ArticleJournal of cellular and molecular medicine2016
Molecular insights into cell toxicity of a novel familial amyloidogenic variant of β2-microglobulin.
Article in Journal of cellular and molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
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- Pathogenic D76N Variant of βBiology · 2021Article
- Quantitative Measurement of the Affinity of Toxic and Nontoxic Misfolded Protein Oligomers for Lipid Bilayers and of its Modulation by Lipid Composition and Trodusquemine.ACS chemical neuroscience · 2021Article
- Natural Compound from Olive Oil Inhibits S100A9 Amyloid Formation and Cytotoxicity: Implications for Preventing Alzheimer's Disease.ACS chemical neuroscience · 2021Article
- Prediction of Transmembrane Regions, Cholesterol, and Ganglioside Binding Sites in Amyloid-Forming Proteins Indicate Potential for Amyloid Pore Formation.Frontiers in molecular neuroscience · 2021Article
- Inhibitory synaptic transmission tuned by CaDevelopment, growth & differentiation · 2020Review
- The Amphipathic GM1 Molecule Stabilizes Amyloid Aggregates, Preventing their Cytotoxicity.Biophysical journal · 2020Article
- The Early Phase of β2-Microglobulin Aggregation: Perspectives From Molecular Simulations.Frontiers in molecular biosciences · 2020Review
- Oleuropein, a Bioactive Compound fromAntioxidants (Basel, Switzerland) · 2019Review
- Article
- Oleuropein aglycone stabilizes the monomeric α-synuclein and favours the growth of non-toxic aggregates.Scientific reports · 2018Article
- Catechol-Containing Hydroxylated Biomimetic 4-Thiaflavanes as Inhibitors of Amyloid Aggregation.Biomimetics (Basel, Switzerland) · 2017Article
- A specific nanobody prevents amyloidogenesis of D76N βScientific reports · 2017Article
- Biochemical and Electrophysiological Modification of Amyloid Transthyretin on Cardiomyocytes.Biophysical journal · 2016Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The first genetic variant of β2 -microglobulin (b2M) associated with a familial form of systemic amyloidosis has been recently described. The mutated protein, carrying a substitution of Asp at position 76 with an Asn (D76N b2M), exhibits a strongly enhanced amyloidogenic tendency to aggregate with respect to the wild-type protein. In this study, we characterized the D76N b2M aggregation path and performed an unprecedented analysis of the biochemical mechanisms underlying aggregate cytotoxicity. We showed that, contrarily to what expected from other amyloid studies, early aggregates of the mutant are not the most toxic species, despite their higher surface hydrophobicity. By modulating ganglioside GM1 content in cell membrane or synthetic lipid bilayers, we confirmed the pivotal role of this lipid as aggregate recruiter favouring their cytotoxicity. We finally observed that the aggregates bind to the cell membrane inducing an alteration of its elasticity (with possible functional unbalance and cytotoxicity) in GM1-enriched domains only, thus establishing a link between aggregate-membrane contact and cell damage.
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