anti-CAD (Caspase-activated Dnase DFF40), pAb

CHF 315.00
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YIF-LF-PA0057100 µlCHF 315.00
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Product Details
Synonyms CAD; DFFB; CPAN; DFF-40; Caspase-activated DNase; Caspase-activated Nuclease; Caspase-activated Deoxyribonuclease; DNA Fragmentation Factor Subunit β; DNA Fragmentation Factor 40 kDa Subunit
Product Type Polyclonal Antibody
Immunogen/Antigen Synthetic peptide.

Western Blot (1:2,000)
Immunoprecipitation not tested.

Crossreactivity Human
Purity Detail Protein A purified.
Formulation Liquid. HEPES with 0.15M NaCl, 0.01% BSA, 0.03% sodium azide, and 50% glycerol.
Other Product Data

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Our product description may differ slightly from the original manufacturers product datasheet.

Declaration Manufactured by AbFrontier
Shipping and Handling
Shipping BLUE ICE
Short Term Storage +4°C
Long Term Storage -20°C
Use/Stability Stable for at least 1 year after receipt when stored at -20°C.
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Product Specification Sheet
Datasheet Download PDF

CAD (caspase-activated DNase), a 40kDa nuclear protein, is primarily responsible for cell-autonomous DNA degradation during apoptosis. CAD is present in healthy cells where it is held in an inactive state through the association with its inhibitor ICAD. The ICAD protein is inactivated in apoptotic cells via caspase-3 cleavage thereby releasing CAD, which subsequently cleaves chromosomal DNA. CAD is a magnesium-dependent endonuclease specific for double stranded DNA that generates double strand breaks with 3'-hydroxyl ends. The nuclease preferentially attacks chromatin in the internucleosomal linker DNA. However, the nuclease hypersensitive sites can be detected and CAD is potentially involved in large-scale DNA fragmentation as well. CAD-mediated DNA fragmentation triggers chromatin condensation that is another hallmark of apoptosis. Nuclease that induces DNA fragmentation and chromatin condensation during apoptosis. Degrades naked DNA and induces apoptotic morphology.

Product References

1) Nagata S Annu Rev Immunol. 2005;vol.23: pp.853-75. (General)
2) Nagata S et al, Cell Death Differ. 2003; vol.10(1): pp.108-16. (General)
3) Widlak P Acta Biochim Pol. 2000; vol.47(4): pp.1037-44. (General)
4) Degen WG et al, Cell Death Differ. 2000; vol.7(7): pp.616-27. (General)

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