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  • Articles  (12)
  • Nature Publishing Group (NPG)  (8)
  • Institute of Physics  (4)
  • American Geophysical Union
  • 2010-2014  (12)
  • Biology  (12)
  • Medicine  (12)
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  • Articles  (12)
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  • 1
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    Evaluation of the deformation and corresponding dosimetric implications in prostate cancer treatment (2012)
    Institute of Physics
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    Publication Date: 2012-08-03
    Print ISSN: 0031-9155
    Electronic ISSN: 1361-6560
    Topics: Biology , Medicine , Physics
    Published by Institute of Physics
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  • 2
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    Direct dose mapping versus energy/mass transfer mapping for 4D dose accumulation: fundamental differences and dosimetric consequences (2013)
    Institute of Physics
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    Publication Date: 2013-12-13
    Print ISSN: 0031-9155
    Electronic ISSN: 1361-6560
    Topics: Biology , Medicine , Physics
    Published by Institute of Physics
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  • 3
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    Voxel-based statistical analysis of uncertainties associated with deformable image registration (2013)
    Institute of Physics
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    Publication Date: 2013-09-03
    Print ISSN: 0031-9155
    Electronic ISSN: 1361-6560
    Topics: Biology , Medicine , Physics
    Published by Institute of Physics
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  • 4
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    Molecular genetics: The sound of silence (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-04-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hurst, Laurence D -- England -- Nature. 2011 Mar 31;471(7340):582-3. doi: 10.1038/471582a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21455166" target="_blank"〉PubMed〈/a〉
    Keywords: Continental Population Groups/genetics ; Crohn Disease/*genetics ; Humans ; MicroRNAs/*genetics/metabolism ; Models, Genetic ; Point Mutation/*genetics ; RNA Splicing/genetics ; RNA, Messenger/*genetics/metabolism
    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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  • 5
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    Mitochondrial Atpif1 regulates haem synthesis in developing erythroblasts (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-11-09
    Description: Defects in the availability of haem substrates or the catalytic activity of the terminal enzyme in haem biosynthesis, ferrochelatase (Fech), impair haem synthesis and thus cause human congenital anaemias. The interdependent functions of regulators of mitochondrial homeostasis and enzymes responsible for haem synthesis are largely unknown. To investigate this we used zebrafish genetic screens and cloned mitochondrial ATPase inhibitory factor 1 (atpif1) from a zebrafish mutant with profound anaemia, pinotage (pnt (tq209)). Here we describe a direct mechanism establishing that Atpif1 regulates the catalytic efficiency of vertebrate Fech to synthesize haem. The loss of Atpif1 impairs haemoglobin synthesis in zebrafish, mouse and human haematopoietic models as a consequence of diminished Fech activity and elevated mitochondrial pH. To understand the relationship between mitochondrial pH, redox potential, [2Fe-2S] clusters and Fech activity, we used genetic complementation studies of Fech constructs with or without [2Fe-2S] clusters in pnt, as well as pharmacological agents modulating mitochondrial pH and redox potential. The presence of [2Fe-2S] cluster renders vertebrate Fech vulnerable to perturbations in Atpif1-regulated mitochondrial pH and redox potential. Therefore, Atpif1 deficiency reduces the efficiency of vertebrate Fech to synthesize haem, resulting in anaemia. The identification of mitochondrial Atpif1 as a regulator of haem synthesis advances our understanding of the mechanisms regulating mitochondrial haem homeostasis and red blood cell development. An ATPIF1 deficiency may contribute to important human diseases, such as congenital sideroblastic anaemias and mitochondriopathies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3504625/" 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/PMC3504625/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shah, Dhvanit I -- Takahashi-Makise, Naoko -- Cooney, Jeffrey D -- Li, Liangtao -- Schultz, Iman J -- Pierce, Eric L -- Narla, Anupama -- Seguin, Alexandra -- Hattangadi, Shilpa M -- Medlock, Amy E -- Langer, Nathaniel B -- Dailey, Tamara A -- Hurst, Slater N -- Faccenda, Danilo -- Wiwczar, Jessica M -- Heggers, Spencer K -- Vogin, Guillaume -- Chen, Wen -- Chen, Caiyong -- Campagna, Dean R -- Brugnara, Carlo -- Zhou, Yi -- Ebert, Benjamin L -- Danial, Nika N -- Fleming, Mark D -- Ward, Diane M -- Campanella, Michelangelo -- Dailey, Harry A -- Kaplan, Jerry -- Paw, Barry H -- K01 DK085217/DK/NIDDK NIH HHS/ -- P01 HL032262/HL/NHLBI NIH HHS/ -- P30 DK072437/DK/NIDDK NIH HHS/ -- R01 DK052380/DK/NIDDK NIH HHS/ -- R01 DK070838/DK/NIDDK NIH HHS/ -- R01 DK096051/DK/NIDDK NIH HHS/ -- R01 HL082945/HL/NHLBI NIH HHS/ -- T32 GM007223/GM/NIGMS NIH HHS/ -- England -- Nature. 2012 Nov 22;491(7425):608-12. doi: 10.1038/nature11536. Epub 2012 Nov 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Division of Hematology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23135403" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Sideroblastic/genetics/metabolism/pathology ; Animals ; Disease Models, Animal ; Erythroblasts/cytology/*metabolism ; *Erythropoiesis ; Ferrochelatase/metabolism ; Genetic Complementation Test ; Heme/*biosynthesis ; Humans ; Hydrogen-Ion Concentration ; Mice ; Mitochondria/*metabolism/pathology ; Mitochondrial Proteins/deficiency/genetics/*metabolism ; Oxidation-Reduction ; Proteins/genetics/*metabolism ; Zebrafish/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    Primate-specific endogenous retrovirus-driven transcription defines naive-like stem cells (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-10-16
    Description: Naive embryonic stem cells hold great promise for research and therapeutics as they have broad and robust developmental potential. While such cells are readily derived from mouse blastocysts it has not been possible to isolate human equivalents easily, although human naive-like cells have been artificially generated (rather than extracted) by coercion of human primed embryonic stem cells by modifying culture conditions or through transgenic modification. Here we show that a sub-population within cultures of human embryonic stem cells (hESCs) and induced pluripotent stem cells (hiPSCs) manifests key properties of naive state cells. These naive-like cells can be genetically tagged, and are associated with elevated transcription of HERVH, a primate-specific endogenous retrovirus. HERVH elements provide functional binding sites for a combination of naive pluripotency transcription factors, including LBP9, recently recognized as relevant to naivety in mice. LBP9-HERVH drives hESC-specific alternative and chimaeric transcripts, including pluripotency-modulating long non-coding RNAs. Disruption of LBP9, HERVH and HERVH-derived transcripts compromises self-renewal. These observations define HERVH expression as a hallmark of naive-like hESCs, and establish novel primate-specific transcriptional circuitry regulating pluripotency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Jichang -- Xie, Gangcai -- Singh, Manvendra -- Ghanbarian, Avazeh T -- Rasko, Tamas -- Szvetnik, Attila -- Cai, Huiqiang -- Besser, Daniel -- Prigione, Alessandro -- Fuchs, Nina V -- Schumann, Gerald G -- Chen, Wei -- Lorincz, Matthew C -- Ivics, Zoltan -- Hurst, Laurence D -- Izsvak, Zsuzsanna -- England -- Nature. 2014 Dec 18;516(7531):405-9. doi: 10.1038/nature13804. Epub 2014 Oct 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Delbruck-Center for Molecular Medicine, Robert-Rossle-Strasse 10, 13125 Berlin, Germany. ; 1] Max-Delbruck-Center for Molecular Medicine, Robert-Rossle-Strasse 10, 13125 Berlin, Germany [2] Key Laboratory of Computational Biology, CAS-MPG Partner Institute for Computational Biology, 320 Yueyang Road, Shanghai 200031, China. ; University of Bath, Department of Biology and Biochemistry, Bath, Somerset BA2 7AY, UK. ; 1] Max-Delbruck-Center for Molecular Medicine, Robert-Rossle-Strasse 10, 13125 Berlin, Germany [2] Paul-Ehrlich-Institute, Division of Medical Biotechnology, Paul-Ehrlich-Strasse 51-59, 63225 Langen, Germany. ; Paul-Ehrlich-Institute, Division of Medical Biotechnology, Paul-Ehrlich-Strasse 51-59, 63225 Langen, Germany. ; Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25317556" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; DNA Transposable Elements ; Embryonic Stem Cells/*cytology/*metabolism ; Endogenous Retroviruses/genetics/*metabolism ; Gene Expression Profiling ; Genetic Markers ; Humans ; Induced Pluripotent Stem Cells/cytology/*physiology/virology ; RNA, Long Noncoding/metabolism ; Transcription Factors/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Metabolic trade-offs and the maintenance of the fittest and the flattest (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-03-29
    Description: How is diversity maintained? Environmental heterogeneity is considered to be important, yet diversity in seemingly homogeneous environments is nonetheless observed. This, it is assumed, must either be owing to weak selection, mutational input or a fitness advantage to genotypes when rare. Here we demonstrate the possibility of a new general mechanism of stable diversity maintenance, one that stems from metabolic and physiological trade-offs. The model requires that such trade-offs translate into a fitness landscape in which the most fit has unfit near-mutational neighbours, and a lower fitness peak also exists that is more mutationally robust. The 'survival of the fittest' applies at low mutation rates, giving way to 'survival of the flattest' at high mutation rates. However, as a consequence of quasispecies-level negative frequency-dependent selection and differences in mutational robustness we observe a transition zone in which both fittest and flattest coexist. Although diversity maintenance is possible for simple organisms in simple environments, the more trade-offs there are, the wider the maintenance zone becomes. The principle may be applied to lineages within a species or species within a community, potentially explaining why competitive exclusion need not be observed in homogeneous environments. This principle predicts the enigmatic richness of metabolic strategies in clonal bacteria and questions the safety of lethal mutagenesis as an antimicrobial treatment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beardmore, Robert E -- Gudelj, Ivana -- Lipson, David A -- Hurst, Laurence D -- G0802611/Medical Research Council/United Kingdom -- England -- Nature. 2011 Apr 21;472(7343):342-6. doi: 10.1038/nature09905. Epub 2011 Mar 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Mathematics, Imperial College London, Huxley Building, 180 Queen's Gate, London SW7 2A7, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21441905" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Biological/genetics ; *Biodiversity ; *Biological Evolution ; *Genetic Fitness/genetics ; Genotype ; Metabolism/*genetics ; *Models, Biological ; Models, Genetic ; Mutagenesis/genetics ; Saccharomyces cerevisiae ; *Selection, Genetic/genetics ; Stochastic Processes
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Distinct physiological and behavioural functions for parental alleles of imprinted Grb10 (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-01-29
    Description: Imprinted genes, defined by their preferential expression of a single parental allele, represent a subset of the mammalian genome and often have key roles in embryonic development, but also postnatal functions including energy homeostasis and behaviour. When the two parental alleles are unequally represented within a social group (when there is sex bias in dispersal and/or variance in reproductive success), imprinted genes may evolve to modulate social behaviour, although so far no such instance is known. Predominantly expressed from the maternal allele during embryogenesis, Grb10 encodes an intracellular adaptor protein that can interact with several receptor tyrosine kinases and downstream signalling molecules. Here we demonstrate that within the brain Grb10 is expressed from the paternal allele from fetal life into adulthood and that ablation of this expression engenders increased social dominance specifically among other aspects of social behaviour, a finding supported by the observed increase in allogrooming by paternal Grb10-deficient animals. Grb10 is, therefore, the first example of an imprinted gene that regulates social behaviour. It is also currently alone in exhibiting imprinted expression from each of the parental alleles in a tissue-specific manner, as loss of the peripherally expressed maternal allele leads to significant fetal and placental overgrowth. Thus Grb10 is, so far, a unique imprinted gene, able to influence distinct physiological processes, fetal growth and adult behaviour, owing to actions of the two parental alleles in different tissues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3031026/" 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/PMC3031026/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garfield, Alastair S -- Cowley, Michael -- Smith, Florentia M -- Moorwood, Kim -- Stewart-Cox, Joanne E -- Gilroy, Kerry -- Baker, Sian -- Xia, Jing -- Dalley, Jeffrey W -- Hurst, Laurence D -- Wilkinson, Lawrence S -- Isles, Anthony R -- Ward, Andrew -- 093875/Wellcome Trust/United Kingdom -- G0300415/Medical Research Council/United Kingdom -- G0300415(66812)/Medical Research Council/United Kingdom -- G11786/Biotechnology and Biological Sciences Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2011 Jan 27;469(7331):534-8. doi: 10.1038/nature09651.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology & Biochemistry and Centre for Regenerative Medicine, University of Bath, Claverton Down, Bath BA2 7AY, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21270893" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Animals ; Behavior, Animal/*physiology ; Central Nervous System/embryology ; Female ; GRB10 Adaptor Protein/*genetics/*metabolism ; Gene Expression Regulation, Developmental ; Genomic Imprinting/*genetics ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mutation ; Social Dominance
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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    The BC component of ABC toxins is an RHS-repeat-containing protein encapsulation device (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-08-06
    Description: The ABC toxin complexes produced by certain bacteria are of interest owing to their potent insecticidal activity and potential role in human disease. These complexes comprise at least three proteins (A, B and C), which must assemble to be fully toxic. The carboxy-terminal region of the C protein is the main cytotoxic component, and is poorly conserved between different toxin complexes. A general model of action has been proposed, in which the toxin complex binds to the cell surface via the A protein, is endocytosed, and subsequently forms a pH-triggered channel, allowing the translocation of C into the cytoplasm, where it can cause cytoskeletal disruption in both insect and mammalian cells. Toxin complexes have been visualized using single-particle electron microscopy, but no high-resolution structures of the components are available, and the role of the B protein in the mechanism of toxicity remains unknown. Here we report the three-dimensional structure of the complex formed between the B and C proteins, determined to 2.5 A by X-ray crystallography. These proteins assemble to form an unprecedented, large hollow structure that encapsulates and sequesters the cytotoxic, C-terminal region of the C protein like the shell of an egg. The shell is decorated on one end by a beta-propeller domain, which mediates attachment of the B-C heterodimer to the A protein in the native complex. The structure reveals how C auto-proteolyses when folded in complex with B. The C protein is the first example, to our knowledge, of a structure that contains rearrangement hotspot (RHS) repeats, and illustrates a marked structural architecture that is probably conserved across both this widely distributed bacterial protein family and the related eukaryotic tyrosine-aspartate (YD)-repeat-containing protein family, which includes the teneurins. The structure provides the first clues about the function of these protein repeat families, and suggests a generic mechanism for protein encapsulation and delivery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Busby, Jason N -- Panjikar, Santosh -- Landsberg, Michael J -- Hurst, Mark R H -- Lott, J Shaun -- England -- Nature. 2013 Sep 26;501(7468):547-50. doi: 10.1038/nature12465. Epub 2013 Aug 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉AgResearch Structural Biology Laboratory, School of Biological Sciences, The University of Auckland, Auckland 1142, New Zealand.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23913273" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Bacterial Toxins/*chemistry/metabolism ; Consensus Sequence ; Conserved Sequence ; Crystallography, X-Ray ; Insecticides/chemistry ; Models, Molecular ; Molecular Sequence Data ; Protein Subunits/chemistry/metabolism ; Proteolysis ; *Repetitive Sequences, Amino Acid ; Yersinia/*chemistry
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
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    Evolutionary biology: A gut feeling for isolation (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-08-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hurst, Gregory D D -- Jiggins, Chris D -- England -- Nature. 2013 Aug 22;500(7463):412-3. doi: 10.1038/500412a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23969458" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteria/*classification ; Gastrointestinal Tract/*microbiology ; Germ-Free Life/*physiology ; Hymenoptera/*microbiology/*physiology ; *Symbiosis
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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