 As we have seen, many of the molecules necessary for glucocorticoid-induced apoptosis are constitutively expressed in the cytoplasm. These include: GR, Apaf-1, and caspase precursors. Thus, it is very important that there be regulatory mechanisms in place to stop apoptosis in a healthy cell. (this concept is very applicable to other forms of apoptosis, as well.)
The most well-known inhibitor of glucocorticoid-induced apoptosis is Bcl-2. This molecule binds to Bax, preventing it from forming pores in the mitochondria. Apoptosis can only proceed when Bcl-2 is outnumbered by Bax.
Current research suggests that heat shock proteins may also act to inhibit apoptosis.
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