愛滋病毒Vpr 蛋白之功能研究及其與HAX-1 和脊椎肌肉萎縮基因之作用(1/3)
Date Issued
2002
Date
2002
Author(s)
黃立民
DOI
902314B002160
Abstract
HIV-1 Vpr, a 96-amino-acid 14-kDa
protein, has several important and interesting
functions, including nuclear translocation of
the pre-integration complex, cell cycle arrest
at the G2/M phase, transactivation,
enhancement of virus replication, and
apoptosis. To understand the role of Vpr in
HIV-1 life cycle and pathogenesis, yeast
two-hybrid system had been used and cDNA
encoding HAX-1 or SMN1 protein was
identified. Interaction between Vpr and
HAX-1 (or SMN1) was characterized by in
vitro protein-protein binding assay.
Furthermore, over-expressed HAX-1 or
N-terminal of HAX-1 in HeLa cells blocks
the nuclear transport of a Vpr-GFP fusion
protein while C-terminal of HAX-1 fail to
block Vpr-GFP nuclear transport. We
hypothesize that cytoplasmic retention of
HIV-1 regulatory protein Vpr by
protein-protein interaction with human
cytoplasmic protein HAX-1 may cause
functional changes in the host cell that affect
HIV-1 pathogenesis.
It is difficult to evaluate the interaction
of Vpr and SMN1 since little is known about
SMN1 how to cause the degeneration of
motor neuron the developing to spinal
muscular atrophy disease. Newly studies find
that Vpr induces apoptosis in neuronal cells,
and the correlations between SMN1 and
antiapoptosis protein, NAIP (neuronal
apoptosis inhibitory protein) and Bcl-2, has
been proved. In coming project we will try to
verify the possible functional mechanism.
This article provides guidance for report writing
under the Grant of National Science Council
beginning from fiscal year 1998.
Subjects
HIV-1
yeast two - hybrid system
SDGs
Publisher
臺北市：國立臺灣大學醫學院小兒科
Type
report
File(s)![Thumbnail Image]()
Loading...
Name
902314B002160.pdf
Size
269.84 KB
Format
Adobe PDF
Checksum
(MD5):f0c4fa24f60661a781d89c97d34caa9b