Translocation and accumulation of exogeneous hepatitis B virus preS surface proteins in the cell nucleus

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dc.contributor.authorEun Wie Cho-
dc.contributor.authorJung Hyun Park-
dc.contributor.authorOok Joon Yoo-
dc.contributor.authorKil Lyong Kim-
dc.date.accessioned2017-04-19T08:57:50Z-
dc.date.available2017-04-19T08:57:50Z-
dc.date.issued2001-
dc.identifier.issn0021-9533-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/5410-
dc.description.abstractRecurrent reports about protease-sensitive sites in the junction of the preS and S region of the hepatitis B virus large surface protein have raised the question about a possible biological role of S protein-depleted, independent preS protein fragments in the virus life cycle. In the present study, this question was addressed by exogenous introduction of fluorescence-labeled recombinant preS proteins into permeabilized HepG2 cells. While maltose-binding proteins (MBP) were evenly distributed throughout the cytoplasm, MBP-preS fusion proteins selectively accumulated in the nucleus. Using truncated preS proteins, the effective domain for this nuclear accumulation was localized around the preS2 region. The mode of this action differs from conventional nuclear translocation mechanism in its energy- and mediator-independency and in that it is not saturated regardless of the increase of preS protein concentration. The biological meaning of this phenomenon has to be further studied. However, in regard to hepatitis B virus infection, this observation might provide a clue for unveiling the still poorly characterized events after initial internalization of the virus, which might make use of the nuclear translocation effect of the preS2 region to facilitate the infection.-
dc.publisherCompany Biologists Ltd-
dc.titleTranslocation and accumulation of exogeneous hepatitis B virus preS surface proteins in the cell nucleus-
dc.title.alternativeTranslocation and accumulation of exogeneous hepatitis B virus preS surface proteins in the cell nucleus-
dc.typeArticle-
dc.citation.titleJournal of Cell Science-
dc.citation.number6-
dc.citation.endPage1123-
dc.citation.startPage1115-
dc.citation.volume114-
dc.contributor.affiliatedAuthorEun Wie Cho-
dc.contributor.affiliatedAuthorJung Hyun Park-
dc.contributor.affiliatedAuthorKil Lyong Kim-
dc.contributor.alternativeName조은위-
dc.contributor.alternativeName박정현-
dc.contributor.alternativeName유욱준-
dc.contributor.alternativeName김길룡-
dc.identifier.bibliographicCitationJournal of Cell Science, vol. 114, no. 6, pp. 1115-1123-
dc.subject.keywordhepatitis B virus-
dc.subject.keywordPreS2 region-
dc.subject.keywordenergy-independent translocation-
dc.subject.localhepatitis B virus (HBV)-
dc.subject.localHepatitis B Virus-
dc.subject.localHepatitis B virus (HBV)-
dc.subject.localhepatitis B virus-
dc.subject.localhepatitis B Virus (HBV)-
dc.subject.localHepatitis B virus-
dc.subject.localPreS2 region-
dc.subject.localenergy-independent translocation-
dc.description.journalClassY-
Appears in Collections:
Division of Biomedical Research > Rare Disease Research Center > 1. Journal Articles
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