| |  Online-Ressource |
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| Verfasst von: | Klemke, Martin [VerfasserIn]  |
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| | Wabnitz, Guido H. [VerfasserIn] |
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| | Funke, Faustina [VerfasserIn] |
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| | Funk, Beate [VerfasserIn] |
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| | Kirchgessner, Henning [VerfasserIn] |
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| | Samstag, Yvonne [VerfasserIn] |
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| Titel: | Oxidation of cofilin mediates T cell hyporesponsiveness under oxidative stress conditions |
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| Verf.angabe: | Martin Klemke, Guido H. Wabnitz, Faustina Funke, Beate Funk, Henning Kirchgessner, Yvonne Samstag |
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| E-Jahr: | 2008 |
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| Jahr: | 4 September 2008 |
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| Umfang: | 10 S. |
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| Teil: | volume:29 |
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| | year:2008 |
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| | number:3 |
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| | pages:404-413 |
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| | extent:10 |
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| Fussnoten: | Gesehen am 16.07.2021 |
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| Titel Quelle: | Enthalten in: Immunity |
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| Ort Quelle: | [Cambridge, Mass.] : Cell Press, 1994 |
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| Jahr Quelle: | 2008 |
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| Band/Heft Quelle: | 29(2008), 3, Seite 404-413 |
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| ISSN Quelle: | 1097-4180 |
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| Abstract: | Oxidative stress leads to impaired T cell activation. A central integrator of T cell activation is the actin-remodelling protein cofilin. Cofilin is activated through dephosphorylation at Ser3. Activated cofilin enables actin dynamics through severing and depolymerization of F-actin. Binding of cofilin to actin is required for formation of the immune synapse and T cell activation. Here, we showed that oxidatively stressed human T cells were impaired in chemotaxis- and costimulation-induced F-actin modulation. Although cofilin was dephosphorylated, steady-state F-actin levels increased under oxidative stress conditions. Mass spectrometry revealed that cofilin itself was a target for oxidation. Cofilin oxidation induced formation of an intramolecular disulfide bridge and loss of its Ser3 phosphorylation. Importantly, dephosphorylated oxidized cofilin, although still able to bind to F-actin, did not mediate F-actin depolymerization. Impairing actin dynamics through oxidation of cofilin provides a molecular explanation for the T cell hyporesponsiveness caused by oxidative stress. |
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| DOI: | doi:10.1016/j.immuni.2008.06.016 |
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| URL: | Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.
Volltext ; Verlag: https://doi.org/10.1016/j.immuni.2008.06.016 |
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| | Volltext: https://www.sciencedirect.com/science/article/pii/S1074761308003695 |
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| | DOI: https://doi.org/10.1016/j.immuni.2008.06.016 |
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| Datenträger: | Online-Ressource |
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| Sprache: | eng |
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| Sach-SW: | Actin Depolymerizing Factors |
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| | Actins |
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| | CD28 Antigens |
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| | CD3 Complex |
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| | Chemotaxis, Leukocyte |
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| | Humans |
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| | Hydrogen Peroxide |
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| | Lim Kinases |
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| | Lymphocyte Activation |
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| | Neutrophil Activation |
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| | Neutrophils |
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| | Oxidation-Reduction |
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| | Oxidative Stress |
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| | Phosphorylation |
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| | T-Lymphocytes |
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| K10plus-PPN: | 1763034895 |
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| Verknüpfungen: | → Zeitschrift |
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Oxidation of cofilin mediates T cell hyporesponsiveness under oxidative stress conditions / Klemke, Martin [VerfasserIn]; 4 September 2008 (Online-Ressource)
