Severe SMA mice show organ impairment that cannot be rescued by therapy with the HDACi JNJ-26481585.
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Selective Neuromuscular Denervation in Taiwanese Severe SMA Mouse Can Be Reversed by Morpholino Antisense OligonucleotidesThe DcpS inhibitor RG3039 improves survival, function and motor unit pathologies in two SMA mouse models.Efficient SMN Rescue following Subcutaneous Tricyclo-DNA Antisense Oligonucleotide TreatmentImprovement of neuromuscular synaptic phenotypes without enhanced survival and motor function in severe spinal muscular atrophy mice selectively rescued in motor neuronsHistopathological Defects in Intestine in Severe Spinal Muscular Atrophy Mice Are Improved by Systemic Antisense Oligonucleotide Treatment.SMN expression is required in motor neurons to rescue electrophysiological deficits in the SMNΔ7 mouse model of SMA.Genetic inhibition of JNK3 ameliorates spinal muscular atrophy.Mechanistic principles of antisense targets for the treatment of spinal muscular atrophyChronic Treatment with the AMPK Agonist AICAR Prevents Skeletal Muscle Pathology but Fails to Improve Clinical Outcome in a Mouse Model of Severe Spinal Muscular Atrophy.Severe impairment of male reproductive organ development in a low SMN expressing mouse model of spinal muscular atrophyPlacental development in a mouse model of spinal muscular atrophy.Decreased function of survival motor neuron protein impairs endocytic pathways.Spinal muscular atrophy: an update on therapeutic progressSurvival Motor Neuron (SMN) protein is required for normal mouse liver development.Dysregulation of ubiquitin homeostasis and β-catenin signaling promote spinal muscular atrophy.Cardiac pathology in spinal muscular atrophy: a systematic review.Spinal muscular atrophy: a motor neuron disorder or a multi-organ disease?Diverse role of survival motor neuron protein.How the discovery of ISS-N1 led to the first medical therapy for spinal muscular atrophyRestoration of SMN in Schwann cells reverses myelination defects and improves neuromuscular function in spinal muscular atrophy.Downregulation of Survivin contributes to cell-cycle arrest during postnatal cardiac development in a severe spinal muscular atrophy mouse model.Spinal muscular atrophy: antisense oligonucleotide therapy opens the door to an integrated therapeutic landscape.Predominant expression of exon 7 skipped SMN mRNAs in lung based on analysis of transcriptome sequencing datasets.Survival of motor neurone protein is required for normal postnatal development of the spleen.AP-1 confers resistance to anti-cancer therapy by activating XIAP.Light modulation ameliorates expression of circadian genes and disease progression in spinal muscular atrophy mice
P2860
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P2860
Severe SMA mice show organ impairment that cannot be rescued by therapy with the HDACi JNJ-26481585.
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年学术文章
@wuu
2012年学术文章
@zh-cn
2012年学术文章
@zh-hans
2012年学术文章
@zh-my
2012年学术文章
@zh-sg
2012年學術文章
@yue
2012年學術文章
@zh
2012年學術文章
@zh-hant
name
Severe SMA mice show organ imp ...... y with the HDACi JNJ-26481585.
@en
type
label
Severe SMA mice show organ imp ...... y with the HDACi JNJ-26481585.
@en
prefLabel
Severe SMA mice show organ imp ...... y with the HDACi JNJ-26481585.
@en
P2093
P2860
P356
P1476
Severe SMA mice show organ imp ...... y with the HDACi JNJ-26481585.
@en
P2093
Albrecht Berkessel
Anja Sterner-Kock
Bastian Ackermann
Brunhilde Wirth
Eilidh Somers
Jan Krämer
Julia Schreml
Kristina Roßbach
Lutz Garbes
Mario Paterno
P2860
P2888
P304
P356
10.1038/EJHG.2012.222
P577
2012-10-17T00:00:00Z
P6179
1014828880