Regulation of Mitochondrial Biogenesis in Skeletal Muscle by CaMK
By Hai Wu, S. Kanatous, F. Thurmond, T. Gallardo, E. Isotani, R. Bassel-Duby, R. S. Williams. Science, 2002
723 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/09f42736d8703901f207c7d71c898a881c9ef202
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In Cancer Research
- B. Spiegelman
- J. Hawley
- J. Zierath
- R. Scarpulla
- Jiandie D. Lin
- B. Egan
- Gerald I. Shulman
- K. Petersen
In Molecular Biology
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- Christoph Handschin
- Gerald I. Shulman
- J. Zierath
- J. Hawley
- Jiandie D. Lin
- D. Kelly
In Physiology
- B. Spiegelman
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- J. Hawley
- Christoph Handschin
- J. Zierath
- Johan Auwerx
- Gerald I. Shulman
- Jiandie D. Lin
Citations in the corpus
- Resveratrol improves mitochondrial function and protects against metabolic disease by activating SIRT1 and PGC-1alpha. (2006, background): “Comparable changes in muscle fiber types have been recapitulated in genetically engineered mouse models that trigger calcium regulatory pathways (Wu et al., 2002), mimic PPARb/d activation (Wang et al.”
- Metabolic control through the PGC-1 family of transcription coactivators. (2005, background): “…Huss et al., 2002; Huss et al., 2004; Kamei et al., 2003; ERRα,β,γ + + mitochondrial genes Mootha et al., 2004; Schreiber et al., 2004 TRβ + + cpt-1 induction Wu et al., 2002; Zhang et al., 2004b; Shin et al., 2003 LXRα,β + + lipoprotein secretion Lin et al., 2005; Oberkofler et al., 2003 FXR + ND…”
- Transcriptional paradigms in mammalian mitochondrial biogenesis and function. (2008, background): “Calcium signaling has also been associated with a PGC-1-dependent pathway of mitochondrial biogenesis in skeletal muscle (155, 235).”
- Regulation of Muscle Fiber Type and Running Endurance by PPARδ (2004, background): “…described here are remarkably similar to those of transgenic mice expressing either calcineurin, calmodulin-dependent kinase, or PGC-1 a (Naya et al. 2000; Lin et al. 2002; Wu et al. 2002), indicating that PPAR d could be one of the hypothetical downstream transcription factors of these pathways.”
- Transcriptional regulatory circuits controlling mitochondrial biogenesis and function. (2004, background): “First, overexpression of CaMK in the skeletal muscle of transgenic mice triggers a robust mitochondrial biogenesis associated with an induction of PGC-1 expression (Wu et al. 2002).”
- Regulation of mitochondrial biogenesis (2010, background): “In addition, mRNA expression of cytochrome b and carnitine palmitoyltransferase-1 was increased in the transgenic mice [23].”
- The Mitochondrial Basis of Aging (2016, background): “…by a number of physiological adaptations; however, one of the most beneficial effects appears to be stimulation of mitochondrial biogenesis in a wide variety of tissues, including the brain (Arany et al., 2005; Egan and Zierath, 2013; Rowe et al., 2014; Steiner et al., 2011; Wu et al., 2002).”
- Exercise metabolism and the molecular regulation of skeletal muscle adaptation. (2013, background): “CaMKs and calcium signaling influence glucose transport (Wright et al., 2004), lipid uptake and oxidation (Raney and Turcotte, 2008), and skeletal muscle plasticity (Wu et al., 2002).”
- Disordered lipid metabolism and the pathogenesis of insulin resistance. (2007, neutral): “Together, these data suggest that alterations in nuclear-encoded genes that regulate mitochondrial biogenesis such as PPAR- coactivator 1 (PGC-1 ), AMP kinase (7, 132), and calmodulin IV kinase (125) may form the genetic basis for inheritance of at least some forms of T2DM.”
- Cell and Molecular Biology (2009, background): “, 1999), specifically CaMKII and CaMKIV (Rose et al., 2007; Wu et al., 2002) and calcineurin, a calcium–calmodulin (CaM)-dependent protein phosphatase (Bigard et al.”
- Transcriptional control of mitochondrial biogenesis and function. (2009, background): “Second, transgenic mice expressing constitutively active calcineurin or CAMKIV in muscle show increased mtDNA content, mitochondrial volume, and PGC-1α levels (143, 144).”
- Deficiency of subsarcolemmal mitochondria in obesity and type 2 diabetes. (2005, methodology): “subsarcolemmal mitochondria, using a previously published method (28).”