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PPARGC1A — SIRT1

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: PPARGC1A → SIRT1 (increases, SIRT1 Activity, PPARGC1A Activity) Rodgers et al., Nature 2005*
  Evidence: We find that once SIRT1 is induced, it interacts with and deacetylates PGC-1alpha at specific lysine residues in an NAD(+)-dependent manner. SIRT1 induces gluconeogenic genes and hepatic glucose output through PGC-1alpha, but does not regulate the effects of PGC-1alpha on mitochondrial genes.
• NCI Pathway Database Signaling events mediated by HDAC Class III: SIRT1/PGC1A complex (SIRT1-PPARGC1A) → SIRT1 (SIRT1) (modification, collaborate) Rodgers et al., Nature 2005*
  Evidence: physical interaction, other species
• NCI Pathway Database Signaling events mediated by HDAC Class III: SIRT1/PGC1A complex (SIRT1-PPARGC1A) → PGC1A (PPARGC1A) (modification, collaborate) Rodgers et al., Nature 2005*
  Evidence: physical interaction, other species
• NCI Pathway Database Signaling events mediated by HDAC Class III: SIRT1 (SIRT1) → PGC1A (PPARGC1A) (modification, collaborate) Rodgers et al., Nature 2005*
  Evidence: physical interaction, other species
• WikiPathways Energy Metabolism: SIRT1 → PPARGC1A (activation)
• WikiPathways SREBF and miR33 in cholesterol and lipid homeostasis: SIRT1 → PPARGC1A (activation)

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: PPARGC1A — SIRT1 (colocalization, imaging technique) Amat et al., J Biol Chem 2009*
• IRef Hprd Interaction: Complex of HNF4A-HNF4A-SIRT1-PPARGC1A-SIRT1-PPARGC1A-HNF4A-SIRT1-PPARGC1A (in vivo) Rodgers et al., Nature 2005*
• IRef Hprd Interaction: SIRT1 — PPARGC1A (in vitro) Rodgers et al., Nature 2005*
• IRef Hprd Interaction: SIRT1 — PPARGC1A (in vivo) Rodgers et al., Nature 2005*
• STRING interaction: SIRT1 — PPARGC1A (interaction, mapped from intact)
• STRING interaction: SIRT1 — PPARGC1A (interaction, mapped from intact)
• STRING interaction: PPARGC1A — SIRT1 (interaction, mapped from grid bind dip)
• STRING interaction: PPARGC1A — SIRT1 (interaction, mapped from grid bind dip)

Text-mined interactions from Literome

Rodgers et al., Nature 2005 : SIRT1 induces gluconeogenic genes and hepatic glucose output through PGC-1alpha , but does not regulate the effects of PGC-1alpha on mitochondrial genes
Purushotham et al., Cell Metab 2009 (Fatty Liver...) : SIRT1 interacts with PPARalpha and is required to activate PPARalpha coactivator PGC-1alpha
Amat et al., J Biol Chem 2009 : Conversely, SIRT1 activation or overexpression in differentiated C2C12 myotubes increased PGC-1alpha mRNA expression ... Conversely, SIRT1 activation or overexpression in differentiated C2C12 myotubes increased PGC-1alpha mRNA expression ... In the presence of MyoD, SIRT1 promoted a positive autoregulatory PGC-1alpha expression loop, such that overexpression of PGC-1alpha increased PGC-1alpha promoter activity in the presence of co-expressed MyoD and SIRT1 ... Collectively, these data indicate that SIRT1 controls PGC-1alpha gene expression in skeletal muscle and that MyoD is a key mediator of this action ... The involvement of MyoD in SIRT1 dependent PGC-1alpha expression may help to explain the ability of SIRT1 to drive muscle-specific gene expression and metabolism
Zhu et al., Neuropharmacology 2010 (Brain Edema...) : Icariin protects against brain injury by enhancing SIRT1 dependent PGC-1alpha expression in experimental stroke
Goh et al., Curr Diabetes Rev 2010 (Diabetes Mellitus, Type 2...) : At the molecular forefront, energy sensing signaling pathways in T2DM, such as PGC1alpha, AMPK, O-GlcNAc and most recently SIRT1 have been shown to play key roles in oxidative stress, mitochondrial dysfunction, inflammation and glucolipotoxicity, which are the hallmarks of insulin resistance and T2DM, Furthermore, SIRT1 , PGC1alpha and O-GlcNAc also regulate gene expression and may play a role in the epigenetic machinery, thus providing an explanation to how metabolism switches to either a ` thrift ' or ` spend ' mode depending on food availability ... At the molecular forefront, energy sensing signaling pathways in T2DM, such as PGC1alpha, AMPK, O-GlcNAc and most recently SIRT1 have been shown to play key roles in oxidative stress, mitochondrial dysfunction, inflammation and glucolipotoxicity, which are the hallmarks of insulin resistance and T2DM, Furthermore, SIRT1 , PGC1alpha and O-GlcNAc also regulate gene expression and may play a role in the epigenetic machinery, thus providing an explanation to how metabolism switches to either a ` thrift ' or ` spend ' mode depending on food availability