Energy metabolism and cytochrome oxidase activity: linking metabolism to gene expression

Canadian Journal of Zoology, Volume 92, Issue 7, Page 557-568, July 2014. Modification of mitochondrial content demands the synthesis of hundreds of proteins encoded by nuclear and mitochondrial genomes. The responsibility for coordination of this process falls to nuclear-encoded master regulators of transcription. DNA-binding proteins and coactivators integrate information from energy-sensing pathways and hormones to alter mitochondrial gene expression. In mammals, the signaling cascade for mitochondrial biogenesis can be described as follows: hormonal signals and energetic information are sensed by protein-modifying enzymes that in turn regulate the post-translational modification of transcription factors. Once activated, transcription-factor complexes form on promoter elements of many of the nuclear-encoded mitochondrial genes, recruiting proteins that remodel chromatin and initiate transcription. One master regulator in mammals, PGC-1α, is well studied because of its role in determining the metabolic phenotype of muscles, but also due to its importance in mitochondria-related metabolic diseases. However, relatively little is known about the role of this pathway in other vertebrates. These uncertainties raise broader questions about the evolutionary origins of the pathway and its role in generating the diversity in muscle metabolic phenotypes seen in nature.
Source: Canadian Journal of Zoology - Category: Zoology Tags: article Source Type: research

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Authors: Meunier L, Larrey D Abstract Some drugs may induce hepatotoxic lesions, such as steatosis or steatohepatitis found in Non-Alcoholic Fatty Liver Disease (NAFLD). Among these drugs there are some anti-tumoral molecules, such as methotrexate, 5-fluorouracil, irinotecan, tamoxifen and l-asparaginase. The hepatotoxic phenotype developed from treatment with such drugs is known as "CASH" for "Chemotherapy-induced Acute Steatohepatitis". The mechanism of toxicity is essentially based on mitochondrial toxicity. These lesions are chronic and often reversible when the treatment is stopped. Contrib...
Source: Annals of Hepatology - Category: Gastroenterology Tags: Ann Hepatol Source Type: research
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Source: Mitochondrion - Category: Biochemistry Source Type: research
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Source: Genes - Category: Genetics & Stem Cells Authors: Tags: Article Source Type: research
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Source: Fight Aging! - Category: Research Authors: Tags: Investment Source Type: blogs
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Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - Category: Molecular Biology Source Type: research
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Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
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Source: Phytomedicine - Category: Drugs & Pharmacology Source Type: research
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Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - Category: Molecular Biology Source Type: research
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Source: Molecules - Category: Chemistry Authors: Tags: Article Source Type: research
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Source: Current Alzheimer Research - Category: Neurology Authors: Tags: Curr Alzheimer Res Source Type: research
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