metabolism ; Oxygenases/genetics/metabolism ; Pseudomonas/enzymology/genetics ; 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)
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