Which statement is false regarding the mechanism that removes sialic acid residues from serum glycoproteins? It may be due to asialoglycoprotein receptor catalytic activity. X The exact mechanism is unclear. It may be due to extracellular enzymes slowly releasing Neu5Ac residues. It may be due to the production of the enzyme neuraminidase by invading organisms.
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Suppose you are studying a mutant that you know is impaired in secretion, but you do not know the exact nature of the defect. You analyze the sugar content of some of the proteins purified from the mutant that you know should be N-glycosylated and find that fucose, galactose, and sialic acid residues are absent. Instead, only N-acetylglucosamine and mannose residues are evident. Where do you think the defect in secretion lies?
Adi S.
Jennifer S.
Patients with Hunter's syndrome or with Hurler's syndrome rarely live beyond their teens. These patients accumulate glycosaminoglycans in lysosomes due to the lack of specific lysosomal enzymes necessary for their degradation. When cells from patients with the two syndromes are fused, glycosaminoglycans are degraded properly, indicating that the cells are missing different degradative enzymes. Even if the cells are just cultured together, they still correct each other's defects. Most surprising of all, the medium from a culture of Hurler's cells corrects the defect in Hunter's cells (and vice versa). The corrective factors in the media are inactivated by treatment with proteases, by treatment with periodate, which destroys carbohydrate, and by treatment with alkaline phosphatase, which removes phosphates. A. What do you suppose the corrective factors are? Beginning with the donor patient's cells, describe the route by which the factors reach the medium and subsequently enter the recipient cells to correct the lysosomal defects. B. Why do you suppose the treatments with protease, periodate, and alkaline phosphatase inactivate the corrective factors? C. Would you expect a similar sort of correction scheme to work for mutant cytosolic enzymes?
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