The DAXX tax: C9orf72 DNA repeat expansions drive gain- and loss-of-function pathology in c9FTD/ALS

Feilin Liu; Wilfried Rossoll

doi:10.1016/j.neuron.2023.03.028

The DAXX tax: C9orf72 DNA repeat expansions drive gain- and loss-of-function pathology in c9FTD/ALS

Feilin Liu, Wilfried Rossoll

Neuroscience

Research output: Contribution to journal › Comment/debate › peer-review

Abstract

In this issue of Neuron, Liu et al.¹ identify DAXX as a C9orf72 hexanucleotide repeat expansion DNA-binding protein that initiates epigenetic modifications and chromatin remodeling, contributing to C9orf72 haploinsufficiency by inhibiting its stress-inducible expression and mediating both loss- and toxic gain-of-function pathology.

Original language	English (US)
Pages (from-to)	1165-1167
Number of pages	3
Journal	Neuron
Volume	111
Issue number	8
DOIs	https://doi.org/10.1016/j.neuron.2023.03.028
State	Published - Apr 19 2023

ASJC Scopus subject areas

General Neuroscience

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10.1016/j.neuron.2023.03.028

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title = "The DAXX tax: C9orf72 DNA repeat expansions drive gain- and loss-of-function pathology in c9FTD/ALS",

abstract = "In this issue of Neuron, Liu et al.1 identify DAXX as a C9orf72 hexanucleotide repeat expansion DNA-binding protein that initiates epigenetic modifications and chromatin remodeling, contributing to C9orf72 haploinsufficiency by inhibiting its stress-inducible expression and mediating both loss- and toxic gain-of-function pathology.",

author = "Feilin Liu and Wilfried Rossoll",

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AU - Rossoll, Wilfried

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AB - In this issue of Neuron, Liu et al.1 identify DAXX as a C9orf72 hexanucleotide repeat expansion DNA-binding protein that initiates epigenetic modifications and chromatin remodeling, contributing to C9orf72 haploinsufficiency by inhibiting its stress-inducible expression and mediating both loss- and toxic gain-of-function pathology.

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The DAXX tax: C9orf72 DNA repeat expansions drive gain- and loss-of-function pathology in c9FTD/ALS

Abstract

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