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Iron oxide nanoparticle-induced autophagic flux is regulated by interplay between p53-mTOR axis and Bcl-2 signaling in hepatic cells
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SYSNO ASEP 0534433 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Iron oxide nanoparticle-induced autophagic flux is regulated by interplay between p53-mTOR axis and Bcl-2 signaling in hepatic cells Author(s) Uzhytchak, Mariia (FZU-D) ORCID
Smolková, Barbora (FZU-D) ORCID
Lunova, Mariia (FZU-D) ORCID
Jirsa, M. (CZ)
Frtús, Adam (FZU-D) ORCID
Kubinová, Šárka (FZU-D) RID, ORCID
Dejneka, Alexandr (FZU-D) RID, ORCID
Lunov, Oleg (FZU-D) ORCIDNumber of authors 8 Article number 1015 Source Title Cells. - : MDPI
Roč. 9, č. 4 (2020), s. 1-24Number of pages 24 s. Language eng - English Country CH - Switzerland Keywords nano-bio interactions ; iron oxide nanoparticles ; autophagy ; lysosomes ; magnetic resonance imaging ; p53 Subject RIV BO - Biophysics OECD category Biophysics R&D Projects LTC19040 GA MŠMT - Ministry of Education, Youth and Sports (MEYS) Method of publishing Open access Institutional support FZU-D - RVO:68378271 UT WOS 000535559500226 EID SCOPUS 85084030549 DOI 10.3390/cells9041015 Annotation Iron oxide-based nanoparticles have been repeatedly shown to affect lysosomal-mediated signaling. Recently, nanoparticles have demonstrated an ability to modulate autophagic flux via lysosome-dependent signaling. However, the precise underlying mechanisms of such modulation as well as the impact of cellular genetic background remain enigmatic. In this study, we investigated how lysosomal-mediated signaling is a ected by iron oxide nanoparticle uptake in three distinct hepatic cell lines. We found that nanoparticle-induced lysosomal dysfunction alters sub-cellular localization of pmTOR and p53 proteins. Our data indicate that alterations in the sub-cellular localization of p53 protein induced by nanoparticle greatly affect the autophagic flux.
Workplace Institute of Physics Contact Kristina Potocká, potocka@fzu.cz, Tel.: 220 318 579 Year of Publishing 2021 Electronic address http://hdl.handle.net/11104/0312628
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