Reference health
FoxO restricts growth and differentiation of cells with elevated TORC1 activity under nutrient restriction
39/39 checkable references clean · checked 2026-07-22
Every reference with a DOI in the deposited reference list resolved to a known work in Crossref or DataCite at the dated check, and none carried a retraction, withdrawal, or removal notice.
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The 39 checked references that resolve
resolves10.1371/journal.pgen.1000990
Dynamic Switch of Negative Feedback Regulation in Drosophila Akt–TOR Signaling
resolves10.1083/jcb.200710100
FOXO-regulated transcription restricts overgrowth of <i>Tsc</i> mutant organs
resolves10.1146/annurev.physiol.70.113006.100533
Insulin-Like Signaling, Nutrient Homeostasis, and Life Span
resolves10.1126/science.1068094
Living with Lethal PIP3 Levels: Viability of Flies Lacking PTEN Restored by a PH Domain Mutation in Akt/PKB
resolves10.1242/dev.126.23.5365
PTEN affects cell size, cell proliferation and apoptosis during <i>Drosophila</i> eye development
resolves10.1038/sj.onc.1203739
The conserved PI3′K/PTEN/Akt signaling pathway regulates both cell size and survival in Drosophila
resolves10.1101/gad.13.24.3244
Drosophila tumor suppressor PTEN controls cell size and number by antagonizing the Chico/PI3-kinase signaling pathway
resolves10.1006/dbio.2000.9680
Drosophila PTEN Regulates Cell Growth and Proliferation through PI3K-Dependent and -Independent Pathways
resolves10.1016/S0092-8674(01)00333-6
Drosophila Tsc1 Functions with Tsc2 to Antagonize Insulin Signaling in Regulating Cell Growth, Cell Proliferation, and Organ Size
resolves10.1016/S0092-8674(01)00332-4
The Drosophila Tuberous Sclerosis Complex Gene Homologs Restrict Cell Growth and Cell Proliferation
resolves10.1101/gad.239102
Lethality of <i>Drosophila</i> lacking TSC tumor suppressor function rescued by reducing dS6K signaling
resolves10.7554/eLife.00380
Nutrient restriction enhances the proliferative potential of cells lacking the tumor suppressor PTEN in mitotic tissues
resolves10.1074/jbc.M414499200
The Tuberous Sclerosis Protein TSC2 Is Not Required for the Regulation of the Mammalian Target of Rapamycin by Amino Acids and Certain Cellular Stresses
resolves10.1016/j.cell.2014.01.024
Regulation of TORC1 in Response to Amino Acid Starvation via Lysosomal Recruitment of TSC2
resolves10.1016/j.celrep.2014.07.018
The TSC Complex Is Required for the Benefits of Dietary Protein Restriction on Stress Resistance In Vivo
resolves10.1242/dev.127.4.851
Analysis of <i>Drosophila</i> photoreceptor axon guidance in eye-specific mosaics
resolves10.1101/gad.341505
4E-BP functions as a metabolic brake used under stress conditions but not during normal growth
resolves10.1186/1475-4924-2-20
The Drosophila Forkhead transcription factor FOXO mediates the reduction in cell number associated with reduced insulin signaling
resolves10.1101/gad.1211604
Epithelial polarity and proliferation control: links from the <i>Drosophila</i> neoplastic tumor suppressors
resolves10.1093/genetics/141.3.1025
The ecdysone-inducible Broad-complex and E74 early genes interact to regulate target gene transcription and Drosophila metamorphosis.
resolves10.7554/eLife.03091
Nutritional control of body size through FoxO-Ultraspiracle mediated ecdysone biosynthesis
resolves10.1016/j.ccr.2010.10.019
FoxOs Enforce a Progression Checkpoint to Constrain mTORC1-Activated Renal Tumorigenesis
resolves10.1038/ncb995
Rheb is an essential regulator of S6K in controlling cell growth in Drosophila
resolves10.1111/j.1474-9726.2011.00707.x
dFOXO‐independent effects of reduced insulin‐like signaling in <i>Drosophila</i>
resolves10.1101/gad.845700
Genetic and biochemical characterization of dTOR, the <i>Drosophila</i> homolog of the target of rapamycin
resolves10.1016/0092-8674(95)90150-7
Drosophila homologs of baculovirus inhibitor of apoptosis proteins function to block cell death
resolves10.1371/journal.pbio.1000566
A dp53-Dependent Mechanism Involved in Coordinating Tissue Growth in Drosophila
The 1 reference without a DOI — listed, not checked
no DOI — not checkedSignaling crosstalk between the mTOR complexes
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