The identification of a novel isoform of EphA4 and ITS expression in SOD1G93A mice

Zhao, Jing, Boyd, Andrew W. and Bartlett, Perry F. (2017) The identification of a novel isoform of EphA4 and ITS expression in SOD1G93A mice. Neuroscience, 347 11-21. doi:10.1016/j.neuroscience.2017.01.038


Author Zhao, Jing
Boyd, Andrew W.
Bartlett, Perry F.
Title The identification of a novel isoform of EphA4 and ITS expression in SOD1G93A mice
Formatted title
The identification of a novel isoform of EphA4 and ITS expression in SOD1G93A mice
Journal name Neuroscience   Check publisher's open access policy
ISSN 1873-7544
0306-4522
Publication date 2017-04-07
Year available 2017
Sub-type Article (original research)
DOI 10.1016/j.neuroscience.2017.01.038
Open Access Status Not yet assessed
Volume 347
Start page 11
End page 21
Total pages 11
Place of publication Kidlington, Oxford, United Kingdom
Publisher Pergamon Press
Language eng
Subject 2800 Neuroscience
Abstract 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 SOD1 compared to wild-type mice suggesting that both forms are modulated during the disease process.
Formatted abstract
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.
Keyword Amyotrophic lateral sclerosis
EphA4 receptor
Isoforms
SOD1G93A mice
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
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