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Signal transduction in Alzheimer disease: p21-activated kinase signaling requires C-terminal cleavage of APP at Asp664
The deficits in Alzheimer disease (AD) stem at least partly from neurotoxic β-amyloid peptides generated from the amyloid precursor protein (APP). APP may also be cleaved intracellularly at Asp664 to yield a second neurotoxic peptide, C31. Previously, we showed that cleavage of APP at the C-terminus...
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| Hoofdauteurs: | , , , , , , |
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| Formaat: | Artigo |
| Taal: | Inglês |
| Gepubliceerd in: |
2007
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| Onderwerpen: | |
| Online toegang: | https://ncbi.nlm.nih.gov/pmc/articles/PMC2553705/ https://ncbi.nlm.nih.gov/pubmed/17986220 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1111/j.1471-4159.2007.05031.x |
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