Normal hypertrophy accompanied by phosphoryation and activation of AMP-activated protein kinase alpha1 following overload in LKB1 knockout mice. - Wikidata - awgldk - TriplyDB

Normal hypertrophy accompanied by phosphoryation and activation of AMP-activated protein kinase alpha1 following overload in LKB1 knockout mice.

Normal hypertrophy accompanied by phosphoryation and activation of AMP-activated protein kinase alpha1 following overload in LKB1 knockout mice.

http://www.wikidata.org/entity/Q46803372

about

Inhibitory effect of ethanol on AMPK phosphorylation is mediated in part through elevated ceramide levels Skeletal muscle dysfunction in muscle-specific LKB1 knockout mice.How to explain exercise-induced phenotype from molecular data: rethink and reconstruction based on AMPK and mTOR signaling.A limited role for PI(3,4,5)P3 regulation in controlling skeletal muscle mass in response to resistance exercise.CaMKII regulates contraction- but not insulin-induced glucose uptake in mouse skeletal muscle.Molecular brakes regulating mTORC1 activation in skeletal muscle following synergist ablation.Impaired adaptive response to mechanical overloading in dystrophic skeletal muscle Muscle fiber type-dependent differences in the regulation of protein synthesis.Constitutive activation of CaMKKα signaling is sufficient but not necessary for mTORC1 activation and growth in mouse skeletal muscle.Using molecular biology to maximize concurrent training.Glycogen content regulates peroxisome proliferator activated receptor-∂ (PPAR-∂) activity in rat skeletal muscle Moderate alcohol consumption does not impair overload-induced muscle hypertrophy and protein synthesis.Role of exercise therapy in prevention of decline in aging muscle function: glucocorticoid myopathy and unloading.Bone and skeletal muscle: Key players in mechanotransduction and potential overlapping mechanisms.Iron deficiency causes a shift in AMP-activated protein kinase (AMPK) subunit composition in rat skeletal muscle.AMP-activated protein kinase and its downstream transcriptional pathways Reduced AMPK-ACC and mTOR signaling in muscle from older men, and effect of resistance exercise.Skeletal muscle-specific overexpression of SIRT1 does not enhance whole-body energy expenditure or insulin sensitivity in young mice.Cellular mechanisms regulating protein synthesis and skeletal muscle hypertrophy in animals.Mitochondrial and performance adaptations to exercise training in mice lacking skeletal muscle LKB1 Adiponectin activates AMP-activated protein kinase in muscle cells via APPL1/LKB1-dependent and phospholipase C/Ca2+/Ca2+/calmodulin-dependent protein kinase kinase-dependent pathways.LKB1 and AMP-activated protein kinase control of mTOR signalling and growth.The transcriptional coactivator PGC-1α is dispensable for chronic overload-induced skeletal muscle hypertrophy and metabolic remodeling.AMP-activated protein kinase control of fat metabolism in skeletal muscle.Constitutively active CaMKKα stimulates skeletal muscle glucose uptake in insulin-resistant mice in vivo.Changes in muscle mass with mechanical load: possible cellular mechanisms.The signaling underlying FITness.Adenosine Monophosphate-Activated Protein Kinase (AMPK) as a New Target for Antidiabetic Drugs: A Review on Metabolic, Pharmacological and Chemical Considerations.LKB1 and AMPK family signaling: the intimate link between cell polarity and energy metabolism.Lipogenic regulators are elevated with age and chronic overload in rat skeletal muscle.Recent progress toward understanding the molecular mechanisms that regulate skeletal muscle mass.Overload-mediated skeletal muscle hypertrophy is not impaired by loss of myofiber STAT3.The influence of iron deficiency on the functioning of skeletal muscles: experimental evidence and clinical implications.Kv1.3 inhibitors have differential effects on glucose uptake and AMPK activity in skeletal muscle cell lines and mouse ex vivo skeletal muscle.AMPKγ3 is dispensable for skeletal muscle hypertrophy induced by functional overload.The unfolded protein response is activated in skeletal muscle by high-fat feeding: potential role in the downregulation of protein synthesis.LKB1 is required for hepatic bile acid transport and canalicular membrane integrity in mice.Acute doxorubicin cardiotoxicity is associated with p53-induced inhibition of the mammalian target of rapamycin pathway.CaMKK is an upstream signal of AMP-activated protein kinase in regulation of substrate metabolism in contracting skeletal muscle.AMPKα2 deficiency uncovers time dependency in the regulation of contraction-induced palmitate and glucose uptake in mouse muscle.

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P2860

Normal hypertrophy accompanied by phosphoryation and activation of AMP-activated protein kinase alpha1 following overload in LKB1 knockout mice.

http://www.wikidata.org/entity/Q46803372

description

2008 nî lūn-bûn

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2008年の論文

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年学术文章

@zh-sg

2008年學術文章

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2008年學術文章

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2008年學術文章

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name

Normal hypertrophy accompanied ...... verload in LKB1 knockout mice.

@en

Normal hypertrophy accompanied ...... verload in LKB1 knockout mice.

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type

label

Normal hypertrophy accompanied ...... verload in LKB1 knockout mice.

@en

Normal hypertrophy accompanied ...... verload in LKB1 knockout mice.

@nl

prefLabel

Normal hypertrophy accompanied ...... verload in LKB1 knockout mice.

@en

Normal hypertrophy accompanied ...... verload in LKB1 knockout mice.

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JPHYSIOL.2007.143685

P1433

The Journal of Physiology

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Normal hypertrophy accompanied ...... overload in LKB1 knockout mice

@en

P2093

Keith Baar

http://www.w3.org/2001/XMLSchema#string

Kirsty J Mustard

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P2860

Complexes between the LKB1 tumor suppressor, STRAD alpha/beta and MO25 alpha/beta are upstream kinases in the AMP-activated protein kinase cascade

AMP-Activated Protein Kinase in Metabolic Control and Insulin Signaling

Phosphorylation and regulation of Akt/PKB by the rictor-mTOR complex

AMP kinase is required for mitochondrial biogenesis in skeletal muscle in response to chronic energy deprivation.

The AMP-activated protein kinase alpha2 catalytic subunit controls whole-body insulin sensitivity

CBS domains form energy-sensing modules whose binding of adenosine ligands is disrupted by disease mutations

Rheb GTPase is a direct target of TSC2 GAP activity and regulates mTOR signaling

TSC2 is phosphorylated and inhibited by Akt and suppresses mTOR signalling

Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo

AMP-activated protein kinase suppresses protein synthesis in rat skeletal muscle through down-regulated mammalian target of rapamycin (mTOR) signaling

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1731-1741

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10.1113/JPHYSIOL.2007.143685

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6

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586

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David Grahame Hardie

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2008-01-17T00:00:00Z

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