TY  - JOUR
A2  - Ahn, Sang-hoon
AB  - The hepatitis B virus (HBV) genome encodes the X protein (HBx), a ubiquitous transactivator that is required for HBV replication. Expression of the HBx protein has been associated with the development of HBV infection-related hepatocellular carcinoma (HCC). Previously, we generated a 3D structure of HBx by combined homology and ab initio in silico modelling. This structure showed a striking similarity to the human thymine DNA glycosylase (TDG), a key enzyme in the base excision repair (BER) pathway. To further explore this finding, we investigated whether both proteins interfere with or complement each other’s functions. Here we show that TDG does not affect HBV replication, but that HBx strongly inhibits TDG-initiated base excision repair (BER), a major DNA repair pathway. Inhibition of the BER pathway may contribute substantially to the oncogenic effect of HBV infection.
AU  - van de Klundert, Maarten A. A
AU  - van Hemert, Formijn J
AU  - Zaaijer, Hans L
AU  - Kootstra, Neeltje A
CY  - San Francisco, USA
DA  - 20121108
DO  - 10.1371/journal.pone.0048940
KW  - Research Article ; Biology ; Computer Science ; Medicine ; Infectious Diseases ; Molecular Biology ; Oncology ; Computer Science
LA  - eng
PB  - Public Library of Science
PY  - 20121108
SN  - 1932-6203
SP  - e48940
TI  - The Hepatitis B Virus X Protein Inhibits Thymine DNA Glycosylase Initiated Base Excision Repair (Inhibition of BER by the HBV Protein X)
Y2  - 2021-04-19T11:32:04+02:00
ER  -