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It is an X-linked recessive disorder that results in defective glucose-6-phosphate dehydrogenase enzyme. [1] Glucose-6-phosphate dehydrogenase is an enzyme that protects red blood cells, which carry oxygen from the lungs to tissues throughout the body. A defect of the enzyme results in the premature breakdown of red blood cells.
Glucose 6-phosphatase-β is a ubiquitously expressed, 346-amino acid membrane protein that shares 36% sequence identity with glucose 6-phosphatase-α. Within the glucose 6-phosphatase-β enzyme, sequence alignments predict that its active site contains His167, His114, and Arg79.
The last step of normal gluconeogenesis, like the last step of glycogenolysis, is the dephosphorylation of G6P by glucose-6-phosphatase to free glucose and PO 4. Thus glucose-6-phosphatase mediates the final, key, step in both of the two main processes of glucose production during fasting. The effect is amplified because the resulting high ...
A glycogen storage disease (GSD, also glycogenosis and dextrinosis) is a metabolic disorder caused by a deficiency of an enzyme or transport protein affecting glycogen synthesis, glycogen breakdown, or glucose breakdown, typically in muscles and/or liver cells.
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G6PD reduces NADP + to NADPH while oxidizing glucose-6-phosphate. [2] Glucose-6-phosphate dehydrogenase is also an enzyme in the Entner–Doudoroff pathway, a type of glycolysis. Clinically, an X-linked genetic deficiency of G6PD makes a human prone to non-immune hemolytic anemia. [3]
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If glycogenolysis is taking place in the liver, G-6-P can be converted to glucose by the enzyme glucose 6-phosphatase (G6Pase); the glucose produced in the liver is then released to the bloodstream for use in other organs. Muscle cells in contrast do not have the enzyme glucose 6-phosphatase, so they cannot share their glycogen stores with the ...