Molecular piracy by Kaposis Sarcoma-Associated Herpesvirus: dysregulation of wnt signaling and the unfolded protein response

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K07952
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Biological pharmacy
• Research Institution: Kyoto Pharmaceutical University
• Principal Investigator: Fujimuro Masahiro 京都薬科大学, 薬学部, 教授 (20360927)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: ウイルス / 小胞体ストレス / Wntシグナル / リンパ腫 / アポトーシス / ヘルペスウイルス

Outline of Final Research Achievements

Kaposi’s sarcoma associated herpesvirus (KSHV) is　an oncogenic DNA virus and classified in the gamma-herpesvirus subfamily. Kaposi's sarcoma and AIDS-related primary effusion lymphoma (PEL) is caused by KSHV infection. We have demonstrated that LANA protein suppresses the phosphorylation ability of GSK-3beta and stabilizes the protein-X by binding to the GSK-3beta. In addition, KSHV encoded vCyclin and LANA suppressed the unfolded protein response (UPR) such as IRE1 and PERK transcription, suggesting that KSHV achieves anti-apoptosis through the suppression of pro-apoptotic UPR. Furthermore, we found that diallyl trisulfide, methylseleninic acid, and sodium selenite are the novel and effective drugs against PEL.

Free Research Field

細胞生物学