Rapamycin nanoparticles target defective autophagy in muscular dystrophy to enhance both strength and cardiac function - Wikidata - awgldk - TriplyDB

Rapamycin nanoparticles target defective autophagy in muscular dystrophy to enhance both strength and cardiac function

Rapamycin nanoparticles target defective autophagy in muscular dystrophy to enhance both strength and cardiac function

http://www.wikidata.org/entity/Q30576097

about

SIRT1: A Novel Target for the Treatment of Muscular Dystrophies Oxidative Stress-Mediated Skeletal Muscle Degeneration: Molecules, Mechanisms, and Therapies Disrupted autophagy undermines skeletal muscle adaptation and integrity A cell-penetrating ester of the neural metabolite lanthionine ketimine stimulates autophagy through the mTORC1 pathway: Evidence for a mechanism of action with pharmacological implications for neurodegenerative pathologies Skeletal muscle homeostasis in duchenne muscular dystrophy: modulating autophagy as a promising therapeutic strategy.Internalization and fate of silica nanoparticles in C2C12 skeletal muscle cells: evidence of a beneficial effect on myoblast fusion.Rapamycin and chloroquine: the in vitro and in vivo effects of autophagy-modifying drugs show promising results in valosin containing protein multisystem proteinopathy.Nanotechnology inspired tools for mitochondrial dysfunction related diseases.Four-week rapamycin treatment improves muscular dystrophy in a fukutin-deficient mouse model of dystroglycanopathy "Get the Balance Right": Pathological Significance of Autophagy Perturbation in Neuromuscular Disorders Immune-mediated pathology in Duchenne muscular dystrophy.mTOR in health and in sickness.Nanotherapy for Duchenne muscular dystrophy.Autophagy regulates satellite cell ability to regenerate normal and dystrophic muscles.Modulation of Protein Quality Control and Proteasome to Autophagy Switch in Immortalized Myoblasts from Duchenne Muscular Dystrophy Patients.Nanomedicine approaches for sirolimus delivery: a review of pharmaceutical properties and preclinical studies.Deficit in PINK1/PARKIN-mediated mitochondrial autophagy at late stages of dystrophic cardiomyopathy.Autophagic dysfunction and autophagosome escape in the mdx mus musculus model of Duchenne muscular dystrophy.The Dystrophin Glycoprotein Complex Regulates the Epigenetic Activation of Muscle Stem Cell Commitment.

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P2860

Rapamycin nanoparticles target defective autophagy in muscular dystrophy to enhance both strength and cardiac function

http://www.wikidata.org/entity/Q30576097

description

2014 nî lūn-bûn

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2014 թուականի Փետրուարին հրատարակուած գիտական յօդուած

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2014 թվականի փետրվարին հրատարակված գիտական հոդված

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2014年の論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年论文

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name

Rapamycin nanoparticles target ...... strength and cardiac function

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Rapamycin nanoparticles target ...... strength and cardiac function

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Rapamycin nanoparticles target ...... strength and cardiac function

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Rapamycin nanoparticles target ...... strength and cardiac function

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Rapamycin nanoparticles target ...... strength and cardiac function

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Rapamycin nanoparticles target ...... strength and cardiac function

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Allison J Li

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Conrad C Weihl

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Grace Hu

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Gregory M Lanza

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Jon N Marsh

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Kristin P Bibee

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Paul T Golumbek

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P2860

Guidelines for the use and interpretation of assays for monitoring autophagy

Hypernitrosylated ryanodine receptor calcium release channels are leaky in dystrophic muscle

Exon skipping and dystrophin restoration in patients with Duchenne muscular dystrophy after systemic phosphorodiamidate morpholino oligomer treatment: an open-label, phase 2, dose-escalation study

Local restoration of dystrophin expression with the morpholino oligomer AVI-4658 in Duchenne muscular dystrophy: a single-blind, placebo-controlled, dose-escalation, proof-of-concept study

The big picture on nanomedicine: the state of investigational and approved nanomedicine products

TOR signaling in growth and metabolism

FKBP12 binding to RyR1 modulates excitation-contraction coupling in mouse skeletal myotubes

Genome remodelling in a basal-like breast cancer metastasis and xenograft

Dystrophin: the protein product of the Duchenne muscular dystrophy locus

Amelioration of Duchenne muscular dystrophy in mdx mice by elimination of matrix-associated fibrin-driven inflammation coupled to the αMβ2 leukocyte integrin receptor

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