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PI3 — TP53

Text-mined interactions from Literome

Cuddihy et al., Mol Cell Biol 1999 : Furthermore, the specific phosphatidylinositol-3 (PI-3) kinase inhibitor LY294002 inhibited the induction of phosphorylation of Ser18 of p53 by adriamycin to a higher degree in PKR+/+ cells than in PKR-/- cells
Latonen et al., Cell Signal 2003 : p53 and MDM2 are regulated by PI-3-kinases on multiple levels under stress induced by UV radiation and proteasome dysfunction
Guo et al., Mol Cell Biol 2004 : We found that ( i ) p19(Arf) or p53 deficiency led to a significant increase in PI 3-kinase activity, which in turn upregulated RhoA and Rac1 activities ; ( ii ) deletion of p19Arf or p53 led to an increase in cell growth rate that was in part dependent on RhoA, Rac1, and Cdc42 activities ; ( iii ) p19(Arf) or p53 deficiency caused an enhancement of the growth related transcription factor NF-kappa B and cyclin D1 activities that are partly dependent on RhoA or Cdc42 but not on Rac1 ; ( iv ) forced expression of the activating mutants of Rac1, RhoA, or Cdc42 caused a hyperproliferative phenotype of the p19Arf ( -/- ) and p53 ( -/- ) cells and promoted transformation of both cells ; ( v ) RhoA appeared to contribute to p53 regulated cell proliferation by modulating cell cycle machinery, while hyperactivation of RhoA further suppressed a p53 independent apoptotic signal ; and ( vi ) multiple pathways regulated by RhoA, including that of Rho-kinase, were required for RhoA to fully promote the transformation of p53 ( -/- ) cells
Cordero-Herrera et al., Nutr Cancer 2013 : In this study, the in vitro anticancer effects of ECG on SW480 colon cancer cell line was investigated by analyzing the cell cycle, apoptosis, key proteins involved in cellular survival/proliferation, namely AKT/phosphatidylinositol-3-kinase (PI3K) and mitogen activated protein kinases ( MAPKs ), and the role of p53 in these processes