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Biological Activity for DBeQ
DBeQ is a selective and reversible inhibitor of p97 ATPase (VCP, IC50 = 1.5 μM). Induces executioner caspases (caspase-3 and caspase-7) rapidly. Blocks the degradation of endoplasmic reticulum-associated degradation (ERAD) reporters; also blocks autophagosome maturation and promotes accumulation of LC3-II.
Compound Libraries for DBeQ
Technical Data for DBeQ
|Storage||Store at +4°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.
Solubility Data for DBeQ
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions for DBeQ
The following data is based on the product molecular weight 340.42. Batch specific molecular weights may vary from batch to batch due to the degree 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||2.94 mL||14.69 mL||29.38 mL|
|5 mM||0.59 mL||2.94 mL||5.88 mL|
|10 mM||0.29 mL||1.47 mL||2.94 mL|
|50 mM||0.06 mL||0.29 mL||0.59 mL|
References for DBeQ
References are publications that support the biological activity of the product.
Chou et al (2011) Reversible inhibitor of p97, DBeQ, impairs both ubiquitin-dependent and autophagic protein clearance pathways. Proc.Natl.Acad.Sci.USA 108 4834 PMID: 21383145
Chou and Deshaies (2011) Development of p97 AAA ATPase inhibitors. Autophagy 7 1091 PMID: 21606684
If you know of a relevant reference for DBeQ, please let us know.
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Reviews for DBeQ
Average Rating: 3 (Based on 1 Review.)
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Treated Dictyostelium cells with DbeQ at 15 uM and 1.5 uM concentrations for 1 hour or 24 hours, and monitored p-4E-BP1 levels as a readout for mTORc1 activity. Did not see any significant difference from control
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Cancer Metabolism Poster
Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the main targets for cancer metabolism researchers. Genetic changes and epigenetic modifications in cancer cells alter the regulation of cellular metabolic pathways. These distinct metabolic circuits could provide viable cancer therapeutic targets.