BACKGROUND 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).
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6. Huang, S.J. and Cidlowski, J.A. (2002) FASEB J.16, 825–832.
7. Deng, X. et al. (2001) J. Biol. Chem.276, 23681–23688.
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