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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
Version:
Publisher's version

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Publisher copy:
10.1074/jbc.RA118.005364

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Grant:
MC_PC_16034
MC_EX_MR/N50192X/1
MR/N013255/1/2720366
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
Pubs id:
pubs:983969
URN:
uri:d224331f-e6c1-4d4a-bd56-75f2851078fd
UUID:
uuid:d224331f-e6c1-4d4a-bd56-75f2851078fd
Local pid:
pubs:983969

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