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Gene Review

PIK3CB  -  phosphatidylinositol-4,5-bisphosphate 3...

Bos taurus

Synonyms: PI3K, PI3Kbeta
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Disease relevance of PIK3CB

  • Recombinant adenoviruses were used to test whether the downstream target of PI3K activation, Akt kinase, was required for protection against apoptosis [1].
  • Previous studies have suggested that ERK1/2, phosphatidylinositol 3-kinase (PI3K), Akt, and mammalian target of rapamycin (mTOR) are activated by hypoxia and play a role in a variety of cell responses [2].
  • The phosphatidylinositol 3-kinase (PI3-K)/Akt pathway is involved in various malignancies, but the role of PI3-K/Akt pathway in Epstein-Barr virus (EBV) infected Burkitt's lymphoma (BL) cells remains unclear [3].

High impact information on PIK3CB

  • 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) [4].
  • The underlying mechanism by which PLCgamma antagonized tube formation appeared to be by competing with PI3K for their common substrate, phosphatidylinositol-4,5-bisphosphate [4].
  • Phosphatidylinositol 3-kinase (PI3K) is an important component of various receptor tyrosine kinase complexes in mammalian cells and a key enzyme required for cell division and vacuolar protein sorting in yeast [5].
  • The polypeptides encoded by soybean PI3K cDNAs show significant sequence homology (50-60% similarity and 20-40% identity) to both PI3Ks and phosphatidylinositol 4-kinases from mammalian and yeast cells [5].
  • Expression of the root form of PI3K is repressed during nodule organogenesis and is reinduced in mature nodules [5].

Biological context of PIK3CB


Anatomical context of PIK3CB

  • The results show that there are two types of PI 3-kinase in bovine thymus [11].
  • Inhibitor studies also suggest an important role for the lipid kinase, PI-3K, in the continuous proliferation of T. parva-transformed lymphocytes [12].
  • Role of Cbl in shear-activation of PI 3-kinase and JNK in endothelial cells [13].
  • In conclusion, shear stress of BAEC increases eNOS transcriptional rate and upregulates eNOS mRNA levels by a process that requires calmodulin-independent [Ca2+]i signaling and a PTX-sensitive G-protein, is inhibited by PI 3-kinase, and is independent of microtubule integrity and tyrosine kinase activity [14].
  • In summary, IGF-I protects granulosa cells from apoptosis by activation of the PI3K/Akt pathway [1].

Associations of PIK3CB with chemical compounds

  • Finally, shear stress caused an activation of PI 3-kinase only in BAECs seeded onto fibronectin, vitronectin, or laminin, but not poly-l-lysine [13].
  • The betagamma cascade subsequently activates PI3-Kbeta-dependent signaling that is coupled to PDK1 and the downstream effector PKCzeta, and results in an increase in 5-HT release [15].
  • Neither U0126 nor LY294002 pretreatment affected TNF-induced activation of NF-kappaB, suggesting that the MAP kinase or PI3-kinase/Akt-mediated anti-apoptotic effect induced by TNF was not relevant to NF-kappaB activation [16].
  • High glucose- or peroxynitrite-treated cells also showed significant increases in tyrosine nitration on the p85 subunit of PI 3-kinase that blocked PI 3-kinase and Akt-1 kinase activity [17].
  • In summary, H(2)O(2) causes endothelial NO* release mediated by cooperative effects between PI 3-kinase/Akt-dependent eNOS serine 1179 phosphorylation and activation of MEK/ERK1/2 [18].

Analytical, diagnostic and therapeutic context of PIK3CB

  • We have employed a co-culture approach to dissect the molecular signals that are dependent on the spatial relationship between ECs and SMCs, and have identified the importance of the PI3K/Akt pathway in EC-induced SMC differentiation [9].
  • Activation of the MAPK and PI 3-K was detected by Western blot analysis, using specific antiphosphosignaling protein antibodies [19].
  • Treatment of ROS with insulin, followed by immunoprecipitation with either anti-IRbeta or anti-PY, resulted in increased PI3K activity [20].
  • PI 3-kinase immunoprecipitated by anti-p85 antibody converted PI to PI-3-P and PI-4-P to PI-3,4-P2, as determined by HPLC analysis of the deacylated products [21].
  • High-performance liquid chromatography on an ion exchange column (Partisil-SAX; Whatman, Maidstone, United Kingdom) was used to identify PI-3K reaction products [22].


  1. Cell cycle progression and activation of Akt kinase are required for insulin-like growth factor I-mediated suppression of apoptosis in granulosa cells. Hu, C.L., Cowan, R.G., Harman, R.M., Quirk, S.M. Mol. Endocrinol. (2004) [Pubmed]
  2. Activation of phosphatidylinositol 3-kinase, Akt, and mammalian target of rapamycin is necessary for hypoxia-induced pulmonary artery adventitial fibroblast proliferation. Gerasimovskaya, E.V., Tucker, D.A., Stenmark, K.R. J. Appl. Physiol. (2005) [Pubmed]
  3. 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]
  4. Regulating angiogenesis at the level of PtdIns-4,5-P2. Im, E., Kazlauskas, A. EMBO J. (2006) [Pubmed]
  5. A phosphatidylinositol 3-kinase is induced during soybean nodule organogenesis and is associated with membrane proliferation. Hong, Z., Verma, D.P. Proc. Natl. Acad. Sci. U.S.A. (1994) [Pubmed]
  6. Effects of bezafibrate on the expression of endothelial nitric oxide synthase gene and its mechanisms in cultured bovine endothelial cells. Wang, Y., Wang, Y., Yang, Q., Yan, J.T., Zhao, C., Cianflone, K., Wang, D.W. Atherosclerosis (2006) [Pubmed]
  7. Dissimilar effects of LY 294002 and PD 098059 in IGF-I-mediated inhibition of TGF-beta(1) expression and apoptosis in bovine mammary epithelial cells. Zarzyńska, J., Motyl, T. J. Physiol. Pharmacol. (2005) [Pubmed]
  8. Sphingosine 1-phosphate and isoform-specific activation of phosphoinositide 3-kinase beta. Evidence for divergence and convergence of receptor-regulated endothelial nitric-oxide synthase signaling pathways. Igarashi, J., Michel, T. J. Biol. Chem. (2001) [Pubmed]
  9. Endothelial cell activation of the smooth muscle cell phosphoinositide 3-kinase/Akt pathway promotes differentiation. Brown, D.J., Rzucidlo, E.M., Merenick, B.L., Wagner, R.J., Martin, K.A., Powell, R.J. J. Vasc. Surg. (2005) [Pubmed]
  10. Sphingosine 1-phosphate activates Akt, nitric oxide production, and chemotaxis through a Gi protein/phosphoinositide 3-kinase pathway in endothelial cells. Morales-Ruiz, M., Lee, M.J., Zöllner, S., Gratton, J.P., Scotland, R., Shiojima, I., Walsh, K., Hla, T., Sessa, W.C. J. Biol. Chem. (2001) [Pubmed]
  11. Two types of phosphatidylinositol 3-kinase from bovine thymus. Monomer and heterodimer form. Shibasaki, F., Homma, Y., Takenawa, T. J. Biol. Chem. (1991) [Pubmed]
  12. Theileria parva: taking control of host cell proliferation and survival mechanisms. Dobbelaere, D.A., Fernandez, P.C., Heussler, V.T. Cell. Microbiol. (2000) [Pubmed]
  13. Role of Cbl in shear-activation of PI 3-kinase and JNK in endothelial cells. Miao, H., Yuan, S., Wang, Y., Tsygankov, A., Chien, S. Biochem. Biophys. Res. Commun. (2002) [Pubmed]
  14. Induction of nitric oxide synthase mRNA by shear stress requires intracellular calcium and G-protein signals and is modulated by PI 3 kinase. Malek, A.M., Jiang, L., Lee, I., Sessa, W.C., Izumo, S., Alper, S.L. Biochem. Biophys. Res. Commun. (1999) [Pubmed]
  15. Calcium receptor-induced serotonin secretion by parafollicular cells: role of phosphatidylinositol 3-kinase-dependent signal transduction pathways. Liu, K.P., Russo, A.F., Hsiung, S.C., Adlersberg, M., Franke, T.F., Gershon, M.D., Tamir, H. J. Neurosci. (2003) [Pubmed]
  16. Inhibition of phosphatidylinositol-3 kinase/Akt or mitogen-activated protein kinase signaling sensitizes endothelial cells to TNF-alpha cytotoxicity. Zhang, L., Himi, T., Morita, I., Murota, S. Cell Death Differ. (2001) [Pubmed]
  17. Oxidative stress inactivates VEGF survival signaling in retinal endothelial cells via PI 3-kinase tyrosine nitration. el-Remessy, A.B., Bartoli, M., Platt, D.H., Fulton, D., Caldwell, R.B. J. Cell. Sci. (2005) [Pubmed]
  18. Akt-dependent phosphorylation of serine 1179 and mitogen-activated protein kinase kinase/extracellular signal-regulated kinase 1/2 cooperatively mediate activation of the endothelial nitric-oxide synthase by hydrogen peroxide. Cai, H., Li, Z., Davis, M.E., Kanner, W., Harrison, D.G., Dudley, S.C. Mol. Pharmacol. (2003) [Pubmed]
  19. Proliferation of CECs requires dual signaling through both MAPK/ERK and PI 3-K/Akt pathways. Zubilewicz, A., Hecquet, C., Jeanny, J., Soubrane, G., Courtois, Y., Mascarelli, F. Invest. Ophthalmol. Vis. Sci. (2001) [Pubmed]
  20. Interaction of the insulin receptor beta-subunit with phosphatidylinositol 3-kinase in bovine ROS. Rajala, R.V., Anderson, R.E. Invest. Ophthalmol. Vis. Sci. (2001) [Pubmed]
  21. Phosphatidylinositol 3-kinase in bovine photoreceptor rod outer segments. Guo, X., Ghalayini, A.J., Chen, H., Anderson, R.E. Invest. Ophthalmol. Vis. Sci. (1997) [Pubmed]
  22. Phosphatidylinositol 3-kinase in bovine lens and its stimulation by insulin and IGF-1. Chandrasekher, G., Bazan, H.E. Invest. Ophthalmol. Vis. Sci. (2000) [Pubmed]
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