Cytokine stimulation of energy expenditure through p38 MAP kinase activation of PPARgamma coactivator-1.
By P. Puigserver, James Rhee, Jiandie D. Lin, Zhidan Wu, J.Cliff Yoon, Chen-Yu Zhang, S. Krauss, Vamsi K. Mootha, Bradford B. Lowell, B. Spiegelman. Molecules and Cells, 2001
785 citations recorded by the source corpus.
Subfields: Epidemiology, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/6723fd53f8b934c61162376c12cb67dac7e622ec
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In Epidemiology
- A. Chawla
- J. Odegaard
- Jianping Ye
- P. Murray
- B. Spiegelman
- Lata Mukundan
- Christoph Handschin
- Jiandie D. Lin
In Molecular Biology
In Physiology
Citations in the corpus
- Butyrate Improves Insulin Sensitivity and Increases Energy Expenditure in Mice (2009, background): “Their activities may contribute to elevation of the PGC-1α protein through enhancing protein stability (26-28).”
- Exercise metabolism and the molecular regulation of skeletal muscle adaptation. (2013, background): “PGC-1a activity is highly regulated by numerous posttranslational modifications including phosphorylation and deacetylation (Puigserver et al., 2001; Jäger et al., 2007; Cantó et al., 2009).”
- Oxidative metabolism and PGC-1beta attenuate macrophage-mediated inflammation. (2006, background): “By interacting with tissue-specific transcription factors, the PGC-1 proteins regulate various cellular processes, including thermogenesis, muscle fiber type specification, gluconeogenesis, lipogenesis, and cytokine signaling (Lin et al., 2002,2005b;Puigserver et al., 1998,2001;Yoon et al., 2001).”
- Transcriptional control of mitochondrial biogenesis: the central role of PGC-1alpha. (2008, background): “PGC-1a phosphorylation by p38MAPK, for example, is most likely involved in mediating the effects of cytokines.(65,66) An interesting observation made recently is that, in addition to increasing PGC-1a expression, AMPK can directly phosphorylate PGC-1a, this phosphorylation being required for the PGC”
- Mitochondrial biogenesis and mitochondrial DNA maintenance of mammalian cells under oxidative stress. (2005, background): “It was reported that P can be activated by a p38 MAPK-sensitive pathw nd that PPAR gene expression is dependent on APK activation (Puigserver et al., 2001).”