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Gene Review

Pi3K59F  -  Phosphotidylinositol 3 kinase 59F

Drosophila melanogaster

Synonyms: CG5373, DmVps34, Dmel\CG5373, PI(3)K, PI3K, ...
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Disease relevance of Pi3K59F

  • In contrast to the mild effects of removing HM site phosphorylation at normal levels of PI3K activity, loss of TORC2 activity strongly inhibited hyperplasia caused by elevated pathway activity, as in mutants of the tumor suppressor PTEN [1].
  • Our results raise the possibility that neurofibroma formation in individuals with neurofibromatosis might result in part from a Ras-PI3K-Akt-dependent inhibition of FOXO within Schwann cells [2].
  • In step mutant animals both cell size and cell number are reduced, resulting in decreased body size and body weight in larvae, pupae and adults. step acts upstream of PI(3)K and is required for the proper regulation of Akt and the transcription factor FOXO [3].
  • TRB3 expression is remarkably reduced in prostate cancer PC-3 cells after inhibition of PI 3-kinase [4].
  • We also report that PI3K controls the expression and localization of synaptic markers in human neuroblastoma cells, suggesting that PI3K synaptogenic activity is conserved in humans [5].

High impact information on Pi3K59F

  • Thus, Dp110 integrates inputs from its phosphotyrosine-binding adaptor and Ras to achieve maximal PI(3)K signalling in specific biological situations [6].
  • The Drosophila class I PI(3)K, Dp110, is activated by nutrient-responsive insulin signalling and modulates growth, oogenesis and metabolism [6].
  • In contrast, using both laser ablation and a novel wounding assay that allows localized treatment with inhibitory drugs, we show that PI3K is essential for hemocyte chemotaxis toward wounds and that Pvf signals and PDGF/VEGF receptor expression are not required for this rapid chemotactic response [7].
  • In the last few years, the PI3K signal transduction pathway has emerged as one of the main signaling routes utilized by cells to control their increase in size [8].
  • We report here the cloning of a novel PI 3-kinase, p170, from cDNA of insulin-sensitive mouse 3T3-L1 adipocytes [9].

Biological context of Pi3K59F

  • FOXO-independent suppression of programmed cell death by the PI3K/Akt signaling pathway in Drosophila [10].
  • Rheb plays a key role in the regulation of cell growth in response to growth factors, nutrients, and amino acids linking PI3K and TOR signaling [11].
  • Using chromosomal loss-of-function mutations and transgenes encoding dominant-negative and constitutively active proteins, we show that this nonautonomous effect of Ras(V12) is mediated by the Ras effector phosphatidylinositol 3-kinase (PI3K) and its downstream kinase Akt [2].
  • Recent molecular genetic studies initiated in the fruitfly, Drosophila melanogaster, have highlighted two new cell-type-specific mechanisms regulating PI3K/Akt signalling and its downstream effects [12].
  • The mutant larvae showed impaired upregulation of ecdysone signaling during development, accompanied by a failure to downregulate the PI3K pathway [13].

Anatomical context of Pi3K59F

  • In this study, we show that elevated signaling through PI3K and Akt can prevent developmentally controlled death in the salivary glands of the fruit fly [10].
  • Thus DOCK180 contained a phosphoinositide-binding domain, as did the other guanine nucleotide exchange factors with a Dbl homology domain, and was translocated to the plasma membrane on the activation of PI-3K [14].
  • We show here that the levels of phosphoinositide 3 kinase (PI3K) regulate synapse number in both Drosophila larval motor neurons and adult brain projection neurons [5].
  • Previous work in our laboratory has indicated that the steroid hormone ecdysone triggers programmed autophagy in the fat body of Drosophila larvae by downregulating the class I phosphoinositide 3-kinase (PI3K) pathway [13].

Associations of Pi3K59F with chemical compounds

  • Biochemical characterization of the enzyme, by expression of the complete coding sequence as a glutathione S-transferase fusion protein in Sf9 cells, demonstrates that PI3K_59F is a PtdIns-specific PI3K that can utilize either Mg2+ or Mn2+ [15].
  • These data demonstrate that the kinase and adaptor properties of ILK function together, in a Pi3 kinase-dependent manner, to regulate integrin-mediated cell attachment and signal transduction [16].
  • TRB3 expression is furthermore controlled by nutrient supplies: Both the lack of glucose or amino acids results in a substantial increase in TRB3 protein levels in a PI 3-kinase-dependent manner [4].


  1. Re-evaluating AKT regulation: role of TOR complex 2 in tissue growth. Hietakangas, V., Cohen, S.M. Genes Dev. (2007) [Pubmed]
  2. Phosphatidylinositol 3-kinase and Akt nonautonomously promote perineurial glial growth in Drosophila peripheral nerves. Lavery, W., Hall, V., Yager, J.C., Rottgers, A., Wells, M.C., Stern, M. J. Neurosci. (2007) [Pubmed]
  3. The cytohesin Steppke is essential for insulin signalling in Drosophila. Fuss, B., Becker, T., Zinke, I., Hoch, M. Nature (2006) [Pubmed]
  4. TRB3 is a PI 3-kinase dependent indicator for nutrient starvation. Schwarzer, R., Dames, S., Tondera, D., Klippel, A., Kaufmann, J. Cell. Signal. (2006) [Pubmed]
  5. Age-independent synaptogenesis by phosphoinositide 3 kinase. Mart??n-Pe??a, A., Acebes, A., Rodr??guez, J.R., Sorribes, A., de Polavieja, G.G., Fern??ndez-F??nez, P., Ferr??s, A. J. Neurosci. (2006) [Pubmed]
  6. Input from Ras is required for maximal PI(3)K signalling in Drosophila. Orme, M.H., Alrubaie, S., Bradley, G.L., Walker, C.D., Leevers, S.J. Nat. Cell Biol. (2006) [Pubmed]
  7. Distinct mechanisms regulate hemocyte chemotaxis during development and wound healing in Drosophila melanogaster. Wood, W., Faria, C., Jacinto, A. J. Cell Biol. (2006) [Pubmed]
  8. Regulation of cell size in growth, development and human disease: PI3K, PKB and S6K. Kozma, S.C., Thomas, G. Bioessays (2002) [Pubmed]
  9. Mouse p170 is a novel phosphatidylinositol 3-kinase containing a C2 domain. Virbasius, J.V., Guilherme, A., Czech, M.P. J. Biol. Chem. (1996) [Pubmed]
  10. FOXO-independent suppression of programmed cell death by the PI3K/Akt signaling pathway in Drosophila. Liu, Y., Lehmann, M. Dev. Genes Evol. (2006) [Pubmed]
  11. Rheb Activation of mTOR and S6K1 Signaling. Hanrahan, J., Blenis, J. Meth. Enzymol. (2005) [Pubmed]
  12. Extracellular and subcellular regulation of the PI3K/Akt cassette: new mechanisms for controlling insulin and growth factor signalling. Wilson, C., Vereshchagina, N., Reynolds, B., Meredith, D., Boyd, C.A., Goberdhan, D.C. Biochem. Soc. Trans. (2007) [Pubmed]
  13. How a RING finger protein and a steroid hormone control autophagy. Lindmo, K., Stenmark, H. Autophagy. (2006) [Pubmed]
  14. Membrane recruitment of DOCK180 by binding to PtdIns(3,4,5)P3. Kobayashi, S., Shirai, T., Kiyokawa, E., Mochizuki, N., Matsuda, M., Fukui, Y. Biochem. J. (2001) [Pubmed]
  15. Molecular cloning and biochemical characterization of a Drosophila phosphatidylinositol-specific phosphoinositide 3-kinase. Linassier, C., MacDougall, L.K., Domin, J., Waterfield, M.D. Biochem. J. (1997) [Pubmed]
  16. Integration of cell attachment, cytoskeletal localization, and signaling by integrin-linked kinase (ILK), CH-ILKBP, and the tumor suppressor PTEN. Attwell, S., Mills, J., Troussard, A., Wu, C., Dedhar, S. Mol. Biol. Cell (2003) [Pubmed]
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