Restoring calcium homeostasis in Purkinje cells arrests neurodegeneration and neuroinflammation in the ARSACS mouse model-Reference-Cited by-同舟云学术

Restoring calcium homeostasis in Purkinje cells arrests neurodegeneration and neuroinflammation in the ARSACS mouse model

Published:2023-06-22 Issue:12 Volume:8 Page:
ISSN:2379-3708
Container-title:JCI Insight
language:en
Short-container-title:

Author:

Del Bondio Andrea,Longo Fabiana^ORCID,De Ritis Daniele,Spirito Erica,Podini Paola,Brais Bernard,Bachi Angela^ORCID,Quattrini Angelo,Maltecca Francesca

Funder

Ministero della Salute

Ataxia Charlevoix-Saguenay Foundation

Publisher

American Society for Clinical Investigation

Subject

General Medicine

Link

https://insight.jci.org/articles/view/163576/files/pdf

Reference55 articles.

1. Recessive ataxias

2. A novel homozygous SACS mutation identified by whole exome sequencing-genotype phenotype correlations of all published cases

3. ARSACS, a spastic ataxia common in northeastern Québec, is caused by mutations in a new gene encoding an 11.5-kb ORF

4. The ataxia protein sacsin is a functional co-chaperone that protects against polyglutamine-expanded ataxin-1

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1. A human microglial cell model of autosomal recessive spastic ataxia of Charlevoix-Saguenay;Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease;2024-12

2. HDAC inhibitor SAHA resolved intermediate filament bundling and defective autophagy caused by the lack of sacsin in ARSACS.;2024-08-17

3. Toll-like receptor 4 deficiency in Purkinje neurons drives cerebellar ataxia by impairing the BK channel-mediated after-hyperpolarization and cytosolic calcium homeostasis;Cell Death & Disease;2024-08-15

4. Proteomics and lipidomic analysis reveal dysregulated pathways associated with loss of sacsin;Frontiers in Neuroscience;2024-06-07

5. Subcellular, biochemical and biophysical alterations in two glial cell models of ARSACS;2024-04-15