Postnatal knockdown of dok-7 gene expression in mice causes structural defects in neuromuscular synapses and myasthenic pathology.
about
DOK7 gene therapy enhances motor activity and life span in ALS model mice.The carboxyl-terminal region of Dok-7 plays a key, but not essential, role in activation of muscle-specific receptor kinase MuSK and neuromuscular synapse formation.The beta-adrenergic agonist salbutamol modulates neuromuscular junction formation in zebrafish models of human myasthenic syndromes.
P2860
Postnatal knockdown of dok-7 gene expression in mice causes structural defects in neuromuscular synapses and myasthenic pathology.
description
2016 nî lūn-bûn
@nan
2016年の論文
@ja
2016年学术文章
@wuu
2016年学术文章
@zh-cn
2016年学术文章
@zh-hans
2016年学术文章
@zh-my
2016年学术文章
@zh-sg
2016年學術文章
@yue
2016年學術文章
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2016年學術文章
@zh-hant
name
Postnatal knockdown of dok-7 g ...... pses and myasthenic pathology.
@en
type
label
Postnatal knockdown of dok-7 g ...... pses and myasthenic pathology.
@en
prefLabel
Postnatal knockdown of dok-7 g ...... pses and myasthenic pathology.
@en
P2093
P2860
P356
P1433
P1476
Postnatal knockdown of dok-7 g ...... pses and myasthenic pathology.
@en
P2093
Sadanori Miyoshi
Takahiro Eguchi
Tohru Tezuka
Yuji Yamanashi
P2860
P304
P356
10.1111/GTC.12370
P577
2016-04-18T00:00:00Z