Apoptosis and Autophagy

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Bcl-2 exerts a survival function in response to a wide range of apoptotic stimuli through inhibition of mitochondrial cytochrome c release (1). It has been implicated in modulating mitochondrial calcium homeostasis and proton flux (2). Several phosphorylation sites have been identified within Bcl-2 including Thr56, Ser70, Thr74 and Ser87 (3). It has been suggested that these phosphorylation sites may be targets of the ASK1/MKK7/JNK1 pathway, and that phosphorylation of Bcl-2 may be a marker for mitotic events (4,5). Mutation of Bcl-2 at Thr56 or Ser87 inhibits its anti-apoptotic activity during glucocorticoid-induced apoptosis of T lymphocytes (6). Interleukin 3 and JNK-induced Bcl-2 phosphorylation at Ser70 may be required for its enhanced anti-apoptotic functions (7).

1. Murphy, K.M. et al. (2000) Cell Death Differ 7, 102-11.
2. Zhu, L. et al. (1999) J Biol Chem 274, 33267-73.
3. Maundrell, K. et al. (1997) J Biol Chem 272, 25238-42.
4. Yamamoto, K. et al. (1999) Mol Cell Biol 19, 8469-78.
5. Ling, Y.H. et al. (1998) J Biol Chem 273, 18984-91.
6. Huang, S.T. and Cidlowski, J.A. (2002) FASEB J 16, 825-32.
7. Deng, X. et al. (2001) J Biol Chem 276, 23681-8.

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Bcl-2 (D17C4) Rabbit mAb (Mouse Preferred)

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