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  • Animals  (23)
  • Female  (11)
  • Nuclear Structure  (6)
  • 2010-2014  (21)
  • 1980-1984  (11)
  • 1
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    Isobaric multiplet mass equation for A=7 and 8 (2011)
    American Physical Society (APS)
    Details
    Publication Date: 2011-11-19
    Description: Author(s): R. J. Charity, J. M. Elson, J. Manfredi, R. Shane, L. G. Sobotka, Z. Chajecki, D. Coupland, H. Iwasaki, M. Kilburn, J. Lee, W. G. Lynch, A. Sanetullaev, M. B. Tsang, J. Winkelbauer, M. Youngs, S. T. Marley, D. V. Shetty, A. H. Wuosmaa, T. K. Ghosh, and M. E. Howard [Phys. Rev. C 84, 051308] Published Fri Nov 18, 2011
    Keywords: Nuclear Structure
    Print ISSN: 0556-2813
    Electronic ISSN: 1089-490X
    Topics: Physics
    Published by American Physical Society (APS)
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  • 2
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    Investigations of three-, four-, and five-particle decay channels of levels in light nuclei created using a ^{9}C beam (2011)
    American Physical Society (APS)
    Details
    Publication Date: 2011-07-21
    Description: Author(s): R. J. Charity, J. M. Elson, J. Manfredi, R. Shane, L. G. Sobotka, B. A. Brown, Z. Chajecki, D. Coupland, H. Iwasaki, M. Kilburn, Jenny Lee, W. G. Lynch, A. Sanetullaev, M. B. Tsang, J. Winkelbauer, M. Youngs, S. T. Marley, D. V. Shetty, A. H. Wuosmaa, T. K. Ghosh, and M. E. Howard The interactions of an E / A =70 -MeV 9 C beam with a Be target was used to populate levels in Be, B, and C isotopes, which undergo decay into many-particle exit channels. The decay products were detected in the HiRA array and the level energies were identified from their invariant mass. Correlations bet... [Phys. Rev. C 84, 014320] Published Wed Jul 20, 2011
    Keywords: Nuclear Structure
    Print ISSN: 0556-2813
    Electronic ISSN: 1089-490X
    Topics: Physics
    Published by American Physical Society (APS)
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  • 3
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    Two-proton decay from the isobaric analog state in B8 (2014)
    American Physical Society (APS)
    Details
    Publication Date: 2014-08-22
    Description: Author(s): K. W. Brown, W. W. Buhro, R. J. Charity, J. M. Elson, W. Reviol, L. G. Sobotka, Z. Chajecki, W. G. Lynch, J. Manfredi, R. Shane, R. H. Showalter, M. B. Tsang, D. Weisshaar, J. R. Winkelbauer, S. Bedoor, and A. H. Wuosmaa The isobaric analog state (IAS) in B8 is confirmed to decay by two-proton emission to the isobaric analog state in Li6, which emits a 3.563 MeV γ ray. Upper limits on the yield to isospin breaking decay channels are also reported. The three-body correlations from the two-proton decay from B8IAS to L... [Phys. Rev. C 90, 027304] Published Thu Aug 21, 2014
    Keywords: Nuclear Structure
    Print ISSN: 0556-2813
    Electronic ISSN: 1089-490X
    Topics: Physics
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  • 4
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    Chemoprevention of colorectal cancer by targeting APC-deficient cells for apoptosis (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-03-30
    Description: Cancer chemoprevention uses natural, synthetic, or biological substances to reverse, suppress, or prevent either the initial phase of carcinogenesis or the progression of neoplastic cells to cancer. It holds promise for overcoming problems associated with the treatment of late-stage cancers. However, the broad application of chemoprevention is compromised at present by limited effectiveness and potential toxicity. To overcome these challenges, here we developed a new chemoprevention approach that specifically targets premalignant tumour cells for apoptosis. We show that a deficiency in the adenomatous polyposis coli (APC) gene and subsequent activation of beta-catenin lead to the repression of cellular caspase-8 inhibitor c-FLIP (also known as CFLAR) expression through activation of c-Myc, and that all-trans-retinyl acetate (RAc) independently upregulates tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) death receptors and suppresses decoy receptors. Thus, the combination of TRAIL and RAc induces apoptosis in APC-deficient premalignant cells without affecting normal cells in vitro. In addition, we show that short-term and non-continuous TRAIL and RAc treatment induce apoptosis specifically in intestinal polyps, strongly inhibit tumour growth, and prolong survival in multiple intestinal neoplasms C57BL/6J-Apc(Min)/J (Apc(Min)) mice. With our approach, we further demonstrate that TRAIL and RAc induce significant cell death in human colon polyps, providing a potentially selective approach for colorectal cancer chemoprevention by targeting APC-deficient cells for apoptosis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3425353/" 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/PMC3425353/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Ling -- Ren, Xiaoyang -- Alt, Eckhard -- Bai, Xiaowen -- Huang, Shaoyi -- Xu, Zhengming -- Lynch, Patrick M -- Moyer, Mary P -- Wen, Xian-Feng -- Wu, Xiangwei -- AI063063/AI/NIAID NIH HHS/ -- R01 AI063063/AI/NIAID NIH HHS/ -- England -- Nature. 2010 Apr 15;464(7291):1058-61. doi: 10.1038/nature08871. Epub 2010 Mar 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Head and Neck Surgery, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20348907" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein/*deficiency/genetics ; Animals ; Apoptosis/*drug effects ; CASP8 and FADD-Like Apoptosis Regulating Protein/metabolism ; Cell Proliferation/drug effects ; Colorectal Neoplasms/genetics/metabolism/*pathology/*prevention & control ; Gene Expression Regulation/drug effects ; Genes, APC ; Humans ; Intestinal Polyps/drug therapy/pathology ; Mice ; Mice, Inbred C57BL ; Precancerous Conditions/drug therapy/genetics/metabolism/pathology ; Proto-Oncogene Proteins c-myc/metabolism ; Receptors, TNF-Related Apoptosis-Inducing Ligand/metabolism ; Signal Transduction/drug effects ; Survival Rate ; TNF-Related Apoptosis-Inducing Ligand/administration & ; dosage/pharmacology/therapeutic use ; Time Factors ; Vitamin A/administration & dosage/*analogs & derivatives/pharmacology/therapeutic ; use ; beta Catenin/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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    Functional and evolutionary insights from the genomes of three parasitoid Nasonia species (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-16
    Description: We report here genome sequences and comparative analyses of three closely related parasitoid wasps: Nasonia vitripennis, N. giraulti, and N. longicornis. Parasitoids are important regulators of arthropod populations, including major agricultural pests and disease vectors, and Nasonia is an emerging genetic model, particularly for evolutionary and developmental genetics. Key findings include the identification of a functional DNA methylation tool kit; hymenopteran-specific genes including diverse venoms; lateral gene transfers among Pox viruses, Wolbachia, and Nasonia; and the rapid evolution of genes involved in nuclear-mitochondrial interactions that are implicated in speciation. Newly developed genome resources advance Nasonia for genetic research, accelerate mapping and cloning of quantitative trait loci, and will ultimately provide tools and knowledge for further increasing the utility of parasitoids as pest insect-control agents.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2849982/" 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/PMC2849982/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Werren, John H -- Richards, Stephen -- Desjardins, Christopher A -- Niehuis, Oliver -- Gadau, Jurgen -- Colbourne, John K -- Nasonia Genome Working Group -- Beukeboom, Leo W -- Desplan, Claude -- Elsik, Christine G -- Grimmelikhuijzen, Cornelis J P -- Kitts, Paul -- Lynch, Jeremy A -- Murphy, Terence -- Oliveira, Deodoro C S G -- Smith, Christopher D -- van de Zande, Louis -- Worley, Kim C -- Zdobnov, Evgeny M -- Aerts, Maarten -- Albert, Stefan -- Anaya, Victor H -- Anzola, Juan M -- Barchuk, Angel R -- Behura, Susanta K -- Bera, Agata N -- Berenbaum, May R -- Bertossa, Rinaldo C -- Bitondi, Marcia M G -- Bordenstein, Seth R -- Bork, Peer -- Bornberg-Bauer, Erich -- Brunain, Marleen -- Cazzamali, Giuseppe -- Chaboub, Lesley -- Chacko, Joseph -- Chavez, Dean -- Childers, Christopher P -- Choi, Jeong-Hyeon -- Clark, Michael E -- Claudianos, Charles -- Clinton, Rochelle A -- Cree, Andrew G -- Cristino, Alexandre S -- Dang, Phat M -- Darby, Alistair C -- de Graaf, Dirk C -- Devreese, Bart -- Dinh, Huyen H -- Edwards, Rachel -- Elango, Navin -- Elhaik, Eran -- Ermolaeva, Olga -- Evans, Jay D -- Foret, Sylvain -- Fowler, Gerald R -- Gerlach, Daniel -- Gibson, Joshua D -- Gilbert, Donald G -- Graur, Dan -- Grunder, Stefan -- Hagen, Darren E -- Han, Yi -- Hauser, Frank -- Hultmark, Da -- Hunter, Henry C 4th -- Hurst, Gregory D D -- Jhangian, Shalini N -- Jiang, Huaiyang -- Johnson, Reed M -- Jones, Andrew K -- Junier, Thomas -- Kadowaki, Tatsuhiko -- Kamping, Albert -- Kapustin, Yuri -- Kechavarzi, Bobak -- Kim, Jaebum -- Kim, Jay -- Kiryutin, Boris -- Koevoets, Tosca -- Kovar, Christie L -- Kriventseva, Evgenia V -- Kucharski, Robert -- Lee, Heewook -- Lee, Sandra L -- Lees, Kristin -- Lewis, Lora R -- Loehlin, David W -- Logsdon, John M Jr -- Lopez, Jacqueline A -- Lozado, Ryan J -- Maglott, Donna -- Maleszka, Ryszard -- Mayampurath, Anoop -- Mazur, Danielle J -- McClure, Marcella A -- Moore, Andrew D -- Morgan, Margaret B -- Muller, Jean -- Munoz-Torres, Monica C -- Muzny, Donna M -- Nazareth, Lynne V -- Neupert, Susanne -- Nguyen, Ngoc B -- Nunes, Francis M F -- Oakeshott, John G -- Okwuonu, Geoffrey O -- Pannebakker, Bart A -- Pejaver, Vikas R -- Peng, Zuogang -- Pratt, Stephen C -- Predel, Reinhard -- Pu, Ling-Ling -- Ranson, Hilary -- Raychoudhury, Rhitoban -- Rechtsteiner, Andreas -- Reese, Justin T -- Reid, Jeffrey G -- Riddle, Megan -- Robertson, Hugh M -- Romero-Severson, Jeanne -- Rosenberg, Miriam -- Sackton, Timothy B -- Sattelle, David B -- Schluns, Helge -- Schmitt, Thomas -- Schneider, Martina -- Schuler, Andreas -- Schurko, Andrew M -- Shuker, David M -- Simoes, Zila L P -- Sinha, Saurabh -- Smith, Zachary -- Solovyev, Victor -- Souvorov, Alexandre -- Springauf, Andreas -- Stafflinger, Elisabeth -- Stage, Deborah E -- Stanke, Mario -- Tanaka, Yoshiaki -- Telschow, Arndt -- Trent, Carol -- Vattathil, Selina -- Verhulst, Eveline C -- Viljakainen, Lumi -- Wanner, Kevin W -- Waterhouse, Robert M -- Whitfield, James B -- Wilkes, Timothy E -- Williamson, Michael -- Willis, Judith H -- Wolschin, Florian -- Wyder, Stefan -- Yamada, Takuji -- Yi, Soojin V -- Zecher, Courtney N -- Zhang, Lan -- Gibbs, Richard A -- 5R01GM070026-04/GM/NIGMS NIH HHS/ -- 5R01HG000747-14/HG/NHGRI NIH HHS/ -- 5R24GM084917-02/GM/NIGMS NIH HHS/ -- AI028309-13A2/AI/NIAID NIH HHS/ -- R01 AI055624/AI/NIAID NIH HHS/ -- R01 GM064864/GM/NIGMS NIH HHS/ -- R01 GM064864-04/GM/NIGMS NIH HHS/ -- R01 GM064864-05A2/GM/NIGMS NIH HHS/ -- R01 GM070026/GM/NIGMS NIH HHS/ -- R01 GM070026-04S1/GM/NIGMS NIH HHS/ -- R01 GM079484/GM/NIGMS NIH HHS/ -- R01 GM085163/GM/NIGMS NIH HHS/ -- R01 GM085163-01/GM/NIGMS NIH HHS/ -- R01 GM085233/GM/NIGMS NIH HHS/ -- R01 HG000747/HG/NHGRI NIH HHS/ -- R01 HG000747-14/HG/NHGRI NIH HHS/ -- R01GM064864/GM/NIGMS NIH HHS/ -- R24 GM084917/GM/NIGMS NIH HHS/ -- R24 GM084917-01/GM/NIGMS NIH HHS/ -- R24 GM084917-02/GM/NIGMS NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- U54 HG003273-03/HG/NHGRI NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Jan 15;327(5963):343-8. doi: 10.1126/science.1178028.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20075255" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthropods/parasitology ; *Biological Evolution ; DNA Methylation ; DNA Transposable Elements ; Female ; Gene Transfer, Horizontal ; Genes, Insect ; Genetic Speciation ; Genetic Variation ; *Genome, Insect ; Host-Parasite Interactions ; Insect Proteins/genetics/metabolism ; Insect Viruses/genetics ; Insects/genetics ; Male ; Molecular Sequence Data ; Quantitative Trait Loci ; Recombination, Genetic ; Sequence Analysis, DNA ; Wasp Venoms/chemistry/toxicity ; Wasps/*genetics/physiology ; Wolbachia/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 6
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    Hsp72 preserves muscle function and slows progression of severe muscular dystrophy (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-04-13
    Description: Duchenne muscular dystrophy (DMD) is a severe and progressive muscle wasting disorder caused by mutations in the dystrophin gene that result in the absence of the membrane-stabilizing protein dystrophin. Dystrophin-deficient muscle fibres are fragile and susceptible to an influx of Ca(2+), which activates inflammatory and muscle degenerative pathways. At present there is no cure for DMD, and existing therapies are ineffective. Here we show that increasing the expression of intramuscular heat shock protein 72 (Hsp72) preserves muscle strength and ameliorates the dystrophic pathology in two mouse models of muscular dystrophy. Treatment with BGP-15 (a pharmacological inducer of Hsp72 currently in clinical trials for diabetes) improved muscle architecture, strength and contractile function in severely affected diaphragm muscles in mdx dystrophic mice. In dko mice, a phenocopy of DMD that results in severe spinal curvature (kyphosis), muscle weakness and premature death, BGP-15 decreased kyphosis, improved the dystrophic pathophysiology in limb and diaphragm muscles and extended lifespan. We found that the sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase (SERCA, the main protein responsible for the removal of intracellular Ca(2+)) is dysfunctional in severely affected muscles of mdx and dko mice, and that Hsp72 interacts with SERCA to preserve its function under conditions of stress, ultimately contributing to the decreased muscle degeneration seen with Hsp72 upregulation. Treatment with BGP-15 similarly increased SERCA activity in dystrophic skeletal muscles. Our results provide evidence that increasing the expression of Hsp72 in muscle (through the administration of BGP-15) has significant therapeutic potential for DMD and related conditions, either as a self-contained therapy or as an adjuvant with other potential treatments, including gene, cell and pharmacological therapies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gehrig, Stefan M -- van der Poel, Chris -- Sayer, Timothy A -- Schertzer, Jonathan D -- Henstridge, Darren C -- Church, Jarrod E -- Lamon, Severine -- Russell, Aaron P -- Davies, Kay E -- Febbraio, Mark A -- Lynch, Gordon S -- GTB07001/Telethon/Italy -- MC_U137761449/Medical Research Council/United Kingdom -- England -- Nature. 2012 Apr 4;484(7394):394-8. doi: 10.1038/nature10980.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basic and Clinical Myology Laboratory, Department of Physiology, University of Melbourne, Victoria, 3010, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22495301" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium-Transporting ATPases/metabolism ; Diaphragm/drug effects/physiology ; Disease Models, Animal ; *Disease Progression ; Female ; Gene Expression Regulation/drug effects ; HSP72 Heat-Shock Proteins/biosynthesis/genetics/*metabolism ; Kyphosis/drug therapy ; Longevity/drug effects ; Male ; Mice ; Mice, Inbred mdx ; Mice, Transgenic ; Muscle, Skeletal/drug effects/*physiology/physiopathology ; Muscular Dystrophy, Duchenne/genetics/*metabolism/pathology/*physiopathology ; Oximes/pharmacology ; Piperidines/pharmacology ; Rats
    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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    Editorial expression of concern: Non-adaptive origins of interactome complexity (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-12-04
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4757426/" 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/PMC4757426/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fernandez, Ariel -- Lynch, Michael -- England -- Nature. 2014 Dec 18;516(7531):440. doi: 10.1038/nature13141. Epub 2014 Nov 26.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25470052" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Evolution, Molecular ; *Genetic Drift ; Humans ; Metabolic Networks and Pathways/*physiology ; Proteins/*metabolism
    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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    Regulatory evolution through divergence of a phosphoswitch in the transcription factor CEBPB (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-11-15
    Description: There is an emerging consensus that gene regulation evolves through changes in cis-regulatory elements and transcription factors. Although it is clear how nucleotide substitutions in cis-regulatory elements affect gene expression, it is not clear how amino-acid substitutions in transcription factors influence gene regulation. Here we show that amino-acid changes in the transcription factor CCAAT/enhancer binding protein-beta (CEBPB, also known as C/EBP-beta) in the stem-lineage of placental mammals changed the way it responds to cyclic AMP/protein kinase A (cAMP/PKA) signalling. By functionally analysing resurrected ancestral proteins, we identify three amino-acid substitutions in an internal regulatory domain of CEBPB that are responsible for the novel function. These amino-acid substitutions reorganize the location of key phosphorylation sites, introducing a new site and removing two ancestral sites, reversing the response of CEBPB to GSK-3beta-mediated phosphorylation from repression to activation. We conclude that changing the response of transcription factors to signalling pathways can be an important mechanism of gene regulatory evolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lynch, Vincent J -- May, Gemma -- Wagner, Gunter P -- England -- Nature. 2011 Nov 13;480(7377):383-6. doi: 10.1038/nature10595.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Yale Systems Biology Institute and Department of Ecology and Evolutionary Biology, Yale University, New Haven, Connecticut 06511, USA. vincent.j.lynch@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22080951" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; CCAAT-Enhancer-Binding Protein-beta/*chemistry/genetics/*metabolism ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; *Evolution, Molecular ; Female ; Forkhead Transcription Factors/metabolism ; *Gene Expression Regulation ; Glycogen Synthase Kinase 3/metabolism ; HeLa Cells ; Humans ; Mammals ; Models, Molecular ; Phosphorylation/genetics ; Placenta ; Pregnancy ; Protein Conformation ; Protein Structure, Tertiary ; Structure-Activity Relationship
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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    The genomic and transcriptomic architecture of 2,000 breast tumours reveals novel subgroups (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-04-24
    Description: The elucidation of breast cancer subgroups and their molecular drivers requires integrated views of the genome and transcriptome from representative numbers of patients. We present an integrated analysis of copy number and gene expression in a discovery and validation set of 997 and 995 primary breast tumours, respectively, with long-term clinical follow-up. Inherited variants (copy number variants and single nucleotide polymorphisms) and acquired somatic copy number aberrations (CNAs) were associated with expression in ~40% of genes, with the landscape dominated by cis- and trans-acting CNAs. By delineating expression outlier genes driven in cis by CNAs, we identified putative cancer genes, including deletions in PPP2R2A, MTAP and MAP2K4. Unsupervised analysis of paired DNA-RNA profiles revealed novel subgroups with distinct clinical outcomes, which reproduced in the validation cohort. These include a high-risk, oestrogen-receptor-positive 11q13/14 cis-acting subgroup and a favourable prognosis subgroup devoid of CNAs. Trans-acting aberration hotspots were found to modulate subgroup-specific gene networks, including a TCR deletion-mediated adaptive immune response in the 'CNA-devoid' subgroup and a basal-specific chromosome 5 deletion-associated mitotic network. Our results provide a novel molecular stratification of the breast cancer population, derived from the impact of somatic CNAs on the transcriptome.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3440846/" 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/PMC3440846/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Curtis, Christina -- Shah, Sohrab P -- Chin, Suet-Feung -- Turashvili, Gulisa -- Rueda, Oscar M -- Dunning, Mark J -- Speed, Doug -- Lynch, Andy G -- Samarajiwa, Shamith -- Yuan, Yinyin -- Graf, Stefan -- Ha, Gavin -- Haffari, Gholamreza -- Bashashati, Ali -- Russell, Roslin -- McKinney, Steven -- METABRIC Group -- Langerod, Anita -- Green, Andrew -- Provenzano, Elena -- Wishart, Gordon -- Pinder, Sarah -- Watson, Peter -- Markowetz, Florian -- Murphy, Leigh -- Ellis, Ian -- Purushotham, Arnie -- Borresen-Dale, Anne-Lise -- Brenton, James D -- Tavare, Simon -- Caldas, Carlos -- Aparicio, Samuel -- A7199/Cancer Research UK/United Kingdom -- P50HG02790/HG/NHGRI NIH HHS/ -- Cancer Research UK/United Kingdom -- England -- Nature. 2012 Apr 18;486(7403):346-52. doi: 10.1038/nature10983.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncology, University of Cambridge, Hills Road, Cambridge CB2 2XZ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22522925" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/classification/diagnosis/*genetics/*pathology ; DNA Copy Number Variations/*genetics ; Female ; *Gene Expression Profiling ; *Gene Expression Regulation, Neoplastic ; Gene Regulatory Networks/genetics ; Genes, Neoplasm/genetics ; Genome, Human/*genetics ; Genomics ; Humans ; Kaplan-Meier Estimate ; MAP Kinase Kinase 4/genetics ; Polymorphism, Single Nucleotide/genetics ; Prognosis ; Protein Phosphatase 2/genetics ; Treatment Outcome
    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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    Microbiota-liberated host sugars facilitate post-antibiotic expansion of enteric pathogens (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-09-03
    Description: The human intestine, colonized by a dense community of resident microbes, is a frequent target of bacterial pathogens. Undisturbed, this intestinal microbiota provides protection from bacterial infections. Conversely, disruption of the microbiota with oral antibiotics often precedes the emergence of several enteric pathogens. How pathogens capitalize upon the failure of microbiota-afforded protection is largely unknown. Here we show that two antibiotic-associated pathogens, Salmonella enterica serovar Typhimurium (S. typhimurium) and Clostridium difficile, use a common strategy of catabolizing microbiota-liberated mucosal carbohydrates during their expansion within the gut. S. typhimurium accesses fucose and sialic acid within the lumen of the gut in a microbiota-dependent manner, and genetic ablation of the respective catabolic pathways reduces its competitiveness in vivo. Similarly, C. difficile expansion is aided by microbiota-induced elevation of sialic acid levels in vivo. Colonization of gnotobiotic mice with a sialidase-deficient mutant of Bacteroides thetaiotaomicron, a model gut symbiont, reduces free sialic acid levels resulting in C. difficile downregulating its sialic acid catabolic pathway and exhibiting impaired expansion. These effects are reversed by exogenous dietary administration of free sialic acid. Furthermore, antibiotic treatment of conventional mice induces a spike in free sialic acid and mutants of both Salmonella and C. difficile that are unable to catabolize sialic acid exhibit impaired expansion. These data show that antibiotic-induced disruption of the resident microbiota and subsequent alteration in mucosal carbohydrate availability are exploited by these two distantly related enteric pathogens in a similar manner. This insight suggests new therapeutic approaches for preventing diseases caused by antibiotic-associated pathogens.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3825626/" 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/PMC3825626/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ng, Katharine M -- Ferreyra, Jessica A -- Higginbottom, Steven K -- Lynch, Jonathan B -- Kashyap, Purna C -- Gopinath, Smita -- Naidu, Natasha -- Choudhury, Biswa -- Weimer, Bart C -- Monack, Denise M -- Sonnenburg, Justin L -- R01 AI089722/AI/NIAID NIH HHS/ -- R01 DK085025/DK/NIDDK NIH HHS/ -- R01-DK085025/DK/NIDDK NIH HHS/ -- T32 AI007328/AI/NIAID NIH HHS/ -- England -- Nature. 2013 Oct 3;502(7469):96-9. doi: 10.1038/nature12503. Epub 2013 Sep 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23995682" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/*pharmacology ; Bacteroides/physiology ; Carbohydrate Metabolism/*drug effects ; Clostridium difficile/*physiology ; Enterocolitis, Pseudomembranous/*microbiology ; Female ; Fucose/metabolism ; Gene Expression Profiling ; Gene Expression Regulation, Bacterial ; Intestinal Mucosa/metabolism/*microbiology ; Male ; Metagenome/drug effects/physiology ; Mice ; N-Acetylneuraminic Acid/metabolism ; Neuraminidase/genetics/metabolism ; Salmonella Infections/*microbiology ; Salmonella typhimurium/*physiology ; Specific Pathogen-Free Organisms
    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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