1/100 - 1/1000. Perform heat mediated antigen retrieval before commencing with IHC staining protocol using 10mM Citrate buffer (pH6.0) or Tris-EDTA buffer (pH8.0).
1/100 - 1/1000.
May be involved in learning and memory reactions by increasing the turnover of the excitatory neurotransmitter glutamate.
Involvement in disease
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.