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  • 1
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    Bmf: a proapoptotic BH3-only protein regulated by interaction with the myosin V actin motor complex, activated by anoikis (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-09-08
    Description: Bcl-2 family members bearing only the BH3 domain are essential inducers of apoptosis. We identified a BH3-only protein, Bmf, and show that its BH3 domain is required both for binding to prosurvival Bcl-2 proteins and for triggering apoptosis. In healthy cells, Bmf is sequestered to myosin V motors by association with dynein light chain 2. Certain damage signals, such as loss of cell attachment (anoikis), unleash Bmf, allowing it to translocate and bind prosurvival Bcl-2 proteins. Thus, at least two mammalian BH3-only proteins, Bmf and Bim, function to sense intracellular damage by their localization to distinct cytoskeletal structures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Puthalakath, H -- Villunger, A -- O'Reilly, L A -- Beaumont, J G -- Coultas, L -- Cheney, R E -- Huang, D C -- Strasser, A -- CA 80188/CA/NCI NIH HHS/ -- R29 DC003299/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 2001 Sep 7;293(5536):1829-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Walter and Eliza Hall Institute of Medical Research, Melbourne, P.O. Royal Melbourne Hospital, 3050 VIC, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11546872" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; *Anoikis ; Apoptosis Regulatory Proteins ; Calmodulin-Binding Proteins/*metabolism ; Carrier Proteins/*chemistry/genetics/*metabolism ; Cell Line ; Cytoskeleton/metabolism ; *Drosophila Proteins ; Dyneins ; Gene Expression Profiling ; Humans ; *Membrane Proteins ; Mice ; Molecular Motor Proteins/*metabolism ; Molecular Sequence Data ; Mutation ; Myeloid Cell Leukemia Sequence 1 Protein ; *Myosin Type V ; Neoplasm Proteins/genetics/metabolism ; Nerve Tissue Proteins/*metabolism ; Protein Binding ; Protein Structure, Tertiary ; Protein Transport ; *Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-bcl-2/chemistry/genetics/metabolism ; RNA, Messenger/analysis/genetics ; Transfection ; Two-Hybrid System Techniques
    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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    XIAP discriminates between type I and type II FAS-induced apoptosis (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-07-25
    Description: FAS (also called APO-1 and CD95) and its physiological ligand, FASL, regulate apoptosis of unwanted or dangerous cells, functioning as a guardian against autoimmunity and cancer development. Distinct cell types differ in the mechanisms by which the 'death receptor' FAS triggers their apoptosis. In type I cells, such as lymphocytes, activation of 'effector caspases' by FAS-induced activation of caspase-8 suffices for cell killing, whereas in type II cells, including hepatocytes and pancreatic beta-cells, caspase cascade amplification through caspase-8-mediated activation of the pro-apoptotic BCL-2 family member BID (BH3 interacting domain death agonist) is essential. Here we show that loss of XIAP (X-chromosome linked inhibitor of apoptosis protein) function by gene targeting or treatment with a second mitochondria-derived activator of caspases (SMAC, also called DIABLO; direct IAP-binding protein with low pI) mimetic drug in mice rendered hepatocytes and beta-cells independent of BID for FAS-induced apoptosis. These results show that XIAP is the critical discriminator between type I and type II apoptosis signalling and suggest that IAP inhibitors should be used with caution in cancer patients with underlying liver conditions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2956120/" 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/PMC2956120/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jost, Philipp J -- Grabow, Stephanie -- Gray, Daniel -- McKenzie, Mark D -- Nachbur, Ueli -- Huang, David C S -- Bouillet, Philippe -- Thomas, Helen E -- Borner, Christoph -- Silke, John -- Strasser, Andreas -- Kaufmann, Thomas -- CA 43540/CA/NCI NIH HHS/ -- CA 80188/CA/NCI NIH HHS/ -- R01 CA043540/CA/NCI NIH HHS/ -- R01 CA043540-09/CA/NCI NIH HHS/ -- R01 CA043540-22/CA/NCI NIH HHS/ -- R01 CA080188-01/CA/NCI NIH HHS/ -- R01 CA080188-08/CA/NCI NIH HHS/ -- England -- Nature. 2009 Aug 20;460(7258):1035-9. doi: 10.1038/nature08229. Epub 2009 Jul 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Walter and Eliza Hall Institute of Medical Research, Melbourne University, Parkville, Victoria 3050, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19626005" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/antagonists & inhibitors/immunology/*metabolism ; *Apoptosis ; BH3 Interacting Domain Death Agonist Protein/deficiency/genetics ; Biomimetic Materials/pharmacology ; Caspase Inhibitors ; Enzyme Activation ; Fas Ligand Protein/metabolism ; Female ; Hepatitis/metabolism/pathology ; Hepatocytes/cytology/drug effects/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Signal Transduction ; Thymus Gland/cytology/drug effects ; X-Linked Inhibitor of Apoptosis Protein/antagonists & ; inhibitors/deficiency/genetics/*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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  • 3
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    Apoptosis initiated when BH3 ligands engage multiple Bcl-2 homologs, not Bax or Bak (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-02-10
    Description: A central issue in the regulation of apoptosis by the Bcl-2 family is whether its BH3-only members initiate apoptosis by directly binding to the essential cell-death mediators Bax and Bak, or whether they can act indirectly, by engaging their pro-survival Bcl-2-like relatives. Contrary to the direct-activation model, we show that Bax and Bak can mediate apoptosis without discernable association with the putative BH3-only activators (Bim, Bid, and Puma), even in cells with no Bim or Bid and reduced Puma. Our results indicate that BH3-only proteins induce apoptosis at least primarily by engaging the multiple pro-survival relatives guarding Bax and Bak.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Willis, Simon N -- Fletcher, Jamie I -- Kaufmann, Thomas -- van Delft, Mark F -- Chen, Lin -- Czabotar, Peter E -- Ierino, Helen -- Lee, Erinna F -- Fairlie, W Douglas -- Bouillet, Philippe -- Strasser, Andreas -- Kluck, Ruth M -- Adams, Jerry M -- Huang, David C S -- CA43540/CA/NCI NIH HHS/ -- CA80188/CA/NCI NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Feb 9;315(5813):856-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3050, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17289999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins/chemistry/genetics/*metabolism ; BH3 Interacting Domain Death Agonist Protein/chemistry/genetics/*metabolism ; Cell Line ; Cells, Cultured ; Humans ; Ligands ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Mice, Knockout ; Models, Biological ; Mutation ; Myeloid Cell Leukemia Sequence 1 Protein ; Neoplasm Proteins/metabolism ; Protein Structure, Tertiary ; Proteins/metabolism ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins c-bcl-2/*metabolism ; Tumor Suppressor Proteins/genetics/metabolism ; bcl-2 Homologous Antagonist-Killer Protein/metabolism ; bcl-2-Associated X Protein/chemistry/*metabolism ; bcl-Associated Death Protein/metabolism ; bcl-X Protein/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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    Transcriptional architecture and chromatin landscape of the core circadian clock in mammals (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-01
    Description: The mammalian circadian clock involves a transcriptional feed back loop in which CLOCK and BMAL1 activate the Period and Cryptochrome genes, which then feedback and repress their own transcription. We have interrogated the transcriptional architecture of the circadian transcriptional regulatory loop on a genome scale in mouse liver and find a stereotyped, time-dependent pattern of transcription factor binding, RNA polymerase II (RNAPII) recruitment, RNA expression, and chromatin states. We find that the circadian transcriptional cycle of the clock consists of three distinct phases: a poised state, a coordinated de novo transcriptional activation state, and a repressed state. Only 22% of messenger RNA (mRNA) cycling genes are driven by de novo transcription, suggesting that both transcriptional and posttranscriptional mechanisms underlie the mammalian circadian clock. We also find that circadian modulation of RNAPII recruitment and chromatin remodeling occurs on a genome-wide scale far greater than that seen previously by gene expression profiling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3694775/" 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/PMC3694775/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koike, Nobuya -- Yoo, Seung-Hee -- Huang, Hung-Chung -- Kumar, Vivek -- Lee, Choogon -- Kim, Tae-Kyung -- Takahashi, Joseph S -- F32 DA024556/DA/NIDA NIH HHS/ -- R01 NS053616/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Oct 19;338(6105):349-54. doi: 10.1126/science.1226339. Epub 2012 Aug 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, The University of Texas Southwestern Medical Center, Dallas, TX 75390-9111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22936566" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/metabolism ; Animals ; CLOCK Proteins/metabolism ; Chromatin/*metabolism ; Chromatin Assembly and Disassembly/genetics ; Circadian Clocks/*genetics ; Cryptochromes/*genetics ; DNA, Intergenic ; Enhancer Elements, Genetic ; *Epigenesis, Genetic ; Gene Expression Profiling ; Genetic Loci ; Histones/metabolism ; Liver/metabolism/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Period Circadian Proteins/genetics ; RNA Polymerase II/metabolism ; RNA, Messenger/genetics ; *Transcription, Genetic ; *Transcriptional Activation
    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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    C57BL/6N mutation in cytoplasmic FMRP interacting protein 2 regulates cocaine response (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-12-21
    Description: The inbred mouse C57BL/6J is the reference strain for genome sequence and for most behavioral and physiological phenotypes. However, the International Knockout Mouse Consortium uses an embryonic stem cell line derived from a related C57BL/6N substrain. We found that C57BL/6N has a lower acute and sensitized response to cocaine and methamphetamine. We mapped a single causative locus and identified a nonsynonymous mutation of serine to phenylalanine (S968F) in Cytoplasmic FMRP interacting protein 2 (Cyfip2) as the causative variant. The S968F mutation destabilizes CYFIP2, and deletion of the C57BL/6N mutant allele leads to acute and sensitized cocaine-response phenotypes. We propose that CYFIP2 is a key regulator of cocaine response in mammals and present a framework to use mouse substrains to identify previously unknown genes and alleles regulating behavior.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4500108/" 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/PMC4500108/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kumar, Vivek -- Kim, Kyungin -- Joseph, Chryshanthi -- Kourrich, Said -- Yoo, Seung-Hee -- Huang, Hung Chung -- Vitaterna, Martha H -- de Villena, Fernando Pardo-Manuel -- Churchill, Gary -- Bonci, Antonello -- Takahashi, Joseph S -- F32 DA024556/DA/NIDA NIH HHS/ -- F32DA024556/DA/NIDA NIH HHS/ -- U01 MH061915/MH/NIMH NIH HHS/ -- U01MH61915/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Dec 20;342(6165):1508-12. doi: 10.1126/science.1245503.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390-9111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24357318" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; Central Nervous System Stimulants/administration & dosage ; Cocaine/*administration & dosage ; Cocaine-Related Disorders/*genetics/*psychology ; *Drug-Seeking Behavior ; Methamphetamine/administration & dosage ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Motor Activity/drug effects ; Mutation ; Nerve Tissue Proteins/genetics/*physiology ; Phenylalanine/genetics ; Polymorphism, Single Nucleotide ; Psychomotor Performance/drug effects ; Quantitative Trait Loci ; Serine/genetics
    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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    Reelin promotes peripheral synapse elimination and maturation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-02
    Description: Reelin is an extracellular protein that is crucial for layer formation in the embryonic brain. Here, we demonstrate that Reelin functions postnatally to regulate the development of the neuromuscular junction. Reelin is required for motor end-plate maturation and proper nerve-muscle connectivity, and it directly promotes synapse elimination. Unlike layer formation, neuromuscular junction development requires a function of Reelin that is not mediated by Disabled1 or very-low-density lipoprotein receptors and apolipoprotein E receptor 2 receptors but by a distinct mechanism involving its protease activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Quattrocchi, Carlo C -- Huang, Cheng -- Niu, Sanyong -- Sheldon, Michael -- Benhayon, David -- Cartwright, Joiner Jr -- Mosier, Dennis R -- Keller, Flavio -- D'Arcangelo, Gabriella -- New York, N.Y. -- Science. 2003 Aug 1;301(5633):649-53.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Cain Foundation Laboratories, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12893944" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Axons/metabolism ; Cell Adhesion Molecules, Neuronal/genetics/metabolism/pharmacology/*physiology ; Culture Media, Conditioned ; Diaphragm/innervation ; Extracellular Matrix Proteins/genetics/metabolism/pharmacology/*physiology ; LDL-Receptor Related Proteins ; Mice ; Mice, Neurologic Mutants ; Microscopy, Confocal ; Microscopy, Electron ; Motor Endplate/ultrastructure ; Motor Neurons/metabolism ; Muscle, Skeletal/innervation ; Mutation ; Nerve Tissue Proteins/genetics/metabolism ; Neuromuscular Junction/*growth & ; development/metabolism/*physiology/ultrastructure ; Receptors, LDL/genetics/metabolism ; Receptors, Lipoprotein/genetics/metabolism ; Schwann Cells/metabolism ; Serine Endopeptidases ; Serine Proteinase Inhibitors/pharmacology ; Sulfones/pharmacology ; Synapses/*physiology/ultrastructure
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 7
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    Anticonvulsant medications extend worm life-span (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-01-18
    Description: Genetic studies have elucidated mechanisms that regulate aging, but there has been little progress in identifying drugs that delay aging. Here, we report that ethosuximide, trimethadione, and 3,3-diethyl-2-pyrrolidinone increase mean and maximum life-span of Caenorhabditis elegans and delay age-related declines of physiological processes, indicating that these compounds retard the aging process. These compounds, two of which are approved for human use, are anticonvulsants that modulate neural activity. These compounds also regulated neuromuscular activity in nematodes. These findings suggest that the life-span-extending activity of these compounds is related to the anticonvulsant activity and implicate neural activity in the regulation of aging.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Evason, Kimberley -- Huang, Cheng -- Yamben, Idella -- Covey, Douglas F -- Kornfeld, Kerry -- P50 AG05681/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2005 Jan 14;307(5707):258-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15653505" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*drug effects ; Aldicarb/pharmacology ; Animals ; Anticonvulsants/*pharmacology/therapeutic use ; Caenorhabditis elegans/*drug effects/genetics/growth & development/physiology ; Caenorhabditis elegans Proteins/genetics/physiology ; Disorders of Sex Development ; Dose-Response Relationship, Drug ; Drug Evaluation, Preclinical ; Epilepsy, Absence/drug therapy ; Ethosuximide/*pharmacology/therapeutic use ; Female ; Forkhead Transcription Factors ; Genes, Helminth ; Humans ; Lactams/*pharmacology ; Longevity/*drug effects ; Movement/drug effects ; Muscles/drug effects/innervation/physiology ; Mutation ; Neurons/drug effects/physiology ; Oviposition/drug effects ; Pharynx/drug effects/physiology ; Reproduction/drug effects ; Synaptic Transmission/drug effects ; Transcription Factors/genetics/physiology ; Trimethadione/*pharmacology/therapeutic use ; Vulva
    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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  • 8
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    A FOXO3-IRF7 gene regulatory circuit limits inflammatory sequelae of antiviral responses (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-09-18
    Description: Antiviral responses must be tightly regulated to defend rapidly against infection while minimizing inflammatory damage. Type 1 interferons (IFN-I) are crucial mediators of antiviral responses and their transcription is regulated by a variety of transcription factors; principal among these is the family of interferon regulatory factors (IRFs). The IRF gene regulatory networks are complex and contain multiple feedback loops. The tools of systems biology are well suited to elucidate the complex interactions that give rise to precise coordination of the interferon response. Here we have used an unbiased systems approach to predict that a member of the forkhead family of transcription factors, FOXO3, is a negative regulator of a subset of antiviral genes. This prediction was validated using macrophages isolated from Foxo3-null mice. Genome-wide location analysis combined with gene deletion studies identified the Irf7 gene as a critical target of FOXO3. FOXO3 was identified as a negative regulator of Irf7 transcription and we have further demonstrated that FOXO3, IRF7 and IFN-I form a coherent feed-forward regulatory circuit. Our data suggest that the FOXO3-IRF7 regulatory circuit represents a novel mechanism for establishing the requisite set points in the interferon pathway that balances the beneficial effects and deleterious sequelae of the antiviral response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3556990/" 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/PMC3556990/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Litvak, Vladimir -- Ratushny, Alexander V -- Lampano, Aaron E -- Schmitz, Frank -- Huang, Albert C -- Raman, Ayush -- Rust, Alistair G -- Bergthaler, Andreas -- Aitchison, John D -- Aderem, Alan -- HHSN272200700038C/AI/NIAID NIH HHS/ -- HHSN272200700038C/PHS HHS/ -- HHSN272200800058C/AI/NIAID NIH HHS/ -- HSN272200800058C/PHS HHS/ -- R01 AI025032/AI/NIAID NIH HHS/ -- R01 AI032972/AI/NIAID NIH HHS/ -- R01AI025032/AI/NIAID NIH HHS/ -- R01AI032972/AI/NIAID NIH HHS/ -- U19 AI100627/AI/NIAID NIH HHS/ -- U54 GM103511/GM/NIGMS NIH HHS/ -- U54 RR022220/RR/NCRR NIH HHS/ -- U54GM103511/GM/NIGMS NIH HHS/ -- England -- Nature. 2012 Oct 18;490(7420):421-5. doi: 10.1038/nature11428. Epub 2012 Sep 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Seattle Biomedical Research Institute, Seattle, Washington 98109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22982991" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Forkhead Transcription Factors/deficiency/genetics/*metabolism ; Gene Deletion ; Gene Expression Regulation/*immunology ; Inflammation/genetics/*immunology/*pathology ; Interferon Regulatory Factor-7/deficiency/genetics/*metabolism ; Interferon Type I/immunology ; Lung/immunology/pathology/virology ; Macrophages/immunology ; Mice ; Mice, Inbred C57BL ; Reproducibility of Results ; Vesiculovirus/*immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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    Helminth infection reactivates latent gamma-herpesvirus via cytokine competition at a viral promoter (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-06-28
    Description: Mammals are coinfected by multiple pathogens that interact through unknown mechanisms. We found that helminth infection, characterized by the induction of the cytokine interleukin-4 (IL-4) and the activation of the transcription factor Stat6, reactivated murine gamma-herpesvirus infection in vivo. IL-4 promoted viral replication and blocked the antiviral effects of interferon-gamma (IFNgamma) by inducing Stat6 binding to the promoter for an important viral transcriptional transactivator. IL-4 also reactivated human Kaposi's sarcoma-associated herpesvirus from latency in cultured cells. Exogenous IL-4 plus blockade of IFNgamma reactivated latent murine gamma-herpesvirus infection in vivo, suggesting a "two-signal" model for viral reactivation. Thus, chronic herpesvirus infection, a component of the mammalian virome, is regulated by the counterpoised actions of multiple cytokines on viral promoters that have evolved to sense host immune status.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4531374/" 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/PMC4531374/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reese, T A -- Wakeman, B S -- Choi, H S -- Hufford, M M -- Huang, S C -- Zhang, X -- Buck, M D -- Jezewski, A -- Kambal, A -- Liu, C Y -- Goel, G -- Murray, P J -- Xavier, R J -- Kaplan, M H -- Renne, R -- Speck, S H -- Artyomov, M N -- Pearce, E J -- Virgin, H W -- AI032573/AI/NIAID NIH HHS/ -- AI084887/AI/NIAID NIH HHS/ -- CA119917/CA/NCI NIH HHS/ -- CA164062/CA/NCI NIH HHS/ -- CA52004/CA/NCI NIH HHS/ -- P30 CA021765/CA/NCI NIH HHS/ -- R01 AI032573/AI/NIAID NIH HHS/ -- R01 AI084887/AI/NIAID NIH HHS/ -- R01 AI095282/AI/NIAID NIH HHS/ -- R01 CA052004/CA/NCI NIH HHS/ -- R01 CA119917/CA/NCI NIH HHS/ -- R01 CA164062/CA/NCI NIH HHS/ -- U54 AI057160/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2014 Aug 1;345(6196):573-7. doi: 10.1126/science.1254517. Epub 2014 Jun 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. ; Emory University Vaccine Center, Atlanta, GA 30322, USA. ; Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL 32610, USA. ; Departments of Pediatrics and Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202, USA. ; Center for Computational and Integrative Biology and Gastrointestinal Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. ; Departments of Infectious Diseases and Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. ; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. virgin@wustl.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24968940" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gammaherpesvirinae/genetics/*physiology ; Gene Expression Regulation, Viral ; Herpesvirus 8, Human/genetics/*physiology ; Humans ; Interferon-gamma/*immunology/pharmacology ; Interleukin-4/*metabolism/pharmacology ; Macrophages/immunology ; Mice ; Mice, Inbred C57BL ; Nematospiroides dubius/immunology ; Ovum/immunology ; Promoter Regions, Genetic ; STAT6 Transcription Factor/*metabolism ; Schistosoma mansoni/*immunology ; Schistosomiasis mansoni/*immunology ; Strongylida Infections/immunology ; Virus Activation/drug effects/genetics/*physiology ; Virus Latency/physiology ; Virus Replication/physiology
    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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  • 10
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    A viral RNA structural element alters host recognition of nonself RNA (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-02-01
    Description: Although interferon (IFN) signaling induces genes that limit viral infection, many pathogenic viruses overcome this host response. As an example, 2'-O methylation of the 5' cap of viral RNA subverts mammalian antiviral responses by evading restriction of Ifit1, an IFN-stimulated gene that regulates protein synthesis. However, alphaviruses replicate efficiently in cells expressing Ifit1 even though their genomic RNA has a 5' cap lacking 2'-O methylation. We show that pathogenic alphaviruses use secondary structural motifs within the 5' untranslated region (UTR) of their RNA to alter Ifit1 binding and function. Mutations within the 5'-UTR affecting RNA structural elements enabled restriction by or antagonism of Ifit1 in vitro and in vivo. These results identify an evasion mechanism by which viruses use RNA structural motifs to avoid immune restriction.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4209899/" 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/PMC4209899/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hyde, Jennifer L -- Gardner, Christina L -- Kimura, Taishi -- White, James P -- Liu, Gai -- Trobaugh, Derek W -- Huang, Cheng -- Tonelli, Marco -- Paessler, Slobodan -- Takeda, Kiyoshi -- Klimstra, William B -- Amarasinghe, Gaya K -- Diamond, Michael S -- AI049820/AI/NIAID NIH HHS/ -- P41GM66326/GM/NIGMS NIH HHS/ -- P41RR02301/RR/NCRR NIH HHS/ -- R01 AI083383/AI/NIAID NIH HHS/ -- R01 AI104972/AI/NIAID NIH HHS/ -- U19 AI083019/AI/NIAID NIH HHS/ -- UL1 TR000071/TR/NCATS NIH HHS/ -- UL1TR000071/TR/NCATS NIH HHS/ -- New York, N.Y. -- Science. 2014 Feb 14;343(6172):783-7. doi: 10.1126/science.1248465. Epub 2014 Jan 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24482115" target="_blank"〉PubMed〈/a〉
    Keywords: 5' Untranslated Regions/immunology ; Alphavirus/*pathogenicity/physiology ; Alphavirus Infections/*immunology/virology ; Animals ; Carrier Proteins/antagonists & inhibitors/genetics/immunology ; Host-Pathogen Interactions/*immunology ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Mutation ; Nucleic Acid Conformation ; RNA Caps/*chemistry/*immunology ; RNA, Viral/*chemistry/*immunology ; Virus Replication
    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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