enzyme plays a key role in urea synthesis by regulating provision of glutamate for synthesis of N-acetylglutamate, the obligatory cofactor of carbamoylphosphate synthetase
kidney enzyme increases during acidosis, skeletal muscle enzyme does not. Under some conditions the enzyme from skeletal muscle is able to catabolize Gln to Glu and further to CO2
enzyme is involved in deamination of Gln to Glu, which is utilized for energy production via the TCA cycle. Glutaminase mRNA increases around the 3rd week of life
glutamine synthesis pathway, overview, the intestinal and brain phosphate-activated glutaminase plays a role in the pathogenesis of hepatic encephalopathy, overview, PAG is increased in cirrhotics showing minimal hepatic encephalopathy and, therefore, could be implicated in the production of systemic hyperammonemia in these patients, PAG localized into the astrocytes is responsible for ammonia and free-radical production, PAG regulation mechanism, overview
intestinal glutaminase activity is increased in liver cirrhosis and correlates with minimal hepatic encephalopathy, relationship between enzyme activity, liver function, and porto-systemic shunts, overview
the enzyme plays a key role in energy and nitrogen metabolism, glutamate is a major excitatory neurotransmitter in neurons, especially in the cerebral cortex
neurotransmitter glutamate has been thought to derive mainly from glutamine via the action of glutaminase type 1, the GLS1 pathway is essential for maintaining the function of active synapses, knockout mice lacking brain/kidney phosphate-activated glutaminase have impaired glutamatergic synaptic transmission, altered breathing, disorganized goal-directed behavior and die shortly after birth
enzyme participates in an ATP-consuming cycle, plays a catabolic role in the degradation of glutamine to carbon skeletons, maintaining the optimal balance between glutamine and glutamate
the brain-specific BNIP-2-homology protein, BHIP-H is involved in enzyme regulation in neurons, loss of BNIP-H function could render glutamate excitotoxicity or/and deregulated glutamatergic activation, leading to ataxia, dystonia or other neurological disorders
the brain-specific BNIP-2-homology protein, BHIP-H is involved in enzyme regulation in neurons, loss of BNIP-H function could render glutamate excitotoxicity or/and deregulated glutamatergic activation, leading to ataxia, dystonia or other neurological disorders
the spatial segregation of tissue-specific isozymes in pancreas alpha- and beta-cells may have important functional implications, facilitating a differential regulation of glutamate production in insulin- and glucagon-secreting cells, overview