COP1 Antibody (N-term)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| FC, WB, E |
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Primary Accession | Q5EG05 |
Other Accession | P29466, NP_443121.1, NP_001017534.1 |
Reactivity | Human |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 22625 Da |
Antigen Region | 37-65 aa |
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 |
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. |
Dilution | WB~~1:1000 FC~~1:10~50 |
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. |
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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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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