ArticleScientific reports2018
Adult mouse eIF2Bε Arg191His astrocytes display a normal integrated stress response in vitro.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- White matter disorders at the intersection of transcription, RNA processing and translation.Nature reviews. Neurology · 2026Review
- Consensus-Based Expert Recommendations for Diagnosis and Clinical Management of Vanishing White Matter.Neurology · 2025Review
- The translational landscape of reactive astrocytes reveals the impact of eIF2B-mediated dysregulation in VWM disease.NAR molecular medicine · 2025Article
- eIF2B localization and its regulation during the integrated stress response is cell-type specific.iScience · 2024Article
- Signaling plasticity in the integrated stress response.Frontiers in cell and developmental biology · 2023Review
- Neuron-specific translational control shift ensures proteostatic resilience during ER stress.The EMBO journal · 2022Article
- Guanabenz ameliorates disease in vanishing white matter mice in contrast to sephin1.Annals of clinical and translational neurology · 2022Article
- Human iPSC-Derived Astrocytes: A Powerful Tool to Study Primary Astrocyte Dysfunction in the Pathogenesis of Rare Leukodystrophies.International journal of molecular sciences · 2021Review
- Vanishing white matter: deregulated integrated stress response as therapy target.Annals of clinical and translational neurology · 2019Article
- Modeling vanishing white matter disease with patient-derived induced pluripotent stem cells reveals astrocytic dysfunction.CNS neuroscience & therapeutics · 2019Article
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vanishing white matter (VWM) is a genetic childhood white matter disorder, characterized by chronic as well as episodic, stress provoked, neurological deterioration. Treatment is unavailable and patients often die within a few years after onset. VWM is caused by recessive mutations in the eukaryotic initiation factor 2B (eIF2B). eIF2B regulates protein synthesis rates in every cell of the body. In normal cells, various types of cellular stress inhibit eIF2B activity and induce the integrated stress response (ISR). We have developed a VWM mouse model homozygous for the pathogenic Arg191His mutation in eIF2Bε (2b5
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