(Des-Glu²²)-Amyloid β-Protein (1-40) |
| Katalog-Nr.GA20095 |
The Osaka mutation was the first deletion-type mutation to be identified in APP and Aβ. The Aβ E22delta mutant is more resistant to degradation by two major Aβ-degrading enzymes, neprilysin and insulin-degrading enzyme. Synthetic mutant Aβ showed unusual aggregation properties with enhanced oligomerization but no fibrillization. It also inhibited hippocampal long-term potentiation more efficiently than wild-type Aβ. A transgenic mouse model containing APP with the E693delta mutation has been developed. APP(OSK)-Tg mice exhibit intraneuronal Aβ E22delta oligomers and memory impairment as early as eight months of age.
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Cas No.: 1678416-36-8
Sample solution is provided at 25 µL, 10mM.
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The Osaka mutation was the first deletion-type mutation to be identified in APP and Aβ.The Aβ E22delta mutant is more resistant to degradation by two major Aβ-degrading enzymes, neprilysin and insulin-degrading enzyme. Synthetic mutant A
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