Influence of Mabs on PrPSc Formation Using In Vitro and Cell-Free Systems
Identifieur interne : 000B67 ( Main/Exploration ); précédent : 000B66; suivant : 000B68Influence of Mabs on PrPSc Formation Using In Vitro and Cell-Free Systems
Auteurs : Binggong Chang [États-Unis] ; Robert Petersen [États-Unis] ; Thomas Wisniewski [États-Unis] ; Richard Rubenstein [États-Unis]Source :
- PLoS ONE [ 1932-6203 ] ; 2012.
Abstract
PrPSc is believed to serve as a template for the conversion of PrPC to the abnormal isoform. This process requires contact between the two proteins and implies that there may be critical contact sites that are important for conversion. We hypothesized that antibodies binding to either PrPcor PrPSc would hinder or prevent the formation of the PrPC–PrPSc complex and thus slow down or prevent the conversion process. Two systems were used to analyze the effect of different antibodies on PrPSc formation: (i) neuroblastoma cells persistently infected with the 22L mouse-adapted scrapie stain, and (ii) protein misfolding cyclic amplification (PMCA), which uses PrPSc as a template or seed, and a series of incubations and sonications, to convert PrPC to PrPSc. The two systems yielded similar results, in most cases, and demonstrate that PrP-specific monoclonal antibodies (Mabs) vary in their ability to inhibit the PrPC–PrPSc conversion process. Based on the numerous and varied Mabs analyzed, the inhibitory effect does not appear to be epitope specific, related to PrPC conformation, or to cell membrane localization, but is influenced by the targeted PrP region (amino vs carboxy).
Url:
DOI: 10.1371/journal.pone.0041626
PubMed: 22848548
PubMed Central: 3407222
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Influence of Mabs on PrP<sup>Sc</sup> Formation Using <italic>In Vitro</italic> and Cell-Free Systems</title><author><name sortKey="Chang, Binggong" sort="Chang, Binggong" uniqKey="Chang B" first="Binggong" last="Chang">Binggong Chang</name><affiliation wicri:level="2"><nlm:aff id="aff1"><addr-line>Departments of Neurology and Physiology/Pharmacology, State University New York Downstate Medical Center, Brooklyn, New York, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Departments of Neurology and Physiology/Pharmacology, State University New York Downstate Medical Center, Brooklyn, New York</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Petersen, Robert" sort="Petersen, Robert" uniqKey="Petersen R" first="Robert" last="Petersen">Robert Petersen</name><affiliation wicri:level="2"><nlm:aff id="aff2"><addr-line>Departments of Pathology, Neuroscience, and Neurology, Case Western Reserve University, Cleveland, Ohio, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Departments of Pathology, Neuroscience, and Neurology, Case Western Reserve University, Cleveland, Ohio</wicri:regionArea><placeName><region type="state">Ohio</region></placeName></affiliation></author><author><name sortKey="Wisniewski, Thomas" sort="Wisniewski, Thomas" uniqKey="Wisniewski T" first="Thomas" last="Wisniewski">Thomas Wisniewski</name><affiliation wicri:level="2"><nlm:aff id="aff3"><addr-line>Departments of Neurology, Psychiatry and Pathology, New York University School of Medicine, New York, New York, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Departments of Neurology, Psychiatry and Pathology, New York University School of Medicine, New York, New 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type="main">Influence of Mabs on PrP<sup>Sc</sup> Formation Using <italic>In Vitro</italic> and Cell-Free Systems</title><author><name sortKey="Chang, Binggong" sort="Chang, Binggong" uniqKey="Chang B" first="Binggong" last="Chang">Binggong Chang</name><affiliation wicri:level="2"><nlm:aff id="aff1"><addr-line>Departments of Neurology and Physiology/Pharmacology, State University New York Downstate Medical Center, Brooklyn, New York, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Departments of Neurology and Physiology/Pharmacology, State University New York Downstate Medical Center, Brooklyn, New York</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Petersen, Robert" sort="Petersen, Robert" uniqKey="Petersen R" first="Robert" last="Petersen">Robert Petersen</name><affiliation wicri:level="2"><nlm:aff id="aff2"><addr-line>Departments of Pathology, Neuroscience, and Neurology, Case Western Reserve University, Cleveland, Ohio, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Departments of Pathology, Neuroscience, and Neurology, Case Western Reserve University, Cleveland, Ohio</wicri:regionArea><placeName><region type="state">Ohio</region></placeName></affiliation></author><author><name sortKey="Wisniewski, Thomas" sort="Wisniewski, Thomas" uniqKey="Wisniewski T" first="Thomas" last="Wisniewski">Thomas Wisniewski</name><affiliation wicri:level="2"><nlm:aff id="aff3"><addr-line>Departments of Neurology, Psychiatry and Pathology, New York University School of Medicine, New York, New York, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Departments of Neurology, Psychiatry and Pathology, New York University School of Medicine, New York, New York</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Rubenstein, Richard" sort="Rubenstein, Richard" uniqKey="Rubenstein R" first="Richard" last="Rubenstein">Richard Rubenstein</name><affiliation wicri:level="2"><nlm:aff id="aff1"><addr-line>Departments of Neurology and Physiology/Pharmacology, State University New York Downstate Medical Center, Brooklyn, New York, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Departments of Neurology and Physiology/Pharmacology, State University New York Downstate Medical Center, Brooklyn, New York</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author></analytic><series><title level="j">PLoS ONE</title><idno type="eISSN">1932-6203</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>PrP<sup>Sc</sup> is believed to serve as a template for the conversion of PrP<sup>C</sup> to the abnormal isoform. This process requires contact between the two proteins and implies that there may be critical contact sites that are important for conversion. We hypothesized that antibodies binding to either PrP<sup>c</sup>or PrP<sup>Sc</sup> would hinder or prevent the formation of the PrP<sup>C</sup>–PrP<sup>Sc</sup> complex and thus slow down or prevent the conversion process. Two systems were used to analyze the effect of different antibodies on PrP<sup>Sc</sup> formation: (i) neuroblastoma cells persistently infected with the 22L mouse-adapted scrapie stain, and (ii) protein misfolding cyclic amplification (PMCA), which uses PrP<sup>Sc</sup> as a template or seed, and a series of incubations and sonications, to convert PrP<sup>C</sup> to PrP<sup>Sc</sup>. The two systems yielded similar results, in most cases, and demonstrate that PrP-specific monoclonal antibodies (Mabs) vary in their ability to inhibit the PrP<sup>C</sup>–PrP<sup>Sc</sup> conversion process. Based on the numerous and varied Mabs analyzed, the inhibitory effect does not appear to be epitope specific, related to PrP<sup>C</sup> conformation, or to cell membrane localization, but is influenced by the targeted PrP region (amino vs carboxy).</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Caughey, Bw" uniqKey="Caughey B">BW Caughey</name></author><author><name sortKey="Dong, A" uniqKey="Dong A">A Dong</name></author><author><name sortKey="Bhat, Ks" uniqKey="Bhat K">KS Bhat</name></author><author><name sortKey="Ernst, D" uniqKey="Ernst D">D Ernst</name></author><author><name sortKey="Hayes, Sf" uniqKey="Hayes S">SF Hayes</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gasset, M" uniqKey="Gasset M">M Gasset</name></author><author><name sortKey="Baldwin, Ma" uniqKey="Baldwin M">MA Baldwin</name></author><author><name sortKey="Fletterick, Rj" uniqKey="Fletterick R">RJ 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Balachandran</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Ohio</li><li>État de New York</li></region></list><tree><country name="États-Unis"><region name="État de New York"><name sortKey="Chang, Binggong" sort="Chang, Binggong" uniqKey="Chang B" first="Binggong" last="Chang">Binggong Chang</name></region><name sortKey="Petersen, Robert" sort="Petersen, Robert" uniqKey="Petersen R" first="Robert" last="Petersen">Robert Petersen</name><name sortKey="Rubenstein, Richard" sort="Rubenstein, Richard" uniqKey="Rubenstein R" first="Richard" last="Rubenstein">Richard Rubenstein</name><name sortKey="Wisniewski, Thomas" sort="Wisniewski, Thomas" uniqKey="Wisniewski T" first="Thomas" last="Wisniewski">Thomas Wisniewski</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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