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COP1 Antibody (N-term) Blocking peptide

Synthetic peptide

     
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Product Information
Primary Accession Q5EG05
Clone Names 81006031
Peptide ID 81006031
Additional Information
Gene ID 114769
Other Names Caspase recruitment domain-containing protein 16, Caspase recruitment domain-only protein 1, CARD-only protein 1, Caspase-1 inhibitor COP, Pseudo interleukin-1 beta converting enzyme, Pseudo-ICE, Pseudo-IL1B-converting enzyme, CARD16, COP, COP1
Format Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.
StorageMaintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.
PrecautionsThis product is for research use only. Not for use in diagnostic or therapeutic procedures.
Protein Information
Name CARD16
Synonyms COP, COP1
Function Caspase inhibitor. Acts as a regulator of procaspase- 1/CASP1 activation implicated in the regulation of the proteolytic maturation of pro-interleukin-1 beta (IL1B) and its release during inflammation. Inhibits the release of IL1B in response to LPS in monocytes. Also induces NF-kappa-B activation during the pro- inflammatory cytokine response. Also able to inhibit CASP1- mediated neuronal cell death, TNF-alpha, hypoxia-, UV-, and staurosporine-mediated cell death but not ER stress-mediated cell death. Acts by preventing activation of caspases CASP1 and CASP4, possibly by preventing the interaction between CASP1 and RIPK2.
Tissue Location Widely expressed. Expressed at higher level in placenta, spleen, lymph node and bone marrow. Weakly or not expressed in thymus.
Research Areas
Citations (0)

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Background

Caspase inhibitor. Acts as a regulator of procaspase-1/CASP1 activation implicated in the regulation of the proteolytic maturation of pro-interleukin-1 beta (IL1B) and its release during inflammation. Inhibits the release of IL1B in response to LPS in monocytes. Also induces NF-kappa-B activation during the pro-inflammatory cytokine response. Also able to inhibit CASP1-mediated neuronal cell death, TNF-alpha, hypoxia-, UV-, and staurosporine-mediated cell death but not ER stress-mediated cell death. Acts by preventing activation of caspases CASP1 and CASP4, possibly by preventing the interaction between CASP1 and RIPK2.

References

Bailey, S.D., et al. Diabetes Care (2010) In press :Talmud, P.J., et al. Am. J. Hum. Genet. 85(5):628-642(2009)Wang, X., et al. Biochim. Biophys. Acta 1762(8):742-754(2006)Wang, X., et al. J. Neurosci. 25(50):11645-11654(2005)Lamkanfi, M., et al. J. Biol. Chem. 279(50):51729-51738(2004)

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$ 80.00
Cat# BP11328a
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