Product Pathways - Autophagy Signaling
Phospho-Beclin-1 (Ser93/96) Antibody #12476
|12476S||100 µl (10 western blots)||---||In Stock||---|
|12476||carrier free and custom formulation / quantity||email request|
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Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting
Species predicted to react based on 100% sequence homology: Mouse, Rat, Monkey, Bovine, Dog, Pig.
Specificity / Sensitivity
Phospho-Beclin-1 (Ser93/96) Antibody recognizes overexpressed levels of Beclin-1 protein only when phosphorylated at Ser93 and Ser96 (Ser91 and Ser94 in mouse). This antibody may react with single phosphorylated Beclin-1 at either Ser93 or Ser96, as well as the double phosphorylated protein. This antibody cross-reacts with a protein of unknown origin at ~40 kDa.
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Ser93/96 of human Beclin-1 protein. Antibodies are purified by protein A and peptide affinity chromatography.
Western blot analysis of extracts from 293T cells, mock transfected or transfected with a construct expressing human Beclin-1 (hBeclin-1), untreated or treated with carbonyl cyanide 3-chlorophenylhydrazone (CCCP, 100 μM, 2 hr) as indicated, using Phospho-Beclin-1 (Ser93/96) Antibody (upper) or Beclin-1 (D40C5) Rabbit mAb #3495 (lower).
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).
To induce autophagy, AMP-activated protein kinase (AMPK) directly phosphorylates Beclin-1 at conserved Ser93 and Ser96 residues in human (Ser91 and Ser94 in mouse) (8).
- Reggiori, F. and Klionsky, D.J. (2002) Eukaryot Cell 1, 11-21.
- Kametaka, S. et al. (1998) J Biol Chem 273, 22284-91.
- Liang, X.H. et al. (1999) Nature 402, 672-6.
- Liang, X.H. et al. (1998) J Virol 72, 8586-96.
- Aita, V.M. et al. (1999) Genomics 59, 59-65.
- Liang, X.H. et al. (2001) Cancer Res 61, 3443-9.
- Yue, Z. et al. (2003) Proc Natl Acad Sci USA 100, 15077-82.
- Kim, J. et al. (2013) Cell 152, 290-303.
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For Research Use Only. Not For Use In Diagnostic Procedures.
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