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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.
This gene encodes the catalytic subunit of glucose 6-phosphatase (G6Pase). G6Pase is located in the endoplasmic reticulum (ER) and catalyzes the hydrolysis of glucose 6-phosphate to glucose and phosphate in the last step of the gluconeogenic and glycogenolytic pathways. [5]
Mutations in the PKLR gene therefore cause a deficiency in the pyruvate kinase enzyme. [3] [9] 180 different mutations have been found on the gene coding for the L and R isoenzymes, 124 of which are single-nucleotide missense mutations. [10] Pyruvate kinase deficiency is most commonly an autosomal recessive trait. [11]
Glucose-6-phosphatase, catalytic subunit (glucose 6-phosphatase alpha) is an enzyme that in humans is encoded by the G6PC gene. [ 5 ] [ 6 ] Glucose-6-phosphatase is an integral membrane protein of the endoplasmic reticulum that catalyzes the hydrolysis of D-glucose 6-phosphate to D-glucose and orthophosphate.
Dogs can develop carcinomas of epithelial cells and organs, sarcomas of connective tissues and bones, and lymphomas or leukemias of the circulatory system. Selective breeding of dogs has led certain pure-bred breeds to be at high-risk for specific kinds of cancer. [1] Veterinary oncology is the medical study of cancer in animals, and can be ...
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.
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 ...
G6PD (glucose-6-phosphate dehydrogenase) deficiency exacerbated by administration of oxidant drugs (e.g., primaquine, dapsone, quinidine) can also result in Heinz bodies. G6PD deficient red cells in combination with high levels of oxidants causes a cross-linking of sulfhydryl groups on globin chains which causes a denaturing and formation of ...