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

• Inhibitors of PPARalpha, PI3 kinase and MAPK, respectively, markedly attenuate bezafibrate-induced upregulation of eNOS [6].
• The results clearly showed that inhibition of PI3-K reverses the ability of IGF-I to suppress TGF-beta(1) expression and apoptosis [7].
• Vascular endothelial growth factor activated both PI3-Kalpha and PI3-Kbeta via tyrosine kinase pathways and promoted eNOS phosphorylation that was unaffected by Gbetagamma inhibition [8].
• CONCLUSIONS: ECs direct SMCs towards a differentiated phenotype through activation of the SMC PI 3-kinase/Akt pathway [9].
• Inhibition of G(i) signaling, and phosphoinositide 3-kinase (PI 3-kinase) activity resulted in a decrease in SPP-induced endothelial cell chemotaxis [10].

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].

References