Cleaved Caspase-8 (Asp374) (E6H8S) Rabbit mAb #98134
- WB
- IP
- IF
- F
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 18, 41, 43 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- IF-Immunofluorescence
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Simple Western™ | 1:50 - 1:250 |
| Immunoprecipitation | 1:200 |
| Immunofluorescence (Immunocytochemistry) | 1:400 |
| Flow Cytometry (Fixed/Permeabilized) | 1:400 - 1:1600 |
Storage
Protocol
Specificity / Sensitivity
Species Reactivity:
Source / Purification
Background
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).
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- Mandal, R. et al. (2020) Biochim Biophys Acta Rev Cancer 1873, 188357.
- Han, J.H. et al. (2021) Int J Mol Sci 22, 3318. doi: 10.3390/ijms22073318.
- Newton, K. et al. (2019) Nature 574, 428-431.
- Feng, S. et al. (2007) Cell Signal 19, 2056-67.
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- Alvarez-Diaz, S. et al. (2016) Immunity 45, 513-526.
- Man, S.M. et al. (2013) J Immunol 191, 5239-46.
- Antonopoulos, C. et al. (2015) J Biol Chem 290, 20167-84.
- Fritsch, M. et al. (2019) Nature 575, 683-687.
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