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Transplants of fibroblasts secreting high levels of β-glucuronidase decrease lesions in the brains of mice with Sly syndrome, a lysososmal storage disease (771–774).
p53 mutation partially rescues developmental arrest in Brca1 and Brca2 null mice, suggesting a role for familial breast cancer genes in DNA damage repair.
Accumulating evidence from several studies points to the normal function of presenilin 1 and suggests how the mutant protein contributes to deposition of amyloid plaques in Alzheimer's disease (pages 756–760).