Abstract
The virus-derived protein Apoptin has the ability to induce p53-independent apoptosis in a variety of human cancer cells while leaving normal cells unharmed. It thus represents a potential anti-cancer therapeutic agent of the future but a proper understanding of Apoptin-induced signalling events is necessary prior to clinical application. The tumor-specific nuclear translocation and phosphorylation of Apoptin by a cellular kinase such as protein kinase C seem to be required for its function but otherwise the mode of tumor selectivity remains unknown. Apoptin has been shown to interact with several cellular proteins including Akt and the anaphase-promoting complex that regulate its activity and promote caspase-dependent apoptosis. This chapter summarizes the available data on tumor-specific pathways sensed by Apoptin and the mechanism of Apoptin-induced cell death.
| Original language | English |
|---|---|
| Pages (from-to) | 11-37 |
| Number of pages | 27 |
| Journal | Advances in Experimental Medicine And Biology |
| Volume | 818 |
| Early online date | 16 Jun 2014 |
| DOIs | |
| Publication status | Published - 2014 |
Keywords
- Active Transport, Cell Nucleus
- Animals
- Antineoplastic Agents
- Apoptosis
- Capsid Proteins
- Caspases
- Cell Nucleus
- Humans
- Neoplasms
- Protein Kinase C
- Signal Transduction
- Tumor Suppressor Protein p53
