FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2174233513> ?p ?o ?g. }

• W2174233513 endingPage "e0143218" @default.
• W2174233513 startingPage "e0143218" @default.
• W2174233513 abstract "The central molecular event underlying prion diseases involves conformational change of the cellular form of the prion protein (PrPC), which is a sialoglycoprotein, into the disease-associated, transmissible form denoted PrPSc. Recent studies revealed a correlation between the sialylation status of PrPSc and incubation time to disease and introduced a new hypothesis that progression of prion diseases could be controlled or reversed by altering the sialylation level of PrPC. Of the four known mammalian sialidases, the enzymes that cleave off sialic acid residues, only NEU1, NEU3 and NEU4 are expressed in the brain. To test whether cellular sialidases control the steady-state sialylation level of PrPC and to identify the putative sialidase responsible for desialylating PrPC, we analyzed brain-derived PrPC from knockout mice deficient in Neu1, Neu3, Neu4, or from Neu3/Neu4 double knockouts. Surprisingly, no differences in the sialylation of PrPC or its proteolytic product C1 were noticed in any of the knockout mice tested as compared to the age-matched controls. However, significantly higher amounts of the C1 fragment relative to full-length PrPC were detected in the brains of Neu1 knockout mice as compared to WT mice or to the other knockout mice. Additional experiments revealed that in neuroblastoma cell line the sialylation pattern of C1 could be changed by an inhibitor of sialylatransferases. In summary, this study suggests that targeting cellular sialidases is apparently not the correct strategy for altering the sialylation levels of PrPC, whereas modulating the activity of sialylatransferases might offer a more promising approach. Our findings also suggest that catabolism of PrPC involves its α-cleavage followed by desialylation of the resulting C1 fragments by NEU1 and consequent fast degradation of the desialylated products." @default.
• W2174233513 created "2016-06-24" @default.
• W2174233513 creator A5024244401 @default.
• W2174233513 creator A5032924150 @default.
• W2174233513 creator A5033935218 @default.
• W2174233513 creator A5042499250 @default.
• W2174233513 creator A5047910628 @default.
• W2174233513 creator A5049008682 @default.
• W2174233513 creator A5055400963 @default.
• W2174233513 creator A5073944883 @default.
• W2174233513 creator A5074222588 @default.
• W2174233513 creator A5083296707 @default.
• W2174233513 creator A5089679919 @default.
• W2174233513 date "2015-11-16" @default.
• W2174233513 modified "2023-10-11" @default.
• W2174233513 title "Loss of Cellular Sialidases Does Not Affect the Sialylation Status of the Prion Protein but Increases the Amounts of Its Proteolytic Fragment C1" @default.
• W2174233513 cites W107050974 @default.
• W2174233513 cites W1562167215 @default.
• W2174233513 cites W1971078992 @default.
• W2174233513 cites W1972407931 @default.
• W2174233513 cites W1979971930 @default.
• W2174233513 cites W1981200521 @default.
• W2174233513 cites W1982056508 @default.
• W2174233513 cites W1990952979 @default.
• W2174233513 cites W1991934962 @default.
• W2174233513 cites W1997725693 @default.
• W2174233513 cites W2000507134 @default.
• W2174233513 cites W2005583362 @default.
• W2174233513 cites W2005926287 @default.
• W2174233513 cites W2006443434 @default.
• W2174233513 cites W2012222860 @default.
• W2174233513 cites W2024954984 @default.
• W2174233513 cites W2027937601 @default.
• W2174233513 cites W2031682941 @default.
• W2174233513 cites W2041274762 @default.
• W2174233513 cites W2048512065 @default.
• W2174233513 cites W2052544294 @default.
• W2174233513 cites W2053636966 @default.
• W2174233513 cites W2065698593 @default.
• W2174233513 cites W2067188727 @default.
• W2174233513 cites W2067975188 @default.
• W2174233513 cites W2069066758 @default.
• W2174233513 cites W2079898180 @default.
• W2174233513 cites W2087197243 @default.
• W2174233513 cites W2092014857 @default.
• W2174233513 cites W2095764561 @default.
• W2174233513 cites W2107811485 @default.
• W2174233513 cites W2110588674 @default.
• W2174233513 cites W2111278119 @default.
• W2174233513 cites W2112921913 @default.
• W2174233513 cites W2113892605 @default.
• W2174233513 cites W2115923529 @default.
• W2174233513 cites W2123332780 @default.
• W2174233513 cites W2126586049 @default.
• W2174233513 cites W2127674627 @default.
• W2174233513 cites W2127981299 @default.
• W2174233513 cites W2138063446 @default.
• W2174233513 cites W2147838967 @default.
• W2174233513 cites W2148130200 @default.
• W2174233513 cites W2148235564 @default.
• W2174233513 cites W2148965649 @default.
• W2174233513 cites W2150824641 @default.
• W2174233513 cites W2167503783 @default.
• W2174233513 cites W2304202484 @default.
• W2174233513 cites W2324660492 @default.
• W2174233513 cites W4244789804 @default.
• W2174233513 doi "https://doi.org/10.1371/journal.pone.0143218" @default.
• W2174233513 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4646690" @default.
• W2174233513 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26569607" @default.
• W2174233513 hasPublicationYear "2015" @default.
• W2174233513 type Work @default.
• W2174233513 sameAs 2174233513 @default.
• W2174233513 citedByCount "15" @default.
• W2174233513 countsByYear W21742335132016 @default.
• W2174233513 countsByYear W21742335132017 @default.
• W2174233513 countsByYear W21742335132018 @default.
• W2174233513 countsByYear W21742335132019 @default.
• W2174233513 countsByYear W21742335132022 @default.
• W2174233513 crossrefType "journal-article" @default.
• W2174233513 hasAuthorship W2174233513A5024244401 @default.
• W2174233513 hasAuthorship W2174233513A5032924150 @default.
• W2174233513 hasAuthorship W2174233513A5033935218 @default.
• W2174233513 hasAuthorship W2174233513A5042499250 @default.
• W2174233513 hasAuthorship W2174233513A5047910628 @default.
• W2174233513 hasAuthorship W2174233513A5049008682 @default.
• W2174233513 hasAuthorship W2174233513A5055400963 @default.
• W2174233513 hasAuthorship W2174233513A5073944883 @default.
• W2174233513 hasAuthorship W2174233513A5074222588 @default.
• W2174233513 hasAuthorship W2174233513A5083296707 @default.
• W2174233513 hasAuthorship W2174233513A5089679919 @default.
• W2174233513 hasBestOaLocation W21742335131 @default.
• W2174233513 hasConcept C104317684 @default.
• W2174233513 hasConcept C108625454 @default.
• W2174233513 hasConcept C134164806 @default.
• W2174233513 hasConcept C153911025 @default.
• W2174233513 hasConcept C170493617 @default.
• W2174233513 hasConcept C181199279 @default.
• W2174233513 hasConcept C182704531 @default.

• next