mTOR controls mitochondrial oxidative function through a YY1–PGC-1α transcriptional complex

By John T. Cunningham, J. T. Rodgers, Daniel H Arlow, F. Vazquez, Vamsi K. Mootha, P. Puigserver. Nature, 2007

1,397 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/a1a4a9cf6d88e2a29d37dab11564d51d1dd57acf

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Citations in the corpus

Akt stimulates hepatic SREBP1c and lipogenesis through parallel mTORC1-dependent and independent pathways (2011, background): “As mitochondria are the major site of β-oxidation and mTORC1 signaling has been proposed to promote mitochondrial biogenesis (Cunningham et al., 2007), we also measured levels of mitochondrial markers.”
Transcriptional control of mitochondrial biogenesis and function. (2009, background): “These protein surfaces include leucine-rich motifs that mediate interactions with nuclear receptors (16, 45, 94, 95); a conserved DHDY motif that binds HCF and presumably enables interactions with GABP (17, 33, 34); and less well-characterized interfaces for NRF-1, YY1, and other transcription facto”
Reprogramming of fatty acid metabolism in cancer (2019, background): “Furthermore, mTORC1 and mTORC2 downstream of oncogenic PI3K promote oxidative phosphorylation through PGC-1α-dependent mitochondrial biosynthesis, and synthesis of cardiolipins, which enhance respiration and improve mitochondrial activity.(91,102) Therefore, hyperactive PI3K signalling provides a cl”
PGC-1α, Inflammation, and Oxidative Stress: An Integrative View in Metabolism (2020, background): “Interestingly, PGC-1α is able to self-regulate its own transcription through YingYang1 (YY1), in a direct interaction that requires the presence of mTOR, thus stimulating mitochondrial activity [28].”
Mitochondrial DNA: more than an evolutionary bystander (2014, background): “2006), and mTOR inhibition reduced the association of PGC-1a with the transcription factor YY1, leading to lower expression of several genes encoding mitochondrial proteins (Cunningham et al. 2007).”
mTOR signaling in growth control and disease (2012, background): “Additional evidence is needed to support this connection because the YY1 response element was not identified as a motif enriched in the promoters of mTORC1-regulated genes (Düvel et al., 2010) and little endogenous mTORC1 is found in the nucleus (Sancak et al., 2010; Sancak et al., 2008; Zoncu et a”
mTOR Signaling in Growth, Metabolism, and Disease (2017, background): “Paradoxically, however, chronic pharmacological inhibition of mTORC1 using rapamycin has the opposite effect, causing insulin resistance and impaired glucose homeostasis (Figure 4D; Cunningham et al., 2007).”
Regulation of Immune Responses by mTOR (2011, background): “Indeed, mTORC1 inhibition leads to an increase in autophagy, whereas mitochondrial biosynthesis is enhanced in the setting of increased mTORC1 activation (39, 40).”
Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate (2012, background): “…1970; Tallal et al., 1970). mTORC1 has also been shown to have direct effects on promoting mitochondrial biogenesis, in part via a transcriptional complex that promotes the function of PGC-1a (Bentzinger et al., 2008; Cunningham et al., 2007; Ramanathan and Schreiber, 2009; Schieke et al., 2006).”