Restoration of p53 activity is a promising chemotherapeutic approach, and because of the high binding affinity between HAUSP, MDM2 and p53, blocking HAUSP activity should have the net effect of robust p53 stabilization. HAUSP is inhibited by belt-like binding of vIRF4 from Kaposi's sarcoma–associated herpesvirus. Two peptides derived from vIRF4 can additively inhibit HAUSP, leading to p53-dependent cell cycle arrest and xenograft tumor regression.
- Hye-Ra Lee
- Won-Chan Choi
- Jae U Jung