Anti-GLUD1 antibody

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

GLUD1 also known as glutamate dehydrogenase 1 is an enzyme that catalyzes the reversible oxidative deamination of glutamate to α-ketoglutarate and ammonia playing an important role in amino acid metabolism. The molecular mass of GLUD1 is approximately 61 kDa. It is expressed in many tissues with notably high levels in liver kidney and neural tissues. GLUD1 is essential for maintaining the balance between amino acid and carbohydrate metabolism.

Biological function summary

GLUD1 facilitates nitrogen and carbon homeostasis through its role in amino acid breakdown and energy metabolism. Although not part of a complex GLUD1's activity impacts central metabolic processes influencing cellular energy status and neurotransmitter regulation. The enzyme contributes to the glutamate-glutamine cycle which is important for neurotransmission in the brain. Its regulation by ADP GDP and other molecules enables cells to adapt to energetic demands.

Pathways

GLUD1 is integral to the tricarboxylic acid (TCA) cycle and urea cycle impacting both energy production and detoxification of ammonia. In the TCA cycle GLUD1 influences the availability of α-ketoglutarate interfacing with enzymes such as isocitrate dehydrogenase. In the urea cycle it aids in converting ammonia to urea in the liver. Additionally GLUD1's function connects with glutamine synthetase in managing amino acid synthesis and degradation.

Associated diseases and disorders

GLUD1 is associated with congenital hyperinsulinism and hepatic encephalopathy. Hyperinsulinism often results from mutations in GLUD1 which lead to excessive insulin release due to increased leucine sensitivity. In hepatic encephalopathy GLUD1's role in ammonia detoxification becomes important with impaired function potentially leading to elevated ammonia levels and neurological dysfunction. Understanding GLUD1's interactions with other proteins such as those in insulin signaling pathways could further elucidate its impact on these medical conditions.