![Figure 6. The antiapoptotic phenotype and alterations in BCL-2 family members in MCL. The prosurvival BCL-2 family members (BCL-2, BCL-XL, MCL-1, BCL-W, and A1/BFL1) bind and sequester the apoptosis-inducing members BAX and BAK. The BH3-only proteins (BIM, PUMA, NOXA, BAD, BID, BMF, BIK, and HRK) can be activated by cytotoxic signals and selectively engage prosurvival members, which leads to release of BAX and BAK, leading to permeabilization of the mitochondrion, the release of proapoptotic factors, caspase activation, and, finally, cell death.136,137 BCL2L11/BIM is frequently deleted (blue symbol [Δ]), whereas some antiapoptotic family members are commonly overexpressed (red symbols) in MCL, including BCL-2. In addition, PI3K/AKT/mTOR signaling can inactivate BAD through phosphorylation and stabilize of MCL-1 protein. Illustration by Paulette Dennis.](https://ash.silverchair-cdn.com/ash/content_public/journal/blood/117/1/10.1182_blood-2010-04-189977/4/zh89991063490006.jpeg?Expires=1724250078&Signature=e~1zVv22gFX9mOHE8E0f5uoJrbO3xt7m0cb2k-kLyAHyaRZ6J2AydjRbIJRPJHD99iGVZ1FM60V0KVeiLruwqRfy77RY6NKxOIgGzXHLh4Hv2moCLkyZi0R8EUbLYy9mSLLt461RAHu334LRo81mXMb0oxb7L9FlaiaXiWFEaaJHx9AemWYNF740XSXgq189MM4AtefOFSVfPH5WJql1YayyF7g01dqIzqOtU0KkESxX3S3iSFg4q9c3eBH7My7STBJaUJ4yGY27YAdFCH06jUJIcJGm-gTexAfCn-4bPonm9u8CGJnhYzDSsGcTv7FHb2iW7ZixytPBpEDDITmI4w__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA)
The antiapoptotic phenotype and alterations in BCL-2 family members in MCL. The prosurvival BCL-2 family members (BCL-2, BCL-XL, MCL-1, BCL-W, and A1/BFL1) bind and sequester the apoptosis-inducing members BAX and BAK. The BH3-only proteins (BIM, PUMA, NOXA, BAD, BID, BMF, BIK, and HRK) can be activated by cytotoxic signals and selectively engage prosurvival members, which leads to release of BAX and BAK, leading to permeabilization of the mitochondrion, the release of proapoptotic factors, caspase activation, and, finally, cell death.136,137 BCL2L11/BIM is frequently deleted (blue symbol [Δ]), whereas some antiapoptotic family members are commonly overexpressed (red symbols) in MCL, including BCL-2. In addition, PI3K/AKT/mTOR signaling can inactivate BAD through phosphorylation and stabilize of MCL-1 protein. Illustration by Paulette Dennis.
