Cell Signaling Technology

Product Pathways - Apoptosis

Bcl-2 (50E3) Rabbit mAb #2870

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP H M R (Mk) (C) (B) (Dg) Endogenous 26 Rabbit IgG

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
Reactivity Key:  H=Human  M=Mouse  R=Rat  Mk=Monkey  C=Chicken  B=Bovine  Dg=Dog
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

Bcl-2 (50E3) Rabbit mAb detects endogenous levels of total Bcl-2 protein. This antibody does not cross-react with other Bcl-2 family members.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues at the carboxy terminus of Bcl-2.

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell types using Bcl-2 (50E3) Rabbit mAb.

Western Blotting

Western Blotting

Western blot analysis of extracts from HeLa cells, transfected with 100 nM SignalSilence® Control siRNA (Fluorescein Conjugate) #6201 (-), SignalSilence® Bcl-2 siRNA I (+) or SignalSilence® Bcl-2 siRNA II #6516 (+), using Bcl-2 (50E3) Rabbit mAb and α-Tubulin (11H10) Rabbit mAb #2125. Bcl-2 (50E3) Rabbit mAb #2870 confirms silencing of Bcl-2 expression, while the α-tubulin (11H10) rabbit mAb is used to control for loading and specificity of Bcl-2 siRNA.

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).

  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.

Application References

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For Research Use Only. Not For Use In Diagnostic Procedures.

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