Anti-Mouse ICAD (NT)

Leinco Technologies
Product Code: LEI-I-312
Product Group: Primary Antibodies
CodeSizePrice
LEI-I-312-20ug20 ug£199.00
Quantity:
LEI-I-312-0.1mg0.1 mg£591.00
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.

Images

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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:I-326
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 DNA fragmentation factor (DFF) was identified recently which is cleaved by caspase-3 during apoptosis. Mouse homologue of human DFF was identified as a DNase inhibitor designated ICAD, for inhibitor of caspase-activated DNase. Upon cleavage of DFF/ICAD, a caspase activated deoxyribonuclease (CAD) is released and activated and eventually causes the degradation of DNA in the nuclei. Therefore, the cleavage of CAD inhibitor molecule DFF/ICAD, which causes DNase activation and DNA degradation, is the hallmark of apoptotic cell death.
Target:
ICAD

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. Wyllie, A. (1998) Nature 391(6662):20-1.

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