|Application ||FC, WB, E|
|Other Accession||P29466, NP_443121.1, NP_001017534.1|
|Calculated MW||22625 Da|
|Antigen Region||37-65 aa|
|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|
|Target/Specificity||This COP1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 37-65 amino acids from the N-terminal region of human COP1.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||COP1 Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|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.|
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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.
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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