Defects in synaptic transmission at the neuromuscular junction precede motor deficits in a TDP‐43 Q331K transgenic mouse model of amyotrophic lateral sclerosis-Reference-Cited by-同舟云学术

Defects in synaptic transmission at the neuromuscular junction precede motor deficits in a TDP‐43 Q331K transgenic mouse model of amyotrophic lateral sclerosis

Published:2018-01-02 Issue:5 Volume:32 Page:2676-2689
ISSN:0892-6638
Container-title:The FASEB Journal
language:en
Short-container-title:FASEB j.

Author:

Chand Kirat K.¹,Lee Kah Meng¹,Lee John D.¹,Qiu Hao¹,Willis Emily F.¹,Lavidis Nickolas A.¹,Hilliard Massimo A.¹,Noakes Peter G.¹

Affiliation:

1. School of Biomedical Sciences Brisbane Queensland Australia

Publisher

Wiley

Subject

Genetics,Molecular Biology,Biochemistry,Biotechnology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1096/fj.201700835R

Reference74 articles.

1. Amyotrophic Lateral Sclerosis: From Current Developments in the Laboratory to Clinical Implications

2. Expanded GGGGCC Hexanucleotide Repeat in Noncoding Region of C9ORF72 Causes Chromosome 9p-Linked FTD and ALS

3. Mutations in the FUS/TLS Gene on Chromosome 16 Cause Familial Amyotrophic Lateral Sclerosis

4. Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis

5. TDP-43 Mutations in Familial and Sporadic Amyotrophic Lateral Sclerosis

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