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  • 1
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Analytical chemistry 31 (1959), S. 1563-1564 
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 79 (1957), S. 5077-5078 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1420-9039
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mathematics , Physics
    Notes: Zusammenfassung Eine Untersuchung wurde durchgeführt über die adiabatische Strömung der Luft zwischen zwei parallelen Platten, bei einem Druckunterschied quer über die sich bewegende Platte. Die Lösung lässt eine thermale Keilwirkung der hydrodynamischen Schmierung erwarten und gibt eine quantitative Analyse des allgemeineren Problems, wo ein Druckunterschied quer über die Gleitplatte vorhanden ist. Die Ergebnisse deuten an, dass der Beitrag des hydrodynamischen Druckes oft äusserst klein sein kann (für mässige Geschwindigkeiten) im Vergleich zum hydrodynamischen Druck in den dem Druck ausgesetzten Lagern. Im Falle von stillstehenden Platten ist die adiabatische Lösung gleich der isothermen Lösung; weswegen keine Temperaturerhöhung stattfindet.
    Type of Medium: Electronic Resource
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  • 4
    Publication Date: 2013-11-08
    Description: Human immunodeficiency virus (HIV)-1 is able to replicate in primary human macrophages without stimulating innate immunity despite reverse transcription of genomic RNA into double-stranded DNA, an activity that might be expected to trigger innate pattern recognition receptors. We reasoned that if correctly orchestrated HIV-1 uncoating and nuclear entry is important for evasion of innate sensors then manipulation of specific interactions between HIV-1 capsid and host factors that putatively regulate these processes should trigger pattern recognition receptors and stimulate type 1 interferon (IFN) secretion. Here we show that HIV-1 capsid mutants N74D and P90A, which are impaired for interaction with cofactors cleavage and polyadenylation specificity factor subunit 6 (CPSF6) and cyclophilins (Nup358 and CypA), respectively, cannot replicate in primary human monocyte-derived macrophages because they trigger innate sensors leading to nuclear translocation of NF-kappaB and IRF3, the production of soluble type 1 IFN and induction of an antiviral state. Depletion of CPSF6 with short hairpin RNA expression allows wild-type virus to trigger innate sensors and IFN production. In each case, suppressed replication is rescued by IFN-receptor blockade, demonstrating a role for IFN in restriction. IFN production is dependent on viral reverse transcription but not integration, indicating that a viral reverse transcription product comprises the HIV-1 pathogen-associated molecular pattern. Finally, we show that we can pharmacologically induce wild-type HIV-1 infection to stimulate IFN secretion and an antiviral state using a non-immunosuppressive cyclosporine analogue. We conclude that HIV-1 has evolved to use CPSF6 and cyclophilins to cloak its replication, allowing evasion of innate immune sensors and induction of a cell-autonomous innate immune response in primary human macrophages.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3928559/" 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/PMC3928559/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rasaiyaah, Jane -- Tan, Choon Ping -- Fletcher, Adam J -- Price, Amanda J -- Blondeau, Caroline -- Hilditch, Laura -- Jacques, David A -- Selwood, David L -- James, Leo C -- Noursadeghi, Mahdad -- Towers, Greg J -- 090940/Wellcome Trust/United Kingdom -- G0501446/Medical Research Council/United Kingdom -- G0900950/Medical Research Council/United Kingdom -- G9721629/Medical Research Council/United Kingdom -- MC_PC_12024/Medical Research Council/United Kingdom -- MC_U105181010/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- England -- Nature. 2013 Nov 21;503(7476):402-5. doi: 10.1038/nature12769. Epub 2013 Nov 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University College London, Medical Research Council Centre for Medical Molecular Virology, Division of Infection and Immunity, University College London, 90 Gower Street, London WC1E 6BT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24196705" target="_blank"〉PubMed〈/a〉
    Keywords: Capsid Proteins/genetics/metabolism ; Cyclophilins/metabolism ; Cyclosporine/metabolism ; HIV Infections/immunology/metabolism/pathology/virology ; HIV-1/*immunology/metabolism ; Humans ; *Immune Evasion ; Immunity, Innate/*immunology ; Interferon Regulatory Factor-3/metabolism ; Interferon Type I/immunology/secretion ; Macrophages/cytology/*immunology/pathology/*virology ; Molecular Chaperones/metabolism ; Monocytes/cytology ; NF-kappa B/metabolism ; Nuclear Pore Complex Proteins/metabolism ; Receptors, Pattern Recognition ; Virus Internalization ; Virus Replication/immunology ; mRNA Cleavage and Polyadenylation Factors/deficiency/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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