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

Sent on Wednesday, 2014 August 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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1.	Science. 2014 Aug 8;345(6197):679-84. doi: 10.1126/science.1254790. Inflammation. 25-Hydroxycholesterol suppresses interleukin-1-driven inflammation downstream of type I interferon. Reboldi A1, Dang EV1, McDonald JG2, Liang G2, Russell DW2, Cyster JG3. Author information: 1Howard Hughes Medical Institute, Department of Microbiology and Immunology, University of California, San Francisco, CA 94143, USA. 2Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. 3Howard Hughes Medical Institute, Department of Microbiology and Immunology, University of California, San Francisco, CA 94143, USA. jason.cyster@ucsf.edu. Abstract Type I interferon (IFN) protects against viruses, yet it also has a poorly understood suppressive influence on inflammation. Here, we report that activated mouse macrophages lacking the IFN-stimulated gene cholesterol 25-hydroxylase (Ch25h) and that are unable to produce the oxysterol 25-hydroxycholesterol (25-HC) overproduce inflammatory interleukin-1 (IL-1) family cytokines. 25-HC acts by antagonizing sterol response element-binding protein (SREBP) processing to reduce Il1b transcription and to broadly repress IL-1-activating inflammasomes. In accord with these dual actions of 25-HC, Ch25h-deficient mice exhibit increased sensitivity to septic shock, exacerbated experimental autoimmune encephalomyelitis, and a stronger ability to repress bacterial growth. These findings identify an oxysterol, 25-HC, as a critical mediator in the negative-feedback pathway of IFN signaling on IL-1 family cytokine production and inflammasome activity. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 25104388 [PubMed - indexed for MEDLINE]
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2.	Science. 2014 Aug 8;345(6197):676-9. doi: 10.1126/science.1254070. Nitrogen cycling. The environmental controls that govern the end product of bacterial nitrate respiration. Kraft B1, Tegetmeyer HE2, Sharma R3, Klotz MG4, Ferdelman TG1, Hettich RL3, Geelhoed JS5, Strous M6. Author information: 1Max Planck Institute for Marine Microbiology, 28359 Bremen, Germany. 2Max Planck Institute for Marine Microbiology, 28359 Bremen, Germany. Institute for Genome Research and Systems Biology, Center for Biotechnology, University of Bielefeld, 33615 Bielefeld, Germany. 3UT-ORNL Graduate School of Genome Science and Technology, University of Tennessee, Knoxville, TN 37996, USA. Chemical Science Division, Oak Ridge National Laboratory, Oak Ridge, TN 37830, USA. 4Department of Biological Sciences, University of North Carolina, Charlotte, NC 28223, USA. State Key Laboratory of Marine Environmental Science, Xiamen University, Xiamen 361005, China. 5Max Planck Institute for Marine Microbiology, 28359 Bremen, Germany. NIOZ Royal Netherlands Institute for Sea Research, 4401NT Yerseke, Netherlands. 6Max Planck Institute for Marine Microbiology, 28359 Bremen, Germany. Institute for Genome Research and Systems Biology, Center for Biotechnology, University of Bielefeld, 33615 Bielefeld, Germany. Department of Geoscience, University of Calgary, Calgary, Alberta T2N 1N4, Canada. mstrous@ucalgary.ca. Abstract In the biogeochemical nitrogen cycle, microbial respiration processes compete for nitrate as an electron acceptor. Denitrification converts nitrate into nitrogenous gas and thus removes fixed nitrogen from the biosphere, whereas ammonification converts nitrate into ammonium, which is directly reusable by primary producers. We combined multiple parallel long-term incubations of marine microbial nitrate-respiring communities with isotope labeling and metagenomics to unravel how specific environmental conditions select for either process. Microbial generation time, supply of nitrite relative to nitrate, and the carbon/nitrogen ratio were identified as key environmental controls that determine whether nitrite will be reduced to nitrogenous gas or ammonium. Our results define the microbial ecophysiology of a biogeochemical feedback loop that is key to global change, eutrophication, and wastewater treatment. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 25104387 [PubMed - indexed for MEDLINE]
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What's new for 'JKB_daily1' in PubMed

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

Sent on Friday, 2014 August 15
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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Items 1 - 7 of 7

1.	Science. 2014 Aug 1;345(6196):1251343. doi: 10.1126/science.1251343. Mobile DNA in cancer. Extensive transduction of nonrepetitive DNA mediated by L1 retrotransposition in cancer genomes. Tubio JM1, Li Y1, Ju YS1, Martincorena I1, Cooke SL1, Tojo M2, Gundem G1, Pipinikas CP3, Zamora J1, Raine K1, Menzies A1, Roman-Garcia P1, Fullam A1, Gerstung M1, Shlien A1, Tarpey PS1, Papaemmanuil E1, Knappskog S4, Van Loo P5, Ramakrishna M1, Davies HR1, Marshall J1, Wedge DC1, Teague JW1, Butler AP1, Nik-Zainal S6, Alexandrov L1, Behjati S1, Yates LR1, Bolli N7, Mudie L1, Hardy C1, Martin S1, McLaren S1, O'Meara S1, Anderson E1, Maddison M1, Gamble S1; ICGC Breast Cancer Group; ICGC Bone Cancer Group; ICGC Prostate Cancer Group, Foster C8, Warren AY9, Whitaker H10, Brewer D11, Eeles R12, Cooper C11, Neal D10, Lynch AG10, Visakorpi T13, Isaacs WB14, van't Veer L15, Caldas C10, Desmedt C16, Sotiriou C16, Aparicio S17, Foekens JA18, Eyfjörd JE19, Lakhani SR20, Thomas G21, Myklebost O22, Span PN23, Børresen-Dale AL22, Richardson AL24, Van de Vijver M25, Vincent-Salomon A26, Van den Eynden GG27, Flanagan AM28, Futreal PA29, Janes SM3, Bova GS13, Stratton MR1, McDermott U1, Campbell PJ30. Collaborators: Provenzano E, van de Vijver M, Richardson AL, Purdie C, Pinder S, MacGrogan G, Vincent-Salomon A, Larsimont D, Grabau D, Sauer T, Garred Ø, Ehinger A, Van den Eynden GG, van Deurzen CH, Salgado R, Brock JE, Lakhani SR, Giri DD, Arnould L, Jacquemier J, Treilleux I, Caldas C, Chin SF, Fatima A, Thompson AM, Stenhouse A, Foekens J, Martens J, Sieuwerts A, Brinkman A, Stunnenberg H, Span PN, Sweep F, Desmedt C, Sotiriou C, Thomas G, Broeks A, Langerod A, Aparicio S, Simpson P, van 't Veer L, Eyfjörd JE, Hilmarsdottir H, Jonasson JG, Børresen-Dale AL, Lee MT, Wong BH, Tan BK, Hooijer GK, Cooper C, Eeles R, Wedge D, Van Loo P, Gundem G, Alexandrov L, Kremeyer B, Butler A, Lynch A, Edwards S, Camacho N, Massie C, Kote-Jarai Z, Dennis N, Merson S, Zamora J, Kay J, Corbishley C, Thomas S, Nik-Zainai S, O'Meara S, Matthews L, Clark J, Hurst R, Mithen R, Cooke S, Raine K, Jones D, Menzies A, Stebbings L, Hinton J, Teague J, McLaren S , Mudie L, Hardy C, Anderson E, Joseph O, Goody V, Robinson B, Maddison M, Gamble S, Greenman C, Berney D, Hazell S, Livni N, Fisher C, Ogden C, Kumar P, Thompson A, Woodhouse C, Nicol D, Mayer E, Dudderidge T, Shah N, Gnanapragasam V, Campbell P, Futreal A, Easton D, Warren AY, Foster C, Stratton M, Whitaker H, McDermott U, Brewer D, Neal D. Author information: 1Wellcome Trust Sanger Institute, Hinxton, Cambridgeshire, UK. 2Department of Physiology, School of Medicine-Center for Resesarch in Molecular Medicine and Chronic Diseases, Instituto de Investigaciones Sanitarias, University of Santiago de Compostela, Spain. 3Lungs for Living Research Centre, Rayne Institute, University College London (UCL), London, UK. 4Wellcome Trust Sanger Institute, Hinxton, Cambridgeshire, UK. Department of Clinical Science, University of Bergen, Bergen, Norway. Department of Oncology, Haukeland University Hospital, Bergen, Norway. 5Wellcome Trust Sanger Institute, Hinxton, Cambridgeshire, UK. Human Genome Laboratory, Department of Human Genetics, VIB and KU Leuven, Leuven, Belgium. 6Wellcome Trust Sanger Institute, Hinxton, Cambridgeshire, UK. Cambridge University Hospitals National Health Service (NHS) Foundation Trust, Cambridge, UK. 7Wellcome Trust Sanger Institute, Hinxton, Cambridgeshire, UK. Department of Haematology, University of Cambridge, Cambridge, UK. 8University of Liverpool and HCA Pathology Laboratories, London, UK. 9Cambridge University Hospitals National Health Service (NHS) Foundation Trust, Cambridge, UK. 10Cancer Research UK (CRUK) Cambridge Institute, University of Cambridge, Cambridge, UK. 11Institute of Cancer Research, Sutton, London, UK. University of East Anglia, Norwich, UK. 12Institute of Cancer Research, Sutton, London, UK. 13Institute of Biosciences and Medical Technology-BioMediTech, University of Tampere and Tampere University Hospital, Tampere, Finland. 14Johns Hopkins University, Baltimore, MD, USA. 15Netherlands Cancer Institute, Amsterdam, Netherlands. 16Breast Cancer Translational Research Laboratory, Institut Jules Bordet, Université Libre de Bruxelles, Brussels, Belgium. 17British Columbia Cancer Agency, Vancouver, Canada. 18Department of Medical Oncology, Erasmus Medical Center Cancer Institute, Erasmus University Medical Center, Rotterdam, Netherlands. 19Cancer Research Laboratory, University of Iceland, Reykjavik, Iceland. 20School of Medicine, University of Queensland, Brisbane, Australia. Pathology Queensland, Royal Brisbane and Women's Hospital, Brisbane, Australia. UQ Centre for Clinical Research, University of Queensland, Brisbane, Australia. 21Université Lyon 1, Institut National du Cancer (INCa)-Synergie, Lyon, France. 22Institute for Cancer Research, Oslo University Hospital, Oslo, Norway. 23Department of Radiation Oncology and Department of Laboratory Medicine, Radboud University Medical Center, Nijmegen, Netherlands. 24Dana-Farber Cancer Institute, Boston, MA, USA. 25Department of Pathology, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, Netherlands. 26Institut Bergonié, 229 cours de l'Argone, 33076 Bordeaux, France. Institut Curie, Department of Tumor Biology, 26 rue d'Ulm, 75248 Paris cédex 05, France. 27Translational Cancer Research Unit and Department of Pathology, GZA Hospitals, Antwerp, Belgium. 28Royal National Orthopaedic Hospital, Middlesex, UK. UCL Cancer Institute, University College London, London, UK. 29Wellcome Trust Sanger Institute, Hinxton, Cambridgeshire, UK. MD Anderson Cancer Center, Houston, TX, USA. 30Wellcome Trust Sanger Institute, Hinxton, Cambridgeshire, UK. Cambridge University Hospitals National Health Service (NHS) Foundation Trust, Cambridge, UK. Department of Haematology, University of Cambridge, Cambridge, UK. pc8@sanger.ac.uk. Abstract Long interspersed nuclear element-1 (L1) retrotransposons are mobile repetitive elements that are abundant in the human genome. L1 elements propagate through RNA intermediates. In the germ line, neighboring, nonrepetitive sequences are occasionally mobilized by the L1 machinery, a process called 3' transduction. Because 3' transductions are potentially mutagenic, we explored the extent to which they occur somatically during tumorigenesis. Studying cancer genomes from 244 patients, we found that tumors from 53% of the patients had somatic retrotranspositions, of which 24% were 3' transductions. Fingerprinting of donor L1s revealed that a handful of source L1 elements in a tumor can spawn from tens to hundreds of 3' transductions, which can themselves seed further retrotranspositions. The activity of individual L1 elements fluctuated during tumor evolution and correlated with L1 promoter hypomethylation. The 3' transductions disseminated genes, exons, and regulatory elements to new locations, most often to heterochromatic regions of the genome. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 25082706 [PubMed - indexed for MEDLINE]
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2.	Science. 2014 Aug 1;345(6196):578-82. doi: 10.1126/science.1256942. Epub 2014 Jul 17. Coinfection. Virus-helminth coinfection reveals a microbiota-independent mechanism of immunomodulation. Osborne LC1, Monticelli LA1, Nice TJ2, Sutherland TE3, Siracusa MC1, Hepworth MR4, Tomov VT5, Kobuley D1, Tran SV1, Bittinger K6, Bailey AG6, Laughlin AL6, Boucher JL7, Wherry EJ8, Bushman FD6, Allen JE3, Virgin HW2, Artis D9. Author information: 1Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. 2Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. 3Institute of Immunology and Infection Research, Centre for Immunity, Infection and Evolution, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3JT, UK. 4Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Department of Medicine, Division of Gastroenterology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. 5Department of Medicine, Division of Gastroenterology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. 6Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. 7Laboratoire de Chimie et Biochimie Pharmacologiques et Toxicologiques, Université Paris Descartes, Paris, France. 8Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. 9Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. dartis@mail.med.upenn.edu. Comment in Immunology. How helminths go viral. [Science. 2014] Immunology. How helminths go viral.Maizels RM, Gause WC. Science. 2014 Aug 1; 345(6196):517-8. Epub 2014 Jul 31. Abstract The mammalian intestine is colonized by beneficial commensal bacteria and is a site of infection by pathogens, including helminth parasites. Helminths induce potent immunomodulatory effects, but whether these effects are mediated by direct regulation of host immunity or indirectly through eliciting changes in the microbiota is unknown. We tested this in the context of virus-helminth coinfection. Helminth coinfection resulted in impaired antiviral immunity and was associated with changes in the microbiota and STAT6-dependent helminth-induced alternative activation of macrophages. Notably, helminth-induced impairment of antiviral immunity was evident in germ-free mice, but neutralization of Ym1, a chitinase-like molecule that is associated with alternatively activated macrophages, could partially restore antiviral immunity. These data indicate that helminth-induced immunomodulation occurs independently of changes in the microbiota but is dependent on Ym1. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 25082704 [PubMed - indexed for MEDLINE]
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3.	Science. 2014 Aug 1;345(6196):573-7. doi: 10.1126/science.1254517. Epub 2014 Jun 26. Coinfection. Helminth infection reactivates latent γ-herpesvirus via cytokine competition at a viral promoter. Reese TA1, Wakeman BS2, Choi HS3, Hufford MM4, Huang SC1, Zhang X1, Buck MD1, Jezewski A1, Kambal A1, Liu CY1, Goel G5, Murray PJ6, Xavier RJ5, Kaplan MH4, Renne R3, Speck SH2, Artyomov MN1, Pearce EJ1, Virgin HW7. Author information: 1Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. 2Emory University Vaccine Center, Atlanta, GA 30322, USA. 3Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL 32610, USA. 4Departments of Pediatrics and Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202, USA. 5Center for Computational and Integrative Biology and Gastrointestinal Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. 6Departments of Infectious Diseases and Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. 7Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. virgin@wustl.edu. Comment in Immunology. How helminths go viral. [Science. 2014] Immunology. How helminths go viral.Maizels RM, Gause WC. Science. 2014 Aug 1; 345(6196):517-8. Epub 2014 Jul 31. Abstract 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 γ-herpesvirus infection in vivo. IL-4 promoted viral replication and blocked the antiviral effects of interferon-γ (IFNγ) 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 IFNγ reactivated latent murine γ-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. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 24968940 [PubMed - indexed for MEDLINE]
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4.	Nature. 2014 Jun 26;510(7506):473. doi: 10.1038/510473d. Embryo screening: update German view of genetic testing. Propping P, Schott H. Author information: University of Bonn, Germany.
	PMID: 24965640 [PubMed - indexed for MEDLINE]
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5.	Nature. 2014 Jun 26;510(7506):473. doi: 10.1038/510473b. Ancient cultures: maize is not a clue to Puerto Rican origins. Pagán-Jiménez JR1, Rodríguez-Ramos R2, Oliver JR3. Author information: 1Leiden University, the Netherlands. 2University of Puerto Rico, Utuado, Puerto Rico. 3University College London, UK.
	PMID: 24965639 [PubMed - indexed for MEDLINE]
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6.	Nature. 2014 Apr 24;508(7497):451-3. Medical genomics: Gather and use genetic data in health care. Ginsburg G.
	PMID: 24765668 [PubMed - indexed for MEDLINE]
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7.	Nature. 2014 Apr 24;508(7497):488-93. doi: 10.1038/nature13151. Origins and functional evolution of Y chromosomes across mammals. Cortez D1, Marin R1, Toledo-Flores D2, Froidevaux L3, Liechti A3, Waters PD4, Grützner F2, Kaessmann H1. Author information: 11] Center for Integrative Genomics, University of Lausanne, 1015 Lausanne, Switzerland [2] Swiss Institute of Bioinformatics, 1015 Lausanne, Switzerland. 2The Robinson Research Institute, School of Molecular and Biomedical Science, University of Adelaide, Adelaide, South Australia 5005, Australia. 3Center for Integrative Genomics, University of Lausanne, 1015 Lausanne, Switzerland. 4School of Biotechnology and Biomolecular Sciences, UNSW Australia, Sydney, New South Wales 2052, Australia. Comment in Genetics: The vital Y chromosome. [Nature. 2014] Genetics: The vital Y chromosome.Clark AG. Nature. 2014 Apr 24; 508(7497):463-5. Abstract Y chromosomes underlie sex determination in mammals, but their repeat-rich nature has hampered sequencing and associated evolutionary studies. Here we trace Y evolution across 15 representative mammals on the basis of high-throughput genome and transcriptome sequencing. We uncover three independent sex chromosome originations in mammals and birds (the outgroup). The original placental and marsupial (therian) Y, containing the sex-determining gene SRY, emerged in the therian ancestor approximately 180 million years ago, in parallel with the first of five monotreme Y chromosomes, carrying the probable sex-determining gene AMH. The avian W chromosome arose approximately 140 million years ago in the bird ancestor. The small Y/W gene repertoires, enriched in regulatory functions, were rapidly defined following stratification (recombination arrest) and erosion events and have remained considerably stable. Despite expression decreases in therians, Y/W genes show notable conservation of proto-sex chromosome expression patterns, although various Y genes evolved testis-specificities through differential regulatory decay. Thus, although some genes evolved novel functions through spatial/temporal expression shifts, most Y genes probably endured, at least initially, because of dosage constraints.
	PMID: 24759410 [PubMed - indexed for MEDLINE]
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What's new for 'JKB_daily1' in PubMed

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

Sent on Wednesday, 2014 August 13
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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1.	N Engl J Med. 2014 Jul 31;371(5):411-23. doi: 10.1056/NEJMoa1314981. Spread of artemisinin resistance in Plasmodium falciparum malaria. Ashley EA1, Dhorda M, Fairhurst RM, Amaratunga C, Lim P, Suon S, Sreng S, Anderson JM, Mao S, Sam B, Sopha C, Chuor CM, Nguon C, Sovannaroth S, Pukrittayakamee S, Jittamala P, Chotivanich K, Chutasmit K, Suchatsoonthorn C, Runcharoen R, Hien TT, Thuy-Nhien NT, Thanh NV, Phu NH, Htut Y, Han KT, Aye KH, Mokuolu OA, Olaosebikan RR, Folaranmi OO, Mayxay M, Khanthavong M, Hongvanthong B, Newton PN, Onyamboko MA, Fanello CI, Tshefu AK, Mishra N, Valecha N, Phyo AP, Nosten F, Yi P, Tripura R, Borrmann S, Bashraheil M, Peshu J, Faiz MA, Ghose A, Hossain MA, Samad R, Rahman MR, Hasan MM, Islam A, Miotto O, Amato R, MacInnis B, Stalker J, Kwiatkowski DP, Bozdech Z, Jeeyapant A, Cheah PY, Sakulthaew T, Chalk J, Intharabut B, Silamut K, Lee SJ, Vihokhern B, Kunasol C, Imwong M, Tarning J, Taylor WJ, Yeung S, Woodrow CJ, Flegg JA, Das D, Smith J, Venkatesan M, Plowe CV, Stepniewska K, Guerin PJ, Dondorp AM, Day NP, White NJ; Tracking Resistance to Artemisinin Collaboration (TRAC). Author information: 1The authors' affiliations are listed in the Appendix. Comment in Treatment of malaria--a continuing challenge. [N Engl J Med. 2014] Treatment of malaria--a continuing challenge.Greenwood B. N Engl J Med. 2014 Jul 31; 371(5):474-5. Abstract BACKGROUND: Artemisinin resistance in Plasmodium falciparum has emerged in Southeast Asia and now poses a threat to the control and elimination of malaria. Mapping the geographic extent of resistance is essential for planning containment and elimination strategies. METHODS: Between May 2011 and April 2013, we enrolled 1241 adults and children with acute, uncomplicated falciparum malaria in an open-label trial at 15 sites in 10 countries (7 in Asia and 3 in Africa). Patients received artesunate, administered orally at a daily dose of either 2 mg per kilogram of body weight per day or 4 mg per kilogram, for 3 days, followed by a standard 3-day course of artemisinin-based combination therapy. Parasite counts in peripheral-blood samples were measured every 6 hours, and the parasite clearance half-lives were determined. RESULTS: The median parasite clearance half-lives ranged from 1.9 hours in the Democratic Republic of Congo to 7.0 hours at the Thailand-Cambodia border. Slowly clearing infections (parasite clearance half-life >5 hours), strongly associated with single point mutations in the "propeller" region of the P. falciparum kelch protein gene on chromosome 13 (kelch13), were detected throughout mainland Southeast Asia from southern Vietnam to central Myanmar. The incidence of pretreatment and post-treatment gametocytemia was higher among patients with slow parasite clearance, suggesting greater potential for transmission. In western Cambodia, where artemisinin-based combination therapies are failing, the 6-day course of antimalarial therapy was associated with a cure rate of 97.7% (95% confidence interval, 90.9 to 99.4) at 42 days. CONCLUSIONS: Artemisinin resistance to P. falciparum, which is now prevalent across mainland Southeast Asia, is associated with mutations in kelch13. Prolonged courses of artemisinin-based combination therapies are currently efficacious in areas where standard 3-day treatments are failing. (Funded by the U.K. Department of International Development and others; ClinicalTrials.gov number, NCT01350856.). Free Article
	PMID: 25075834 [PubMed - in process]
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2.	N Engl J Med. 2014 Jul 31;371(5):403-10. doi: 10.1056/NEJMoa1315860. Spiroindolone KAE609 for falciparum and vivax malaria. White NJ1, Pukrittayakamee S, Phyo AP, Rueangweerayut R, Nosten F, Jittamala P, Jeeyapant A, Jain JP, Lefèvre G, Li R, Magnusson B, Diagana TT, Leong FJ. Author information: 1From the Mahidol-Oxford Tropical Medicine Research Unit (N.J.W., F.N., A.J.) and the Department of Clinical Tropical Medicine (S.P., P.J.), Faculty of Tropical Medicine, Mahidol University, Bangkok, and the Shoklo Malaria Research Unit, Faculty of Tropical Medicine, Mahidol-Oxford Tropical Medicine Research Unit, Mahidol University (A.P.P., F.N.), and Mae Sot General Hospital (R.R.), Mae Sot - all in Thailand; the Centre for Tropical Medicine, Nuffield Department of Medicine, University of Oxford, Oxford, United Kingdom (N.J.W., F.N.); Novartis Healthcare, Hyderabad, India (J.P.J.); Novartis, Basel, Switzerland (G.L., B.M.); Novartis Institute of Biomedical Research, Beijing (R.L.); and Novartis Institute for Tropical Diseases, Singapore (T.T.D., F.J.L.). Comment in Treatment of malaria--a continuing challenge. [N Engl J Med. 2014] Treatment of malaria--a continuing challenge.Greenwood B. N Engl J Med. 2014 Jul 31; 371(5):474-5. Abstract BACKGROUND: KAE609 (cipargamin; formerly NITD609, Novartis Institute for Tropical Diseases) is a new synthetic antimalarial spiroindolone analogue with potent, dose-dependent antimalarial activity against asexual and sexual stages of Plasmodium falciparum. METHODS: We conducted a phase 2, open-label study at three centers in Thailand to assess the antimalarial efficacy, safety, and adverse-event profile of KAE609, at a dose of 30 mg per day for 3 days, in two sequential cohorts of adults with uncomplicated P. vivax malaria (10 patients) or P. falciparum malaria (11). The primary end point was the parasite clearance time. RESULTS: The median parasite clearance time was 12 hours in each cohort (interquartile range, 8 to 16 hours in patients with P. vivax malaria and 10 to 16 hours in those with P. falciparum malaria). The median half-lives for parasite clearance were 0.95 hours (range, 0.68 to 2.01; interquartile range, 0.85 to 1.14) in the patients with P. vivax malaria and 0.90 hours (range, 0.68 to 1.64; interquartile range, 0.78 to 1.07) in those with P. falciparum malaria. By comparison, only 19 of 5076 patients with P. falciparum malaria (<1%) who were treated with oral artesunate in Southeast Asia had a parasite clearance half-life of less than 1 hour. Adverse events were reported in 14 patients (67%), with nausea being the most common. The adverse events were generally mild and did not lead to any discontinuations of the drug. The mean terminal half-life for the elimination of KAE609 was 20.8 hours (range, 11.3 to 37.6), supporting a once-daily oral dosing regimen. CONCLUSIONS: KAE609, at dose of 30 mg daily for 3 days, cleared parasitemia rapidly in adults with uncomplicated P. vivax or P. falciparum malaria. (Funded by Novartis and others; ClinicalTrials.gov number, NCT01524341.). Free Article
	PMID: 25075833 [PubMed - in process]
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3.	Nat Genet. 2014 Jun;46(6):530-1. doi: 10.1038/ng.2993. Exploring new models of easiRNA biogenesis. Sarazin A, Voinnet O. Author information: Department of Biology at the Swiss Federal Institute of Technology Zürich, Zürich, Switzerland. Comment on miRNAs trigger widespread epigenetically activated siRNAs from transposons in Arabidopsis. [Nature. 2014] miRNAs trigger widespread epigenetically activated siRNAs from transposons in Arabidopsis.Creasey KM, Zhai J, Borges F, Van Ex F, Regulski M, Meyers BC, Martienssen RA. Nature. 2014 Apr 17; 508(7496):411-5. Epub 2014 Mar 16. Abstract Although silent transposons in plants can be reactivated by stress or during development, their potential deleterious effects are prevented by transposon-derived epigenetically activated small interfering RNAs (easiRNAs). A new study shows how serendipitous interactions between reactivated transposons and endogenous microRNAs might initiate easiRNA biogenesis, establishing an unexpected link between these two classes of silencing small RNAs.
	PMID: 24866189 [PubMed - in process]
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4.	Nat Genet. 2014 Jun;46(6):567-72. doi: 10.1038/ng.2987. Epub 2014 May 18. Genome sequence of the cultivated cotton Gossypium arboreum. Li F1, Fan G2, Wang K1, Sun F2, Yuan Y 1, Song G1, Li Q3, Ma Z4, Lu C5, Zou C5, Chen W6, Liang X6, Shang H5, Liu W6, Shi C6, Xiao G7, Gou C6, Ye W5, Xu X6, Zhang X5, Wei H5, Li Z5, Zhang G8, Wang J6, Liu K5, Kohel RJ9, Percy RG9, Yu JZ9, Zhu YX7, Wang J10, Yu S5. Author information: 11] State Key Laboratory of Cotton Biology, Institute of Cotton Research of the Chinese Academy of Agricultural Sciences, Anyang, China. [2]. 21] BGI-Shenzhen, Shenzhen, China. [2]. 31] State Key Laboratory of Protein and Plant Gene Research, College of Life Sciences, Peking University, Beijing, China. [2]. 41] Key Laboratory for Crop Germplasm Resources of Hebei, Agricultural University of Hebei, Baoding, China. [2]. 5State Key Laboratory of Cotton Biology, Institute of Cotton Research of the Chinese Academy of Agricultural Sciences, Anyang, China. 6BGI-Shenzhen, Shenzhen, China. 7State Key Laboratory of Protein and Plant Gene Research, College of Life Sciences, Peking University, Beijing, China. 8Key Laboratory for Crop Germplasm Resources of Hebei, Agricultural University of Hebei, Baoding, China. 9Crop Germplasm Research Unit, Southern Plains Agricultural Research Center, US Department of Agriculture-Agricultural Research Service (USDA-ARS), College Station, Texas, USA. 101] BGI-Shenzhen, Shenzhen, China. [2] Department of Biology, University of Copenhagen, Copenhagen, Denmark. [3] King Abdulaziz University, Jeddah, Saudi Arabia. [4] Macau University of Science and Technology, Macau, China. [5] Department of Medicine, University of Hong Kong, Hong Kong. [6] State Key Laboratory of Pharmaceutical Biotechnology, University of Hong Kong, Hong Kong. Abstract The complex allotetraploid nature of the cotton genome (AADD; 2n = 52) makes genetic, genomic and functional analyses extremely challenging. Here we sequenced and assembled the Gossypium arboreum (AA; 2n = 26) genome, a putative contributor of the A subgenome. A total of 193.6 Gb of clean sequence covering the genome by 112.6-fold was obtained by paired-end sequencing. We further anchored and oriented 90.4% of the assembly on 13 pseudochromosomes and found that 68.5% of the genome is occupied by repetitive DNA sequences. We predicted 41,330 protein-coding genes in G. arboreum. Two whole-genome duplications were shared by G. arboreum and Gossypium raimondii before speciation. Insertions of long terminal repeats in the past 5 million years are responsible for the twofold difference in the sizes of these genomes. Comparative transcriptome studies showed the key role of the nucleotide binding site (NBS)-encoding gene family in resistance to Verticillium dahliae and the involvement of ethylene in the development of cotton fiber cells.
	PMID: 24836287 [PubMed - in process]
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5.	Nat Genet. 2014 Jun;46(6):588-94. doi: 10.1038/ng.2981. Epub 2014 May 4. Pan-cancer genetic analysis identifies PARK2 as a master regulator of G1/S cyclins. Gong Y1, Zack TI2, Morris LG3, Lin K4, Hukkelhoven E5, Raheja R5, Tan IL4, Turcan S1, Veeriah S1, Meng S1, Viale A6, Schumacher SE7, Palmedo P8, Beroukhim R9, Chan TA10. Author information: 1Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, New York, New York, USA. 21] Broad Institute, Cambridge, Massachusetts, USA. [2] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA. [3] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA. [4] Center for Cancer Genome Characterization, Dana-Farber Cancer Institute, Boston, Massachusetts, USA. [5] Biophysics Program, Harvard University, Boston, Massachusetts, USA. 3Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, New York, USA. 4Weill Cornell College of Medicine, New York, New York, USA. 5Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, New York, New York, USA. 6Genomics Core, Memorial Sloan-Kettering Cancer Center, New York, New York, USA. 7Broad Institute, Cambridge, Massachusetts, USA. 81] Broad Institute, Cambridge, Massachusetts, USA. [2] Center for Biomedical Informatics, Harvard University, Boston, Massachusetts, USA. 91] Broad Institute, Cambridge, Massachusetts, USA. [2] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA. [3] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA. [4] Center for Cancer Genome Characterization, Dana-Farber Cancer Institute, Boston, Massachusetts, USA. 101] Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, New York, New York, USA. [2] Department of Radiation Oncology, Memorial Sloan-Kettering Cancer Center, New York, New York, USA. [3] Brain Tumor Center, Memorial Sloan-Kettering Cancer Center, New York, New York, USA. Comment in PARK2 orchestrates cyclins to avoid cancer. [Nat Genet. 2014] PARK2 orchestrates cyclins to avoid cancer.Bartek J, Hodny Z. Nat Genet. 2014 Jun; 46(6):527-8. Abstract Coordinate control of different classes of cyclins is fundamentally important for cell cycle regulation and tumor suppression, yet the underlying mechanisms are incompletely understood. Here we show that the PARK2 tumor suppressor mediates this coordination. The PARK2 E3 ubiquitin ligase coordinately controls the stability of both cyclin D and cyclin E. Analysis of approximately 5,000 tumor genomes shows that PARK2 is a very frequently deleted gene in human cancer and uncovers a striking pattern of mutual exclusivity between PARK2 deletion and amplification of CCND1, CCNE1 or CDK4-implicating these genes in a common pathway. Inactivation of PARK2 results in the accumulation of cyclin D and acceleration of cell cycle progression. Furthermore, PARK2 is a component of a new class of cullin-RING-containing ubiquitin ligases targeting both cyclin D and cyclin E for degradation. Thus, PARK2 regulates cyclin-CDK complexes, as does the CDK inhibitor p16, but acts as a master regulator of the stability of G1/S cyclins.
	PMID: 24793136 [PubMed - in process]
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6.	Nat Genet. 2014 Jun;46(6):558-66. doi: 10.1038/ng.2965. Epub 2014 Apr 28. Deep transcriptome profiling of mammalian stem cells supports a regulatory role for retrotransposons in pluripotency maintenance. Fort A1, Hashimoto K1, Yamada D2, Salimullah M3, Keya CA3, Saxena A1, Bonetti A3, Voineagu I1, Bertin N1, Kratz A3, Noro Y3, Wong CH4, de Hoon M3, Andersson R5, Sandelin A5, Suzuki H3, Wei CL4, Koseki H2; FANTOM Consortium, Hasegawa Y3, Forrest AR3, Carninci P3. Author information: 11] Division of Genomic Technologies, RIKEN Center for Life Science Technologies, Yokohama, Japan. [2]. 2Laboratory for Developmental Genetics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan. 3Division of Genomic Technologies, RIKEN Center for Life Science Technologies, Yokohama, Japan. 4Sequencing Technology Group, Joint Genome Institute, Lawrence Berkeley National Laboratory, Walnut Creek, California, USA. 5Bioinformatics Centre, Department of Biology and Biotech Research and Innovation Centre, University of Copenhagen, Copenhagen, Denmark. Abstract The importance of microRNAs and long noncoding RNAs in the regulation of pluripotency has been documented; however, the noncoding components of stem cell gene networks remain largely unknown. Here we investigate the role of noncoding RNAs in the pluripotent state, with particular emphasis on nuclear and retrotransposon-derived transcripts. We have performed deep profiling of the nuclear and cytoplasmic transcriptomes of human and mouse stem cells, identifying a class of previously undetected stem cell-specific transcripts. We show that long terminal repeat (LTR)-derived transcripts contribute extensively to the complexity of the stem cell nuclear transcriptome. Some LTR-derived transcripts are associated with enhancer regions and are likely to be involved in the maintenance of pluripotency.
	PMID: 24777452 [PubMed - in process]
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7.	Nat Genet. 2014 Jun;46(6):607-12. doi: 10.1038/ng.2953. Epub 2014 Apr 20. Integrated genomic characterization of adrenocortical carcinoma. Assié G1, Letouzé E2, Fassnacht M3, Jouinot A4, Luscap W4, Barreau O5, Omeiri H4, Rodriguez S4, Perlemoine K4, René-Corail F4, Elarouci N6, Sbiera S7, Kroiss M8, Allolio B9, Waldmann J10, Quinkler M11, Mannelli M12, Mantero F13, Papathomas T14, De Krijger R14, Tabarin A15, Kerlan V16, Baudin E17, Tissier F18, Dousset B19, Groussin L5, Amar L20, Clauser E21, Bertagna X22, Ragazzon B4, Beuschlein F23, Libé R22, de Reyniès A2, Bertherat J24. Author information: 11] INSERM U1016, Institut Cochin, Paris, France. [2] CNRS UMR 8104, Paris, France. [3] Université Paris Descartes, Sorbonne Paris Cité, Paris, France. [4] Center for Rare Adrenal Diseases, Department of Endocrinology, Assistance Publique-Hôpitaux de Paris, Hôpital Cochin, Paris, France. [5]. 21] Programme Cartes d'Identité des Tumeurs (CIT), Ligue Nationale Contre Le Cancer, Paris, France. [2]. 31] Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, University of Munich, Munich, Germany. [2] Endocrine and Diabetes Unit, Department of Internal Medicine I, University Hospital of Würzburg, Würzburg, Germany. [3] Comprehensive Cancer Center Mainfranken, University of Würzburg, Würzburg, Germany. 41] INSERM U1016, Institut Cochin, Paris, France. [2] CNRS UMR 8104, Paris, France. [3] Université Paris Descartes, Sorbonne Paris Cité, Paris, France. 51] INSERM U1016, Institut Cochin, Paris, France. [2] CNRS UMR 8104, Paris, France. [3] Université Paris Descartes, Sorbonne Paris Cité, Paris, France. [4] Center for Rare Adrenal Diseases, Department of Endocrinology, Assistance Publique-Hôpitaux de Paris, Hôpital Cochin, Paris, France. 6Programme Cartes d'Identité des Tumeurs (CIT), Ligue Nationale Contre Le Cancer, Paris, France. 71] Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, University of Munich, Munich, Germany. [2] Endocrine and Diabetes Unit, Department of Internal Medicine I, University Hospital of Würzburg, Würzburg, Germany. 8Comprehensive Cancer Center Mainfranken, University of Würzburg, Würzburg, Germany. 9Endocrine and Diabetes Unit, Department of Internal Medicine I, University Hospital of Würzburg, Würzburg, Germany. 10Visceral, Thoracic and Vascular Surgery, University Hospital Giessen and Marburg, Marburg, Germany. 11Department of Clinical Endocrinology, Charité Campus Mitte, Charité University Medicine, Berlin, Germany. 12Department of Experimental and Clinical Biomedical Sciences, University of Florence, Florence, Italy. 13Endocrinology Unit, Department of Medicine, University of Padova, Padova, Italy. 14Department of Pathology, Josephine Nefkens Institute, Erasmus MC University Medical Center, Rotterdam, The Netherlands. 151] Department of Endocrinology, Diabetes and Metabolic Diseases, University Hospital of Bordeaux, Bordeaux, France. [2] Rare Adrenal Cancer Network COMETE, Paris, France. 161] Rare Adrenal Cancer Network COMETE, Paris, France. [2] Department of Endocrinology, Diabetes and Metabolic Diseases, University Hospital of Brest, Brest, France. 171] Rare Adrenal Cancer Network COMETE, Paris, France. [2] Department of Nuclear Medicine and Endocrine Oncology, Institut Gustave Roussy, Université Paris-Sud, Villejuif, France. 181] INSERM U1016, Institut Cochin, Paris, France. [2] CNRS UMR 8104, Paris, France. [3] Université Paris Descartes, Sorbonne Paris Cité, Paris, France. [4] Department of Pathology, Assistance Publique-Hôpitaux de Paris, Hôpital Pitié-Salpétrière, Pierre et Marie Curie Université, Paris, France. 191] INSERM U1016, Institut Cochin, Paris, France. [2] CNRS UMR 8104, Paris, France. [3] Université Paris Descartes, Sorbonne Paris Cité, Paris, France. [4] Center for Rare Adrenal Diseases, Department of Endocrinology, Assistance Publique-Hôpitaux de Paris, Hôpital Cochin, Paris, France. [5] Department of Digestive and Endocrine Surgery, Assistance Publique-Hôpitaux de Paris, Hôpital Cochin, Paris, France. 20Hypertension Unit, Assistance Publique-Hôpitaux de Paris, Hôpital Européen Georges Pompidou, Paris, France. 21Oncogenetic Laboratory, Assistance Publique-Hôpitaux de Paris, Hôpital Cochin, Paris, France. 221] INSERM U1016, Institut Cochin, Paris, France. [2] CNRS UMR 8104, Paris, France. [3] Université Paris Descartes, Sorbonne Paris Cité, Paris, France. [4] Center for Rare Adrenal Diseases, Department of Endocrinology, Assistance Publique-Hôpitaux de Paris, Hôpital Cochin, Paris, France. [5] Rare Adrenal Cancer Network COMETE, Paris, France. 23Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, University of Munich, Munich, Germany. 241] INSERM U1016, Institut Cochin, Paris, France. [2] CNRS UMR 8104, Paris, France. [3] Université Paris Descartes, Sorbonne Paris Cité, Paris, France. [4] Center for Rare Adrenal Diseases, Department of Endocrinology, Assistance Publique-Hôpitaux de Paris, Hôpital Cochin, Paris, France. [5] Rare Adrenal Cancer Network COMETE, Paris, France. [6]. Abstract Adrenocortical carcinomas (ACCs) are aggressive cancers originating in the cortex of the adrenal gland. Despite overall poor prognosis, ACC outcome is heterogeneous. We performed exome sequencing and SNP array analysis of 45 ACCs and identified recurrent alterations in known driver genes (CTNNB1, TP53, CDKN2A, RB1 and MEN1) and in genes not previously reported in ACC (ZNRF3, DAXX, TERT and MED12), which we validated in an independent cohort of 77 ACCs. ZNRF3, encoding a cell surface E3 ubiquitin ligase, was the most frequently altered gene (21%) and is a potential new tumor suppressor gene related to the β-catenin pathway. Our integrated genomic analyses further identified two distinct molecular subgroups with opposite outcome. The C1A group of ACCs with poor outcome displayed numerous mutations and DNA methylation alterations, whereas the C1B group of ACCs with good prognosis displayed specific deregulation of two microRNA clusters. Thus, aggressive and indolent ACCs correspond to two distinct molecular entities driven by different oncogenic alterations.
	PMID: 24747642 [PubMed - in process]
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8.	Dev Comp Immunol. 2014 Feb;42(2):278-85. doi: 10.1016/j.dci.2013.09.011. Epub 2013 Sep 29. Production and characterisation of a monoclonal antibody that recognises the chicken CSF1 receptor and confirms that expression is restricted to macrophage-lineage cells. Garcia-Morales C1, Rothwell L, Moffat L, Garceau V, Balic A, Sang HM, Kaiser P, Hume DA. Author information: 1The Roslin Institute & Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Midlothian EH25 9RG, UK. Abstract Macrophages contribute to innate and acquired immunity as well as many aspects of homeostasis and development. Studies of macrophage biology and function in birds have been hampered by a lack of definitive cell surface markers. As in mammals, avian macrophages proliferate and differentiate in response to CSF1 and IL34, acting through the shared receptor, CSF1R. CSF1R mRNA expression in the chicken is restricted to macrophages and their progenitors. To expedite studies of avian macrophage biology, we produced an avian CSF1R-Fc chimeric protein and generated a monoclonal antibody (designated ROS-AV170) against the chicken CSF1R using the chimeric protein as immunogen. Specific binding of ROS-AV170 to CSF1R was confirmed by FACS, ELISA and immunohistochemistry on tissue sections. CSF1 down-regulated cell surface expression of the CSF1R detected with ROS-AV170, but the antibody did not block CSF1 signalling. Expression of CSF1R was detected on the surface of bone marrow progenitors only after culture in the absence of CSF1, and was induced during macrophage differentiation. Constitutive surface expression of CSF1R distinguished monocytes from other myeloid cells, including heterophils and thrombocytes. This antibody will therefore be of considerable utility for the study of chicken macrophage biology. Copyright © 2013. Published by Elsevier Ltd.
	PMID: 24084378 [PubMed - in process]
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