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Caspase-8 (F5K9P) Rabbit mAb #8873

Filter:
  • WB
  • IHC
Western Blotting Image 1: Caspase-8 (F5K9P) Rabbit mAb
Western blot analysis of extracts from HCT 116 and CRISPR/Cas9 caspase-8 knockout (KO) HCT 116 cells, untreated (-) or treated with Staurosporine #9953 (1 μM, 4 hr; +), using Caspase-8 (F5K9P) Rabbit mAb (upper) or GAPDH (D16H11) XP® Rabbit mAb #5174 (lower).

To Purchase # 8873

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 
  • Related Products

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).

Pathways

Explore pathways related to this product.


For Research Use Only. Not For Use In Diagnostic Procedures.
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