The Senescence‐Related Mitochondrial/Oxidative Stress Pathway is Repressed in Human Induced Pluripotent Stem Cells
By A. Prigione, B. Fauler, R. Lurz, Hans Lehrach. Stem Cells, 2010
601 citations recorded by the source corpus.
Subfields: Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/358908364f84770b24a952e7dc3eb282457b76dc
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In Molecular Biology
- Sheng Ding
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In Physiology
Citations in the corpus
- Proliferation, survival and metabolism: the role of PI3K/AKT/mTOR signalling in pluripotency and cell fate determination (2016, background): “Compared with differentiated cells, which utilise oxidative phosphorylation as the primary metabolic pathway, these PSCs possess largely underdeveloped and immature mitochondria that are few in number, thus maintaining high rates of glycolysis even under aerobic culture conditions, although a recent”
- The return of metabolism: biochemistry and physiology of the pentose phosphate pathway (2014, background): “Biological Reviews published by John Wiley & Sons Ltd on behalf of Cambridge Philosophical Society. and TKT ) is augmented (Folmes et al., 2011; Prigione et al., 2011; Varum et al., 2011).”
- Metabolic Plasticity in Stem Cell Homeostasis and Differentiation (2012, unknown): “In addition, reduction of the mtDNA copy number in the setting of constant nuclear encoded mitochondrial gene expression and upregulation in mitochondrial biogenesis genes underlies reprogramming (Prigione et al., 2010).”
- Reprogramming of human primary somatic cells by OCT4 and chemical compounds. (2010, background): “It has been shown that differentiated somatic cells typically use mitochondrial oxidation while pluripotent cells mainly use glycolysis for cell proliferation (Manning and Cantley, 2007; Kondoh et al., 2007; Vander Heiden et al., 2009; Prigione et al., 2010).”
- Somatic oxidative bioenergetics transitions into pluripotency-dependent glycolysis to facilitate nuclear reprogramming (2011, background): “In fact, mitochondrial regression and reduction of mtDNA as a result of nuclear reprogramming are consistent with the undeveloped mitochondrial morphology of ESC (Kondoh et al., 2007; Armstrong et al., 2010; Prigione et al., 2010; Zeuschner et al., 2010).”