Leinco Technologies

Anti-Human DFF45 (NT)

Product Code:
 
LEI-D244
Product Group:
 
Primary Antibodies
Host Type:
 
Rabbit
Antibody Clonality:
 
Polyclonal
Regulatory Status:
 
RUO
Target Species:
 
Human
Application:
 
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.
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CodeSizePrice
LEI-D244-20ug20 ug£199.00
Quantity:
LEI-D244-0.1mg0.1 mg£591.00
Quantity:
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This product comes from: US.
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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:D272
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 human 45 kDa DNA fragmentation factor (DFF45) was identified recently that was cleaved by caspase-3 during apoptosis. Mouse homologue of human DFF45 was identified as a DNase inhibitor designated ICAD. DFF45/ICAD have short forms that were termed DFF35 and ICADs, respectively. Upon cleavage of DFF45/ICAD, the caspase activated deoxyribonuclease (DFF40/CAD) is released and activated and eventually causes the degradation of DNA in the nuclei. Therefore, the cleavage of DFF45/ICAD, which causes DFF40/CAD activation and DNA degradation, is the hallmark of apoptotic cell death.
Target:
DFF45

References

1. Liu, X. et al. (1997) Cell 89:175-184 2. Enari, M. et al. (1998) Nature 391:43-50 3. Sakahira, H. et al. (1998) Nature 391:96-99 4. Gu, J. et al. (1999) J Biol Chem 274:20759-62