The University of Osaka · Medicine
Professor Keiji Ueda's research lab focuses on viral oncogenesis and the molecular mechanisms underlying persistent viral infections, particularly hepatitis B virus (HBV) and Kaposi's sarcoma-associated herpesvirus (KSHV). The lab investigates viral genome replication, latency, and the role of viral and cellular factors in pathogenesis, with a strong emphasis on how viral proteins and regulatory elements manipulate host cell machinery. Key research directions include the function of viral structural proteins in virion assembly, the role of latency-associated antigens in genome maintenance, and the transcriptional regulation of viral oncogenes. The lab also explores viral oncogene-induced cellular transformation and apoptosis, particularly in the context of hepatocarcinogenesis driven by viral integration.
Figures are computed from collected data and may differ slightly.
The infectious particles of hepatitis B virus are called Dane particles and consist of viral nucleic acid encapsulated within a core particle that is enveloped by virus-coded surface proteins. The major S protein constitutes a significant fraction of these surface proteins. In addition, there are two other related proteins (large S and middle S), but their role in envelope formation has not yet been elucidated. We modified the translation initiation codon ATG of each of the envelope proteins by
During latency, Kaposi's sarcoma-associated herpesvirus (KSHV) is thought to replicate once and to be partitioned in synchrony with the cell cycle of the host. In this replication cycle, the KSHV terminal repeat (TR) sequence functions as a replication origin, assisted by the latency-associated nuclear antigen (LANA). Thus, TR seems to function as a cis element for the replication and partitioning of the KSHV genome. Viral replication and partitioning are also likely to require cellular factors
The replication and transcription activator (RTA) of Kaposi's sarcoma-associated herpesvirus (KSHV), or human herpesvirus 8, a homologue of Epstein-Barr virus BRLF1 or Rta, is a strong transactivator and inducer of lytic replication. RTA acting alone can induce lytic replication of KSHV in infected cell lines that originated from primary effusion lymphomas, leading to virus production. During the lytic replication process, RTA activates many kinds of genes, including polyadenylated nuclear RNA,
Induction of hepatocellular carcinoma in woodchucks by woodchuck hepatitis virus is associated with the activation of N-myc gene expression, usually by viral DNA integration in cis to the N-myc locus. We have examined the consequences of N-myc up-regulation in rodent hepatic cells in culture. Mouse alpha ML hepatocytes infected with a retroviral vector overexpressing the woodchuck N-myc2 gene display a higher proliferation rate than parental alpha ML cells but are morphologically unchanged and d
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