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A disease of actin transport?
Author(s) -
William A. Wells
Publication year - 2003
Publication title -
the journal of cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.414
H-Index - 380
eISSN - 1540-8140
pISSN - 0021-9525
DOI - 10.1083/jcb1634iti3
Subject(s) - smn1 , spinal muscular atrophy , biology , sma* , actin , microbiology and biotechnology , paralysis , disease , loss function , rna splicing , motor neuron , neuromuscular disease , neuroscience , spinal cord , gene , genetics , pathology , phenotype , rna , medicine , mathematics , surgery , combinatorics
![Graphic][1] SMA neurons (right) have less actin.Spinal muscular atrophy (SMA), a motoneuron disease that results in paralysis and death usually before age 3, is caused by loss of the SMN1 gene. But what does the established splicing function of SMN1 have to do with motoneurons?

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