Myc Stimulates Nuclearly Encoded Mitochondrial Genes and Mitochondrial Biogenesis
By Feng Li, Yunyue Wang, K. Zeller, J. Potter, Diane R. Wonsey, Kathryn A. O’Donnell, Jung-whan Kim, Jason T. Yustein, Linda A. Lee, C. V. Dang. Molecular and Cellular Biology, 2005
629 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/08f30760177e6a6c2b6be0c6332503b7265b9934
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In Molecular Biology
- C. V. Dang
- G. Semenza
- Ralph J. Deberardinis
- Navdeep S. Chandel
- Craig B. Thompson
- M. V. Vander Heiden
- Ping Gao
- Huafeng Zhang
Citations in the corpus
- Myc regulates a transcriptional program that stimulates mitochondrial glutaminolysis and leads to glutamine addiction (2008, background): “Despite this, Myctransformed cells display an increased mitochondrial mass and increased rate of O2 consumption (21).”
- Metabolic control of mitochondrial biogenesis through the PGC-1 family regulatory network (2010, background): “Finally, c-myc is associated with the expression of certain NRF-1 target genes [32] and myc null fibroblasts are deficient in mitochondrial content [33].”
- Cancer's molecular sweet tooth and the Warburg effect. (2006, background): “In immortalized rat fibroblasts, Myc is able to enhance aerobic glycolysis; however, activation of MYC in a human B cell model resulted in increased respiration that was associated with increased mitochondrial biogenesis (5).”
- Transcriptional paradigms in mammalian mitochondrial biogenesis and function. (2008, background): “In addition, Myc null fibroblasts were found deficient in mitochondrial content, and c-Myc expression in these cells partially restored mitochondrial mass (121).”
- MYC, Metabolism, and Cancer. (2015, background): “Correspondingly, loss of Myc function through Cre recombinase treatment of T cells with a floxed allele of Myc or in knockout fibroblasts was associated with severely deficient mitochondrial mass and morphology (173).”
- HIF-1 inhibits mitochondrial biogenesis and cellular respiration in VHL-deficient renal cell carcinoma by repression of C-MYC activity. (2007, background): “Previous studies demonstrated that TFAM is a C-MYC target gene in lymphoid cells (Li et al., 2005), but TFAM mRNA levels were not correlated with C-MYC activity or VHL status in RCC4 cells (data not shown).”
- Reprogramming of glucose, fatty acid and amino acid metabolism for cancer progression (2015, background): “An early study has demonstrated that cMyc also induces genes involved in mitochondrial structure and function and stimulates mitochondrial biogenesis [10].”
- Hypoxia-Inducible Factor 1 and Dysregulated c-Myc Cooperatively Induce Vascular Endothelial Growth Factor and Metabolic Switches Hexokinase 2 and Pyruvate Dehydrogenase Kinase 1 (2007, background): “Previously, we have also reported that c-Myc promotes mitochondrial biogenesis and respiration, in addition to its induction of glycolytic enzyme genes (38, 46, 59, 78).”
- Hypoxia-inducible factors in stem cells and cancer (2009, positive): “It has been previously shown that cMyc promotes mitochondrial biogenesis [93].”
- Mitochondrial complex III ROS regulate adipocyte differentiation (2011, positive): “Mitochondrial biogenesis was assessed by measuring mitochondrial DNA copy number as previously described (Li et al., 2005).”
- Transcriptional control of mitochondrial biogenesis and function. (2009, background): “Consistent with the binding and gene expression studies, c-Myc null cells have diminished mitochondrial mass (90).”
- Links between metabolism and cancer. (2012, background): “Myc was subsequently shown to activate genes involved in mitochondrial biogenesis and function as well as those involved in glutamine metabolism (Li et al. 2005; Wise et al. 2008; Gao et al. 2009).”
- Glucose-independent glutamine metabolism via TCA cycling for proliferation and survival in B-cells (2012, positive): “In this regard, our previous studies documented the ability of MYC to induce mitochondrial biogenesis, function, and enhanced oxygen consumption (Li et al., 2005), which persisted under hypoxia (Figure 7C).”