Activation of SAT1 engages polyamine metabolism with p53-mediated ferroptotic responses
By Yang Ou, Shang-Jui Wang, Dawei Li, Bo Chu, W. Gu. Proceedings of the National Academy of Sciences of the United States of America, 2016
716 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/a83add43994dec955a2aa0d3b98a77e3cdc52b61
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Citations in the corpus
- Targeting p53 pathways: mechanisms, structures and advances in therapy (2023, background): “130 ALOX12 was also reported to be required for p53-mediated ferroptosis.”
- ROS Generation and Antioxidant Defense Systems in Normal and Malignant Cells (2019, background): “Additionally, PA metabolism was linked to p53-mediated ferroptosis in response to oxidative stress [116].”
- The Tumor Suppressor p53 Limits Ferroptosis by Blocking DPP4 Activity. (2017, neutral): “, 2015), or transcriptional induction of spermidine/spermine N(1)-acetyltransferase 1 and glutaminase 2, two genes involved in lipid peroxidation (Jennis et al., 2016; Ou et al., 2016).”
- Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease. (2017, neutral): “…have been implicated as modulators of sensitivity to ferroptosis or markers of ferroptosis in diverse contexts: SAT1, which lies downstream of p53 (Ou et al., 2016) is involved in polyamine metabolism; kiss of death (KOD) in Arabidopsis (Distefano et al., 2017) and FANCD2 in bone marrow stromal…”
- The Tumor Suppressor Protein p53 and the Ferroptosis Network (2018, neutral): “However, only ferrostatin-1, but not other cell death inhibitors (Z-VAD-FMK, necrostatin-1, and 3-methyladenine), can inhibit ROS-induced cell death in SAT1 Tet-on cells [13].”
- The interaction between ferroptosis and lipid metabolism in cancer (2020, background): “On the one hand, P53 can promote the accumulation of lipid hydroperoxides to enhance ferroptosis by increasing the expression levels of 15-LOX by promoting the expression of spermidine/ spermine N1-acetyltransferase1 (STA1), or increasing the expression of GLS2, and activating the function of 12-LOX”