William O. Kline

skeletal muscle by chronic electrical stimulation in vivo Induction of neuronal type nitric oxide synthase in

William O. Kline, Pál L. Vághy, T. Vassilakopoulos, G. Deckman et autres

Metabolomic profiling reveals severe skeletal muscle group-specific perturbations of metabolism in aged FBN rats

Sean M. Garvey, Janis E. Dugle, Adam D. Kennedy, Jonathan E. McDunn et autres

Mammalian skeletal muscles exhibit age-related adaptive and pathological remodeling. Several muscles in particular undergo progressive atrophy and degeneration beyond median lifespan. To better understand myocellular responses to aging, we used semi-quantitative global metabolomic profiling to characterize trends in metabolic changes between 15-month-old …

gb, us (code pays fourni par la source)

NBD delivery improves the disease phenotype of the golden retriever model of Duchenne muscular dystrophy

Joe N. Kornegay, Jennifer M. Peterson, Daniel J. Bogan, William O. Kline et autres

BACKGROUND: Duchenne muscular dystrophy (DMD) is caused by mutations in the dystrophin gene and afflicts skeletal and cardiac muscles. Previous studies showed that DMD is associated with constitutive activation of NF-κB, and in dystrophin-deficient mdx and utrophin/dystrophin (utrn (-/-) ;mdx) double knock …

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Peptide-Based Inhibition of NF-κB Rescues Diaphragm Muscle Contractile Dysfunction in a Murine Model of Duchenne Muscular Dystrophy

Jennifer M. Peterson, William O. Kline, Benjamin D. Canan, Daniel J. Ricca et autres

Deterioration of diaphragm function is one of the prominent factors that contributes to the susceptibility of serious respiratory infections and development of respiratory failure in patients with Duchenne Muscular Dystrophy (DMD). The NF-κB signaling pathway has been implicated as a contributing factor …

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TNF Inhibits Notch-1 in Skeletal Muscle Cells by Ezh2 and DNA Methylation Mediated Repression: Implications in Duchenne Muscular Dystrophy

Swarnali Acharyya, Sudarshana M. Sharma, Alfred S.L. Cheng, Katherine J. Ladner et autres

BACKGROUND: Classical NF-kappaB signaling functions as a negative regulator of skeletal myogenesis through potentially multiple mechanisms. The inhibitory actions of TNFalpha on skeletal muscle differentiation are mediated in part through sustained NF-kappaB activity. In dystrophic muscles, NF-kappaB activity is compartmentalized to myofibers …

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Rapamycin inhibits the growth and muscle-sparing effects of clenbuterol

William O. Kline, Frank J. Panaro, Hayung Yang, Sue C. Bodine

Clenbuterol and other beta2-adrenergic agonists are effective at inducing muscle growth and attenuating muscle atrophy through unknown mechanisms. This study tested the hypothesis that clenbuterol-induced growth and muscle sparing is mediated through the activation of Akt and mammalian target of rapamycin (mTOR) …

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Erratum: Absence of the lipid phosphatase SHIP2 confers resistance to dietary obesity

Mark W. Sleeman, Katherine E. Wortley, K-M V Lai, Lori C. Gowen et autres

Absence of the lipid phosphatase SHIP2 confers resistance to dietary obesity

Mark W. Sleeman, Katherine E. Wortley, Ka‐Man Venus Lai, Lori C. Gowen et autres

us (code pays fourni par la source)

Conditional Activation of Akt in Adult Skeletal Muscle Induces Rapid Hypertrophy

Ka‐Man Venus Lai, Michael Gonzalez, William T. Poueymirou, William O. Kline et autres

Skeletal muscle atrophy is a severe morbidity caused by a variety of conditions, including cachexia, cancer, AIDS, prolonged bedrest, and diabetes. One strategy in the treatment of atrophy is to induce the pathways normally leading to skeletal muscle hypertrophy. The pathways that …

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The IGF-1/PI3K/Akt Pathway Prevents Expression of Muscle Atrophy-Induced Ubiquitin Ligases by Inhibiting FOXO Transcription Factors

Trevor N. Stitt, Doreen Drujan, Brian A. Clarke, Frank J. Panaro et autres

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Short Article The IGF-1/PI3K/Akt Pathway Prevents Expression of Muscle Atrophy-Induced Ubiquitin Ligases by Inhibiting FOXO Transcription Factors

Trevor N. Stitt, Doreen Drujan, Brian A. Clarke, Frank J. Panaro et autres

Summary membrane phospholipid phosphatidylinositol-4,5-bis- phosphate to phosphatidylinositol-3,4,5-trisphosphate, Skeletalmusclesizedependsuponadynamicbalance creating a lipid binding site on the cell membrane forbetween anabolic (or hypertrophic) and catabolic (or a serine/threonine kinase called Akt (or PKB—protein atrophic) processes. Previously, no link between the kinase B). The subsequent …

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

Sue C. Bodine, Trevor N. Stitt, Michael Gonzalez, William O. Kline et autres

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