DNA damage rather than type I IFN signaling is the primary mediator of neural dysfunction in Aicardi-Goutières syndrome after RNASEH2 disruption
- PMID: 34914915
- DOI: 10.1016/j.neuron.2021.11.019
DNA damage rather than type I IFN signaling is the primary mediator of neural dysfunction in Aicardi-Goutières syndrome after RNASEH2 disruption
Abstract
Mutations in genes that function in nucleic metabolism have been shown to be linked to Aicardi-Goutières syndrome. In this issue of Neuron, Aditi et al. (2021) provide evidence that DNA damage-dependent signaling rather than type I interferon signaling underlies neurodegeneration in this class of neurodevelopmental/neuroinflammatory disease.
Copyright © 2021 Elsevier Inc. All rights reserved.
Comment on
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Genome instability independent of type I interferon signaling drives neuropathology caused by impaired ribonucleotide excision repair.Neuron. 2021 Dec 15;109(24):3962-3979.e6. doi: 10.1016/j.neuron.2021.09.040. Epub 2021 Oct 15. Neuron. 2021. PMID: 34655526 Free PMC article.
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