Spinal muscular atrophy astrocytes exhibit abnormal calcium regulation and reduced growth factor production - sprookjes - yvandenbroek - TriplyDB

Spinal muscular atrophy astrocytes exhibit abnormal calcium regulation and reduced growth factor production

Spinal muscular atrophy astrocytes exhibit abnormal calcium regulation and reduced growth factor production

http://www.wikidata.org/entity/Q37614887

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Human Stem Cell-Derived Astrocytes: Specification and Relevance for Neurological Disorders Is spinal muscular atrophy a disease of the motor neurons only: pathogenesis and therapeutic implications?iPSC-Based Models to Unravel Key Pathogenetic Processes Underlying Motor Neuron Disease Development A large animal model of spinal muscular atrophy and correction of phenotype.Utility of Induced Pluripotent Stem Cells for the Study and Treatment of Genetic Diseases: Focus on Childhood Neurological Disorders Established Stem Cell Model of Spinal Muscular Atrophy Is Applicable in the Evaluation of the Efficacy of Thyrotropin-Releasing Hormone Analog.Immune dysregulation may contribute to disease pathogenesis in spinal muscular atrophy mice Sensory neurons do not induce motor neuron loss in a human stem cell model of spinal muscular atrophy Defining the therapeutic window in a severe animal model of spinal 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 Therapeutic opportunities and challenges of induced pluripotent stem cells-derived motor neurons for treatment of amyotrophic lateral sclerosis and motor neuron disease.Spinal muscular atrophy: from tissue specificity to therapeutic strategies SMN deficiency disrupts gastrointestinal and enteric nervous system function in mice SMN expression is required in motor neurons to rescue electrophysiological deficits in the SMNΔ7 mouse model of SMA.CUG-BP1 regulates RyR1 ASI alternative splicing in skeletal muscle atrophy.Decay in survival motor neuron and plastin 3 levels during differentiation of iPSC-derived human motor neurons.AAV9-mediated central nervous system-targeted gene delivery via cisterna magna route in mice.Impact of a cytomegalovirus kinase inhibitor on infection and neuronal progenitor cell differentiation Calcium binding is essential for plastin 3 function in Smn-deficient motoneurons.Human stem cell models of neurodegeneration: a novel approach to study mechanisms of disease development.Human-induced pluripotent stem cells pave the road for a better understanding of motor neuron disease.Human-induced pluripotent stem cells: potential for neurodegenerative diseases.Developing therapies for spinal muscular atrophy.Establishing a reference dataset for the authentication of spinal muscular atrophy cell lines using STR profiling and digital PCR.Astrocyte-produced miR-146a as a mediator of motor neuron loss in spinal muscular atrophy.Restoration of SMN in Schwann cells reverses myelination defects and improves neuromuscular function in spinal muscular atrophy.New insights into SMA pathogenesis: immune dysfunction and neuroinflammation.SMN deficiency does not induce oxidative stress in SMA iPSC-derived astrocytes or motor neurons.Astrocytes influence the severity of spinal muscular atrophy.An Efficient Platform for Astrocyte Differentiation from Human Induced Pluripotent Stem Cells Differentiation defects in primary motoneurons from a SMARD1 mouse model that are insensitive to treatment with low dose PEGylated IGF1 SMN-dependent intrinsic defects in Schwann cells in mouse models of spinal muscular atrophy.Decreased Motor Neuron Support by SMA Astrocytes due to Diminished MCP1 Secretion.The Importance of Non-neuronal Cell Types in hiPSC-Based Disease Modeling and Drug Screening.Oligodendrocyte development and CNS myelination are unaffected in a mouse model of severe spinal muscular atrophy.Astrocytes in a dish: Using pluripotent stem cells to model neurodegenerative and neurodevelopmental disorders.[Neuronal cells derived from induced pluripotent stem cells to model motoneuron diseases].Plastin 3 Promotes Motor Neuron Axonal Growth and Extends Survival in a Mouse Model of Spinal Muscular Atrophy.Purinergic Receptors in Neurological Diseases With Motor Symptoms: Targets for Therapy.

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Spinal muscular atrophy astrocytes exhibit abnormal calcium regulation and reduced growth factor production

http://www.wikidata.org/entity/Q37614887

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

@pt

bilimsel makale

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scientific article published on 10 July 2013

@en

vedecký článok

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vetenskaplig artikel

@sv

videnskabelig artikel

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vědecký článek

@cs

name

Spinal muscular atrophy astroc ...... duced growth factor production

@en

Spinal muscular atrophy astroc ...... uced growth factor production.

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type

label

Spinal muscular atrophy astroc ...... duced growth factor production

@en

Spinal muscular atrophy astroc ...... uced growth factor production.

@nl

prefLabel

Spinal muscular atrophy astroc ...... duced growth factor production

@en

Spinal muscular atrophy astroc ...... uced growth factor production.

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Spinal muscular atrophy astroc ...... duced growth factor production

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Allison D Ebert

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Cheryl L Stucky

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Jered V McGivern

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Joshua A Nord

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Marie-Elizabeth A Barabas

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Teresa N Patitucci

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P2860

Developing motor neurons rescued from programmed and axotomy-induced cell death by GDNF

The contribution of mouse models to understanding the pathogenesis of spinal muscular atrophy

Non-cell autonomous effect of glia on motor neurons in an embryonic stem cell-based ALS model

The astrocyte odyssey

Purinergic signalling in neuron-glia interactions

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

GDNF: a potent survival factor for motoneurons present in peripheral nerve and muscle

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

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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1418-1428

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scholarly article

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10.1002/GLIA.22522

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9

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61

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2013-07-10T00:00:00Z

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23839956

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spinal muscular atrophy

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3941074

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