Meeting the (N-terminal) end with acetylation.
editorial · Level V
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- Record sourced from PubMed, PMID 21854977.
- Also identified by DOI 10.1016/j.cell.2011.07.024.
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Abstract
Cell-fate decisions are tightly linked to cellular energy status. In this issue, Yi et al. (2011) introduce a mechanism by which Bcl-xL lowers the threshold for apoptosis by suppressing acetyl-CoA production, which, in turn, suppresses the N-alpha-acetylation important for activation of the proapoptotic protease caspase-2.