ArticleInternational journal of molecular sciences2022
The J Domain of Sacsin Disrupts Intermediate Filament Assembly.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- S100B Mitigates Cytoskeletal and Mitochondrial Alterations in a Glial Cell Model of Autosomal Recessive Spastic Ataxia of Charlevoix-Saguenay.Molecular neurobiology · 2025Article
- Selection of Clinical Outcome Assessments for Trial Readiness in ARSACS - 2-year Progression and Responsiveness to Change Part 1: Disease Severity, Swallowing, Upper Limb Function, and Participation.Cerebellum (London, England) · 2025Article
- FGF-Mediated Axon Guidance: Role of Downstream Signaling Pathways in Cytoskeletal Control.Cells · 2025Review
- Single-cell RNA sequencing of the carotid artery and femoral artery of rats exposed to hindlimb unloading.Cellular and molecular life sciences : CMLS · 2025Article
- A Novel Mutation in Sacsin, p.Val1335IIe, May Cause Late-Onset Sacsinopathy Due to Haploinsufficiency.Current issues in molecular biology · 2023Article
- Neurofilaments in health and Charcot-Marie-Tooth disease.Frontiers in cell and developmental biology · 2023Review
- Genetics of Autosomal Recessive Spastic Ataxia of Charlevoix-Saguenay (ARSACS) and Role of Sacsin in Neurodegeneration.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Autosomal Recessive Spastic Ataxia of the Charlevoix Saguenay (ARSACS) is caused by mutation in the SACS gene resulting in loss of function of the protein sacsin. A key feature is the formation of abnormal bundles of neurofilaments (NF) in neurons and vimentin intermediate filaments (IF) in cultured fibroblasts, suggesting a role of sacsin in IF homeostasis. Sacsin contains a J domain (SacsJ) homologous to Hsp40, that can interact with Hsp70 chaperones. The SacsJ domain resolved NF bundles in cultured
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Registered trials
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