Cell Signaling Technology

Product Pathways - Apoptosis

Beclin-1 (2A4) Mouse mAb #4122

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP H Endogenous 60 Mouse IgG1

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
Reactivity Key:  H=Human
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

Beclin-1 (2A4) Mouse mAb recognizes endogenous levels of total human Beclin-1 protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a recombinant protein specific to a central region within human Beclin-1 protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using Beclin-1 (2A4) Mouse mAb.

Background

Autophagy is a catabolic process for the autophagosomic-lysosomal degradation of proteins activated in response to nutrient deprivation and in neurodegenerative conditions (1). One of the proteins critical to this process is Beclin-1, the mammalian orthologue of the yeast autophagy protein Apg6/Vps30 (2). Beclin-1 can complement defects in yeast autophagy caused by loss of Apg6 and can also stimulate autophagy when overexpressed in mammalian cells (3). Mammalian Beclin-1 was originally isolated in a yeast two-hybrid screen for Bcl-2 interacting proteins and has been shown to interact with Bcl-2 and Bcl-xL, but not with Bax or Bak (4). While Beclin-1 is generally ubiquitously expressed, research studies have shown it is monoallelically deleted in 40-75% of sporadic human breast and ovarian cancers (5). Beclin-1 is localized within cytoplasmic structures including the mitochondria, although overexpression of Beclin-1 reveals some nuclear staining and CRM1-dependent nuclear export (6). Investigators have demonstrated that Beclin-1 -/- mice die early in embryogenesis and Beclin-1 -/+ mice have a high incidence of spontaneous tumors. Stem cells from the null mice demonstrate an altered autophagic response, although responses to apoptosis appeared normal (7). Researchers have also found that overexpression of Beclin-1 in virally infected neurons in vivo resulted in significant protection against Sindbis virus-induced disease and neuronal apoptosis (4).

  1. Reggiori, F. and Klionsky, D.J. (2002) Eukaryot Cell 1, 11-21.
  2. Kametaka, S. et al. (1998) J Biol Chem 273, 22284-91.
  3. Liang, X.H. et al. (1999) Nature 402, 672-6.
  4. Liang, X.H. et al. (1998) J Virol 72, 8586-96.
  5. Aita, V.M. et al. (1999) Genomics 59, 59-65.
  6. Liang, X.H. et al. (2001) Cancer Res 61, 3443-9.
  7. Yue, Z. et al. (2003) Proc Natl Acad Sci USA 100, 15077-82.

Application References

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

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