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(Thr²)-Amyloid β-Protein (1-42)

Name
(Thr²)-Amyloid β-Protein (1-42)
Molecular structural formula
Purity
95%
Formula
C204H313N55O61S1
MW
4544.06
Sequence
Asp-Thr-Glu-Phe-Arg-His-Asp-Ser-Gly-Tyr-Glu-Val-His-His-Gln-Lys-Leu-Val-Phe-Phe-Ala-Glu-Asp-Val-Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met-Val-Gly-Gly-Val-Val-Ile-Ala
Sequence Shortening
DTEFRHDSGYEVHHQKLVFFAEDVGSNKGAIIGLMVGGVVIA
References
[1]. The A673T mutation in the amyloid precursor protein reduces the production of β-amyloid protein from its β-carboxyl terminal fragment in cells. [2]. A2T and A2V Aβ peptides exhibit different aggregation kinetics, primary nucleation, morphology, structure, and LTP inhibition. [3]. Alzheimer's Protective Cross-Interaction between Wild-Type and A2T Variants Alters Aβ 42 Dimer Structure. [4].Pathogenic Aβ A2V versus protective Aβ A2T mutation: Early stage aggregation and membrane interaction.
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A mutation very close to the β-secretase cleavage site of APP (A673V). Contrary to the protective Icelandic mutation A2T, the recessive A2V mutation may increase the risk of Alzheimer’s disease. Cantu et al. observed that APP A673V is associated with the early onset of AD-type dementia in homozygous individuals, whereas it has a protective effect in the heterozygous state.