{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T05:13:07Z","timestamp":1791090787755,"version":"4.1.0"},"reference-count":26,"publisher":"Cold Spring Harbor Laboratory","issue":"20","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes Dev."],"published-print":{"date-parts":[[2004,10,15]]},"abstract":"\n Signaling by insulin and target of rapamycin are both required for cell growth, but their interrelationships remain poorly defined. It was reported that Akt, an essential component of the insulin pathway, stimulates growth by phosphorylating and inhibiting tuberous sclerosis complex 2 (TSC2). Here we evaluate this model genetically in\n Drosophila<\/jats:italic>\n by engineering\n Tsc2<\/jats:italic>\n mutants in which the Akt phosphorylation sites are changed to nonphosphorylatable or phospho-mimicking residues. Strikingly, such mutants completely rescue the lethality and cell growth defects of\n Tsc2<\/jats:italic>\n -null mutants. Taken together, our data suggest that Tsc2 is not a critical substrate of Akt in normal\n Drosophila<\/jats:italic>\n development.\n <\/jats:p>","DOI":"10.1101\/gad.1240504","type":"journal-article","created":{"date-parts":[[2004,10,1]],"date-time":"2004-10-01T20:25:21Z","timestamp":1096662321000},"page":"2479-2484","source":"Crossref","is-referenced-by-count":97,"title":["Tsc2 is not a critical target of Akt during normal\n Drosophila<\/i>\n development"],"prefix":"10.1101","volume":"18","author":[{"given":"Jixin","family":"Dong","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Duojia","family":"Pan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"246","published-online":{"date-parts":[[2004,10,1]]},"reference":[{"key":"2021111607210742000_18.20.2479.1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M205838200"},{"key":"2021111607210742000_18.20.2479.2","doi-asserted-by":"crossref","first-page":"6242","DOI":"10.1128\/MCB.16.11.6242","volume":"16","year":"1996","journal-title":"Mol. 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