ZBP-89 Promotes Growth Arrest through Stabilization of p53

• DOI: 10.1128/mcb.21.14.4670-4683.2001
• Publication Date: 2002-07-27T10:06:23Z
• Authors: Longchuan Bai; Juanita L. Merchant
• Keywords: p14arf

Transcription factor p53 can induce growth arrest and/or apoptosis in cells through activation or repression of downstream target genes. Recently, we reported that ZBP-89 cooperates with histone acetyltransferase coactivator p300 the regulation p21(waf1), a cyclin-dependent kinase inhibitor whose associated gene is p53. Therefore, examined whether might also inhibit cell by activating In present study, demonstrate elevated levels and human gastrointestinal lines. The protein accumulated within 4 h, 16 serum starvation without changes p14ARF levels, demonstrating physiological increase cellular these two proteins. Overexpression stabilized enhanced its transcriptional activity direct protein-protein interactions. DNA binding C-terminal domains zinc finger domain mediated interaction. A point mutation domain, R273H, greatly reduced ZBP-89-mediated stabilization but not their physical Furthermore, formed complex MDM2 therefore did prevent MDM2-p53 However, heterokaryon assays demonstrated retained nucleus. Collectively, data indicate regulates proliferation part ability to directly bind retard nuclear export. Our findings further our understanding how modulates reveals novel mechanism which stabilized.