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Cell
Article
License: Elsevier Non-Commercial
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Cell
Article . 2011
License: Elsevier Non-Commercial
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Cell
Article . 2011 . Peer-reviewed
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SnapShot: Neuromuscular Junction

Authors: Burden, Steven J.;

SnapShot: Neuromuscular Junction

Abstract

Agrin MuSK Dok-7Rapsyn AChR AChE ChAT Nav1.4Auto-antibodiesto AChRsAuto-antibodiesto MuSKHypomorphic mutations in thesegenes impair postsynaptic differentiation. The number of AChRs at synapses is reduced, which compromises the reliability of synaptic transmission and leads to muscle weakness and fatigue. Mutations in these genes impairsynaptic transmission, leading tomuscle weakness and fatigue. ChAT encodes the enzyme forsynthesizing ACh, and Nav1.4encodes a voltage-activatedsodium channel expressed inskeletal muscle. Cause accelerated degradationof AChRs and structural disorganization of the synapse,leading to Myasthenia GravisCause structural disorganizationof the synapse, leading toMyasthenia Gravis.

Related Organizations
Keywords

Biochemistry, Genetics and Molecular Biology(all), Cell Membrane, Neuromuscular Junction, Animals, Humans

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
44
Top 10%
Top 10%
Top 10%
hybrid