Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/83587
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dc.contributor.authorKovács, Tiboren
dc.contributor.authorBilles, Viktoren
dc.contributor.authorKomlós, Marcellen
dc.contributor.authorHotzi, Bernadetteen
dc.contributor.authorManzéger, Annaen
dc.contributor.authorTarnóci, Annaen
dc.contributor.authorPapp, Diánaen
dc.contributor.authorSzikszai, Fannien
dc.contributor.authorSzinyákovics, Jankaen
dc.contributor.authorRácz, Ákosen
dc.contributor.authorNoszál, Bélaen
dc.contributor.authorVeszelka, Szilviaen
dc.contributor.authorWalter, Fruzsina R.en
dc.contributor.authorDeli, Mária A.en
dc.contributor.authorHackler, Laszloen
dc.contributor.authorAlfoldi, Roberten
dc.contributor.authorHuzian, Orsolyaen
dc.contributor.authorPuskas, Laszlo G.en
dc.contributor.authorLiliom, Hannaen
dc.contributor.authorTárnok, Krisztiánen
dc.contributor.authorSchlett, Katalinen
dc.contributor.authorBorsy, Adriennen
dc.contributor.authorWelker, Ervinen
dc.contributor.authorKovács, Attila L.en
dc.contributor.authorPádár, Zsolten
dc.contributor.authorErdős, Attilaen
dc.contributor.authorLegradi, Adamen
dc.contributor.authorBjelik, Annamariaen
dc.contributor.authorGulya, Károlyen
dc.contributor.authorGulyás, Balázsen
dc.contributor.authorVellai, Tiboren
dc.date.accessioned2017-06-13T07:49:30Zen
dc.date.accessioned2019-12-06T15:26:13Z-
dc.date.available2017-06-13T07:49:30Zen
dc.date.available2019-12-06T15:26:13Z-
dc.date.issued2017en
dc.identifier.citationKovács, T., Billes, V., Komlós, M., Hotzi, B., Manzéger, A., Tarnóci, A., et al. (2017). The small molecule AUTEN-99 (autophagy enhancer-99) prevents the progression of neurodegenerative symptoms. Scientific Reports, 7, 42014-.en
dc.identifier.issn2045-2322en
dc.identifier.urihttps://hdl.handle.net/10356/83587-
dc.description.abstractAutophagy functions as a main route for the degradation of superfluous and damaged constituents of the cytoplasm. Defects in autophagy are implicated in the development of various age-dependent degenerative disorders such as cancer, neurodegeneration and tissue atrophy, and in accelerated aging. To promote basal levels of the process in pathological settings, we previously screened a small molecule library for novel autophagy-enhancing factors that inhibit the myotubularin-related phosphatase MTMR14/Jumpy, a negative regulator of autophagic membrane formation. Here we identify AUTEN-99 (autophagy enhancer-99), which activates autophagy in cell cultures and animal models. AUTEN-99 appears to effectively penetrate through the blood-brain barrier, and impedes the progression of neurodegenerative symptoms in Drosophila models of Parkinson’s and Huntington’s diseases. Furthermore, the molecule increases the survival of isolated neurons under normal and oxidative stress-induced conditions. Thus, AUTEN-99 serves as a potent neuroprotective drug candidate for preventing and treating diverse neurodegenerative pathologies, and may promote healthy aging.en
dc.description.sponsorshipMOH (Min. of Health, S’pore)en
dc.format.extent17 p.en
dc.language.isoenen
dc.relation.ispartofseriesScientific Reportsen
dc.rights© 2017 The Author(s) (Nature Publishing Group). This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/en
dc.subjectDrug discoveryen
dc.subjectDiseasesen
dc.titleThe small molecule AUTEN-99 (autophagy enhancer-99) prevents the progression of neurodegenerative symptomsen
dc.typeJournal Articleen
dc.contributor.schoolLee Kong Chian School of Medicine (LKCMedicine)en
dc.identifier.doi10.1038/srep42014en
dc.description.versionPublished versionen
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item.grantfulltextopen-
Appears in Collections:LKCMedicine Journal Articles

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