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    Amyotrophic lateral sclerosis (ALS) is characterized by the degeneration of motor neurons, leading to progressive muscle atrophy and fatal paralysis. Mutations in more than 20 genes, including full-length EphA4 (EphA4-FL), have been implicated in this pathogenesis. The present study aimed to identify novel isoforms of EphA4-FL and to investigate the expression of EphA4-FL and its isoforms in the superoxide dismutase 1 (SOD1) mutant mouse model of ALS. Two novel transcripts were verified in mouse and humans. In transfected cells, both transcripts could be translated into proteins, which respectively contained the N- and C-termini of EphA4-FL, referred as EphA4-N and EphA4-C. EphA4-N, which was expressed on the surface of transfected cells, was shown to act as a dominant negative receptor by significantly suppressing the activation of EphA4-FL in vitro. The expression of both EphA4-FL and EphA4-N was significantly higher in the nervous tissue of SOD1G93A compared to wild-type mice suggesting that both forms are modulated during the disease process. Copyright © 2017 IBRO. Published by Elsevier Ltd. All rights reserved.


    Jing Zhao, Andrew W Boyd, Perry F Bartlett. The identification of a novel isoform of EphA4 and ITS expression in SOD1G93A mice. Neuroscience. 2017 Apr 07;347:11-21

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    PMID: 28153688

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