Selenite Inhibits the c-Jun N-terminal Kinase/Stress-activated Protein Kinase (JNK/SAPK) through a Thiol Redox Mechanism*

Selenium, an essential biological trace element, has been shown to modulate functions of many regulatory proteins involved in signal transduction and to affect a variety of cellular activities including cell growth, survival, and death. The molecular mechanism by which selenium exerts its action on the cellular events, however, remains unclear. In our present study, we observed that selenite suppresses both the c-Jun N-terminal …