期刊
NATURE MEDICINE
卷 6, 期 4, 页码 397-404出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/74656
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资金
- NIA NIH HHS [AG05131, AG12282] Funding Source: Medline
- NINDS NIH HHS [NS37776] Funding Source: Medline
The amyloid beta -protein precursor gives rise to the amyloid beta -protein, the principal constituent of senile plaques and a cytotoxic fragment involved in the pathogenesis of Alzheimer disease. Here we show that amyloid beta -protein precursor was proteolytically cleaved by caspases in the C terminus to generate a second unrelated peptide, called C31. The resultant C31 peptide was a potent inducer of apoptosis. Both caspase-cleaved amyloid beta -protein precursor and activated caspase-9 were present in brains of Alzheimer disease patients but not in control brains. These findings indicate the possibility that caspase cleavage of amyloid beta -protein precursor with the generation of C31 may be involved in the neuronal death associated with Alzheimer disease.
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