Product Pathways - Autophagy Signaling
Phospho-Beclin-1 (Ser15) (D4B7R) Rabbit mAb #84966
|84966S||100 µl ( 10 western blots )||￥4,050.00||现货查询 购买询价 防伪查询|
|84966||carrier free & custom formulation / quantity||email request|
|W||1:1000||Human,Mouse,||Transfected Only||60||Rabbit IgG|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting,
Specificity / Sensitivity
Phospho-Beclin-1 (Ser15) (D4B7R) Rabbit mAb recognizes transfected levels of Beclin-1 protein only when phosphorylated at Ser15 (which corresponds to Ser14 in mouse).
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Ser15 of human Beclin-1 protein.
Western blot analysis of extracts from 293T cells, mock transfected (-) or transfected with constructs expressing full-length human Beclin-1 protein (hBeclin-1; +), mouse Beclin-1 protein (mBeclin-1; +), or mouse ULK1 protein (mULK1; +), using Phospho-Beclin-1 (Ser15) (D4B7R) Rabbit mAb (upper), Beclin-1 (D40C5) Rabbit mAb #3495 (middle) or β-Actin (D6A8) Rabbit mAb #8457 (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).
Autophagy inducers, including amino-acid starvation and mTOR inhibition, lead to phosphorylation of mouse Beclin-1 at Ser14 (equivalent to human Ser15) by the serine/threonine kinase ULK1. This results in an increase in VPS34 lipid kinase activity and leads to the induction of autophagy (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.
- Russell, R.C. et al. (2013) Nat Cell Biol 15, 741-50.
Have you published research involving the use of our products? If so we'd love to hear about it. Please let us know!
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For Research Use Only. Not For Use In Diagnostic Procedures.
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