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  • 1
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    Vitamin D receptor as an intestinal bile acid sensor (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-05-23
    Description: The vitamin D receptor (VDR) mediates the effects of the calcemic hormone 1alpha,25-dihydroxyvitamin D3 [1,25(OH)2D3]. We show that VDR also functions as a receptor for the secondary bile acid lithocholic acid (LCA), which is hepatotoxic and a potential enteric carcinogen. VDR is an order of magnitude more sensitive to LCA and its metabolites than are other nuclear receptors. Activation of VDR by LCA or vitamin D induced expression in vivo of CYP3A, a cytochrome P450 enzyme that detoxifies LCA in the liver and intestine. These studies offer a mechanism that may explain the proposed protective effects of vitamin D and its receptor against colon cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Makishima, Makoto -- Lu, Timothy T -- Xie, Wen -- Whitfield, G Kerr -- Domoto, Hideharu -- Evans, Ronald M -- Haussler, Mark R -- Mangelsdorf, David J -- New York, N.Y. -- Science. 2002 May 17;296(5571):1313-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Pharmacology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9050, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12016314" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Aryl Hydrocarbon Hydroxylases ; Binding, Competitive ; COS Cells ; Cell Line ; Colonic Neoplasms/prevention & control ; Cytochrome P-450 CYP3A ; Cytochrome P-450 Enzyme System/genetics/metabolism ; DNA-Binding Proteins/metabolism ; Dimerization ; Gene Expression Regulation, Enzymologic ; Histone Acetyltransferases ; Humans ; Intestine, Small/*metabolism ; Ligands ; Lithocholic Acid/analogs & derivatives/*metabolism/pharmacology ; Male ; Mice ; Nuclear Receptor Coactivator 1 ; Oxidoreductases, N-Demethylating/genetics/metabolism ; Promoter Regions, Genetic ; Rats ; Receptors, Calcitriol/agonists/genetics/*metabolism ; Receptors, Cytoplasmic and Nuclear/metabolism ; Receptors, Steroid/metabolism ; Transcription Factors/metabolism ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Cloning and characterization of inducible nitric oxide synthase from mouse macrophages (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-04-10
    Description: Nitric oxide (NO) conveys a variety of messages between cells, including signals for vasorelaxation, neurotransmission, and cytotoxicity. In some endothelial cells and neurons, a constitutive NO synthase is activated transiently by agonists that elevate intracellular calcium concentrations and promote the binding of calmodulin. In contrast, in macrophages, NO synthase activity appears slowly after exposure of the cells to cytokines and bacterial products, is sustained, and functions independently of calcium and calmodulin. A monospecific antibody was used to clone complementary DNA that encoded two isoforms of NO synthase from immunologically activated mouse macrophages. Liquid chromatography-mass spectrometry was used to confirm most of the amino acid sequence. Macrophage NO synthase differs extensively from cerebellar NO synthase. The macrophage enzyme is immunologically induced at the transcriptional level and closely resembles the enzyme in cytokine-treated tumor cells and inflammatory neutrophils.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xie, Q W -- Cho, H J -- Calaycay, J -- Mumford, R A -- Swiderek, K M -- Lee, T D -- Ding, A -- Troso, T -- Nathan, C -- AI30165/AI/NIAID NIH HHS/ -- CA43610/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 Apr 10;256(5054):225-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Beatrice and Samuel A. Seaver Laboratory, Department of Medicine, Cornell University Medical College, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1373522" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Oxidoreductases/biosynthesis/*genetics ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Cells, Cultured ; Cloning, Molecular ; Codon ; Enzyme Induction ; Interferon-gamma/pharmacology ; Isoenzymes/biosynthesis/*genetics ; Kinetics ; Lipopolysaccharides ; Macrophages/drug effects/*enzymology ; Mammary Neoplasms, Experimental ; Mice ; Molecular Sequence Data ; Molecular Weight ; Neutrophils/drug effects/enzymology ; Nitric Oxide Synthase ; Oligodeoxyribonucleotides ; Poly A/genetics ; RNA/genetics ; RNA, Messenger ; Rats ; Sequence Homology, Nucleic Acid ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Epigenetic reprogramming by adenovirus e1a (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-23
    Description: Adenovirus e1a induces quiescent human cells to replicate. We found that e1a causes global relocalization of the RB (retinoblastoma) proteins (RB, p130, and p107) and p300/CBP histone acetyltransferases on promoters, the effect of which is to restrict the acetylation of histone 3 lysine-18 (H3K18ac) to a limited set of genes, thereby stimulating cell cycling and inhibiting antiviral responses and cellular differentiation. Soon after expression, e1a binds transiently to promoters of cell cycle and growth genes, causing enrichment of p300/CBP, PCAF (p300/CBP-associated factor), and H3K18ac; depletion of RB proteins; and transcriptional activation. e1a also associates transiently with promoters of antiviral genes, causing enrichment for RB, p130, and H4K16ac; increased nucleosome density; and transcriptional repression. At later times, e1a and p107 bind mainly to promoters of development and differentiation genes, repressing transcription. The temporal order of e1a binding requires its interactions with p300/CBP and RB proteins. Our data uncover a defined epigenetic reprogramming leading to cellular transformation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2693122/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2693122/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferrari, Roberto -- Pellegrini, Matteo -- Horwitz, Gregory A -- Xie, Wei -- Berk, Arnold J -- Kurdistani, Siavash K -- CA25235/CA/NCI NIH HHS/ -- R37 CA025235/CA/NCI NIH HHS/ -- R37 CA025235-30/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Aug 22;321(5892):1086-8. doi: 10.1126/science.1155546.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, University of California, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18719284" target="_blank"〉PubMed〈/a〉
    Keywords: Adenovirus E1A Proteins/genetics/*metabolism ; Adenoviruses, Human/genetics/*metabolism ; CREB-Binding Protein/metabolism ; Cell Transformation, Viral ; Crk-Associated Substrate Protein/genetics/metabolism ; *Epigenesis, Genetic ; Gene Expression Profiling ; Gene Expression Regulation ; Histones/metabolism ; Humans ; Mutation ; Promoter Regions, Genetic ; Protein Binding ; RNA, Messenger/genetics/metabolism ; Retinoblastoma Protein/genetics/metabolism ; Retinoblastoma-Like Protein p107/genetics/metabolism ; Transcription, Genetic ; p300-CBP Transcription Factors/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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  • 4
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    Dnmt3a-dependent nonpromoter DNA methylation facilitates transcription of neurogenic genes (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-24
    Description: DNA methylation at proximal promoters facilitates lineage restriction by silencing cell type-specific genes. However, euchromatic DNA methylation frequently occurs in regions outside promoters. The functions of such nonproximal promoter DNA methylation are unclear. Here we show that the de novo DNA methyltransferase Dnmt3a is expressed in postnatal neural stem cells (NSCs) and is required for neurogenesis. Genome-wide analysis of postnatal NSCs indicates that Dnmt3a occupies and methylates intergenic regions and gene bodies flanking proximal promoters of a large cohort of transcriptionally permissive genes, many of which encode regulators of neurogenesis. Surprisingly, Dnmt3a-dependent nonproximal promoter methylation promotes expression of these neurogenic genes by functionally antagonizing Polycomb repression. Thus, nonpromoter DNA methylation by Dnmt3a may be used for maintaining active chromatin states of genes critical for development.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3539760/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3539760/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Hao -- Coskun, Volkan -- Tao, Jifang -- Xie, Wei -- Ge, Weihong -- Yoshikawa, Kazuaki -- Li, En -- Zhang, Yi -- Sun, Yi Eve -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jul 23;329(5990):444-8. doi: 10.1126/science.1190485.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Medical Pharmacology, University of California Los Angeles (UCLA), Los Angeles, CA 90095, USA. haowu7@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20651149" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Brain/cytology/growth & development/*metabolism ; Chromatin Immunoprecipitation ; DNA (Cytosine-5-)-Methyltransferase/*metabolism ; *DNA Methylation ; DNA, Intergenic ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Genome ; Histones/genetics/metabolism ; Mice ; Mice, Knockout ; Nervous System/growth & development ; Neurogenesis/*genetics ; Neuroglia/cytology ; Neurons/*cytology/metabolism ; Polycomb-Group Proteins ; Promoter Regions, Genetic ; Repressor Proteins/metabolism ; Stem Cells/*metabolism ; *Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Inhibition of viral replication by interferon-gamma-induced nitric oxide synthase (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-09-10
    Description: Interferons (IFNs) induce antiviral activity in many cell types. The ability of IFN-gamma to inhibit replication of ectromelia, vaccinia, and herpes simplex-1 viruses in mouse macrophages correlated with the cells' production of nitric oxide (NO). Viral replication was restored in IFN-gamma-treated macrophages exposed to inhibitors of NO synthase. Conversely, epithelial cells with no detectable NO synthesis restricted viral replication when transfected with a complementary DNA encoding inducible NO synthase or treated with organic compounds that generate NO. In mice, an inhibitor of NO synthase converted resolving ectromelia virus infection into fulminant mousepox. Thus, induction of NO synthase can be necessary and sufficient for a substantial antiviral effect of IFN-gamma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karupiah, G -- Xie, Q W -- Buller, R M -- Nathan, C -- Duarte, C -- MacMicking, J D -- CA43610/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 Sep 10;261(5127):1445-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral Diseases, 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/7690156" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Oxidoreductases/*biosynthesis/metabolism ; Animals ; Arginine/analogs & derivatives/pharmacology ; Cell Line ; Cells, Cultured ; Ectromelia virus/drug effects/*physiology ; Ectromelia, Infectious/microbiology ; Enzyme Induction ; Female ; Humans ; Interferon-gamma/*pharmacology ; Macrophages/*microbiology ; Mice ; Mice, Inbred C57BL ; Nitric Oxide/metabolism/pharmacology ; Nitric Oxide Synthase ; Simplexvirus/drug effects/physiology ; Transfection ; Vaccinia virus/drug effects/physiology ; *Virus Replication/drug effects ; omega-N-Methylarginine
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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