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  • Transcription, Genetic
  • American Association for the Advancement of Science (AAAS)  (14)
  • American Chemical Society (ACS)
  • National Academy of Sciences
  • PANGAEA
  • 1985-1989  (14)
  • 1986  (14)
Collection
Publisher
  • American Association for the Advancement of Science (AAAS)  (14)
  • American Chemical Society (ACS)
  • National Academy of Sciences
  • PANGAEA
Years
  • 1985-1989  (14)
Year
  • 1
    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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  • 2
    Publication Date: 1986-10-10
    Description: An inversion of chromosome 14 present in the tumor cells of a patient with childhood acute lymphoblastic leukemia of B-cell lineage was shown to be the result of a site-specific recombination event between an immunoglobulin heavy-chain variable gene and the joining segment of a T-cell receptor alpha chain. This rearrangement resulted in the formation of a hybrid gene, part immunoglobulin and part T-cell receptor. Furthermore, this hybrid gene was transcribed into messenger RNA with a completely open reading frame. Thus, two loci felt to be normally activated at distinct and disparate points in lymphocyte development were unified and expressed in this tumor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Denny, C T -- Hollis, G F -- Hecht, F -- Morgan, R -- Link, M P -- Smith, S D -- Kirsch, I R -- New York, N.Y. -- Science. 1986 Oct 10;234(4773):197-200.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3092355" target="_blank"〉PubMed〈/a〉
    Keywords: *B-Lymphocytes ; Cell Differentiation ; Child ; *Chromosome Inversion ; Chromosomes, Human, 13-15 ; Humans ; Immunoglobulin Heavy Chains/*genetics ; Leukemia, Lymphoid/*genetics/pathology ; Models, Genetic ; Receptors, Antigen, T-Cell/*genetics ; Recombination, Genetic ; T-Lymphocytes ; Transcription, Genetic
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  • 3
    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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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-12-12
    Description: The suppression of the c-myc nuclear oncogene is associated with growth arrest and may therefore be directly controlled by naturally occurring growth inhibitors. The effect of tumor necrosis factor (TNF) and of interferon-gamma (IFN-gamma) on c-myc expression was investigated in HeLa cells, which respond to these cytokines by a specific arrest in the G0/G1 phase of the cell cycle. Northern blot and nuclear transcription analyses indicated that each cytokine reduced within 1 to 3 hours the c-myc messenger RNA levels as a result of transcriptional inhibition. Adding the two cytokines together at saturating levels resulted in enhanced inhibition of c-myc transcription and of the c-myc messenger RNA steady-state levels. While the reduction of c-myc messenger RNA by IFN-gamma was dependent on new protein synthesis, the inhibitory effect of TNF on c-myc messenger RNA was direct and was not abrogated by cycloheximide. The differential effect of the protein synthesis inhibitor and the cooperative inhibitory effects of the two cytokines when added together suggest that IFN-gamma and TNF reduce c-myc transcription through different molecular mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yarden, A -- Kimchi, A -- New York, N.Y. -- Science. 1986 Dec 12;234(4782):1419-21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3097823" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Survival ; Cycloheximide/pharmacology ; Gene Expression Regulation/*drug effects ; Glycoproteins/*pharmacology ; HeLa Cells/metabolism ; Humans ; Interferon-gamma/*pharmacology ; *Oncogenes ; RNA, Messenger/metabolism ; Transcription, Genetic ; Tumor Necrosis Factor-alpha
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  • 5
    Publication Date: 1986-01-17
    Description: Alterations of c-myc, c-rasHa, or c-myb oncogenes were found in more than one-third of human solid tumors. Amplification of c-myc occurred in advanced, widespread tumors or in aggressive primary tumors. Apparent allelic deletions of c-rasHa and c-myb can be correlated with progression and metastasis of carcinomas and sarcomas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yokota, J -- Tsunetsugu-Yokota, Y -- Battifora, H -- Le Fevre, C -- Cline, M J -- CA15619/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Jan 17;231(4735):261-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3941898" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Child ; DNA, Neoplasm/genetics/isolation & purification ; Female ; Humans ; Leukemia/genetics ; Male ; Middle Aged ; Neoplasms/*genetics ; Oncogenes ; Phenotype ; Polymorphism, Genetic ; *Proto-Oncogenes ; Sarcoma/genetics ; Transcription, Genetic
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  • 6
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-05-02
    Description: A novel procedure for saturation mutagenesis of cloned DNA was used to obtain more than 100 single base substitutions within the promoter of the mouse beta-major globin gene. The effects of these promoter substitutions on transcription were determined by transfecting the cloned mutant genes into HeLa cells on plasmids containing an SV40 transcription enhancer, and measuring the levels of correctly initiated beta-globin transcripts after 2 days. Mutations in three regions of the promoter resulted in a significant decrease in the level of transcription: (i) the CACCC box, located between -87 and -95, (ii) the CCAAT box, located between -72 and -77, and (iii) the TATA box, located between -26 and -30 relative to the start site of transcription. In contrast, two different mutations in nucleotides immediately upstream from the CCAAT box resulted in a 3- to 3.5-fold increase in transcription. With two minor exceptions, single base substitutions in all other regions of the promoter had no effect on transcription. These results precisely delineate the cis-acting sequences required for accurate and efficient initiation of beta-globin transcription, and they establish a general approach for the fine structure genetic analysis of eukaryotic regulatory sequences.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Myers, R M -- Tilly, K -- Maniatis, T -- New York, N.Y. -- Science. 1986 May 2;232(4750):613-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3457470" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cloning, Molecular ; DNA/genetics ; Genes ; Genetic Engineering ; Globins/biosynthesis/*genetics ; HeLa Cells ; Humans ; Mice ; Mutation ; *Promoter Regions, Genetic ; Transcription, Genetic
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  • 7
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    American Association for the Advancement of Science (AAAS)
    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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  • 8
    Publication Date: 1986-12-12
    Description: Hereditary hypogonadism in the hypogonadal (hpg) mouse is caused by a deletional mutation of at least 33.5 kilobases encompassing the distal half of the gene for the common biosynthetic precursor of gonadotropin-releasing hormone (GnRH) and GnRH-associated peptide (GAP). The partially deleted gene is transcriptionally active as revealed by in situ hybridization histochemistry of hpg hypothalamic tissue sections, but immunocytochemical analysis failed to show the presence of antigen corresponding to any part of the precursor protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mason, A J -- Hayflick, J S -- Zoeller, R T -- Young, W S 3rd -- Phillips, H S -- Nikolics, K -- Seeburg, P H -- New York, N.Y. -- Science. 1986 Dec 12;234(4782):1366-71.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3024317" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Brain Chemistry ; Chromosome Deletion ; Chromosome Mapping ; DNA Restriction Enzymes/metabolism ; Gonadotropin-Releasing Hormone/*genetics ; Histocytochemistry ; Hypogonadism/*genetics ; Mice ; Nucleic Acid Hybridization ; Protein Precursors/*genetics ; Transcription, Genetic
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  • 9
    Publication Date: 1986-10-24
    Description: Expression of the yeast his3 and other amino acid biosynthetic genes is induced during conditions of amino acid starvation. The coordination of this response is mediated by a positive regulatory protein called GCN4, which binds specifically to regulatory sites upstream of all coregulated genes and stimulates their transcription. The nucleotide sequence requirements of the his3 regulatory site were determined by analysis of numerous point mutations obtained by a novel method of cloning oligonucleotides. Almost all single base pair mutations within the nine base pair sequence ATGACTCTT significantly reduce his3 induction in vivo and GCN4 binding in vitro, whereas changes outside this region have minimal effects. One mutation, which generates a sequence that most closely resembles the consensus for 15 coregulated genes, increases both the level of induction and the affinity for GCN4 protein. The palindromic nature of the optimal sequence, ATGACTCAT, suggest that GCN4 protein binds as a dimer to adjacent half-sites that possibly overlap.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hill, D E -- Hope, I A -- Macke, J P -- Struhl, K -- GM 30186/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 Oct 24;234(4775):451-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3532321" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; DNA, Fungal/genetics ; *DNA-Binding Proteins ; Enzyme Induction ; Fungal Proteins/*physiology ; Genes, Regulator ; Histidine/*genetics ; Mutation ; *Protein Kinases ; Saccharomyces cerevisiae/*genetics ; *Saccharomyces cerevisiae Proteins ; Sequence Homology, Nucleic Acid ; Transcription Factors/*physiology ; Transcription, Genetic
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  • 10
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    American Association for the Advancement of Science (AAAS)
    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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  • 11
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-08-15
    Description: Chiral metal complexes provide unique molecular probes for DNA. Chiral reagents that "recognize" different local structures along the DNA strand have been designed by a process in which the asymmetry in shape and size of the complex is matched to that of the DNA helical groove. As a result, the chiral metal complexes provide very sensitive probes for local helical structure, both left- and right-handed. Direct coordination of chiral complexes to the DNA bases adds an element of sequence selectivity to the probe design. With a suitable reactive metal center, reagents that target chemically specific sites along the strand may be developed. One such chiral reagent, which cleaves left-handed DNA sites with photoactivation, has been useful in mapping this distinct conformation and examining its biological role. The conformation-specific molecular cleaver, much like a DNA-binding enzyme, recognizes and reacts at discrete sites along the DNA strand. These site-specific chiral metal complexes provide exciting new tools for probing the local variations in DNA structure and its role in the regulation of gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barton, J K -- GM33309/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 Aug 15;233(4765):727-34.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3016894" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; *DNA/genetics ; Genes, Regulator ; Intercalating Agents ; *Metals ; Models, Molecular ; *Nucleic Acid Conformation ; Plasmids ; RNA, Messenger/genetics ; Ruthenium ; Simian virus 40/genetics ; Transcription, Genetic
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  • 12
    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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  • 13
    Publication Date: 1986-10-03
    Description: Viral infection of mammalian cells entails the regulated induction of viral gene expression. The induction of many viral genes, including the herpes simplex virus gene encoding thymidine kinase (tk), depends on viral regulatory proteins that act in trans. Because recognition of the tk promoter by cellular transcription factors is well understood, its trans induction by viral regulatory proteins may serve as a useful model for the regulation of eukaryotic gene expression. A comprehensive set of mutations was therefore introduced into the chromosome of herpes simplex virus at the tk promoter to directly analyze the effects of promoter mutations on tk transcription. The promoter domains required for efficient tk expression under conditions of trans induction corresponded to those important for recognition by cellular transcription factors. Thus, trans induction of tk expression may be catalyzed initially by the interaction of viral regulatory proteins with cellular transcription factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coen, D M -- Weinheimer, S P -- McKnight, S L -- New York, N.Y. -- Science. 1986 Oct 3;234(4772):53-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3018926" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Gene Expression Regulation ; Genes, Viral ; Mutation ; *Promoter Regions, Genetic ; RNA, Messenger/genetics ; Simplexvirus/genetics/growth & development ; Transcription, Genetic ; *Virus Activation ; Xenopus
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  • 14
    Publication Date: 1986-12-05
    Description: A nonrepetitive complementary RNA probe specific for an intervening sequence of the rat pro-opiomelanocortin (POMC) gene primary transcript was used to analyze the hormonal regulation of POMC gene transcription in individual cell nuclei in the rat pituitary by in situ hybridization. This probe recognized only full-length POMC heterogeneous nuclear RNA, as verified by Northern blots of pituitary RNA. When pituitary sections were hybridized with this 3H-labeled POMC intron A probe, silver grains were predominantly localized over the nuclei of cells that expressed POMC in the anterior and intermediate lobes. Adrenalectomy increased both the average grain density over corticotroph nuclei and the number of cells in the anterior pituitary with significant numbers of silver grains over their nucleus. Dexamethasone administration to intact or adrenalectomized rats results in the rapid (within 30 minutes) disappearance of silver grains over the nuclei of corticotrophs in the anterior lobe, suggesting that POMC gene transcription had been inhibited. However, adrenalectomy or dexamethasone administration did not alter the silver grain density over nuclei of intermediate lobe melanotrophs. Thus, this in situ hybridization assay utilizing an intervening sequence-specific POMC probe can measure rapid physiological changes in POMC heterogeneous nuclear RNA in individual cell nuclei.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fremeau, R T Jr -- Lundblad, J R -- Pritchett, D B -- Wilcox, J N -- Roberts, J L -- AM27484/AM/NIADDK NIH HHS/ -- NS07786/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1986 Dec 5;234(4781):1265-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3775385" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Nucleus/metabolism ; DNA/genetics ; Dexamethasone/pharmacology ; Gene Expression Regulation/drug effects ; Genes ; Male ; Nucleic Acid Hybridization ; Pituitary Gland, Anterior/metabolism ; Pro-Opiomelanocortin/*biosynthesis/genetics ; RNA, Messenger/genetics ; Rats ; Rats, Inbred Strains ; Transcription, Genetic
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