Key features and details
- Assay type: Quantitative
- Detection method: Fluorescent
- Platform: Microplate reader
- Sample type: Adherent cells, Other biological fluids, Plasma, Serum, Suspension cells, Tissue
- Sensitivity: 0.5 µM
Product nameDihydroxyacetone Phosphate (DHAP) Assay Kit (Fluorometric)
Sample typeSerum, Plasma, Other biological fluids, Tissue, Adherent cells, Suspension cells
Sensitivity> 0.5 µM
Species reactivityReacts with: Mammals, Other species
Dihydroxyacetone Phosphate (DHAP) Assay Kit (Fluorometric) (ab197003) is suitable for measuring low levels of DHAP typically found in a variety of samples. In this kit, triose phosphate isomerase (TPI) converts dihydroxyacetone phosphate (DHAP) to glyceraldehyde-3-phosphate (GAP), which subsequently undergoes a series of reaction and reduces the probe to generate fluorescence. The fluorescence intensity generated is directly proportional to the amount of dihydroxyacetone Phosphate.
Detection limit: 0.5 µM DHAP.
This product is manufactured by BioVision, an Abcam company and was previously called K673 PicoProbe™ Dihydroxyacetone Phosphate (DHAP) Fluorometric Assay Kit. K673-100 is the same size as the 100 test size of ab197003.
Dihydroxyacetone Phosphate (DHAP) is an important intermediate in both lipid biosynthesis and glycolysis. In glycolysis, fructose-1,6- diphosphate is converted to dydroxyacetone phosphate (DHAP) and glyceraldehyde-3-phosphate (GAP) by aldolase. Both DHAP and GAP serve as the intracellular pool for triose phosphate. DHAP can be further converted into GAP by Triose Phosphate Isomerase (TPI).
In humans, TPI deficiency is a rare autosomal disease. It causes hemolytic anemia, neurological diseases, and even death due to blockage of the glycolytic pathway and accumulation of DHAP in erythrocytes.
Storage instructionsStore at -20°C. Please refer to protocols.
Components 100 tests DHAP Assay Buffer 1 x 25ml DHAP Developer 1 vial DHAP Enzyme Mix 1 vial DHAP Standard 1 vial PicoProbe 1 x 400µl
ab197003 has been referenced in 3 publications.
- Haythorne E et al. Altered glycolysis triggers impaired mitochondrial metabolism and mTORC1 activation in diabetic β-cells. Nat Commun 13:6754 (2022). PubMed: 36376280
- Parvaiz N et al. Discovery of beta-lactamase CMY-10 inhibitors for combination therapy against multi-drug resistant Enterobacteriaceae. PLoS One 16:e0244967 (2021). PubMed: 33449932
- Jiang H et al. The Mitochondria-Targeted Metabolic Tubular Injury in Diabetic Kidney Disease. Cell Physiol Biochem 52:156-171 (2019). PubMed: 30816665