ArticlePloS one2014
β2-Microglobulin amyloid fibril-induced membrane disruption is enhanced by endosomal lipids and acidic pH.
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 22 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- Article
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- Human wild-type and D76N βFASEB bioAdvances · 2023Article
- Amyloid seeding as a disease mechanism and treatment target in transthyretin cardiac amyloidosis.Heart failure reviews · 2022Review
- Dynamic protein structures in normal function and pathologic misfolding in systemic amyloidosis.Biophysical chemistry · 2022Review
- Global Proteotoxicity Caused by Human βInternational journal of molecular sciences · 2021Article
- Identification of transmissible proteotoxic oligomer-like fibrils that expand conformational diversity of amyloid assemblies.Communications biology · 2021Article
- The Double-Edged Sword of Beta2-Microglobulin in Antibacterial Properties and Amyloid Fibril-Mediated Cytotoxicity.International journal of molecular sciences · 2021Review
- Article
- The hydrophobic effect characterises the thermodynamic signature of amyloid fibril growth.PLoS computational biology · 2020Article
- Structure and Aggregation Mechanisms in Amyloids.Molecules (Basel, Switzerland) · 2020Review
- Looking Beyond the Core: The Role of Flanking Regions in the Aggregation of Amyloidogenic Peptides and Proteins.Frontiers in neuroscience · 2020Review
- Extracellular matrix components modulate different stages in βThe Journal of biological chemistry · 2019Article
- A new era for understanding amyloid structures and disease.Nature reviews. Molecular cell biology · 2018Review
- The structure of a βNature communications · 2018Article
- Why are Functional Amyloids Non-Toxic in Humans?Biomolecules · 2017Review
- Iowa Mutant Apolipoprotein A-I (ApoA-IIowa) Fibrils Target Lysosomes.Scientific reports · 2016Article
- RepA-WH1, the agent of an amyloid proteinopathy in bacteria, builds oligomeric pores through lipid vesicles.Scientific reports · 2016Article
- Amyloid Assemblies of Influenza A Virus PB1-F2 Protein Damage Membrane and Induce Cytotoxicity.The Journal of biological chemistry · 2016Article
- Amyloid Fibres: Inert End-Stage Aggregates or Key Players in Disease?Trends in biochemical sciences · 2015Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Although the molecular mechanisms underlying the pathology of amyloidoses are not well understood, the interaction between amyloid proteins and cell membranes is thought to play a role in several amyloid diseases. Amyloid fibrils of β2-microglobulin (β2m), associated with dialysis-related amyloidosis (DRA), have been shown to cause disruption of anionic lipid bilayers in vitro. However, the effect of lipid composition and the chemical environment in which β2m-lipid interactions occur have not been investigated previously. Here we examine membrane damage resulting from the interaction of β2m monomers and fibrils with lipid bilayers. Using dye release, tryptophan fluorescence quenching and fluorescence confocal microscopy assays we investigate the effect of anionic lipid composition and pH on the susceptibility of liposomes to fibril-induced membrane damage. We show that β2m fibril-induced membrane disruption is modulated by anionic lipid composition and is enhanced by acidic pH. Most strikingly, the greatest degree of membrane disruption is observed for liposomes containing bis(monoacylglycero)phosphate (BMP) at acidic pH, conditions likely to reflect those encountered in the endocytic pathway. The results suggest that the interaction between β2m fibrils and membranes of endosomal origin may play a role in the molecular mechanism of β2m amyloid-associated osteoarticular tissue destruction in DRA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.