Ecdysone analog that acts as an inducer of ecdysone-inducible gene expression systems in mammalian cells and transgenic animals. Stimulates Bcl-XL mRNA transcription and inhibits TRAIL- and hFasL-induced apoptosis in RKO cells.
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solubility||Soluble in DMSO|
Preparing Stock Solutions
The following data is based on the product molecular weight 496.63. Batch specific molecular weights may vary from batch to batch due to solvent of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||2.01 mL||10.07 mL||20.14 mL|
|5 mM||0.4 mL||2.01 mL||4.03 mL|
|10 mM||0.2 mL||1.01 mL||2.01 mL|
|50 mM||0.04 mL||0.2 mL||0.4 mL|
References are publications that support the biological activity of the product.
Patrick et al (2001) Muristerone A-induced nerve growth factor release from genetically engineered human dermal fibroblasts for peripheral nerve tissue engineering. Tissue Eng. 7 303 PMID: 11429150
No et al (1996) Ecdysone-inducible gene expression in mammalian cells and transgenic mice. Proc.Natl.Acad.Sci.USA 93 3346
Bosser and Zornig (2005) Agonists of an ecdysone-inducible mammalian expression system inhibit Fas-ligand- and TRAIL-induced apoptosis in the human colon carcinoma cell line RKO. Cell Death Diff. 13 189
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Parkinson's disease (PD) causes chronic disability and is the second most common neurodegenerative condition. This poster outlines the neurobiology of the disease, as well as highlighting current therapeutic treatments for symptomatic PD, and emerging therapeutic strategies to delay PD onset and progression.
Programmed Cell Death Poster
There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.