Metabolic sensors such as AMPK and SIRT1, gatekeepers of the activity of the master regulator of mitochondria, PGC1α, are vital links in a regulatory network for metabolic homeostasis.

A key inducer of PGC-1α signaling is adenosine monophosphate-activated kinase (AMPK). Thus, the AMPK-PGC-1α signaling axis coordinates metabolic and oxidative damage responses in the central nervous system (CNS).

The metabolic stress-induced activation of AMPK upregulates PGC-1α expression, promoting mitochondrial biogenesis. PGC-1α was confirmed to enhance the transcriptional capacity of p53. Under conditions of metabolic stress, p53 recruits PGC-1α to promote its metabolic function.

Our data identify a novel AMPK-mediated regulatory pathway that regulates PGC-1α gene expression. This could represent a potential therapeutic target to control PGC-1α expression in skeletal muscle. Skeletal muscle exhibits remarkable plasticity in …

50AMP-activated protein kinase (AMPK) is considered a master regu-lator of cellular metabolism (14) and has been shown to control PGC-1a and mitochondrial enzyme gene expression in skeletal mus-cle (15).

We employed genetic approaches (stable/inducible overexpression, CRISPR/Cas9 knockout), pharmacological interventions with a novel inhibitor of AMP-activated protein kinase (AMPK) in glioblastoma cell culture systems and a proteomic approach to investigate mechanisms of metabolic plasticity.

Sep 9, 2010 · Further, we have shown that nitric oxide interacts with the metabolic sensor enzyme, AMPK. Therefore, we tested the hypothesis that nitric oxide and AMPK act synergistically to upregulate PGC-1α mRNA expression …

Metabolic sensors such as AMPK and SIRT1, gatekeepers of the activity of the master regulator of mitochondria, PGC-1alpha, are vital links in a regulatory network for metabolic homeostasis. Together, these players explain many of the beneficial …

Two metabolic sensors, AMP-activated protein kinase (AMPK) and SIRT1 have been described to directly affect PGC-1α activity through phosphorylation and deacetylation, respectively.

Jul 17, 2007 · In this work, we demonstrate two important points: first, that AMPK requires PGC-1α for many of its most important effects on GLUT4 and mitochondrial gene expression in skeletal muscle, both in culture and in vivo. Second, AMPK binds to and activates PGC-1α in muscle by direct phosphorylation on two critical residues, threonine-177 and serine ...