Redox regulation of PI 3‐kinase signalling via inactivation of PTEN

By N. Leslie, D. Bennett, Y. Lindsay, Hazel Stewart, A. Gray, C. Downes. EMBO Journal, 2003

630 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/ac34c7d1695af42eeb8e0008221eef33275f8879

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Citations in the corpus

Ca2+ signalling checkpoints in cancer: remodelling Ca2+ for cancer cell proliferation and survival (2008, background): “, yet under certain acute conditions, they can enhance PKB activity through oxidative inactivation of the phosphatidylinositol (3,4,5)-trisphosphate phosphatase PTEN”
ROS Generation and Antioxidant Defense Systems in Normal and Malignant Cells (2019, background): “Moreover, oxidative stress inhibits PTEN-induced PI3K/AKT signaling, which promotes both the expression of cell survival genes and ROS production [219].”
ROS Function in Redox Signaling and Oxidative Stress (2014, background): “Increased levels of oxidized PTEN can be measured in cells shortly after stimulation with various growth factors involved in PI3K activation [28].”
Akt determines replicative senescence and oxidative or oncogenic premature senescence and sensitizes cells to oxidative apoptosis (2008, background): “Likewise, U251 human glioblastoma cells deficient in PTEN were relatively sensitive to PEITC and PEITC plus rapamycin (Figure 7A; Figures S11A and S11B).”
Phosphoinositides: tiny lipids with giant impact on cell regulation. (2013, background): “It is also of great interest that PTEN is very sensitive to oxidative damage, and hydrogen peroxide rapidly inactivates its enzymatic activity (384, 842, 874, 888, 1297).”
Mitochondrial reactive oxygen species and cancer (2014, background): “This results in inactivation of PTEN and perpetual activation of the PI3K pathway [36,37].”
Superoxide dismutases: Dual roles in controlling ROS damage and regulating ROS signaling (2018, neutral): “For example, activation of the PI3K/AKT signaling transduction pathway, one of the major targets of ROS, can promote proliferation, metabolic adaption, and cell mobility (Cantley, 2002; Leslie et al., 2003; Pelicano et al., 2006; Sullivan and Chandel, 2014).”
Intracellular messenger function of hydrogen peroxide and its regulation by peroxiredoxins. (2005, background): “Given that H2O2-dependent increases in the abundance of PIP3 and in the activity of Akt were detected in PTEN-expressing glioma cells but not in PTEN-null glioma cells, the H2O2-induced accumulation of PIP3 is likely to be chiefly attributable to oxidative inhibition of PTEN [21 ,22].”
Tenets of PTEN tumor suppression. (2008, background): “Inactivation of PTEN was observed with either hydrogen peroxide (H2O2) or endogenous ROS production in macrophages, where ROS are generated in response to cellular stress and receptor activation, and is associated with an oxidant-dependent activation of downstream signaling (Kwon et al., 2004; Lesli”