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Oncogene-induced Nrf2 transcription promotes ROS detoxification and tumorigenesis
Oncogene-directed increased expression of Nrf2 is a new mechanism for the activation of the NRF2 antioxidant program, and is evident in primary cells and tissues of mice expressing K-RasG12D and B-RafV619E, and in human pancreatic cancer.
Foxp3 Reprograms T Cell Metabolism to Function in Low-Glucose, High-Lactate Environments.
Distinct Signaling of Coreceptors Regulates Specific Metabolism Pathways and Impacts Memory Development in CAR T Cells.
Non-cyclooxygenase-derived prostanoids (F2-isoprostanes) are formed in situ on phospholipids.
- J. Morrow, J. Awad, H. Boss, I. Blair, L. Roberts
- Biology, ChemistryProceedings of the National Academy of Sciences…
- 15 November 1992
The formation of these phospholipid species in lipid bilayers may contribute in an important way to alterations in fluidity and integrity of cellular membranes, well-known sequelae of oxidant injury.
Akt-mTORC1 signaling regulates Acly to integrate metabolic input to control of macrophage activation
It is proposed that Akt-mTORC1 signaling calibrates metabolic state to energetically demanding aspects of M2 activation, which may define a new role for metabolism in supporting macrophage activation.
Akt-dependent metabolic reprogramming regulates tumor cell histone acetylation.
Association of CYP3A4 genotype with treatment-related leukemia.
- C. Felix, A. Walker, T. Rebbeck
- Biology, MedicineProceedings of the National Academy of Sciences…
- 27 October 1998
The data suggest that individuals with CYP3A4-W genotype may be at increased risk for treatment-related leukemia and that epipodophyllotoxin metabolism by CYP 3A4 may contribute to the secondary cancer risk.
Evidence for Intramyocardial Disruption of Lipid Metabolism and Increased Myocardial Ketone Utilization in Advanced Human Heart Failure
These findings indicate increased ketone utilization in the severely failing human heart independent of diabetes mellitus, and they support the role of ketone bodies as an alternative fuel and myocardial ketone oxidation as a key metabolic adaptation in the failing humanheart.
DNA topoisomerase II in therapy-related acute promyelocytic leukemia.
Drug-induced cleavage of DNA by topoisomerase II mediates the formation of chromosomal translocation breakpoints in mitoxantrone-related APL and in APL that occurs after therapy with other topoisomersase II poisons.