Transcriptional regulation of gene expression in human skeletal muscle during recovery from exercise.
By H. Pilegaard, G. Ordway, Bengt Saltin, P. Neufer. American Journal of Physiology. Endocrinology and Metabolism, 2000
617 citations recorded by the source corpus.
Subfields: Cell Biology, Physiology, Rehabilitation
View Paper: https://www.semanticscholar.org/paper/6dcb6a19f9ef2b9cf0e2f036ecb6376b13a6d118
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cell Biology
In Physiology
In Rehabilitation
Citations in the corpus
- The Molecular Bases of Training Adaptation (2007, methodology): “The results showing an up-regulation of these genes in endurance-trained subjects are in agreement with previous findings (Pilegaard et al. 2000; Gavin et al. 2004; Cartoni et al. 2005; Mahoney et al. 2005) and provide further support for their proposed roles in exercise-induced regulation of mitoch”
- Exercise induces transient transcriptional activation of the PGC‐1α gene in human skeletal muscle (2003, methodology): “Reverse transcription of both nascent RNA (from the nuclear runon reactions) and of total RNA was performed using the Superscript II RNase H-system (Invitrogen) as previously described (Hildebrandt & Neufer, 2000; Pilegaard et al. 2000).”
- The role of FoxO in the regulation of metabolism (2008, background): “…levels in both human and rodent skeletal muscle increase under very similar circumstances, such as insulin resistance, fasting and exercise, the effects of fasting or exercise on FoxO1 in skeletal muscle remain controversial (Pilegaard et al., 2000; Peters et al., 2001; Tsintzas et al., 2006).”
- Acute exercise remodels promoter methylation in human skeletal muscle. (2012, background): “Exercise increases the messenger RNA (mRNA) expression and protein levels of a plethora of genes regulating mitochondrial function and fuel usage, including PGC-1a, transcription factor A, mitochondrial (TFAM); peroxisome proliferator-activated receptor d (PPAR-d); and pyruvate dehydrogenase kinase,”