Mcl-1 deficiency results in peri-implantaion embryonic lethality

Article Abstract:

Mcl-1 deficiency brings on peri-implantaion lethality in the embryo. Mcl-1 is a Bcl-2 family member. Null blastocysts did not hatch or attach in vitro, likely an indication of a trophectoderm defect. The inner cell mass, however, could grow in culture. The blastocysts showed no evidence of greater apoptosis, but had a delay in maturation beyond precompaction.

Mice, mutant strains, Mutant mice, Embryology, Experimental, Embryological research, Polycystic kidney disease

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tBID, a membrane-targeted death ligand, oligomerizes BAK to release cytochrome c

Article Abstract:

The physiologically active p15 BID has been studied. The BH3 domain of tBID is not necessary for targeting. It remains on the mitochondrial surface where it is necessary to trigger BAK to release cytochrome c. An activation cascade of apoptosis-promoting proteins from BID to BAK integrates the pathway from surface death receptors to the efflux of cytochrome c, which cannot be reversed. A pore into which the intramembranous oligomerization is induced is proposed.

Physiological aspects, Cell receptors, Cytochrome c

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BCL-2 family members and the mitochondria in apoptosis

Article Abstract:

A review of information available on BCL-2 family members, many of which have a carboxy-terminal hydrophobic domain, and mitochondria in apoptosis is presented with some history and various proposed models. A rather large proportion of the pro- versus anti-apoptotic BCL-2 members localize to compartmentalize subcellular material when a death signal is lacking. BCL-2 family members are upstream of irreversible cell damage and put much of their effort into the mitochondria level, giving them a central role in the life-or-death status of a cell.

Cellular signal transduction

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