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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Alternative cleavage of Alzheimer-associated presenilins during apoptosis by a caspase-3 family protease.

Most cases of early-onset familial Alzheimer's disease (FAD) are caused by mutations in the genes encoding the presenilin 1 ( PS1) and PS2 proteins, both of which undergo regulated endoproteolytic processing. During apoptosis, PS1 and PS2 were shown to be cleaved at sites distal to their normal cleavage sites by a caspase-3 family protease. In cells expressing PS2 containing the asparagine-141 FAD mutant, the ratio of alternative to normal PS2 cleavage fragments was increased relative to wild-type PS2-expressing cells, suggesting a potential role for apoptosis-associated cleavage of presenilins in the pathogenesis of Alzheimer's disease.[1]

References

  1. Alternative cleavage of Alzheimer-associated presenilins during apoptosis by a caspase-3 family protease. Kim, T.W., Pettingell, W.H., Jung, Y.K., Kovacs, D.M., Tanzi, R.E. Science (1997) [Pubmed]
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