Render Target: STATIC
Render Timestamp: 2024-11-21T13:07:51.670Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-08-01 15:28:10.318
Product last modified at: 2024-11-08T12:45:15.656Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

Phospho-Beclin-1 (Ser30) Antibody #54101

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 60
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50

    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 (Ser30) Antibody recognizes endogenous levels of Beclin-1 protein only when phosphorylated at Ser30.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic phospho-peptide corresponding to residues surrounding Ser30 of human Beclin-1 protein. Antibodies are purified by 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).
    ULK1 phosphorylates Beclin-1 at Ser30 to induce autophagy in response to amino acid starvation, mTORC1 inhibition, and hypoxia (8).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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