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Render Timestamp: 2024-11-13T11:05:47.239Z
Commit: 3c1f305a63297e594ac8d7bb5424007d592d68be
XML generation date: 2024-09-20 06:22:10.684
Product last modified at: 2024-11-09T00:15:08.777Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464
  1. Products /
  2. Primary Antibodies /
  3. Phospho-Beclin-1 (Ser90) Antibody

Phospho-Beclin-1 (Ser90) Antibody #86455

Filter:
  • WB

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 60
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    Phospho-Beclin-1 (Ser90) Antibody recognizes endogenous levels of Beclin-1 protein only when phosphorylated at Ser90. The antibody may not react with Beclin-1 when dually phosphorylated at Ser90 and Ser93. Background bands of unknown origin were detected at 100, 35, and 10 kDa in some cell lines.

    Species Reactivity:

    Human

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic phospho-peptide corresponding to residues surrounding Ser90 of human Beclin-1 protein. Antibodies are purified by protein A and peptide affinity chromatography.

    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).
    Several studies have indicated that autophagy is enhanced by phosphorylation of Beclin-1 at Ser90 triggered by stress-responsive kinases including MAPKAPK-2/MAPKAPK-3, DAPK3, and CaMKII (8-10).

    Database Links

    UniProt ID: Q14457


    Entrez-Gene Id: 8678


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