Phospho-Bcl-2 (Thr56) Antibody #2875
- WB
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 28 |
| SOURCE | Rabbit |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
Storage
Protocol
Specificity / Sensitivity
Phospho-Bcl-2 (Thr56) Antibody detects endogenous levels of Bcl-2 only when phosphorylated at threonine 56. It does not cross-react with non-phosphorylated Bcl-2 or with other Bcl-2 family members at endogenous levels.
Species Reactivity:
Human
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Thr56 of human Bcl-2. Antibodies are purified by protein A and peptide affinity chromatography.
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).
- Murphy, K.M. et al. (2000) Cell Death Differ 7, 102-11.
- Zhu, L. et al. (1999) J Biol Chem 274, 33267-73.
- Maundrell, K. et al. (1997) J Biol Chem 272, 25238-42.
- Yamamoto, K. et al. (1999) Mol Cell Biol 19, 8469-78.
- Ling, Y.H. et al. (1998) J Biol Chem 273, 18984-91.
- Huang, S.T. and Cidlowski, J.A. (2002) FASEB J 16, 825-32.
- Deng, X. et al. (2001) J Biol Chem 276, 23681-8.
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