What's new for 'JKB_daily1' in PubMed

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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Saturday, 2012 January 28
Search: (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))

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PubMed Results

Items 1 - 4 of 4

1.	Science. 2011 Dec 16;334(6062):1518-24. Detecting novel associations in large data sets. Reshef DN, Reshef YA, Finucane HK, Grossman SR, McVean G, Turnbaugh PJ, Lander ES, Mitzenmacher M, Sabeti PC. Source Department of Computer Science, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. dnreshef@mit.edu Comment in Science. 2011 Dec 16;334(6062):1502-3. Abstract Identifying interesting relationships between pairs of variables in large data sets is increasingly important. Here, we present a measure of dependence for two-variable relationships: the maximal information coefficient (MIC). MIC captures a wide range of associations both functional and not, and for functional relationships provides a score that roughly equals the coefficient of determination (R(2)) of the data relative to the regression function. MIC belongs to a larger class of maximal information-based nonparametric exploration (MINE) statistics for identifying and classifying relationships. We apply MIC and MINE to data sets in global health, gene expression, major-league baseball, and the human gut microbiota and identify known and novel relationships.
	PMID: 22174245 [PubMed - indexed for MEDLINE]
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2.	Science. 2011 Dec 16;334(6062):1487. Genetics. China bets on the variome to uncover hereditary diseases. Hvistendahl M.
	PMID: 22174225 [PubMed - indexed for MEDLINE]
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3.	Lancet. 2011 Nov 26;378(9806):1838. Genomic future beckons for cancer management. Qadir Z.
	PMID: 22125803 [PubMed - indexed for MEDLINE]
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4.	Science. 2011 Dec 16;334(6062):1553-7. Epub 2011 Nov 17. Host proteasomal degradation generates amino acids essential for intracellular bacterial growth. Price CT, Al-Quadan T, Santic M, Rosenshine I, Abu Kwaik Y. Source Department of Microbiology and Immunology, College of Medicine, University of Louisville, KY 40202, USA. Abstract Legionella pneumophila proliferates in environmental amoeba and human cells within the Legionella-containing vacuole (LCV). The exported AnkB F-box effector of L. pneumophila is anchored into the LCV membrane by host-mediated farnesylation. Here, we report that host proteasomal degradation of Lys(48)-linked polyubiquitinated proteins, assembled on the LCV by AnkB, generates amino acids required for intracellular bacterial proliferation. The severe defect of the ankB null mutant in proliferation within amoeba and human cells is rescued by supplementation of a mixture of amino acids or cysteine, serine, pyruvate, or citrate, similar to rescue by genetic complementation. Defect of the ankB mutant in intrapulmonary proliferation in mice is rescued upon injection of a mixture of amino acids or cysteine. Therefore, Legionella promotes eukaryotic proteasomal degradation to generate amino acids needed as carbon and energy sources for bacterial proliferation within evolutionarily distant hosts.
	PMID: 22096100 [PubMed - indexed for MEDLINE]
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What's new for 'JKB_daily1' in PubMed

This message contains My NCBI what's new results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).
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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Friday, 2012 January 27
Search: (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))

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PubMed Results

Items 1 - 12 of 12

1.	Science. 2012 Jan 13;335(6065):229-32. iRhom2 regulation of TACE controls TNF-mediated protection against Listeria and responses to LPS. McIlwain DR, Lang PA, Maretzky T, Hamada K, Ohishi K, Maney SK, Berger T, Murthy A, Duncan G, Xu HC, Lang KS, Häussinger D, Wakeham A, Itie-Youten A, Khokha R, Ohashi PS, Blobel CP, Mak TW. Source Campell Family Institute for Breast Cancer Research, Ontario Cancer Institute, University Health Network (UHN), 620 University Avenue, Toronto, Ontario M5G 2C1, Canada. Comment in Science. 2012 Jan 13;335(6065):179-80. Abstract Innate immune responses are vital for pathogen defense but can result in septic shock when excessive. A key mediator of septic shock is tumor necrosis factor-α (TNFα), which is shed from the plasma membrane after cleavage by the TNFα convertase (TACE). We report that the rhomboid family member iRhom2 interacted with TACE and regulated TNFα shedding. iRhom2 was critical for TACE maturation and trafficking to the cell surface in hematopoietic cells. Gene-targeted iRhom2-deficient mice showed reduced serum TNFα in response to lipopolysaccharide (LPS) and could survive a lethal LPS dose. Furthermore, iRhom2-deficient mice failed to control the replication of Listeria monocytogenes. Our study has identified iRhom2 as a regulator of innate immunity that may be an important target for modulating sepsis and pathogen defense.
	PMID: 22246778 [PubMed - indexed for MEDLINE]
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2.	Science. 2012 Jan 13;335(6065):225-8. Tumor necrosis factor signaling requires iRhom2 to promote trafficking and activat ion of TACE. Adrain C, Zettl M, Christova Y, Taylor N, Freeman M. Source Medical Research Council Laboratory of Molecular Biology, Hills Road, Cambridge CB2 0QH, UK. Comment in Science. 2012 Jan 13;335(6065):179-80. Abstract The cytokine tumor necrosis factor (TNF) is the primary trigger of inflammation. Like many extracellular signaling proteins, TNF is synthesized as a transmembrane protein; the active signal is its ectodomain, which is shed from cells after cleavage by an ADAM family metalloprotease, ADAM17 (TNFα-converting enzyme, TACE). We report that iRhom2 (RHBDF2), a proteolytically inactive member of the rhomboid family, is required for TNF release in mice. iRhom2 binds TACE and promotes its exit from the endoplasmic reticulum. The failure of TACE to exit the endoplasmic reticulum in the absence of iRhom2 prevents the furin-mediated maturation and trafficking of TACE to the cell surface, the site of TNF cleavage. Given the role of TNF in autoimmune and inflammatory diseases, iRhom2 may represent an attractive therapeutic target.
	PMID: 22246777 [PubMed - indexed for MEDLINE]
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3.	Science. 2012 Jan 13;335(6065):181. Retrospective. Paul Mead Doty (1920-2011). Meselson M. Source Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA. msm@wjh.harvard.edu
	PMID: 22246766 [PubMed - indexed for MEDLINE]
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4.	Science. 2012 Jan 13;335(6065):179-80. Cell biology. Sheddase gets guidance. Lichtenthaler SF. Source DZNE-German Center for Neurodegenerative Diseases Munich, 80336 Munich, Germany. stefan.lichtenthaler@dzne.lmu.de Comment on Science. 2012 Jan 13;335(6065):229-32. Science. 2012 Jan 13;335(6065):225-8.
	PMID: 22246765 [PubMed - indexed for MEDLINE]
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5.	Nature. 2011 Nov 23;479(7374):487-92. doi: 10.1038/nature10640. The genome of Tetranychus urticae reveals herbivorous pe st adaptations. Grbić M, Van Leeuwen T, Clark RM, Rombauts S, Rouzé P, Grbić V, Osborne EJ, Dermauw W, Ngoc PC, Ortego F, Hernández-Crespo P, Diaz I, Martinez M, Navajas M, Sucena É, Magalhães S, Nagy L, Pace RM, Djuranović S, Smagghe G, Iga M, Christiaens O, Veenstra JA, Ewer J, Villalobos RM, Hutter JL, Hudson SD, Velez M, Yi SV, Zeng J, Pires-daSilva A, Roch F, Cazaux M, Navarro M, Zhurov V, Acevedo G, Bjelica A, Fawcett JA, Bonnet E, Martens C, Baele G, Wissler L, Sanchez-Rodriguez A, Tirry L, Blais C, Demeestere K, Henz SR, Gregory TR, Mathieu J, Verdon L, Farinelli L, Schmutz J, Lindquist E, Feyereisen R, Van de Peer Y. Source Department of Biology, The University of Western Ontario, London N6A 5B7, Canada. mgrbic@uwo.ca Abstract The spider mite Tetranychus urticae is a cosmopolitan agricultural pest with an extensive host plant range and an extreme record of pesticide resistance. Here we present the completely sequenced and annotated spider mite genome, representing the first complete chelicerate genome. At 90 megabases T. urticae has the smallest sequenced arthropod genome. Compared with other arthropods, the spider mite genome shows unique changes in the hormonal environment and organization of the Hox complex, and also reveals evolutionary innovation of silk production. We find strong signatures of polyphagy and detoxification in gene families associated with feeding on different hosts and in new gene families acquired by lateral gene transfer. Deep transcriptome analysis of mites feeding on different plants shows how this pest responds to a changing host environment. The T. urticae genome thus offers new insights into arthropod evolution and plant-herbivore interactions, and provides unique opportunities for developing novel plant protection strategies. ©2011 Macmillan Publishers Limited. All rights reserved
	PMID: 22113690 [PubMed - indexed for MEDLINE]
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6.	Nature. 2011 Oct 30;479(7374):534-7. doi: 10.1038/nature10531. Somatic retrotransposition alters the genetic landscape of the human brain. Baillie JK, Barnett MW, Upton KR, Gerhardt DJ, Richmond TA, De Sapio F, Brennan PM, Rizzu P, Smith S, Fell M, Talbot RT, Gustincich S, Freeman TC, Mattick JS, Hume DA, Heutink P, Carninci P, Jeddeloh JA, Faulkner GJ. Source Division of Genetics and Genomics, The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Edinburgh EH25 9RG, UK. Abstract Retrotransposons are mobile genetic elements that use a germline 'copy-and-paste' mechanism to spread throughout metazoan genomes. At least 50 per cent of the human genome is derived from retrotransposons, with three active families (L1, Alu and SVA) associated with insertional mutagenesis and disease. Epigenetic and post-transcriptional suppression block retrotransposition in somatic cells, excluding early embryo development and some malignancies. Recent reports of L1 expression and copy number variation in the human brain suggest that L1 mobilization may also occur during later development. However, the corresponding integration sites have not been mapped. Here we apply a high-throughput method to identify numerous L1, Alu and SVA germline mutations, as well as 7,743 putative somatic L1 insertions, in the hippocampus and caudate nucleus of three individuals. Surprisingly, we also found 13,692 somatic Alu insertions and 1,350 SVA insertions. Our results demonstrate that retrotransposons mobilize to protein-coding genes differentially expressed and active in the brain. Thus, somatic genome mosaicism driven by retrotransposition may reshape the genetic circuitry that underpins normal and abnormal neurobiological processes. ©2011 Macmillan Publishers Limited. All rights reserved PMCID: PMC3224101 [Available on 2012/4/30]
	PMID: 22037309 [PubMed - indexed for MEDLINE]
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7.	Nature. 2011 Oct 26;478(7370):458-9. doi: 10.1038/478458d. Genome sequencing: Aboriginal people agreed to DNA study. Muller C. Comment on Nature. 2011 Sep 29;477(7366):522-3.
	PMID: 22031428 [PubMed - indexed for MEDLINE]
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8.	Nature. 2011 Oct 26;479(7374):529-33. doi: 10.1038/nature10553. Ascaris suum draft genome. Jex AR, Liu S, Li B, Young ND, Hall RS, Li Y, Yang L, Zeng N, Xu X, Xiong Z, Chen F, Wu X, Zhang G, Fang X, Kang Y, Anderson GA, Harris TW, Campbell BE, Vlaminck J, Wang T, Cantacessi C, Schwarz EM, Ranganathan S, Geldhof P, Nejsum P, Sternberg PW, Yang H, Wang J, Wang J, Gasser RB. Source Faculty of Veterinary Science, The University of Melbourne, Parkville, Victoria 3010, Australia. ajex@unimelb.edu.au Abstract Parasitic diseases have a devastating, long-term impact on human health, welfare and food production worldwide. More than two billion people are infected with geohelminths, including the roundworms Ascaris (common roundworm), Necator and Ancylostoma (hookworms), and Trichuris (whipworm), mainly in developing or impoverished nations of Asia, Africa and Latin America. In humans, the diseases caused by these parasites result in about 135,000 deaths annually, with a global burden comparable with that of malaria or tuberculosis in disability-adjusted life years. Ascaris alone infects around 1.2 billion people and, in children, causes nutritional deficiency, impaired physical and cognitive development and, in severe cases, death. Ascaris also causes major production losses in pigs owing to reduced growth, failure to thrive and mortality. The Ascaris-swine model makes it possible to study the parasite, its relationship with the host, and ascariasis at the molecular level. To enable such molecular studies, we report the 273 megabase draft genome of Ascaris suum and compare it with other nematode genomes. This genome has low repeat content (4.4%) and encodes about 18,500 protein-coding genes. Notably, the A. suum secretome (about 750 molecules) is rich in peptidases linked to the penetration and degradation of host tissues, and an assemblage of molecules likely to modulate or evade host immune responses. This genome provides a comprehensive resource to the scientific community and underpins the development of new and urgently needed interventions (drugs, vaccines and diagnostic tests) against ascariasis and other nematodiases. ©2011 Macmillan Publishers Limited. All rights reserved
	PMID: 22031327 [PubMed - indexed for MEDLINE]
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9.	Nature. 2011 Oct 19;479(7374):517-20. doi: 10.1038/nature10548. Changes in plant community composition lag behind climate warming in lowland forests. Bertrand R, Lenoir J, Piedallu C, Riofrío-Dillon G, de Ruffray P, Vidal C, Pierrat JC, Gégout JC. Source AgroParisTech, ENGREF, UMR1092 Laboratoire d'Étude des Ressources Forêt-Bois (LERFoB), 14 rue Girardet, F-54000 Nancy, France. romain.bertrand@engref.agroparistech.fr Abstract Climate change is driving latitudinal and altitudinal shifts in species distribution worldwide, leading to novel species assemblages. Lags between these biotic responses and contemporary climate changes have been reported for plants and animals. Theoretically, the magnitude of these lags should be greatest in lowland areas, where the velocity of climate change is expected to be much greater than that in highland areas. We compared temperature trends to temperatures reconstructed from plant assemblages (observed in 76,634 surveys) over a 44-year period in France (1965-2008). Here we report that forest plant communities had responded to 0.54 °C of the effective increase of 1.07 °C in highland areas (500-2,600 m above sea level), while they had responded to only 0.02 °C of the 1.11 °C warming trend in lowland areas. There was a larger temperature lag (by 3.1 times) between the climate and plant community composition in lowland forests than in highland forests. The explanation of such disparity lies in the following properties of lowland, as compared to highland, forests: the higher proportion of species with greater ability for local persistence as the climate warms, the reduced opportunity for short-distance escapes, and the greater habitat fragmentation. Although mountains are currently considered to be among the ecosystems most threatened by climate change (owing to mountaintop extinction), the current inertia of plant communities in lowland forests should also be noted, as it could lead to lowland biotic attrition. ©2011 Macmillan Publishers Limited. All rights reserved
	PMID: 22012261 [PubMed - indexed for MEDLINE]
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10.	Nature. 2011 Oct 12;478(7370):476-82. doi: 10.1038/nature10530. A high-resolution map of human evolutionary constraint using 29 mammals. Lindblad-Toh K, Garber M, Zuk O, Lin MF, Parker BJ, Washietl S, Kheradpour P, Ernst J, Jordan G, Mauceli E, Ward LD, Lowe CB, Holloway AK, Clamp M, Gnerre S, Alföldi J, Beal K, Chang J, Clawson H, Cuff J, Di Palma F, Fitzgerald S, Flicek P, Guttman M, Hubisz MJ, Jaffe DB, Jungreis I, Kent WJ, Kostka D, Lara M, Martins AL, Massingham T, Moltke I, Raney BJ, Rasmussen MD, Robinson J, Stark A, Vilella AJ, Wen J, Xie X, Zody MC; Broad Institute Sequencing Platform and Whole Genome Assembly Team, Baldwin J, Bloom T, Chin CW, Heiman D, Nicol R, Nusbaum C, Young S, Wilkinson J, Worley KC, Kovar CL, Muzny DM, Gibbs RA; Baylor College of Medicine Human Genome Sequencing Center Sequencing Team, Cree A, Dihn HH, Fowler G, Jhangiani S, Joshi V, Lee S, Lewis LR, Nazareth LV, Okwuonu G, Santibanez J, Warren WC, Mardis ER, Weinstock GM, Wilson RK; Genome Institute at Washington University, Delehaunty K, Dooling D, Fronik C, Fulton L, Fulton B, Graves T, Minx P, Sodergren E, Birney E, Margulies EH, Herrero J, Green ED, Haussler D, Siepel A, Goldman N, Pollard KS, Pedersen JS, Lander ES, Kellis M. Source Broad Institute of Harvard and Massachusetts Institute of Technology, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA. kersli@broadinstitute.org Comment in Nat Rev Genet. 2011 Dec;12(12):806-7. Abstract The comparison of related genomes has emerged as a powerful lens for genome interpretation. Here we report the sequencing and comparative analysis of 29 eutherian genomes. We confirm that at least 5.5% of the human genome has undergone purifying selection, and locate constrained elements covering ∼4.2% of the genome. We use evolutionary signatures and comparisons with experimental data sets to suggest candidate functions for ∼60% of constrained bases. These elements reveal a small number of new coding exons, candidate stop codon readthrough events and over 10,000 regions of overlapping synonymous constraint within protein-coding exons. We find 220 candidate RNA structural families, and nearly a million elements overlapping potential promoter, enhancer and insulator regions. We report specific amino acid residues that have undergone positive selection, 280,000 non-coding elements exapted from mobile elements and more than 1,000 primate- and human-accelerated elements. Overlap with disease-associated variants indicates that our findings will be relevant for studies of human biology, health and disease. PMCID: PMC3207357 [Available on 2012/4/27]
	PMID: 21993624 [PubMed - indexed for MEDLINE]
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11.	Nature. 2011 Oct 2;478(7370):529-33. doi: 10.1038/nature10509. Inhibition of BET recruitment to chromatin as an effective treatment for MLL-fusion leukaemia. Dawson MA, Prinjha RK, Dittmann A, Giotopoulos G, Bantscheff M, Chan WI, Robson SC, Chung CW, Hopf C, Savitski MM, Huthmacher C, Gudgin E, Lugo D, Beinke S, Chapman TD, Roberts EJ, Soden PE, Auger KR, Mirguet O, Doehner K, Delwel R, Burnett AK, Jeffrey P, Drewes G, Lee K, Huntly BJ, Kouzarides T. Source Department of Haematology, Cambridge Institute for Medical Research and Addenbrookes Hospital, University of Cambridge, Cambridge CB2 0XY, UK. Abstract Recurrent chromosomal translocations involving the mixed lineage leukaemia (MLL) gene initiate aggressive forms of leukaemia, which are often refractory to conventional therapies. Many MLL-fusion partners are members of the super elongation complex (SEC), a critical regulator of transcriptional elongation, suggesting that aberrant control of this process has an important role in leukaemia induction. Here we use a global proteomic strategy to demonstrate that MLL fusions, as part of SEC and the polymerase-associated factor complex (PAFc), are associated with the BET family of acetyl-lysine recognizing, chromatin 'adaptor' proteins. These data provided the basis for therapeutic intervention in MLL-fusion leukaemia, via the displacement of the BET family of proteins from chromatin. We show that a novel small molecule inhibitor of the BET family, GSK1210151A (I-BET151), has profound efficacy against human and murine MLL-fusion leukaemic cell lines, through the induction of early cell cycle arrest and apoptosis. I-BET151 treatment in two human leukaemia cell lines with different MLL fusions alters the expression of a common set of genes whose function may account for these phenotypic changes. The mode of action of I-BET151 is, at least in part, due to the inhibition of transcription at key genes (BCL2, C-MYC and CDK6) through the displacement of BRD3/4, PAFc and SEC components from chromatin. In vivo studies indicate that I-BET151 has significant therapeutic value, providing survival benefit in two distinct mouse models of murine MLL-AF9 and human MLL-AF4 leukaemia. Finally, the efficacy of I-BET151 against human leukaemia stem cells is demonstrated, providing further evidence of its potent therapeutic potential. These findings establish the displacement of BET proteins from chromatin as a promising epigenetic therapy for these aggressive leukaemias.
	PMID: 21964340 [PubMed - indexed for MEDLINE]
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12.	Nature. 2011 Sep 25;478(7370):515-8. doi: 10.1038/nature10429. STING is a direct innate immune sensor of cyclic di-GMP. Burdette DL, Monroe KM, Sotelo-Troha K, Iwig JS, Eckert B, Hyodo M, Hayakawa Y, Vance RE. Source Department of Molecular & Cell Biology, University of California, Berkeley, California 94720, USA. Abstract The innate immune system detects infection by using germline-encoded receptors that are specific for conserved microbial molecules. The recognition of microbial ligands leads to the production of cytokines, such as type I interferons (IFNs), that are essential for successful pathogen elimination. Cytosolic detection of pathogen-derived DNA is one major mechanism of inducing IFN production, and this process requires signalling through TANK binding kinase 1 (TBK1) and its downstream transcription factor, IFN-regulatory factor 3 (IRF3). In addition, a transmembrane protein called STING (stimulator of IFN genes; also known as MITA, ERIS, MPYS and TMEM173) functions as an essential signalling adaptor, linking the cytosolic detection of DNA to the TBK1-IRF3 signalling axis. Recently, unique nucleic acids called cyclic dinucleotides, which function as conserved signalling molecules in bacteria, have also been shown to induce a STING-dependent type I IFN response. However, a mammalian sensor of cyclic dinucleotides has not been identified. Here we report evidence that STING itself is an innate immune sensor of cyclic dinucleotides. We demonstrate that STING binds directly to radiolabelled cyclic diguanylate monophosphate (c-di-GMP), and we show that unlabelled cyclic dinucleotides, but not other nucleotides or nucleic acids, compete with c-di-GMP for binding to STING. Furthermore, we identify mutations in STING that selectively affect the response to cyclic dinucleotides without affecting the response to DNA. Thus, STING seems to function as a direct sensor of cyclic dinucleotides, in addition to its established role as a signalling adaptor in the IFN response to cytosolic DNA. Cyclic dinucleotides have shown promise as novel vaccine adjuvants and immunotherapeutics, and our results provide insight into the mechanism by which cyclic dinucleotides are sensed by the innate immune system. PMCID: PMC3203314 [Available on 2012/4/27]
	PMID: 21947006 [PubMed - indexed for MEDLINE]
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What's new for 'JKB_daily1' in PubMed

This message contains My NCBI what's new results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).
Do not reply directly to this message.

Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Thursday, 2012 January 26
Search: (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))

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PubMed Results

Items 1 - 17 of 17

1.	Science. 2011 Dec 23;334(6063):1657-8. Essays on science and society. Lessons from a science education portal. Micklos D, Lauter S, Nisselle A. Source DNA Learning Center, Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA. micklos@cshi.edu
	PMID: 22194567 [PubMed - indexed for MEDLINE]
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2.	Science. 2011 Dec 23;334(6063):1630-1. Breakthrough of the year. Areas to watch. [No authors listed]
	PMID: 22194549 [PubMed - indexed for MEDLINE]
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3.	Science. 2011 Dec 23;334(6063):1614. HIV/AIDS research. Tissue says blood is misleading, confusing HIV cure efforts. Cohen J.
	PMID: 22194536 [PubMed - indexed for MEDLINE]
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4.	Science. 2012 Jan 6;335(6064):89-92. Epub 2011 Dec 15. Equilibrative nucleoside transporter 3 deficiency perturbs lysos ome function and macrophage homeostasis. Hsu CL, Lin W, Seshasayee D, Chen YH, Ding X, Lin Z, Suto E, Huang Z, Lee WP, Park H, Xu M, Sun M, Rangell L, Lutman JL, Ulufatu S, Stefanich E, Chalouni C, Sagolla M, Diehl L, Fielder P, Dean B, Balazs M, Martin F. Source Immunology, Genentech Inc., 1 DNA Way, South San Francisco, CA 94080, USA. Abstract Lysosomal storage diseases (LSDs) are a group of heterogeneous disorders caused by defects in lysosomal enzymes or transporters, resulting in accumulation of undegraded macromolecules or metabolites. Macrophage numbers are expanded in several LSDs, leading to histiocytosis of unknown pathophysiology. Here, we found that mice lacking the equilibrative nucleoside transporter 3 (ENT3) developed a spontaneous and progressive macrophage-dominated histiocytosis. In the absence of ENT3, defective apoptotic cell clearance led to lysosomal nucleoside buildup, elevated intralysosomal pH, and altered macrophage function. The macrophage accumulation was partly due to increased macrophage colony-stimulating factor and receptor expression and signaling secondary to the lysosomal defects. These studies suggest a cellular and molecular basis for the development of histiocytosis in several human syndromes associated with ENT3 mutations and potentially other LSDs.
	PMID: 22174130 [PubMed - indexed for MEDLINE]
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5.	Science. 2011 Dec 2;334(6060):1230-2. Improving validation practices in "omics" research. Ioannidis JP, Khoury MJ. Source Stanford Prevention Research Center, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA. Abstract "Omics" research poses acute challenges regarding how to enhance validation practices and eventually the utility of this rich information. Several strategies may be useful, including routine replication, public data and protocol availability, funding incentives, reproducibility rewards or penalties, and targeted repeatability checks.
	PMID: 22144616 [PubMed - indexed for MEDLINE]
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6.	Nature. 2011 Oct 16;479(7371):117-21. doi: 10.1038/nature10558. Non-canonical inflammasome activation targets caspase-11 . Kayagaki N, Warming S, Lamkanfi M, Vande Walle L, Louie S, Dong J, Newton K, Qu Y, Liu J, Heldens S, Zhang J, Lee WP, Roose-Girma M, Dixit VM. Source Department of Physiological Chemistry, Genentech Inc., South San Francisco, California 94080, USA. kayagaki@gene.com Comment in Nature. 2011 Nov 3;479(7371):48-50. Nat Rev Immunol. 2011 Dec;11(12):801. Abstract Caspase-1 activation by inflammasome scaffolds comprised of intracellular nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) and the adaptor ASC is believed to be essential for production of the pro-inflammatory cytokines interleukin (IL)-1β and IL-18 during the innate immune response. Here we show, with C57BL/6 Casp11 gene-targeted mice, that caspase-11 (also known as caspase-4) is critical for caspase-1 activation and IL-1β production in macrophages infected with Escherichia coli, Citrobacter rodentium or Vibrio cholerae. Strain 129 mice, like Casp11(-/-) mice, exhibited defects in IL-1β production and harboured a mutation in the Casp11 locus that attenuated caspase-11 expression. This finding is important because published targeting of the Casp1 gene was done using strain 129 embryonic stem cells. Casp1 and Casp11 are too close in the genome to be segregated by recombination; consequently, the published Casp1(-/-) mice lack both caspase-11 and caspase-1. Interestingly, Casp11(-/-) macrophages secreted IL-1β normally in response to ATP and monosodium urate, indicating that caspase-11 is engaged by a non-canonical inflammasome. Casp1(-/-)Casp11(129mt/129mt) macrophages expressing caspase-11 from a C57BL/6 bacterial artificial chromosome transgene failed to secrete IL-1β regardless of stimulus, confirming an essential role for caspase-1 in IL-1β production. Caspase-11 rather than caspase-1, however, was required for non-canonical inflammasome-triggered macrophage cell death, indicating that caspase-11 orchestrates both caspase-1-dependent and -independent outputs. Caspase-1 activation by non-canonical stimuli required NLRP3 and ASC, but caspase-11 processing and cell death did not, implying that there is a distinct activator of caspase-11. Lastly, loss of caspase-11 rather than caspase-1 protected mice from a lethal dose of lipopolysaccharide. These data highlight a unique pro-inflammatory role for caspase-11 in the innate immune response to clinically significant bacterial infections.
	PMID: 22002608 [PubMed - indexed for MEDLINE]
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7.	Nature. 2011 Oct 12;478(7368):S16-8. doi: 10.1038/478S16a. Translational research: The American way. Maxmen A.
	PMID: 21993821 [PubMed - indexed for MEDLINE]
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8.	Nature. 2011 Oct 12;478(7368):156. doi: 10.1038/478156a. More than teeth. [No authors listed]
	PMID: 21993719 [PubMed - indexed for MEDLINE]
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9.	Nature. 2011 Oct 12;479(7372):223-7. doi: 10.1038/nature10533. Genome sequencing reveals insights into physiology and longevity of the naked mole rat. Kim EB, Fang X, Fushan AA, Huang Z, Lobanov AV, Han L, Marino SM, Sun X, Turanov AA, Yang P, Yim SH, Zhao X, Kasaikina MV, Stoletzki N, Peng C, Polak P, Xiong Z, Kiezun A, Zhu Y, Chen Y, Kryukov GV, Zhang Q, Peshkin L, Yang L, Bronson RT, Buffenstein R, Wang B, Han C, Li Q, Chen L, Zhao W, Sunyaev SR, Park TJ, Zhang G, Wang J, Gladyshev VN. Source Department of Bioinspired Science, Ewha Womans University, Seoul, 120-750, Korea. Abstract The naked mole rat (Heterocephalus glaber) is a strictly subterranean, extraordinarily long-lived eusocial mammal. Although it is the size of a mouse, its maximum lifespan exceeds 30 years, making this animal the longest-living rodent. Naked mole rats show negligible senescence, no age-related increase in mortality, and high fecundity until death. In addition to delayed ageing, they are resistant to both spontaneous cancer and experimentally induced tumorigenesis. Naked mole rats pose a challenge to the theories that link ageing, cancer and redox homeostasis. Although characterized by significant oxidative stress, the naked mole rat proteome does not show age-related susceptibility to oxidative damage or increased ubiquitination. Naked mole rats naturally reside in large colonies with a single breeding female, the 'queen', who suppresses the sexual maturity of her subordinates. They also live in full darkness, at low oxygen and high carbon dioxide concentrations, and are unable to sustain thermogenesis nor feel certain types of pain. Here we report the sequencing and analysis of the naked mole rat genome, which reveals unique genome features and molecular adaptations consistent with cancer resistance, poikilothermy, hairlessness and insensitivity to low oxygen, and altered visual function, circadian rythms and taste sensing. This information provides insights into the naked mole rat's exceptional longevity and ability to live in hostile conditions, in the dark and at low oxygen. The extreme traits of the naked mole rat, together with the reported genome and transcriptome information, offer opportunities for understanding ageing and advancing other areas of biological and biomedical research.
	PMID: 21993625 [PubMed - indexed for MEDLINE]
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10.	Nature. 2011 Oct 6;478(7367):143-5. Education: Inspiration for informatics. Gewin V.
	PMID: 21985005 [PubMed - indexed for MEDLINE]
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11.	Nature. 2011 Oct 9;479(7371):122-6. doi: 10.1038/nature10507. Macrophage skewing by Phd2 haplodeficiency prevents ischaemia by inducing arteriogenesis. Takeda Y, Costa S, Delamarre E, Roncal C, Leite de Oliveira R, Squadrito ML, Finisguerra V, Deschoemaeker S, Bruyère F, Wenes M, Hamm A, Serneels J, Magat J, Bhattacharyya T, Anisimov A, Jordan BF, Alitalo K, Maxwell P, Gallez B, Zhuang ZW, Saito Y, Simons M, De Palma M, Mazzone M. Source Laboratory of Molecular Oncology and Angiogenesis, Vesalius Research Center, VIB, Leuven B-3000, Belgium. Abstract PHD2 serves as an oxygen sensor that rescues blood supply by regulating vessel formation and shape in case of oxygen shortage. However, it is unknown whether PHD2 can influence arteriogenesis. Here we studied the role of PHD2 in collateral artery growth by using hindlimb ischaemia as a model, a process that compensates for the lack of blood flow in case of major arterial occlusion. We show that Phd2 (also known as Egln1) haplodeficient (Phd2(+/-)) mice displayed preformed collateral arteries that preserved limb perfusion and prevented tissue necrosis in ischaemia. Improved arteriogenesis in Phd2(+/-) mice was due to an expansion of tissue-resident, M2-like macrophages and their increased release of arteriogenic factors, leading to enhanced smooth muscle cell (SMC) recruitment and growth. Both chronic and acute deletion of one Phd2 allele in macrophages was sufficient to skew their polarization towards a pro-arteriogenic phenotype. Mechanistically, collateral vessel preconditioning relied on the activation of canonical NF-κB pathway in Phd2(+/-) macrophages. These results unravel how PHD2 regulates arteriogenesis and artery homeostasis by controlling a specific differentiation state in macrophages and suggest new treatment options for ischaemic disorders.
	PMID: 21983962 [PubMed - indexed for MEDLINE]
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12.	Nature. 2011 Oct 5;478(7367):127-31. doi: 10.1038/nature10456. Pathogenic exon-trapping by SVA retrotransposon and rescue in Fukuyama muscular dystrophy. Taniguchi-Ikeda M, Kobayashi K, Kanagawa M, Yu CC, Mori K, Oda T, Kuga A, Kurahashi H, Akman HO, DiMauro S, Kaji R, Yokota T, Takeda S, Toda T. Source Division of Neurology/Molecular Brain Science, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan. Comment in Nature. 2011 Oct 6;478(7367):46-7. Abstract Fukuyama muscular dystrophy (FCMD; MIM253800), one of the most common autosomal recessive disorders in Japan, was the first human disease found to result from ancestral insertion of a SINE-VNTR-Alu (SVA) retrotransposon into a causative gene. In FCMD, the SVA insertion occurs in the 3' untranslated region (UTR) of the fukutin gene. The pathogenic mechanism for FCMD is unknown, and no effective clinical treatments exist. Here we show that aberrant messenger RNA (mRNA) splicing, induced by SVA exon-trapping, underlies the molecular pathogenesis of FCMD. Quantitative mRNA analysis pinpointed a region that was missing from transcripts in patients with FCMD. This region spans part of the 3' end of the fukutin coding region, a proximal part of the 3' UTR and the SVA insertion. Correspondingly, fukutin mRNA transcripts in patients with FCMD and SVA knock-in model mice were shorter than the expected length. Sequence analysis revealed an abnormal splicing event, provoked by a strong acceptor site in SVA and a rare alternative donor site in fukutin exon 10. The resulting product truncates the fukutin carboxy (C) terminus and adds 129 amino acids encoded by the SVA. Introduction of antisense oligonucleotides (AONs) targeting the splice acceptor, the predicted exonic splicing enhancer and the intronic splicing enhancer prevented pathogenic exon-trapping by SVA in cells of patients with FCMD and model mice, rescuing normal fukutin mRNA expression and protein production. AON treatment also restored fukutin functions, including O-glycosylation of α-dystroglycan (α-DG) and laminin binding by α-DG. Moreover, we observe exon-trapping in other SVA insertions associated with disease (hypercholesterolemia, neutral lipid storage disease) and human-specific SVA insertion in a novel gene. Thus, although splicing into SVA is known, we have discovered in human disease a role for SVA-mediated exon-trapping and demonstrated the promise of splicing modulation therapy as the first radical clinical treatment for FCMD and other SVA-mediated diseases.
	PMID: 21979053 [PubMed - indexed for MEDLINE]
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13.	Nature. 2011 Oct 5;478(7367):76-81. doi: 10.1038/nature10449. Complement factor H binds malondialdehyde epitopes and protects from oxidative stress. Weismann D, Hartvigsen K, Lauer N, Bennett KL, Scholl HP, Charbel Issa P, Cano M, Brandstätter H, Tsimikas S, Skerka C, Superti-Furga G, Handa JT, Zipfel PF, Witztum JL, Binder CJ. Source Center for Molecular Medicine of the Austrian Academy of Sciences, 1090 Vienna, Austria. Comment in Nature. 2011 Oct 6;478(7367):42-3. Abstract Oxidative stress and enhanced lipid peroxidation are linked to many chronic inflammatory diseases, including age-related macular degeneration (AMD). AMD is the leading cause of blindness in Western societies, but its aetiology remains largely unknown. Malondialdehyde (MDA) is a common lipid peroxidation product that accumulates in many pathophysiological processes, including AMD. Here we identify complement factor H (CFH) as a major MDA-binding protein that can block both the uptake of MDA-modified proteins by macrophages and MDA-induced proinflammatory effects in vivo in mice. The CFH polymorphism H402, which is strongly associated with AMD, markedly reduces the ability of CFH to bind MDA, indicating a causal link to disease aetiology. Our findings provide important mechanistic insights into innate immune responses to oxidative stress, which may be exploited in the prevention of and therapy for AMD and other chronic inflammatory diseases.
	PMID: 21979047 [PubMed - indexed for MEDLINE]
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14.	Nature. 2011 Oct 5;478(7367):46-7. doi: 10.1038/478046a. Muscular dystrophy: A hidden ancestral legacy trumped. Nakamori M, Thornton C. Comment on Nature. 2011 Oct 6;478(7367):127-31.
	PMID: 21979043 [PubMed - indexed for MEDLINE]
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15.	Nature. 2011 Oct 5;478(7367):22-4. doi: 10.1038/478022a. Human genetics: Genomes on prescription. Maher B.
	PMID: 21979025 [PubMed - indexed for MEDLINE]
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16.	Nature. 2011 Oct 5;478(7367):19. doi: 10.1038/478019a. Nature readers flirt with personal genomics. Mah er B.
	PMID: 21979023 [PubMed - indexed for MEDLINE]
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17.	Nature. 2011 Oct 4;478(7367):17. doi: 10.1038/478017a. Secrets of the human genome disclosed. Hayden E C.
	PMID: 21979022 [PubMed - indexed for MEDLINE]
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