|Application ||WB, IF, ICC, E|
|Other Accession||P51878, 212276423|
|Calculated MW||49736 Da|
|Application Notes||Casp-5 antibody can be used for the detection of caspase-5 by Western blot at 0.5 - 2 µg/mL. Antibody can also be used for immunocytochemistry starting at 2 µg/mL. For immunofluorescence start at 2 µg/mL.|
|Other Names||Caspase-5 Antibody: ICH-3, ICEREL-III, ICE(rel)III, ICH3, Caspase-5, Protease ICH-3, CASP-5, caspase 5, apoptosis-related cysteine peptidase|
|Target/Specificity||CASP5; Depending on cell lines or tissues used, other cleavage products may be observed.|
|Reconstitution & Storage||Caspase-5 antibody can be stored at 4℃ for three months and -20℃, 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.|
|Precautions||Caspase-5 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Mediator of programmed cell death (apoptosis).|
|Tissue Location||Expressed in barely detectable amounts in most tissues except brain, highest levels being found in lung, liver and skeletal muscle|
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Provided below are standard protocols that you may find useful for product applications.
Caspase-5 Antibody: Caspases are a family of cysteine proteases that can be divided into the apoptotic and inflammatory caspase subfamilies. Unlike the apoptotic caspases, members of the inflammatory subfamily are generally not involved in cell death but are associated with the immune response to microbial pathogens. Members of this subfamily include caspase-1, -4, -5, and -12. Activation of these caspases results in the cleavage and activation of proinflammatory cytokines such as IL-1β and IL-18. Caspase-5 can interact with caspase-1; both are constituents of the NALP1 inflammasome, a complex that can trigger the cleavage of pro-IL-1β. Expression of caspase-5 can be regulated by lipopolysaccharide (LPS) and IFN-gamma.
Martinon F and Tschopp J. Inflammatory caspases: linking an intracellular innate immune system to autoinflammatory diseases. Cell 2004; 117:561-74.
Kuida K, Lippke JA, Ku G, et al. Altered cytokine export and apoptosis in mice deficient in interleukin-1 β converting enzyme. Science 1995; 267:2000-3.
Gracie JA, Robertson SE, and McInnes IB. Interleukin-18. J. Leukoc. Biol. 2003; 73:213-224.
Martinon F, Burns K, and Tschopp J. The inflammasome: a molecular platform triggering activation of the inflammatory caspases and processing of proIL-1beta. Mol. Cell. 2002; 10:417-26.
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