MCL-1

Myeloid cell leukemia-1 (MCL-1) shares sequence homology with BCL-2, and its expression promotes cell viability. P53 and MCL-1 demonstrate opposing effects on mitochondrial apoptosis by mediating BCL-2 antagonist killer (Bak) activity. Cell death or apoptosis manifests in two major execution programs downstream of the death signal: 1) signaling of the caspase pathway, or 2) organelle dysfunction, of which mitochondrial dysfunction is the best characterized. As the BCL-2 family members reside upstream of irreversible cellular damage and focus much of their efforts at the level of mitochondria, they play a pivotal role in deciding whether a cell will live or die.