Increased IGF-1 in muscle modulates the phenotype of severe SMA mice - Wikidata - thesis-toulmin - TriplyDB

Increased IGF-1 in muscle modulates the phenotype of severe SMA mice

Increased IGF-1 in muscle modulates the phenotype of severe SMA mice

http://www.wikidata.org/entity/Q34767012

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Spinal muscular atrophy: from gene discovery to clinical trials Pathological impact of SMN2 mis-splicing in adult SMA mice Muscle expression of mutant androgen receptor accounts for systemic and motor neuron disease phenotypes in spinal and bulbar muscular atrophy Assays for the identification and prioritization of drug candidates for spinal muscular atrophy ROCK inhibition as a therapy for spinal muscular atrophy: understanding the repercussions on multiple cellular targets Analysis of the fibroblast growth factor system reveals alterations in a mouse model of spinal muscular atrophy SMN-inducing compounds for the treatment of spinal muscular atrophy.Limited phenotypic effects of selectively augmenting the SMN protein in the neurons of a mouse model of severe spinal muscular atrophy.SMA-MAP: a plasma protein panel for spinal muscular atrophy SMN regulates axonal local translation via miR-183/mTOR pathway Spinal muscular atrophy: from tissue specificity to therapeutic strategies Glucose metabolism and pancreatic defects in spinal muscular atrophy Peripheral SMN restoration is essential for long-term rescue of a severe spinal muscular atrophy mouse model.Systemic administration of a recombinant AAV1 vector encoding IGF-1 improves disease manifestations in SMA mice Antisense oligonucleotides shed new light on the pathogenesis and treatment of spinal muscular atrophy.Plastin 3 Expression Does Not Modify Spinal Muscular Atrophy Severity in the ∆7 SMA Mouse Neurogenic and myogenic contributions to hereditary motor neuron disease.Therapy development for spinal muscular atrophy in SMN independent targets.Transcriptional profiling of differentially vulnerable motor neurons at pre-symptomatic stage in the Smn (2b/-) mouse model of spinal muscular atrophy.Human axonal survival of motor neuron (a-SMN) protein stimulates axon growth, cell motility, C-C motif ligand 2 (CCL2), and insulin-like growth factor-1 (IGF1) production.Survival motor neuron protein in motor neurons determines synaptic integrity in spinal muscular atrophy IPLEX administration improves motor neuron survival and ameliorates motor functions in a severe mouse model of spinal muscular atrophy.Differential neuronal vulnerability identifies IGF-2 as a protective factor in ALS.The therapeutic potential of IGF-I in skeletal muscle repair.Spinal muscular atrophy: an update on therapeutic progress More than a bystander: the contributions of intrinsic skeletal muscle defects in motor neuron diseases.Spinal muscular atrophy and the antiapoptotic role of survival of motor neuron (SMN) protein.Spinal muscular atrophy: a motor neuron disorder or a multi-organ disease?Motor neuron degeneration in spinal and Bulbar Muscular Atrophy is a skeletal muscle-driven process: Relevance to therapy development and implications for related motor neuron diseases.Developing therapies for spinal muscular atrophy.Differential roles of α-, β-, and γ-actin in axon growth and collateral branch formation in motoneurons.Diverse role of survival motor neuron protein.Polyethylene glycol-coupled IGF1 delays motor function defects in a mouse model of spinal muscular atrophy with respiratory distress type 1.Severe SMA mice show organ impairment that cannot be rescued by therapy with the HDACi JNJ-26481585.Stem Cells and Tissue Niche: Two Faces of the Same Coin of Muscle Regeneration.Pharmacologically induced mouse model of adult spinal muscular atrophy to evaluate effectiveness of therapeutics after disease onset.SMA-causing missense mutations in survival motor neuron (Smn) display a wide range of phenotypes when modeled in Drosophila.Differential induction of muscle atrophy pathways in two mouse models of spinal muscular atrophy.Spinal muscular atrophy: antisense oligonucleotide therapy opens the door to an integrated therapeutic landscape.Bisphenol A Represses Dopaminergic Neuron Differentiation from Human Embryonic Stem Cells through Downregulating the Expression of Insulin-like Growth Factor 1.

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Increased IGF-1 in muscle modulates the phenotype of severe SMA mice

http://www.wikidata.org/entity/Q34767012

description

2011 nî lūn-bûn

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2011 թուականի Փետրուարին հրատարակուած գիտական յօդուած

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2011 թվականի փետրվարին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

Increased IGF-1 in muscle modulates the phenotype of severe SMA mice

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Increased IGF-1 in muscle modulates the phenotype of severe SMA mice

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Increased IGF-1 in muscle modulates the phenotype of severe SMA mice

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type

label

Increased IGF-1 in muscle modulates the phenotype of severe SMA mice

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Increased IGF-1 in muscle modulates the phenotype of severe SMA mice

@en

Increased IGF-1 in muscle modulates the phenotype of severe SMA mice

@nl

prefLabel

Increased IGF-1 in muscle modulates the phenotype of severe SMA mice

@ast

Increased IGF-1 in muscle modulates the phenotype of severe SMA mice

@en

Increased IGF-1 in muscle modulates the phenotype of severe SMA mice

@nl

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Human Molecular Genetics

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Increased IGF-1 in muscle modulates the phenotype of severe SMA mice

@en

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Celeste E Lipkes

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

Charlotte J Sumner

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

Claribel D Wee

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

Dong W Choe

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James P Van Meerbeke

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Lingling Kong

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Marta Bosch-Marcé

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Tara L Martinez

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P2860

Alternative splicing events are a late feature of pathology in a mouse model of spinal muscular atrophy

Modeling spinal muscular atrophy in Drosophila

Synaptic defects in the spinal and neuromuscular circuitry in a mouse model of spinal muscular atrophy

The changing natural history of spinal muscular atrophy type 1

Early heart failure in the SMNDelta7 model of spinal muscular atrophy and correction by postnatal scAAV9-SMN delivery

Sustained improvement of spinal muscular atrophy mice treated with trichostatin A plus nutrition

Congenital heart disease is a feature of severe infantile spinal muscular atrophy

Trichostatin A increases SMN expression and survival in a mouse model of spinal muscular atrophy.

Arrhythmia and cardiac defects are a feature of spinal muscular atrophy model mice.

Cardiac defects contribute to the pathology of spinal muscular atrophy models

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1844-1853

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scholarly article

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10.1093/HMG/DDR067

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9

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20

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2011-02-16T00:00:00Z

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49840016

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21325354

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3071675

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