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  • Humans  (5)
  • Air temperature at 10 m height; Air temperature at 2 m height; Anemometer, Thies Clima, Combined Wind Transmitter 4.3324.31.673; AWI_Meteo; Barometer, Paroscientific, Digiquartz 6000-16B, SN 136669; DATE/TIME; Dronning Maud Land, Antarctica; Georg von Neumayer; GVN; Humidity, relative; Hygrometer, Vaisala, HMP233; Hygrometer, Vaisala, HMT337 in T2 housing; Long-wave downward radiation; Meteorological Long-Term Observations @ AWI; Monitoring station; MONS; Neumayer_based; NEUMAYER III; Pyranometer, Eppley, CM11, SN 903250; Pyranometer, Eppley, CM11, SN 903252; Pyrgeometer, Kipp & Zonen, CGR4, SN 080058; Short-wave downward radiation, 525 - 3000 nm; Short-wave downward radiation, 696 - 3000 nm; Station pressure; Sunshine duration; Sunshine indicator, Kipp & Zonen, CSD 3, SN 080096; Thermometer, Thies Clima, Ventilated Air Temperature Transmitter 2.1265.xx.000 (modified); Total Ultraviolet Radiometer, Eppley, TUVR, SN 28276; Ultraviolet radiation; Wind direction at 10 m height; Wind direction at 2 m height; Wind speed at 10 m height; Wind speed at 2 m height
  • Nature Publishing Group (NPG)  (5)
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  • 1
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    A comprehensive catalogue of somatic mutations from a human cancer genome (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-12-18
    Description: All cancers carry somatic mutations. A subset of these somatic alterations, termed driver mutations, confer selective growth advantage and are implicated in cancer development, whereas the remainder are passengers. Here we have sequenced the genomes of a malignant melanoma and a lymphoblastoid cell line from the same person, providing the first comprehensive catalogue of somatic mutations from an individual cancer. The catalogue provides remarkable insights into the forces that have shaped this cancer genome. The dominant mutational signature reflects DNA damage due to ultraviolet light exposure, a known risk factor for malignant melanoma, whereas the uneven distribution of mutations across the genome, with a lower prevalence in gene footprints, indicates that DNA repair has been preferentially deployed towards transcribed regions. The results illustrate the power of a cancer genome sequence to reveal traces of the DNA damage, repair, mutation and selection processes that were operative years before the cancer became symptomatic.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3145108/" 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/PMC3145108/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pleasance, Erin D -- Cheetham, R Keira -- Stephens, Philip J -- McBride, David J -- Humphray, Sean J -- Greenman, Chris D -- Varela, Ignacio -- Lin, Meng-Lay -- Ordonez, Gonzalo R -- Bignell, Graham R -- Ye, Kai -- Alipaz, Julie -- Bauer, Markus J -- Beare, David -- Butler, Adam -- Carter, Richard J -- Chen, Lina -- Cox, Anthony J -- Edkins, Sarah -- Kokko-Gonzales, Paula I -- Gormley, Niall A -- Grocock, Russell J -- Haudenschild, Christian D -- Hims, Matthew M -- James, Terena -- Jia, Mingming -- Kingsbury, Zoya -- Leroy, Catherine -- Marshall, John -- Menzies, Andrew -- Mudie, Laura J -- Ning, Zemin -- Royce, Tom -- Schulz-Trieglaff, Ole B -- Spiridou, Anastassia -- Stebbings, Lucy A -- Szajkowski, Lukasz -- Teague, Jon -- Williamson, David -- Chin, Lynda -- Ross, Mark T -- Campbell, Peter J -- Bentley, David R -- Futreal, P Andrew -- Stratton, Michael R -- 077012/Z/05/Z/Wellcome Trust/United Kingdom -- 088340/Wellcome Trust/United Kingdom -- 093867/Wellcome Trust/United Kingdom -- England -- Nature. 2010 Jan 14;463(7278):191-6. doi: 10.1038/nature08658. Epub 2009 Dec 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20016485" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Cell Line, Tumor ; DNA Damage/genetics ; DNA Mutational Analysis ; DNA Repair/genetics ; Gene Dosage/genetics ; Genes, Neoplasm/*genetics ; Genome, Human/*genetics ; Humans ; Loss of Heterozygosity/genetics ; Male ; Melanoma/etiology/genetics ; MicroRNAs/genetics ; Mutagenesis, Insertional/genetics ; Mutation/*genetics ; Neoplasms/etiology/*genetics ; Polymorphism, Single Nucleotide/genetics ; Precision Medicine ; Sequence Deletion/genetics ; Ultraviolet Rays
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    A trans-acting locus regulates an anti-viral expression network and type 1 diabetes risk (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-09-10
    Description: Combined analyses of gene networks and DNA sequence variation can provide new insights into the aetiology of common diseases that may not be apparent from genome-wide association studies alone. Recent advances in rat genomics are facilitating systems-genetics approaches. Here we report the use of integrated genome-wide approaches across seven rat tissues to identify gene networks and the loci underlying their regulation. We defined an interferon regulatory factor 7 (IRF7)-driven inflammatory network (IDIN) enriched for viral response genes, which represents a molecular biomarker for macrophages and which was regulated in multiple tissues by a locus on rat chromosome 15q25. We show that Epstein-Barr virus induced gene 2 (Ebi2, also known as Gpr183), which lies at this locus and controls B lymphocyte migration, is expressed in macrophages and regulates the IDIN. The human orthologous locus on chromosome 13q32 controlled the human equivalent of the IDIN, which was conserved in monocytes. IDIN genes were more likely to associate with susceptibility to type 1 diabetes (T1D)-a macrophage-associated autoimmune disease-than randomly selected immune response genes (P = 8.85 x 10(-6)). The human locus controlling the IDIN was associated with the risk of T1D at single nucleotide polymorphism rs9585056 (P = 7.0 x 10(-10); odds ratio, 1.15), which was one of five single nucleotide polymorphisms in this region associated with EBI2 (GPR183) expression. These data implicate IRF7 network genes and their regulatory locus in the pathogenesis of T1D.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3657719/" 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/PMC3657719/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heinig, Matthias -- Petretto, Enrico -- Wallace, Chris -- Bottolo, Leonardo -- Rotival, Maxime -- Lu, Han -- Li, Yoyo -- Sarwar, Rizwan -- Langley, Sarah R -- Bauerfeind, Anja -- Hummel, Oliver -- Lee, Young-Ae -- Paskas, Svetlana -- Rintisch, Carola -- Saar, Kathrin -- Cooper, Jason -- Buchan, Rachel -- Gray, Elizabeth E -- Cyster, Jason G -- Cardiogenics Consortium -- Erdmann, Jeanette -- Hengstenberg, Christian -- Maouche, Seraya -- Ouwehand, Willem H -- Rice, Catherine M -- Samani, Nilesh J -- Schunkert, Heribert -- Goodall, Alison H -- Schulz, Herbert -- Roider, Helge G -- Vingron, Martin -- Blankenberg, Stefan -- Munzel, Thomas -- Zeller, Tanja -- Szymczak, Silke -- Ziegler, Andreas -- Tiret, Laurence -- Smyth, Deborah J -- Pravenec, Michal -- Aitman, Timothy J -- Cambien, Francois -- Clayton, David -- Todd, John A -- Hubner, Norbert -- Cook, Stuart A -- 061858/Wellcome Trust/United Kingdom -- 076113/Wellcome Trust/United Kingdom -- 089989/Wellcome Trust/United Kingdom -- MC_U120061454/Medical Research Council/United Kingdom -- MC_U120085815/Medical Research Council/United Kingdom -- MC_U120097112/Medical Research Council/United Kingdom -- P301/10/0290/British Heart Foundation/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2010 Sep 23;467(7314):460-4. doi: 10.1038/nature09386. Epub 2010 Sep 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Delbruck-Center for Molecular Medicine (MDC), Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20827270" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Chromosomes, Human, Pair 13/genetics ; Chromosomes, Mammalian/genetics ; Diabetes Mellitus, Type 1/*genetics/immunology ; Gene Regulatory Networks/genetics ; Genetic Loci/*genetics ; Genetic Predisposition to Disease/*genetics ; Genome-Wide Association Study ; Humans ; Immunity, Innate/*genetics ; Inflammation/genetics/immunology ; Interferon Regulatory Factor-7/immunology ; Macrophages/immunology/metabolism ; Organ Specificity ; Polymorphism, Single Nucleotide/genetics ; Quantitative Trait Loci/genetics ; Rats ; Receptors, G-Protein-Coupled/genetics/metabolism ; Viruses/*immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    Human MX2 is an interferon-induced post-entry inhibitor of HIV-1 infection (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-09-21
    Description: Animal cells harbour multiple innate effector mechanisms that inhibit virus replication. For the pathogenic retrovirus human immunodeficiency virus type 1 (HIV-1), these include widely expressed restriction factors, such as APOBEC3 proteins, TRIM5-alpha, BST2 (refs 4, 5) and SAMHD1 (refs 6, 7), as well as additional factors that are stimulated by type 1 interferon (IFN). Here we use both ectopic expression and gene-silencing experiments to define the human dynamin-like, IFN-induced myxovirus resistance 2 (MX2, also known as MXB) protein as a potent inhibitor of HIV-1 infection and as a key effector of IFN-alpha-mediated resistance to HIV-1 infection. MX2 suppresses infection by all HIV-1 strains tested, has equivalent or reduced effects on divergent simian immunodeficiency viruses, and does not inhibit other retroviruses such as murine leukaemia virus. The Capsid region of the viral Gag protein dictates susceptibility to MX2, and the block to infection occurs at a late post-entry step, with both the nuclear accumulation and chromosomal integration of nascent viral complementary DNA suppressed. Finally, human MX1 (also known as MXA), a closely related protein that has long been recognized as a broadly acting inhibitor of RNA and DNA viruses, including the orthomyxovirus influenza A virus, does not affect HIV-1, whereas MX2 is ineffective against influenza virus. MX2 is therefore a cell-autonomous, anti-HIV-1 resistance factor whose purposeful mobilization may represent a new therapeutic approach for the treatment of HIV/AIDS.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3808269/" 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/PMC3808269/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goujon, Caroline -- Moncorge, Olivier -- Bauby, Helene -- Doyle, Tomas -- Ward, Christopher C -- Schaller, Torsten -- Hue, Stephane -- Barclay, Wendy S -- Schulz, Reiner -- Malim, Michael H -- 098850/Wellcome Trust/United Kingdom -- DA033773/DA/NIDA NIH HHS/ -- G1000196/Medical Research Council/United Kingdom -- G1001081/Medical Research Council/United Kingdom -- R01 DA033773/DA/NIDA NIH HHS/ -- Department of Health/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2013 Oct 24;502(7472):559-62. doi: 10.1038/nature12542. Epub 2013 Sep 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Infectious Diseases, King's College London, London SE1 9RT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24048477" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cell Nucleus/genetics/virology ; Cells, Cultured ; HIV Infections/immunology/metabolism/*prevention & control/*virology ; HIV-1/classification/enzymology/genetics/*physiology ; Humans ; Interferons/*immunology ; Myxovirus Resistance Proteins/deficiency/genetics/*metabolism ; RNA, Viral/biosynthesis/genetics/metabolism ; Reverse Transcription/genetics ; Species Specificity ; Substrate Specificity ; Virus Integration ; Virus Replication
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Intrinsic honesty and the prevalence of rule violations across societies (2016)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2016-03-10
    Description: Deception is common in nature and humans are no exception. Modern societies have created institutions to control cheating, but many situations remain where only intrinsic honesty keeps people from cheating and violating rules. Psychological, sociological and economic theories suggest causal pathways to explain how the prevalence of rule violations in people's social environment, such as corruption, tax evasion or political fraud, can compromise individual intrinsic honesty. Here we present cross-societal experiments from 23 countries around the world that demonstrate a robust link between the prevalence of rule violations and intrinsic honesty. We developed an index of the 'prevalence of rule violations' (PRV) based on country-level data from the year 2003 of corruption, tax evasion and fraudulent politics. We measured intrinsic honesty in an anonymous die-rolling experiment. We conducted the experiments with 2,568 young participants (students) who, due to their young age in 2003, could not have influenced PRV in 2003. We find individual intrinsic honesty is stronger in the subject pools of low PRV countries than those of high PRV countries. The details of lying patterns support psychological theories of honesty. The results are consistent with theories of the cultural co-evolution of institutions and values, and show that weak institutions and cultural legacies that generate rule violations not only have direct adverse economic consequences, but might also impair individual intrinsic honesty that is crucial for the smooth functioning of society.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4817241/" 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/PMC4817241/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gachter, Simon -- Schulz, Jonathan F -- England -- Nature. 2016 Mar 24;531(7595):496-9. doi: 10.1038/nature17160. Epub 2016 Mar 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Nottingham, University Park, Nottingham NG7 2RD, UK. ; CESifo, Schackstrasse 4, 80539 Munich, Germany. ; IZA, Schaumburg-Lippe-Strasse 5-9, 53113 Bonn, Germany. ; Yale University, 1 Prospect Street, New Haven, Connecticut 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26958830" target="_blank"〉PubMed〈/a〉
    Keywords: Cultural Evolution ; *Deception ; Female ; Fraud/statistics & numerical data ; Humans ; *Internationality ; Male ; Models, Psychological ; Politics ; *Societies/economics ; Students/*psychology ; Taxes/statistics & numerical data ; *Virtues ; Young Adult
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Improving survival by exploiting tumour dependence on stabilized mutant p53 for treatment (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-05-27
    Description: Missense mutations in p53 generate aberrant proteins with abrogated tumour suppressor functions that can also acquire oncogenic gain-of-function activities that promote malignant progression, invasion, metastasis and chemoresistance. Mutant p53 (mutp53) proteins undergo massive constitutive stabilization specifically in tumours, which is the key requisite for the acquisition of gain-of-functions activities. Although currently 11 million patients worldwide live with tumours expressing highly stabilized mutp53, it is unknown whether mutp53 is a therapeutic target in vivo. Here we use a novel mutp53 mouse model expressing an inactivatable R248Q hotspot mutation (floxQ) to show that tumours depend on sustained mutp53 expression. Upon tamoxifen-induced mutp53 ablation, allotransplanted and autochthonous tumours curb their growth, thus extending animal survival by 37%, and advanced tumours undergo apoptosis and tumour regression or stagnation. The HSP90/HDAC6 chaperone machinery, which is significantly upregulated in cancer compared with normal tissues, is a major determinant of mutp53 stabilization. We show that long-term HSP90 inhibition significantly extends the survival of mutp53 Q/- (R248Q allele) and H/H (R172H allele) mice by 59% and 48%, respectively, but not their corresponding p53(-/-) littermates. This mutp53-dependent drug effect occurs in H/H mice treated with 17DMAG+SAHA and in H/H and Q/- mice treated with the potent Hsp90 inhibitor ganetespib. Notably, drug activity correlates with induction of mutp53 degradation, tumour apoptosis and prevention of T-cell lymphomagenesis. These proof-of-principle data identify mutp53 as an actionable cancer-specific drug target.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4506213/" 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/PMC4506213/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alexandrova, E M -- Yallowitz, A R -- Li, D -- Xu, S -- Schulz, R -- Proia, D A -- Lozano, G -- Dobbelstein, M -- Moll, U M -- 1R01CA176647/CA/NCI NIH HHS/ -- P30 CA016672/CA/NCI NIH HHS/ -- R01 CA176647/CA/NCI NIH HHS/ -- T32 HD007505/HD/NICHD NIH HHS/ -- England -- Nature. 2015 Jul 16;523(7560):352-6. doi: 10.1038/nature14430. Epub 2015 May 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Stony Brook University, Stony Brook, New York 11794, USA. ; Institute of Molecular Oncology, University of Gottingen, 37077 Gottingen, Germany. ; Synta Pharmaceuticals Corp., Lexington, Massachusetts 02421, USA. ; Department of Cancer Genetics, University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA. ; 1] Department of Pathology, Stony Brook University, Stony Brook, New York 11794, USA [2] Institute of Molecular Oncology, University of Gottingen, 37077 Gottingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26009011" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Allografts ; Animals ; Apoptosis/drug effects ; Cell Line, Tumor ; Disease Models, Animal ; Female ; HSP90 Heat-Shock Proteins/antagonists & inhibitors/metabolism ; Histone Deacetylases/metabolism ; Humans ; Lymphoma/*drug therapy/genetics/*metabolism/pathology ; Male ; Mice ; Molecular Targeted Therapy/*methods ; Mutant Proteins/*antagonists & inhibitors/genetics/metabolism ; Neoplasm Transplantation ; *Protein Stability/drug effects ; Survival Rate ; Tamoxifen/pharmacology/therapeutic use ; Triazoles/pharmacology/therapeutic use ; Tumor Suppressor Protein p53/*antagonists & inhibitors/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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