FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2524938670> ?p ?o ?g. }

• W2524938670 endingPage "70" @default.
• W2524938670 startingPage "53" @default.
• W2524938670 abstract "Oxidative damage and aggregation of cellular proteins is a hallmark of neuronal cell death after neurotrauma and chronic neurodegenerative conditions. Autophagy and ubiquitin protease system are involved in degradation of protein aggregates, and interruption of their function is linked to apoptotic cell death in these diseases. Oxidative modification of cysteine groups in key molecular proteins has been linked to modification of cellular systems and cell death in these conditions. Glutathione and thioredoxin systems provide reducing protons that can effectively reverse protein modifications and promote cell survival. The central role of Thioredoxin in inhibition of apoptosis is well identified. Additionally, its involvement in initiation of autophagy has been suggested recently. We therefore aimed to investigate the involvement of Thioredoxin system in autophagy-apoptosis processes. A model of serum deprivation in SH-SY5Y was used that is associated with autophagy and apoptosis. Using pharmacological and RNA-editing technology we show that Thioredoxin reductase deficiency in this model enhances oxidative stress and interrupts the early protective autophagy and promotes apoptosis. This was associated with decreased protein-degradation in lysosomes due to altered lysosomal acidification and accumulation of autophagosomes as well as impairment in proteasome pathway. We further confirmed that the extent of oxidative stress is a determining factor in autophagy- apoptosis interplay, as upregulation of cellular reducing capacity by N-acetylcysteine prevented impairment in autophagy and proteasome systems thus promoted cell viability. Our study provides evidence that excessive oxidative stress inhibits protein degradation systems and affects the final stages of autophagy by inhibiting autolysosome maturation: a novel mechanistic link between protein aggregation and conversion of autophagy to apoptosis that can be applicable to neurodegenerative diseases." @default.
• W2524938670 created "2016-10-07" @default.
• W2524938670 creator A5000421313 @default.
• W2524938670 creator A5002676860 @default.
• W2524938670 creator A5003487434 @default.
• W2524938670 creator A5028507507 @default.
• W2524938670 creator A5053429168 @default.
• W2524938670 creator A5059244618 @default.
• W2524938670 creator A5070474392 @default.
• W2524938670 date "2016-12-01" @default.
• W2524938670 modified "2023-10-09" @default.
• W2524938670 title "Perturbation of redox balance after thioredoxin reductase deficiency interrupts autophagy-lysosomal degradation pathway and enhances cell death in nutritionally stressed SH-SY5Y cells" @default.
• W2524938670 cites W1481679469 @default.
• W2524938670 cites W1788190869 @default.
• W2524938670 cites W1929735444 @default.
• W2524938670 cites W1963661977 @default.
• W2524938670 cites W1966597938 @default.
• W2524938670 cites W1968962277 @default.
• W2524938670 cites W1970256894 @default.
• W2524938670 cites W1970564748 @default.
• W2524938670 cites W1972542282 @default.
• W2524938670 cites W1975774056 @default.
• W2524938670 cites W1975915247 @default.
• W2524938670 cites W1977930150 @default.
• W2524938670 cites W1978524153 @default.
• W2524938670 cites W1980680117 @default.
• W2524938670 cites W1984799406 @default.
• W2524938670 cites W1986216304 @default.
• W2524938670 cites W1986535251 @default.
• W2524938670 cites W1987280803 @default.
• W2524938670 cites W1992266464 @default.
• W2524938670 cites W1992643412 @default.
• W2524938670 cites W1998319919 @default.
• W2524938670 cites W1998684235 @default.
• W2524938670 cites W2005997790 @default.
• W2524938670 cites W2012034410 @default.
• W2524938670 cites W2016356853 @default.
• W2524938670 cites W2029342214 @default.
• W2524938670 cites W2032096651 @default.
• W2524938670 cites W2044621729 @default.
• W2524938670 cites W2046245413 @default.
• W2524938670 cites W2065126270 @default.
• W2524938670 cites W2068218660 @default.
• W2524938670 cites W2088869582 @default.
• W2524938670 cites W2088940576 @default.
• W2524938670 cites W2092320787 @default.
• W2524938670 cites W2093295909 @default.
• W2524938670 cites W2101534102 @default.
• W2524938670 cites W2109195911 @default.
• W2524938670 cites W2110056576 @default.
• W2524938670 cites W2112329697 @default.
• W2524938670 cites W2114287704 @default.
• W2524938670 cites W2114806766 @default.
• W2524938670 cites W2116240218 @default.
• W2524938670 cites W2123671636 @default.
• W2524938670 cites W2125461230 @default.
• W2524938670 cites W2129040637 @default.
• W2524938670 cites W2130191536 @default.
• W2524938670 cites W2133397461 @default.
• W2524938670 cites W2142596760 @default.
• W2524938670 cites W2151047843 @default.
• W2524938670 cites W2152614869 @default.
• W2524938670 cites W215368981 @default.
• W2524938670 cites W2155086974 @default.
• W2524938670 cites W2156696931 @default.
• W2524938670 cites W2157940538 @default.
• W2524938670 cites W2215852242 @default.
• W2524938670 cites W2264489409 @default.
• W2524938670 cites W2270549539 @default.
• W2524938670 cites W2342851162 @default.
• W2524938670 cites W2418442725 @default.
• W2524938670 cites W4251161705 @default.
• W2524938670 doi "https://doi.org/10.1016/j.freeradbiomed.2016.09.026" @default.
• W2524938670 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27693380" @default.
• W2524938670 hasPublicationYear "2016" @default.
• W2524938670 type Work @default.
• W2524938670 sameAs 2524938670 @default.
• W2524938670 citedByCount "31" @default.
• W2524938670 countsByYear W25249386702017 @default.
• W2524938670 countsByYear W25249386702018 @default.
• W2524938670 countsByYear W25249386702019 @default.
• W2524938670 countsByYear W25249386702020 @default.
• W2524938670 countsByYear W25249386702021 @default.
• W2524938670 countsByYear W25249386702022 @default.
• W2524938670 countsByYear W25249386702023 @default.
• W2524938670 crossrefType "journal-article" @default.
• W2524938670 hasAuthorship W2524938670A5000421313 @default.
• W2524938670 hasAuthorship W2524938670A5002676860 @default.
• W2524938670 hasAuthorship W2524938670A5003487434 @default.
• W2524938670 hasAuthorship W2524938670A5028507507 @default.
• W2524938670 hasAuthorship W2524938670A5053429168 @default.
• W2524938670 hasAuthorship W2524938670A5059244618 @default.
• W2524938670 hasAuthorship W2524938670A5070474392 @default.
• W2524938670 hasConcept C185592680 @default.
• W2524938670 hasConcept C190283241 @default.
• W2524938670 hasConcept C203522944 @default.
• W2524938670 hasConcept C27740335 @default.
• W2524938670 hasConcept C2776151105 @default.

• next