Talk:Bcl-2-associated death promoter

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comment[edit]

Your last sentence "After activation, it is able to form a heterodimer with anti-apoptotic proteins and prevent them from stopping apoptosis" needs more nuance & sources (binding to bcl-2 for example). Bad can be stopped if it becomes phosporylated at specific sites (example AKT phosphorylates BAD at s136, this sequesters BAD to cytoplasmic 14-3-3 proteins, keeping it away from anti-apoptotic proteins such as bcl-2). Daviddecraene 11:13, 20 December 2006 (UTC)[reply]

In addition: here is a direct link to a paper on BH3-only proteins: BH3-only proteins — evolutionarily conserved proapoptotic Bcl-2 family members essential for initiating programmed cell death. Daviddecraene 11:21, 20 December 2006 (UTC)[reply]