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Fnip1 physically interacts with AMPK, an energy-sensing enzyme that stimulates mitochondria and ATP production in response to energy deficit, while inhibiting mammalian target of rapamycin (mTOR)-mediated cell growth. Fnip1-deficient iNKT cells contain reduced mitochondrial number and hyperactive mTOR, which resulted in decreased ATP levels and increased sensitivity to apoptosis. Our findings indicate that Fnip1 is vital for maintaining metabolic balance during iNKT cell development.<\/jats:p>","DOI":"10.1073\/pnas.1406473111","type":"journal-article","created":{"date-parts":[[2014,5,1]],"date-time":"2014-05-01T07:10:14Z","timestamp":1398928214000},"page":"7066-7071","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":48,"title":["Metabolic regulator Fnip1 is crucial for iNKT lymphocyte development"],"prefix":"10.1073","volume":"111","author":[{"given":"Heon","family":"Park","sequence":"first","affiliation":[{"name":"Department of Immunology,"},{"name":"Howard Hughes Medical Institute, University of Washington, Seattle, WA 98109; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark","family":"Tsang","sequence":"additional","affiliation":[{"name":"Department of Comparative Medicine, University of Washington, Seattle, WA 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