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  • Gene Expression Regulation  (54)
  • American Association for the Advancement of Science (AAAS)  (54)
  • American Chemical Society
  • Periodicals Archive Online (PAO)
  • 1985-1989  (54)
  • 1980-1984
  • 1965-1969
  • 1988  (37)
  • 1986  (17)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (54)
  • American Chemical Society
  • Periodicals Archive Online (PAO)
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  • 1985-1989  (54)
  • 1980-1984
  • 1965-1969
Year
  • 1
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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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    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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  • 3
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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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  • 4
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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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  • 5
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    A transcriptional enhancer 3' of C beta 2 in the T cell receptor beta locus (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-08
    Description: Run-on transcription experiments were used to demonstrate that transcription of T cell receptor beta chain V genes is activated by DNA rearrangement, in a manner similar to immunoglobulin genes. A transcriptional enhancer likely to be involved in this activation has been identified. A 25-kilobase region from J beta 1 to V beta 14 was tested for enhancer activity by transient transfections, and an enhancer was found 7.5 kilobases 3' of C beta 2. The beta enhancer has low activity relative to the simian virus 40 viral enhancer, does not display a preference for V beta promoters, has a T cell-specific activity, and binds two purified immunoglobulin heavy chain enhancer factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDougall, S -- Peterson, C L -- Calame, K -- GM29361/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Jul 8;241(4862):205-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, UCLA School of Medicine 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2968651" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; *Enhancer Elements, Genetic ; Gene Expression Regulation ; Genes, Immunoglobulin ; Immunoglobulin Heavy Chains/genetics ; In Vitro Techniques ; Mice ; Nuclear Proteins/physiology ; Receptors, Antigen, T-Cell/*genetics ; Receptors, Antigen, T-Cell, alpha-beta ; *Regulatory Sequences, Nucleic Acid ; Transcription Factors/physiology ; Transcription, Genetic
    Print ISSN: 0036-8075
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  • 6
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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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  • 7
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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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  • 8
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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)
    Details
    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
    Print ISSN: 0036-8075
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  • 9
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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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  • 10
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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)
    Details
    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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  • 11
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    jun Is bustin' out all over (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 12
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    Evolution's link to development explored (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 13
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    Activation of developmentally mutated human globin genes by cell fusion (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 14
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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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  • 15
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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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  • 16
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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)
    Details
    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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  • 17
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    Structural heterogeneity and functional domains of murine immunoglobulin G Fc receptors (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-11-07
    Description: Binding of antibodies to effector cells by way of receptors to their constant regions (Fc receptors) is central to the pathway that leads to clearance of antigens by the immune system. The structure and function of this important class of receptors on immune cells is addressed through the molecular characterization of Fc receptors (FcR) specific for the murine immunoglobulin G isotype. Structural diversity is encoded by two genes that by alternative splicing result in expression of molecules with highly conserved extracellular domains and different transmembrane and intracytoplasmic domains. The proteins encoded by these genes are members of the immunoglobulin supergene family, most homologous to the major histocompatibility complex molecule E beta. Functional reconstitution of ligand binding by transfection of individual FcR genes demonstrates that the requirements for ligand binding are encoded in a single gene. These studies demonstrate the molecular basis for the functional heterogeneity of FcR's, accounting for the possible transduction of different signals in response to a single ligand.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ravetch, J V -- Luster, A D -- Weinshank, R -- Kochan, J -- Pavlovec, A -- Portnoy, D A -- Hulmes, J -- Pan, Y C -- Unkeless, J C -- AI 24322/AI/NIAID NIH HHS/ -- GM 36306/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 Nov 7;234(4777):718-25.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2946078" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; DNA/genetics ; Gene Expression Regulation ; Histocompatibility Antigens Class II/genetics ; Immunoglobulin G ; Lymphocytes/*physiology ; Macrophages/*physiology ; Membrane Proteins ; Mice ; Protein Conformation ; *Receptors, Fc/genetics ; Receptors, IgG ; Transcription, Genetic ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
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    Tissue-specific and ectopic expression of genes introduced into transgenic mice by retroviruses (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-12-12
    Description: Recombinant retroviruses containing the complete genomic human beta globin gene (under the control of its own promoter) and the bacterial neomycin phosphotransferase gene (under the control of the normal or enhancerless viral promoter) were used to derive transgenic mouse strains by infection of preimplantation embryos. Expression of the beta globin gene in hematopoietic tissues was observed in all transgenic strains. In addition, one strain showed ectopic expression of beta globin in the same tissues that also expressed high levels of RNA from the viral promoter. It is likely that expression from the long terminal repeat (LTR), in contrast to expression from the internal promoter, is dependent on the site of integration. Thus, retroviral vectors can be used for tissue-specific expression of foreign genes in transgenic mice, as well as for the identification of loci that allow developmental activation of a provirus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Soriano, P -- Cone, R D -- Mulligan, R C -- Jaenisch, R -- HD-19105/HD/NICHD NIH HHS/ -- P01-CA38497/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Dec 12;234(4782):1409-13.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3024318" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gene Expression Regulation ; Globins/genetics ; Humans ; Kanamycin Kinase ; Mice/genetics ; Phosphotransferases/genetics ; Promoter Regions, Genetic ; RNA, Viral/immunology ; Repetitive Sequences, Nucleic Acid ; Retroviridae/*genetics
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  • 19
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    Mammalian metallothionein is functional in yeast (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-02-21
    Description: Expression of two monkey metallothioneins in yeast leads to complementation of both known functions of the endogenous yeast copperthionein gene, namely copper detoxification and autoregulation of transcription. The metallothionein-like proteins of higher and lower eukaryotes are therefore functionally analogous despite their dissimilar primary sequences.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thiele, D J -- Walling, M J -- Hamer, D H -- New York, N.Y. -- Science. 1986 Feb 21;231(4740):854-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3080806" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Copper/metabolism ; Gene Expression Regulation ; Genetic Complementation Test ; Haplorhini ; Metallothionein/genetics/*physiology ; Saccharomyces cerevisiae/*physiology ; Species Specificity ; Structure-Activity Relationship ; Transformation, Genetic
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  • 20
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    The cellular src gene product regulates junctional cell-to-cell communication (1988)
    American Association for the Advancement of Science (AAAS)
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    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 21
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    Cone cell-specific genes expressed in retinoblastoma (1988)
    American Association for the Advancement of Science (AAAS)
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    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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  • 22
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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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  • 23
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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)
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    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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  • 24
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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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  • 25
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    Molecular characterization of a functional cDNA encoding the serotonin 1c receptor (1988)
    American Association for the Advancement of Science (AAAS)
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    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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  • 26
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    Inactivation of the retinoblastoma susceptibility gene in human breast cancers (1988)
    American Association for the Advancement of Science (AAAS)
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    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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  • 27
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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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  • 28
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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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  • 31
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    Separation of DNA binding from the transcription-activating function of a eukaryotic regulatory protein (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-02-14
    Description: The yeast GAL4 protein (881 amino acids) binds to specific DNA sites upstream of target genes and activates transcription. Derivatives of this protein bearing as few as 74 amino terminal residues bind to these sites but fail to activate transcription. When appropriately positioned in front of a gene these derivatives act as repressors. These and related findings support the idea that GAL4 activates transcription by touching other DNA-bound proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keegan, L -- Gill, G -- Ptashne, M -- GM07598/GM/NIGMS NIH HHS/ -- GM32308/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 Feb 14;231(4739):699-704.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3080805" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; DNA, Fungal/genetics/metabolism ; DNA, Recombinant ; DNA-Binding Proteins/*genetics/metabolism ; Fungal Proteins/genetics ; Galactose ; Gene Expression Regulation ; Repressor Proteins/genetics ; Saccharomyces cerevisiae/*genetics ; Transcription Factors/*genetics/metabolism ; *Transcription, Genetic ; beta-Galactosidase/genetics
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  • 32
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    Binding of the Sp1 transcription factor by the human Harvey ras1 proto-oncogene promoter (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-06-13
    Description: Members of the ras gene family encode proteins that when overproduced or mutated can transform immortalized mammalian cells. It is therefore important to understand the mechanisms by which the ras genes are regulated. The promoter region of the human Harvey ras proto-oncogene c-Ha-ras1 initiates RNA transcription at multiple sites and contains repeated copies of the hexanucleotide GGGCGG and its inverted complement CCGCCC, referred to as GC boxes. These GC boxes consist of sequences identical to those found in the SV40 early promoter, where the human cellular transcriptional factor Sp1 binds. Footprinting analysis with deoxyribonuclease I was used to show that Sp1 binds to six GC box sequences within the c-Ha-ras1 promoter. An in vivo transfection assay showed competition between the 21-base pair repeats of the SV40 promoter and the c-Ha-ras1 promoter for common regulatory factors. In this system the presence of Sp1 is apparently required for c-Ha-ras1 transcription. Analysis of deletions of the c-Ha-ras1 promoter region by means of a transient expression assay revealed that the three Sp1 binding sites closest to the RNA start sites were sufficient for full transcriptional activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ishii, S -- Kadonaga, J T -- Tjian, R -- Brady, J N -- Merlino, G T -- Pastan, I -- New York, N.Y. -- Science. 1986 Jun 13;232(4756):1410-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3012774" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Binding, Competitive ; DNA/metabolism ; DNA-Binding Proteins/metabolism ; Gene Expression Regulation ; HeLa Cells ; Humans ; *Promoter Regions, Genetic ; *Proto-Oncogenes ; Simian virus 40/genetics ; Transcription Factors/*genetics/metabolism
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    The hypogonadal mouse: reproductive functions restored by gene therapy (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-12-12
    Description: The hypogonadal (hpg) mouse lacks a complete gonadotropin-releasing hormone (GnRH) gene and consequently cannot reproduce. Introduction of an intact GnRH gene into the genome of these mutant mice resulted in complete reversal of the hypogonadal phenotype. Transgenic hpg/hpg homozygotes of both sexes were capable of mating and producing offspring. Pituitary and serum concentrations of luteinizing hormone, follicle-stimulating hormone, and prolactin were restored to those of normal animals. Immunocytochemistry and in situ hybridization showed that GnRH expression was restored in the appropriate hypothalamic neurons of the transgenic hpg animals, an indication of neural-specific expression of the introduced gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mason, A J -- Pitts, S L -- Nikolics, K -- Szonyi, E -- Wilcox, J N -- Seeburg, P H -- Stewart, T A -- New York, N.Y. -- Science. 1986 Dec 12;234(4782):1372-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3097822" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Follicle Stimulating Hormone/blood ; Gene Expression Regulation ; *Genetic Engineering ; Gonadotropin-Releasing Hormone/genetics ; Histocytochemistry ; Hypogonadism/*genetics ; Hypothalamus/analysis/cytology ; Infertility/genetics/*therapy ; Luteinizing Hormone/blood ; Male ; Mice ; Mutation ; Neurons/analysis ; Phenotype ; Prolactin/blood ; Tissue Distribution
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    Tissue-specific expression in transgenic mice of a fused gene containing RSV terminal sequences (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-03-28
    Description: Transgenic mice were generated with pRSV-CAT, a chimeric gene construct containing the long terminal repeat of Rous sarcoma virus (RSV) linked to the bacterial gene encoding chloramphenicol acetyltransferase (CAT). CAT expression, detected in adult animals of five independent strains, was preferentially directed to organs rich in tendon, bone, and muscle. This pattern reflects the disease specificity of the intact virus and suggests that the tissue tropism of RSV is determined at least in part by the presence of endogenous tissue-specific factors that can promote expression of genetic information linked to the long terminal repeat. In two of the mouse strains, insertion of the pRSV-CAT DNA resulted in developmental abnormalities. One of these strains was characterized by a dominant trait of embryonic lethality, the other by a recessive trait of fused toes in all four feet.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Overbeek, P A -- Lai, S P -- Van Quill, K R -- Westphal, H -- New York, N.Y. -- Science. 1986 Mar 28;231(4745):1574-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3006249" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/genetics ; Age Factors ; Animals ; Avian Sarcoma Viruses/*genetics ; Chloramphenicol O-Acetyltransferase ; DNA, Viral/*genetics ; Gene Expression Regulation ; Genes, Regulator ; Limb Deformities, Congenital ; Mice ; Repetitive Sequences, Nucleic Acid ; Tissue Distribution ; Transcription, Genetic ; Transfection
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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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  • 36
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    Expression cloning of a lymphocyte homing receptor cDNA: ubiquitin is the reactive species (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-02-21
    Description: The lymphocyte cell surface receptor for the high endothelial venules (HEV's) of peripheral lymph nodes is specifically recognized by the monoclonal antibody MEL-14. Three independent complementary DNA (cDNA) clones, each of which encodes the protein ubiquitin, were detected by virtue of the expression of the MEL-14 antigenic determinant on cDNA-beta-galactosidase bacterial fusion proteins. The antigenic determinant defined by MEL-14 resides in the carboxyl terminal 13-amino-acid proteolytic peptide of ubiquitin, but is undetected in intact undenatured ubiquitin and other cellular ubiquitinated proteins. Antisera and monoclonal antibodies to ubiquitin determinants bind to the surface of both HEV-receptor positive and negative cell lines. The MEL-14-identified cDNA clones hydridize to RNA transcripts that encode tandemly repeated ubiquitins. Sequence analysis of these polyubiquitin cDNA's does not identify a leader sequence for export to the cell surface. The expression of the MEL-14 epitope of ubiquitin depends upon its local environment. The steady-state levels of expression of the ubiquitin messenger RNA's do not correlate with either the tissue derivation of the RNA or the expression of the lymphocyte HEV receptor. Regulation of the expression of the HEV receptor is not likely to reflect the transcriptional control of ubiquitin genes, but rather to reflect control of the expression of the HEV core polypeptide or its level or form of ubiquitination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉St John, T -- Gallatin, W M -- Siegelman, M -- Smith, H T -- Fried, V A -- Weissman, I L -- AI19512/AI/NIAID NIH HHS/ -- CA 09151/CA/NCI NIH HHS/ -- GM 31461/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 Feb 21;231(4740):845-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3003914" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal/*immunology ; Antibody Specificity ; Base Sequence ; Cloning, Molecular ; Endothelium/metabolism ; Gene Expression Regulation ; High Mobility Group Proteins/*genetics ; Lymphatic System/metabolism ; Lymphocytes/*physiology ; Mice ; Receptors, Cell Surface/*genetics/immunology/metabolism ; Ubiquitins/*genetics/immunology/metabolism
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    The structure, function, and expression of interleukin-2 receptors on normal and malignant lymphocytes (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-05-09
    Description: Antigen or mitogen-induced activation of resting T cells induces the synthesis of interleukin-2 (IL-2) as well as the expression of specific cell surface receptors for this lymphokine. Failure of the production of either IL-2 or its receptor results in a failure of the T-cell immune response. The receptor is composed of a 33,000-dalton (251-amino acid) peptide precursor that is post-translationally glycosylated into the mature 55,000-dalton form. In contrast to resting T cells, human T-cell lymphotrophic virus I (HTLV-I)-associated adult T-cell leukemia cells constitutively express large numbers of IL-2 receptors. Because IL-2 receptors are present on the malignant T cells but not on normal resting cells, clinical trials have been initiated in which patients with adult T-cell leukemia are treated with a monoclonal antibody that binds to the IL-2 receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Waldmann, T A -- New York, N.Y. -- Science. 1986 May 9;232(4751):727-32.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3008337" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology ; Animals ; Antibodies, Monoclonal/therapeutic use ; B-Lymphocytes/physiology ; Clinical Trials as Topic ; Cloning, Molecular ; DNA/genetics ; Deltaretrovirus/physiology ; Gene Expression Regulation ; Humans ; Interleukin-2/physiology ; Leukemia/*immunology/therapy ; Lymphocytes/microbiology/*physiology ; Mice/immunology ; Receptors, Immunologic/genetics/isolation & purification/*physiology ; Receptors, Interleukin-2 ; T-Lymphocytes/physiology
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    Long-term cultures of HTLV-III--infected T cells: a model of cytopathology of T-cell depletion in AIDS (1986)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1986-02-21
    Description: Long-term cultures were established of HTLV-III-infected T4 cells from patients with the acquired immune deficiency syndrome (AIDS) and of T4 cells from normal donors after infection of the cells in vitro. By initially reducing the number of cells per milliliter of culture medium it was possible to grow the infected cells for 50 to 60 days. As with uninfected T cells, immunologic activation of the HTLV-III-infected cells with phytohemagglutinin led to patterns of gene expression typical of T-cell differentiation, such as production of interleukin-2 and expression of interleukin-2 receptors, but in the infected cells immunologic activation also led to expression of HTLV-III, which was followed by cell death. The results revealed a cytopathogenic mechanism that may account for T4 cell depletion in AIDS patients and suggest how repeated antigenic stimulation by infectious agents, such as malaria in Africa, or by allogeneic blood or semen, may be important determinants of the latency period in AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zagury, D -- Bernard, J -- Leonard, R -- Cheynier, R -- Feldman, M -- Sarin, P S -- Gallo, R C -- New York, N.Y. -- Science. 1986 Feb 21;231(4740):850-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2418502" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology/microbiology/*pathology ; Antigens, Differentiation, T-Lymphocyte ; Antigens, Surface/analysis ; Cell Differentiation ; Cells, Cultured ; Cytopathogenic Effect, Viral ; Deltaretrovirus/*growth & development ; Gene Expression Regulation ; Humans ; Interleukin-2/biosynthesis ; RNA-Directed DNA Polymerase/metabolism ; Receptors, Immunologic/biosynthesis ; Receptors, Interleukin-2 ; T-Lymphocytes/immunology/*microbiology
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  • 39
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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)
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    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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    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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    Induction of altered c-src product during neural differentiation of embryonal carcinoma cells (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-11-14
    Description: The expression of the cellular src gene product pp60c-src was examined in an embryonal carcinoma cell line that differentiates in vitro into neuronlike cells after being treated with retinoic acid. Quantitative and qualitative changes in c-src expression accompanied the events associated with neuronal differentiation. The levels of pp60c-src increased 8- to 20-fold during the period when the cells elaborated neuritic processes and expressed neuron-specific proteins. The electrophoretic mobility of pp60c-src induced in these cells was retarded in comparison with that in untreated cells or in treated cells before neurite elaboration. The shift in electrophoretic mobility was due to an alteration in the amino terminal 16,000 daltons of pp60c-src and similar to an alteration of c-src protein found in neural tissues and in pure primary cultures of neuronal cells. These results indicate that expression of pp60c-src induced by retinoic acid in these embryonal carcinoma cells mimics the expression of c-src in developing neurons. Therefore, this embryonal carcinoma cell line provides a model system to investigate the function of the src protein in neuronal differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lynch, S A -- Brugge, J S -- Levine, J M -- CA 28146/CA/NCI NIH HHS/ -- NS 21198/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1986 Nov 14;234(4778):873-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3095923" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Differentiation/drug effects ; Cell Line ; Embryonal Carcinoma Stem Cells ; Gene Expression Regulation ; Neoplastic Stem Cells/cytology/*metabolism ; Neurons/cytology ; Oncogene Protein pp60(v-src) ; Phosphorylation ; Protein-Tyrosine Kinases/metabolism ; Retroviridae Proteins/genetics/*metabolism ; Tretinoin/pharmacology
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    A surprising action for the AIDS virus (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-02-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1986 Feb 21;231(4740):798.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3003912" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*microbiology ; Deltaretrovirus/*genetics ; Gene Expression Regulation ; Humans ; Protein Biosynthesis ; Transcription, Genetic
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  • 45
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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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  • 46
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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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  • 48
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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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    Trans-activator gene of HTLV-II induces IL-2 receptor and IL-2 cellular gene expression (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-05-16
    Description: The human T-lymphotropic viruses types I and II (HTLV-I and -II) have been etiologically linked with certain T-cell leukemias and lymphomas that characteristically display membrane receptors for interleukin-2. The relation of these viruses to this growth factor receptor has remained unexplained. It is demonstrated here that introduction of the trans-activator (tat) gene of HTLV-II into the Jurkat T-lymphoid cell line results in the induction of both interleukin-2 receptor and interleukin-2 gene expression. The coexpression of these cellular genes may play a role in the altering T-cell growth following retroviral infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greene, W C -- Leonard, W J -- Wano, Y -- Svetlik, P B -- Peffer, N J -- Sodroski, J G -- Rosen, C A -- Goh, W C -- Haseltine, W A -- 1R01CA369974-01AI/CA/NCI NIH HHS/ -- CA07580/CA/NCI NIH HHS/ -- CA40658/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 May 16;232(4752):877-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3010456" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Deltaretrovirus/*genetics ; Gene Expression Regulation ; *Genes, Viral ; Humans ; Interleukin-2/biosynthesis/*genetics ; Leukemia/microbiology ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; Receptors, Immunologic/*genetics ; Receptors, Interleukin-2
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    Two elements in the bovine leukemia virus long terminal repeat that regulate gene expression (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-03-21
    Description: The bovine leukemia virus, like the human T-cell leukemia viruses (HTLV-I and HTLV-II), are unusual biologically in that viral transcripts are not detected in tumors or infected tissues. The bovine leukemia virus long terminal repeat (BLV LTR) functions as a transcriptional promoter only in cell lines productively infected with BLV. Deletion mapping indicated that at least two regions of the LTR, on the 5' and 3' sides of the RNA start site, influenced gene expression. An analysis has now been made of the effects of coupling sequences from these LTR regions to a heterologous core promoter derived from the SV40 early promoter unit. Through the use of the transient expression of the bacterial chloramphenicol acetyltransferase (CAT) gene to monitor transcriptional activity in vivo, two independent, regulatory elements were identified in the BLV LTR. One was present in a fragment of 75 base pairs derived from the U3 region of the LTR and behaved much like other enhancer elements. It may be a major determinant of BLV expression in productively infected cell lines, since it enhanced transcription controlled by the heterologous core promoter only in these cells. The second element was contained in a 250-bp fragment derived from LTR sequences in the R region, located downstream from the RNA start site. Its activation of CAT expression was not dependent on BLV infection and was evident only when the fragment was located immediately downstream from the RNA start site. BLV expression thus appears to be regulated in part by a cell-specific enhancer element upstream from the core promoter and a novel sequence downstream from the RNA initiation site in the viral LTR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Derse, D -- Casey, J W -- CA07392/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Mar 21;231(4744):1437-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3006241" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cell Line ; Cercopithecus aethiops ; DNA, Recombinant ; DNA, Viral/genetics ; Deltaretrovirus/genetics ; *Enhancer Elements, Genetic ; Gene Expression Regulation ; *Genes, Regulator ; Genes, Viral ; Humans ; Leukemia Virus, Bovine/*genetics ; Plasmids ; *Promoter Regions, Genetic ; RNA, Messenger/genetics ; *Repetitive Sequences, Nucleic Acid ; Retroviridae/*genetics ; Transcription, Genetic
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    Differentiation-linked leukemogenesis in lymphocytes (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-11-07
    Description: Most human lymphoid malignancies preserve a pattern of gene expression reflecting their proliferative activity and the development level of clonal expansion and maturation arrest. Characteristics of leukemia and other cancer cells frequently considered to reflect aberrant differentiation may more often reflect clonal selection of cell types that are normally infrequent and transitory. The differentiation status of progenitor or mature lymphoid cells influences which genetic elements are at risk of being exploited, via mutation, recombination, or deletion, for clonal advantage. These alterations may frequently arise spontaneously as a consequence of the unique developmental and functional programs of lymphoid cells and have as a major phenotypic consequence the stabilization of transitory cellular phenotypes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greaves, M F -- New York, N.Y. -- Science. 1986 Nov 7;234(4777):697-704.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3535067" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Surface/analysis ; Cell Cycle ; Cell Differentiation ; Clone Cells ; Gene Expression Regulation ; Hematopoiesis ; Humans ; Leukemia/genetics/*pathology ; Leukemia, Lymphoid/genetics/pathology ; Leukemia, Myeloid, Acute/genetics/pathology ; Lymphocytes/pathology/*physiology ; Phenotype ; Proto-Oncogenes ; Receptors, Antigen, T-Cell/genetics
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    A perspective on degenerative brain disease (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-06-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kolata, G -- New York, N.Y. -- Science. 1986 Jun 6;232(4755):1197.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3704645" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Diseases/*etiology ; Cricetinae ; Gene Expression Regulation ; *Genes ; Humans ; Mice ; Prions/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 54
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    Purification and biochemical characterization of the promoter-specific transcription factor, Sp1 (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-10-03
    Description: The biochemical analysis of cellular trans-activators involved in promoter recognition provides an important step toward understanding the mechanisms of gene expression in animal cells. The promoter selective transcription factor, Sp1, has been purified from human cells to more than 95 percent homogeneity by sequence-specific DNA affinity chromatography. Isolation and renaturation of proteins purified from sodium dodecyl sulfate polyacrylamide gels allowed the identification of two polypeptides (105 and 95 kilodaltons) as those responsible for recognizing and interacting specifically with the GC-box promoter elements characteristic of Sp1 binding sites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Briggs, M R -- Kadonaga, J T -- Bell, S P -- Tjian, R -- T32 ES07075/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1986 Oct 3;234(4772):47-52.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3529394" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Chromatography, Affinity ; Chromatography, High Pressure Liquid ; Cricetinae ; Cricetulus ; DNA/metabolism ; DNA-Binding Proteins/*isolation & purification/metabolism ; Electrophoresis, Polyacrylamide Gel ; Gene Expression Regulation ; HeLa Cells/metabolism ; Humans ; Sp1 Transcription Factor ; Transcription Factors/*isolation & purification/metabolism ; Transcription, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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