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mTOR-independent autophagy counteracts apoptosis in herpes simplex virus type 1-infected U251 glioma cells
dc.creator | Tovilović-Kovačević, Gordana | |
dc.creator | Ristić, Biljana | |
dc.creator | Šiljić, Marina | |
dc.creator | Nikolić, Valentina | |
dc.creator | Kravić-Stevović, Tamara | |
dc.creator | Dulović, Marija | |
dc.creator | Milenković, Marina | |
dc.creator | Knežević, Aleksandra | |
dc.creator | Bošnjak, Mihajlo | |
dc.creator | Bumbaširević, Vladimir | |
dc.creator | Stanojević, Maja | |
dc.creator | Trajković, Vladimir | |
dc.date.accessioned | 2023-11-24T10:02:35Z | |
dc.date.available | 2900-01-01 | |
dc.date.issued | 2013 | |
dc.identifier.issn | 1286-4579 | |
dc.identifier.uri | http://radar.ibiss.bg.ac.rs/handle/123456789/6345 | |
dc.description.abstract | We investigated the role of autophagy, a stress-inducible lysosomal self-digestion of cellular components, in modulation of herpes simplex virus type 1 (HSV-1)-triggered death of U251 human glioma cells. HSV-1 caused apoptotic death in U251 cells, characterized by phosphatidylserine externalization, caspase activation and DNA fragmentation. HSV-1-induced apoptosis was associated with the induction of autophagic response, as confirmed by the conversion of cytosolic LC3-I to autophagosome-associated LC3-II, increase in intracellular acidification, presence of autophagic vesicles, and increase in proteolysis of the selective autophagic target p62. HSV-1-triggered autophagy was not associated with the significant increase in the expression of proautophagic protein beclin-1 or downregulation of the major autophagy suppressor mammalian target of rapamycin (mTOR). Moreover, the phosphorylation of mTOR and its direct substrate p70 S6 kinase was augmented by HSV-1 infection, while the mTOR stimulator Akt and inhibitor AMPK-activated protein kinase (AMPK) were accordingly activated and suppressed, respectively. An shRNA-mediated knockdown of the autophagy-essential LC3b, as well as pharmacological inhibition of autophagy with bafilomycin A1 or 3-methyladenine, markedly accelerated apoptotic changes and ensuing cell death in HSV-1-infected glioma cells. These data indicate that AMPK/Akt/mTOR-independent autophagy could prolong survival of HSV-1-infected U251 glioma cells by counteracting the coinciding apoptotic response. | sr |
dc.language.iso | en | sr |
dc.publisher | Elsevier Masson SAS | sr |
dc.relation | info:eu-repo/grantAgreement/MESTD/Integrated and Interdisciplinary Research (IIR or III)/41025/RS// | sr |
dc.relation | info:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/175024/RS// | sr |
dc.relation | info:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/173053/RS// | sr |
dc.rights | restrictedAccess | sr |
dc.source | Microbes and Infection | sr |
dc.subject | HSV-1 | sr |
dc.subject | Autophagy | sr |
dc.subject | Apoptosis | sr |
dc.subject | mTOR | sr |
dc.subject | AMP-activated protein kinase | sr |
dc.subject | Akt | sr |
dc.title | mTOR-independent autophagy counteracts apoptosis in herpes simplex virus type 1-infected U251 glioma cells | sr |
dc.type | article | sr |
dc.rights.license | ARR | sr |
dc.rights.holder | © 2013 by Institut Pasteur | sr |
dc.citation.issue | 8-9 | |
dc.citation.volume | 15 | |
dc.identifier.doi | 10.1016/j.micinf.2013.04.012 | |
dc.identifier.pmid | 23669212 | |
dc.identifier.scopus | 2-s2.0-84880618303 | |
dc.identifier.wos | 000322932500009 | |
dc.citation.spage | 615 | |
dc.citation.epage | 624 | |
dc.type.version | publishedVersion | sr |
dc.citation.rank | M22 |