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CD55 — INS

Text-mined interactions from Literome

Cahill et al., J Biol Chem 2001 (MAP Kinase Signaling System) : In HepG2 cells, insulin signaling to PI 3-kinase/AKT inhibits the ability of a GAL4 DNA binding domain/DAF-16 fusion protein to activate transcription via the insulin-like growth factor binding protein-1-insulin response element, but not the GAL4 DNA binding site, which suggests that insulin inhibits the interaction of DAF-16 with its cognate DNA site ... Elimination of the DAF-16/1433 association by mutation of the AKT/14-3-3 sites in DAF-16, prevents 14-3-3 inhibition of DAF-16 DNA binding and insulin inhibition of DAF-16 function
Matyash et al., PLoS Biol 2004 : This hormonal control of DAF-16 activation is, however, independent of insulin signalling and has no influence on life span
Wolff et al., Cell 2006 : In C. elegans, the sole insulin/IGF-1 receptor, DAF-2, negatively regulates the FOXO transcription factor, DAF-16
Berdichevsky et al., Cell 2006 : By contrast, low insulin-like signaling does not promote SIR-2.1/DAF-16 interaction, and sir-2.1 and the 14-3-3 genes are not required for the regulation of life span by the insulin-like signaling pathway
Iser et al., Dev Biol 2007 : These results suggest that insulin signaling may regulate DAF-16 through cell-intrinsic and endocrine pathways
Shaw et al., Curr Biol 2007 : The TGF-beta Dauer pathway 's regulation of longevity appears to be mediated at least in part through insulin interactions with the IIS pathway and the regulation of DAF-16 localization
Hansen et al., PLoS Genet 2008 : Long lived daf-2 insulin/IGF-1 receptor mutants require both autophagy and the transcription factor DAF-16/FOXO for their longevity, but we find that autophagy takes place in the absence of DAF-16
Jones et al., PLoS Biol 2009 : These functions of CeRictor are not mediated through the regulation of AKT kinases or their major downstream target, the insulin regulated FOXO transcription factor DAF-16
Kenyon et al., Ann N Y Acad Sci 2010 : DAF-16 is also required for inhibition of insulin/insulin-like growth factor 1 (IGF-1) signaling to extend lifespan ... However, the mechanisms by which inhibition of insulin/IGF-1 signaling and germline loss activate DAF-16/FOXO are distinct
Edmonds et al., Dev Cell 2010 : Reduction in insulin signaling activates DAF-16/FOXO , which represses the transcription of germline and intestinal genes required to deliver PUFAs to oocytes in lipoprotein complexes
Mansisidor et al., PLoS Genet 2011 : Inhibition of insulin signaling results in the activation of DAF-16/FOXO and SKN-1/Nrf transcription factors and increased animal fitness
Putker et al., Mol Cell 2013 : We show that disulfide formation with transportin-1 is required for nuclear localization and the activation of FOXO4/DAF-16 induced by ROS, but not by the loss of insulin signaling
Tissenbaum et al., Genetics 1998 : These data show that insulin signaling, mediated by DAF-2 through the AGE-1 phosphatidylinositol-3-OH kinase, regulates reproduction and embryonic development, as well as dauer diapause and life span, and that DAF-16 transduces these signals