Render Target: STATIC
Render Timestamp: 2024-12-12T12:05:46.379Z
Commit: 611277b6de3cd1bb065350b6ef8d63df412b7185
XML generation date: 2024-11-12 23:02:10.016
Product last modified at: 2024-11-13T08:01:00.168Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77

Phospho-Bad (Ser112) (7E11) Mouse mAb #9296

Filter:
  • WB

    Supporting Data

    REACTIVITY H M R Mk
    SENSITIVITY Endogenous
    MW (kDa) 23
    Source/Isotype Mouse IgG1
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 
    • Mk-Monkey 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:2000

    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 #48694.

    Protocol

    Specificity / Sensitivity

    Phospho-Bad (Ser112) (7E11) Mouse mAb detects endogenous levels of Bad only when phosphorylated at serine112. The Ser112 nomenclature is based upon the mouse sequence. The analogous phosphorylation site is Ser75 in human and Ser113 in rat. This antibody does not detect Bad phosphorylated at other sites, nor does it detect related family members.

    Species Reactivity:

    Human, Mouse, Rat, Monkey

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Ser112 of mouse Bad.

    Background

    Bad is a proapoptotic member of the Bcl-2 family that promotes cell death by displacing Bax from binding to Bcl-2 and Bcl-xL (1,2). Survival factors, such as IL-3, inhibit the apoptotic activity of Bad by activating intracellular signaling pathways that result in the phosphorylation of Bad at Ser112 and Ser136 (2). Phosphorylation at these sites promotes binding of Bad to 14-3-3 proteins to prevent an association between Bad with Bcl-2 and Bcl-xL (2). Akt phosphorylates Bad at Ser136 to promote cell survival (3,4). Bad is phosphorylated at Ser112 both in vivo and in vitro by p90RSK (5,6) and mitochondria-anchored PKA (7). Phosphorylation at Ser155 in the BH3 domain by PKA plays a critical role in blocking the dimerization of Bad and Bcl-xL (8-10).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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