Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-6301
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dc.contributor.authorZeyen, Lisa-
dc.contributor.authorDöring, Tatjana-
dc.contributor.authorStieler, Jens T.-
dc.contributor.authorPrange, Reinhild-
dc.date.accessioned2021-08-24T09:23:29Z-
dc.date.available2021-08-24T09:23:29Z-
dc.date.issued2020-
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/6311-
dc.description.abstractHepatitis B virus (HBV) is a leading cause of liver disease. Its success as a human pathogen is related to the immense production of subviral envelope particles (SVPs) contributing to viral persistence by interfering with immune functions. To explore cellular pathways involved in SVP formation and egress, we investigated host–pathogen interactions. Yeast-based proteomics revealed Sec24A, a component of the coat protein complex II (COPII), as an interaction partner of the HBV envelope S domain. To understand how HBV co-opts COPII as a proviral machinery, we studied roles of key Sec proteins in HBV-expressing liver cells. Silencing of Sar1, Sec23, and Sec24, which promote COPII assembly concomitant with cargo loading, strongly diminished endoplasmic reticulum (ER) envelope export and SVP secretion. By analysing Sec paralog specificities, we unexpectedly found that the HBV envelope is a selective interaction partner of Sec24A and Sec23B whose functions could not be substituted by their related isoforms. In support, we found that HBV replication upregulated Sec24A and Sec23B transcription. Furthermore, HBV encountered the Sec24A/Sec23B complex via an interaction that involved the N-terminal half of Sec24A and a di-arginine motif of its S domain, mirroring a novel ER export code. Accordingly, an interference with the COPII/HBV cross-talk might display a tool to effectively inhibit SVP release.en_GB
dc.language.isoengde
dc.rightsCC BY*
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleHepatitis B subviral envelope particles use the COPII machinery for intracellular transport via selective exploitation of Sec24A and Sec23Ben_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-6301-
jgu.type.dinitypearticleen_GB
jgu.type.versionPublished versionde
jgu.type.resourceTextde
jgu.organisation.departmentFB 04 Medizinde
jgu.organisation.number2700-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titleCellular microbiologyde
jgu.journal.volume22de
jgu.journal.issue6de
jgu.pages.alternativee13181de
jgu.publisher.year2020-
jgu.publisher.nameWiley-Blackwellde
jgu.publisher.placeOxfordde
jgu.publisher.urihttps://doi.org/10.1111/cmi.13181de
jgu.publisher.issn1462-5822de
jgu.organisation.placeMainz-
jgu.subject.ddccode610de
jgu.publisher.doi10.1111/cmi.13181
jgu.organisation.rorhttps://ror.org/023b0x485
Appears in collections:JGU-Publikationen

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