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  • 1
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    Suppression of inflammation by a synthetic histone mimic (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-11-12
    Description: Interaction of pathogens with cells of the immune system results in activation of inflammatory gene expression. This response, although vital for immune defence, is frequently deleterious to the host due to the exaggerated production of inflammatory proteins. The scope of inflammatory responses reflects the activation state of signalling proteins upstream of inflammatory genes as well as signal-induced assembly of nuclear chromatin complexes that support mRNA expression. Recognition of post-translationally modified histones by nuclear proteins that initiate mRNA transcription and support mRNA elongation is a critical step in the regulation of gene expression. Here we present a novel pharmacological approach that targets inflammatory gene expression by interfering with the recognition of acetylated histones by the bromodomain and extra terminal domain (BET) family of proteins. We describe a synthetic compound (I-BET) that by 'mimicking' acetylated histones disrupts chromatin complexes responsible for the expression of key inflammatory genes in activated macrophages, and confers protection against lipopolysaccharide-induced endotoxic shock and bacteria-induced sepsis. Our findings suggest that synthetic compounds specifically targeting proteins that recognize post-translationally modified histones can serve as a new generation of immunomodulatory drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nicodeme, Edwige -- Jeffrey, Kate L -- Schaefer, Uwe -- Beinke, Soren -- Dewell, Scott -- Chung, Chun-Wa -- Chandwani, Rohit -- Marazzi, Ivan -- Wilson, Paul -- Coste, Herve -- White, Julia -- Kirilovsky, Jorge -- Rice, Charles M -- Lora, Jose M -- Prinjha, Rab K -- Lee, Kevin -- Tarakhovsky, Alexander -- England -- Nature. 2010 Dec 23;468(7327):1119-23. doi: 10.1038/nature09589. Epub 2010 Nov 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre de Recherche GSK, 27 Avenue du Quebec, 91140 Villebon Sur Yvette, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21068722" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation/drug effects ; Animals ; Anti-Inflammatory Agents/chemistry/*pharmacology/therapeutic use ; Benzodiazepines ; Cells, Cultured ; Epigenomics ; Gene Expression Regulation/*drug effects ; Genome-Wide Association Study ; Heterocyclic Compounds with 4 or More Rings/chemistry/*pharmacology/therapeutic ; use ; Histone Deacetylase Inhibitors/pharmacology ; Hydroxamic Acids/pharmacology ; *Inflammation/drug therapy/prevention & control ; Kaplan-Meier Estimate ; Lipopolysaccharides/pharmacology ; Macrophages/*drug effects ; Mice ; Mice, Inbred C57BL ; Models, Molecular ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/metabolism ; Salmonella Infections/drug therapy/immunology/physiopathology/prevention & ; control ; Salmonella typhimurium ; Sepsis/drug therapy/prevention & control ; Shock, Septic/drug therapy/prevention & control
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Essential role of the histone methyltransferase G9a in cocaine-induced plasticity (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-09
    Description: Cocaine-induced alterations in gene expression cause changes in neuronal morphology and behavior that may underlie cocaine addiction. In mice, we identified an essential role for histone 3 lysine 9 (H3K9) dimethylation and the lysine dimethyltransferase G9a in cocaine-induced structural and behavioral plasticity. Repeated cocaine administration reduced global levels of H3K9 dimethylation in the nucleus accumbens. This reduction in histone methylation was mediated through the repression of G9a in this brain region, which was regulated by the cocaine-induced transcription factor DeltaFosB. Using conditional mutagenesis and viral-mediated gene transfer, we found that G9a down-regulation increased the dendritic spine plasticity of nucleus accumbens neurons and enhanced the preference for cocaine, thereby establishing a crucial role for histone methylation in the long-term actions of cocaine.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2820240/" 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/PMC2820240/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maze, Ian -- Covington, Herbert E 3rd -- Dietz, David M -- LaPlant, Quincey -- Renthal, William -- Russo, Scott J -- Mechanic, Max -- Mouzon, Ezekiell -- Neve, Rachael L -- Haggarty, Stephen J -- Ren, Yanhua -- Sampath, Srihari C -- Hurd, Yasmin L -- Greengard, Paul -- Tarakhovsky, Alexander -- Schaefer, Anne -- Nestler, Eric J -- P01 DA008227/DA/NIDA NIH HHS/ -- P01 DA008227-120001/DA/NIDA NIH HHS/ -- P01 DA008227-129001/DA/NIDA NIH HHS/ -- P01 DA008227-13/DA/NIDA NIH HHS/ -- P01 DA008227-14/DA/NIDA NIH HHS/ -- P01 DA008227-15/DA/NIDA NIH HHS/ -- P01 DA008227-16/DA/NIDA NIH HHS/ -- P01 DA008227-170003/DA/NIDA NIH HHS/ -- P01 DA008227-180003/DA/NIDA NIH HHS/ -- P01 DA010044/DA/NIDA NIH HHS/ -- P01 DA010044-14/DA/NIDA NIH HHS/ -- P01 DA010044-140005/DA/NIDA NIH HHS/ -- P01 DA010044-149002/DA/NIDA NIH HHS/ -- P01 DA010044-14S1/DA/NIDA NIH HHS/ -- P01 DA010044-14S10005/DA/NIDA NIH HHS/ -- P01 DA010044-14S19002/DA/NIDA NIH HHS/ -- P01 DA010044-15/DA/NIDA NIH HHS/ -- P01 DA010044-150005/DA/NIDA NIH HHS/ -- P01 DA010044-159002/DA/NIDA NIH HHS/ -- P01 DA08227/DA/NIDA NIH HHS/ -- P0110044/PHS HHS/ -- R01 DA007359/DA/NIDA NIH HHS/ -- R01 DA007359-02/DA/NIDA NIH HHS/ -- R01 DA007359-17/DA/NIDA NIH HHS/ -- R01 DA007359-18/DA/NIDA NIH HHS/ -- R01 DA007359-19/DA/NIDA NIH HHS/ -- R01 DA007359-20/DA/NIDA NIH HHS/ -- R01 DA007359-21/DA/NIDA NIH HHS/ -- R01 DA007359-22/DA/NIDA NIH HHS/ -- R01 DA014133/DA/NIDA NIH HHS/ -- R01 DA07359/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2010 Jan 8;327(5962):213-6. doi: 10.1126/science.1179438.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20056891" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/*drug effects ; Cocaine/*administration & dosage/pharmacology ; Cocaine-Related Disorders/etiology/metabolism ; Dendritic Spines/physiology ; Down-Regulation ; Enzyme Repression ; Gene Expression Profiling ; Gene Expression Regulation ; Histone-Lysine N-Methyltransferase/genetics/*metabolism ; Histones/*metabolism ; Lysine/metabolism ; Male ; Methylation ; Mice ; Mice, Inbred C57BL ; *Neuronal Plasticity ; Neurons/drug effects/*metabolism ; Nucleus Accumbens/cytology/drug effects/*metabolism ; Oligonucleotide Array Sequence Analysis ; Proto-Oncogene Proteins c-fos/genetics/metabolism ; Reward ; Self Administration ; Transcription, Genetic
    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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  • 3
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    Suppression of the antiviral response by an influenza histone mimic (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-03-16
    Description: Viral infection is commonly associated with virus-driven hijacking of host proteins. Here we describe a novel mechanism by which influenza virus affects host cells through the interaction of influenza non-structural protein 1 (NS1) with the infected cell epigenome. We show that the NS1 protein of influenza A H3N2 subtype possesses a histone-like sequence (histone mimic) that is used by the virus to target the human PAF1 transcription elongation complex (hPAF1C). We demonstrate that binding of NS1 to hPAF1C depends on the NS1 histone mimic and results in suppression of hPAF1C-mediated transcriptional elongation. Furthermore, human PAF1 has a crucial role in the antiviral response. Loss of hPAF1C binding by NS1 attenuates influenza infection, whereas hPAF1C deficiency reduces antiviral gene expression and renders cells more susceptible to viruses. We propose that the histone mimic in NS1 enables the influenza virus to affect inducible gene expression selectively, thus contributing to suppression of the antiviral response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3598589/" 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/PMC3598589/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marazzi, Ivan -- Ho, Jessica S Y -- Kim, Jaehoon -- Manicassamy, Balaji -- Dewell, Scott -- Albrecht, Randy A -- Seibert, Chris W -- Schaefer, Uwe -- Jeffrey, Kate L -- Prinjha, Rab K -- Lee, Kevin -- Garcia-Sastre, Adolfo -- Roeder, Robert G -- Tarakhovsky, Alexander -- 1K99AI095320-01/AI/NIAID NIH HHS/ -- CA129325/CA/NCI NIH HHS/ -- HHSN266200700010C/PHS HHS/ -- R01 CA129325/CA/NCI NIH HHS/ -- R01AI046954/AI/NIAID NIH HHS/ -- R01AI068058/AI/NIAID NIH HHS/ -- U19AI083025/AI/NIAID NIH HHS/ -- England -- Nature. 2012 Mar 14;483(7390):428-33. doi: 10.1038/nature10892.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immune Cell Epigenetics and Signaling, The Rockefeller University, 1230 York Avenue, New York, New York 10065, USA. imarazzi@rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22419161" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Gene Expression Regulation/immunology ; Histones/chemistry/*metabolism ; Humans ; Influenza A Virus, H3N2 Subtype/genetics/*metabolism/pathogenicity ; Influenza, Human/*genetics/*immunology/pathology/virology ; *Molecular Mimicry ; Molecular Sequence Data ; Nuclear Proteins/antagonists & inhibitors/metabolism ; Protein Binding ; Transcription, Genetic/immunology ; Viral Nonstructural Proteins/chemistry/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    A role for CD5 in TCR-mediated signal transduction and thymocyte selection (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-07-28
    Description: CD5 is a transmembrane protein that is expressed on the surface of T cells and a subset of B cells. The absence of CD5 rendered thymocytes hyperresponsive to stimulation through the T cell antigen receptor (TCR) in vitro. Selection of T cells expressing three distinct transgenic TCRs was also abnormal in CD5-deficient mice. These observations indicate that CD5 can influence the fate of developing thymocytes by acting as a negative regulator of TCR-mediated signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tarakhovsky, A -- Kanner, S B -- Hombach, J -- Ledbetter, J A -- Muller, W -- Killeen, N -- Rajewsky, K -- New York, N.Y. -- Science. 1995 Jul 28;269(5223):535-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genetics, University of Cologne, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7542801" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/*immunology ; Antigens, CD3/metabolism ; Antigens, CD5 ; Female ; *Lymphocyte Activation ; Male ; Mice ; Mice, Transgenic ; Phosphorylation ; Protein-Tyrosine Kinases/metabolism ; Receptors, Antigen, T-Cell/*immunology ; *Signal Transduction ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes/*immunology ; Thymus Gland/immunology ; ZAP-70 Protein-Tyrosine Kinase
    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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    Immunodeficiency in protein kinase cbeta-deficient mice (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-09
    Description: Cross-linking of the antigen receptor on lymphocytes by antigens or antibodies to the receptor results in activation of enzymes of the protein kinase C (PKC) family. Mice homozygous for a targeted disruption of the gene encoding the PKC-betaI and PKC-betaII isoforms develop an immunodeficiency characterized by impaired humoral immune responses and reduced cellular responses of B cells, which is similar to X-linked immunodeficiency in mice. Thus PKC-betaI and PKC-betaII play an important role in B cell activation and may be functionally linked to Bruton's tyrosine kinase in antigen receptor-mediated signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leitges, M -- Schmedt, C -- Guinamard, R -- Davoust, J -- Schaal, S -- Stabel, S -- Tarakhovsky, A -- New York, N.Y. -- Science. 1996 Aug 9;273(5276):788-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Delbruck-Laboratorium in der Max-Planck-Gesellschaft, Carl-von-Linne-Weg 10, D-50829 Koln, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8670417" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology ; Gene Targeting ; Genetic Linkage ; Immunoglobulin G/blood ; Immunoglobulin M/blood/immunology ; Immunoglobulins/*blood ; Immunologic Deficiency Syndromes/enzymology/*immunology ; Lymphocyte Activation ; Lymphocyte Count ; Mice ; Protein Kinase C/deficiency/genetics/*physiology ; Protein Kinase C beta ; Protein-Tyrosine Kinases/genetics/metabolism ; Receptors, Antigen, B-Cell/immunology ; Signal Transduction ; T-Lymphocytes/immunology ; X Chromosome
    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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  • 6
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    CD5-mediated negative regulation of antigen receptor-induced growth signals in B-1 B cells (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-13
    Description: A subset of B lymphocytes present primarily in the peritoneal and pleural cavities is defined by the expression of CD5 and is elevated in autoimmune diseases. Upon signaling through membrane immunoglobulin M (mIgM), splenic B lymphocytes (B-2) proliferate, whereas peritoneal B cells (B-1) undergo apoptosis. However, in CD5-deficient mice, B-1 cells responded to mIgM crosslinking by developing a resistance to apoptosis and entering the cell cycle. In wild-type B-1 cells, prevention of association between CD5 and mIgM rescued their growth response to mIgM crosslinking. Thus the B cell receptor-mediated signaling is negatively regulated by CD5 in normal B-1 cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bikah, G -- Carey, J -- Ciallella, J R -- Tarakhovsky, A -- Bondada, S -- AG05731/AG/NIA NIH HHS/ -- AI21490/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 13;274(5294):1906-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology and Center on Aging, University of Kentucky, Lexington, KY 40536, USA. sbonda@pop.uky.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8943203" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD5/*physiology ; Apoptosis ; B-Lymphocyte Subsets/*cytology/*immunology/metabolism ; Calcium/metabolism ; Cell Division ; Cell Nucleus/metabolism ; Cross-Linking Reagents ; Female ; Immunoglobulin M/immunology/metabolism ; *Lymphocyte Activation ; Male ; Mice ; Mice, Inbred C57BL ; Mutation ; NF-kappa B/metabolism ; Peritoneal Cavity/cytology ; Receptors, Antigen, B-Cell/immunology/metabolism/*physiology ; *Signal Transduction
    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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  • 7
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    BAFF activates Akt and Erk through BAFF-R in an IKK1-dependent manner in primary mouse B cells (2008)
    National Academy of Sciences
    Details
    Publication Date: 2008-08-19
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 8
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    Abnormal development of secondary lymphoid tissues in lymphotoxin  -deficient mice (1997)
    National Academy of Sciences
    Details
    Publication Date: 1997-08-19
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 9
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    A sensitized genetic system for the analysis of murine B lymphocyte signal transduction pathways dependent on Bruton's tyrosine kinase (2000)
    National Academy of Sciences
    Details
    Publication Date: 2000-05-30
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 10
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    Ezh2, the histone methyltransferase of PRC2, regulates the balance between self-renewal and differentiation in the cerebral cortex (2010)
    National Academy of Sciences
    Details
    Publication Date: 2010-08-23
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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