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  • 1
    Publication Date: 2013-12-10
    Description: Evolution drives, and is driven by, demography. A genotype moulds its phenotype's age patterns of mortality and fertility in an environment; these two patterns in turn determine the genotype's fitness in that environment. Hence, to understand the evolution of ageing, age patterns of mortality and reproduction need to be compared for species across the tree of life. However, few studies have done so and only for a limited range of taxa. Here we contrast standardized patterns over age for 11 mammals, 12 other vertebrates, 10 invertebrates, 12 vascular plants and a green alga. Although it has been predicted that evolution should inevitably lead to increasing mortality and declining fertility with age after maturity, there is great variation among these species, including increasing, constant, decreasing, humped and bowed trajectories for both long- and short-lived species. This diversity challenges theoreticians to develop broader perspectives on the evolution of ageing and empiricists to study the demography of more species.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4157354/" 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/PMC4157354/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, Owen R -- Scheuerlein, Alexander -- Salguero-Gomez, Roberto -- Camarda, Carlo Giovanni -- Schaible, Ralf -- Casper, Brenda B -- Dahlgren, Johan P -- Ehrlen, Johan -- Garcia, Maria B -- Menges, Eric S -- Quintana-Ascencio, Pedro F -- Caswell, Hal -- Baudisch, Annette -- Vaupel, James W -- P01 AG-031719/AG/NIA NIH HHS/ -- P01 AG031719/AG/NIA NIH HHS/ -- England -- Nature. 2014 Jan 9;505(7482):169-73. doi: 10.1038/nature12789. Epub 2013 Dec 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Max-Planck Odense Center on the Biodemography of Aging, Campusvej 55, 5230 Odense M, Denmark [2] Department of Biology, University of Southern Denmark, Campusvej 55, 5230 Odense M, Denmark [3]. ; 1] Max Planck Institute for Demographic Research, Konrad-Zuse-Strasse 1, 18057 Rostock, Germany [2]. ; 1] Max Planck Institute for Demographic Research, Konrad-Zuse-Strasse 1, 18057 Rostock, Germany [2] School of Biological Sciences, Centre for Biodiversity and Conservation Science, University of Queensland, Brisbane QLD 4072, Australia. ; Institut National d'Etudes Demographiques, 133 Boulevard Davout, 75980 Paris Cedex 20, France. ; Max Planck Institute for Demographic Research, Konrad-Zuse-Strasse 1, 18057 Rostock, Germany. ; Department of Biology, University of Pennsylvania, 433 South University Avenue, Philadelphia, Pennsylvania 19104-6018, USA. ; 1] Max-Planck Odense Center on the Biodemography of Aging, Campusvej 55, 5230 Odense M, Denmark [2] Department of Biology, University of Southern Denmark, Campusvej 55, 5230 Odense M, Denmark. ; Department of Ecology, Environment and Plant Sciences, Stockholm University, Lilla Frescativagen 5, 10691 Stockholm, Sweden. ; Pyrenean Institute of Ecology (CSIC), Avenida Montanana 1005, 50059 Zaragoza, Spain. ; Archbold Biological Station, 123 Main Drive, Venus, Florida 33960, USA. ; Department of Biology, University of Central Florida, 4110 Libra Drive, Orlando, Florida 32816-2368, USA. ; 1] Department of Biology, University of Southern Denmark, Campusvej 55, 5230 Odense M, Denmark [2] Max Planck Institute for Demographic Research, Konrad-Zuse-Strasse 1, 18057 Rostock, Germany [3] Woods Hole Oceanographic Institution, Biology Department MS-34, Woods Hole, Massachusetts 02543 USA [4] Institute for Biodiversity and Ecosystem Dynamics, University of Amsterdam, PO Box 94248, 1090GE Amsterdam, The Netherlands. ; 1] Max-Planck Odense Center on the Biodemography of Aging, Campusvej 55, 5230 Odense M, Denmark [2] Max Planck Institute for Demographic Research, Konrad-Zuse-Strasse 1, 18057 Rostock, Germany [3] Duke Population Research Institute, Duke University, Durham, North Carolina 27705, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24317695" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; Biological Evolution ; Chlorophyta ; Fertility/*physiology ; Longevity/*physiology ; *Phylogeny ; Plants ; Reproduction/physiology
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  • 2
    Publication Date: 2011-03-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nekaris, K Anne-Isola -- Nijman, Vincent -- Godfrey, Laurie R -- England -- Nature. 2011 Mar 24;471(7339):448. doi: 10.1038/471448c.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21430762" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthropology/*methods ; Culture ; Extinction, Biological ; Humans ; *Interdisciplinary Studies ; *Primates/physiology/psychology ; Tool Use Behavior
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  • 3
    Publication Date: 2011-02-11
    Description: Telomere dysfunction activates p53-mediated cellular growth arrest, senescence and apoptosis to drive progressive atrophy and functional decline in high-turnover tissues. The broader adverse impact of telomere dysfunction across many tissues including more quiescent systems prompted transcriptomic network analyses to identify common mechanisms operative in haematopoietic stem cells, heart and liver. These unbiased studies revealed profound repression of peroxisome proliferator-activated receptor gamma, coactivator 1 alpha and beta (PGC-1alpha and PGC-1beta, also known as Ppargc1a and Ppargc1b, respectively) and the downstream network in mice null for either telomerase reverse transcriptase (Tert) or telomerase RNA component (Terc) genes. Consistent with PGCs as master regulators of mitochondrial physiology and metabolism, telomere dysfunction is associated with impaired mitochondrial biogenesis and function, decreased gluconeogenesis, cardiomyopathy, and increased reactive oxygen species. In the setting of telomere dysfunction, enforced Tert or PGC-1alpha expression or germline deletion of p53 (also known as Trp53) substantially restores PGC network expression, mitochondrial respiration, cardiac function and gluconeogenesis. We demonstrate that telomere dysfunction activates p53 which in turn binds and represses PGC-1alpha and PGC-1beta promoters, thereby forging a direct link between telomere and mitochondrial biology. We propose that this telomere-p53-PGC axis contributes to organ and metabolic failure and to diminishing organismal fitness in the setting of telomere dysfunction.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3741661/" 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/PMC3741661/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sahin, Ergun -- Colla, Simona -- Liesa, Marc -- Moslehi, Javid -- Muller, Florian L -- Guo, Mira -- Cooper, Marcus -- Kotton, Darrell -- Fabian, Attila J -- Walkey, Carl -- Maser, Richard S -- Tonon, Giovanni -- Foerster, Friedrich -- Xiong, Robert -- Wang, Y Alan -- Shukla, Sachet A -- Jaskelioff, Mariela -- Martin, Eric S -- Heffernan, Timothy P -- Protopopov, Alexei -- Ivanova, Elena -- Mahoney, John E -- Kost-Alimova, Maria -- Perry, Samuel R -- Bronson, Roderick -- Liao, Ronglih -- Mulligan, Richard -- Shirihai, Orian S -- Chin, Lynda -- DePinho, Ronald A -- P30 DK046200/DK/NIDDK NIH HHS/ -- P30DK079638/DK/NIDDK NIH HHS/ -- R01 CA084628/CA/NCI NIH HHS/ -- R01 DK035914/DK/NIDDK NIH HHS/ -- R01 DK056690/DK/NIDDK NIH HHS/ -- R01 DK063356/DK/NIDDK NIH HHS/ -- R01 DK089185/DK/NIDDK NIH HHS/ -- U24 DK-59635/DK/NIDDK NIH HHS/ -- England -- Nature. 2011 Feb 17;470(7334):359-65. doi: 10.1038/nature09787. Epub 2011 Feb 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21307849" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/biosynthesis ; Aging/metabolism/pathology ; Animals ; Cardiomyopathies/chemically induced/metabolism/pathology/physiopathology ; Cell Proliferation ; DNA, Mitochondrial/analysis ; Doxorubicin/toxicity ; Gluconeogenesis ; Hematopoietic Stem Cells/metabolism/pathology ; Liver/cytology/metabolism ; Mice ; Mitochondria/*metabolism/*pathology ; Myocardium/cytology/metabolism ; RNA/genetics ; Reactive Oxygen Species/metabolism ; Telomerase/deficiency/genetics ; Telomere/enzymology/genetics/*metabolism/*pathology ; Transcription Factors/antagonists & inhibitors/metabolism ; Tumor Suppressor Protein p53/deficiency/genetics/metabolism
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  • 4
    Publication Date: 2011-04-02
    Description: Cpdm (chronic proliferative dermatitis) mice develop chronic dermatitis and an immunodeficiency with increased serum IgM, symptoms that resemble those of patients with X-linked hyper-IgM syndrome and hypohydrotic ectodermal dysplasia (XHM-ED), which is caused by mutations in NEMO (NF-kappaB essential modulator; also known as IKBKG). Spontaneous null mutations in the Sharpin (SHANK-associated RH domain interacting protein in postsynaptic density) gene are responsible for the cpdm phenotype in mice. SHARPIN shows significant similarity to HOIL-1L (also known as RBCK1), a component of linear ubiquitin chain assembly complex (LUBAC), which induces NF-kappaB activation through conjugation of linear polyubiquitin chains to NEMO. Here, we identify SHARPIN as an additional component of LUBAC. SHARPIN-containing complexes can linearly ubiquitinate NEMO and activated NF-kappaB. Thus, we re-define LUBAC as a complex containing SHARPIN, HOIL-1L, and HOIP (also known as RNF31). Deletion of SHARPIN drastically reduced the amount of LUBAC, which resulted in attenuated TNF-alpha- and CD40-mediated activation of NF-kappaB in mouse embryonic fibroblasts (MEFs) or B cells from cpdm mice. Considering the pleomorphic phenotype of cpdm mice, these results confirm the predicted role of LUBAC-mediated linear polyubiquitination in NF-kappaB activation induced by various stimuli, and strongly suggest the involvement of LUBAC-induced NF-kappaB activation in various disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tokunaga, Fuminori -- Nakagawa, Tomoko -- Nakahara, Masaki -- Saeki, Yasushi -- Taniguchi, Masami -- Sakata, Shin-ichi -- Tanaka, Keiji -- Nakano, Hiroyasu -- Iwai, Kazuhiro -- England -- Nature. 2011 Mar 31;471(7340):633-6. doi: 10.1038/nature09815.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biophysics and Biochemistry, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21455180" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD40 Ligand/metabolism ; Carrier Proteins/metabolism ; Cells, Cultured ; HEK293 Cells ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Mice ; Multiprotein Complexes/*chemistry/*metabolism ; NF-kappa B/*metabolism ; Nerve Tissue Proteins/deficiency/genetics/*metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Ubiquitin/*metabolism ; Ubiquitin-Protein Ligase Complexes/chemistry/metabolism ; Ubiquitin-Protein Ligases/metabolism
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  • 5
    Publication Date: 2011-08-05
    Description: The role of African savannahs in the evolution of early hominins has been debated for nearly a century. Resolution of this issue has been hindered by difficulty in quantifying the fraction of woody cover in the fossil record. Here we show that the fraction of woody cover in tropical ecosystems can be quantified using stable carbon isotopes in soils. Furthermore, we use fossil soils from hominin sites in the Awash and Omo-Turkana basins in eastern Africa to reconstruct the fraction of woody cover since the Late Miocene epoch (about 7 million years ago). (13)C/(12)C ratio data from 1,300 palaeosols at or adjacent to hominin sites dating to at least 6 million years ago show that woody cover was predominantly less than approximately 40% at most sites. These data point to the prevalence of open environments at the majority of hominin fossil sites in eastern Africa over the past 6 million years.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cerling, Thure E -- Wynn, Jonathan G -- Andanje, Samuel A -- Bird, Michael I -- Korir, David Kimutai -- Levin, Naomi E -- Mace, William -- Macharia, Anthony N -- Quade, Jay -- Remien, Christopher H -- England -- Nature. 2011 Aug 3;476(7358):51-6. doi: 10.1038/nature10306.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Utah, Salt Lake City, Utah 84112, USA. thure.cerling@utah.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21814275" target="_blank"〉PubMed〈/a〉
    Keywords: Africa, Eastern ; Animals ; *Biological Evolution ; Calibration ; Carbon Isotopes/analysis ; *Ecosystem ; Fossils ; Gait/physiology ; Hominidae/anatomy & histology/*physiology ; Paleontology ; Plant Leaves/growth & development ; Poaceae/growth & development ; Population Dynamics ; Soil/chemistry ; *Trees/growth & development ; Tropical Climate ; Wilderness ; Wood
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  • 6
    Publication Date: 2011-05-13
    Description: The generation of functional hepatocytes independent of donor liver organs is of great therapeutic interest with regard to regenerative medicine and possible cures for liver disease. Induced hepatic differentiation has been achieved previously using embryonic stem cells or induced pluripotent stem cells. Particularly, hepatocytes generated from a patient's own induced pluripotent stem cells could theoretically avoid immunological rejection. However, the induction of hepatocytes from induced pluripotent stem cells is a complicated process that would probably be replaced with the arrival of improved technology. Overexpression of lineage-specific transcription factors directly converts terminally differentiated cells into some other lineages, including neurons, cardiomyocytes and blood progenitors; however, it remains unclear whether these lineage-converted cells could repair damaged tissues in vivo. Here we demonstrate the direct induction of functional hepatocyte-like (iHep) cells from mouse tail-tip fibroblasts by transduction of Gata4, Hnf1alpha and Foxa3, and inactivation of p19(Arf). iHep cells show typical epithelial morphology, express hepatic genes and acquire hepatocyte functions. Notably, transplanted iHep cells repopulate the livers of fumarylacetoacetate-hydrolase-deficient (Fah(-/-)) mice and rescue almost half of recipients from death by restoring liver functions. Our study provides a novel strategy to generate functional hepatocyte-like cells for the purpose of liver engineering and regenerative medicine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Pengyu -- He, Zhiying -- Ji, Shuyi -- Sun, Huawang -- Xiang, Dao -- Liu, Changcheng -- Hu, Yiping -- Wang, Xin -- Hui, Lijian -- England -- Nature. 2011 May 11;475(7356):386-9. doi: 10.1038/nature10116.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy for Sciences, Yueyang Road 320, 200031 Shanghai, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21562492" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation/genetics ; Cell Lineage ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p16/deficiency/genetics ; DNA-Binding Proteins/deficiency ; Fibroblasts/*cytology/*metabolism ; GATA4 Transcription Factor/genetics/metabolism ; Gene Expression Profiling ; Hepatocyte Nuclear Factor 1-alpha/genetics/metabolism ; Hepatocyte Nuclear Factor 3-gamma/genetics/metabolism ; Hepatocytes/*cytology/*metabolism/physiology/transplantation ; Hydrolases/deficiency/genetics ; Liver/cytology/enzymology/physiology/physiopathology ; Liver Diseases/enzymology/pathology/physiopathology/therapy ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Regenerative Medicine/methods ; Survival Rate ; Tail/cytology ; Tissue Engineering/methods ; Transduction, Genetic
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  • 7
    Publication Date: 2011-02-26
    Description: Mammalian prions cause fatal neurodegenerative conditions including Creutzfeldt-Jakob disease in humans and scrapie and bovine spongiform encephalopathy in animals. Prion infections are typically associated with remarkably prolonged but highly consistent incubation periods followed by a rapid clinical phase. The relationship between prion propagation, generation of neurotoxic species and clinical onset has remained obscure. Prion incubation periods in experimental animals are known to vary inversely with expression level of cellular prion protein. Here we demonstrate that prion propagation in brain proceeds via two distinct phases: a clinically silent exponential phase not rate-limited by prion protein concentration which rapidly reaches a maximal prion titre, followed by a distinct switch to a plateau phase. The latter determines time to clinical onset in a manner inversely proportional to prion protein concentration. These findings demonstrate an uncoupling of infectivity and toxicity. We suggest that prions themselves are not neurotoxic but catalyse the formation of such species from PrP(C). Production of neurotoxic species is triggered when prion propagation saturates, leading to a switch from autocatalytic production of infectivity (phase 1) to a toxic (phase 2) pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sandberg, Malin K -- Al-Doujaily, Huda -- Sharps, Bernadette -- Clarke, Anthony R -- Collinge, John -- MC_U123160656/Medical Research Council/United Kingdom -- MC_U123192748/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- England -- Nature. 2011 Feb 24;470(7335):540-2. doi: 10.1038/nature09768.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Prion Unit and Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21350487" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biocatalysis ; Biological Assay ; Disease Models, Animal ; Gene Expression ; Kinetics ; Mice ; Mice, Transgenic ; Models, Biological ; PrPC Proteins/analysis/biosynthesis/genetics/metabolism ; PrPSc Proteins/biosynthesis/*metabolism/*pathogenicity/toxicity ; Prion Diseases/*metabolism/*pathology/physiopathology/transmission ; Survival Rate ; Time Factors ; Toxicity Tests
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  • 8
    Publication Date: 2011-10-28
    Description: Sauropod dinosaurs were the largest vertebrates ever to walk the Earth, and as mega-herbivores they were important parts of terrestrial ecosystems. In the Late Jurassic-aged Morrison depositional basin of western North America, these animals occupied lowland river-floodplain settings characterized by a seasonally dry climate. Massive herbivores with high nutritional and water needs could periodically experience nutritional and water stress under these conditions, and thus the common occurrence of sauropods in this basin has remained a paradox. Energetic arguments and mammalian analogues have been used to suggest that migration allowed sauropods access to food and water resources over a wide region or during times of drought or both, but there has been no direct support for these hypotheses. Here we compare oxygen isotope ratios (delta(18)O) of tooth-enamel carbonate from the sauropod Camarasaurus with those of ancient soil, lake and wetland (that is, 'authigenic') carbonates that formed in lowland settings. We demonstrate that certain populations of these animals did in fact undertake seasonal migrations of several hundred kilometres from lowland to upland environments. This ability to describe patterns of sauropod movement will help to elucidate the role that migration played in the ecology and evolution of gigantism of these and associated dinosaurs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fricke, Henry C -- Hencecroth, Justin -- Hoerner, Marie E -- England -- Nature. 2011 Oct 26;480(7378):513-5. doi: 10.1038/nature10570.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Geology, Colorado College, Colorado Springs, Colorado 80903, USA. hfricke@coloradocollege.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22031326" target="_blank"〉PubMed〈/a〉
    Keywords: *Animal Migration ; Animals ; Dental Enamel/chemistry ; Dinosaurs/*physiology ; Oxygen Isotopes/analysis ; Seasons ; Soil/analysis
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  • 9
    Publication Date: 2011-06-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Apostolou, Effie -- Hochedlinger, Konrad -- England -- Nature. 2011 Jun 8;474(7350):165-6. doi: 10.1038/474165a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21654792" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cellular Reprogramming/genetics/immunology ; Graft Rejection/*genetics/*immunology ; Induced Pluripotent Stem Cells/cytology/*immunology/metabolism/*transplantation ; Mice ; Teratoma/genetics/immunology ; Transplantation, Homologous/immunology ; Transplantation, Isogeneic/immunology ; Up-Regulation/genetics/immunology
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  • 10
    Publication Date: 2011-02-19
    Description: Toll-like receptors (TLRs) function as initiators of inflammation through their ability to sense pathogen-associated molecular patterns and products of tissue damage. Transcriptional activation of many TLR-responsive genes requires an initial de-repression step in which nuclear receptor co-repressor (NCoR) complexes are actively removed from the promoters of target genes to relieve basal repression. Ligand-dependent SUMOylation of liver X receptors (LXRs) has been found to suppress TLR4-induced transcription potently by preventing the NCoR clearance step, but the underlying mechanisms remain enigmatic. Here we provide evidence that coronin 2A (CORO2A), a component of the NCoR complex of previously unknown function, mediates TLR-induced NCoR turnover by a mechanism involving interaction with oligomeric nuclear actin. SUMOylated LXRs block NCoR turnover by binding to a conserved SUMO2/SUMO3-interaction motif in CORO2A and preventing actin recruitment. Intriguingly, the LXR transrepression pathway can itself be inactivated by inflammatory signals that induce calcium/calmodulin-dependent protein kinase IIgamma (CaMKIIgamma)-dependent phosphorylation of LXRs, leading to their deSUMOylation by the SUMO protease SENP3 and release from CORO2A. These findings uncover a CORO2A-actin-dependent mechanism for the de-repression of inflammatory response genes that can be differentially regulated by phosphorylation and by nuclear receptor signalling pathways that control immunity and homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3464905/" 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/PMC3464905/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Wendy -- Ghisletti, Serena -- Saijo, Kaoru -- Gandhi, Meghal -- Aouadi, Myriam -- Tesz, Greg J -- Zhang, Dawn X -- Yao, Joyee -- Czech, Michael P -- Goode, Bruce L -- Rosenfeld, Michael G -- Glass, Christopher K -- 1F31DK083913/DK/NIDDK NIH HHS/ -- CA52599/CA/NCI NIH HHS/ -- DK074868/DK/NIDDK NIH HHS/ -- DK085853/DK/NIDDK NIH HHS/ -- HC088093/HC/NHLBI NIH HHS/ -- P01 DK074868/DK/NIDDK NIH HHS/ -- P50 HL056989/HL/NHLBI NIH HHS/ -- R01 CA052599/CA/NCI NIH HHS/ -- R01 CA097134/CA/NCI NIH HHS/ -- R01 DK091183/DK/NIDDK NIH HHS/ -- R01 HL065445/HL/NHLBI NIH HHS/ -- R01 NS034934/NS/NINDS NIH HHS/ -- R37 DK039949/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Feb 17;470(7334):414-8. doi: 10.1038/nature09703.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0651, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21331046" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/chemistry/*metabolism ; Animals ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism ; Cell Line ; *Gene Expression Regulation/drug effects ; Gene Knockdown Techniques ; HeLa Cells ; Homeostasis/genetics ; Humans ; Inflammation/*genetics ; Lipopolysaccharides/pharmacology ; Mice ; Microfilament Proteins/chemistry/deficiency/genetics/*metabolism ; Orphan Nuclear Receptors/metabolism ; Peptide Hydrolases/metabolism ; Peritonitis/chemically induced/metabolism ; Phosphorylation ; Promoter Regions, Genetic/genetics ; Protein Structure, Tertiary ; Signal Transduction ; Sumoylation ; Thioglycolates/pharmacology ; Toll-Like Receptors/metabolism
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