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Journal article

Proteolytic shedding of the prion protein via activation of metallopeptidase ADAM10 reduces cellular binding and toxicity of amyloid-β oligomers

Abstract:

The cellular prion protein (PrPC) is a key neuronal receptor for β-amyloid oligomers (AβO), mediating their neurotoxicity, which contributes to the neurodegeneration in Alzheimer's disease (AD). Similarly to the amyloid precursor protein (APP), PrPC is proteolytically cleaved from the cell surface by a disintegrin and metalloprotease, ADAM10. We hypothesized that ADAM10-modulated PrPC shedding would alter the cellular binding and cytotoxicity of AβO. Here, we found that in human neuroblastoma...

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Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1074/jbc.RA118.005364

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Wellcome Trust More from this funder
Publisher:
American Society for Biochemistry and Molecular Biology Publisher's website
Journal:
Journal of Biological Chemistry Journal website
Volume:
294
Issue:
17
Pages:
7085-7097
Publication date:
2019-03-14
Acceptance date:
2019-03-14
DOI:
EISSN:
1083-351X
Pmid:
30872401
Source identifiers:
983969
Language:
English
Keywords:
Pubs id:
pubs:983969
UUID:
uuid:d224331f-e6c1-4d4a-bd56-75f2851078fd
Local pid:
pubs:983969
Deposit date:
2019-06-17

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