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  • 1
    Publication Date: 1984-02-03
    Description: Cattle grazing St. Augustine grass growing on peaty muck soils in the Florida Everglades developed anemia associated with the presence of Heinz bodies and suboptimal concentrations of selenium in blood. Selenium supplementation corrected the anemia, prevented Heinz body formation, increased the body weight of cows and calves, and elevated blood selenium. This may be the first recorded example of widespread anemia in a population due to selenium deficiency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morris, J G -- Cripe, W S -- Chapman, H L Jr -- Walker, D F -- Armstrong, J B -- Alexander, J D Jr -- Miranda, R -- Sanchez, A Jr -- Sanchez, B -- Blair-West, J R -- New York, N.Y. -- Science. 1984 Feb 3;223(4635):491-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6691160" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Hemolytic/drug therapy/etiology/*veterinary ; Animal Feed ; Animals ; Body Weight ; Cattle ; Cattle Diseases/drug therapy/*etiology ; Heinz Bodies/*ultrastructure ; Hematocrit ; Hemoglobins/analysis ; Selenium/administration & dosage/blood/*deficiency
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2005-10-08
    Description: To investigate the role of astrocytes in regulating synaptic transmission, we generated inducible transgenic mice that express a dominant-negative SNARE domain selectively in astrocytes to block the release of transmitters from these glial cells. By releasing adenosine triphosphate, which accumulates as adenosine, astrocytes tonically suppressed synaptic transmission, thereby enhancing the dynamic range for long-term potentiation and mediated activity-dependent, heterosynaptic depression. These results indicate that astrocytes are intricately linked in the regulation of synaptic strength and plasticity and provide a pathway for synaptic cross-talk.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pascual, Olivier -- Casper, Kristen B -- Kubera, Cathryn -- Zhang, Jing -- Revilla-Sanchez, Raquel -- Sul, Jai-Yoon -- Takano, Hajime -- Moss, Stephen J -- McCarthy, Ken -- Haydon, Philip G -- New York, N.Y. -- Science. 2005 Oct 7;310(5745):113-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Conte Center for Integration at the Tripartite Synapse, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16210541" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/*metabolism ; Adenosine A1 Receptor Antagonists ; Adenosine Triphosphatases/antagonists & inhibitors ; Adenosine Triphosphate/analogs & derivatives/metabolism/pharmacology ; Animals ; Astrocytes/drug effects/*physiology ; Cells, Cultured ; Excitatory Postsynaptic Potentials ; Hippocampus/drug effects/physiology ; In Vitro Techniques ; Long-Term Potentiation/drug effects ; Mice ; Mice, Transgenic ; Neuronal Plasticity/drug effects ; Purinergic P1 Receptor Antagonists ; Purinergic P2 Receptor Antagonists ; Receptor, Adenosine A1/metabolism ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/metabolism ; Receptors, Purinergic P1/metabolism ; Receptors, Purinergic P2/metabolism ; Synapses/*physiology ; *Synaptic Transmission/drug effects ; Xanthines/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2008-04-05
    Description: The timing of the first human migration into the Americas and its relation to the appearance of the Clovis technological complex in North America at about 11,000 to 10,800 radiocarbon years before the present (14C years B.P.) remains contentious. We establish that humans were present at Paisley 5 Mile Point Caves, in south-central Oregon, by 12,300 14C years B.P., through the recovery of human mitochondrial DNA (mtDNA) from coprolites, directly dated by accelerator mass spectrometry. The mtDNA corresponds to Native American founding haplogroups A2 and B2. The dates of the coprolites are 〉1000 14C years earlier than currently accepted dates for the Clovis complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gilbert, M Thomas P -- Jenkins, Dennis L -- Gotherstrom, Anders -- Naveran, Nuria -- Sanchez, Juan J -- Hofreiter, Michael -- Thomsen, Philip Francis -- Binladen, Jonas -- Higham, Thomas F G -- Yohe, Robert M 2nd -- Parr, Robert -- Cummings, Linda Scott -- Willerslev, Eske -- New York, N.Y. -- Science. 2008 May 9;320(5877):786-9. doi: 10.1126/science.1154116. Epub 2008 Apr 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Ancient Genetics, University of Copenhagen, Universitetsparken 15, 2100 Copenhagen, Denmark.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18388261" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Canidae/genetics ; *DNA, Mitochondrial ; *Emigration and Immigration ; *Feces ; *Fossils ; Humans ; Molecular Sequence Data ; North America ; Oregon ; Polymerase Chain Reaction ; Polymorphism, Single Nucleotide ; Sciuridae/genetics ; Sigmodontinae/genetics ; Time
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2008-10-31
    Description: The nephron is the basic structural and functional unit of the vertebrate kidney. It is composed of a glomerulus, the site of ultrafiltration, and a renal tubule, along which the filtrate is modified. Although widely regarded as a vertebrate adaptation, 'nephron-like' features can be found in the excretory systems of many invertebrates, raising the possibility that components of the vertebrate excretory system were inherited from their invertebrate ancestors. Here we show that the insect nephrocyte has remarkable anatomical, molecular and functional similarity to the glomerular podocyte, a cell in the vertebrate kidney that forms the main size-selective barrier as blood is ultrafiltered to make urine. In particular, both cell types possess a specialized filtration diaphragm, known as the slit diaphragm in podocytes or the nephrocyte diaphragm in nephrocytes. We find that fly (Drosophila melanogaster) orthologues of the major constituents of the slit diaphragm, including nephrin, NEPH1 (also known as KIRREL), CD2AP, ZO-1 (TJP1) and podocin, are expressed in the nephrocyte and form a complex of interacting proteins that closely mirrors the vertebrate slit diaphragm complex. Furthermore, we find that the nephrocyte diaphragm is completely lost in flies lacking the orthologues of nephrin or NEPH1-a phenotype resembling loss of the slit diaphragm in the absence of either nephrin (as in human congenital nephrotic syndrome of the Finnish type, NPHS1) or NEPH1. These changes markedly impair filtration function in the nephrocyte. The similarities we describe between invertebrate nephrocytes and vertebrate podocytes provide evidence suggesting that the two cell types are evolutionarily related, and establish the nephrocyte as a simple model in which to study podocyte biology and podocyte-associated diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2687078/" 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/PMC2687078/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weavers, Helen -- Prieto-Sanchez, Silvia -- Grawe, Ferdinand -- Garcia-Lopez, Amparo -- Artero, Ruben -- Wilsch-Brauninger, Michaela -- Ruiz-Gomez, Mar -- Skaer, Helen -- Denholm, Barry -- 072441/Wellcome Trust/United Kingdom -- 079221/Wellcome Trust/United Kingdom -- Arthritis Research UK/United Kingdom -- England -- Nature. 2009 Jan 15;457(7227):322-6. doi: 10.1038/nature07526. Epub 2008 Oct 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, University of Cambridge, Downing Street, Cambridge CB2 3EJ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18971929" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Drosophila Proteins/genetics/*metabolism ; Drosophila melanogaster/anatomy & histology/*cytology/physiology ; Immunoglobulins/genetics/metabolism ; Membrane Proteins/deficiency/genetics/metabolism ; Muscle Proteins/genetics/metabolism ; Podocytes/*cytology/metabolism/*physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2010-06-25
    Description: The early development of teleost paired fins is strikingly similar to that of tetrapod limb buds and is controlled by similar mechanisms. One early morphological divergence between pectoral fins and limbs is in the fate of the apical ectodermal ridge (AER), the distal epidermis that rims the bud. Whereas the AER of tetrapods regresses after specification of the skeletal progenitors, the AER of teleost fishes forms a fold that elongates. Formation of the fin fold is accompanied by the synthesis of two rows of rigid, unmineralized fibrils called actinotrichia, which keep the fold straight and guide the migration of mesenchymal cells within the fold. The actinotrichia are made of elastoidin, the components of which, apart from collagen, are unknown. Here we show that two zebrafish proteins, which we name actinodin 1 and 2 (And1 and And2), are essential structural components of elastoidin. The presence of actinodin sequences in several teleost fishes and in the elephant shark (Callorhinchus milii, which occupies a basal phylogenetic position), but not in tetrapods, suggests that these genes have been lost during tetrapod species evolution. Double gene knockdown of and1 and and2 in zebrafish embryos results in the absence of actinotrichia and impaired fin folds. Gene expression profiles in embryos lacking and1 and and2 function are consistent with pectoral fin truncation and may offer a potential explanation for the polydactyly observed in early tetrapod fossils. We propose that the loss of both actinodins and actinotrichia during evolution may have led to the loss of lepidotrichia and may have contributed to the fin-to-limb transition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Jing -- Wagh, Purva -- Guay, Danielle -- Sanchez-Pulido, Luis -- Padhi, Bhaja K -- Korzh, Vladimir -- Andrade-Navarro, Miguel A -- Akimenko, Marie-Andree -- MC_U137761446/Medical Research Council/United Kingdom -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2010 Jul 8;466(7303):234-7. doi: 10.1038/nature09137. Epub 2010 Jun 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CAREG, Department of Biology, University of Ottawa, Ottawa, Ontario K1N 6N5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20574421" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Structures/*anatomy & histology/embryology/*physiology ; Animals ; *Biological Evolution ; Collagen/chemistry/metabolism ; Ectoderm/embryology/metabolism ; Embryo, Nonmammalian/anatomy & histology/embryology/metabolism ; Evolution, Molecular ; Extremities/anatomy & histology/embryology/*physiology ; Fish Proteins/*deficiency/genetics/metabolism ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Gene Knockdown Techniques ; Limb Buds/anatomy & histology/embryology/metabolism ; Models, Biological ; Phylogeny ; Zebrafish/*anatomy & histology/embryology/genetics/*metabolism ; Zebrafish Proteins/deficiency/genetics/metabolism
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  • 6
    Publication Date: 2010-11-26
    Description: Tumorigenesis is a multistep process that results from the sequential accumulation of mutations in key oncogene and tumour suppressor pathways. Personalized cancer therapy that is based on targeting these underlying genetic abnormalities presupposes that sustained inactivation of tumour suppressors and activation of oncogenes is essential in advanced cancers. Mutations in the p53 tumour-suppressor pathway are common in human cancer and significant efforts towards pharmaceutical reactivation of defective p53 pathways are underway. Here we show that restoration of p53 in established murine lung tumours leads to significant but incomplete tumour cell loss specifically in malignant adenocarcinomas, but not in adenomas. We define amplification of MAPK signalling as a critical determinant of malignant progression and also a stimulator of Arf tumour-suppressor expression. The response to p53 restoration in this context is critically dependent on the expression of Arf. We propose that p53 not only limits malignant progression by suppressing the acquisition of alterations that lead to tumour progression, but also, in the context of p53 restoration, responds to increased oncogenic signalling to mediate tumour regression. Our observations also underscore that the p53 pathway is not engaged by low levels of oncogene activity that are sufficient for early stages of lung tumour development. These data suggest that restoration of pathways important in tumour progression, as opposed to initiation, may lead to incomplete tumour regression due to the stage-heterogeneity of tumour cell populations.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3003305/" 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/PMC3003305/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feldser, David M -- Kostova, Kamena K -- Winslow, Monte M -- Taylor, Sarah E -- Cashman, Chris -- Whittaker, Charles A -- Sanchez-Rivera, Francisco J -- Resnick, Rebecca -- Bronson, Roderick -- Hemann, Michael T -- Jacks, Tyler -- P30 CA014051/CA/NCI NIH HHS/ -- P30 CA014051-37/CA/NCI NIH HHS/ -- P30 CA014051-38/CA/NCI NIH HHS/ -- P30 CA014051-39/CA/NCI NIH HHS/ -- P30 CA014051-40/CA/NCI NIH HHS/ -- P30-CA14051/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Nov 25;468(7323):572-5. doi: 10.1038/nature09535.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Koch Institute for Integrative Cancer Research, Department of Biology, and Howard Hughes Medical Institute, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21107428" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/metabolism/*physiopathology ; Adenoma/metabolism/*physiopathology ; Animals ; Cell Proliferation ; *Disease Progression ; Lung Neoplasms/*physiopathology ; Mice ; Mice, Inbred C57BL ; Mitogen-Activated Protein Kinases/metabolism ; Signal Transduction ; Tumor Suppressor Protein p53/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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  • 7
    Publication Date: 2011-11-19
    Description: Natural products that elicit discomfort or pain represent invaluable tools for probing molecular mechanisms underlying pain sensation. Plant-derived irritants have predominated in this regard, but animal venoms have also evolved to avert predators by targeting neurons and receptors whose activation produces noxious sensations. As such, venoms provide a rich and varied source of small molecule and protein pharmacophores that can be exploited to characterize and manipulate key components of the pain-signalling pathway. With this in mind, here we perform an unbiased in vitro screen to identify snake venoms capable of activating somatosensory neurons. Venom from the Texas coral snake (Micrurus tener tener), whose bite produces intense and unremitting pain, excites a large cohort of sensory neurons. The purified active species (MitTx) consists of a heteromeric complex between Kunitz- and phospholipase-A2-like proteins that together function as a potent, persistent and selective agonist for acid-sensing ion channels (ASICs), showing equal or greater efficacy compared with acidic pH. MitTx is highly selective for the ASIC1 subtype at neutral pH; under more acidic conditions (pH 〈 6.5), MitTx massively potentiates (〉100-fold) proton-evoked activation of ASIC2a channels. These observations raise the possibility that ASIC channels function as coincidence detectors for extracellular protons and other, as yet unidentified, endogenous factors. Purified MitTx elicits robust pain-related behaviour in mice by activation of ASIC1 channels on capsaicin-sensitive nerve fibres. These findings reveal a mechanism whereby snake venoms produce pain, and highlight an unexpected contribution of ASIC1 channels to nociception.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3226747/" 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/PMC3226747/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bohlen, Christopher J -- Chesler, Alexander T -- Sharif-Naeini, Reza -- Medzihradszky, Katalin F -- Zhou, Sharleen -- King, David -- Sanchez, Elda E -- Burlingame, Alma L -- Basbaum, Allan I -- Julius, David -- F31NS065597/NS/NINDS NIH HHS/ -- P40 RR018300-09/RR/NCRR NIH HHS/ -- P40RR018300-09/RR/NCRR NIH HHS/ -- P41 GM103481/GM/NIGMS NIH HHS/ -- P41RR001614/RR/NCRR NIH HHS/ -- R01NS065071/NS/NINDS NIH HHS/ -- Canadian Institutes of Health Research/Canada -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Nov 16;479(7373):410-4. doi: 10.1038/nature10607.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of California, San Francisco, California 94158-2517, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22094702" target="_blank"〉PubMed〈/a〉
    Keywords: Acid Sensing Ion Channels ; Amino Acid Sequence ; Animals ; Capsaicin/pharmacology ; Cells, Cultured ; Elapid Venoms/*chemistry/*pharmacology ; *Elapidae ; Hindlimb/drug effects/physiopathology ; Humans ; Hydrogen-Ion Concentration ; Ion Channel Gating/drug effects ; Male ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Nerve Tissue Proteins/agonists/deficiency/genetics/*metabolism ; Nociception/drug effects/physiology ; Oocytes ; Pain/*chemically induced/metabolism/physiopathology ; *Protein Multimerization ; Protein Structure, Quaternary ; Protons ; Rats ; Sensory Receptor Cells/drug effects/metabolism ; Sodium Channel Agonists ; Sodium Channels/deficiency/genetics/*metabolism ; TRPV Cation Channels/metabolism ; Xenopus laevis
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2011-11-25
    Description: The spider mite Tetranychus urticae is a cosmopolitan agricultural pest with an extensive host plant range and an extreme record of pesticide resistance. Here we present the completely sequenced and annotated spider mite genome, representing the first complete chelicerate genome. At 90 megabases T. urticae has the smallest sequenced arthropod genome. Compared with other arthropods, the spider mite genome shows unique changes in the hormonal environment and organization of the Hox complex, and also reveals evolutionary innovation of silk production. We find strong signatures of polyphagy and detoxification in gene families associated with feeding on different hosts and in new gene families acquired by lateral gene transfer. Deep transcriptome analysis of mites feeding on different plants shows how this pest responds to a changing host environment. The T. urticae genome thus offers new insights into arthropod evolution and plant-herbivore interactions, and provides unique opportunities for developing novel plant protection strategies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grbic, Miodrag -- Van Leeuwen, Thomas -- Clark, Richard M -- Rombauts, Stephane -- Rouze, Pierre -- Grbic, Vojislava -- Osborne, Edward J -- Dermauw, Wannes -- Ngoc, Phuong Cao Thi -- Ortego, Felix -- Hernandez-Crespo, Pedro -- Diaz, Isabel -- Martinez, Manuel -- Navajas, Maria -- Sucena, Elio -- Magalhaes, Sara -- Nagy, Lisa -- Pace, Ryan M -- Djuranovic, Sergej -- Smagghe, Guy -- Iga, Masatoshi -- Christiaens, Olivier -- Veenstra, Jan A -- Ewer, John -- Villalobos, Rodrigo Mancilla -- Hutter, Jeffrey L -- Hudson, Stephen D -- Velez, Marisela -- Yi, Soojin V -- Zeng, Jia -- Pires-daSilva, Andre -- Roch, Fernando -- Cazaux, Marc -- Navarro, Marie -- Zhurov, Vladimir -- Acevedo, Gustavo -- Bjelica, Anica -- Fawcett, Jeffrey A -- Bonnet, Eric -- Martens, Cindy -- Baele, Guy -- Wissler, Lothar -- Sanchez-Rodriguez, Aminael -- Tirry, Luc -- Blais, Catherine -- Demeestere, Kristof -- Henz, Stefan R -- Gregory, T Ryan -- Mathieu, Johannes -- Verdon, Lou -- Farinelli, Laurent -- Schmutz, Jeremy -- Lindquist, Erika -- Feyereisen, Rene -- Van de Peer, Yves -- England -- Nature. 2011 Nov 23;479(7374):487-92. doi: 10.1038/nature10640.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, The University of Western Ontario, London N6A 5B7, Canada. mgrbic@uwo.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22113690" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological/*genetics/physiology ; Animals ; Ecdysterone/analogs & derivatives/genetics ; Evolution, Molecular ; Fibroins/genetics ; Gene Expression Regulation ; Gene Transfer, Horizontal/genetics ; Genes, Homeobox/genetics ; Genome/*genetics ; Genomics ; Herbivory/*genetics/physiology ; Molecular Sequence Data ; Molting/genetics ; Multigene Family/genetics ; Nanostructures/chemistry ; Plants/parasitology ; Silk/biosynthesis/chemistry ; Tetranychidae/*genetics/*physiology ; Transcriptome/genetics
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  • 9
    Publication Date: 2013-03-15
    Description: Tapeworms (Cestoda) cause neglected diseases that can be fatal and are difficult to treat, owing to inefficient drugs. Here we present an analysis of tapeworm genome sequences using the human-infective species Echinococcus multilocularis, E. granulosus, Taenia solium and the laboratory model Hymenolepis microstoma as examples. The 115- to 141-megabase genomes offer insights into the evolution of parasitism. Synteny is maintained with distantly related blood flukes but we find extreme losses of genes and pathways that are ubiquitous in other animals, including 34 homeobox families and several determinants of stem cell fate. Tapeworms have specialized detoxification pathways, metabolism that is finely tuned to rely on nutrients scavenged from their hosts, and species-specific expansions of non-canonical heat shock proteins and families of known antigens. We identify new potential drug targets, including some on which existing pharmaceuticals may act. The genomes provide a rich resource to underpin the development of urgently needed treatments and control.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3964345/" 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/PMC3964345/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsai, Isheng J -- Zarowiecki, Magdalena -- Holroyd, Nancy -- Garciarrubio, Alejandro -- Sanchez-Flores, Alejandro -- Brooks, Karen L -- Tracey, Alan -- Bobes, Raul J -- Fragoso, Gladis -- Sciutto, Edda -- Aslett, Martin -- Beasley, Helen -- Bennett, Hayley M -- Cai, Jianping -- Camicia, Federico -- Clark, Richard -- Cucher, Marcela -- De Silva, Nishadi -- Day, Tim A -- Deplazes, Peter -- Estrada, Karel -- Fernandez, Cecilia -- Holland, Peter W H -- Hou, Junling -- Hu, Songnian -- Huckvale, Thomas -- Hung, Stacy S -- Kamenetzky, Laura -- Keane, Jacqueline A -- Kiss, Ferenc -- Koziol, Uriel -- Lambert, Olivia -- Liu, Kan -- Luo, Xuenong -- Luo, Yingfeng -- Macchiaroli, Natalia -- Nichol, Sarah -- Paps, Jordi -- Parkinson, John -- Pouchkina-Stantcheva, Natasha -- Riddiford, Nick -- Rosenzvit, Mara -- Salinas, Gustavo -- Wasmuth, James D -- Zamanian, Mostafa -- Zheng, Yadong -- Taenia solium Genome Consortium -- Cai, Xuepeng -- Soberon, Xavier -- Olson, Peter D -- Laclette, Juan P -- Brehm, Klaus -- Berriman, Matthew -- 085775/Wellcome Trust/United Kingdom -- 098051/Wellcome Trust/United Kingdom -- BBG0038151/Biotechnology and Biological Sciences Research Council/United Kingdom -- MOP#84556/Canadian Institutes of Health Research/Canada -- TW008588/TW/FIC NIH HHS/ -- England -- Nature. 2013 Apr 4;496(7443):57-63. doi: 10.1038/nature12031. Epub 2013 Mar 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Parasite Genomics, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23485966" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological/*genetics ; Animals ; Biological Evolution ; Cestoda/drug effects/*genetics/physiology ; Cestode Infections/drug therapy/metabolism ; Conserved Sequence/genetics ; Echinococcus granulosus/genetics ; Echinococcus multilocularis/drug effects/genetics/metabolism ; Genes, Helminth/genetics ; Genes, Homeobox/genetics ; Genome, Helminth/*genetics ; HSP70 Heat-Shock Proteins/genetics ; Humans ; Hymenolepis/genetics ; Metabolic Networks and Pathways/genetics ; Molecular Targeted Therapy ; Parasites/drug effects/*genetics/physiology ; Proteome/genetics ; Stem Cells/cytology/metabolism ; Taenia solium/genetics
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  • 10
    Publication Date: 2013-07-19
    Description: The epigenetic regulation of imprinted genes by monoallelic DNA methylation of either maternal or paternal alleles is critical for embryonic growth and development. Imprinted genes were recently shown to be expressed in mammalian adult stem cells to support self-renewal of neural and lung stem cells; however, a role for imprinting per se in adult stem cells remains elusive. Here we show upregulation of growth-restricting imprinted genes, including in the H19-Igf2 locus, in long-term haematopoietic stem cells and their downregulation upon haematopoietic stem cell activation and proliferation. A differentially methylated region upstream of H19 (H19-DMR), serving as the imprinting control region, determines the reciprocal expression of H19 from the maternal allele and Igf2 from the paternal allele. In addition, H19 serves as a source of miR-675, which restricts Igf1r expression. We demonstrate that conditional deletion of the maternal but not the paternal H19-DMR reduces adult haematopoietic stem cell quiescence, a state required for long-term maintenance of haematopoietic stem cells, and compromises haematopoietic stem cell function. Maternal-specific H19-DMR deletion results in activation of the Igf2-Igfr1 pathway, as shown by the translocation of phosphorylated FoxO3 (an inactive form) from nucleus to cytoplasm and the release of FoxO3-mediated cell cycle arrest, thus leading to increased activation, proliferation and eventual exhaustion of haematopoietic stem cells. Mechanistically, maternal-specific H19-DMR deletion leads to Igf2 upregulation and increased translation of Igf1r, which is normally suppressed by H19-derived miR-675. Similarly, genetic inactivation of Igf1r partly rescues the H19-DMR deletion phenotype. Our work establishes a new role for this unique form of epigenetic control at the H19-Igf2 locus in maintaining adult stem cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3896866/" 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/PMC3896866/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Venkatraman, Aparna -- He, Xi C -- Thorvaldsen, Joanne L -- Sugimura, Ryohichi -- Perry, John M -- Tao, Fang -- Zhao, Meng -- Christenson, Matthew K -- Sanchez, Rebeca -- Yu, Jaclyn Y -- Peng, Lai -- Haug, Jeffrey S -- Paulson, Ariel -- Li, Hua -- Zhong, Xiao-bo -- Clemens, Thomas L -- Bartolomei, Marisa S -- Li, Linheng -- GM51279/GM/NIGMS NIH HHS/ -- R01 GM087376/GM/NIGMS NIH HHS/ -- R37 GM051279/GM/NIGMS NIH HHS/ -- England -- Nature. 2013 Aug 15;500(7462):345-9. doi: 10.1038/nature12303. Epub 2013 Jul 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stowers Institute for Medical Research, Kansas City, Missouri 64110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23863936" target="_blank"〉PubMed〈/a〉
    Keywords: Adult Stem Cells/*cytology/*physiology ; Animals ; Epigenesis, Genetic/genetics ; Gene Expression Regulation, Developmental ; *Genomic Imprinting ; Insulin-Like Growth Factor II/*genetics/*metabolism ; Mice ; RNA, Long Noncoding/*genetics/*metabolism ; Receptor, IGF Type 1/genetics ; Signal Transduction ; Transcriptional Activation
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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