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  • Articles  (50)
  • Gene Expression Regulation
  • 1990-1994  (50)
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  • Science. 247(4950): 1543-5.  (1)
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  • Articles  (50)
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  • 1
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    Enhancer point mutation results in a homeotic transformation in Drosophila (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-13
    Description: In Drosophila, the misexpression or altered activity of genes from the bithorax complex results in homeotic transformations. One of these genes, abd-A, normally specifies the identity of the second through fourth abdominal segments (A2 to A4). In the dominant Hyperabdominal mutations (Hab), portions of the third thoracic segment (T3) are transformed toward A2 as the result of ectopic abd-A expression. Sequence analysis and deoxyribonuclease I footprinting demonstrate that the misexpression of abd-A in two independent Hab mutations results from the same single base change in a binding site for the gap gene Kruppel protein. These results establish that the spatial limits of the homeotic genes are directly regulated by gap gene products.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shimell, M J -- Simon, J -- Bender, W -- O'Connor, M B -- New York, N.Y. -- Science. 1994 May 13;264(5161):968-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Biochemistry, University of California, Irvine 92717.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7909957" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Binding Sites ; DNA-Binding Proteins/genetics/metabolism ; *Drosophila Proteins ; Drosophila melanogaster/embryology/*genetics ; Enhancer Elements, Genetic/*genetics ; Gene Expression Regulation ; *Genes, Homeobox ; Genes, Insect ; Kruppel-Like Transcription Factors ; Molecular Sequence Data ; *Nuclear Proteins ; *Point Mutation ; Proteins/*genetics ; Regulatory Sequences, Nucleic Acid ; *Repressor Proteins ; Transcription Factors/genetics/metabolism
    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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    Mediation of c-Myc-induced apoptosis by p53 (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-30
    Description: The cellular proto-oncogene c-myc is involved in cell proliferation and transformation but is also implicated in the induction of programmed cell death (apoptosis). The same characteristics have been described for the tumor suppressor gene p53, the most commonly mutated gene in human cancer. In quiescent mouse fibroblasts expressing wild-type p53 protein, activation of c-Myc was found to induce apoptosis and cell cycle reentry, preceded by stabilization of p53. In contrast, in quiescent p53-null fibroblasts, activation of c-Myc induced cell cycle reentry but not apoptosis. These results suggest that p53 mediates apoptosis as a safeguard mechanism to prevent cell proliferation induced by oncogene activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hermeking, H -- Eick, D -- New York, N.Y. -- Science. 1994 Sep 30;265(5181):2091-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Klinische Molekularbiologie und Tumorgenetik Forschungszentrum fur Umwelt und Gesundheit, GSF, Munchen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8091232" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; *Apoptosis ; Cell Line ; Estradiol/pharmacology ; G1 Phase ; Gene Expression Regulation ; Genes, myc ; Genes, p53 ; Mice ; Proto-Oncogene Proteins c-myc/*metabolism ; Tamoxifen/analogs & derivatives/pharmacology ; Transfection ; Tumor Suppressor Protein p53/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Mining treasures from 'junk DNA' (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nowak, R -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):608-10.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7508142" target="_blank"〉PubMed〈/a〉
    Keywords: Biological Evolution ; DNA/*genetics ; DNA, Satellite ; Gene Expression Regulation ; *Genome, Human ; Humans ; *Introns ; Pseudogenes ; RNA/*genetics/metabolism ; Repetitive Sequences, Nucleic Acid
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Role of a conserved retinoic acid response element in rhombomere restriction of Hoxb-1 (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-16
    Description: After activation in mesoderm and neuroectoderm, expression of the Hoxb-1 gene is progressively restricted to rhombomere (r) 4 in the hindbrain. Analysis of the chick and mouse Hoxb-1 genes identified positive and negative regulatory regions that cooperate to mediate segment-restricted expression during rhombomere formation. An enhancer generates expression extending into r3 and r5, and a repressor limits this domain to r4. The repressor contains a conserved retinoic acid response element, point mutations in which allow expression to spread into adjacent rhombomeres. Retinoids and their nuclear receptors may therefore participate in sharpening segment-restricted expression of Hoxb-1 during rhombomere boundary formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Studer, M -- Popperl, H -- Marshall, H -- Kuroiwa, A -- Krumlauf, R -- New York, N.Y. -- Science. 1994 Sep 16;265(5179):1728-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lab of Developmental Neurobiology, National Institute for Medical Research, Mill Hill, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7916164" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Chick Embryo ; Enhancer Elements, Genetic ; Gene Expression Regulation ; *Genes, Homeobox ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; Neural Crest/metabolism ; Oligonucleotides/metabolism ; Point Mutation ; Receptors, Cytoplasmic and Nuclear/metabolism ; Receptors, Retinoic Acid/metabolism ; *Regulatory Sequences, Nucleic Acid ; Retinoid X Receptors ; Rhombencephalon/*embryology/metabolism ; *Transcription Factors ; Tretinoin/*pharmacology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Loss of circadian behavioral rhythms and per RNA oscillations in the Drosophila mutant timeless (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-18
    Description: Eclosion, or emergence of adult flies from the pupa, and locomotor activity of adults occur rhythmically in Drosophila melanogaster, with a circadian period of about 24 hours. Here, a clock mutation, timeless (tim), is described that produces arrhythmia for both behaviors. The effects of tim on behavioral rhythms are likely to involve products of the X chromosome-linked clock gene period (per), because tim alters circadian oscillations of per RNA. Genetic mapping places tim on the left arm of the second chromosome between dumpy (dp) and decapentaplegic (dpp).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sehgal, A -- Price, J L -- Man, B -- Young, M W -- New York, N.Y. -- Science. 1994 Mar 18;263(5153):1603-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, National Science Foundation Science and Technology Center for Biological Timing, Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128246" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks/*genetics ; Chromosome Mapping ; Circadian Rhythm/*genetics ; Drosophila Proteins ; Drosophila melanogaster/genetics/*physiology ; Gene Expression Regulation ; *Genes, Insect ; Metamorphosis, Biological ; Motor Activity ; Mutagenesis, Insertional ; Mutation ; Nuclear Proteins/*genetics/physiology ; Period Circadian Proteins ; RNA, Messenger/genetics/*metabolism
    Print ISSN: 0036-8075
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  • 6
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    Regulation of alternative splicing in vivo by overexpression of antagonistic splicing factors (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-16
    Description: The opposing effects of SF2/ASF and heterogeneous nuclear ribonucleoprotein (hnRNP) A1 influence alternative splicing in vitro. SF2/ASF or hnRNP A1 complementary DNAs were transiently overexpressed in HeLa cells, and the effect on alternative splicing of several cotransfected reporter genes was measured. Increased expression of SF2/ASF activated proximal 5' splice sites, promoted inclusion of a neuron-specific exon, and prevented abnormal exon skipping. Increased expression of hnRNP A1 activated distal 5' splice sites. Therefore, variations in the intracellular levels of antagonistic splicing factors influence different modes of alternative splicing in vivo and may be a natural mechanism for tissue-specific or developmental regulation of gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caceres, J F -- Stamm, S -- Helfman, D M -- Krainer, A R -- New York, N.Y. -- Science. 1994 Sep 16;265(5179):1706-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, NY 11724.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8085156" target="_blank"〉PubMed〈/a〉
    Keywords: Adenovirus E1A Proteins/genetics ; *Alternative Splicing ; Base Sequence ; DNA, Complementary/genetics ; Exons ; Gene Expression Regulation ; Genes, Reporter ; HeLa Cells ; *Heterogeneous-Nuclear Ribonucleoprotein Group A-B ; Heterogeneous-Nuclear Ribonucleoproteins ; Humans ; Molecular Sequence Data ; Nuclear Proteins/*genetics/*metabolism ; RNA-Binding Proteins ; Ribonucleoproteins/genetics/*metabolism ; Serine-Arginine Splicing Factors ; Transfection ; Tropomyosin/genetics
    Print ISSN: 0036-8075
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  • 7
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    Chromosome ends catch fire (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1994 Sep 16;265(5179):1656-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7521969" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Aging ; Cell Division ; Cell Transformation, Neoplastic ; Ciliophora/enzymology/genetics ; DNA Nucleotidylexotransferase/*metabolism ; Gene Expression Regulation ; Humans ; Molecular Sequence Data ; Neoplasms/enzymology/etiology ; RNA/metabolism ; Telomere/chemistry/*physiology ; Yeasts/enzymology/genetics
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Involvement of the IRF-1 transcription factor in antiviral responses to interferons (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-24
    Description: The mechanisms underlying interferon (IFN)-induced antiviral states are not well understood. Interferon regulatory factor-1 (IRF-1) is an IFN-inducible transcriptional activator, whereas IRF-2 suppresses IRF-1 action. The inhibition of encephalomyocarditis virus (EMCV) replication by IFN-alpha and especially by IFN-gamma was impaired in cells from mice with a null mutation in the IRF-1 gene (IRF-1-/- mice). The IRF-1-/- mice were less resistant than normal mice to EMCV infection, as revealed by accelerated mortality and a larger virus titer in target organs. The absence of IRF-1 did not clearly affect replication of two other types of viruses. Thus, IRF-1 is necessary for the antiviral action of IFNs against some viruses, but IFNs activate multiple activation pathways through diverse target genes to induce the antiviral state.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kimura, T -- Nakayama, K -- Penninger, J -- Kitagawa, M -- Harada, H -- Matsuyama, T -- Tanaka, N -- Kamijo, R -- Vilcek, J -- Mak, T W -- R35CA49731/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1921-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular and Cellular Biology, Osaka University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8009222" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cardiovirus Infections/*immunology/microbiology ; Cells, Cultured ; DNA-Binding Proteins/genetics/*physiology ; Encephalomyocarditis virus/physiology ; Gene Expression Regulation ; Interferon Regulatory Factor-1 ; Interferon-alpha/*pharmacology ; Interferon-gamma/*pharmacology ; Mice ; Mutation ; Phosphoproteins/genetics/*physiology ; Simplexvirus/physiology ; Transcription Factors/genetics/*physiology ; Vesicular stomatitis Indiana virus/physiology ; *Virus Replication
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Knockout mice: round two (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 Jul 1;265(5168):26-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8016653" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antiporters/genetics ; DNA Nucleotidyltransferases/genetics/metabolism ; DNA Polymerase I/genetics/metabolism ; Gene Deletion ; Gene Expression Regulation ; Genetic Engineering/*methods ; *Integrases ; Mice ; Mice, Knockout/*genetics ; Mice, Transgenic ; Repressor Proteins/genetics ; Stem Cells ; T-Lymphocytes/enzymology ; Tetracycline/pharmacology ; *Viral Proteins
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Time is the essence: molecular analysis of the biological clock (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Page, T L -- NS15264/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 18;263(5153):1570-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Vanderbilt University, Nashville, TN 37235.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128243" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks/*genetics ; Circadian Rhythm/*genetics ; Drosophila Proteins ; Drosophila melanogaster/genetics/*physiology ; Gene Expression Regulation ; Gene Expression Regulation, Fungal ; Genes, Fungal ; Genes, Insect ; Neurospora crassa/genetics/*physiology ; Nuclear Proteins/*genetics/physiology ; Period Circadian Proteins ; RNA, Messenger/genetics/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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    Mineralocorticoids, glucocorticoids, receptors and response elements (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Funder, J W -- New York, N.Y. -- Science. 1993 Feb 19;259(5098):1132-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Baker Medical Research Institute, Prahran, Victoria, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8382375" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Binding Sites ; DNA/*metabolism ; DNA-Binding Proteins/*metabolism ; Gene Expression Regulation ; Glucocorticoids/*physiology ; Mineralocorticoids/*physiology ; Models, Biological ; Molecular Sequence Data ; Receptors, Glucocorticoid/*metabolism ; Receptors, Mineralocorticoid ; Receptors, Steroid/*metabolism ; *Transcription, Genetic
    Print ISSN: 0036-8075
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  • 12
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    Tumor rejection after direct costimulation of CD8+ T cells by B7-transfected melanoma cells (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-15
    Description: A variety of tumors are potentially immunogenic but do not stimulate an effective anti-tumor immune response in vivo. Tumors may be capable of delivering antigen-specific signals to T cells, but may not deliver the costimulatory signals necessary for full activation of T cells. Expression of the costimulatory ligand B7 on melanoma cells was found to induce the rejection of a murine melanoma in vivo. This rejection was mediated by CD8+ T cells; CD4+ T cells were not required. These results suggest that B7 expression renders tumor cells capable of effective antigen presentation, leading to their eradication in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Townsend, S E -- Allison, J P -- CA57986/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Jan 15;259(5093):368-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7678351" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; Antigens, CD80 ; Antigens, Surface/genetics/*immunology ; CD4-Positive T-Lymphocytes/immunology ; Cross Reactions ; Female ; Gene Expression Regulation ; Genetic Vectors ; Ligands ; *Lymphocyte Activation ; Melanoma/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Nude ; T-Lymphocytes, Regulatory/*immunology ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
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  • 13
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    Controlling signal transduction with synthetic ligands (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-11-12
    Description: Dimerization and oligomerization are general biological control mechanisms contributing to the activation of cell membrane receptors, transcription factors, vesicle fusion proteins, and other classes of intra- and extracellular proteins. Cell permeable, synthetic ligands were devised that can be used to control the intracellular oligomerization of specific proteins. To demonstrate their utility, these ligands were used to induce intracellular oligomerization of cell surface receptors that lacked their transmembrane and extracellular regions but contained intracellular signaling domains. Addition of these ligands to cells in culture resulted in signal transmission and specific target gene activation. Monomeric forms of the ligands blocked the pathway. This method of ligand-regulated activation and termination of signaling pathways has the potential to be applied wherever precise control of a signal transduction pathway is desired.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Spencer, D M -- Wandless, T J -- Schreiber, S L -- Crabtree, G R -- New York, N.Y. -- Science. 1993 Nov 12;262(5136):1019-24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7694365" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Carrier Proteins/*metabolism ; Cross-Linking Reagents ; Gene Expression Regulation ; Heat-Shock Proteins/*metabolism ; Ligands ; Membrane Proteins/*metabolism ; Models, Biological ; Molecular Sequence Data ; Polymers ; Receptors, Antigen, T-Cell/*metabolism ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; T-Lymphocytes/*metabolism ; Tacrolimus/*analogs & derivatives/chemical synthesis/chemistry/metabolism ; Tacrolimus Binding Proteins ; Transcriptional Activation ; Transfection ; Tumor Cells, Cultured
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  • 14
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    Regulation of CREB phosphorylation in the suprachiasmatic nucleus by light and a circadian clock (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-09
    Description: Mammalian circadian rhythms are regulated by a pacemaker within the suprachiasmatic nuclei (SCN) of the hypothalamus. The molecular mechanisms controlling the synchronization of the circadian pacemaker are unknown; however, immediate early gene (IEG) expression in the SCN is tightly correlated with entrainment of SCN-regulated rhythms. Antibodies were isolated that recognize the activated, phosphorylated form of the transcription factor cyclic adenosine monophosphate response element binding protein (CREB). Within minutes after exposure of hamsters to light, CREB in the SCN became phosphorylated on the transcriptional regulatory site, Ser133. CREB phosphorylation was dependent on circadian time: CREB became phosphorylated only at times during the circadian cycle when light induced IEG expression and caused phase shifts of circadian rhythms. These results implicate CREB in neuronal signaling in the hypothalamus and suggest that circadian clock gating of light-regulated molecular responses in the SCN occurs upstream of phosphorylation of CREB.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ginty, D D -- Kornhauser, J M -- Thompson, M A -- Bading, H -- Mayo, K E -- Takahashi, J S -- Greenberg, M E -- F31 MH10241/MH/NIMH NIH HHS/ -- F32 NS08764/NS/NINDS NIH HHS/ -- NS 28829/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 Apr 9;260(5105):238-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8097062" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; *Circadian Rhythm ; Colforsin/pharmacology ; Cricetinae ; Cyclic AMP Response Element-Binding Protein/immunology/*metabolism ; Darkness ; Gene Expression Regulation ; Genes, fos ; Glutamates/pharmacology ; Glutamic Acid ; *Light ; Molecular Sequence Data ; PC12 Cells ; Phosphorylation ; Potassium Chloride/pharmacology ; Suprachiasmatic Nucleus/drug effects/*metabolism
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  • 15
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    A link between cyclin A expression and adhesion-dependent cell cycle progression (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-03
    Description: Cell adhesion has an essential role in regulating proliferation during the G1 phase of the cell cycle, and loss of this adhesion requirement is a classic feature of oncogenic transformation. The appearance of cyclin A messenger RNA and protein in late G1 was dependent on cell adhesion in both NRK and NIH 3T3 fibroblasts. In contrast, the expression of Cdc2, Cdk2, cyclin D1, and cyclin E was independent of adhesion in both cell lines. Transfection of NRK cells with a cyclin A complementary DNA resulted in adhesion-independent accumulation of cyclin A protein and cyclin A-associated kinase activity. These transfected cells also entered S phase and complete multiple rounds of cell division in the absence of cell adhesion. Thus, cyclin A is a target of the adhesion-dependent signals that control cell proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guadagno, T M -- Ohtsubo, M -- Roberts, J M -- Assoian, R K -- GM48224/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Dec 3;262(5139):1572-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biophysics, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8248807" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; CDC2 Protein Kinase/biosynthesis ; *CDC2-CDC28 Kinases ; Cell Adhesion/*physiology ; Cell Cycle/*physiology ; Cell Line ; Cyclin-Dependent Kinase 2 ; *Cyclin-Dependent Kinases ; Cyclins/*biosynthesis ; Fibroblasts/cytology/metabolism ; Gene Expression Regulation ; Humans ; Mice ; Protein Kinases/biosynthesis ; *Protein-Serine-Threonine Kinases ; Rats ; Transfection
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  • 16
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    The many roads that lead to Ras (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feig, L A -- New York, N.Y. -- Science. 1993 May 7;260(5109):767-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Sackler School of Graduate Biomedical Sciences, Tufts University School of Medicine, Boston, MA 02111.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8484117" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/metabolism ; *Cell Cycle Proteins ; Fungal Proteins/genetics/*metabolism ; GTP-Binding Proteins/genetics/*metabolism ; Gene Expression Regulation ; Genes, ras ; Guanosine Diphosphate/*metabolism ; Guanosine Triphosphate/*metabolism ; Humans ; Membrane Proteins/genetics/metabolism ; Proto-Oncogene Proteins/genetics/metabolism ; Proto-Oncogene Proteins c-vav ; Proto-Oncogene Proteins p21(ras)/genetics/*metabolism ; Saccharomyces cerevisiae/genetics/metabolism ; Saccharomyces cerevisiae Proteins ; Son of Sevenless Proteins ; rap GTP-Binding Proteins ; *ras-GRF1
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  • 17
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    Neuroblast specification and formation regulated by wingless in the Drosophila CNS (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-09-17
    Description: The Drosophila central nervous system (CNS) develops from a heterogeneous population of neural stem cells (neuroblasts), yet the genes regulating neuroblast determination remain unknown. The segmentation gene wingless is regionally expressed in the neuroectoderm from which neuroblasts develop. A conditional wingless mutation is used to inactivate CNS function without affecting segmentation. The stripe of wingless-expressing neuroectoderm generates apparently normal neuroblasts after wingless inactivation; however, adjacent anterior and posterior neuroectoderm requires wingless nonautonomously for subsequent neuroblast determination and formation. Loss of wingless results in the absence or duplication of identified neuroblasts, highlighting its role in generating neuroblast diversity in the CNS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chu-LaGraff, Q -- Doe, C Q -- New York, N.Y. -- Science. 1993 Sep 17;261(5128):1594-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Structural Biology, University of Illinois, Urbana 61801.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8372355" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Central Nervous System/embryology ; Drosophila/embryology/*genetics ; *Drosophila Proteins ; Gene Expression Regulation ; *Genes, Insect ; Mutation ; Neurons/*cytology ; Phenotype ; Proto-Oncogene Proteins/*genetics/physiology ; Stem Cells/*cytology ; Wnt1 Protein
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  • 18
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    The cell's nucleus shapes up (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffman, M -- New York, N.Y. -- Science. 1993 Feb 26;259(5099):1257-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8446894" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport ; Cell Nucleus/*ultrastructure ; Gene Expression Regulation ; In Vitro Techniques ; Nuclear Matrix/*ultrastructure ; *RNA Processing, Post-Transcriptional ; RNA Splicing ; RNA, Messenger/genetics/metabolism ; Rats ; Spliceosomes/metabolism/ultrastructure
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  • 19
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    Spatial control of the gap gene knirps in the Drosophila embryo by posterior morphogen system (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-02-21
    Description: The gap genes of Drosophila are the first zygotic genes to respond to the maternal positional signals and establish the body pattern along the anterior-posterior axis. The gap gene knirps, required for patterning in the posterior region of the embryo, can be activated throughout the wild-type embryo and is normally repressed from the anterior and posterior sides. These results provide direct molecular evidence that the posterior morphogen system interacts in a fundamentally different manner than do hunchback and bicoid, which are responsible for anterior pattern formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pankratz, M J -- Busch, M -- Hoch, M -- Seifert, E -- Jackle, H -- New York, N.Y. -- Science. 1992 Feb 21;255(5047):986-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck Institut fur Biophysikalische Chemie, Abteilung Molekulare Entwicklungsbiologie, Gottingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1546296" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Binding Sites ; Cloning, Molecular ; Drosophila melanogaster/embryology/*genetics ; Gene Expression Regulation ; Genes ; Molecular Sequence Data ; Morphogenesis ; Regulatory Sequences, Nucleic Acid
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  • 20
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    Hidden messages in genetic maps (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-10-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Farr, C J -- Goodfellow, P N -- New York, N.Y. -- Science. 1992 Oct 2;258(5079):49.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genetics Department, University of Cambridge, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1439767" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chromosome Mapping ; Conserved Sequence ; Dosage Compensation, Genetic ; Gene Expression Regulation ; *Genome ; Humans ; Mammals/*genetics ; Rats ; *X Chromosome ; *Y Chromosome
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  • 21
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    Molecular characterization of helix-loop-helix peptides (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-02-21
    Description: A class of regulators of eukaryotic gene expression contains a conserved amino acid sequence responsible for protein oligomerization and binding to DNA. This structure consists of an arginine- and lysine-rich basic region followed by a helix-loop-helix motif, which together mediate specific binding to DNA. Peptides were prepared that span this motif in the MyoD protein; in solution, they formed alpha-helical dimers and tetramers. They bound to DNA as dimers and their alpha-helical content increased on binding. Parallel and antiparallel four-helix models of the DNA-bound dimer were constructed. Peptides containing disulfide bonds were engineered to test the correctness of the two models. A disulfide that is compatible with the parallel model promotes specific interaction with DNA, whereas a disulfide compatible with the antiparallel model abolishes specific binding. Electron paramagnetic resonance (EPR) measurements of nitroxide-labeled peptides provided intersubunit distance measurements that also supported the parallel model.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anthony-Cahill, S J -- Benfield, P A -- Fairman, R -- Wasserman, Z R -- Brenner, S L -- Stafford, W F 3rd -- Altenbach, C -- Hubbell, W L -- DeGrado, W F -- GM13731/GM/NIGMS NIH HHS/ -- GM14321/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Feb 21;255(5047):979-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biotechnology Department, DuPont Merck Pharmaceutical Co., Wilmington, DE 19880-0328.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1312255" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Circular Dichroism ; DNA-Binding Proteins/*chemistry ; Disulfides ; Electron Spin Resonance Spectroscopy ; Enhancer Elements, Genetic ; Gene Expression Regulation ; Humans ; Models, Molecular ; Molecular Sequence Data ; Protein Conformation ; Regulatory Sequences, Nucleic Acid ; Sequence Alignment ; Transcription Factors/*chemistry
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  • 22
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    DNA binding activity of recombinant SRY from normal males and XY females (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-24
    Description: The protein encoded by the human testis determining gene, SRY, contains a high mobility group (HMG) box related to that present in the T cell-specific, DNA-binding protein TCF-1. Recombinant SRY protein was able to bind to the same core sequence AACAAAG recognized by TCF-1 in a sequence dependent manner. In five XY females point mutations were found in the region encoding the HMG box. In four cases DNA binding activity of mutant SRY protein was negligible; in the fifth case DNA binding was reduced. These results imply that the DNA binding activity of SRY is required for sex determination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harley, V R -- Jackson, D I -- Hextall, P J -- Hawkins, J R -- Berkovitz, G D -- Sockanathan, S -- Lovell-Badge, R -- Goodfellow, P N -- MC_U117562207/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 1992 Jan 24;255(5043):453-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Molecular Genetics Laboratory, Imperial Cancer Research Fund, London, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1734522" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; DNA-Binding Proteins/*metabolism ; Female ; Gene Expression Regulation ; Humans ; In Vitro Techniques ; Male ; Mice ; Molecular Sequence Data ; *Nuclear Proteins ; Oligonucleotide Probes ; Recombinant Proteins/metabolism ; Sequence Alignment ; Sex-Determining Region Y Protein ; Transcription Factors/metabolism
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  • 23
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    Competition for overlapping sites in the regulatory region of the Drosophila gene Kruppel (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-04-03
    Description: A 730-base pair element regulates expression of the Drosophila gap gene Kruppel (Kr) in response to the fly anterior morphogen bicoid (bcd). Two hormone receptor-like proteins, encoded by the genes knirps (kni) and tailless (tll), bind specifically to the element. In vitro, kni protein competes with the homeodomain-containing bcd protein in binding to a 16-base pair target sequence. In vivo experiments suggest that both kni and tll act as competitive repressors of bcd-mediated activation of Kr. These results suggest a mechanism by which developmental genes can be regulated in response to an activating morphogen gradient antagonized by repressors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoch, M -- Gerwin, N -- Taubert, H -- Jackle, H -- New York, N.Y. -- Science. 1992 Apr 3;256(5053):94-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur Biophysikalische Chemie, Abteilung Molekulare Entwicklungsbiologie, Gottingen, Federal Republic of Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1348871" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Binding, Competitive ; Chloramphenicol O-Acetyltransferase/genetics/metabolism ; DNA-Binding Proteins/*genetics/metabolism ; Drosophila/embryology/*genetics ; *Drosophila Proteins ; Embryo, Nonmammalian/physiology ; Female ; Gene Expression Regulation ; *Genes, Homeobox ; Genes, Regulator ; Molecular Sequence Data ; *Regulatory Sequences, Nucleic Acid ; Repressor Proteins/*genetics/metabolism ; Restriction Mapping ; beta-Galactosidase/genetics/metabolism
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  • 24
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    Function of the homeodomain protein GHF1 in pituitary cell proliferation (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-07-12
    Description: Mutations that cause pituitary dwarfism in the mouse reside in the gene encoding the transcription factor growth hormone factor 1 (GHF1 or pit1). These dwarf mice (dw and dwJ) are deficient in growth hormone (GH) and prolactin (PRL) synthesis and exhibit pituitary hypoplasia, suggesting a stem cell defect. With antisense oligonucleotide technology, a cell culture model of this genetic defect was developed. Specific inhibition of GHF1 synthesis by complementary oligonucleotides led to a marked decrease in GH and PRL expression and to a marked decrease in proliferation of somatotrophic cell lines. These results provide direct evidence that the homeodomain protein GHF1 is required not only for the establishment and maintenance of the differentiated phenotype but for cell proliferation as well.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Castrillo, J L -- Theill, L E -- Karin, M -- DK38527/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1991 Jul 12;253(5016):197-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, 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/1677216" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antisense Elements (Genetics) ; Base Sequence ; *Cell Division ; Cells, Cultured ; DNA/biosynthesis ; DNA-Binding Proteins/*physiology ; Dwarfism/genetics ; Gene Expression Regulation ; *Genes, Homeobox ; Growth Hormone/genetics ; In Vitro Techniques ; Mice ; Molecular Sequence Data ; Pituitary Gland/*cytology/physiology ; Prolactin/genetics ; Transcription Factor Pit-1 ; Transcription Factors/*physiology
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  • 25
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    A genetic model for interaction of the homeodomain recognition helix with DNA (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-01-25
    Description: The Bicoid homeodomain protein controls anterior development in the Drosophila embryo by binding to DNA and regulating gene expression. With the use of genetic assays in yeast, the interaction between the Bicoid homeodomain and a series of mutated DNA sites was studied. These experiments defined important features of homeodomain binding sites, identified specific amino acid-base pair contacts, and suggested a model for interaction of the recognition alpha-helices of Bicoid and Antennapedia-class homeodomain proteins with DNA. The model is in general agreement with results of crystallographic and magnetic resonance studies, but differs in important details. It is likely that genetic studies of protein-DNA interaction will continue to complement conventional structural approaches.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanes, S D -- Brent, R -- New York, N.Y. -- Science. 1991 Jan 25;251(4992):426-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Massachusetts General Hospital, Boston 02114.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1671176" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; DNA/*metabolism ; DNA-Binding Proteins/*genetics/metabolism ; Drosophila ; Gene Expression Regulation ; Genes, Homeobox/*genetics ; *Homeodomain Proteins ; Insect Hormones/*genetics/metabolism ; *Models, Genetic ; Molecular Sequence Data ; *Trans-Activators ; Transcription, Genetic
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  • 26
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    Three Europeans find their own road to fame (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-11-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1991 Nov 22;254(5035):1116-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1957163" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle ; Europe ; Gene Expression Regulation ; History, 20th Century ; Humans ; Neoplasms/etiology/*physiopathology ; Oncogenic Viruses/pathogenicity
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  • 27
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    Establishment of the mesoderm-neuroectoderm boundary in the Drosophila embryo (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-04
    Description: A gradient of the maternal morphogen dorsal establishes asymmetric patterns of gene expression along the dorsal-ventral axis of early embryos and activates the regulatory genes twist and snail, which are responsible for the differentiation of the ventral mesoderm. Expression of snail is restricted to the presumptive mesoderm, and the sharp lateral limits of this expression help to define the mesoderm-neuroectoderm boundary by repressing the expression of regulatory genes that are responsible for the differentiation of the neuroectoderm. The snail gene encodes a zinc finger protein, and neuroectodermal genes that are normally restricted to ventral-lateral regions of early embryos are expressed throughout ventral regions of snail- mutants. The formation of the sharp snail border involves dosage-sensitive interactions between dorsal and twist, which encode regulatory proteins that are related to the mammalian transcription factors NF-kB and MyoD, respectively.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kosman, D -- Ip, Y T -- Levine, M -- Arora, K -- GM 46638/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Oct 4;254(5028):118-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biology Department, 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/1925551" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA Probes ; DNA-Binding Proteins/metabolism ; Drosophila Proteins ; Drosophila melanogaster/*embryology ; Ectoderm/cytology/*physiology ; Embryonic Induction ; Gene Expression Regulation ; Mesoderm/cytology/*physiology ; *Morphogenesis ; Nervous System/*embryology ; Nuclear Proteins/metabolism ; *Transcription Factors ; Twist Transcription Factor ; Zinc Fingers
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  • 28
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    Global suppression of protein folding defects and inclusion body formation (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-07-05
    Description: Amino acid substitutions at a site in the center of the bacteriophage protein P22 tailspike polypeptide chain suppress temperature-sensitive folding mutations at many sites throughout the chain. Characterization of the intracellular folding and chain assembly process reveals that the suppressors act in the folding pathway, inhibiting the aggregation of an early folding intermediate into the kinetically trapped inclusion body state. The suppressors alone increase the folding efficiency of the otherwise wild-type polypeptide chain without altering the stability or activity of the native state. These amino acid substitutions identify an unexpected aspect of the protein folding grammar--sequences within the chain that carry information inhibiting unproductive off-pathway conformations. Such mutations may serve to increase the recovery of protein products of cloned genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mitraki, A -- Fane, B -- Haase-Pettingell, C -- Sturtevant, J -- King, J -- GMS17,980/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Jul 5;253(5015):54-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1648264" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Coliphages ; DNA Mutational Analysis ; Electrophoresis, Polyacrylamide Gel ; Gene Expression Regulation ; Inclusion Bodies/*chemistry ; Molecular Sequence Data ; Mutation ; *Protein Conformation ; Viral Proteins/*chemistry ; Viral Tail Proteins
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    Regulation of the apolipoprotein AI gene by ARP-1, a novel member of the steroid receptor superfamily (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-02-01
    Description: Apolipoprotein AI (apoAI) is a lipid-binding protein that participates in the transport of cholesterol and other lipids in the plasma. A complementary DNA clone for a protein that bound to regulatory elements of the apoAI gene was isolated. This protein, designated apoAI regulatory protein-1 (ARP-1), is a novel member of the steroid hormone receptor superfamily. ARP-1 bound to DNA as a dimer, and its dimerization domain was localized to the COOH-terminal region. ARP-1 also bound to a thyroid hormone-responsive element and to regulatory regions of the apoB, apoCIII, insulin, and ovalbumin genes. In cotransfection experiments, ARP-1 downregulated the apoAI gene. The involvement of ARP-1 in the regulation of apoAI gene expression suggests that it may participate in lipid metabolism and cholesterol homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ladias, J A -- Karathanasis, S K -- New York, N.Y. -- Science. 1991 Feb 1;251(4993):561-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiology, Children's Hospital, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1899293" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Apolipoprotein A-I ; Apolipoproteins A/*genetics ; Base Sequence ; COUP Transcription Factor II ; COUP Transcription Factors ; Cloning, Molecular ; DNA/metabolism ; DNA-Binding Proteins/*metabolism ; Gene Expression Regulation ; Humans ; Lipoproteins, HDL/*genetics ; Molecular Sequence Data ; Oligonucleotide Probes ; Receptors, Steroid/*metabolism ; Regulatory Sequences, Nucleic Acid ; *Transcription Factors
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    FTZ-F1, a steroid hormone receptor-like protein implicated in the activation of fushi tarazu (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-05-10
    Description: The Drosophila homeobox segmentation gene fushi tarazu (ftz) is expressed in a seven-stripe pattern during early embryogenesis. This characteristic pattern is largely specified by the zebra element located immediately upstream of the ftz transcriptional start site. The FTZ-F1 protein, one of multiple DNA binding factors that interacts with the zebra element, is implicated in the activation of ftz transcription, especially in stripes 1, 2, 3, and 6. An FTZ-F1 complementary DNA has been cloned by recognition site screening of a Drosophila expression library. The identity of the FTZ-F1 complementary DNA clone was confirmed by immunological cross-reaction with antibodies to FTZ-F1 and by sequence analysis of peptides from purified FTZ-F1 protein. The predicted amino acid sequence of FTZ-F1 revealed that the protein is a member of the nuclear hormone receptor superfamily. This finding raises the possibility that a hormonal ligand affects the expression of a homeobox segmentation gene early in embryonic development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lavorgna, G -- Ueda, H -- Clos, J -- Wu, C -- New York, N.Y. -- Science. 1991 May 10;252(5007):848-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Biochemistry, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1709303" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Blotting, Northern ; Blotting, Southern ; Blotting, Western ; Chromosome Mapping ; Cloning, Molecular ; Drosophila Proteins ; Drosophila melanogaster ; Fushi Tarazu Transcription Factors ; Gene Expression Regulation ; Genes, Homeobox ; *Homeodomain Proteins ; Insect Hormones/*chemistry ; Molecular Sequence Data ; Open Reading Frames ; RNA/analysis ; Receptors, Steroid/genetics ; Sequence Homology, Nucleic Acid ; Transcription, Genetic ; Zinc Fingers
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    CCAAT-enhancer binding protein: a component of a differentiation switch (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-01-18
    Description: The CCAAT-enhancer binding protein (C/EBP) has now been found to promote the terminal differentiation of adipocytes. During the normal course of adipogenesis, C/EBP expression is restricted to a terminal phase wherein proliferative growth is arrested, and specialized cell phenotype is first manifested. A conditional form of C/EBP was developed, making it feasible to test its capacity to regulate the differentiation of cultured adipocytes. Premature expression of C/EBP in adipoblasts caused a direct cessation of mitotic growth. Moreover, when abetted by the effects of three adipogenic hormones, C/EBP promoted terminal cell differentiation. Since C/EBP is expressed in a variety of tissues, it may have a fundamental role in regulating the balance between cell growth and differentiation in higher animals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Umek, R M -- Friedman, A D -- McKnight, S L -- New York, N.Y. -- Science. 1991 Jan 18;251(4991):288-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Research Laboratories, Department of Embryology, Carnegic Institution of Washington, Baltimore, MD 21210.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1987644" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/*cytology ; Animals ; CCAAT-Enhancer-Binding Proteins ; *Cell Differentiation ; Cell Division ; DNA-Binding Proteins/*physiology ; Gene Expression Regulation ; L Cells (Cell Line) ; Mice ; Nuclear Proteins/*physiology ; Receptors, Steroid/physiology ; Regulatory Sequences, Nucleic Acid ; Structure-Activity Relationship
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    Cross-regulatory interactions between the proneural achaete and scute genes of Drosophila (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-03-22
    Description: The achaete (ac) and scute (sc) genes of Drosophila allow cells to become sensory organ mother cells. Although ac and sc have similar patterns of expression, deletion of either gene removes specific subsets of sensory organs. This specificity was shown to reside in the peculiar regulation of ac and sc expression. These genes are first activated in complementary spatial domains in response to different cis-regulatory sequences. Each gene product then stimulates expression of the other gene, thus generating similar patterns of expression. Therefore, removal of one gene leads to the absence of both proneural gene products and sensory organs in the sites specified by its cis-regulatory sequences.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martinez, C -- Modolell, J -- New York, N.Y. -- Science. 1991 Mar 22;251(5000):1485-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centro de Biologia Molecular, Consejo Superior de Investigaciones Cientificas, Universidad Autonoma de Madrid, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1900954" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drosophila melanogaster/embryology/*genetics ; Gene Expression Regulation ; Nervous System/*embryology ; Promoter Regions, Genetic
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    Regulation of a segmentation stripe by overlapping activators and repressors in the Drosophila embryo (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-11-29
    Description: Gene expression stripes in Drosophila melanogaster embryos provide a model for how eukaryotic promoters are turned on and off in response to combinations of transcriptional regulators. Genetic studies suggested that even-skipped (eve) stripe 2 is controlled by three gap genes, hunchback (hb), Kruppel (Kr), and giant (gt), and by the maternal morphogen bicoid (bcd). A direct link is established between binding sites for these regulatory proteins in the stripe 2 promoter element and the expression of the stripe during early embryogenesis. The bcd and hb protein binding sites mediate activation, whereas neighboring gt and Kr protein sites repress expression and establish the stripe borders. The stripe 2 element has the properties of a genetic on-off switch.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stanojevic, D -- Small, S -- Levine, M -- GM 34431/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Nov 29;254(5036):1385-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Fairchild Center, Columbia University, New York, NY 10027.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1683715" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Chromosome Deletion ; Drosophila melanogaster/embryology/*genetics ; Embryo, Nonmammalian/physiology ; Gene Expression Regulation ; *Genes ; Genes, Homeobox ; Molecular Sequence Data ; Morphogenesis ; Mutagenesis, Site-Directed ; Oligodeoxyribonucleotides ; Promoter Regions, Genetic
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    Regulation of interleukin-2 gene enhancer activity by the T cell accessory molecule CD28 (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-01-18
    Description: The mechanism by which cell surface molecules regulate T cell production of lymphokines is poorly understood. Production of interleukin-2 (IL-2) can be regulated by signal transduction pathways distinct from those induced by the T cell antigen receptor. Stimulation of CD28, a molecule expressed on most human T cells, induced the formation of a protein complex that bound to a site on the IL-2 gene distinct from previously described binding sites and increased IL-2 enhancer activity fivefold. The CD28-responsive complex bound to the IL-2 gene between -164 and -154 base pairs from the transcription start site. The sequence of this element is similar to regions conserved in the 5' flanking regions of several other lymphokine genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fraser, J D -- Irving, B A -- Crabtree, G R -- Weiss, A -- GM39553/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Jan 18;251(4991):313-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1846244" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD28 ; Antigens, Differentiation, T-Lymphocyte/*physiology ; Base Sequence ; Cell Line ; DNA Mutational Analysis ; *Enhancer Elements, Genetic ; Gene Expression Regulation ; Humans ; In Vitro Techniques ; Interleukin-2/*genetics ; Molecular Sequence Data ; Oligonucleotides/chemistry ; *Regulatory Sequences, Nucleic Acid ; Signal Transduction ; T-Lymphocytes/*physiology ; Transcription, Genetic
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    Role of nucleosomal cores and histone H1 in regulation of transcription by RNA polymerase II (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-11
    Description: The relation between chromatin structure and transcriptional activity was examined by in vitro transcription analysis of chromatin reconstituted in the absence or presence of histone H1. To maintain well-defined template DNA, purified components were used in the reconstitution of chromatin. Reconstitution of nucleosomal cores to an average density of 1 nucleosome per 200 base pairs of DNA resulted in a mild reduction of basal RNA polymerase II transcription to 25 to 50 percent of that obtained with naked DNA templates. This nucleosome-mediated repression was due to nucleosomal cores located at the RNA start site and could not be counteracted by the sequence-specific transcription activators Sp1 and GAL4-VP16. When H1 was incorporated into the chromatin at 0.5 to 1.0 molecule per nucleosome (200 base pairs of DNA), RNA synthesis was reduced to 1 to 4 percent of that observed with chromatin containing only nucleosomal cores, and this H1-mediated repression could be counteracted by the addition of Sp1 or GAL4-VP16 (antirepression). With naked DNA templates, transcription was increased by a factor of 3 and 8 by Sp1 and GAL4-VP-16, respectively (true activation). With H1-repressed chromatin templates, however, the magnitude of transcriptional activation mediated by Sp1 and GAL4-VP16 was 90 and more than 200 times higher, respectively, because of the combined effects of true activation and antirepression. The data provide direct biochemical evidence that support and clarify previously proposed models in which there is depletion or reconfiguration of nucleosomal cores and histone H1 at the promoter regions of active genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Laybourn, P J -- Kadonaga, J T -- New York, N.Y. -- Science. 1991 Oct 11;254(5029):238-45.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, 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/1718039" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromatin/physiology ; DNA/genetics ; Gene Expression Regulation ; Histones/*physiology ; Nucleosomes/*physiology ; RNA/genetics ; RNA Polymerase II/*metabolism ; *Transcription, Genetic
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    Oct-3 and the beginning of mammalian development (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-07-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosner, M H -- Vigano, M A -- Rigby, P W -- Arnheiter, H -- Staudt, L M -- New York, N.Y. -- Science. 1991 Jul 12;253(5016):144-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1853199" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA Replication ; DNA-Binding Proteins/*physiology ; Embryo, Mammalian/*physiology ; Gene Expression Regulation ; Mice ; Octamer Transcription Factor-3 ; Stem Cells/physiology ; Teratoma/genetics/pathology ; Transcription Factors/*physiology
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    The myoD gene family: nodal point during specification of the muscle cell lineage (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-02-15
    Description: The myoD gene converts many differentiated cell types into muscle. MyoD is a member of the basic-helix-loop-helix family of proteins; this 68-amino acid domain in MyoD is necessary and sufficient for myogenesis. MyoD binds cooperatively to muscle-specific enhancers and activates transcription. The helix-loop-helix motif is responsible for dimerization, and, depending on its dimerization partner, MyoD activity can be controlled. MyoD senses and integrates many facets of cell state. MyoD is expressed only in skeletal muscle and its precursors; in nonmuscle cells myoD is repressed by specific genes. MyoD activates its own transcription; this may stabilize commitment to myogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weintraub, H -- Davis, R -- Tapscott, S -- Thayer, M -- Krause, M -- Benezra, R -- Blackwell, T K -- Turner, D -- Rupp, R -- Hollenberg, S -- New York, N.Y. -- Science. 1991 Feb 15;251(4995):761-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Fred Hutchinson Cancer Research Center, Seattle, WA 98104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1846704" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/genetics ; DNA-Binding Proteins/*genetics/physiology ; Gene Expression Regulation ; *Genes, Regulator ; Humans ; Multigene Family ; Muscle Proteins/*genetics/physiology ; Muscles/*cytology/embryology ; MyoD Protein
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    Diversity of G proteins in signal transduction (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-05-10
    Description: The heterotrimeric guanine nucleotide-binding proteins (G proteins) act as switches that regulate information processing circuits connecting cell surface receptors to a variety of effectors. The G proteins are present in all eukaryotic cells, and they control metabolic, humoral, neural, and developmental functions. More than a hundred different kinds of receptors and many different effectors have been described. The G proteins that coordinate receptor-effector activity are derived from a large gene family. At present, the family is known to contain at least sixteen different genes that encode the alpha subunit of the heterotrimer, four that encode beta subunits, and multiple genes encoding gamma subunits. Specific transient interactions between these components generate the pathways that modulate cellular responses to complex chemical signals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Simon, M I -- Strathmann, M P -- Gautam, N -- New York, N.Y. -- Science. 1991 May 10;252(5007):802-8.〈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/1902986" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Differentiation/physiology ; Chromosome Mapping ; GTP-Binding Proteins/*chemistry ; Gene Expression Regulation ; Molecular Sequence Data ; Signal Transduction/*physiology
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    Control of doublesex alternative splicing by transformer and transformer-2 in Drosophila (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-05-10
    Description: Sex-specific alternative processing of doublesex (dsx) precursor messenger RNA (pre-mRNA) regulates somatic sexual differentiation in Drosophila melanogaster. Cotransfection analyses in which the dsx gene and the female-specific transformer (tra) and transformer-2 (tra-2) complementary DNAs were expressed in Drosophila Kc cells revealed that female-specific splicing of the dsx transcript was positively regulated by the products of the tra and tra-2 genes. Furthermore, analyses of mutant constructs of dsx showed that a portion of the female-specific exon sequence was required for regulation of dsx pre-messenger RNA splicing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoshijima, K -- Inoue, K -- Higuchi, I -- Sakamoto, H -- Shimura, Y -- New York, N.Y. -- Science. 1991 May 10;252(5007):833-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biophysics, Faculty of Science, Kyoto University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1902987" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Chromosome Mapping ; Drosophila melanogaster/*genetics ; Gene Expression Regulation ; Genes/physiology ; Genes, Regulator/physiology ; Molecular Sequence Data ; *RNA Splicing ; RNA, Messenger/biosynthesis ; Repetitive Sequences, Nucleic Acid ; Sex Differentiation/*physiology ; Transfection
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    Transcriptional repression mediated by the WT1 Wilms tumor gene product (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-10-07
    Description: The wt1 gene, a putative tumor suppressor gene located at the Wilms tumor (WT) locus on chromosome 11p13, encodes a zinc finger-containing protein that binds to the same DNA sequence as EGR-1, a mitogen-inducible immediate-early gene product that activates transcription. The transcriptional regulatory potential of WT1 has not been demonstrated. In transient transfection assays, the WT1 protein functioned as a repressor of transcription when bound to the EGR-1 site. The repression function was mapped to the glutamine- and proline-rich NH2-terminus of WT1; fusion of this domain to the zinc finger region of EGR-1 converted EGR-1 into a transcriptional repressor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Madden, S L -- Cook, D M -- Morris, J F -- Gashler, A -- Sukhatme, V P -- Rauscher, F J 3rd -- CA-0917-15/CA/NCI NIH HHS/ -- CA-23413/CA/NCI NIH HHS/ -- CA-52009/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Sep 27;253(5027):1550-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wistar Institute of Anatomy and Biology, Philadelphia, PA 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1654597" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Line ; Chromosomes, Human, Pair 11 ; DNA/genetics ; DNA-Binding Proteins/*genetics ; Gene Expression Regulation ; *Genes, Tumor Suppressor ; Humans ; Kidney Neoplasms/*genetics ; Molecular Sequence Data ; Repressor Proteins/*genetics ; *Transcription, Genetic ; Wilms Tumor/*genetics ; Zinc Fingers/*genetics
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    beta-Arrestin: a protein that regulates beta-adrenergic receptor function (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-06-22
    Description: Homologous or agonist-specific desensitization of beta-adrenergic receptors is thought to be mediated by a specific kinase, the beta-adrenergic receptor kinase (beta ARK). However, recent data suggest that a cofactor is required for this kinase to inhibit receptor function. The complementary DNA for such a cofactor was cloned and found to encode a 418-amino acid protein homologous to the retinal protein arrestin. The protein, termed beta-arrestin, was expressed and partially purified. It inhibited the signaling function of beta ARK-phosphorylated beta-adrenergic receptors by more than 75 percent, but not that of rhodopsin. It is proposed that beta-arrestin in concert with beta ARK effects homologous desensitization of beta-adrenergic receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lohse, M J -- Benovic, J L -- Codina, J -- Caron, M G -- Lefkowitz, R J -- DK19318/DK/NIDDK NIH HHS/ -- HL16037/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 22;248(4962):1547-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, Biochemistry and Cell Biology, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2163110" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens/*genetics/isolation & purification/pharmacology ; Arrestin ; Blotting, Northern ; Chromatography, Ion Exchange ; Cloning, Molecular ; *Cyclic AMP-Dependent Protein Kinases ; DNA/genetics ; Eye Proteins/*genetics/isolation & purification/pharmacology ; Gene Expression Regulation ; Molecular Sequence Data ; Phosphodiesterase Inhibitors/*pharmacology ; Phosphorylation ; Protein Kinases/*pharmacology ; RNA, Messenger/analysis ; Receptors, Adrenergic, beta/*drug effects/physiology ; Transfection ; beta-Adrenergic Receptor Kinases
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 42
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    D1 and D2 dopamine receptor-regulated gene expression of striatonigral and striatopallidal neurons (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-07
    Description: The striatum, which is the major component of the basal ganglia in the brain, is regulated in part by dopaminergic input from the substantia nigra. Severe movement disorders result from the loss of striatal dopamine in patients with Parkinson's disease. Rats with lesions of the nigrostriatal dopamine pathway caused by 6-hydroxydopamine (6-OHDA) serve as a model for Parkinson's disease and show alterations in gene expression in the two major output systems of the striatum to the globus pallidus and substantia nigra. Striatopallidal neurons show a 6-OHDA-induced elevation in their specific expression of messenger RNAs (mRNAs) encoding the D2 dopamine receptor and enkephalin, which is reversed by subsequent continuous treatment with the D2 agonist quinpirole. Conversely, striatonigral neurons show a 6-OHDA-induced reduction in their specific expression of mRNAs encoding the D1 dopamine receptor and substance P, which is reversed by subsequent daily injections of the D1 agonist SKF-38393. This treatment also increases dynorphin mRNA in striatonigral neurons. Thus, the differential effects of dopamine on striatonigral and striatopallidal neurons are mediated by their specific expression of D1 and D2 dopamine receptor subtypes, respectively.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gerfen, C R -- Engber, T M -- Mahan, L C -- Susel, Z -- Chase, T N -- Monsma, F J Jr -- Sibley, D R -- New York, N.Y. -- Science. 1990 Dec 7;250(4986):1429-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell Biology, National Institute of Mental Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2147780" target="_blank"〉PubMed〈/a〉
    Keywords: 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine/pharmacology ; Animals ; Cerebral Cortex/physiology ; Corpus Striatum/drug effects/*metabolism ; Ergolines/pharmacology ; Gene Expression Regulation ; Globus Pallidus/drug effects/*metabolism ; Hydroxydopamines/pharmacology ; Models, Neurological ; Neurons/drug effects/*metabolism ; Oligonucleotide Probes ; Oxidopamine ; Quinpirole ; RNA, Messenger/drug effects/*genetics ; Rats ; Receptors, Dopamine/*genetics ; Receptors, Dopamine D1 ; Receptors, Dopamine D2 ; Substantia Nigra/drug effects/*metabolism ; Thalamus/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 43
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    Spontaneous order, evolution, and life (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-03-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Waldrop, M M -- New York, N.Y. -- Science. 1990 Mar 30;247(4950):1543-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2321014" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Gene Expression Regulation ; Humans ; *Origin of Life
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 44
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    The cellular functions of small GTP-binding proteins (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-10
    Description: A substantial number of novel guanine nucleotide binding regulatory proteins have been identified over the last few years but the function of many of them is largely unknown. This article will discuss a particular family of these proteins, structurally related to the Ras oncoprotein. Approximately 30 Ras-related small guanosine triphosphate (GTP)-binding proteins are known, and from yeast to man they appear to be involved in controlling a diverse set of essential cellular functions including growth, differentiation, cytoskeletal organization, and intracellular vesicle transport and secretion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hall, A -- New York, N.Y. -- Science. 1990 Aug 10;249(4969):635-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Chester Beatty Laboratories, Institute of Cancer Research, London, Great Britain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2116664" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Fungal Proteins/metabolism ; GTP-Binding Proteins/*physiology ; Gene Expression Regulation ; *Genes, ras ; Models, Biological ; Oncogene Protein p21(ras)/*physiology ; *ras Proteins
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  • 45
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    Sequence-specific binding of human Ets-1 to the T cell receptor alpha gene enhancer (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-09
    Description: Expression of the human T cell receptor (TCR) alpha gene is regulated by a T cell-specific transcriptional enhancer that is located 4.5 kilobases (kb) 3' to the C alpha gene segment. The core enhancer contains two nuclear protein binding sites, T alpha 1 and T alpha 2, which are essential for full enhancer activity. T alpha 1 contains a consensus cyclic adenosine monophosphate (cAMP) response element (CRE) and binds a set of ubiquitously expressed CRE binding proteins. In contrast, the transcription factors that interact with the T alpha 2 site have not been defined. In this report, a lambda gt11 expression protocol was used to isolate a complementary DNA (cDNA) that programs the expression of a T alpha 2 binding protein. DNA sequence analysis demonstrated that this clone encodes the human ets-1 proto-oncogene. Lysogen extracts produced with this cDNA clone contained a beta-galactosidase-Ets-1 fusion protein that bound specifically to a synthetic T alpha 2 oligonucleotide. The Ets-1 binding site was localized to a 17-base pair (bp) region from the 3' end of T alpha 2. Mutation of five nucleotides within this sequence abolished both Ets-1 binding and the activity of the TCR alpha enhancer in T cells. These results demonstrate that Ets-1 binds in a sequence-specific fashion to the human TCR alpha enhancer and suggest that this developmentally regulated proto-oncogene functions in regulating TCR alpha gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ho, I C -- Bhat, N K -- Gottschalk, L R -- Lindsten, T -- Thompson, C B -- Papas, T S -- Leiden, J M -- AI-29673/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 9;250(4982):814-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Ann Arbor, MI.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2237431" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Binding, Competitive ; Cloning, Molecular ; DNA/genetics ; DNA Mutational Analysis ; *Enhancer Elements, Genetic ; Gene Expression Regulation ; Gene Rearrangement, T-Lymphocyte ; Humans ; Immunoblotting ; Molecular Sequence Data ; Proto-Oncogene Protein c-ets-1 ; Proto-Oncogene Proteins/genetics/*metabolism ; Proto-Oncogene Proteins c-ets ; *Proto-Oncogenes ; Receptors, Antigen, T-Cell/genetics/*metabolism ; Transcription Factors ; Transcription, Genetic
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  • 46
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    Long-term synaptic changes produced by a cellular analog of classical conditioning in Aplysia (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-27
    Description: A change in synaptic strength arising from the activation of two neuronal pathways at approximately the same time is a form of associative plasticity and may underlie classical or Pavlovian conditioning. A cellular analog of a classical conditioning protocol produces short-term associative plasticity at the connections between sensory and motor neurons in Aplysia. A similar training protocol produced long-term (24-hour) enhancement of excitatory postsynaptic potentials (EPSPs). EPSPs produced by sensory neurons in which activity was paired with a reinforcing stimulus were significantly larger than unpaired controls 24 hours after training. Thus, associative plasticity at the sensory to motor neuron connection can occur in a long-term form in addition to the short-term form. In this system, it should be possible to analyze the molecular mechanisms underlying long-term associative plasticity and classical conditioning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buonomano, D V -- Byrne, J H -- F31 MH09895/MH/NIMH NIH HHS/ -- K02 MH00649/MH/NIMH NIH HHS/ -- R01 NS19895/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jul 27;249(4967):420-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Anatomy, University of Texas Medical School, Houston 77225.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2165631" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/physiology ; Animals ; Aplysia/*physiology ; Calcium/physiology ; Conditioning, Classical/*physiology ; Cyclic AMP/physiology ; Electric Stimulation ; Gene Expression Regulation ; Motor Neurons/physiology ; Neuronal Plasticity/physiology ; Neurons, Afferent/physiology ; Synapses/*physiology
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  • 47
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    Partner found for the myc protein (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1990 Sep 28;249(4976):1503-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2218492" target="_blank"〉PubMed〈/a〉
    Keywords: Cloning, Molecular ; Gene Expression Regulation ; Humans ; Neoplasms/etiology/*genetics ; Proto-Oncogene Proteins c-myc/*genetics
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  • 48
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    Regulation of progesterone receptor-mediated transcription by phosphorylation (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-21
    Description: The progesterone receptor (PR) in the chicken oviduct is a phosphoprotein that regulates gene transcription in the presence of progesterone. Treatment with progesterone in vivo stimulates phosphorylation of the progesterone receptor. With transient transfection assays, the present work has tested whether phosphorylation participates in the regulation of PR-mediated transcription. Treatment with 8-bromo-cyclic adenosine monophosphate (8-Br cAMP), a stimulator of cAMP-dependent protein kinase [protein kinase A (PKA)], mimicked progesterone-dependent, receptor-mediated transcription in the absence of progesterone. Inhibition of PKA blocked hormone action. Treatment with okadaic acid, an inhibitor of protein phosphatases 1 and 2A, stimulated transcription in a manner similar to that of progesterone. These observations suggest that phosphorylation of the PR or other proteins in the transcription complex can modulate PR-mediated transcription in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Denner, L A -- Weigel, N L -- Maxwell, B L -- Schrader, W T -- O'Malley, B W -- HD-07857/HD/NICHD NIH HHS/ -- HD-22061/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1990 Dec 21;250(4988):1740-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2176746" target="_blank"〉PubMed〈/a〉
    Keywords: 8-Bromo Cyclic Adenosine Monophosphate/pharmacology ; Animals ; Cell Line ; Chickens ; Female ; Gene Expression Regulation ; Kinetics ; Oviducts/metabolism ; Phosphoprotein Phosphatases/antagonists & inhibitors ; Phosphorylation ; Progesterone/*pharmacology ; Receptors, Progesterone/*metabolism ; *Transcription, Genetic/drug effects ; Transfection
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  • 49
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    Expression and activity of the POU transcription factor SCIP (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-14
    Description: POU proteins have been shown to transcriptionally active cell-specific genes and to participate in the determination of cell fate. It is therefore thought that these proteins function in development through the stable activation of genes that define specific developmental pathways. Evidence is provided here for an alternative mode of action. The primary structure of SCIP, a POU protein expressed by developing Schwann cells of the peripheral nervous system, was deduced and SCIP activity was studied. Both in normal development and in response to nerve transection, SCIP expression was transiently activated only during the period of rapid cell division that separates the premyelinating and myelinating phases of Schwann cell differentiation. In cotransfection assays, SCIP acted as a transcriptional repressor of myelin-specific genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Monuki, E S -- Kuhn, R -- Weinmaster, G -- Trapp, B D -- Lemke, G -- NS 23896/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Sep 14;249(4974):1300-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurobiology Laboratory, Salk Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1975954" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Differentiation/genetics ; Cloning, Molecular ; Cyclic AMP/physiology ; Gene Expression Regulation ; Gene Library ; Genes, Homeobox/genetics/*physiology ; Molecular Sequence Data ; Myelin Sheath/metabolism ; Nerve Tissue Proteins/genetics/*physiology ; Octamer Transcription Factor-6 ; Rats ; Repressor Proteins/genetics/*physiology ; Schwann Cells/*cytology/metabolism ; Transcription Factors/genetics/*physiology ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A cell culture model for T lymphocyte clonal anergy (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-15
    Description: T lymphocytes respond to foreign antigens both by producing protein effector molecules known as lymphokines and by multiplying. Complete activation requires two signaling events, one through the antigen-specific receptor and one through the receptor for a costimulatory molecule. In the absence of the latter signal, the T cell makes only a partial response and, more importantly, enters an unresponsive state known as clonal anergy in which the T cell is incapable of producing its own growth hormone, interleukin-2, on restimulation. Our current understanding at the molecular level of this modulatory process and its relevance to T cell tolerance are reviewed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwartz, R H -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1349-56.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2113314" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/immunology ; Antigens, CD4/immunology ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/immunology ; Cells, Cultured ; Clone Cells/*immunology ; Gene Expression Regulation ; Gene Rearrangement, T-Lymphocyte ; *Immune Tolerance ; Interleukin-2/biosynthesis/genetics ; Mice ; *Models, Biological ; Receptors, Antigen, T-Cell/genetics/immunology ; Second Messenger Systems ; Signal Transduction ; T-Lymphocytes/*immunology ; Thymus Gland/immunology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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