AMP-activated protein kinase (AMPK) action in skeletal muscle via direct phosphorylation of PGC-1alpha.
By Sibylle Jäger, Christoph Handschin, J. St-Pierre, B. Spiegelman. Proceedings of the National Academy of Sciences of the United States of America, 2007
1,034 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/f62cda84e6702f41aac1c0136541cfba563dd538
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Citations in the corpus
- The mitophagy pathway and its implications in human diseases (2023, background): “160 In addition, AMP could be converted to cyclic AMP (cAMP) by adenylate cyclase (AC), which regulates PGC-1 α through the cAMP-PKA-CREB pathway to promote mitochondrial biogenesis.”
- Mitochondrial dysfunction and oxidative stress in metabolic disorders - A Step towards mitochondria based therapeutic strategies (2016, background): “Also, regular exercise triggersmanyother signallingpathways involved in skeletalmuscle mitochondrial biogenesis, dynamics and metabolism in healthy and aged persons [174,175].”
- AMPK in Health and Disease. (2009, background): “Since the constitutively active AMPK fragment 1 (1-312) is not activated by the PT1 compound, it is proposed that PT1 acts by reversing the autoinhibition of the AIS (313-335).”
- Metabolic control of mitochondrial biogenesis through the PGC-1 family regulatory network (2010, background): “This results in increased mitochondrial gene expression supporting the idea that AMPK can mediate at least some of its effects through PGC-1α [67].”
- Interdependence of AMPK and SIRT1 for metabolic adaptation to fasting and exercise in skeletal muscle (2010, background): “In line with this, AMPK acts on mitochondrial gene expression through PGC-1a (Jager et al., 2007), which itself is dispensable for mitochondrial gene induction after exercise (Leick et al.”
- AMP-Activated Protein Kinase–Deficient Mice Are Resistant to the Metabolic Effects of Resveratrol (2009, methodology): “Reactive oxygen species (ROS) levels were determined in muscle extracts using the ROS-sensitive fluorescent dye dichlorodihydrofluorescein (DCF), as previously described (29,30).”
- LKB1 and AMPK control of mTOR signalling and growth (2009, background): “The picture in skeletal muscle is likely to be complex, as both AMPK and mTOR have been reported to stimulate PGC-1a-dependent mitochondrial biogenesis in this tissue, albeit via distinct mechanisms (Cunningham et al. 2007, Jager et al. 2007).”
- Mitochondrial dynamics in health and disease: mechanisms and potential targets (2023, background): “127 PGC-1 α stimulates the biological production of mitochondria through the ampli fi cation of mitochondrial genes encoding nuclear protein, including those involved in mitochondrial fusion and OXPHOS.”
- SIRT1 and other sirtuins in Metabolism (2013, background): “The combined result is increased mitochondrial biogenesis and fatty acid oxidation in the muscle [75,77].”
- AMPK: an emerging drug target for diabetes and the metabolic syndrome. (2009, background): “AMPK activation has been shown to increase mitochondrial genes in skeletal muscle via PGC-1a induction (Jager et al., 2007).”
- Mitochondria: In Sickness and in Health (2012, background): “Sirt1 responds to elevated levels of NAD that occur upon starvation and, together with AMPK, coordinately regulates mitochondrial mass, nutrient oxidation, and ATP production to fit a cell’s particular needs via the transcription cofactor, peroxisome proliferator-activated receptor gamma coactivator”
- SIRT1 is required for AMPK activation and the beneficial effects of resveratrol on mitochondrial function (2012, background): “PGC-1a is also activated by another important metabolic sensor, the AMP-activated protein kinase (AMPK) (Jager et al., 2007).”
- Sirt1 and the Mitochondria (2016, background): “shown to directly phosphorylate PGC-1α (Jäger et al., 2007),”