ArticlePloS one2012
Amyloid beta precursor protein and prion protein have a conserved interaction affecting cell adhesion and CNS development.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 61 citations in OpenAlex.
- Transient cholesterol interactions with the amyloid precursor protein involved in Alzheimer's disease pathogenesis.Biophysical reviews · 2025Review
- Comparing Prion Proteins Across Species: Is Zebrafish a Useful Model?Molecular neurobiology · 2025Review
- Functional investigation suggests CNTNAP5 involvement in glaucomatous neurodegeneration obtained from a GWAS in primary angle closure glaucoma.PLoS genetics · 2024Article
- Post-GWAS functional analyses ofbioRxiv : the preprint server for biology · 2024Article
- Inducing prion protein shedding as a neuroprotective and regenerative approach in pathological conditions of the brain: from theory to facts.Neural regeneration research · 2023Review
- Efficient manipulation of gene expression using Natronobacterium gregoryi Argonaute in zebrafish.BMC biology · 2023Article
- Anchorless risk or released benefit? An updated view on the ADAM10-mediated shedding of the prion protein.Cell and tissue research · 2023Review
- Loxhd1b inhibits the hair cell development in zebrafish: Possible relation to the BDNF/TrkB/ERK pathway.Frontiers in cellular neuroscience · 2022Article
- Amyloid precursor protein (APP) and amyloid β (Aβ) interact with cell adhesion molecules: Implications in Alzheimer's disease and normal physiology.Frontiers in cell and developmental biology · 2022Review
- A Model of Discovery: The Role of Imaging Established and Emerging Non-mammalian Models in Neuroscience.Frontiers in molecular neuroscience · 2022Review
- Article
- Structural Studies Providing Insights into Production and Conformational Behavior of Amyloid-β Peptide Associated with Alzheimer's Disease Development.Molecules (Basel, Switzerland) · 2021Review
- Cellular Prion Protein (PrPc): Putative Interacting Partners and Consequences of the Interaction.International journal of molecular sciences · 2020Review
- Non-Synonymous variants in premelanosome protein (PMEL) cause ocular pigment dispersion and pigmentary glaucoma.Human molecular genetics · 2019Article
- Prion gene paralogs are dispensable for early zebrafish development and have nonadditive roles in seizure susceptibility.The Journal of biological chemistry · 2018Article
- An ancient conserved role for prion protein in learning and memory.Biology open · 2018Article
- Reduced Abundance and Subverted Functions of Proteins in Prion-Like Diseases: Gained Functions Fascinate but Lost Functions Affect Aetiology.International journal of molecular sciences · 2017Review
- Expression of Reactive Oxygen Species-Related Transcripts in Egyptian Children With Autism.Biomarker insights · 2017Article
- The Cellular Prion Protein: A Player in Immunological Quiescence.Frontiers in immunology · 2015Review
- Growth differentiation factor 6 as a putative risk factor in neuromuscular degeneration.PloS one · 2014Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genetic and biochemical mechanisms linking onset or progression of Alzheimer Disease and prion diseases have been lacking and/or controversial, and their etiologies are often considered independent. Here we document a novel, conserved and specific genetic interaction between the proteins that underlie these diseases, amyloid-β precursor protein and prion protein, APP and PRP, respectively. Knockdown of APP and/or PRNP homologs in the zebrafish (appa, appb, prp1, and prp2) produces a dose-dependent phenotype characterized by systemic morphological defects, reduced cell adhesion and CNS cell death. This genetic interaction is surprisingly exclusive in that prp1 genetically interacts with zebrafish appa, but not with appb, and the zebrafish paralog prp2 fails to interact with appa. Intriguingly, appa & appb are largely redundant in early zebrafish development yet their abilities to rescue CNS cell death are differentially contingent on prp1 abundance. Delivery of human APP or mouse Prnp mRNAs rescue the phenotypes observed in app-prp-depleted zebrafish, highlighting the conserved nature of this interaction. Immunoprecipitation revealed that human APP and PrP(C) proteins can have a physical interaction. Our study reports a unique in vivo interdependence between APP and PRP loss-of-function, detailing a biochemical interaction that considerably expands the hypothesized roles of PRP in Alzheimer Disease.
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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.