ERRα Maintains Mitochondrial Oxidative Metabolism and Constitutes an Actionable Target in PGC1α-Elevated Melanomas
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چکیده
منابع مشابه
MYC-dependent oxidative metabolism regulates osteoclastogenesis via nuclear receptor ERRα.
Osteoporosis is a metabolic bone disorder associated with compromised bone strength and an increased risk of fracture. Inhibition of the differentiation of bone-resorbing osteoclasts is an effective strategy for the treatment of osteoporosis. Prior work by our laboratory and others has shown that MYC promotes osteoclastogenesis in vitro, but the underlying mechanisms are not well understood. In...
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Vemurafenib/PLX4032, a selective inhibitor of mutant BRAFV600E, constitutes a paradigm shift in melanoma therapy. Unfortunately, acquired resistance, which unavoidably occurs, represents one major limitation to clinical responses. Recent studies have highlighted that vemurafenib activated oxidative metabolism in BRAFV600E melanomas expressing PGC1α. However, the oxidative state of melanoma resi...
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PGC1α is a transcriptional coactivator that is a central inducer of mitochondrial biogenesis in cells. Recent work highlighted that PGC1α can also modulate the composition and functions of individual mitochondria. Therefore, it is emerging that PGC1α is controlling global oxidative metabolism by performing two types of remodelling: (1) cellular remodelling through mitochondrial biogenesis, and ...
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42 43 A high fat diet can increase adiposity, leptin secretion, and plasma fatty acid concentration. In 44 hypertension, this scenario may accelerate cardiac hypertrophy and development of heart failure, 45 but could be protective by activating peroxisome proliferator-activated receptors and expression 46 of mitochondrial oxidative enzymes. We assessed the effects of a high-fat diet on the 47 d...
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Although the antioxidant and cardioprotective effects of NecroX-5 on various in vitro and in vivo models have been demonstrated, the action of this compound on the mitochondrial oxidative phosphorylation system remains unclear. Here we verify the role of NecroX-5 in protecting mitochondrial oxidative phosphorylation capacity during hypoxia-reoxygenation (HR). Necrox-5 treatment (10 µM) and non-...
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ژورنال
عنوان ژورنال: Molecular Cancer Research
سال: 2017
ISSN: 1541-7786,1557-3125
DOI: 10.1158/1541-7786.mcr-17-0143