ab172730 - Rabbit monoclonal IgG, is suitable for use as an isotype control with this antibody.
Is unsuitable for IP.
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.
Flow cytometry analysis of HeLa (human cervix adenocarcinoma) cells labeling GLUD1 (red) with ab168352 at a 1/2000 dilution. Cells were fixed with 4% paraformaldehyde and permeabilized with 90% methanol. A goat anti-rabbit IgG (Alexa Fluor® 488) (ab150077) was used as the secondary antibody at a 1/2000 dilution. Black - Rabbit monoclonal IgG (ab172730). Blue (unlabeled control) - Cells without incubation with the primary and secondary antibodies.
Li W et al. HIF-2a regulates non-canonical glutamine metabolism via activation of PI3K/mTORC2 pathway in human pancreatic ductal adenocarcinoma. J Cell Mol Med21:2896-2908 (2017).
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