Render Target: STATIC
Render Timestamp: 2024-12-20T11:29:10.614Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-12-10 23:02:06.338
Product last modified at: 2024-12-17T18:51:33.116Z
Cell Signaling Technology Logo
1% for the planet logo
PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

Phospho-Bcl-2 (Ser70) (5H2) Rabbit mAb #2827

Filter:
  • WB
  • F

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 28
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • F-Flow Cytometry 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Flow Cytometry (Fixed/Permeabilized) 1:100 - 1:400

    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 #24152.

    Protocol

    Specificity / Sensitivity

    Phospho-Bcl-2 (Ser70) (5H2) Rabbit mAb detects endogenous levels of Bcl-2 only when phosphorylated at serine 70. The antibody does not cross-react with nonphosphorylated Bcl-2 at endogenous levels or with other Bcl-2 family members.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding serine 70 of human Bcl-2.

    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.
    Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.
    All other trademarks are the property of their respective owners. Visit our Trademark Information page.