ArticlePloS one2009
Loss of anti-Bax function in Gerstmann-Sträussler-Scheinker syndrome-associated prion protein mutants.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Significant modulations of linc001128 and linc0938 with miR-24-3p and miR-30c-5p in Parkinson disease.Scientific reports · 2022Article
- Tau Protein Phosphorylated at Threonine-231 is Expressed Abundantly in the Cerebellum in Prion Encephalopathies.Journal of Alzheimer's disease : JAD · 2021Article
- Human GBP1 binds LPS to initiate assembly of a caspase-4 activating platform on cytosolic bacteria.Nature communications · 2020Article
- Luman contributes to brefeldin A-induced prion protein gene expression by interacting with the ERSE26 element.Scientific reports · 2017Article
- Familial prion protein mutants inhibit Hrd1-mediated retrotranslocation of misfolded proteins by depleting misfolded protein sensor BiP.Human molecular genetics · 2016Article
- Presenilin 2 overexpression is associated with apoptosis in Neuro2a cells.Translational neuroscience · 2016Article
- Yeast as a tool for studying proteins of the Bcl-2 family.Microbial cell (Graz, Austria) · 2015Review
- Disease-associated mutations in the prion protein impair laminin-induced process outgrowth and survival.The Journal of biological chemistry · 2012Article
- A Drosophila model of GSS syndrome suggests defects in active zones are responsible for pathogenesis of GSS syndrome.Human molecular genetics · 2010Article
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Authors and funding
7 authors.
Funding
Abstract
Previously, we have shown the loss of anti-Bax function in Creutzfeldt Jakob disease (CJD)-associated prion protein (PrP) mutants that are unable to generate cytosolic PrP (CyPrP). To determine if the anti-Bax function of PrP modulates the manifestation of prion diseases, we further investigated the anti-Bax function of eight familial Gerstmann-Sträussler-Scheinker Syndrome (GSS)-associated PrP mutants. These PrP mutants contained their respective methionine ((M)) or valine ((V)) at codon 129. All of the mutants lost their ability to prevent Bax-mediated chromatin condensation or DNA fragmentation in primary human neurons. In the breast carcinoma MCF-7 cells, the F198S(V), D202N(V), P102L(V) and Q217R(V) retained, whereas the P102L(M), P105L(V), Y145stop(M) and Q212P(M) PrP mutants lost their ability to inhibit Bax-mediated condensed chromatin. The inhibition of Bax-mediated condensed chromatin depended on the ability of the mutants to generate cytosolic PrP. However, except for the P102L(V), none of the mutants significantly inhibited Bax-mediated caspase activation. These results show that the cytosolic PrP generated from the GSS mutants is not as efficient as wild type PrP in inhibiting Bax-mediated cell death. Furthermore, these results indicate that the anti-Bax function is also disrupted in GSS-associated PrP mutants and is not associated with the difference between CJD and GSS.
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