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  • 1
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    Mitochondrial DNA stress primes the antiviral innate immune response (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-02-03
    Description: Mitochondrial DNA (mtDNA) is normally present at thousands of copies per cell and is packaged into several hundred higher-order structures termed nucleoids. The abundant mtDNA-binding protein TFAM (transcription factor A, mitochondrial) regulates nucleoid architecture, abundance and segregation. Complete mtDNA depletion profoundly impairs oxidative phosphorylation, triggering calcium-dependent stress signalling and adaptive metabolic responses. However, the cellular responses to mtDNA instability, a physiologically relevant stress observed in many human diseases and ageing, remain poorly defined. Here we show that moderate mtDNA stress elicited by TFAM deficiency engages cytosolic antiviral signalling to enhance the expression of a subset of interferon-stimulated genes. Mechanistically, we find that aberrant mtDNA packaging promotes escape of mtDNA into the cytosol, where it engages the DNA sensor cGAS (also known as MB21D1) and promotes STING (also known as TMEM173)-IRF3-dependent signalling to elevate interferon-stimulated gene expression, potentiate type I interferon responses and confer broad viral resistance. Furthermore, we demonstrate that herpesviruses induce mtDNA stress, which enhances antiviral signalling and type I interferon responses during infection. Our results further demonstrate that mitochondria are central participants in innate immunity, identify mtDNA stress as a cell-intrinsic trigger of antiviral signalling and suggest that cellular monitoring of mtDNA homeostasis cooperates with canonical virus sensing mechanisms to fully engage antiviral innate immunity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4409480/" 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/PMC4409480/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉West, A Phillip -- Khoury-Hanold, William -- Staron, Matthew -- Tal, Michal C -- Pineda, Cristiana M -- Lang, Sabine M -- Bestwick, Megan -- Duguay, Brett A -- Raimundo, Nuno -- MacDuff, Donna A -- Kaech, Susan M -- Smiley, James R -- Means, Robert E -- Iwasaki, Akiko -- Shadel, Gerald S -- F31 AG039163/AG/NIA NIH HHS/ -- F32 DK091042/DK/NIDDK NIH HHS/ -- MOP37995/Canadian Institutes of Health Research/Canada -- P01 ES011163/ES/NIEHS NIH HHS/ -- R01 AG047632/AG/NIA NIH HHS/ -- R01 AI054359/AI/NIAID NIH HHS/ -- R01 AI081884/AI/NIAID NIH HHS/ -- T32 AI055403/AI/NIAID NIH HHS/ -- UL1 TR000142/TR/NCATS NIH HHS/ -- England -- Nature. 2015 Apr 23;520(7548):553-7. doi: 10.1038/nature14156. Epub 2015 Feb 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Yale School of Medicine, New Haven, Connecticut 06520, USA. ; Department of Immunobiology, Yale School of Medicine, New Haven, Connecticut 06520, USA. ; Li Ka Shing Institute of Virology, Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta T6G 2S2, Canada. ; Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; 1] Department of Immunobiology, Yale School of Medicine, New Haven, Connecticut 06520, USA [2] Howard Hughes Medical Institute, Chevy Chase, Maryland 20815-6789, USA. ; 1] Department of Pathology, Yale School of Medicine, New Haven, Connecticut 06520, USA [2] Department of Genetics, Yale School of Medicine, New Haven, Connecticut 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25642965" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; DNA, Mitochondrial/*metabolism ; DNA-Binding Proteins/deficiency/genetics/metabolism ; Female ; Gene Expression Regulation/genetics/immunology ; Herpesvirus 1, Human/*immunology ; High Mobility Group Proteins/deficiency/genetics/metabolism ; Humans ; Immunity, Innate/*immunology ; Interferon Regulatory Factor-3/metabolism ; Interferon Type I/immunology ; Membrane Proteins/metabolism ; Mice ; Nucleotidyltransferases/metabolism ; *Stress, Physiological
    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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    Potentiation of bleomycin lethality by anticalmodulin drugs: a role for calmodulin in DNA repair (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-06-22
    Description: Treatment of exponentially growing Chinese hamster ovary cells with bleomycin causes a dose-dependent decrease in cell survival due to DNA damage. This lethal effect can be potentiated by the addition of a nonlethal dose of the anticalmodulin drug N-(4-aminobutyl)-5-chloro-2-naphthalenesulfonamide ( W13 ) but not its inactive analog N-(4-aminobutyl)-2-naphthalenesulfonamide ( W12 ). By preventing the repair of damaged DNA, W13 also inhibits recovery from potentially lethal damage induced by bleomycin. These data suggest a role for calmodulin in the DNA repair pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chafouleas, J G -- Bolton, W E -- Means, A R -- RR-05425/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1984 Jun 22;224(4655):1346-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6203171" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bleomycin/*pharmacology ; Calmodulin/*antagonists & inhibitors/*physiology ; Cell Division/drug effects ; Cell Line ; Cell Survival/drug effects ; Cricetinae ; Cricetulus ; DNA Repair/*drug effects ; Dose-Response Relationship, Drug ; Drug Synergism ; Sulfonamides/pharmacology
    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
    Electronic Resource
    Electronic Resource
    Increased calmodulin affects cell morphology and mRNA levels of cytoskeletal protein genes (1992)
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 21 (1992), S. 45-57 
    Details
    ISSN: 0886-1544
    Keywords: cell shape ; gene expression ; pleiotropic effects ; cell cycle ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: We have previously described stable mouse C127 cell lines in which a CaM mini-gene has been expressed in a bovine papilloma virus-based expression vector (Rasmussen and Means: EMBO J. 6:3961-3968. 1987). Elevation of CaM to levels five-fold higher than in control cells caused an acceleration in cell cycle progression by reducing the length of the G1 period. When these cell lines were originally isolated it was observed that cells in which CaM levels were increased had a flattened morphology. In this study we have examined the localization of actin, vimentin, and tubulin in these cells as compared to the BPV-transformed control cell line in order to determine if changes in shape were accompanied by differences in the cytoskeletal organization. Cell-cycle-dependent changes in the levels of mRNAs for histone H4, glyceraldehyde-3-phosphate dehydrogenase, β-actin, vimentin, and β-tubulin have also been examined. Our results indicate that increased CaM causes differences in the organization of microfilaments, intermediate filaments, and microtubules and that these changes are accompanied by selective differences in the cell-cycle-dependent expression of some mRNAs. Elevated CaM was also correlated with a reduced stability of β-tubulin mRNA. These studies indicate that CaM has pleiotropic effects on cell function and suggest that stable cell lines with altered CaM levels may provide a useful model system for understanding the moiecular basis of CaM-dependent regulation of cellular processes.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cm.970210106
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  • 4
    Electronic Resource
    Electronic Resource
    Coordinate regulation of mRNAs from multiple calmodulin genes during myoblast differentiation in vitro (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 154 (1993), S. 343-349 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Multiple genes encoding identical calmodulin molecules have been found in all mammalian species so far examined, but little is known regarding the factors involved in regulating the expression of this gene family. We have investigated the possibility of differential regulation under conditions of cell cycle withdrawal and differentiation in the nonfusing BC3H1 myoblast. Transcripts from the three genes are expressed in myoblasts and myocytes and each of the mRNA species decreases during BC3H1 differentiation. Calmodulin protein levels also decrease, although with distinct kinetics with respect to the mRNAs. Previous studies indicated that a decrease in transcription is involved (Epstein et al., Molecular Endocrinology 3:193-202, 1989). In this study, an increase in stability for each of the mRNA species is also shown to contribute to overall mRNA levels. The calmodulin mRNAs are also found to decrease under conditions of cell cycle withdrawal when differentiation is blocked. This demonstrates that the expression of mRNA from all three genes is directly coupled with the proliferation state but only indirectly with the differentiation state. Consistent with this, calmodulin expression decreases in serum deprived fibroblasts as they exit the cell cycle. © 1993 Wiley-Liss, Inc.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041540218
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  • 5
    Electronic Resource
    Electronic Resource
    Calmodulin as a mediator of hormone action and cell regulation (1982)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 20 (1982), S. 317-330 
    Details
    ISSN: 0730-2312
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240200402
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  • 6
    Electronic Resource
    Electronic Resource
    Altered synthesis of the 26-kDa heat stress protein family and thermotolerance in cell lines with elevated levels of calcium-binding proteins (1990)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 142 (1990), S. 615-627 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Using a bovine papillorna virus-based vector, mouse mammary adenocarcinoma cells have been transformed to express elevated amounts of functional calmodulin (CaM) (Rasmussen and Means, 1987) and another Ca2+-binding protein, parvalbumin (PV) (Rasmussen and Means, 1989) that is not normally synthesized in these cells. Parental cells (C127) and cells transformed by the vector alone (BPV-1), the vector containing a CaM gene (CM-1), or the vector containing parvalbumin (PV-1) were used to study the effect of increased synthesis of Ca2+-binding proteins on heat-stress protein (HSP) synthesis and cell survival following heating at 43°C. The induction, stability, and repression of the synthesis of most HSPs after 43°C heating was not significantly affected by increased amounts of Ca2+ -binding proteins, but the rate of synthesis of all three isoforms of the 26-kDa HSP (HSP26) was greatly reduced. C127 cells, which have about one half as much CaM as do BPV-1 cells, synthesized the most HSP26. CM-1 cells, which have more than fourfold higher levels of CaM than do BPV-1 cells, had a rate of synthesis of HSP26 approaching that of unheated cells. BPV-1 cells, with a two-fold increase in CaM, were intermediate in HSP26 synthesis. This effect on HSP26 synthesis may be largely related to the Ca2+ -binding capacity of CaM rather than to a specific CaM-regulated function, since PV-1 cells also showed reduced rates of HSP26 synthesis. Survival experiments showed that reduced HSP26 synthesis in cells with increased amounts of Ca2+-binding proteins did not significantly alter intrinsic resistance to continuous 43°C heating. Thermotolerance was not reduced and appeared to develop more rapidly in CM-1 and PV-1 cells. These results suggest that (1) the signal for HSP26 synthesis can be largely abrogated by elevated Ca2+ binding protein levels, and (2) if these HSPs are involved in thermotolerance development, that function may be associated with intracellular Ca2+ homeostasis.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041420323
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  • 7
    Electronic Resource
    Electronic Resource
    Inhibition of human erythroid colony-forming units by interleukin-1 is mediated by gamma interferon (1992)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 150 (1992), S. 59-64 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: IL-1 inhibits erythropoiesis in vivo and in vitro. This inhibition was studied by comparing the effect of recombinant human IL-1 (rhIL-1) on highly purified CFU-erythroid (E) generated from peripheral blood burst-forming units-erythroid (BFU-E) (mean purity 44.4%) with its effect on unpurified marrow CFU-E (mean purity 0.36%). Colony formation by marrow CFU-E was significantly inhibited by rhIL-1, while colony formation by highly purified CFU-E was not inhibited. However, purified CFU-E colonies were inhibited by rhIL-1 in the presence of autologous T-lymphocytes, and also by cell-free conditioned medium prepared from T-lymphocytes stimulated by rhIL-1. This inhibitory effect was ablated by neutralizing antibodies to γinterferon (IFN), but not by antibodies to human IL-1, tumor necrosis factor, or βIFN. Colony formation by highly purified CFU-E was also inhibited by recombinant human γIFN (rhγIFN). IL-1 and γIFN play significant roles in the pathogenesis of the anemia of chronic disease. These studies indicate that rhIL-1 inhibits CFU-E colony formation by an indirect mechanism involving T-lymphocytes and requiring γIFN and that γIFN itself is most probably the direct mediator of this effect.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041500109
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  • 8
    Electronic Resource
    Electronic Resource
    Steroid hormone regulation of specific messenger RNA and protein synthesis in eucaryotic cells (1975)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 85 (1975), S. 343-356 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Evidence is presented that the induction of specific proteins in the chick oviduct by the steroid hormones estrogen and progesterone, involves a primary effect at the level of gene transcription. The intracellular levels of mRNA's which code for the synthesis of the egg-white proteins, ovalbumin and avidin, have been quantitated in a heterologous protein synthesizing system. It is demonstrated that these levels are directly dependent upon the inducing steroid, estrogen or progesterone, respectively. Ovalbumin mRNA has been purified to apparent homogeneity. This ovalbumin mRNA was then used as a template for the synthesis of a complementary DNA copy catalyzed by the enzyme reverse transcriptase which was isolated from avian myeloblastosis virus. This radioactively labeled complementary DNA was used to demonstrate, by means of DNA excess hybridization, that the ovalbumin gene is represented only once in each haploid genome of the chick cell. Next the complementary DNA copy of the ovalbumin mRNA was used as a genetic probe to determine the precise number of sequences of ovalbumin mRNA present at any one time after the administration of estrogen. It was demonstrated that the unstimulated chick contained no sequences of ovalbumin mRNA. Within a very short period of time after estrogen is administered the ovalbumin sequences begin to appear and reach a steady state level of 140,000 molecules per tubular gland cell. It could also be calculated that each ovalbumin molecule is probably translated some 50,000 times during its life which explains why ovalbumin comprises some 60% of the total protein in the oviduct cell. Following withdrawal of the oviduct from estrogen treatment, ovalbumin mRNA sequences again drop to undetectable levels. However, following a single injection of estrogen to these withdrawn animals, new ovalbumin mRNA sequences could be detected within 30 minutes. These data suggest that estrogen controls the activity of the ovalbumin gene via a pure transcriptional control mechanism. It is also demonstrated that the efficiency of the complementary DNA as a means of quantitating specific mRNA sequences is some 1,000 times more sensitive than the best available in vitro translation system. Finally, the efficacy of four popular translation systems is compared. It is suggested that for initial studies involving hormonal control of mRNA levels, the translation system derived from wheat germ is the simplest and most sensitive.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1040850403
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  • 9
    Electronic Resource
    Electronic Resource
    Cholinesterase activity of tissues of adult melanoplus differentialis (Orthoptera, Acrididae)It is a pleasure to thank Dr. E. J. Boell for his helpful supervision of the problem and kindly encouragement. (1942)
    Philadelphia : Wiley-Blackwell
    Journal of Cellular and Comparative Physiology 20 (1942), S. 319-324 
    Details
    ISSN: 0095-9898
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Additional Material: 2 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1030200307
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