| Product Name | Beta-Amyloid (1-42), E22G Arctic Mutation |
| Catalog Number | LT9150 |
| Sequence | DAEFRHDSGYEVHHQKLVFFAGDVGSNKGAIIGLMVGGVVIA |
| Mutation | E22G |
| Molecular Weight | 4442.4 |
| Purity | ≥95% |
| Mechanism & Biological Significance | The Arctic E22G mutation in the Aβ42 background strongly increases aggregation propensity and changes the microscopic pathways of fibril formation. It is a widely studied familial Alzheimer disease variant. |
| Published Research Context | Exact E22G Aβ42 mutant peptide has been generated synthetically and examined in aggregation studies; later work directly compared Arctic Aβ42 with wild-type Aβ42 and showed rapid fibril formation with distinct inhibition behavior toward the BRICHOS anti-amyloid chaperone domain. |
| Research Applications | - Arctic Aβ42 aggregation studies
- secondary nucleation research
- anti-amyloid chaperone/inhibitor studies
- familial Alzheimer disease models
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| Experimental Considerations | Mutation identity and the Aβ C-terminal boundary are integral to this reagent. Compare with sequence-matched wild-type peptide using the same pretreatment, buffer, concentration, incubation time, and aggregation protocol. |
| Selected Scientific References | - O-Acyl isopeptide method for efficient preparation of amyloid β peptide 1-42 mutants
- Amyloid fibril formation of Arctic amyloid-β 1-42 peptide is efficiently inhibited by the BRICHOS domain
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