Prothymosin α plays multifunctional cell robustness roles in genomic, epigenetic, and nongenomic mechanisms
Article first published online: 9 OCT 2012
© 2012 New York Academy of Sciences.
Annals of the New York Academy of Sciences
Volume 1269, Thymosins in Health and Disease I pages 34–43, October 2012
How to Cite
Ueda, H., Matsunaga, H. and Halder, S. K. (2012), Prothymosin α plays multifunctional cell robustness roles in genomic, epigenetic, and nongenomic mechanisms. Annals of the New York Academy of Sciences, 1269: 34–43. doi: 10.1111/j.1749-6632.2012.06675.x
- Issue published online: 9 OCT 2012
- Article first published online: 9 OCT 2012
- linker histone H1;
- estrogen receptor;
- Toll-like receptor-4
Prothymosin α (ProTα) possesses multiple functions for cell robustness. This protein functions intracellularly to stimulate cell proliferation and differentiation through epigenetic or genomic mechanisms. ProTα also regulates the cell defensive mechanisms through an interaction with the Nrf2-Keap1 system. Under the apoptotic conditions, it inhibits apoptosome formation by binding to Apaf-1. Regarding extracellular functions, ProTα is extracellularly released from the nucleus upon necrosis-inducing ischemia stress in a manner of nonclassical release, and thereby inhibits necrosis. However, under the condition of apoptosis, the C-terminus of ProTα is cleaved off and loses binding activity to cargo protein S100A13 for nonclassical release. However, cleaved ProTα is retained in the cytosol and inhibits apoptosome formation. ProTα was recently reported to cause immunological actions through the Toll-like receptor 4. However, the authors also suggest the possible existence of additional receptors for robust cell activities against ischemia stress.