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PPARGC1A — PRKAG2
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Terada et al., Am J Physiol Endocrinol Metab 2004
:
These results suggest that exercise induced
PGC-1alpha expression in skeletal muscle may be
mediated by at least two exercise induced signaling factors :
AMPK activation and Ca2+ elevation
Oliveira et al., Am J Physiol Endocrinol Metab 2004
:
Finally, reduction of
PGC-1alpha resulted in lower Thr172 phosphorylation of
AMPK
Winder et al., Med Sci Sports Exerc 2006
:
There is substantial evidence for a role of AMPK in inducing adaptations to endurance training : 1 ) AMPK is activated in response to muscle contraction ; 2 ) chronic chemical activation of AMPK results in increases in GLUT4, hexokinase 2, UCP-3, and citric acid cycle enzymes ; 3 ) muscle contraction and chemical activation of
AMPK both
result in increases in
PGC-1alpha , a transcriptional coactivator involved in stimulation of mitochondrial biogenesis ; and 4 ) increases in muscle PGC-1 alpha, delta-aminolevulinic acid synthetase, and mitochondrial DNA induced by chronic creatine phosphate depletion in wild-type mice are not observed in dominant negative AMPK mice
Pirinen et al., Mol Cell Biol 2007
(Glucose Intolerance) :
As accelerated polyamine flux caused by SSAT overexpression depleted the ATP pool in adipocytes of SSAT mice and N ( 1 ), N ( 11 ) -diethylnorspermine treated wild-type fetal fibroblasts, we propose that low ATP levels lead to the induction of
AMPK , which in turn
activates PGC-1 alpha in WAT of SSAT mice
Jäger et al., Proc Natl Acad Sci U S A 2007
:
The peroxisome-proliferator activated receptor gamma coactivator 1alpha ( PGC-1alpha ) has emerged as a master regulator of mitochondrial biogenesis ; furthermore, it has been shown that
PGC-1alpha gene expression is
induced by exercise and by chemical activation of
AMPK in skeletal muscle ... Using primary muscle cells and mice deficient in PGC-1alpha, we found that the
effects of
AMPK on gene expression of glucose transporter 4, mitochondrial genes, and
PGC-1alpha itself are almost entirely dependent on the function of PGC-1alpha protein
Irrcher et al., PloS one 2008
:
AMPK activation for 24 hours
increased PGC-1alpha promoter activity with concomitant increases in mRNA expression
Irrcher et al., Am J Physiol Cell Physiol 2009
:
The activation of
AMPK using 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside
increased PGC-1alpha promoter activity and mRNA levels but reduced ROS production ... Thus the net
effect of
AMPK activation on
PGC-1alpha expression was a result of increased transcriptional activation, counterbalanced by reduced ROS production
Łabuzek et al., Neurotoxicology 2010
:
The presented evidence supports the conclusion that
AMPK activated by AICAR is
involved in regulation of ROS and cytokine production ( IL-1 beta, TNF-alpha ( 6h ), IL-10 and TGF-beta ) as well as arginase I and
PGC-1alpha expression
Yu et al., Neuroscience 2010
(Blindness) :
Here, we use primary cultures of rat visual cortical neurons and a rat model of monocular deprivation ( MD ) to investigate whether
AMP activated protein kinase (AMPK) is implicated in mediating activity dependent
regulation of
PGC-1alpha and NRF-1 expression in neurons ... Similarly, pharmacological activation of
AMPK with 5'-aminoimidazole-4-carboxamide riboside ( AICAR ) or resveratrol also markedly
increases PGC-1alpha and NRF-1 mRNA levels in neuron cultures
Fillmore et al., J Appl Physiol 2010
:
The additive increase of mitochondrial markers observed in the white quadriceps may be explained by a combined effect of two separate mechanisms : high-fat diet induced posttranscriptional increase in PGC-1alpha protein and
AMPK mediated
increase in
PGC-1alpha protein via a transcriptional mechanism