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|The FAM FLICA Caspase-1 Kit uses a target sequence (YVAD) sandwiched between a green fluorescent label, carboxyfluorescein (FAM), and a fluoromethylketone (FMK) to make a quick and flexible method to analyze active caspases in apoptotic cells.|
- Reagents in the Kit
- Pack Size: 25 Tests1 vial of FAM-YVAD-FMK FLICA Reagent - lyophilized
10x Apoptosis Wash Buffer, 15 mL
Fixative, 6 mL
Propidium Iodide, 1 mL
Hoechst 33342, 1 mLPack Size: 100 Tests4 vials of FAM-YVAD-FMK FLICA Reagent - lyophilized
10x Apoptosis Wash Buffer, 60 mL
Fixative, 6 mL
Propidium Iodide, 1 mL
Hoechst 33342, 1 mL
- Test Principle
- Caspase FLICA kits measure apoptosis by detecting active caspases in whole, living cells. These kits do not work by using antibodies or as an ELISA. Instead, their methodology is based on a unique cell-permeable and non-cytotoxic reagent called the Fluorochrome Inhibitor of Caspases (FLICA). The FLICA reagent contains a caspase inhibitor sequence linked to a green (Carboxyfluorescein, FAM) fluorescent probe.
The Caspase FLICA Kits are suitable for cells in suspension and adherent cells from many species including mammalian, insect and yeast. Different cell types, e.g. HeLa, primary neurons, macrophages and lymphocytes have also been successfully studied with these kits.
This kit can be used with a flow cytometer, fluorescence microscope or a fluorescence plate reader using black microtitre plates.
- Max Ex/Em
Fluorophore Excitation Max (nm) Emission Max (nm) FAM 494 520
- For research purposes only
- Guaranteed until date of expiry. Please see product label.
- FLICA™ is a trademark of Immunochemistry Technologies, LLC.
Once reconstituted with DMSO, use FLICA reagent immediately, or store at -20oC for 6 months protected from light and thawed no more than twice during that time.
|Application Name||Verified||Min Dilution||Max Dilution|
References for Caspase-1
Hoegen, T. et al. (2011) The NLRP3 Inflammasome Contributes to Brain Injury in Pneumococcal Meningitis and Is Activated through ATP-Dependent Lysosomal Cathepsin B Release.
J Immunol. 187: 5440-51.
Edwards, M.R. et al. (2015) Metabolic dysfunction in lymphocytes promotes postoperative morbidity.
Clin Sci (Lond). Apr 20. [Epub ahead of print]
Inokuchi, T. et al. (2006) Plasma interleukin (IL)-18 (interferon-gamma-inducing factor) and other inflammatory cytokines in patients with gouty arthritis and monosodium urate monohydrate crystal-induced secretion of IL-18.
Cytokine. 33 (1): 21-7.
Hussen, J. et al. (2012) Inflammasome activation in bovine monocytes by extracellular ATP does not require the purinergic receptor P2X7.
Dev Comp Immunol. 38 (2): 312-20.
Wang, Y. et al. (2012) A comparative study of stress-mediated immunological functions with the adjuvanticity of alum.
J Biol Chem. 287 (21): 17152-60.
Wang, Y. et al. (2015) Stress activated DC induce dual homeostatic and inflammasome pathways, which may elicit CD4+ memory T cells and IFN stimulated genes.
J Biol Chem. pii: jbc.M115.645754.
Wree, A. et al. (2014) NLRP3 inflammasome activation results in hepatocyte pyroptosis, liver inflammation, and fibrosis in mice.
Hepatology. 59 (3): 898-910.
Sharma, A.A. et al. (2015) Impaired NLRP3 inflammasome activity during fetal development regulates IL-1β production in human monocytes.
Eur J Immunol. 45 (1): 238-49.
View The Latest Product References
Gabrion, A. et al. (2016) mTOR inhibition counterbalances the inflammatory status of immune cells in Chronic Granulomatous Disease.
J Allergy Clin Immunol. pii: S0091-6749(16)31057-0. [Epub ahead of print]
Burm, S.M. et al. (2015) Inflammasome-induced IL-1β secretion in microglia is characterized by delayed kinetics and is only partially dependent on inflammatory caspases.
J Neurosci. 35 (2): 678-87.
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