R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
Cleaved Caspase-8 (Asp387) (p10 subunit) (E8K5S) Rabbit mAb #16709
Filter:
- WB
- IP
Supporting Data
| REACTIVITY | M |
| SENSITIVITY | Endogenous |
| MW (kDa) | 10 |
| Source/Isotype | Rabbit IgG |
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 | 1:200 |
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.
Protocol
Specificity / Sensitivity
Cleaved Caspase-8 (Asp387) (p10 subunit) (E8K5S) Rabbit mAb recognizes endogenous levels of the p10 subunit of cleaved caspase-8 protein only when cleaved at Asp387.
Species Reactivity:
Mouse
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Asp387 of mouse 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).
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).
- Muzio, M. et al. (1996) Cell 85, 817-27.
- Boldin, M.P. et al. (1996) Cell 85, 803-15.
- Fernandes-Alnemri, T. et al. (1996) Proc Natl Acad Sci U S A 93, 7464-9.
- 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.
- Varfolomeev, E.E. et al. (1998) Immunity 9, 267-76.
- Kaiser, W.J. et al. (2011) Nature 471, 368-72.
- Oberst, A. et al. (2011) Nature 471, 363-7.
- 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.
限制使用
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For Research Use Only. Not For Use In Diagnostic Procedures.
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