Anti-Human CIDE-A (CT)

Leinco Technologies
Product Code: LEI-C1292
Product Group: Primary Antibodies
CodeSizePrice
LEI-C1292-20ug20 ug£199.00
Quantity:
LEI-C1292-0.1mg0.1 mg£591.00
Quantity:
Prices exclude any Taxes / VAT

Overview

Host Type: Rabbit
Antibody Clonality: Polyclonal
Regulatory Status: RUO
Target Species: Human
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:C1136
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. DFF45/ICAD has been identified as inhibitor of caspase activated DNase DFF40/CAD. DFF45 related proteins CIDE-A and CIDE-B (for cell death-inducing DFF-like effector A and B) were recently identified.1 CIDE contains a new type of domain termed CIDE-N, which has high homology with the regulatory domains of DFF45/ICAD and DFF40/CAD.1,2 Expression of CIDE-A induces DNA fragmentation and activates apoptosis, which is inhibited by DFF45. CIDE-A is a DFF45-inhibitable effector that promotes cell death and DNA fragmentation. CIDE-A is expressed in many tissues.
Target:
CIDE-A

References

1. Liu, X. et al. (1997) Cell. 89(2):175-84. 2. Enari, M. et al. (1998) Nature. 391(6662):43-50. 3. Sakahira, H. et al. (2015) Nature. 526(7575):728. 4. Liu, X. et al. (1998) Proc Natl Acad Sci U S A. 95(15):8461-6. 5. Inohara, N. et al. (1998) EMBO J. 17(9):2526-33.

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