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  • 1
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    Genome-wide RNAi screen identifies human host factors crucial for influenza virus replication (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-01-19
    Description: Influenza A virus, being responsible for seasonal epidemics and reoccurring pandemics, represents a worldwide threat to public health. High mutation rates facilitate the generation of viral escape mutants, rendering vaccines and drugs directed against virus-encoded targets potentially ineffective. In contrast, targeting host cell determinants temporarily dispensable for the host but crucial for virus replication could prevent viral escape. Here we report the discovery of 287 human host cell genes influencing influenza A virus replication in a genome-wide RNA interference (RNAi) screen. Using an independent assay we confirmed 168 hits (59%) inhibiting either the endemic H1N1 (119 hits) or the current pandemic swine-origin (121 hits) influenza A virus strains, with an overlap of 60%. Notably, a subset of these common hits was also essential for replication of a highly pathogenic avian H5N1 strain. In-depth analyses of several factors provided insights into their infection stage relevance. Notably, SON DNA binding protein (SON) was found to be important for normal trafficking of influenza virions to late endosomes early in infection. We also show that a small molecule inhibitor of CDC-like kinase 1 (CLK1) reduces influenza virus replication by more than two orders of magnitude, an effect connected with impaired splicing of the viral M2 messenger RNA. Furthermore, influenza-virus-infected p27(-/-) (cyclin-dependent kinase inhibitor 1B; Cdkn1b) mice accumulated significantly lower viral titres in the lung, providing in vivo evidence for the importance of this gene. Thus, our results highlight the potency of genome-wide RNAi screening for the dissection of virus-host interactions and the identification of drug targets for a broad range of influenza viruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karlas, Alexander -- Machuy, Nikolaus -- Shin, Yujin -- Pleissner, Klaus-Peter -- Artarini, Anita -- Heuer, Dagmar -- Becker, Daniel -- Khalil, Hany -- Ogilvie, Lesley A -- Hess, Simone -- Maurer, Andre P -- Muller, Elke -- Wolff, Thorsten -- Rudel, Thomas -- Meyer, Thomas F -- England -- Nature. 2010 Feb 11;463(7282):818-22. doi: 10.1038/nature08760. Epub 2010 Jan 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Department, Max Planck Institute for Infection Biology, Chariteplatz 1, 10117 Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20081832" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Factors/genetics/metabolism ; Cell Line ; Cells, Cultured ; Chick Embryo ; Cyclin-Dependent Kinase Inhibitor p27/deficiency/genetics/metabolism ; Epithelial Cells/virology ; Genome, Human/genetics ; *Host-Pathogen Interactions/genetics/physiology ; Humans ; Influenza A Virus, H1N1 Subtype/classification/*growth & development ; Influenza, Human/*genetics/*virology ; Lung/cytology ; Mice ; Mice, Inbred C57BL ; Protein-Serine-Threonine Kinases/genetics ; Protein-Tyrosine Kinases/genetics ; *RNA Interference ; Virus Replication/*physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Podoplanin maintains high endothelial venule integrity by interacting with platelet CLEC-2 (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-09-03
    Description: Circulating lymphocytes continuously enter lymph nodes for immune surveillance through specialized blood vessels named high endothelial venules, a process that increases markedly during immune responses. How high endothelial venules (HEVs) permit lymphocyte transmigration while maintaining vascular integrity is unknown. Here we report a role for the transmembrane O-glycoprotein podoplanin (PDPN, also known as gp38 and T1alpha) in maintaining HEV barrier function. Mice with postnatal deletion of Pdpn lost HEV integrity and exhibited spontaneous bleeding in mucosal lymph nodes, and bleeding in the draining peripheral lymph nodes after immunization. Blocking lymphocyte homing rescued bleeding, indicating that PDPN is required to protect the barrier function of HEVs during lymphocyte trafficking. Further analyses demonstrated that PDPN expressed on fibroblastic reticular cells, which surround HEVs, functions as an activating ligand for platelet C-type lectin-like receptor 2 (CLEC-2, also known as CLEC1B). Mice lacking fibroblastic reticular cell PDPN or platelet CLEC-2 exhibited significantly reduced levels of VE-cadherin (also known as CDH5), which is essential for overall vascular integrity, on HEVs. Infusion of wild-type platelets restored HEV integrity in Clec-2-deficient mice. Activation of CLEC-2 induced release of sphingosine-1-phosphate from platelets, which promoted expression of VE-cadherin on HEVs ex vivo. Furthermore, draining peripheral lymph nodes of immunized mice lacking sphingosine-1-phosphate had impaired HEV integrity similar to Pdpn- and Clec-2-deficient mice. These data demonstrate that local sphingosine-1-phosphate release after PDPN-CLEC-2-mediated platelet activation is critical for HEV integrity during immune responses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3791160/" 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/PMC3791160/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herzog, Brett H -- Fu, Jianxin -- Wilson, Stephen J -- Hess, Paul R -- Sen, Aslihan -- McDaniel, J Michael -- Pan, Yanfang -- Sheng, Minjia -- Yago, Tadayuki -- Silasi-Mansat, Robert -- McGee, Samuel -- May, Frauke -- Nieswandt, Bernhard -- Morris, Andrew J -- Lupu, Florea -- Coughlin, Shaun R -- McEver, Rodger P -- Chen, Hong -- Kahn, Mark L -- Xia, Lijun -- GM097747/GM/NIGMS NIH HHS/ -- GM103441/GM/NIGMS NIH HHS/ -- HL065590/HL/NHLBI NIH HHS/ -- HL085607/HL/NHLBI NIH HHS/ -- HL093242/HL/NHLBI NIH HHS/ -- HL103432/HL/NHLBI NIH HHS/ -- HL112788/HL/NHLBI NIH HHS/ -- P01 HL085607/HL/NHLBI NIH HHS/ -- P20 GM103527/GM/NIGMS NIH HHS/ -- P20 RR018758/RR/NCRR NIH HHS/ -- R01 GM097747/GM/NIGMS NIH HHS/ -- R01 HL103432/HL/NHLBI NIH HHS/ -- R01 HL112788/HL/NHLBI NIH HHS/ -- S10 RR024598/RR/NCRR NIH HHS/ -- England -- Nature. 2013 Oct 3;502(7469):105-9. doi: 10.1038/nature12501. Epub 2013 Sep 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23995678" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/metabolism ; Cadherins/metabolism ; Endothelium, Lymphatic/immunology/*metabolism ; Female ; Gene Expression Regulation ; Intercellular Junctions/genetics/immunology ; Lectins, C-Type/*metabolism ; Lymph Nodes/metabolism/pathology ; Lysophospholipids/metabolism ; Male ; Membrane Glycoproteins/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Sphingosine/analogs & derivatives/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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  • 3
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    Nanoscale architecture of integrin-based cell adhesions (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-11-26
    Description: Cell adhesions to the extracellular matrix (ECM) are necessary for morphogenesis, immunity and wound healing. Focal adhesions are multifunctional organelles that mediate cell-ECM adhesion, force transmission, cytoskeletal regulation and signalling. Focal adhesions consist of a complex network of trans-plasma-membrane integrins and cytoplasmic proteins that form a 〈200-nm plaque linking the ECM to the actin cytoskeleton. The complexity of focal adhesion composition and dynamics implicate an intricate molecular machine. However, focal adhesion molecular architecture remains unknown. Here we used three-dimensional super-resolution fluorescence microscopy (interferometric photoactivated localization microscopy) to map nanoscale protein organization in focal adhesions. Our results reveal that integrins and actin are vertically separated by a approximately 40-nm focal adhesion core region consisting of multiple protein-specific strata: a membrane-apposed integrin signalling layer containing integrin cytoplasmic tails, focal adhesion kinase and paxillin; an intermediate force-transduction layer containing talin and vinculin; and an uppermost actin-regulatory layer containing zyxin, vasodilator-stimulated phosphoprotein and alpha-actinin. By localizing amino- and carboxy-terminally tagged talins, we reveal talin's polarized orientation, indicative of a role in organizing the focal adhesion strata. The composite multilaminar protein architecture provides a molecular blueprint for understanding focal adhesion functions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3046339/" 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/PMC3046339/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kanchanawong, Pakorn -- Shtengel, Gleb -- Pasapera, Ana M -- Ramko, Ericka B -- Davidson, Michael W -- Hess, Harald F -- Waterman, Clare M -- Z01 HL005105-01/Intramural NIH HHS/ -- Z99 HL999999/Intramural NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Nov 25;468(7323):580-4. doi: 10.1038/nature09621.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21107430" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Cell Adhesion ; Cell Line ; Cell Line, Tumor ; Cell Membrane/metabolism/ultrastructure ; Extracellular Matrix/*metabolism/ultrastructure ; Humans ; Integrins/*metabolism ; Mice ; Models, Biological
    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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  • 4
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    Cardiac angiogenic imbalance leads to peripartum cardiomyopathy (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-05-19
    Description: Peripartum cardiomyopathy (PPCM) is an often fatal disease that affects pregnant women who are near delivery, and it occurs more frequently in women with pre-eclampsia and/or multiple gestation. The aetiology of PPCM, and why it is associated with pre-eclampsia, remain unknown. Here we show that PPCM is associated with a systemic angiogenic imbalance, accentuated by pre-eclampsia. Mice that lack cardiac PGC-1alpha, a powerful regulator of angiogenesis, develop profound PPCM. Importantly, the PPCM is entirely rescued by pro-angiogenic therapies. In humans, the placenta in late gestation secretes VEGF inhibitors like soluble FLT1 (sFLT1), and this is accentuated by multiple gestation and pre-eclampsia. This anti-angiogenic environment is accompanied by subclinical cardiac dysfunction, the extent of which correlates with circulating levels of sFLT1. Exogenous sFLT1 alone caused diastolic dysfunction in wild-type mice, and profound systolic dysfunction in mice lacking cardiac PGC-1alpha. Finally, plasma samples from women with PPCM contained abnormally high levels of sFLT1. These data indicate that PPCM is mainly a vascular disease, caused by excess anti-angiogenic signalling in the peripartum period. The data also explain how late pregnancy poses a threat to cardiac homeostasis, and why pre-eclampsia and multiple gestation are important risk factors for the development of PPCM.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3356917/" 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/PMC3356917/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Patten, Ian S -- Rana, Sarosh -- Shahul, Sajid -- Rowe, Glenn C -- Jang, Cholsoon -- Liu, Laura -- Hacker, Michele R -- Rhee, Julie S -- Mitchell, John -- Mahmood, Feroze -- Hess, Philip -- Farrell, Caitlin -- Koulisis, Nicole -- Khankin, Eliyahu V -- Burke, Suzanne D -- Tudorache, Igor -- Bauersachs, Johann -- del Monte, Federica -- Hilfiker-Kleiner, Denise -- Karumanchi, S Ananth -- Arany, Zoltan -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 May 9;485(7398):333-8. doi: 10.1038/nature11040.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Institute, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22596155" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bromocriptine/pharmacology/therapeutic use ; Cardiomyopathies/blood/drug therapy/*etiology/*physiopathology ; Disease Models, Animal ; Female ; Heart/drug effects/physiopathology ; Humans ; Kaplan-Meier Estimate ; Male ; Mice ; Mice, Knockout ; Myocytes, Cardiac/drug effects/metabolism ; Neovascularization, Pathologic/*complications/drug therapy/*physiopathology ; Neovascularization, Physiologic/drug effects/physiology ; Pre-Eclampsia/physiopathology ; Pregnancy ; Pregnancy Complications, Cardiovascular/blood/drug ; therapy/*etiology/*physiopathology ; Trans-Activators/deficiency/genetics/metabolism ; Transcription Factors ; Vascular Endothelial Growth Factor A/pharmacology/therapeutic use ; Vascular Endothelial Growth Factor ; Receptor-1/blood/genetics/metabolism/pharmacology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Slowing Amazon deforestation through public policy and interventions in beef and soy supply chains (2014)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2014-06-07
    Description: The recent 70% decline in deforestation in the Brazilian Amazon suggests that it is possible to manage the advance of a vast agricultural frontier. Enforcement of laws, interventions in soy and beef supply chains, restrictions on access to credit, and expansion of protected areas appear to have contributed to this decline, as did a decline in the demand for new deforestation. The supply chain interventions that fed into this deceleration are precariously dependent on corporate risk management, and public policies have relied excessively on punitive measures. Systems for delivering positive incentives for farmers to forgo deforestation have been designed but not fully implemented. Territorial approaches to deforestation have been effective and could consolidate progress in slowing deforestation while providing a framework for addressing other important dimensions of sustainable development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nepstad, Daniel -- McGrath, David -- Stickler, Claudia -- Alencar, Ane -- Azevedo, Andrea -- Swette, Briana -- Bezerra, Tathiana -- DiGiano, Maria -- Shimada, Joao -- Seroa da Motta, Ronaldo -- Armijo, Eric -- Castello, Leandro -- Brando, Paulo -- Hansen, Matt C -- McGrath-Horn, Max -- Carvalho, Oswaldo -- Hess, Laura -- New York, N.Y. -- Science. 2014 Jun 6;344(6188):1118-23. doi: 10.1126/science.1248525.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Earth Innovation Institute, 3180 18th Street, Suite 205, San Francisco, CA 94110, USA. dnepstad@earthinnovation.org. ; Earth Innovation Institute, 3180 18th Street, Suite 205, San Francisco, CA 94110, USA. Universidade Federal do Oeste do Para, Bairro Fatima CEP 68040-470 Santarem, Para, Brasil. ; Earth Innovation Institute, 3180 18th Street, Suite 205, San Francisco, CA 94110, USA. ; Instituto de Pesquisa Ambiental da Amazonia, SHIN CA 5, Bloco J2, Sala 309, Bairro, Lago Norte, Brasilia-DF 71503-505. ; Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Brasil. ; Virginia Polytechnic Institute and State University, Blacksburg, VA 24061, USA. ; Instituto de Pesquisa Ambiental da Amazonia, SHIN CA 5, Bloco J2, Sala 309, Bairro, Lago Norte, Brasilia-DF 71503-505. Carnegie Institution for Science, 260 Panama Street, Stanford, CA 94305, USA. ; University of Maryland Department of Geographical Sciences, College Park, MD 20742, USA. ; Earth Research Institute, University of California, Santa Barbara, CA 93106-3060, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24904156" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brazil ; Cattle ; Conservation of Natural Resources/*trends ; Humans ; Meat/*supply & distribution ; *Public Policy ; Soybeans/*supply & distribution
    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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  • 6
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    Metagenomic discovery of biomass-degrading genes and genomes from cow rumen (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-01-29
    Description: The paucity of enzymes that efficiently deconstruct plant polysaccharides represents a major bottleneck for industrial-scale conversion of cellulosic biomass into biofuels. Cow rumen microbes specialize in degradation of cellulosic plant material, but most members of this complex community resist cultivation. To characterize biomass-degrading genes and genomes, we sequenced and analyzed 268 gigabases of metagenomic DNA from microbes adherent to plant fiber incubated in cow rumen. From these data, we identified 27,755 putative carbohydrate-active genes and expressed 90 candidate proteins, of which 57% were enzymatically active against cellulosic substrates. We also assembled 15 uncultured microbial genomes, which were validated by complementary methods including single-cell genome sequencing. These data sets provide a substantially expanded catalog of genes and genomes participating in the deconstruction of cellulosic biomass.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hess, Matthias -- Sczyrba, Alexander -- Egan, Rob -- Kim, Tae-Wan -- Chokhawala, Harshal -- Schroth, Gary -- Luo, Shujun -- Clark, Douglas S -- Chen, Feng -- Zhang, Tao -- Mackie, Roderick I -- Pennacchio, Len A -- Tringe, Susannah G -- Visel, Axel -- Woyke, Tanja -- Wang, Zhong -- Rubin, Edward M -- New York, N.Y. -- Science. 2011 Jan 28;331(6016):463-7. doi: 10.1126/science.1200387.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Energy, Joint Genome Institute, Walnut Creek, CA 94598, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21273488" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Bacteria/enzymology/*genetics/isolation & purification/metabolism ; Bacterial Proteins/chemistry/genetics/metabolism ; *Biomass ; Carbohydrate Metabolism ; Cattle/*microbiology ; Cellulase/genetics/metabolism ; Cellulases/chemistry/*genetics/metabolism ; Cellulose/*metabolism ; Cellulose 1,4-beta-Cellobiosidase/genetics/metabolism ; Genes, Bacterial ; Genome, Bacterial ; *Metagenome ; Metagenomics/methods ; Molecular Sequence Annotation ; Molecular Sequence Data ; Poaceae/microbiology ; Rumen/metabolism/*microbiology ; Sequence Analysis, DNA
    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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