mTOR- and HIF-1α–mediated aerobic glycolysis as metabolic basis for trained immunity
By Shih-Chin Cheng, J. Quintin, R. Cramer, K. Shepardson, Sadia Saeed, Vinod Kumar, E. Giamarellos‐Bourboulis, J. Martens, Nagesha A S Rao, A. Aghajanirefah and 16 more. Science, 2014
2,008 citations recorded by the source corpus.
Subfields: Immunology
View Paper: https://www.semanticscholar.org/paper/44c2b4ad910392e3e0c6d104f24e5ac278bbd71a
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In Immunology
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Citations in the corpus
- Modulation of Myelopoiesis Progenitors Is an Integral Component of Trained Immunity (2018, background): “…progenitor cells, such as glycolysis and cholesterol metabolism, which also accompany the induction of trained innate immunity in mature cells and are involved in innate immune cell adaptation to diverse stimuli (Arts et al., 2016b; Cheng et al., 2014; Mills and O’Neill, 2016; Norata et al., 2015).”
- T cell metabolism drives immunity (2015, background): “This idea has recently been extended to innate immune cells under the novel concept of trained immunity, whereby metabolic priming confers superior immunity to a secondary pathogenic insult (Cheng et al., 2014).”
- Metabolic Induction of Trained Immunity through the Mevalonate Pathway. (2018, neutral): “The increase in lactate suggested activation of the glycolytic pathway similar to b-glucan-trained macrophages (Cheng et al., 2014).”
- Glutaminolysis and Fumarate Accumulation Integrate Immunometabolic and Epigenetic Programs in Trained Immunity (2016, methodology): “We used the previously described in vitro model of trained immunity (Cheng et al., 2014) in which purified monocytes are stimulated for 24 hr with RPMI, b-glucan, or LPS, after which cells are washed and rested for 5 days in cul- ture medium, followed by a second 24 hr stimulation with…”
- Initiation and perpetuation of NLRP3 inflammasome activation and assembly (2015, neutral): “caspase-1) have not been investigated (31, 32).”
- Proliferation, survival and metabolism: the role of PI3K/AKT/mTOR signalling in pluripotency and cell fate determination (2016, background): “On the one hand, mTORC1 upregulates the expression of hypoxia-inducible factor 1 (HIF1), which promotes glycolysis by diverting pyruvate into lactate (Kim et al., 2006; Cheng et al., 2014) and is further enhanced by mTORC2-mediated activation of AKT via S473 phosphorylation.”