Render Target: STATIC
Render Timestamp: 2024-12-11T11:35:19.684Z
Commit: 611277b6de3cd1bb065350b6ef8d63df412b7185
XML generation date: 2024-08-01 15:25:59.614
Product last modified at: 2024-08-28T14:00:07.385Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

Phospho-Bim (Ser69) Antibody #4581

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H M
    SENSITIVITY Endogenous
    MW (kDa) 26
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 

    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-Bim (Ser69) Antibody detects endogenous levels of Bim protein only when phosphorylated at Ser69.

    Species Reactivity:

    Human, Mouse

    The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.

    Species predicted to react based on 100% sequence homology:

    Rat, Monkey, Dog

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Ser69 of human Bim protein (Ser65 in mouse and rat). Antibodies are purified by peptide affinity chromatography.

    Background

    Bim/Bod is a pro-apoptotic protein belonging to the BH3-only group of Bcl-2 family members including Bad, Bid, Bik, Hrk, and Noxa that contain a BH3 domain but lack other conserved BH1 or BH2 domains (1,2). Bim induces apoptosis by binding to and antagonizing anti-apoptotic members of the Bcl-2 family. Interactions have been observed with Bcl-2, Bcl-xL, Mcl-1, Bcl-w, Bfl-1, and BHRF-1 (1,2). Bim functions in regulating apoptosis associated with thymocyte negative selection and following growth factor withdrawal, during which Bim expression is elevated (3-6). Three major isoforms of Bim are generated by alternative splicing: BimEL, BimL, and BimS (1). The shortest form, BimS, is the most cytotoxic and is generally only transiently expressed during apoptosis. The BimEL and BimL isoforms may be sequestered to the dynein motor complex through an interaction with the dynein light chain and released from this complex during apoptosis (7). Apoptotic activity of these longer isoforms may be regulated by phosphorylation (8,9). Environmental stress triggers Bim phosphorylation by JNK and results in its dissociation from the dynein complex and increased apoptotic activity.
    Erk1/2-dependent phosphorylation of BimEL at Ser69 (Ser65 in mouse and rat) in response to growth factor stimulation can promote its proteasome-mediated degradation and enhance cell survival (6,10,11).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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