Glycolysis Stress Test Companion Assay (ab222945)
Key features and details
- Assay type: Cell-based (quantitative)
- Detection method: Fluorescent
- Platform: Microplate reader
- Sample type: Adherent cells
Overview
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Product name
Glycolysis Stress Test Companion Assay -
Detection method
Fluorescent -
Sample type
Adherent cells -
Assay type
Cell-based (quantitative) -
Product overview
Glycolysis Stress Test Companion Assay (ab222945) allows glycolytic characterization at user-defined glucose concentrations in live cells when used in combination with our Glycolysis Assay [Extracellular Acidification] (ab197244).
The assay uses 2-Deoxyglucose (2-DG) and oligomycin to facilitate an in-depth analysis of cellular glycolytic flux: 2-DG blocks glycolysis through competitive hexokinase inhibition allowing quantification of non-glycolytic extracellular acidification (ECA); oligomycin inhibits ATP synthase, therefore preventing aerobic ATP generation and forcing cells to increase glycolytic flux to meet ATP demand. The levels of such compensatory glycolysis achievable under test conditions can reveal underlying glycolytic perturbation not evident under basal conditions and facilitates assessment of ATP-demand limited glycolysis capability. Glucose oxidase is included in the kit to provide a convenient cell-free ECA assay signal control.
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Notes
Learn more about the full range of assays to measure glycolysis, oxygen consumption, fatty acid oxidation and metabolic flux in live cells.
Or review the full metabolism assay guide for other assays for metabolites, metabolic enzymes, mitochondrial function, and oxidative stress.
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Platform
Microplate reader
Properties
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Storage instructions
Please refer to protocols. -
Components 55 tests 2-DG 1 x 600µl Glucose 1 vial Glucose Oxidase Signal Control 1 vial Glucose-free Respiration Buffer 1 tablet Oligomycin 1 vial
Images
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Extracellular acidification of A549 cells treated with 2-DG (purple) and oligomycin (black).
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Glycolytic characterization of A549 cells. -
Increased compensatory glycolysis upon increased ATP demand in monensin-treated HepG2 cells.
