COP1 Antibody | 55-786

COP1 Antibody | 55-786 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human

Homology: N/A

Immunogen: 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.

Research Area: Cell Cycle

Tested Application: WB, Flow

Application: For FACS starting dilution is: 1:10~50
For WB starting dilution is: 1:1000

Specificiy: N/A

Positive Control 1: N/A

Positive Control 2: N/A

Positive Control 3: N/A

Positive Control 4: N/A

Positive Control 5: N/A

Positive Control 6: N/A

Molecular Weight: 23 kDa

Validation: N/A

Isoform: N/A

Purification: This antibody is purified through a protein A column, followed by peptide affinity purification.

Clonality: Polyclonal

Clone: N/A

Isotype: Rabbit Ig

Conjugate: Unconjugated

Physical State: Liquid

Buffer: Supplied in PBS with 0.09% (W/V) sodium azide.

Concentration: batch dependent

Storage Condition: Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.

Alternate Name: 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

User Note: Optimal dilutions for each application to be determined by the researcher.

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.