DDX3X overexpression decreases dipeptide repeat proteins in a mouse model of C9ORF72-ALS/FTD-Reference-Cited by-同舟云学术

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DDX3X overexpression decreases dipeptide repeat proteins in a mouse model of C9ORF72-ALS/FTD

Published:2024-06 Issue: Volume:376 Page:114768
ISSN:0014-4886
Container-title:Experimental Neurology
language:en
Short-container-title:Experimental Neurology

Author:

Fu Xiujuan,Zhang Zhe,Hayes Lindsey R.,Wright Noelle,Asbury Julie,Li Shelley,Ye Yingzhi,Sun Shuying

Funder

National Institutes of Health

ALS Association

Muscular Dystrophy Association

University of Maryland

Publisher

Elsevier BV

Reference41 articles.

1. p62 positive, TDP-43 negative, neuronal cytoplasmic and intranuclear inclusions in the cerebellum and hippocampus define the pathology of C9orf72-linked FTLD and MND/ALS;Al-Sarraj;Acta Neuropathol.,2011

2. Unconventional translation of C9ORF72 GGGGCC expansion generates insoluble polypeptides specific to c9FTD/ALS;Ash;Neuron,2013

3. C9orf72-mediated ALS and FTD: multiple pathways to disease;Balendra;Nat. Rev. Neurol.,2018

4. CRISPR-Cas9 screens identify the RNA helicase DDX3X as a repressor of C9ORF72 (GGGGCC)n repeat-associated non-AUG translation;Cheng;Neuron,2019

5. CRISPR-Cas9 screens identify the RNA helicase DDX3X as a repressor of C9ORF72 (GGGGCC)n repeat-associated non-AUG translation;Cheng;Neuron,2019

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