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Phosphatidylinositol-3-kinase , pathway

Sulpice E, Bryckaert M, Lacour J, Confreres JO, Tobelem G. Platelet factor 4 inhibits FGF2-induced endothelial cell proliferation via the extracellular signal-regulated kinase pathway but not by the phosphatidylinositol 3-kinase pathway. Blood 2002 100(9) 3087-3094. [Pg.334]

Wang, D. Sul, H.S. Insulin stimulation of the fatty acid synthase promoter is mediated by the phosphatidylinositol 3-kinase pathway. Involvement of protein kinase B/Akt. J. Biol. Chem., 273, 25420-25426 (1998)... [Pg.188]

Molecular mechanisms by which PMFs exert their anti-inflammatory and anti-tumor-promoting, as well as anti-tumor-invading activities remain poorly understood. However, Ito and co-workers [80] recently presented an excellent study indicating that nobiletin suppressed the TPA-induced binding activity of activator protein-1 and that it may interfere in the phosphatidylinositol 3-kinase pathway, which divergently regulates the production of MMP and its inhibitor. [Pg.186]

Sato T, Koike L, Miyata Y, Hirata M, Mimaki Y, Sashida Y, Yano M, Ito A. Inhibition of activator protein-1 binding activity and phosphatidylinositol 3-kinase pathway by nobiletin, a polymethoxy flavonoid, results in augmentation of tissue inhibitor of metaUoproteinases-1 production and suppression of production of matrix metalloproteinases-1 and -9 in human fibrosarcoma HT-1080 cells. Cancer Res 2002 62 1025-1029. [Pg.191]

Mehta VB, Besner GE. Heparin-binding epidermal growth factor-like growth factor inhibits cytokine-induced NF-kappa B activation and nitric oxide production via activation of the phosphatidylinositol 3-kinase pathway. J Immunol 2005 175(3) 1911-1918. [Pg.223]

Wicki, A., and Niggli, V. (2001) The Rho/ Rho-kinase and the phosphatidylinositol 3-kinase pathways are essential for spontaneous locomotion ofWalker 256 carcinosarcoma cells. Int. J. Cancer 9, 763-771. [Pg.347]

Ueno, H. et al.. The phosphatidylinositol 3 kinase pathway is required for the survival signal of leukocyte tyrosine kinase. Oncogene, 14, 3067,1997. [Pg.95]

Chen, J., Wang, L., Chen, Y., Sternberg, R, and Cai, J. 2009. Phosphatidylinositol 3 kinase pathway and 4-hydroxy-2-nonenal-induced oxidative injury in the RPE. [Pg.271]

Maserejian NN, Trachtenberg FL, Hauser R et al (2012b) Dental composite restorations and psychosocial function in children. Pediatrics 130(2) 328-338 Masuno H, Kidani T, Sekiya K et al (2002) Bisphenol A in combination with insulin can accelerate the conversion of 3T3-L1 fibroblasts to adipocytes. J Lipid Res 43(5) 676-684 Masuno H, Iwanami J, Kidani T et al (2005) Bisphenol A accelerates terminal differentiation of 3T3-L1 cells into adipocytes through the phosphatidylinositol 3-kinase pathway. Toxicol Sd 84(2) 319-327... [Pg.27]

Lee C, Tomkowicz B, Freedman BD, Collman RG. HIV-1 gpl20-induced TNF-a production by primary human macrophages is mediated by phosphatidylinositol-3 (PI-3) kinase and mitogen-activated protein (MAP) kinase pathways. J Leukoc Biol 2005 78(4) 1016-1023. [Pg.286]

Kim JH, Na HJ, Kim CK, Kim JY, Ha KS, Lee H, Chung HT, Kwon HJ, Kwon YG and Kim YM. 2008. The non-provitamin A carotenoid, lutein, inhibits NF-KB-dependent gene expression through redox-based regulation of the phosphatidylinositol 3-kinase/PTEN/Akt and NF-KB-inducing kinase pathways role of H2O2 in NF-kB activation. Free Radic Biol Med 45(6) 885-896. [Pg.215]

Carrillo, J.J. Ibares, B. Esteban-Gamboa, A. Feliu, J.E. Involvement of both phosphatidylinositol 3-kinase and p44/p42 mitogen-activated protein kinase pathways in the short-term regulation of pyruvate kinase L by insulin. Endocrinology, 142, 1057-1064 (2001)... [Pg.184]

Gary, J.D. Sato, T.K. Stefan, C.J. Bonangelino, C.J. Weisman, L.S. Emr, S.D. Regulation of fabl phosphatidylinositol 3-phosphate 5-kinase pathway by vac7 protein and fig4, a polyphosphoinositide phosphatase family member. Mol. Biol. Cell, 13, 1238-1251 (2002)... [Pg.235]

Glutamate-mediated Ca2+ entry through NMDA at the plasma membrane level and mobilization of Ca2+from intracellular stores through PLC-mediated generation of PtdIns-3/J is indispensable for the basal NF-kB activity. Three cytosolic Ca2+ sensors, calmodulin, protein kinases C (PKC), and the p2 l(ras)/phosphatidylinositol 3-kinase (Ptdlns-3K)/Akt pathways, are simultaneously involved in the steps linking the Ca2+ to NF-kB activity (Lilienbaum and Israel, 2003 Marchetti et al., 2004 Lubin et al., 2005). Calmodulin modulates calcineurin, a Ca2+-dependent protein phosphatase, which plays a role in the basal NF-kB activity, whilst stimulation of both the calmodulin kinase II and Akt kinase pathways results in the up-regulation of the transcriptional potential of the p65 subunit of NF-/cB (Lilienbaum and Israel,... [Pg.141]

Fig. 1. The major inositol lipids. Phosphatidylinositol (Ptdlns), the major membrane inositol phospholipid, is phosphorylated to phosphatidylinositol 4-phosphate (Ptdlns 4-P) by a phosphatidylinositol kinase (a). Ptdlns 4-P is further phosphorylated to phosphatidylinositol 4,5-bisphosphate (Ptdlns 4,5-P2) by a phosphatidylinositol 4-phosphate kinase (b). Ptdlns 4,5-P, is converted back to Ptdlns 4-P by phosphatidylinositol 4,5-bisphosphate phosphomonoesterase (c) and then to Ptdlns by phosphatidylinositol 4-phosphate monoesterase (d). The pathway of phosphorylation and dephosphorylation constitutes a futile cycle and is only interrupted by agonist-induced hydrolysis of Ptdlns 4,5-P,. Fig. 1. The major inositol lipids. Phosphatidylinositol (Ptdlns), the major membrane inositol phospholipid, is phosphorylated to phosphatidylinositol 4-phosphate (Ptdlns 4-P) by a phosphatidylinositol kinase (a). Ptdlns 4-P is further phosphorylated to phosphatidylinositol 4,5-bisphosphate (Ptdlns 4,5-P2) by a phosphatidylinositol 4-phosphate kinase (b). Ptdlns 4,5-P, is converted back to Ptdlns 4-P by phosphatidylinositol 4,5-bisphosphate phosphomonoesterase (c) and then to Ptdlns by phosphatidylinositol 4-phosphate monoesterase (d). The pathway of phosphorylation and dephosphorylation constitutes a futile cycle and is only interrupted by agonist-induced hydrolysis of Ptdlns 4,5-P,.
Gq protein-coupled phosphatidylinositol-Ca " " pathway. The binding of a hormone at a specific receptor site results in the activation of G-protein which, in turn, activates phospholipase C via Gga-OTP-protein. The action of phospholipase C on phosphatidylinositol 4,5-bisphosphate (PIP2) yields inositol trisphosphate (IP3) and diacylglycerol (DAG) which, along with phosphatidylserine (PS), activates protein kinase C. IP3 binds to receptors on SER, releasing Ca " which, in turn, activates another set of protein kinases. -I-, Activation. [Pg.719]

Van de Sande, T., De Schrijver, E., Heyns, W., Verhoeven, G. and Swinnen, J. V., Role of the phosphatidylinositol 3 -kinase/PTEN/Akt kinase pathway in the overexpression of fatty acid synthase in LNCaP prostate cancer cells, Cancer Res 62 (2002) 642-646. [Pg.193]

Phosphatidylinositol kinase is involved in the PI turnover pathway and may be important for the regulation of phosphatidylinositol 4,5-bisphosphate levels. Therefore, we... [Pg.458]

Figure 1, Phosphoinositide Pathway. Enzymes a. phosphatidyl-inositol synthetase (PI synthetase) h. phosphatidylinositol kinase (PI kinase) c. phosphatidylinositol-4-phosphate kinase (pip kinase) d. phospholipase C (R = palmitoyl or other long-chain fatty acid chain). Figure 1, Phosphoinositide Pathway. Enzymes a. phosphatidyl-inositol synthetase (PI synthetase) h. phosphatidylinositol kinase (PI kinase) c. phosphatidylinositol-4-phosphate kinase (pip kinase) d. phospholipase C (R = palmitoyl or other long-chain fatty acid chain).
Shih A, Zhang S, Cao HJ, Boswell S, Wu YH, Tang HY, Lennartz MR, Davis FB, Davis PJ, Lin HY (2004) Inhibitory effect of epidermal growth factor on resveratrol-induced optosis in prostate cancer cells is mediated by protein kinase C-alpha, Mol Cancer Ther 3 1355-1364 Siddiqui lA, Adhami VM, Afaq F, Ahmad N, Mukhtar H (2004) Modulation of phosphatidylinositol-3-kinase/protein kinase B- and mitogen-activated protein kinase-pathways by tea polyphenols in human prostate cancer cells. J Cell Biochem 91 232-242... [Pg.112]

Progress made in recent years has revealed the central role the phosphoinositide 3-kinase pathway plays in the establishment and the maintenance of cell polarity (Figure 7) [246]. The substrate for the Class I phosphoinositide 3-kinase [223] involved in chemotaxis is the membrane lipid phosphatidylinositol-(4, 5) bisphosphate, or PI(4,5)P2, which becomes phosphorylated at its 3 position to phosphatidylinositol-(3, 4, 5) trisphosphate, or PI(3, 4, 5)P3. A second 3-phosphoinositide, PI(3, 4)P2, can be formed by the dephosphorylation of PI(3, 4, 5)P3 at... [Pg.279]


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See also in sourсe #XX -- [ Pg.278 ]

See also in sourсe #XX -- [ Pg.59 ]




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