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Disruption of protein-folding causes neurodegeneration, mental retardation

use) embryonic fibroblasts (MEFs), as well as groups of nerve-like cells called neurospheres. The researchers then compared the behaviour of those cells with that of cells that were similar, except that they lacked -galactosidase, which caused them to accumulate GM1. Regardless of whether the researchers added GM1 or the GM1 accumulated because of loss of -galactosiadase, the excess GM1 caused depletion of calcium from this compartment. Following loss of calcium, the genes responsible for the UPR become activated and eventually cause cell death.


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Contact: Bonnie Cameron
bonnie.cameron@stjude.org
901-495-4815
St. Jude Children's Research Hospital
9-Sep-2004


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