Zur Kurzanzeige

2015-11-26Zeitschriftenartikel DOI: 10.3390/v7122928
Activation of the Mitochondrial Apoptotic Signaling Platform during Rubella Virus Infection
dc.contributor.authorClaus, Claudia
dc.contributor.authorManssen, Lena
dc.contributor.authorHübner, Denise
dc.contributor.authorRoßmark, Sarah
dc.contributor.authorBothe, Viktoria
dc.contributor.authorPetzold, Alice
dc.contributor.authorGroße, Claudia
dc.contributor.authorReins, Mareen
dc.contributor.authorMankertz, Annette
dc.contributor.authorFrey, Teryl K.
dc.contributor.authorLiebert, Uwe G.
dc.date.accessioned2018-05-07T18:45:03Z
dc.date.available2018-05-07T18:45:03Z
dc.date.created2015-12-21
dc.date.issued2015-11-26none
dc.identifier.otherhttp://edoc.rki.de/oa/articles/rerq0Jheqw9Y/PDF/23SrrA9sRm6LQ.pdf
dc.identifier.urihttp://edoc.rki.de/176904/2225
dc.description.abstractMitochondria- as well as p53-based signaling pathways are central for the execution of the intrinsic apoptotic cascade. Their contribution to rubella virus (RV)-induced apoptosis was addressed through time-specific evaluation of characteristic parameters such as permeabilization of the mitochondrial membrane and subsequent release of the pro-apoptotic proteins apoptosis-inducing factor (AIF) and cytochrome c from mitochondria. Additionally, expression and localization pattern of p53 and selected members of the multifunctional and stress-inducible cyclophilin family were examined. The application of pifithrin μ as an inhibitor of p53 shuttling to mitochondria reduced RV-induced cell death to an extent similar to that of the broad spectrum caspase inhibitor z-VAD-fmk (benzyloxycarbonyl-V-A-D-(OMe)-fmk). However, RV progeny generation was not altered. This indicates that, despite an increased survival rate of its cellular host, induction of apoptosis neither supports nor restricts RV replication. Moreover, some of the examined apoptotic markers were affected in a strain-specific manner and differed between the cell culture-adapted strains: Therien and the HPV77 vaccine on the one hand, and a clinical isolate on the other. In summary, the results presented indicate that the transcription-independent mitochondrial p53 program contributes to RV-induced apoptosis.eng
dc.language.isoeng
dc.publisherRobert Koch-Institut, Infektionskrankheiten / Erreger
dc.subjectmPTPeng
dc.subjectp53eng
dc.subjectAIFeng
dc.subjectcyclophilin familyeng
dc.subjectCypAeng
dc.subjectCyp40eng
dc.subjectcytochrome ceng
dc.subjectNIM811eng
dc.subjectPFTμeng
dc.subject.ddc610 Medizin
dc.titleActivation of the Mitochondrial Apoptotic Signaling Platform during Rubella Virus Infection
dc.typeperiodicalPart
dc.identifier.urnurn:nbn:de:0257-10042471
dc.identifier.doi10.3390/v7122928
dc.identifier.doihttp://dx.doi.org/10.25646/2150
local.edoc.container-titleViruses
local.edoc.fp-subtypeArtikel
local.edoc.type-nameZeitschriftenartikel
local.edoc.container-typeperiodical
local.edoc.container-type-nameZeitschrift
local.edoc.container-urlhttp://www.mdpi.com/1999-4915/7/12/2928
local.edoc.container-publisher-nameMDPI
local.edoc.container-volume7
local.edoc.container-issue12
local.edoc.container-year2015

Zur Kurzanzeige