COP1 Antibody (N-term) Blocking peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Primary Accession | Q5EG05 |
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Clone Names | 81006031 |
Gene ID | 114769 |
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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 | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. |
Precautions | This product is for research use only. Not for use in diagnostic or therapeutic procedures. |
Name | CARD16 |
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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. |
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Provided below are standard protocols that you may find useful for product applications.
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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