Errα and Gabpa/b specify PGC-1α-dependent oxidative phosphorylation gene expression that is altered in diabetic muscle
By Vamsi K. Mootha, Christoph Handschin, Daniel H Arlow, Xiaohui S. Xie, J. Pierre, S. Sihag, Wenli Yang, David Altshuler, P. Puigserver, Nick Patterson and 5 more. 2004
656 citations recorded by the source corpus.
Subfields: Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/068d15cfa6fe2e1f1129d1e67ccd10a0e9800d6d
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In Molecular Biology
- B. Spiegelman
- R. Scarpulla
- Christoph Handschin
- Jiandie D. Lin
- Johan Auwerx
- M. Hock
- A. Kralli
- P. Seale
In Physiology
- B. Spiegelman
- R. Scarpulla
- Johan Auwerx
- Christoph Handschin
- Jiandie D. Lin
- P. Seale
- Wenli Yang
- Marc Uldry
Citations in the corpus
- Exercise induces hippocampal BDNF through a PGC-1α/FNDC5 pathway (2013, background): “Treatment of primary cortical neurons with XCT 790 (1 mM), a selective ERRa inhibitor (inverse agonist) which disrupts the ERRa/PGC-1a transcriptional complex (Mootha et al., 2004), significantly reduced Fndc5 gene expression compared to vehicle-treated cells (Figure 4C).”
- Metabolic control of muscle mitochondrial function and fatty acid oxidation through SIRT1/PGC‐1α (2007, background): “In addition, interaction of PGC-1a with PPARa and ERRa transcription factors potently induces fatty acid oxidation genes such as MCAD and CPT-1b (Vega et al, 2000; Huss et al, 2002; Mootha et al, 2004; Schreiber et al, 2004).”
- Complementary action of the PGC-1 coactivators in mitochondrial biogenesis and brown fat differentiation. (2006, methodology): “Total and uncoupled respiration were measured as published (Mootha et al., 2004; St-Pierre et al., 2003).”
- Resveratrol improves mitochondrial function and protects against metabolic disease by activating SIRT1 and PGC-1alpha. (2006, background): “One gene whose decreased expression is consistently implicated in the human or animal diabetic muscle is the peroxisome proliferator-activated receptor g coactivator, PGC1a (Mootha et al., 2004; Patti et al., 2003; Sparks et al., 2005).”
- Transcriptional control of mitochondrial biogenesis and function. (2009, background): “ERRα also acts on mitochondrial gene expression through indirect mechanisms by regulating the expression of GAPBα and PPARα (30, 75). siRNA and pharmacological approaches have shown that endogenous ERRα is required for the ability of exogenously expressed PGC-1α to induce mitochondrial biogenesis an”
- Sirtuin 3, a New Target of PGC-1α, Plays an Important Role in the Suppression of ROS and Mitochondrial Biogenesis (2010, background): “). PGC-1α transactivates transcription of genes involved in oxidative phosphorylation through coactivating ERRα”
- PGC1α Expression Defines a Subset of Human Melanoma Tumors with Increased Mitochondrial Capacity and Resistance to Oxidative Stress (2013, neutral): “In this regard, although small molecules targeting PGC1a do not currently exist, inhibitors of estrogen-related receptors (ERRs), key PGC1 transcription factor partners (Mootha et al., 2004; Chang et al., 2011; Schreiber et al., 2004; Eichner andGiguère, 2011;Wende et al., 2005), could potentially b”
- Transcriptional coactivator PGC-1α controls the energy state and contractile function of cardiac muscle (2005, background): “In addition, the expression of a number of transcription factors known to act in a positive feedback loop with PGC-1α, including PPAR-α and ERR-α (Huss et al., 2004; Mootha et al., 2004), was also decreased (Table 1) in KO mice, likely contributing to the reduction of target gene expression.”
- Metabolic control of mitochondrial biogenesis through the PGC-1 family regulatory network (2010, background): “ERRα may also exert direct control over GABPα transcriptional expression [30].”