Loss of C9orf72 Enhances Autophagic Activity via Deregulated mTOR and TFEB Signaling-Reference-Cited by-同舟云学术

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Loss of C9orf72 Enhances Autophagic Activity via Deregulated mTOR and TFEB Signaling

Published:2016-11-22 Issue:11 Volume:12 Page:e1006443
ISSN:1553-7404
Container-title:PLOS Genetics
language:en
Short-container-title:PLoS Genet

Author:

Ugolino Janet,Ji Yon Ju,Conchina Karen,Chu Justin,Nirujogi Raja Sekhar,Pandey Akhilesh^ORCID,Brady Nathan R.,Hamacher-Brady Anne,Wang Jiou^ORCID

Funder

National Institutes of Health

The Robert Packard Center for ALS Research at Johns Hopkins

National Cancer Institute

Maryland Technology Development Corporation

U.S. Department of Defense (US)

Publisher

Public Library of Science (PLoS)

Subject

Cancer Research,Genetics(clinical),Genetics,Molecular Biology,Ecology, Evolution, Behavior and Systematics

Reference58 articles.

1. Expanded GGGGCC hexanucleotide repeat in noncoding region of C9ORF72 causes chromosome 9p-linked FTD and ALS;M DeJesus-Hernandez;Neuron,2011

2. A Hexanucleotide Repeat Expansion in C9ORF72 Is the Cause of Chromosome 9p21-Linked ALS-FTD;Alan E Renton;Neuron,2011

3. C9orf72 nucleotide repeat structures initiate molecular cascades of disease;AR Haeusler;Nature,2014

4. RNA toxicity from the ALS/FTD C9ORF72 expansion is mitigated by antisense intervention;CJ Donnelly;Neuron,2013

5. The C9orf72 repeat expansion disrupts nucleocytoplasmic transport;K Zhang;Nature,2015

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