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Literature summary for 3.4.24.11 extracted from
- Neprilysin overexpression inhibits plaque formation but fails to reduce pathogenic Abeta oligomers and associated cognitive deficits in human amyloid precursor protein transgenic mice (2009), J. Neurosci., 29, 1977-1986.
Cloned(Commentary)
| Cloned (Comment) | Organism |
|---|---|
| generation of both neprilysin and amyloid precursor protein transgenic mice | Homo sapiens |
Protein Variants
| Protein Variants | Comment | Organism |
|---|---|---|
| additional information | in both neprilysin and amyloid precursor protein transgenic mice, neprilysin overexpression reduces soluble amyloid beta levels by 50% and effectively prevents early amyloid beta deposition in the neocortex and hippocampus. However, it does not reduce levels of amyloid beta trimers and amyloid beta*56 or improve deficits in spatial learning and memory. Neprilysin-dependent degradation of amyloid beta may affect plaques more than oligomers and these structures may form through distinct assembly mechanisms | Homo sapiens |
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Homo sapiens | - |
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