Please use this identifier to cite or link to this item: http://scholarbank.nus.edu.sg/handle/10635/30686
Title: CHARACTERIZATION OF INTERACTIONS BETWEEN HEPATITIS C VIRUS AND HOST PROTEINS AND THEIR EFFECTS ON APOPTOSIS
Authors: NUR KHAIRIAH BINTE MOHD ISMAIL
Keywords: HCV, apoptosis, core, Bcl-2 protein family
Issue Date: 29-Sep-2011
Source: NUR KHAIRIAH BINTE MOHD ISMAIL (2011-09-29). CHARACTERIZATION OF INTERACTIONS BETWEEN HEPATITIS C VIRUS AND HOST PROTEINS AND THEIR EFFECTS ON APOPTOSIS. ScholarBank@NUS Repository.
Abstract: Hepatitis C virus (HCV) is a leading cause of chronic liver disease. Comprehensive understanding of HCV replication and pathogenesis is crucial for the development of successful therapies. The aim of this project is to identify and characterize interactions between HCV and host proteins, specifically in relation to apoptosis. We have identified a Bcl-2 homology 3 (BH3) domain in the HCV core protein that is essential for its proapoptotic property and for specific interaction with the human myeloid cell factor 1 (Mcl-1), a prosurvival member of the Bcl-2 family. Elevated levels of endogenous Bcl-XL, another prosurvival Bcl-2 protein, were detected in HCV-infected Huh7.5 cells. Suppression of Bcl-XL upregulation in HCV-infected cells by small interfering RNA (siRNA) significantly increased apoptosis, suggesting a role for Bcl-XL in modulating HCV-mediated apoptosis. Gene expression profiling of HCV-infected cells by quantitative PCR array analysis was also performed to identify host apoptotic genes that are transcriptionally regulated by infection.
URI: http://scholarbank.nus.edu.sg/handle/10635/30686
Appears in Collections:Ph.D Theses (Open)

Show full item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
NurKhairiahMI.pdf2.73 MBAdobe PDF

OPEN

NoneView/Download

Page view(s)

226
checked on Dec 11, 2017

Download(s)

28
checked on Dec 11, 2017

Google ScholarTM

Check


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.