ArticlePLoS pathogens2010
Oxidation of Helix-3 methionines precedes the formation of PK resistant PrP.
Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 27 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 54 citations in OpenAlex.
- Retraction: Oxidation of Helix-3 Methionines Precedes the Formation of PK Resistant PrPSc.PLoS pathogens · 2024Article
- Retraction: Fatal Prion Disease in a Mouse Model of Genetic E200K Creutzfeldt-Jakob Disease.PLoS pathogens · 2024Article
- Stress and viral insults do not trigger E200K PrP conversion in human cerebral organoids.PloS one · 2022Article
- Methionine oxidation within the prion protein.Prion · 2020Review
- Oxidative and Inflammatory Events in Prion Diseases: Can They Be Therapeutic Targets?Current aging science · 2019Review
- Effects of a naturally occurring amino acid substitution in bovine PrP: a model for inherited prion disease in a natural host species.BMC research notes · 2017Article
- Recombinant PrP and Its Contribution to Research on Transmissible Spongiform Encephalopathies.Pathogens (Basel, Switzerland) · 2017Review
- Correction: Oxidation of Helix-3 Methionines Precedes the Formation of PK Resistant PrPSc.PLoS pathogens · 2017Article
- Disrupting the cortical actin cytoskeleton points to two distinct mechanisms of yeast [PSI+] prion formation.PLoS genetics · 2017Article
- Methionine sulfoxide reductase A affects β-amyloid solubility and mitochondrial function in a mouse model of Alzheimer's disease.American journal of physiology. Endocrinology and metabolism · 2016Article
- Antioxidant peroxiredoxin 6 protein rescues toxicity due to oxidative stress and cellular hypoxia in vitro, and attenuates prion-related pathology in vivo.Neurochemistry international · 2015Article
- PrP charge structure encodes interdomain interactions.Scientific reports · 2015Article
- Aggregation of MBP in chronic demyelination.Annals of clinical and translational neurology · 2015Article
- Oxidative stress conditions increase the frequency of de novo formation of the yeast [PSI+] prion.Molecular microbiology · 2015Article
- Treatment of a multiple sclerosis animal model by a novel nanodrop formulation of a natural antioxidant.International journal of nanomedicine · 2015Article
- Polar substitutions in helix 3 of the prion protein produce transmembrane isoforms that disturb vesicle trafficking.Human molecular genetics · 2013Article
- Age at Death of Creutzfeldt-Jakob disease in subsequent family generation carrying the E200K mutation of the prion protein gene.PloS one · 2013Article
- PrP(ST), a soluble, protease resistant and truncated PrP form features in the pathogenesis of a genetic prion disease.PloS one · 2013Article
- Article
- Failure of prion protein oxidative folding guides the formation of toxic transmembrane forms.The Journal of biological chemistry · 2012Article
Corrections and comments
- Retraction · 2024-12-11Concerns/Issues about Data · Concerns/Issues about Image · Duplication of/in Image · Euphemisms for Duplication · Investigation by Journal/Publisher · Objections by Author(s) · Unreliable Results and/or Conclusions · Upgrade/Update of Prior Notice(s) · · See also: https://pubpeer.com/publications/BFAD087171A428CC203A6893ED5855
- Correction · 2017-05-03Error in Image · Updated to Retraction · · See also: https://pubpeer.com/publications/BFAD087171A428CC203A6893ED5855
- Erratum issued
- Retracted
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While elucidating the peculiar epitope of the alpha-PrP mAb IPC2, we found that PrPSc exhibits the sulfoxidation of residue M213 as a covalent signature. Subsequent computational analysis predicted that the presence of sulfoxide groups at both Met residues 206 and 213 destabilize the alpha-fold, suggesting oxidation may facilitate the conversion of PrPC into PrPSc. To further study the effect of oxidation on prion formation, we generated pAbs to linear PrP peptides encompassing the Helix-3 region, as opposed to the non-linear complexed epitope of IPC2. We now show that pAbs, whose epitopes comprise Met residues, readily detected PrPC, but could not recognize most PrPSc bands unless they were vigorously reduced. Next, we showed that the alpha-Met pAbs did not recognize newly formed PrPSc, as is the case for the PK resistant PrP present in lines of prion infected cells. In addition, these reagents did not detect intermediate forms such as PK sensitive and partially aggregated PrPs present in infected brains. Finally, we show that PrP molecules harboring the pathogenic mutation E200K, which is linked to the most common form of familial CJD, may be spontaneously oxidized. We conclude that the oxidation of methionine residues in Helix-3 represents an early and important event in the conversion of PrPC to PrPSc. We believe that further investigation into the mechanism and role of PrP oxidation will be central in finally elucidating the mechanism by which a normal cell protein converts into a pathogenic entity that causes fatal brain degeneration.
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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.