Render Target: SSR
Render Timestamp: 2024-12-19T21:03:45.313Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-05-10 22:35:40.665
Product last modified at: 2024-12-18T13:15:13.755Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77

Bcl-2 (124) Mouse mAb #15071

Filter:
  • WB
  • IP
  • IHC
  • F

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 26
    Source/Isotype Mouse IgG1
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IHC-Immunohistochemistry 
    • F-Flow Cytometry 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Simple Western™ 1:10 - 1:50
    Immunoprecipitation 1:50
    IHC Leica Bond 1:800 - 1:3200
    Immunohistochemistry (Paraffin) 1:400 - 1:1600
    Flow Cytometry (Fixed/Permeabilized) 1:200 - 1:800

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    For a carrier-free (BSA and azide free) version of this product see product #17447

    Protocol

    Specificity / Sensitivity

    Bcl-2 (124) Mouse mAb recognizes endogenous levels of total Bcl-2 protein.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly47 of human Bcl-2 protein.

    Background

    Bcl-2 exerts a survival function in response to a wide range of apoptotic stimuli through inhibition of mitochondrial cytochrome c release (1). It has been implicated in modulating mitochondrial calcium homeostasis and proton flux (2). Several phosphorylation sites have been identified within Bcl-2, including Thr56, Ser70, Thr74, and Ser87 (3). It has been suggested that these phosphorylation sites may be targets of the ASK1/MKK7/JNK1 pathway and that phosphorylation of Bcl-2 may be a marker for mitotic events (4,5). Mutation of Bcl-2 at Thr56 or Ser87 inhibits its anti-apoptotic activity during glucocorticoid-induced apoptosis of T lymphocytes (6). Interleukin-3 and JNK-induced Bcl-2 phosphorylation at Ser70 may be required for its enhanced anti-apoptotic functions (7).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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