The role of UBR4/HPV16 E7 interaction in cancer

2015 Fiscal Year Final Research Report

• Project/Area Number: 25430119
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Tumor biology
• Research Institution: Kanazawa Medical University
• Principal Investigator: TASAKI Takafumi 金沢医科大学, 総合医学研究所, 准教授 (70629815)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: パピローマウイルス / がん / E7 / UBR4 / 代謝的安定性

Outline of Final Research Achievements

Cervical cancer is caused by certain types of human papilloma virus. The viral E7 is a small 98-amino acid protein that binds various cellular proteins in a host cell. Among these interaction proteins, UBR4 is a huge approx. 5800-amino acids protein. This study found out that the E7 binds to UBR4 via the conservative UBR box domain in UBR4. The UBR box domain is involved in a physiological role of UBR4. Next, we investigated a metabolic stability of the E7 in genetically modified UBR4-deficient cells. The E7 was significantly unstable in the UBR4-lacking cells. Our results suggest that the E7 forms a stable complex with the UBR4 and the complex regulates the viral cancer activity in host cells.

Free Research Field

ユビキチンタンパク質分解システム、ウイルス学