Isocitrate dehydrogenase (IDH) catalyzes the conversion of isocitrate to α-ketoglutarate. In eukaryotes, there are three isozymes of IDH, the mitochondrial IDH2 and IDH3, and the cytoplasmic/ peroxisomal IDH1. All three IDH family members require the presence of a divalent cation (Mg2+ or Mn2+) and either the electron-accepting cofactor NADP+ (IDH1 and IDH2) or NAD+ (IDH3) for their enzymatic activity. IDH1 and IDH2 mutations resulting in neomorphic enzymatic activity are found in certain cancers such as glioblastoma, acute myeloid leukemia, and colon cancer. This neoactivity shows a change in the substrate specificity resulting in the conversion of α-ketoglutarate to 2-hydroxyglutarate. Mutations in IDH family members are also associated with Ollier disease and Maffucci syndrome.
Application
IDH Activity Assay Kit has been used to determine the activity of isocitrate dehydrogenase in samples.[1][2]
Features and Benefits
Compatible with high-throughput handling systems.
Suitability
Suitable for the measurement of isocitrate dehydrogenase (IDH) (NAD+ - dependent, NADP+ -dependent or both IDHs) activity in biological samples including tissue, cells and serum
Principle
The Isocitrate Dehydrogenase Activity Assay kit provides a simple and direct procedure for measuring NADP+-dependent, NAD+-dependent, or both NADP+ and NAD+-dependent IDH activity in a variety of samples. IDH activity is determined using isocitrate as the substrate in an enzyme reaction, which results in a colorimetric (450 nm) product proportional to the enzymatic activity present. One unit of IDH is the amount of enzyme that will generate 1.0 μmole of NADH or NADP per minute at pH 8.0 at 37 °C.
Trilobatin Protects Against Oxidative Injury in Neuronal PC12 Cells Through Regulating Mitochondrial ROS Homeostasis Mediated by AMPK/Nrf2/Sirt3 Signaling Pathway.
Gao J, et al.
Frontiers in Molecular Neuroscience, 11, 267-267 (2018)
Frontiers in molecular neuroscience, 11, 267-267 (2018-08-15)
Oxidative stress-induced neuronal cell damage is a crucial factor in the pathogenesis of mitochondria-associated neurological diseases. Therefore, elimination of overproduction of mitochondrial reactive oxygen species (mtROS) may be a potential strategy for prevention and treatment of neurological diseases. In the
The Journal of nutritional biochemistry, 99, 108833-108833 (2021-08-03)
Breast cancer is the most common malignancy in women worldwide, and environmental factors, especially diet, have a role in the etiology of this disease. This work aimed to investigate the influence of high fat diets (rich in corn oil or
The Journal of pharmacology and experimental therapeutics, 361(2), 292-302 (2017-02-18)
Background: Mitochondrion is an important metabolic and energetic organelle that regulates several cellular processes. Mitochondrial dysfunction has been related to liver diseases including hepatocellular carcinoma. As a result, the energetic demand is not properly supplied and mitochondrial morphologic changes have
Rationale: Recurrent and metastatic cancers often undergo a period of dormancy, which is closely associated with cellular quiescence, a state whereby cells exit the cell cycle and are reversibly arrested in G0 phase. Curative cancer treatment thus requires therapies that
We describe here a rapid and sensitive method to separate and measure D-2-OHG and L-2-OHG enantiomers using high-resolution mass spectrometry (HRMS) detection.
Our team of scientists has experience in all areas of research including Life Science, Material Science, Chemical Synthesis, Chromatography, Analytical and many others.
