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  • 1
    Keywords: Medicine ; Neurosciences ; Ophthalmology ; Neurobiology ; Biomedicine ; Neurosciences ; Ophthalmology ; Neurobiology ; Springer eBooks
    Description / Table of Contents: 1. Introduction -- 2. Fundamental Retinal Circuitry for Circadian Rhythms -- 3. Circadian photoreception: from phototransduction to behaviour -- 4. Role of Melatonin and Dopamine in the Regulation of Retinal Circadian Rhythms -- 5. Circadian Organization of the Vertebrate Retina -- 6. Rhythmicity of the Retinal Pigment Epithelium -- 7. Retinal Circadian Rhythms in Mammals Revealed Using Electroretinography -- 8. Circadian Clock and Light Induced Retinal Damage -- 9. Circadian Rhythms and Vision in Zebrafish -- 10. Circadian Modulation of the Limulus Eye for Day and Night Vision -- 11. Molluscan Ocular Pacemakers: Lessons Learned. ℗ ℗ ℗ ℗ ℗ ℗ ℗ ℗ ℗
    Abstract: The retina plays a critical role in the organization of the circadian system by synchronizing the braiń€™s central clock with the external day through transduction of the daily light/dark cycle.℗ However, the substantial variation in luminance imposed on the retina between day and night also poses a challenge to its role as a sensory tissue ́€“ how is it possible to faithfully encode the enormous dynamic range of luminance that can exceed 10 orders of magnitude? The Retina and Circadian Rhythms summarizes the knowledge accumulated over the last 30 years about the organization of the retinal circadian clock in many different species, concentrating on the roles that this circadian system plays in retinal function. About the Series: The Springer Series in Vision Research is a comprehensive update and overview of cutting edge vision research, exploring, in depth, current breakthroughs at a conceptual level. It details the whole visual system, from molecular processes to anatomy, physiology and behavior and covers both invertebrate and vertebrate organisms from terrestrial and aquatic habitats. Each book in the Series is aimed at all individuals with interests in vision including advanced graduate students, post-doctoral researchers, established vision scientists and clinical investigators.The series editors are N. Justin Marshall, Queensland Brain Institute, The University of Queensland, Australia and Shaun P. Collin, Neuroecology Group within the School of Animal Biology and the Oceans Institute at the University of Western Australia
    Pages: VIII, 238 p. 50 illus., 33 illus. in color. : online resource.
    ISBN: 9781461496137
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  • 2
    Publication Date: 2012-08-17
    Description: In the cores of some clusters of galaxies the hot intracluster plasma is dense enough that it should cool radiatively in the cluster's lifetime, leading to continuous 'cooling flows' of gas sinking towards the cluster centre, yet no such cooling flow has been observed. The low observed star-formation rates and cool gas masses for these 'cool-core' clusters suggest that much of the cooling must be offset by feedback to prevent the formation of a runaway cooling flow. Here we report X-ray, optical and infrared observations of the galaxy cluster SPT-CLJ2344-4243 (ref. 11) at redshift z = 0.596. These observations reveal an exceptionally luminous (8.2 x 10(45) erg s(-1)) galaxy cluster that hosts an extremely strong cooling flow (around 3,820 solar masses a year). Further, the central galaxy in this cluster appears to be experiencing a massive starburst (formation of around 740 solar masses a year), which suggests that the feedback source responsible for preventing runaway cooling in nearby cool-core clusters may not yet be fully established in SPT-CLJ2344-4243. This large star-formation rate implies that a significant fraction of the stars in the central galaxy of this cluster may form through accretion of the intracluster medium, rather than (as is currently thought) assembling entirely via mergers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDonald, M -- Bayliss, M -- Benson, B A -- Foley, R J -- Ruel, J -- Sullivan, P -- Veilleux, S -- Aird, K A -- Ashby, M L N -- Bautz, M -- Bazin, G -- Bleem, L E -- Brodwin, M -- Carlstrom, J E -- Chang, C L -- Cho, H M -- Clocchiatti, A -- Crawford, T M -- Crites, A T -- de Haan, T -- Desai, S -- Dobbs, M A -- Dudley, J P -- Egami, E -- Forman, W R -- Garmire, G P -- George, E M -- Gladders, M D -- Gonzalez, A H -- Halverson, N W -- Harrington, N L -- High, F W -- Holder, G P -- Holzapfel, W L -- Hoover, S -- Hrubes, J D -- Jones, C -- Joy, M -- Keisler, R -- Knox, L -- Lee, A T -- Leitch, E M -- Liu, J -- Lueker, M -- Luong-Van, D -- Mantz, A -- Marrone, D P -- McMahon, J J -- Mehl, J -- Meyer, S S -- Miller, E D -- Mocanu, L -- Mohr, J J -- Montroy, T E -- Murray, S S -- Natoli, T -- Padin, S -- Plagge, T -- Pryke, C -- Rawle, T D -- Reichardt, C L -- Rest, A -- Rex, M -- Ruhl, J E -- Saliwanchik, B R -- Saro, A -- Sayre, J T -- Schaffer, K K -- Shaw, L -- Shirokoff, E -- Simcoe, R -- Song, J -- Spieler, H G -- Stalder, B -- Staniszewski, Z -- Stark, A A -- Story, K -- Stubbs, C W -- Suhada, R -- van Engelen, A -- Vanderlinde, K -- Vieira, J D -- Vikhlinin, A -- Williamson, R -- Zahn, O -- Zenteno, A -- England -- Nature. 2012 Aug 16;488(7411):349-52. doi: 10.1038/nature11379.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MIT Kavli Institute for Astrophysics and Space Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA. mcdonald@space.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22895340" target="_blank"〉PubMed〈/a〉
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2011-07-02
    Description: The intergalactic medium was not completely reionized until approximately a billion years after the Big Bang, as revealed by observations of quasars with redshifts of less than 6.5. It has been difficult to probe to higher redshifts, however, because quasars have historically been identified in optical surveys, which are insensitive to sources at redshifts exceeding 6.5. Here we report observations of a quasar (ULAS J112001.48+064124.3) at a redshift of 7.085, which is 0.77 billion years after the Big Bang. ULAS J1120+0641 has a luminosity of 6.3 x 10(13)L(middle dot in circle) and hosts a black hole with a mass of 2 x 10(9)M(middle dot in circle) (where L(middle dot in circle) and M(middle dot in circle) are the luminosity and mass of the Sun). The measured radius of the ionized near zone around ULAS J1120+0641 is 1.9 megaparsecs, a factor of three smaller than is typical for quasars at redshifts between 6.0 and 6.4. The near-zone transmission profile is consistent with a Lyalpha damping wing, suggesting that the neutral fraction of the intergalactic medium in front of ULAS J1120+0641 exceeded 0.1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mortlock, Daniel J -- Warren, Stephen J -- Venemans, Bram P -- Patel, Mitesh -- Hewett, Paul C -- McMahon, Richard G -- Simpson, Chris -- Theuns, Tom -- Gonzales-Solares, Eduardo A -- Adamson, Andy -- Dye, Simon -- Hambly, Nigel C -- Hirst, Paul -- Irwin, Mike J -- Kuiper, Ernst -- Lawrence, Andy -- Rottgering, Huub J A -- England -- Nature. 2011 Jun 29;474(7353):616-9. doi: 10.1038/nature10159.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Astrophysics Group, Imperial College London, Blackett Laboratory, Prince Consort Road, London SW7 2AZ, UK. mortlock@ic.ac.uk)〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21720366" target="_blank"〉PubMed〈/a〉
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Nature Publishing Group (NPG)
    Publication Date: 2012-02-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McMahon, Clive R -- England -- Nature. 2012 Feb 22;482(7386):471. doi: 10.1038/482471e.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22358824" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conservation of Natural Resources/*methods ; Elephants/*physiology ; Fires/*prevention & control ; *Food Chain
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2013-01-04
    Description: Protein kinase M-zeta (PKM-zeta) is a constitutively active form of atypical protein kinase C that is exclusively expressed in the brain and implicated in the maintenance of long-term memory. Most studies that support a role for PKM-zeta in memory maintenance have used pharmacological PKM-zeta inhibitors such as the myristoylated zeta inhibitory peptide (ZIP) or chelerythrine. Here we use a genetic approach and target exon 9 of the Prkcz gene to generate mice that lack both protein kinase C-zeta (PKC-zeta) and PKM-zeta (Prkcz(-/-) mice). Prkcz(-/-) mice showed normal behaviour in a cage environment and in baseline tests of motor function and sensory perception, but displayed reduced anxiety-like behaviour. Notably, Prkcz(-/-) mice did not show deficits in learning or memory in tests of cued fear conditioning, novel object recognition, object location recognition, conditioned place preference for cocaine, or motor learning, when compared with wild-type littermates. ZIP injection into the nucleus accumbens reduced expression of cocaine-conditioned place preference in Prkcz(-/-) mice. In vitro, ZIP and scrambled ZIP inhibited PKM-zeta, PKC-iota and PKC-zeta with similar inhibition constant (K(i)) values. Chelerythrine was a weak inhibitor of PKM-zeta (K(i) = 76 muM). Our findings show that absence of PKM-zeta does not impair learning and memory in mice, and that ZIP can erase reward memory even when PKM-zeta is not present.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3548047/" 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/PMC3548047/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Anna M -- Kanter, Benjamin R -- Wang, Dan -- Lim, Jana P -- Zou, Mimi E -- Qiu, Chichen -- McMahon, Thomas -- Dadgar, Jahan -- Fischbach-Weiss, Sarah C -- Messing, Robert O -- AA017072/AA/NIAAA NIH HHS/ -- P50 AA017072/AA/NIAAA NIH HHS/ -- T32 GM007618/GM/NIGMS NIH HHS/ -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2013 Jan 17;493(7432):416-9. doi: 10.1038/nature11803. Epub 2013 Jan 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ernest Gallo Clinic and Research Center, Department of Neurology, University of California, San Francisco, 5858 Horton Street, Suite 200, Emeryville, California 94608, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23283171" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anxiety/genetics ; Behavior, Animal ; Benzophenanthridines/pharmacology ; Cocaine ; Conditioning, Classical ; Cues ; Exons/genetics ; Fear ; Female ; *Gene Deletion ; Male ; Memory/*physiology ; Mice ; Protein Kinase C/analysis/*deficiency/*genetics/immunology
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2013-01-11
    Description: Mutational activation of BRAF is the most prevalent genetic alteration in human melanoma, with 〉/=50% of tumours expressing the BRAF(V600E) oncoprotein. Moreover, the marked tumour regression and improved survival of late-stage BRAF-mutated melanoma patients in response to treatment with vemurafenib demonstrates the essential role of oncogenic BRAF in melanoma maintenance. However, as most patients relapse with lethal drug-resistant disease, understanding and preventing mechanism(s) of resistance is critical to providing improved therapy. Here we investigate the cause and consequences of vemurafenib resistance using two independently derived primary human melanoma xenograft models in which drug resistance is selected by continuous vemurafenib administration. In one of these models, resistant tumours show continued dependency on BRAF(V600E)--〉MEK--〉ERK signalling owing to elevated BRAF(V600E) expression. Most importantly, we demonstrate that vemurafenib-resistant melanomas become drug dependent for their continued proliferation, such that cessation of drug administration leads to regression of established drug-resistant tumours. We further demonstrate that a discontinuous dosing strategy, which exploits the fitness disadvantage displayed by drug-resistant cells in the absence of the drug, forestalls the onset of lethal drug-resistant disease. These data highlight the concept that drug-resistant cells may also display drug dependency, such that altered dosing may prevent the emergence of lethal drug resistance. Such observations may contribute to sustaining the durability of the vemurafenib response with the ultimate goal of curative therapy for the subset of melanoma patients with BRAF mutations.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3930354/" 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/PMC3930354/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Das Thakur, Meghna -- Salangsang, Fernando -- Landman, Allison S -- Sellers, William R -- Pryer, Nancy K -- Levesque, Mitchell P -- Dummer, Reinhard -- McMahon, Martin -- Stuart, Darrin D -- R01 CA176839/CA/NCI NIH HHS/ -- R01-CA176839/CA/NCI NIH HHS/ -- T32 HL007185/HL/NHLBI NIH HHS/ -- England -- Nature. 2013 Feb 14;494(7436):251-5. doi: 10.1038/nature11814. Epub 2013 Jan 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Novartis Institutes for Biomedical Research, Emeryville, California 94608, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23302800" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Disease Models, Animal ; Drug Administration Schedule ; Drug Resistance, Neoplasm/*drug effects ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Humans ; Indoles/*administration & dosage/*adverse effects/pharmacology ; MAP Kinase Signaling System/drug effects ; Melanoma/*drug therapy/genetics/*pathology ; Mice ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Mutation ; Neoplasm Transplantation ; Proto-Oncogene Proteins B-raf/chemistry/genetics/metabolism ; Subcutaneous Tissue ; Sulfonamides/*administration & dosage/*adverse effects/pharmacology ; Time Factors ; Xenograft Model Antitumor Assays
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2014-07-06
    Description: The large spectrum of limb morphologies reflects the wide evolutionary diversification of the basic pentadactyl pattern in tetrapods. In even-toed ungulates (artiodactyls, including cattle), limbs are adapted for running as a consequence of progressive reduction of their distal skeleton to symmetrical and elongated middle digits with hoofed phalanges. Here we analyse bovine embryos to establish that polarized gene expression is progressively lost during limb development in comparison to the mouse. Notably, the transcriptional upregulation of the Ptch1 gene, which encodes a Sonic hedgehog (SHH) receptor, is disrupted specifically in the bovine limb bud mesenchyme. This is due to evolutionary alteration of a Ptch1 cis-regulatory module, which no longer responds to graded SHH signalling during bovine handplate development. Our study provides a molecular explanation for the loss of digit asymmetry in bovine limb buds and suggests that modifications affecting the Ptch1 cis-regulatory landscape have contributed to evolutionary diversification of artiodactyl limbs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lopez-Rios, Javier -- Duchesne, Amandine -- Speziale, Dario -- Andrey, Guillaume -- Peterson, Kevin A -- Germann, Philipp -- Unal, Erkan -- Liu, Jing -- Floriot, Sandrine -- Barbey, Sarah -- Gallard, Yves -- Muller-Gerbl, Magdalena -- Courtney, Andrew D -- Klopp, Christophe -- Rodriguez, Sabrina -- Ivanek, Robert -- Beisel, Christian -- Wicking, Carol -- Iber, Dagmar -- Robert, Benoit -- McMahon, Andrew P -- Duboule, Denis -- Zeller, Rolf -- NS 033642/NS/NINDS NIH HHS/ -- England -- Nature. 2014 Jul 3;511(7507):46-51. doi: 10.1038/nature13289. Epub 2014 Jun 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Developmental Genetics, Department Biomedicine, University of Basel, CH-4058 Basel, Switzerland [2]. ; 1] Developmental Genetics, Department Biomedicine, University of Basel, CH-4058 Basel, Switzerland [2] Institut National de la Recherche Agronomique, Genetique Animale et Biologie Integrative, F-78350 Jouy-en-Josas, France [3]. ; Developmental Genetics, Department Biomedicine, University of Basel, CH-4058 Basel, Switzerland. ; School of Life Sciences, Federal Institute of Technology Lausanne, CH-1015 Lausanne, Switzerland. ; Department of Stem Cell Biology and Regenerative Medicine, Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research, Keck School of Medicine, University of Southern California, Los Angeles, California 90089, USA. ; Department for Biosystems Science and Engineering, Federal Institute of Technology Zurich and Swiss Institute of Bioinformatics, CH-4058 Basel, Switzerland. ; 1] Developmental Genetics, Department Biomedicine, University of Basel, CH-4058 Basel, Switzerland [2] Department for Biosystems Science and Engineering, Federal Institute of Technology Zurich and Swiss Institute of Bioinformatics, CH-4058 Basel, Switzerland. ; Institut National de la Recherche Agronomique, Genetique Animale et Biologie Integrative, F-78350 Jouy-en-Josas, France. ; Institut National de la Recherche Agronomique, Domaine Experimental du Pin au Haras, F-61310 Exmes, France. ; Institute of Anatomy, Department Biomedicine, University of Basel, CH-4056 Basel, Switzerland. ; Institute for Molecular Bioscience, The University of Queensland, St Lucia, Queensland 4072, Australia. ; Institut National de la Recherche Agronomique, Biometrie et Intelligence Artificielle, F-31326 Castanet-Tolosan, France. ; 1] Institut National de la Recherche Agronomique, Genetique Animale et Biologie Integrative, F-78350 Jouy-en-Josas, France [2] Institut National de la Recherche Agronomique, Laboratoire d'Ingenierie des Systemes Biologiques et des Procedes, F-31077 Toulouse, France. ; 1] Developmental Genetics, Department Biomedicine, University of Basel, CH-4058 Basel, Switzerland [2] Swiss Institute of Bioinformatics, CH-4058 Basel, Switzerland. ; Institut Pasteur, Genetique Moleculaire de la Morphogenese and Centre National de la Recherche Scientifique URA-2578, F-75015 Paris, France. ; 1] School of Life Sciences, Federal Institute of Technology Lausanne, CH-1015 Lausanne, Switzerland [2] Department of Genetics and Evolution, University of Geneva, CH-1211 Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24990743" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Body Patterning ; Cattle ; Extremities/*anatomy & histology/*embryology ; Female ; Gene Expression Regulation, Developmental/genetics ; Hedgehog Proteins/*metabolism ; Limb Buds/anatomy & histology/embryology ; Male ; Mesoderm/metabolism ; Mice ; Mice, Transgenic ; Receptors, Cell Surface/genetics/*metabolism ; Regulatory Sequences, Nucleic Acid/genetics
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2014-02-21
    Description: Emerging infectious diseases (EIDs) pose a risk to human welfare, both directly and indirectly, by affecting managed livestock and wildlife that provide valuable resources and ecosystem services, such as the pollination of crops. Honeybees (Apis mellifera), the prevailing managed insect crop pollinator, suffer from a range of emerging and exotic high-impact pathogens, and population maintenance requires active management by beekeepers to control them. Wild pollinators such as bumblebees (Bombus spp.) are in global decline, one cause of which may be pathogen spillover from managed pollinators like honeybees or commercial colonies of bumblebees. Here we use a combination of infection experiments and landscape-scale field data to show that honeybee EIDs are indeed widespread infectious agents within the pollinator assemblage. The prevalence of deformed wing virus (DWV) and the exotic parasite Nosema ceranae in honeybees and bumblebees is linked; as honeybees have higher DWV prevalence, and sympatric bumblebees and honeybees are infected by the same DWV strains, Apis is the likely source of at least one major EID in wild pollinators. Lessons learned from vertebrates highlight the need for increased pathogen control in managed bee species to maintain wild pollinators, as declines in native pollinators may be caused by interspecies pathogen transmission originating from managed pollinators.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3985068/" 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/PMC3985068/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Furst, M A -- McMahon, D P -- Osborne, J L -- Paxton, R J -- Brown, M J F -- 094888/Wellcome Trust/United Kingdom -- BB/I000097/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/I000100/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/I000151/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2014 Feb 20;506(7488):364-6. doi: 10.1038/nature12977.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Royal Holloway University of London, School of Biological Sciences, Bourne Building, Egham TW20 0EX, UK [2] IST Austria (Institute of Science and Technology Austria), 3400 Klosterneuburg, Austria. ; Queen's University Belfast, School of Biological Sciences, 97 Lisburn Road, Belfast BT9 7BL, UK. ; 1] Rothamsted Research, Department of Agro-Ecology, Harpenden AL5 2JQ, UK [2] University of Exeter, Environment & Sustainability Institute, Penryn TR10 9EZ, UK. ; 1] Queen's University Belfast, School of Biological Sciences, 97 Lisburn Road, Belfast BT9 7BL, UK [2] Martin-Luther-Universitat Halle-Wittenberg, Institute for Biology/General Zoology, Hoher Weg 8, 06120 Halle (Saale), Germany [3] German Centre for Integrative Biodiversity Research (iDiv), Halle-Jena-Leipzig, Deutscher Platz 5e, 04103 Leipzig, Germany. ; Royal Holloway University of London, School of Biological Sciences, Bourne Building, Egham TW20 0EX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24553241" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Beekeeping/methods ; Bees/classification/*parasitology/physiology/*virology ; Great Britain ; Molecular Sequence Data ; Parasites/genetics/isolation & purification/*pathogenicity ; *Pollination/physiology ; RNA Viruses/genetics/isolation & purification/*pathogenicity ; Risk
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  • 9
    Publication Date: 2014-12-18
    Description: Endocytosis is required for internalization of micronutrients and turnover of membrane components. Endophilin has been assigned as a component of clathrin-mediated endocytosis. Here we show in mammalian cells that endophilin marks and controls a fast-acting tubulovesicular endocytic pathway that is independent of AP2 and clathrin, activated upon ligand binding to cargo receptors, inhibited by inhibitors of dynamin, Rac, phosphatidylinositol-3-OH kinase, PAK1 and actin polymerization, and activated upon Cdc42 inhibition. This pathway is prominent at the leading edges of cells where phosphatidylinositol-3,4-bisphosphate-produced by the dephosphorylation of phosphatidylinositol-3,4,5-triphosphate by SHIP1 and SHIP2-recruits lamellipodin, which in turn engages endophilin. This pathway mediates the ligand-triggered uptake of several G-protein-coupled receptors such as alpha2a- and beta1-adrenergic, dopaminergic D3 and D4 receptors and muscarinic acetylcholine receptor 4, the receptor tyrosine kinases EGFR, HGFR, VEGFR, PDGFR, NGFR and IGF1R, as well as interleukin-2 receptor. We call this new endocytic route fast endophilin-mediated endocytosis (FEME).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boucrot, Emmanuel -- Ferreira, Antonio P A -- Almeida-Souza, Leonardo -- Debard, Sylvain -- Vallis, Yvonne -- Howard, Gillian -- Bertot, Laetitia -- Sauvonnet, Nathalie -- McMahon, Harvey T -- U105178805/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- England -- Nature. 2015 Jan 22;517(7535):460-5. doi: 10.1038/nature14067. Epub 2014 Dec 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] MRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK [2] Institute of Structural and Molecular Biology, University College London &Birkbeck College, London WC1E 6BT, UK. ; Institute of Structural and Molecular Biology, University College London &Birkbeck College, London WC1E 6BT, UK. ; MRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK. ; 1] Institute of Structural and Molecular Biology, University College London &Birkbeck College, London WC1E 6BT, UK [2] Department of Biology, Ecole Normale Superieure de Cachan, 94235 Cachan, France. ; Institut Pasteur, Unite de Pathogenie Moleculaire Microbienne, 28 rue du Docteur Roux, 75724 Paris Cedex 15, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25517094" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Acyltransferases/*metabolism ; Cell Line ; Clathrin ; Dynamins/metabolism ; *Endocytosis ; Humans ; Ligands ; Phosphatidylinositol Phosphates/metabolism ; Pseudopodia/metabolism ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptors, G-Protein-Coupled/metabolism ; Receptors, Interleukin-2/metabolism ; Signal Transduction ; Time Factors
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  • 10
    Publication Date: 2011-07-19
    Description: During early lung development, airway tubes change shape. Tube length increases more than circumference as a large proportion of lung epithelial cells divide parallel to the airway longitudinal axis. We show that this bias is lost in mutants with increased extracellular signal-regulated kinase 1 (ERK1) and ERK2 activity, revealing a link between the ERK1/2 signaling pathway and the control of mitotic spindle orientation. Using a mathematical model, we demonstrate that change in airway shape can occur as a function of spindle angle distribution determined by ERK1/2 signaling, independent of effects on cell proliferation or cell size and shape. We identify sprouty genes, which encode negative regulators of fibroblast growth factor 10 (FGF10)-mediated RAS-regulated ERK1/2 signaling, as essential for controlling airway shape change during development through an effect on mitotic spindle orientation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4260627/" 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/PMC4260627/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tang, Nan -- Marshall, Wallace F -- McMahon, Martin -- Metzger, Ross J -- Martin, Gail R -- 5T32HL007185/HL/NHLBI NIH HHS/ -- R01 CA131201/CA/NCI NIH HHS/ -- R01 CA131261/CA/NCI NIH HHS/ -- R01 CA78711/CA/NCI NIH HHS/ -- R01 DE17744/DE/NIDCR NIH HHS/ -- R01 GM077004/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Jul 15;333(6040):342-5. doi: 10.1126/science.1204831.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy, University of California, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21764747" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Cell Polarity ; Cell Proliferation ; Cell Shape ; Cell Size ; Epithelial Cells/cytology ; Fibroblast Growth Factor 10/genetics/metabolism ; Intracellular Signaling Peptides and Proteins ; Lung/cytology/*embryology/metabolism ; *MAP Kinase Signaling System ; Membrane Proteins/genetics/metabolism ; Mice ; Mice, Knockout ; Mitogen-Activated Protein Kinase 1/*metabolism ; Mitogen-Activated Protein Kinase 3/*metabolism ; Mitosis ; Models, Biological ; *Morphogenesis ; Mutation ; Organogenesis ; Phosphoproteins/genetics/metabolism ; Phosphorylation ; Proto-Oncogene Proteins p21(ras)/genetics/*metabolism ; Respiratory Mucosa/cytology/*embryology ; Spindle Apparatus/*physiology/ultrastructure
    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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