ArticlePLoS pathogens2018
A bispecific immunotweezer prevents soluble PrP oligomers and abolishes prion toxicity.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- Exploring immunotherapeutic strategies for neurodegenerative diseases: a focus on Huntington's disease and Prion diseases.Acta pharmacologica Sinica · 2025Review
- Inducing prion protein shedding as a neuroprotective and regenerative approach in pathological conditions of the brain: from theory to facts.Neural regeneration research · 2023Review
- Genetically engineered cellular models of prion propagation.Cell and tissue research · 2023Review
- Rapid ex vivo reverse genetics identifies the essential determinants of prion protein toxicity.Brain pathology (Zurich, Switzerland) · 2023Article
- Prion therapeutics: Lessons from the past.Prion · 2022Review
- Antibody binding modulates the dynamics of the membrane-bound prion protein.Biophysical journal · 2022Article
- Single-chain tandem macrocyclic peptides as a scaffold for growth factor and cytokine mimetics.Communications biology · 2022Article
- Article
- Ligands binding to the prion protein induce its proteolytic release with therapeutic potential in neurodegenerative proteinopathies.Science advances · 2021Article
- Article
- Cross-Linking Cellular Prion Protein Induces Neuronal Type 2-Like Hypersensitivity.Frontiers in immunology · 2021Article
- Protective anti-prion antibodies in human immunoglobulin repertoires.EMBO molecular medicine · 2020Article
- Engineering a murine cell line for the stable propagation of hamster prions.The Journal of biological chemistry · 2019Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antibodies to the prion protein, PrP, represent a promising therapeutic approach against prion diseases but the neurotoxicity of certain anti-PrP antibodies has caused concern. Here we describe scPOM-bi, a bispecific antibody designed to function as a molecular prion tweezer. scPOM-bi combines the complementarity-determining regions of the neurotoxic antibody POM1 and the neuroprotective POM2, which bind the globular domain (GD) and flexible tail (FT) respectively. We found that scPOM-bi confers protection to prion-infected organotypic cerebellar slices even when prion pathology is already conspicuous. Moreover, scPOM-bi prevents the formation of soluble oligomers that correlate with neurotoxic PrP species. Simultaneous targeting of both GD and FT was more effective than concomitant treatment with the individual molecules or targeting the tail alone, possibly by preventing the GD from entering a toxic-prone state. We conclude that simultaneous binding of the GD and flexible tail of PrP results in strong protection from prion neurotoxicity and may represent a promising strategy for anti-prion immunotherapy.
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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.