EC Number |
Application |
Reference |
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2.7.1.153 | analysis |
low-cost bioassay that readily measures phosphatidylinositol 3-kinase inhibition. The in vivo assay is based on the fact that the overproduction of phosphatidylinositol 3-kinase is toxic in yeast, and uses the ability of commercial phosphatidylinositol 3-kinase inhibitors to rescue cell growth. The use of 0.003% sodium dodecyl sulfate and the elimination of the Snq2 detoxification pump, optimize the bioassay by enhancing its sensitivity. From 9600 extracts tested, 0.6% lead to a recovery of yeast growth reproducibly, selectively, and in a dose-dependent manner |
722828 |
2.7.1.153 | medicine |
application of PI3K/Akt/mTOR inhibitors in T-cell acute lymphoblastic leukemia, T-ALL |
707979 |
2.7.1.153 | medicine |
genetic deletion or selective inhibition of isoform PI3Kdelta diminishes joint erosion to a level comparable to its PI3Kgamma counterpart. The induction and progression of joint destruction is profoundly reduced in the absence of both PI3K isoforms and correlates with a limited ability of neutrophils to migrate into tissue in response to leukotriene B4. fMLP-induced neutrophil extravasation is primarily reliant on PI3Kgamma |
692169 |
2.7.1.153 | medicine |
in human leukemic cell lines and in primary blast cells from acute myelogenous leukemia patients, inhibitor 4-[4-(morpholin-4-yl)-5a,6-dihydro[1]benzofuro[3,2-d]pyrimidin-2-yl]phenol/PI-103 inhibits constitutive and growth factor-induced PI3K/Akt and mTORC1 activation. PI-103 is essentially cytostatic for cell lines and induces cell cycle arrest in the G1 phase. In blast cells, PI-103 inhibits leukemic proliferation, the clonogenicity of leukemic progenitors and induces mitochondrial apoptosis. PI-103 has additive proapoptotic effects with etoposide in blast cells and in immature leukemic cells. PI-103 does not induce apoptosis in normal CD34รพ cells and has moderate effects on their clonogenic and proliferative properties |
693948 |
2.7.1.153 | medicine |
inhibitor 4-[4-(morpholin-4-yl)-5a,6-dihydro[1]benzofuro[3,2-d]pyrimidin-2-yl]phenol, i.e. PI103 is inhibitory to phosphatidylinositol 3-kinases, TORC1 and DNA protein kinase. PI103 potently inhibits proliferation and invasion of a wide variety of human cancer cells in vitro and shows biomarker modulation consistent with inhibition of phosphatidylinositide 3-kinase signaling. PI103 is extensively metabolized, but distributed rapidly to tissues and tumors. This results in tumor growth delay in eight different human cancer xenograft models with various phosphatidylinositide 3-kinase pathway abnormalities. Decreased phosphorylation of AKT is observed in U87MG gliomas, consistent with drug levels achieved |
691604 |
2.7.1.153 | medicine |
p110delta may be a good target for pharmaceutical intervention of T cell-dependent autoimmune pathologies |
675203 |
2.7.1.153 | medicine |
reduction of regulatory subunit p85alpha as a therapeutic target for enhancing insulin-like growth factor 1/insulin signaling, prolongation of cell survival, and protection against apoptosis |
662846 |
2.7.1.153 | medicine |
therapeutic target for Th2-mediated airway disease |
673442 |
2.7.1.153 | medicine |
transition of CD4-/CD8- double-negative to CD4+/CD8+ double-positive thymocytes triggered by anti-CD3 monoclonal antibodies is significantly impaired in mice lacking both major reglulatory subunit p85alpha of phosphatidylinositol 3-kinases and Rag-2 compared with p85alpha+/- Rag-2-/- mice. Inhibition by IC87114 of the major class IA phosphatidylinositol 3-kinase catalytic subunit expressed in lymphocytes, p110, blocks transition of CD4-/CD8- double-negative to CD4+/CD8+ double-positive cells in embryonic day 14.5 fetal thymic organ culture without affecting cell viability |
693450 |
2.7.1.153 | pharmacology |
the PI3Kgamma signaling pathway may represent a suitable target for the development of therapeutic strategies for human diseases characterized by vascular leakage |
709933 |