کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3424592 1227233 2012 10 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Hepatitis B virus regulatory HBx protein binding to DDB1 is required but is not sufficient for maximal HBV replication
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ویروس شناسی
پیش نمایش صفحه اول مقاله
Hepatitis B virus regulatory HBx protein binding to DDB1 is required but is not sufficient for maximal HBV replication
چکیده انگلیسی

Robust hepatitis B virus (HBV) replication is stimulated by the regulatory HBx protein. HBx binds the cellular protein DDB1; however, the importance of this interaction for HBV replication remains unknown. We tested whether HBx binding to DDB1 was required for HBV replication using a plasmid based replication assay in HepG2 cells. Three DDB1 binding-deficient HBx point mutants (HBx69, HBx90/91, HBxR96E) failed to restore wildtype levels of replication from an HBx-deficient plasmid, which established the importance of the HBx-DDB1 interaction for maximal HBV replication. Analysis of overlapping HBx truncation mutants revealed that both the HBx-DDB1 binding domain and the carboxyl region are required for maximal HBV replication both in vitro and in vivo, suggesting the HBx-DDB1 interaction recruits regulatory functions critical for replication. Finally we demonstrate that HBx localizes to the Cul4A-DDB1 complex, and discuss the possible implications for models of HBV replication.


► We studied the requirement of HBx binding to DDB1 in HBV replication.
► HBx binding to DDB1 was required but was not sufficient for virus replication.
► HBx transactivation function from the COOH portion of HBx is also needed.
► The two functions must be provided on the same protein.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Virology - Volume 426, Issue 1, 25 April 2012, Pages 73–82
نویسندگان
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