ArticlePloS one2014
Effect of C-terminal residues of Aβ on copper binding affinity, structural conversion and aggregation.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Peptide-based therapeutics in the management of Alzheimer's disease (AD) and their potential to develop novel strategies.Metabolic brain disease · 2026Review
- A Diruthenium Metallodrug as a Potent Inhibitor of Amyloid-β Aggregation: Synergism of Mechanisms of Action.Inorganic chemistry · 2024Article
- Glucosyl Platinum(II) Complexes Inhibit Aggregation of the C-Terminal Region of the Aβ Peptide.Inorganic chemistry · 2022Article
- Peptides as Potential Therapeutics for Alzheimer's Disease.Molecules (Basel, Switzerland) · 2018Review
- Amyloid-β 1-24 C-terminal truncated fragment promotes amyloid-β 1-42 aggregate formation in the healthy brain.Acta neuropathologica communications · 2016Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many properties of Aβ such as toxicity, aggregation and ROS formation are modulated by Cu2+. Previously, the coordination configuration and interaction of Cu2+ with the Aβ N-terminus has been extensively studied. However, the effect of Aβ C-terminal residues on related properties is still unclear. In the present study, several C-terminus-truncated Aβ peptides, including Aβ1-40, Aβ1-35, Aβ1-29, Aβ1-24 and Aβ1-16, were synthesized to characterize the effect of Aβ C-terminal residues on Cu2+ binding affinity, structure, aggregation ability and ROS formation. Results show that the Aβ C-terminal residues have effect on Cu2+ binding affinity, aggregation ability and inhibitory ability of ROS formation. Compared to the key residues responsible for Aβ aggregation and structure in the absence of Cu2+, it is more likely that residues 36-40, rather than residues 17-21 and 30-35, play a key role on the related properties of Aβ in the presence of Cu2+.
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