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Human hepatitis B virus X protein induces apoptosis in HepG2 cells: role of BH3 domain.

Abstract：

:The smallest protein of hepatitis B virus, HBX, has been implicated in the development of liver diseases by interfering with normal cellular processes. Its role in cell proliferation has been unclear as both pro-apoptotic and anti-apoptotic activities have been reported. We showed molecular evidence that HBX induced apoptosis in HepG2 cells. A Bcl-2 Homology Domain 3 was identified in HBX, which interacted with anti-apoptotic but not pro-apoptotic members of the Bcl-2 family of proteins. HBX induced apoptosis when transfected into HepG2 cells, as demonstrated by both flow cytometry and caspase-3 activity. However, HBX protein may not be stable in apoptotic cells triggered by its own expression as only its mRNA or the fusion protein with the glutathione-S-transferase was detected in transfected cells. Our results suggested that HBX behaved as a pro-apoptotic protein and was able to induce apoptosis.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Lu YW,Chen WN

doi

10.1016/j.bbrc.2005.10.117

subject

Has Abstract

pub_date

2005-12-23 00:00:00

pages

1551-6

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(05)02363-6

journal_volume

338

pub_type

杂志文章

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