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Fluorogenic peptide substrate for caspase-1 (ICE).
(Modifications: Tyr-1 = N-Ac-Tyr, Asp-4 = Asp-(7-amino-4-trifluoromethylcoumarin))
|Storage||Desiccate at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
References are publications that support the biological activity of the product.
Jones et al (1998) Fas-mediated apoptosis in mouse hepatocytes involves the processing and activation of caspases. Hepatology 27 1632 PMID: 9620337
Marks et al (1998) Activation of caspase-3 and apoptosis in cerebellar granule cells. J.Neurosci.Res. 52 334 PMID: 9590441
Keywords: Ac-YVAD-AFC, Ac-YVAD-AFC supplier, Fluorogenic, caspase-1, ICE, Caspases, Proteinases, Proteases, 1572, Tocris Bioscience
Citations are publications that use Tocris products.
Currently there are no citations for Ac-YVAD-AFC.
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Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
This product guide provides a review of the cell cycle and DNA damage research area and lists over 170 products, including research tools for:
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.
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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.