Energy dysfunction in Huntington's disease: insights from PGC-1α, AMPK, and CKB. - Wikidata - wikimedia - TriplyDB

Energy dysfunction in Huntington's disease: insights from PGC-1α, AMPK, and CKB.

Energy dysfunction in Huntington's disease: insights from PGC-1α, AMPK, and CKB.

http://www.wikidata.org/entity/Q38013005

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T1ρ imaging in premanifest Huntington disease reveals changes associated with disease progression.High Protein Diet and Huntington's Disease AMPK-mediated regulation of neuronal metabolism and function in brain diseases.The AMPK enzyme-complex: from the regulation of cellular energy homeostasis to a possible new molecular target in the management of chronic inflammatory disorders.Aberrant activation of AMP-activated protein kinase contributes to the abnormal distribution of HuR in amyotrophic lateral sclerosis.Activation of AMP-activated protein kinase α1 mediates mislocalization of TDP-43 in amyotrophic lateral sclerosis.Localized changes to glycogen synthase kinase-3 and collapsin response mediator protein-2 in the Huntington's disease affected brain.Energy Homeostasis and Abnormal RNA Metabolism in Amyotrophic Lateral Sclerosis Somatic expression of unc-54 and vha-6 mRNAs declines but not pan-neuronal rgef-1 and unc-119 expression in aging Caenorhabditis elegans Towards an Understanding of Energy Impairment in Huntington's Disease Brain.Proteostasis in Huntington's disease: disease mechanisms and therapeutic opportunities.

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Energy dysfunction in Huntington's disease: insights from PGC-1α, AMPK, and CKB.

http://www.wikidata.org/entity/Q38013005

description

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Energy dysfunction in Huntington's disease: insights from PGC-1α, AMPK, and CKB.

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Energy dysfunction in Huntington's disease: insights from PGC-1α, AMPK, and CKB.

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Energy dysfunction in Huntington's disease: insights from PGC-1α, AMPK, and CKB.

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Cellular and Molecular Life Sciences

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Energy dysfunction in Huntington's disease: insights from PGC-1α, AMPK, and CKB.

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Tz-Chuen Ju

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Yow-Sien Lin

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P2860

Early alterations of brain cellular energy homeostasis in Huntington disease models

Intracellular compartmentation, structure and function of creatine kinase isoenzymes in tissues with high and fluctuating energy demands: the 'phosphocreatine circuit' for cellular energy homeostasis

X-linked creatine-transporter gene (SLC6A8) defect: a new creatine-deficiency syndrome.

Arginine:glycine amidinotransferase deficiency: the third inborn error of creatine metabolism in humans

Huntingtin and the molecular pathogenesis of Huntington's disease. Fourth in molecular medicine review series

Estrogen-related receptor alpha directs peroxisome proliferator-activated receptor alpha signaling in the transcriptional control of energy metabolism in cardiac and skeletal muscle

Peroxisome proliferator-activated receptor-gamma coactivator 1alpha (PGC-1alpha) regulates triglyceride metabolism by activation of the nuclear receptor FXR

Leptin regulates tau phosphorylation and amyloid through AMPK in neuronal cells

PGC-1alpha deficiency causes multi-system energy metabolic derangements: muscle dysfunction, abnormal weight control and hepatic steatosis

A cold-inducible coactivator of nuclear receptors linked to adaptive thermogenesis

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s00018-012-1025-2

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4107-4120

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10.1007/S00018-012-1025-2

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24

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69

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2012-05-25T00:00:00Z

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225043580

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22627493

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Huntington disease