Review Article
The Role of BCL2 Family of Apoptosis Regulator Proteins in Acute and Chronic Leukemias
Table 2
This table summarizes the properties of the most well-studied members of BCL2 family.
| | Action | Mechanism of action | Subcellular localization |
| BCL2 | Antiapoptotic | Inhibits apoptosis by preservation of mitochondrial membrane integrity | (i) Outer mitochondrial membrane | (ii) Nuclear envelope | (iii) Membrane of the endoplastic reticulum (ER) |
| BCL-XL | Antiapoptotic | Inhibits cytochrome c release through the mitochondrial pore that inhibits activation of the cytoplasmic caspase cascade by cytochrome c | Transmembrane molecule in the mitochondria |
| BCL-W | Antiapoptotic | Reduced cell apoptosis under cytotoxic conditions | Exclusively on the mitochondrion |
| MCL-1 | Antiapoptotic | Short half-life, interaction with BAK1, Noxa, BCL2L11, Bcl-2-associated death promoter, PCNA | Mitochondria, nucleus |
| BAX | Proapoptotic | Release of apoptogenic factors like cytochrome c, activation of caspase cascade | Cytosol |
| BAK | Proapoptotic | Undergoes conformational changes to form larger aggregates during apoptosis | Integral mitochondrial membrane protein |
| BID | Proapoptotic | Direct activator of Bax | Cytosol and membrane |
| BIM | Proapoptotic | Free Bim binds to Bcl-2 or Bcl-XL and inactivates their antiapoptotic functions | Free BIM in mitochondria |
| BAD | Proapoptotic | Dephosphorylated BAD forms a heterodimer with Bcl-2 and Bcl-xL, inactivating them and thus allowing Bax/Bak-triggered apoptosis | Free BAD in mitochondria |
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