| Product Name | Beta-Amyloid (1-40), H6R England Mutation |
| Catalog Number | LT9144 |
| Sequence | DAEFRRDSGYEVHHQKLVFFAEDVGSNKGAIIGLMVGGVV |
| Mutation | H6R |
| Molecular Weight | 4349.2 |
| Purity | ≥95% |
| Mechanism & Biological Significance | The English H6R familial Alzheimer disease substitution changes His6 to Arg in Aβ40 and alters the N-terminal charge environment, accelerating conformational conversion and shifting oligomer distributions toward higher-order assemblies. |
| Published Research Context | Direct studies synthesized, purified, and characterized H6R Aβ40 and compared it with wild-type Aβ40. The mutant displayed faster secondary-structure transitions and altered oligomerization; earlier work also reported enhanced fibril elongation behavior for H6R Aβ40-based peptides. |
| Research Applications | - familial Alzheimer disease mutation studies
- Aβ40 oligomerization and fibrillization
- PICUP/gel and microscopy studies
- mutant-versus-wild-type structure-function comparisons
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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 | - Effects of the English (H6R) and Tottori (D7N) familial Alzheimer disease mutations on Aβ-protein assembly and toxicity
- The Tottori (D7N) and English (H6R) familial Alzheimer disease mutations accelerate Aβ fibril formation
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