Render Target: STATIC
Render Timestamp: 2024-12-20T10:44:35.599Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-09-30 01:59:49.443
Product last modified at: 2024-12-02T16:45:16.054Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

Caspase-8 (F5K9P) Rabbit mAb #8873

Filter:
  • WB
  • IHC

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 10, 57
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IHC-Immunohistochemistry 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Simple Western™ 1:50 - 1:250
    Immunohistochemistry (Paraffin) 1:50 - 1:200

    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 #46272.

    Protocol

    Specificity / Sensitivity

    Caspase-8 (F5K9P) Rabbit mAb recognizes endogenous levels of total caspase-8 protein, including the p10 subunit of the activated protein.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro394 of human caspase-8 protein.

    Background

    Apoptosis induced through the CD95 receptor (Fas/APO-1) and tumor necrosis factor receptor 1 (TNFR1) activates caspase-8 and leads to the release of the caspase-8 active fragments, p18 and p10 (1-3). Activated caspase-8 cleaves and activates downstream effector caspases such as caspase-1, -3, -6, and -7. Caspase-3 ultimately elicits the morphological hallmarks of apoptosis, including DNA fragmentation and cell shrinkage.

    In addition to functioning as a key initiator caspase for extrinsic apoptosis, more recent studies have identified caspase-8 as a regulator of inflammatory necrotic cell death pathways such as necroptosis and pyroptosis (4,5). Activation of caspase-8 leads to cleavage of RIPK1 and RIPK3 to inhibit necroptosis (6,7). As a result, caspase-8 deficiency in mice, which is embryonic lethal, can be rescued by deletion of the necroptosis proteins RIPK3 or MLKL (8-11). Additionally, in some circumstances, caspase-8 is recruited to the inflammasome to trigger pyroptosis (12,13). Studies have also found that expression of an enzymatically inactive form of caspase-8 (C362S) causes embryonic lethality by inducing necroptosis and pyroptosis (14).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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