Anti-Mouse Caspase Activated Deoxyribonuclease (I17) (CAD)
| Code | Size | Price |
|---|
| LEI-C1145-20ug | 20 ug | £199.00 |
Quantity:
| LEI-C1145-0.1mg | 0.1 mg | £574.00 |
Quantity:
Prices exclude any Taxes / VAT
Overview
Host Type: Rabbit
Antibody Clonality: Polyclonal
Regulatory Status: RUO
Target Species: Mouse
Applications:
- Immunohistochemistry- Paraffin Embedded (IHC-P)
- Western Blot (WB)
Shipping:
Ambient
Storage:
This polyclonal antibody is stable for at least one week when stored at 2-8°C. For long term storage aliquot in working volumes without diluting and store at -20°C in a manual defrost freezer. Avoid Repeated Freeze Thaw Cycles.
Further Information
Concentration:
0.5 mg/ml
Conjugate/Tag/Label:
Purified No Carrier Protein
Format:
This polyclonal antibody is formulated in phosphate buffered saline (PBS) pH 7.4 containing 0.02% sodium azide as a preservative.
Formulation:
This polyclonal antibody is formulated in phosphate buffered saline (PBS) pH 7.4 containing 0.02% sodium azide as a preservative.
Immunogen:
PN:C1126
Long Description:
Apoptosis is related to many diseases and induced by a family of cell death receptors and their ligands. Cell death signals are transduced by death domain containing adapter molecules and members of the caspase family of proteases. These death signals finally cause the degradation of chromosomal DNA by activated DNase. A mouse DNase that causes DNA fragmentation was identified recently and designated CAD (for caspase activated deoxyribonuclease). The human homologue of mouse CAD was more recently identified by two groups independently and termed CPAN and DFF40. Human DFF45 and its mouse homologue ICAD are the inhibitors of CPAN/DFF40 and CAD, respectively. Upon cleavage of DFF45/ICAD by activated caspase, DFF40/CAD is released and activated and eventually causes the degradation of DNA in the nuclei. Activation of CAD/DFF40, which causes DNA degradation, is the hallmark of apoptotic cell death.
Target:
Caspase Activated Deoxyribonuclease
References
1. Enari, M. et al. (1998) Nature 391:43-50 2. Sakahira, H. et al. (1998) Nature391:96-99 3. Liu, X. et al. (1998) Proc Natl Acad Sci USA 95:8461-6 4. Halenbeck, R. et al. (1998) Curr Biol 8:537-40
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