Render Target: STATIC
Render Timestamp: 2024-11-22T12:00:08.272Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-09-30 01:54:05.505
Product last modified at: 2024-11-19T17:00:10.749Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77

Caspase-11 (17D9) Rat mAb #14340

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY M
    SENSITIVITY Endogenous
    MW (kDa) 38, 43
    Source/Isotype Rat IgG2a
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • M-Mouse 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:100

    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.

    Protocol

    Specificity / Sensitivity

    Caspase-11 (17D9) Rat mAb recognizes endogenous levels of total caspase-11 protein.

    Species Reactivity:

    Mouse

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with recombinant protein specific to the p30 subunit terminus of mouse caspase-11 protein.

    Background

    Caspases are a family of aspartate-specific cysteine-dependent proteases that play a critical role in apoptosis as well as inflammatory responses. Pro-inflammatory caspases include caspase-1 and mouse caspase-11 (1). Caspase-11 has about 60% and 55% identity to human caspases-4 and -5, respectively. Caspase-1 cleaves inflammatory cytokines such as pro-IL-1β and IL-18 into their mature forms (2). It is activated by proteolytic cleavage producing a tetramer of its two active subunits, p20 and p10. Canonical activation of caspase-1 occurs through several complex molecular platforms designated “inflammasomes” that include Pycard/Asc, nucleotide-binding oligomerization receptors (NLRs), and AIM2 (3, 4). Non-canonical activation of caspase-1 is triggered by caspase-11, which is transcriptionally induced by toll-like receptor ligands including LPS. Activation of this pathway induces inflammatory cytokines as well as pyroptosis, a form of programmed cell death (5-9).
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