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Status: Bibliographieeintrag

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Verfasst von:Magalhães, Ana Cristina [VerfasserIn]   i
 Islinger, Markus [VerfasserIn]   i
Titel:Peroxisomes are platforms for cytomegalovirus’ evasion from the cellular immune response
Verf.angabe:Ana Cristina Magalhães, Ana Rita Ferreira, Sílvia Gomes, Marta Vieira, Ana Gouveia, Isabel Valença, Markus Islinger, Rute Nascimento, Michael Schrader, Jonathan C. Kagan and Daniela Ribeiro
E-Jahr:2016
Jahr:16 May 2016
Umfang:14 S.
Fussnoten:Gesehen am 09.05.2019
Titel Quelle:Enthalten in: Scientific reports
Ort Quelle:[London] : Springer Nature, 2011
Jahr Quelle:2016
Band/Heft Quelle:6(2016) Artikel-Nummer 26028, 14 Seiten
ISSN Quelle:2045-2322
Abstract:The human cytomegalovirus developed distinct evasion mechanisms from the cellular antiviral response involving vMIA, a virally-encoded protein that is not only able to prevent cellular apoptosis but also to inhibit signalling downstream from mitochondrial MAVS. vMIA has been shown to localize at mitochondria and to trigger their fragmentation, a phenomenon proven to be essential for the signalling inhibition. Here, we demonstrate that vMIA is also localized at peroxisomes, induces their fragmentation and inhibits the peroxisomal-dependent antiviral signalling pathway. Importantly, we demonstrate that peroxisomal fragmentation is not essential for vMIA to specifically inhibit signalling downstream the peroxisomal MAVS. We also show that vMIA interacts with the cytoplasmic chaperone Pex19, suggesting that the virus has developed a strategy to highjack the peroxisomal membrane proteins’ transport machinery. Furthermore, we show that vMIA is able to specifically interact with the peroxisomal MAVS. Our results demonstrate that peroxisomes constitute a platform for evasion of the cellular antiviral response and that the human cytomegalovirus has developed a mechanism by which it is able to specifically evade the peroxisomal MAVS-dependent antiviral signalling.
DOI:doi:10.1038/srep26028
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: https://doi.org/10.1038/srep26028
 Volltext: https://www.nature.com/articles/srep26028
 DOI: https://doi.org/10.1038/srep26028
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1665052481
Verknüpfungen:→ Zeitschrift

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