See the glucocorticoid?Glucocorticoid enters the cell and binds to the GR. The GR changes conformation and the heat shock proteins fall off.
The activated GR/glucocorticoid complex binds to another, forming a homodimer, and this complex enters the nucleus through a transport protein.
The GR interacts with the cell's DNA, upregulating the production of a pro-apoptotic signal, bax. The message leaves the nucleus, is translated by a ribosome, and travels to a mitochondrion, where it binds to the membrane.
Pores form in the mitochondria and cytochrome c is released. Cytochrome c is very important to respiration, so when it leaves the mitochondria, respiration ceases. The cell is now committed to apoptosis.
Cytochrome c, with the help of a another molecule, Apoptosis Activation Factor-1 (Apaf-1), activates the caspases.
The caspases:
Activate endonucleases. Endonucleases destroy the cell's DNA. Cleave PARP. PARP normally repairs damaged DNA. When PARP is cleaved by caspases, it no longer functions, hastening destruction of the DNA by endonucleases. Cleave important enzymes– some are deactivated; others, deregulated. The deregulation of enzymes catalyzing structural protein formation leads to apoptosis' charactersitic blebbing of the cell's membrane
Phosphatidyl serine, a molecule normally found on the inside of the cell's membrane, is flipped to the outside (probably by cytochrome c.) Macrophages thus recognize the cell, and engulf and digest the blebs. The cell's contents are not released, thus there is no inflammation and damage to the surrounding tissues.