Reversible acetylation of PGC-1: connecting energy sensors and effectors to guarantee metabolic flexibility.
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MitohormesisMitochondrial form and functionSelective ion changes during spontaneous mitochondrial transients in intact astrocytesNovel small-molecule PGC-1α transcriptional regulator with beneficial effects on diabetic db/db miceMitochondria: in sickness and in healthTranscriptional coregulators: fine-tuning metabolism.Methyl donor deficiency induces cardiomyopathy through altered methylation/acetylation of PGC-1α by PRMT1 and SIRT1.Regulation of substrate oxidation preferences in muscle by the peptide hormone adropin.A two-way street: reciprocal regulation of metabolism and signalling.Identification of the aryl hydrocarbon receptor target gene TiPARP as a mediator of suppression of hepatic gluconeogenesis by 2,3,7,8-tetrachlorodibenzo-p-dioxin and of nicotinamide as a corrective agent for this effect.Effect of caloric restriction and AMPK activation on hepatic nuclear receptor, biotransformation enzyme, and transporter expression in lean and obese mice.The effect of SIRT1 protein knock down on PGC-1α acetylation during skeletal muscle contractionThe redox basis of epigenetic modifications: from mechanisms to functional consequences.Separation of the gluconeogenic and mitochondrial functions of PGC-1{alpha} through S6 kinase.H9c2 and HL-1 cells demonstrate distinct features of energy metabolism, mitochondrial function and sensitivity to hypoxia-reoxygenation.Protective role of PGC-1α in diabetic nephropathy is associated with the inhibition of ROS through mitochondrial dynamic remodeling.Inhibition of diethylnitrosamine-initiated alcohol-promoted hepatic inflammation and precancerous lesions by flavonoid luteolin is associated with increased sirtuin 1 activity in mice.Deficiencies in acetyl-CoA carboxylase and fatty acid synthase 1 differentially affect eggshell formation and blood meal digestion in Aedes aegyptiCarbohydrate metabolism is perturbed in peroxisome-deficient hepatocytes due to mitochondrial dysfunction, AMP-activated protein kinase (AMPK) activation, and peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) suppression.The transcriptional coactivators, PGC-1α and β, cooperate to maintain cardiac mitochondrial function during the early stages of insulin resistanceLoss of AMP-activated protein kinase-α2 impairs the insulin-sensitizing effect of calorie restriction in skeletal muscle.AMP-activated protein kinase and ATP-citrate lyase are two distinct molecular targets for ETC-1002, a novel small molecule regulator of lipid and carbohydrate metabolism.Metabolic and neuropsychiatric effects of calorie restriction and sirtuinsCalorie restriction: is AMPK a key sensor and effector?Histone methyl transferases and demethylases; can they link metabolism and transcription?Obesity, cancer, and acetyl-CoA metabolism.Protective effect of qiliqiangxin capsule on energy metabolism and myocardial mitochondria in pressure overload heart failure rats.An acetylation rheostat for the control of muscle energy homeostasisThe GCN5-CITED2-PKA signalling module controls hepatic glucose metabolism through a cAMP-induced substrate switch.Pharmacological approaches to restore mitochondrial function.Repressed SIRT1/PGC-1α pathway and mitochondrial disintegration in iPSC-derived RPE disease model of age-related macular degeneration.Heterogeneity in Cancer Metabolism: New Concepts in an Old Field.Lipoic acid: energy metabolism and redox regulation of transcription and cell signalingAMP-activated protein kinase inhibits NF-κB signaling and inflammation: impact on healthspan and lifespan.Mitochondrial sirtuins in the regulation of mitochondrial activity and metabolic adaptation.Circadian rhythms in liver physiology and liver diseases.The diversity of histone versus nonhistone sirtuin substrates.Angiotensin II blockade: how its molecular targets may signal to mitochondria and slow aging. Coincidences with calorie restriction and mTOR inhibition.Peroxisome proliferator-activated receptor α (PPARα) contributes to control of melanogenesis in B16 F10 melanoma cells.Improved Mitochondrial and Methylglyoxal-Related Metabolisms Support Hyperproliferation Induced by 50 Hz Magnetic Field in Neuroblastoma Cells.
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Reversible acetylation of PGC-1: connecting energy sensors and effectors to guarantee metabolic flexibility.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on 07 June 2010
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
Reversible acetylation of PGC- ...... arantee metabolic flexibility.
@en
Reversible acetylation of PGC- ...... arantee metabolic flexibility.
@nl
type
label
Reversible acetylation of PGC- ...... arantee metabolic flexibility.
@en
Reversible acetylation of PGC- ...... arantee metabolic flexibility.
@nl
prefLabel
Reversible acetylation of PGC- ...... arantee metabolic flexibility.
@en
Reversible acetylation of PGC- ...... arantee metabolic flexibility.
@nl
P2860
P356
P1433
P1476
Reversible acetylation of PGC- ...... arantee metabolic flexibility.
@en
P2093
E H Jeninga
K Schoonjans
P2860
P2888
P304
P356
10.1038/ONC.2010.206
P407
P50
P577
2010-06-07T00:00:00Z