Hepatitis B Virus (HBV) signifies a widely disseminated hepatotropic DNA virus, the infection of which places the patient at elevated risks for hepatitis, cirrhosis, and even hepatocarcinoma. The viral genome of HBV is composed of four overlapping open reading frames, tasked with encoding the envelope glycoprotein, pre-core/core, HBx, and polymerase.
The gene HBVgp3 is responsible for the transcription of HBx, serving as the trans-activating factor of the HBV genome. The expression of this gene disrupts normal cellular signaling pathways and modifies the gene expression of host cells. In conjunction with viral genome synergistic effects, it inhibits gene inactivation, triggers carcinogenic genes, and leads to the onset of hepatocarcinoma.
Fig.1 Open reading frames of HBV.1
Generally, HBVgp3 is non-methylated in most hepatocarcinoma cell lines, and is therefore considered a potential intervention target for HBV or hepatocarcinoma. Antibody drugs specifically targeting this area and relevant research are currently being extensively conducted and promoted.
Reference
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