The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

Links

 

Gene Review

PIK3CA  -  phosphatidylinositol-4,5-bisphosphate 3...

Bos taurus

 
 
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.
 

Disease relevance of PIK3CA

 

High impact information on PIK3CA

  • The angiogenic program is regulated by extracellular factors, whose input is integrated at least in part at the level of signal transduction pathways driven by phosphoinositide 3 kinase (PI3K) and phospholipase Cgamma (PLCgamma) [3].
  • The underlying mechanism by which PLCgamma antagonized tube formation appeared to be by competing with PI3K for their common substrate, phosphatidylinositol-4,5-bisphosphate [3].
  • Both GSNO and SNAP increased Akt phosphorylation and activity, which were blocked by cotreatment with the PI3 kinase inhibitor wortmannin [1].
  • These findings indicate that NO promotes endothelial cell migration and neovascularization via cGMP-dependent activation of PI3 kinase and suggest that this pathway is important in mediating NO-induced angiogenesis [1].
  • The mechanism was due to the activation of soluble guanylyl cyclase because 8-bromo-cyclic GMP activated PI3 kinase and the soluble guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-alpha]quinoxalin-1-one (ODQ) blocked NO-induced PI3 kinase activity [1].
 

Biological context of PIK3CA

  • Enhancement of insulin-induced PI3K/Akt/GSK-3beta and ERK signaling by neuronal nicotinic receptor/PKC-alpha/ERK pathway: up-regulation of IRS-1/-2 mRNA and protein in adrenal chromaffin cells [4].
  • Actions of IGF-I to increase cell number were blocked by treatment with the mitogen activated protein kinase kinase (MAPKK) inhibitor PD 98059 whereas the phosphatidylinositol 3-kinase (PI3K) inhibitor LY 294002 had no effect [5].
  • These results demonstrate that PI3-K/Akt pathway is activated constitutively in P3HR-1 cells; it promotes cell growth and the lytic cycle cascade downstream of ZEBRA [2].
 

Anatomical context of PIK3CA

  • We have found that alpha-actinin copurifies with PI 3-kinase from bovine thymus [6].
  • The antibody against PI 3-kinase 85 kDa subunit (p85) also co-immunoprecipitates alpha-actinin from lysates of NIH/3T3 cells [6].
  • Insulin-like growth factor-I promotes resistance of bovine preimplantation embryos to heat shock through actions independent of its anti-apoptotic actions requiring PI3K signaling [5].
  • To elucidate therapeutic targets for BL, this study investigates the effect of PI3-K/Akt pathway in: EBV-positive BL cell lines Raji, P3HR-1, Akata and Daudi; and EBV-negative BL cell lines Ramos and BJAB [2].
  • Transcription factor Ets-1 regulates fibroblast growth factor-1-mediated angiogenesis in vivo: role of Ets-1 in the regulation of the PI3K/AKT/MMP-1 pathway [7].
 

Associations of PIK3CA with chemical compounds

References

  1. Activation of the phosphatidylinositol 3-kinase/protein kinase Akt pathway mediates nitric oxide-induced endothelial cell migration and angiogenesis. Kawasaki, K., Smith, R.S., Hsieh, C.M., Sun, J., Chao, J., Liao, J.K. Mol. Cell. Biol. (2003) [Pubmed]
  2. Functional role of phosphatidylinositol 3-kinase/Akt pathway on cell growth and lytic cycle of Epstein-Barr virus in the Burkitt's lymphoma cell line, P3HR-1. Mori, T., Sairenji, T. Virus Genes (2006) [Pubmed]
  3. Regulating angiogenesis at the level of PtdIns-4,5-P2. Im, E., Kazlauskas, A. EMBO J. (2006) [Pubmed]
  4. Enhancement of insulin-induced PI3K/Akt/GSK-3beta and ERK signaling by neuronal nicotinic receptor/PKC-alpha/ERK pathway: up-regulation of IRS-1/-2 mRNA and protein in adrenal chromaffin cells. Sugano, T., Yanagita, T., Yokoo, H., Satoh, S., Kobayashi, H., Wada, A. J. Neurochem. (2006) [Pubmed]
  5. Insulin-like growth factor-I promotes resistance of bovine preimplantation embryos to heat shock through actions independent of its anti-apoptotic actions requiring PI3K signaling. Jousan, F.D., Hansen, P.J. Mol. Reprod. Dev. (2007) [Pubmed]
  6. Phosphatidylinositol 3-kinase binds to alpha-actinin through the p85 subunit. Shibasaki, F., Fukami, K., Fukui, Y., Takenawa, T. Biochem. J. (1994) [Pubmed]
  7. Transcription factor Ets-1 regulates fibroblast growth factor-1-mediated angiogenesis in vivo: role of Ets-1 in the regulation of the PI3K/AKT/MMP-1 pathway. Forough, R., Weylie, B., Collins, C., Parker, J.L., Zhu, J., Barhoumi, R., Watson, D.K. J. Vasc. Res. (2006) [Pubmed]
  8. Upregulation of endothelial heme oxygenase-1 expression through the activation of the JNK pathway by sublethal concentrations of acrolein. Wu, C.C., Hsieh, C.W., Lai, P.H., Lin, J.B., Liu, Y.C., Wung, B.S. Toxicol. Appl. Pharmacol. (2006) [Pubmed]
  9. Serine 1179 phosphorylation of endothelial nitric oxide synthase caused by 2,4,6-trinitrotoluene through PI3K/Akt signaling in endothelial cells. Sun, Y., Sumi, D., Kumagai, Y. Toxicol. Appl. Pharmacol. (2006) [Pubmed]
  10. Phosphatase PTEN is inactivated in bovine aortic endothelial cells exposed to cyclic strain. Hoshino, Y., Nishimura, K., Sumpio, B.E. J. Cell. Biochem. (2007) [Pubmed]
 
WikiGenes - Universities