Assay by immunoelectrophoresis resulted in a single precipitin arc against anti-peroxidase, anti-Rabbit Serum as well as purified and partially purified Glutamate Dehydrogenase [Bovine Liver].Cross reactivity from other tissues and species may occur but have not been determined.
Due to high sequence homology with GLUD2 there is a potential for cross-reactivity.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Assayed against 1.0ug of Glutamate Dehydrogenase (Bovine Liver) in a standard capture ELISA using ABTS as a substrate for 30 minutes at room temperature.
ELISA: 1/1000 - 1/3900.
Not tested in other applications.
Optimal dilutions/concentrations should be determined by the end user.
May be involved in learning and memory reactions by increasing the turnover of the excitatory neurotransmitter glutamate.
Defects in GLUD1 are the cause of familial hyperinsulinemic hypoglycemia type 6 (HHF6) [MIM:606762]; also known as hyperinsulinism-hyperammonemia syndrome (HHS). Familial hyperinsulinemic hypoglycemia [MIM:256450], also referred to as congenital hyperinsulinism, nesidioblastosis, or persistent hyperinsulinemic hypoglycemia of infancy (PPHI), is the most common cause of persistent hypoglycemia in infancy and is due to defective negative feedback regulation of insulin secretion by low glucose levels. In HHF6 elevated oxidation rate of glutamate to alpha-ketoglutarate stimulates insulin secretion in the pancreatic beta cells, while they impair detoxification of ammonium in the liver.
Belongs to the Glu/Leu/Phe/Val dehydrogenases family.