Matches in SemOpenAlex for { <https://semopenalex.org/work/W3197653539> ?p ?o ?g. }
- W3197653539 endingPage "9646" @default.
- W3197653539 startingPage "9634" @default.
- W3197653539 abstract "Abstract Multiple system atrophy (MSA) is a fatal neurodegenerative disease where the histopathological hallmark is glial cytoplasmic inclusions in oligodendrocytes, rich of aggregated alpha‐synuclein (aSyn). Therefore, therapies targeting aSyn aggregation and toxicity have been studied as a possible disease‐modifying therapy for MSA. Our earlier studies show that inhibition of prolyl oligopeptidase (PREP) with KYP‐2047 reduces aSyn aggregates in several models. Here, we tested the effects of KYP‐2047 on a MSA cellular models, using rat OLN‐AS7 and human MO3.13 oligodendrocyte cells. As translocation of p25α to cell cytosol has been identified as an inducer of aSyn aggregation in MSA models, the cells were transiently transfected with p25α. Similar to earlier studies, p25α increased aSyn phosphorylation and aggregation, and caused tubulin retraction and impaired autophagy in OLN‐AS7 cells. In both cellular models, p25α transfection increased significantly aSyn mRNA levels and also increased the levels of inactive protein phosphatase 2A (PP2A). However, aSyn or p25α did not cause any cellular death in MO3.13 cells, questioning their use as a MSA model. Simultaneous administration of 10 µM KYP‐2047 improved cell viability, decreased insoluble phosphorylated aSyn and normalized autophagy in OLN‐AS7 cells but similar impact was not seen in MO3.13 cells." @default.
- W3197653539 created "2021-09-13" @default.
- W3197653539 creator A5006090131 @default.
- W3197653539 creator A5007898537 @default.
- W3197653539 creator A5017859792 @default.
- W3197653539 creator A5024880489 @default.
- W3197653539 creator A5031186843 @default.
- W3197653539 creator A5039875660 @default.
- W3197653539 creator A5045329840 @default.
- W3197653539 creator A5046574983 @default.
- W3197653539 creator A5054298399 @default.
- W3197653539 creator A5078817501 @default.
- W3197653539 date "2021-09-05" @default.
- W3197653539 modified "2023-10-17" @default.
- W3197653539 title "Prolyl oligopeptidase inhibition reduces alpha‐synuclein aggregation in a cellular model of multiple system atrophy" @default.
- W3197653539 cites W1487661483 @default.
- W3197653539 cites W1496790952 @default.
- W3197653539 cites W1571449885 @default.
- W3197653539 cites W1581206995 @default.
- W3197653539 cites W1717443879 @default.
- W3197653539 cites W1965647575 @default.
- W3197653539 cites W1968014007 @default.
- W3197653539 cites W1997664222 @default.
- W3197653539 cites W1999123976 @default.
- W3197653539 cites W2006288488 @default.
- W3197653539 cites W2016816471 @default.
- W3197653539 cites W2016974059 @default.
- W3197653539 cites W2030025610 @default.
- W3197653539 cites W2031754652 @default.
- W3197653539 cites W2035143687 @default.
- W3197653539 cites W2055185917 @default.
- W3197653539 cites W2057358353 @default.
- W3197653539 cites W2066522549 @default.
- W3197653539 cites W2068288454 @default.
- W3197653539 cites W2073848512 @default.
- W3197653539 cites W2077503584 @default.
- W3197653539 cites W2079766520 @default.
- W3197653539 cites W2081030321 @default.
- W3197653539 cites W2085013728 @default.
- W3197653539 cites W2090048744 @default.
- W3197653539 cites W2091297212 @default.
- W3197653539 cites W2120127860 @default.
- W3197653539 cites W2123133951 @default.
- W3197653539 cites W2153235303 @default.
- W3197653539 cites W2155299862 @default.
- W3197653539 cites W2310305711 @default.
- W3197653539 cites W2387946415 @default.
- W3197653539 cites W2515738886 @default.
- W3197653539 cites W2546550351 @default.
- W3197653539 cites W2560138349 @default.
- W3197653539 cites W2565925499 @default.
- W3197653539 cites W2587082207 @default.
- W3197653539 cites W2592067246 @default.
- W3197653539 cites W2752326209 @default.
- W3197653539 cites W2767014526 @default.
- W3197653539 cites W2803123594 @default.
- W3197653539 cites W2848476480 @default.
- W3197653539 cites W2871293796 @default.
- W3197653539 cites W2889904213 @default.
- W3197653539 cites W2894682893 @default.
- W3197653539 cites W2897524551 @default.
- W3197653539 cites W2901801746 @default.
- W3197653539 cites W2942383121 @default.
- W3197653539 cites W2965362584 @default.
- W3197653539 cites W2986191692 @default.
- W3197653539 cites W2991513562 @default.
- W3197653539 cites W3026560699 @default.
- W3197653539 cites W3086002901 @default.
- W3197653539 cites W3089094591 @default.
- W3197653539 cites W3197653539 @default.
- W3197653539 cites W813117701 @default.
- W3197653539 doi "https://doi.org/10.1111/jcmm.16910" @default.
- W3197653539 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8505845" @default.
- W3197653539 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34486218" @default.
- W3197653539 hasPublicationYear "2021" @default.
- W3197653539 type Work @default.
- W3197653539 sameAs 3197653539 @default.
- W3197653539 citedByCount "8" @default.
- W3197653539 countsByYear W31976535392021 @default.
- W3197653539 countsByYear W31976535392023 @default.
- W3197653539 crossrefType "journal-article" @default.
- W3197653539 hasAuthorship W3197653539A5006090131 @default.
- W3197653539 hasAuthorship W3197653539A5007898537 @default.
- W3197653539 hasAuthorship W3197653539A5017859792 @default.
- W3197653539 hasAuthorship W3197653539A5024880489 @default.
- W3197653539 hasAuthorship W3197653539A5031186843 @default.
- W3197653539 hasAuthorship W3197653539A5039875660 @default.
- W3197653539 hasAuthorship W3197653539A5045329840 @default.
- W3197653539 hasAuthorship W3197653539A5046574983 @default.
- W3197653539 hasAuthorship W3197653539A5054298399 @default.
- W3197653539 hasAuthorship W3197653539A5078817501 @default.
- W3197653539 hasBestOaLocation W31976535391 @default.
- W3197653539 hasConcept C104317684 @default.
- W3197653539 hasConcept C11960822 @default.
- W3197653539 hasConcept C126322002 @default.
- W3197653539 hasConcept C136238340 @default.
- W3197653539 hasConcept C174510640 @default.
- W3197653539 hasConcept C178666793 @default.