Cell Signaling Technology

Product Pathways - Apoptosis / Autophagy

Beclin-1 (D40C5) Rabbit mAb #3495

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP H M R Mk Endogenous 60 Rabbit IgG

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
Reactivity Key:  H=Human  M=Mouse  R=Rat  Mk=Monkey
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 (D40C5) Rabbit mAb detects endogenous levels of total Beclin-1 protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Thr72 of human Beclin-1.

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using Beclin-1 (D40C5) Rabbit mAb.

Western Blotting

Western Blotting

Western blot analysis of extracts from HeLa cells, transfected with 100 nM SignalSilence® Control siRNA (Unconjugated) #6568 (-), SignalSilence® Beclin-1 siRNA I #6222 (+) or SignalSilence® Beclin-1 siRNA II (+), using Beclin-1 (D40C5) XP® Rabbit mAb #3495 (upper) or α-Tubulin (11H10) Rabbit mAb #2125 (lower). The Beclin-1 (D40C5) XP® Rabbit mAb confirms silencing of Beclin-1 expression, while the α-Tubulin (11H10) Rabbit mAb is used to control for loading and specificity of Beclin-1 siRNA.

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, it is monoallelically deleted in 40-75% of sporadic human breast and ovarian cancers (5). It is localized within cytoplasmic structures including the mitochondria, although overexpression of Beclin-1 reveals some nuclear staining and CRM1-dependent nuclear export (6). 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). 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 U S A 100, 15077-82.

Application References

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Companion Products

This product is intended for research purposes only. The product is not intended to be used for therapeutic or diagnostic purposes in humans or animals.

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