Interactions between mitoNEET and NAF-1 in cells

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dc.citation.articleNumbere0175796en_US
dc.citation.issueNumber4en_US
dc.citation.journalTitlePLoS ONEen_US
dc.citation.volumeNumber12en_US
dc.contributor.authorKarmi, Olaen_US
dc.contributor.authorHolt, Sarah H.en_US
dc.contributor.authorSong, Luhuaen_US
dc.contributor.authorTamir, Sagien_US
dc.contributor.authorLuo, Yutingen_US
dc.contributor.authorBai, Fangen_US
dc.contributor.authorAdenwalla, Ammaren_US
dc.contributor.authorDarash-Yahana, Meraven_US
dc.contributor.authorSohn, Yang-Sungen_US
dc.contributor.authorJennings, Patricia A.en_US
dc.contributor.authorAzad, Rajeev K.en_US
dc.contributor.authorOnuchic, José Nelsonen_US
dc.contributor.authorMorcos, Farucken_US
dc.contributor.authorNechushtai, Rachelen_US
dc.contributor.authorMittler, Ronen_US
dc.contributor.orgCenter for Theoretical Biological Physicsen_US
dc.date.accessioned2017-05-03T18:24:05Zen_US
dc.date.available2017-05-03T18:24:05Zen_US
dc.date.issued2017en_US
dc.description.abstractThe NEET proteins mitoNEET (mNT) and nutrient-deprivation autophagy factor-1 (NAF-1) are required for cancer cell proliferation and resistance to oxidative stress. NAF-1 and mNT are also implicated in a number of other human pathologies including diabetes, neurodegeneration and cardiovascular disease, as well as in development, differentiation and aging. Previous studies suggested that mNT and NAF-1 could function in the same pathway in mammalian cells, preventing the over-accumulation of iron and reactive oxygen species (ROS) in mitochondria. Nevertheless, it is unknown whether these two proteins directly interact in cells, and how they mediate their function. Here we demonstrate, using yeast two-hybrid, in vivo bimolecular fluorescence complementation (BiFC), direct coupling analysis (DCA), RNA-sequencing, ROS and iron imaging, and single and double shRNA lines with suppressed mNT, NAF-1 and mNT/NAF-1 expression, that mNT and NAF-1 directly interact in mammalian cells and could function in the same cellular pathway. We further show using an in vitro cluster transfer assay that mNT can transfer its clusters to NAF-1. Our study highlights the possibility that mNT and NAF-1 function as part of an iron-sulfur (2Fe-2S) cluster relay to maintain the levels of iron and Fe-S clusters under control in the mitochondria of mammalian cells, thereby preventing the activation of apoptosis and/or autophagy and supporting cellular proliferation.en_US
dc.identifier.citationKarmi, Ola, Holt, Sarah H., Song, Luhua, et al.. "Interactions between mitoNEET and NAF-1 in cells." <i>PLoS ONE,</i> 12, no. 4 (2017) Public Library of Science: https://doi.org/10.1371/journal.pone.0175796.en_US
dc.identifier.doihttps://doi.org/10.1371/journal.pone.0175796en_US
dc.identifier.urihttps://hdl.handle.net/1911/94139en_US
dc.language.isoengen_US
dc.publisherPublic Library of Scienceen_US
dc.rightsThis is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/en_US
dc.titleInteractions between mitoNEET and NAF-1 in cellsen_US
dc.typeJournal articleen_US
dc.type.dcmiTexten_US
dc.type.publicationpublisher versionen_US
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