The gene S100A8 can protect against it, and a recent study showed that melatonin can antagonize it in partheno-genetic embryos.  This process can be detected via the uptake of 7-AAD during flow cytometry, the exclusion of trypan blue, and the terminal dUTP nick-end labeling, or TUNEL assay.  Binding of the Fas ligand induces it, as does upregulation of proteins like BAX and BAD, while other member
The gene S100A8 can protect against it, and a recent study showed that melatonin can antagonize it in partheno-genetic embryos.  This process can be detected via the uptake of 7-AAD during flow cytometry, the exclusion of trypan blue, and the terminal dUTP nick-end labeling, or TUNEL assay.  Binding of the Fas ligand induces it, as does upregulation of proteins like BAX and BAD, while other members of the Bcl-2 family oppose it.  The exact number of times this process occurs is known for the development of C. elegans, whose ced-3 proteins are the homologues of the Apaf-1-activated human caspases that are responsible for many of its effects.  Also initiated by p53 upon un-repairable DNA damage, FTP, name this process of type I programmed cell death.
The gene S100A8 can protect against it, and a recent study showed that melatonin can antagonize it in partheno-genetic embryos.  
apoptosis [prompt on "programmed cell death"]